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fibrosis</title> <meta name="description" content="Search results for: fibrosis"> <meta name="keywords" content="fibrosis"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button class="d-block d-lg-none navbar-toggler ml-auto" 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id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="fibrosis"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 123</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: fibrosis</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">123</span> The Effect of Acute Rejection and Delayed Graft Function on Renal Transplant Fibrosis in Live Donor Renal Transplantation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Wisam%20Ismail">Wisam Ismail</a>, <a href="https://publications.waset.org/abstracts/search?q=Sarah%20Hosgood"> Sarah Hosgood</a>, <a href="https://publications.waset.org/abstracts/search?q=Michael%20Nicholson"> Michael Nicholson</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The research hypothesis is that early post-transplant allograft fibrosis will be linked to donor factors and that acute rejection and/or delayed graft function in the recipient will be independent risk factors for the development of fibrosis. This research hypothesis is to explore whether acute rejection/delay graft function has an effect on the renal transplant fibrosis within the first year post live donor kidney transplant between 1998 and 2009. Methods: The study has been designed to identify five time points of the renal transplant biopsies [0 (pre-transplant), 1 month, 3 months, 6 months and 12 months] for 300 live donor renal transplant patients over 12 years period between March 1997 – August 2009. Paraffin fixed slides were collected from Leicester General Hospital and Leicester Royal Infirmary. These were routinely sectioned at a thickness of 4 Micro millimetres for standardization. Conclusions: Fibrosis at 1 month after the transplant was found significantly associated with baseline fibrosis (p<0.001) and HTN in the transplant recipient (p<0.001). Dialysis after the transplant showed a weak association with fibrosis at 1 month (p=0.07). The negative coefficient for HTN (-0.05) suggests a reduction in fibrosis in the absence of HTN. Fibrosis at 1 month was significantly associated with fibrosis at baseline (p 0.01 and 95%CI 0.11 to 0.67). Fibrosis at 3, 6 or 12 months was not found to be associated with fibrosis at baseline (p=0.70. 0.65 and 0.50 respectively). The amount of fibrosis at 1 month is significantly associated with graft survival (p=0.01 and 95%CI 0.02 to 0.14). Rejection and severity of rejection were not found to be associated with fibrosis at 1 month. The amount of fibrosis at 1 month was significantly associated with graft survival (p=0.02) after adjusting for baseline fibrosis (p=0.01). Both baseline fibrosis and graft survival were significant predictive factors. The amount of fibrosis at 1 month was not found to be significantly associated with rejection (p=0.64) after adjusting for baseline fibrosis (p=0.01). The amount of fibrosis at 1 month was not found to be significantly associated with rejection severity (p=0.29) after adjusting for baseline fibrosis (p=0.04). Fibrosis at baseline and HTN in the recipient were found to be predictive factors of fibrosis at 1 month. (p 0.02, p <0.001 respectively). Age of the donor, their relation to the patient, the pre-op Creatinine, artery, kidney weight and warm time were not found to be significantly associated with fibrosis at 1 month. In this complex model baseline fibrosis, HTN in the recipient and cold time were found to be predictive factors of fibrosis at 1 month (p=0.01,<0.001 and 0.03 respectively). Donor age was found to be a predictive factor of fibrosis at 6 months. The above analysis was repeated for 3, 6 and 12 months. No associations were detected between fibrosis and any of the explanatory variables with the exception of the donor age which was found to be a predictive factor of fibrosis at 6 months. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title="fibrosis">fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=transplant" title=" transplant"> transplant</a>, <a href="https://publications.waset.org/abstracts/search?q=renal" title=" renal"> renal</a>, <a href="https://publications.waset.org/abstracts/search?q=rejection" title=" rejection"> rejection</a> </p> <a href="https://publications.waset.org/abstracts/69477/the-effect-of-acute-rejection-and-delayed-graft-function-on-renal-transplant-fibrosis-in-live-donor-renal-transplantation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/69477.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">230</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">122</span> Prospective Validation of the FibroTest Score in Assessing Liver Fibrosis in Hepatitis C Infection with Genotype 4</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=G.%20Shiha">G. Shiha</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20Seif"> S. Seif</a>, <a href="https://publications.waset.org/abstracts/search?q=W.%20Samir"> W. Samir</a>, <a href="https://publications.waset.org/abstracts/search?q=K.%20Zalata"> K. Zalata</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Prospective Validation of the FibroTest Score in assessing Liver Fibrosis in Hepatitis C Infection with Genotype 4 FibroTest (FT) is non-invasive score of liver fibrosis that combines the quantitative results of 5 serum biochemical markers (alpha-2-macroglobulin, haptoglobin, apolipoprotein A1, gamma glutamyl transpeptidase (GGT) and bilirubin) and adjusted with the patient's age and sex in a patented algorithm to generate a measure of fibrosis. FT has been validated in patients with chronic hepatitis C (CHC) (Halfon et al., Gastroenterol. Clin Biol.( 2008), 32 6suppl 1, 22-39). The validation of fibro test ( FT) in genotype IV is not well studied. Our aim was to evaluate the performance of FibroTest in an independent prospective cohort of hepatitis C patients with genotype 4. Subject was 122 patients with CHC. All liver biopsies were scored using METAVIR system. Our fibrosis score(FT) were measured, and the performance of the cut-off score were done using ROC curve. Among patients with advanced fibrosis, the FT was identically matched with the liver biopsy in 18.6%, overestimated the stage of fibrosis in 44.2% and underestimated the stage of fibrosis in 37.7% of cases. Also in patients with no/mild fibrosis, identical matching was detected in 39.2% of cases with overestimation in 48.1% and underestimation in 12.7%. So, the overall results of the test were identical matching, overestimation and underestimation in 32%, 46.7% and 21.3% respectively. Using ROC curve it was found that (FT) at the cut-off point of 0.555 could discriminate early from advanced stages of fibrosis with an area under ROC curve (AUC) of 0.72, sensitivity of 65%, specificity of 69%, PPV of 68%, NPV of 66% and accuracy of 67%. As FibroTest Score overestimates the stage of advanced fibrosis, it should not be considered as a reliable surrogate for liver biopsy in hepatitis C infection with genotype 4. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=fibrotest" title="fibrotest">fibrotest</a>, <a href="https://publications.waset.org/abstracts/search?q=chronic%20Hepatitis%20C" title=" chronic Hepatitis C"> chronic Hepatitis C</a>, <a href="https://publications.waset.org/abstracts/search?q=genotype%204" title=" genotype 4"> genotype 4</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20biopsy" title=" liver biopsy"> liver biopsy</a> </p> <a href="https://publications.waset.org/abstracts/4304/prospective-validation-of-the-fibrotest-score-in-assessing-liver-fibrosis-in-hepatitis-c-infection-with-genotype-4" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/4304.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">415</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">121</span> Encoded Nanospheres for the Fast Ratiometric Detection of Cystic Fibrosis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Iv%C3%A1n%20Castell%C3%B3">Iván Castelló</a>, <a href="https://publications.waset.org/abstracts/search?q=Georgiana%20Stoica"> Georgiana Stoica</a>, <a href="https://publications.waset.org/abstracts/search?q=Emilio%20Palomares"> Emilio Palomares</a>, <a href="https://publications.waset.org/abstracts/search?q=Fernando%20Bravo"> Fernando Bravo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> We present herein two colour encoded silica nanospheres (2nanoSi) for the fluorescence quantitative ratiometric determination of trypsin in humans. The system proved to be a faster (minutes) method, with two times higher sensitivity than the state-of-the-art biomarkers based sensors for cystic fibrosis (CF), allowing the quantification of trypsin concentrations in a wide range (0-350 mg/L). Furthermore, as trypsin is directly related to the development of cystic fibrosis, different human genotypes, i.e. healthy homozygotic (> 80 mg/L), CF homozygotic (< 50 mg/L), and heterozygotic (> 50 mg/L), respectively, can be determined using our 2nanoSi nanospheres. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cystic%20fibrosis" title="cystic fibrosis">cystic fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=trypsin" title=" trypsin"> trypsin</a>, <a href="https://publications.waset.org/abstracts/search?q=quantum%20dots" title=" quantum dots"> quantum dots</a>, <a href="https://publications.waset.org/abstracts/search?q=biomarker" title=" biomarker"> biomarker</a>, <a href="https://publications.waset.org/abstracts/search?q=homozygote" title=" homozygote"> homozygote</a>, <a href="https://publications.waset.org/abstracts/search?q=heterozygote" title=" heterozygote"> heterozygote</a> </p> <a href="https://publications.waset.org/abstracts/6006/encoded-nanospheres-for-the-fast-ratiometric-detection-of-cystic-fibrosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/6006.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">484</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">120</span> Comparison between Transient Elastography (FibroScan) and Liver Biopsy for Diagnosis of Hepatic Fibrosis in Chronic Hepatitis C Genotype 4</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Gamal%20Shiha">Gamal Shiha</a>, <a href="https://publications.waset.org/abstracts/search?q=Seham%20Seif"> Seham Seif</a>, <a href="https://publications.waset.org/abstracts/search?q=Shahera%20Etreby"> Shahera Etreby</a>, <a href="https://publications.waset.org/abstracts/search?q=Khaled%20Zalata"> Khaled Zalata</a>, <a href="https://publications.waset.org/abstracts/search?q=Waleed%20Samir"> Waleed Samir</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Transient Elastography (TE; FibroScan®) is a non-invasive technique to assess liver fibrosis. Aim: To compare TE and liver biopsy in hepatitis C virus (HCV) patients, genotype IV and evaluate the effect of steatosis and schistosomiasis on FibroScan. Methods: The fibrosis stage (METAVIR Score) TE, was assessed in 519 patients. The diagnostic performance of FibroScan is assessed by calculating the area under the receiver operating characteristic curves (AUROCs). Results: The cut-off value of ≥ F2 was 8.55 kPa, ≥ F3 was 10.2 kPa and cirrhosis = F4 was 16.3 kPa. The positive predictive value and negative predictive value were 70.1% and 81.7% for the diagnosis of ≥ F2, 62.6% and 96.22% for F ≥ 3, and 27.7% and 100% for F4. No significant difference between schistosomiasis, steatosis degree and FibroScan measurements. Conclusion: Fibroscan could accurately predict liver fibrosis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=chronic%20hepatitis%20C" title="chronic hepatitis C">chronic hepatitis C</a>, <a href="https://publications.waset.org/abstracts/search?q=FibroScan" title=" FibroScan"> FibroScan</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20biopsy" title=" liver biopsy"> liver biopsy</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20fibrosis" title=" liver fibrosis"> liver fibrosis</a> </p> <a href="https://publications.waset.org/abstracts/3662/comparison-between-transient-elastography-fibroscan-and-liver-biopsy-for-diagnosis-of-hepatic-fibrosis-in-chronic-hepatitis-c-genotype-4" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/3662.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">409</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">119</span> Therapeutic Evaluation of Bacopa Monnieri Extract on Liver Fibrosis in Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yu%20Wen%20Wang">Yu Wen Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shyh%20Ming%20Kuo"> Shyh Ming Kuo</a>, <a href="https://publications.waset.org/abstracts/search?q=Hsia%20Ying%20Cheng"> Hsia Ying Cheng</a>, <a href="https://publications.waset.org/abstracts/search?q=Yu%20Chiuan%20Wu"> Yu Chiuan Wu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Liver fibrosis is caused by the activation of hepatic stellate cells in the liver to secrete excessive and deposition of extracellular matrix. In recent years, many treatment strategies have been developed to reduce the activation of hepatic stellate cells and therefore to increase the decomposition of extracellular matrix. Bacopa monnieri, an herbaceous plant of the scrophulariaceae, containing saponins and glycosides, which with antioxidant, anti-inflammation, pain relief and free radical scavenging characteristics. This study was to evaluate the inhibition of hepatic stellate cell activity by Bacopa monnieri extract and its therapeutic potential in treating thioacetamide-induced liver fibrosis in rats. The results showed that the IC50 of Bacopa monnieri extract was 0.39 mg/mL. Bacopa monnieri extract could effectively reduce H2O2-induced hepatic stellate cells inflammation. In the TAA-induced liver fibrosis animal studies, albumin secretion recovered to normal level after treated with Bacopa monnieri extract for 2-w, and fibrosis related proteins, α-SMA and TGF-1levels decreased indicating the extract exerted therapeutic effect on the liver fibrosis. However, inflammatory factors TNF- obviously decreased after 4-w treatment. In summary, we could successfully extract the main component-Bacopaside I from the plant and acquired a potential therapy using this component in treating TAA-induced liver fibrosis in rat. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=anti-inflammatory" title="anti-inflammatory">anti-inflammatory</a>, <a href="https://publications.waset.org/abstracts/search?q=Bacopa%20monnieri" title=" Bacopa monnieri"> Bacopa monnieri</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=hepatic%20stellate%20cells" title=" hepatic stellate cells"> hepatic stellate cells</a>, <a href="https://publications.waset.org/abstracts/search?q=water%20extract" title=" water extract"> water extract</a> </p> <a href="https://publications.waset.org/abstracts/156606/therapeutic-evaluation-of-bacopa-monnieri-extract-on-liver-fibrosis-in-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/156606.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">111</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">118</span> Biopsy or Biomarkers: Which Is the Sample of Choice in Assessment of Liver Fibrosis?</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=S.%20H.%20Atef">S. H. Atef</a>, <a href="https://publications.waset.org/abstracts/search?q=N.%20H.%20Mahmoud"> N. H. Mahmoud</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20Abdrahman"> S. Abdrahman</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20Fattoh"> A. Fattoh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: The aim of the study is to assess the diagnostic value of fibrotest and hyaluronic acid in discriminate between insignificant and significant fibrosis. Also, to find out if these parameters could replace liver biopsy which is currently used for selection of chronic hepatitis C patients eligible for antiviral therapy. Study design: This study was conducted on 52 patients with HCV RNA detected by polymerase chain reaction (PCR) who had undergone liver biopsy and attending the internal medicine clinic at Ain Shams University Hospital. Liver fibrosis was evaluated according to the METAVIR scoring system on a scale of F0 to F4. Biochemical markers assessed were: alpha-2 macroglobulin (α2-MG), apolipoprotein A1 (Apo-A1), haptoglobin, gamma-glutamyl transferase (GGT), total bilirubin (TB) and hyaluronic acid (HA). The fibrotest score was computed after adjusting for age and gender. Predictive values and ROC curves were used to assess the accuracy of fibrotest and HA results. Results: For fibrotest, the observed area under curve for the discrimination between minimal or no fibrosis (F0-F1) and significant fibrosis (F2-F4) was 0.6736 for cutoff value 0.19 with sensitivity of 84.2% and specificity of 85.7%. For HA, the sensitivity was 89.5% and specificity was 85.7% and area under curve was 0.540 at the best cutoff value 71 mg/dL. Multi-use of both parameters, HA at 71 mg/dL with fibrotest score at 0.22 give a sensitivity 89.5%, specificity 100 and efficacy 92.3% (AUC 0.895). Conclusion: The use of both fibrotest score and HA could be as alternative to biopsy in most patients with chronic hepaitis C putting in consideration some limitations of the proposed markers in evaluating liver fibrosis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=fibrotest" title="fibrotest">fibrotest</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20fibrosis" title=" liver fibrosis"> liver fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=HCV%20RNA" title=" HCV RNA"> HCV RNA</a>, <a href="https://publications.waset.org/abstracts/search?q=biochemical%20markers" title=" biochemical markers"> biochemical markers</a> </p> <a href="https://publications.waset.org/abstracts/37231/biopsy-or-biomarkers-which-is-the-sample-of-choice-in-assessment-of-liver-fibrosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/37231.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">287</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">117</span> The Effect of Spark Physical Program (Sports, Play and Active Recreation for Kids) on Quality of Life and Spirometry in 6-18-Year-Old Children with Cystic Fibrosis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Saeedeh%20Eshkil">Saeedeh Eshkil</a>, <a href="https://publications.waset.org/abstracts/search?q=Seyedeh%20Farnaz%20Mousavi"> Seyedeh Farnaz Mousavi</a>, <a href="https://publications.waset.org/abstracts/search?q=Hamid%20Reza%20Kianifar"> Hamid Reza Kianifar</a>, <a href="https://publications.waset.org/abstracts/search?q=Seyed%20Java%20Sayyedi"> Seyed Java Sayyedi</a>, <a href="https://publications.waset.org/abstracts/search?q=Mehdi%20Sohrabi"> Mehdi Sohrabi</a>, <a href="https://publications.waset.org/abstracts/search?q=Elham%20%20Bakhtiari"> Elham Bakhtiari</a>, <a href="https://publications.waset.org/abstracts/search?q=Morteza%20Mashoughi"> Morteza Mashoughi</a>, <a href="https://publications.waset.org/abstracts/search?q=Ezzat%20Khodashenas"> Ezzat Khodashenas</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: The effect of the SPARK physical education program on lung function in cystic fibrosis patients is not yet determined.).SPARK is Sports, play and active recreation for kids, including moving skills, aerobic games, jogging or walking, aerobic dance and jump rope. Regarding the high prevalence of cystic fibrosis and its destructive effects on the lungs, the aim of this study is to evaluate lung function and quality of life before and after undergoing the SPARK physical education program in children with cystic fibrosis. Method: In this quasi-experimental study, all patients with cystic fibrosis aged 6-18 years referred to the cystic fibrosis clinic of Dr. Sheikh Hospital were enrolled. The patients went under 12 weeks of SPARK training program (3 sessions per week, each session 45 minutes). The quality of life questionnaire ( Cystic Fibrosis Questionnaire includes self-examination, parental ) for patients with cystic fibrosis and spirometry indices (FEV1, FVC, FEV1/FVC, FEF25-75) was filled out before and after intervention for all patients. Results The mean and standard deviation of patients' age were 9.85±2.67 years, and 65% of patients were female. The FEV1 was significantly different before and after the SPARK physical education program (P=0.03), and the respiratory component of quality of life significantly increased after intervention (P=0.002). The overall score of quality of life from parents’ point of view was 2.87 ± 0.38, which increased to 2.99 ± 0.38 after the intervention. Conclusion: The SPARK training program may improve the spirometric parameters in children with cystic fibrosis. It also had a significant effect on improving the quality of life of patients, especially in the respiratory component. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cystic%20fibrosis" title="cystic fibrosis">cystic fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=pediatrics" title=" pediatrics"> pediatrics</a>, <a href="https://publications.waset.org/abstracts/search?q=SPARK%20motor%20program" title=" SPARK motor program"> SPARK motor program</a>, <a href="https://publications.waset.org/abstracts/search?q=spirometry" title=" spirometry"> spirometry</a> </p> <a href="https://publications.waset.org/abstracts/191726/the-effect-of-spark-physical-program-sports-play-and-active-recreation-for-kids-on-quality-of-life-and-spirometry-in-6-18-year-old-children-with-cystic-fibrosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/191726.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">21</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">116</span> Sulforaphane Attenuates Fibrosis of Dystrophic Muscle in Mdx Mice via Nrf2-Mediated Inhibition of TGF-β/Smad Signaling</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: A few lines of evidence show that Sulforaphane (SFN) has anti-fibrosis effect in liver tissue via Nrf2-mediated inhibition of TGF-β/Smad signaling. However, its effects on muscular dystrophic fibrosis remain unknown. This work was undertaken to evaluate the effects of SFN on fibrosis in dystrophic muscle. Methods: 3-month-old male mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 3 months. Gastrocnemius, tibial anterior and triceps brachii muscles were collected for related analysis. Fibrosis in skeletal muscles was analyzed by Sirius red staining. Histology and morphology of skeletal muscles were investigated by H&E staining. Moreover, the expressions of Nrf2, NQO1, HO-1, and TGF-β/Smad signaling pathway were detected by western blot, qRT-PCR, immunohistochemistry and immunofluorescence assays. Results: Our results demonstrated that SFN treatment significantly decreased and improved morphological features in mdx muscles. Moreover, SFN increased the expression of muscle phase II enzymes NQO1 and HO-1 and significantly decreased the expression of TGF-β1，p-smad2, p-smad3, α-SMA, fibronectin, collagen I, PAI-1, and TIMP-1 in Nrf2 dependent manner. Additionally, SFN significantly decreased the expression of CD45 and TNF-α. Conclusions: Collectively, these results show that SFN can ameliorate muscle fibrosis in mdx mice by Nrf2-induced inhibition of TGF-β/Smad signaling pathway, which indicate Nrf2 may be useful for the treatment of muscular dystrophy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=TGF-%CE%B2%2Fsmad%20signaling" title=" TGF-β/smad signaling"> TGF-β/smad signaling</a>, <a href="https://publications.waset.org/abstracts/search?q=duchenne%20muscular%20dystrophy" title=" duchenne muscular dystrophy"> duchenne muscular dystrophy</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a> </p> <a href="https://publications.waset.org/abstracts/19674/sulforaphane-attenuates-fibrosis-of-dystrophic-muscle-in-mdx-mice-via-nrf2-mediated-inhibition-of-tgf-vsmad-signaling" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19674.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">441</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">115</span> Effect of Nicorandil in Bile Duct Ligation-Induced Liver Fibrosis in Rats: Role of Hepatic Stellate Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Y.%20S.%20Mohamed">Y. S. Mohamed</a>, <a href="https://publications.waset.org/abstracts/search?q=L.%20A.%20Ahmed"> L. A. Ahmed</a>, <a href="https://publications.waset.org/abstracts/search?q=H.%20A.%20Salem"> H. A. Salem</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20M.%20Agha"> A. M. Agha </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Liver Fibrosis is one of the most serious conditions that affect the Egyptian society. In the present study, the effect of nicorandil was investigated in experimentally-induced liver fibrosis by bile duct ligation in rats. Nicorandil (3mg/kg/day) was given orally 24 h after bile duct ligation for 14 days till the end of the experiment. Nicorandil group showed a significant improvement in liver function tests (ALT and ALP) as well as a significant decrease in oxidative stress biomarkers (TBARS and GSH), area of fibrosis and activity of hepatic stellate cells as indicated by decreased expression of alpha smooth muscle actin.Moreover, nicorandil treatment decreased HSCs proliferation due to its inhibitory effects on protein kinase C(PKC) and Platelet derived growth factor (PDGF) . Oral administration of either glibenclamide (10 mg/kg/day)(a KATP channel blocker) or L-NAME (30 mg/kg/day) (an inhibitor of nitric oxide synthase) blocked the protective effects of nicorandil. However, nicorandil and L-NAME treated group showed more or less results similar to that of untreated bile duct ligated group. In conclusion, nicorandil was effective against the development of bile duct ligated-induced liver fibrosis in rats where activation of the NO pathway plays an important role in the protective effect nicorandil. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hepatic%20stellate%20cells" title="hepatic stellate cells">hepatic stellate cells</a>, <a href="https://publications.waset.org/abstracts/search?q=nicorandil" title=" nicorandil"> nicorandil</a>, <a href="https://publications.waset.org/abstracts/search?q=nitric%20oxide%20donor" title=" nitric oxide donor"> nitric oxide donor</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20fibrosis" title=" liver fibrosis"> liver fibrosis</a> </p> <a href="https://publications.waset.org/abstracts/15870/effect-of-nicorandil-in-bile-duct-ligation-induced-liver-fibrosis-in-rats-role-of-hepatic-stellate-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/15870.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">611</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">114</span> Green Tea Extract: Its Potential Protective Effect on Bleomycin Induced Lung Injuries in Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Azza%20EL-Medany">Azza EL-Medany</a>, <a href="https://publications.waset.org/abstracts/search?q=Jamila%20EL-Medany"> Jamila EL-Medany</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Lung fibrosis is a common side effect of the chemotherapeutic agent, bleomycin. Current evidence suggests that reactive oxygen species may play a key role in the development of lung fibrosis. The present work studied the effect of green tea extract on bleomycin–induced lung fibrosis in rats. Animals were divided into three groups: (1) Saline control group; (2) bleomycin group in which rats were injected with bleomycin (15mg/kg,i.p.) three times a week for four weeks; (3) bleomycin and green tea group in which green tea extract was given to rats (100mg/kg/day, p.o) a week prior to bleomycin and daily during bleomycin injections for 4 weeks until the end of the experiment. Bleomycin–induced pulmonary injury and lung fibrosis that was indicated by increased lung hydroxyproline content, elevated nitric oxide synthase, myeoloperoxidase (MPO), platelet activating factor (PAF), tumor necrosis factor α (TNF_α), transforming growth factor 1β (TGF1β) and angiotensin converting enzyme (ACE) activity in lung tissues. On the other hand, bleomycin induced a reduction in reduced glutathione concentration (GSH). Moreover, bleomycin resulted in a severe histological changes in lung tissues revealed as lymphocytes and neutrophils infiltration, increased collagen deposition and fibrosis. Co-administration of bleomycin and green tea extract reduced bleomycin–induced lung injury as evaluated by the significant reduction in hydroxyproline content, nitric oxide synthase activity, levels of MPO, PAF, TNF-α, and ACE in lung tissues. Furthermore, green tea extract ameliorated bleomycin– induced reduction in GSH concentration. Finally, histological evidence supported the ability of green tea extract to attenuate bleomycin–induced lung fibrosis and consolidation. Thus, the finding of the present study provides that green tea may serve as a novel target for potential therapeutic treatment of lung fibrosis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bleomycin" title="bleomycin">bleomycin</a>, <a href="https://publications.waset.org/abstracts/search?q=lung%20fibrosis" title=" lung fibrosis"> lung fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=green%20tea" title=" green tea"> green tea</a>, <a href="https://publications.waset.org/abstracts/search?q=oxygen%20species" title=" oxygen species"> oxygen species</a> </p> <a href="https://publications.waset.org/abstracts/15399/green-tea-extract-its-potential-protective-effect-on-bleomycin-induced-lung-injuries-in-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/15399.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">452</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">113</span> Curcumin Attenuates Angiogenesis in Liver Fibrosis and Inhibits Angiogenic Properties of Hepatic Stellate Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Feng%20Zhang">Feng Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Li%20Chen"> Li Chen</a>, <a href="https://publications.waset.org/abstracts/search?q=Desong%20Kong"> Desong Kong</a>, <a href="https://publications.waset.org/abstracts/search?q=Xiaoping%20Zhang"> Xiaoping Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Xiaojing%20Zhu"> Xiaojing Zhu</a>, <a href="https://publications.waset.org/abstracts/search?q=Yin%20Lu"> Yin Lu</a>, <a href="https://publications.waset.org/abstracts/search?q=Shizhong%20Zheng"> Shizhong Zheng</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Sinusoidal pathological angiogenesis is a novel therapeutic target for liver fibrosis. We demonstrated that curcumin ameliorated fibrotic injury and sinusoidal angiogenesis in rat liver with fibrosis caused by carbon tetrachloride. Curcumin reduced the expression of angiogenic markers in fibrotic liver. Experiments in vitro showed that the viability and vascularization of rat liver sinusoidal endothelial cells (LSECs) were not impaired by curcumin. Further investigations showed that curcumin inhibited VEGF expression in hepatic stellate cells (HSCs) by disrupting PDGF-βR/ERK and mTOR pathways. HSC motility and vascularization were also suppressed by curcumin via blocking PDGF-βR/FAK/RhoA cascade. Gain- or loss-of-function analyses revealed that activation of PPARγ was required for curcumin to inhibit angiogenic properties of HSCs. We concluded that curcumin attenuated sinusoidal angiogenesis in liver fibrosis possibly by targeting HSCs via a PPARγ activation-dependent mechanism. PPARγ could be a target molecule for reducing pathological angiogenesis during liver fibrosis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=angiogenesis" title="angiogenesis">angiogenesis</a>, <a href="https://publications.waset.org/abstracts/search?q=hepatic%20stellate%20cell" title=" hepatic stellate cell"> hepatic stellate cell</a>, <a href="https://publications.waset.org/abstracts/search?q=curcumin" title=" curcumin"> curcumin</a>, <a href="https://publications.waset.org/abstracts/search?q=peroxisome%20proliferator-activated%20receptor-%CE%B3" title=" peroxisome proliferator-activated receptor-γ"> peroxisome proliferator-activated receptor-γ</a> </p> <a href="https://publications.waset.org/abstracts/2873/curcumin-attenuates-angiogenesis-in-liver-fibrosis-and-inhibits-angiogenic-properties-of-hepatic-stellate-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/2873.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">512</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">112</span> Regression of Fibrosis by Apigenin in Thioacetamide-Induced Liver Fibrosis Rat Model through Suppression of HIF-1/FAK Pathway</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hany%20M.%20Fayed">Hany M. Fayed</a>, <a href="https://publications.waset.org/abstracts/search?q=Rehab%20F.%20Abdel-Rahman"> Rehab F. Abdel-Rahman</a>, <a href="https://publications.waset.org/abstracts/search?q=Alyaa%20F.%20Hessin"> Alyaa F. Hessin</a>, <a href="https://publications.waset.org/abstracts/search?q=Hanan%20A.%20Ogaly"> Hanan A. Ogaly</a>, <a href="https://publications.waset.org/abstracts/search?q=Gihan%20F.%20Asaad"> Gihan F. Asaad</a>, <a href="https://publications.waset.org/abstracts/search?q=Abeer%20A.%20A.%20Salama"> Abeer A. A. Salama</a>, <a href="https://publications.waset.org/abstracts/search?q=Sahar%20Abdelrahman"> Sahar Abdelrahman</a>, <a href="https://publications.waset.org/abstracts/search?q=Mahmoud%20S.%20Arbid"> Mahmoud S. Arbid</a>, <a href="https://publications.waset.org/abstracts/search?q=Marwan%20Abd%20Elbaset%20Mohamed"> Marwan Abd Elbaset Mohamed</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Liver fibrosis is a serious global health problem that occurs as a result of a variety of chronic liver disorders. Apigenin, a flavonoid found in many plants, has several pharmacological properties. The aim of this study was to evaluate the antifibrotic efficacy of apigenin (APG) against experimentally induced hepatic fibrosis in rats via using thioacetamide (TAA) and to explore the possible underlying mechanisms. TAA (100 mg/kg, i.p.) was given three times each week for two weeks to induce liver fibrosis. After TAA injections, APG was given orally (5 and 10 mg/kg) daily for two weeks. Biochemical, molecular, histological and immunohistochemical analyses were performed on blood and liver tissue samples. The functioning of the liver, oxidative stress, inflammation, and liver fibrosis indicators were all evaluated. The findings showed that TAA markedly increased the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), as well as the levels of malondialdehyde (MDA), focal adhesion kinase (FAK), hypoxia-inducible factor-1 (HIF-1), nuclear factor-κB (NF-κB), transforming growth factor-beta (TGF-β), tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) with a reduction in albumin, total protein, A/G ratio, GSH content and interleukin-10 (IL-10). Moreover, TAA elevated the content of collagen I, α -smooth muscle actin (α-SMA), and hydroxyproline in the liver. The treatment with APG in a dose-dependent manner has obviously prevented these alterations and amended the harmful effects induced by TAA. The histopathological and immunohistochemical observations supported this biochemical evidence. The higher dose of APG produced the most significant antifibrotic effect. As a result of these data, APG appears to be a promising antifibrotic drug and could be used as a new herbal medication or dietary supplement in the future for the treatment of liver fibrosis. This effect might be related to the inhibition of the HIF-1/FAK signaling pathway. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=apigenin" title="apigenin">apigenin</a>, <a href="https://publications.waset.org/abstracts/search?q=FAK" title=" FAK"> FAK</a>, <a href="https://publications.waset.org/abstracts/search?q=HIF-1" title=" HIF-1"> HIF-1</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20fibrosis" title=" liver fibrosis"> liver fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=rat" title=" rat"> rat</a>, <a href="https://publications.waset.org/abstracts/search?q=thioacetamide" title=" thioacetamide"> thioacetamide</a> </p> <a href="https://publications.waset.org/abstracts/148178/regression-of-fibrosis-by-apigenin-in-thioacetamide-induced-liver-fibrosis-rat-model-through-suppression-of-hif-1fak-pathway" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/148178.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">134</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">111</span> Analysis of the Lung Microbiome in Cystic Fibrosis Patients Using 16S Sequencing</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Manasvi%20Pinnaka">Manasvi Pinnaka</a>, <a href="https://publications.waset.org/abstracts/search?q=Brianna%20Chrisman"> Brianna Chrisman</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Cystic fibrosis patients often develop lung infections that range anywhere in severity from mild to life-threatening due to the presence of thick and sticky mucus that fills their airways. Since many of these infections are chronic, they not only affect a patient’s ability to breathe but also increase the chances of mortality by respiratory failure. With a publicly available dataset of DNA sequences from bacterial species in the lung microbiome of cystic fibrosis patients, the correlations between different microbial species in the lung and the extent of deterioration of lung function were investigated. 16S sequencing technologies were used to determine the microbiome composition of the samples in the dataset. For the statistical analyses, referencing helped distinguish between taxonomies, and the proportions of certain taxa relative to another were determined. It was found that the Fusobacterium, Actinomyces, and Leptotrichia microbial types all had a positive correlation with the FEV1 score, indicating the potential displacement of these species by pathogens as the disease progresses. However, the dominant pathogens themselves, including Pseudomonas aeruginosa and Staphylococcus aureus, did not have statistically significant negative correlations with the FEV1 score as described by past literature. Examining the lung microbiology of cystic fibrosis patients can help with the prediction of the current condition of lung function, with the potential to guide doctors when designing personalized treatment plans for patients. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bacterial%20infections" title="bacterial infections">bacterial infections</a>, <a href="https://publications.waset.org/abstracts/search?q=cystic%20fibrosis" title=" cystic fibrosis"> cystic fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=lung%20microbiome" title=" lung microbiome"> lung microbiome</a>, <a href="https://publications.waset.org/abstracts/search?q=16S%20sequencing" title=" 16S sequencing"> 16S sequencing</a> </p> <a href="https://publications.waset.org/abstracts/161103/analysis-of-the-lung-microbiome-in-cystic-fibrosis-patients-using-16s-sequencing" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/161103.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">99</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">110</span> MiR-200a/ZEB1 Pathway in Liver Fibrogenesis of Biliary Atresia</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hai-Ying%20Liu">Hai-Ying Liu</a>, <a href="https://publications.waset.org/abstracts/search?q=Yi-Hao%20Chen"> Yi-Hao Chen</a>, <a href="https://publications.waset.org/abstracts/search?q=Shu-Yin%20Pang"> Shu-Yin Pang</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng-Hua%20Wang"> Feng-Hua Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Xiao-Fang%20Peng"> Xiao-Fang Peng</a>, <a href="https://publications.waset.org/abstracts/search?q=Li-Yuan%20Yang"> Li-Yuan Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Zheng-Rong%20Chen"> Zheng-Rong Chen</a>, <a href="https://publications.waset.org/abstracts/search?q=Yi%20Chen"> Yi Chen</a>, <a href="https://publications.waset.org/abstracts/search?q=Bing%20Zhu"> Bing Zhu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objective: Biliary atresia (BA) is characterized by progressive liver fibrosis. Epithelial-mesenchymal transition (EMT) has been implicated as a key mechanism in the pathogenesis of organ fibrosis. MiR-200a has been shown to repress EMT. We aim to explore the role of miR-200a in the fibrogenesis of BA. Methods: We obtained the plasma samples and liver samples from patients with BA or controls to examine the role of miR-200a. Histological liver fibrosis was assessed using the Ishak fibrosis scores. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was performed to detect the expression of miR-200a in plasma. We also evaluated the expression of miR-200a in liver tissues using tyramide signal amplification fluorescence in situ hybridization (TSA-FISH). The expression of EMT related proteins zinc finger E-box-binding homeobox 1 (ZEB1), E-cadherin and α-smooth muscle actin (α-SMA) in the liver sections were detected by immunohistochemical staining. Results: We found that the expression of miR-200a was both elevated in the plasma and liver tissues from BA patients compared with the controls. The hepatic expression of ZEB1 and α-SMA were markedly increased in the liver sections from BA patients compared to the controls, whereas E-cadherin was downregulated in the BA group. Simultaneously, we noted that the hepatic expression of miR-200a, E-cadherin and α-SMA were upregulated with the progression of liver fibrosis in the BA group, while ZEB1 was downregulated with the progression of liver fibrosis in BA patients. Conclusion: These findings suggest EMT has a critical effect on the fibrotic process of BA, and the interaction between miR-200a and ZEB1 may regulate EMT and eventually influence liver fibrogenesis of BA. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=biliary%20atresia" title="biliary atresia">biliary atresia</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20fibrosis" title=" liver fibrosis"> liver fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=MicroRNA" title=" MicroRNA"> MicroRNA</a>, <a href="https://publications.waset.org/abstracts/search?q=epithelial-mesenchymal%20transition" title=" epithelial-mesenchymal transition"> epithelial-mesenchymal transition</a>, <a href="https://publications.waset.org/abstracts/search?q=zinc%20finger%20E-box-binding%20homeobox%201" title=" zinc finger E-box-binding homeobox 1"> zinc finger E-box-binding homeobox 1</a> </p> <a href="https://publications.waset.org/abstracts/53847/mir-200azeb1-pathway-in-liver-fibrogenesis-of-biliary-atresia" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/53847.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">359</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">109</span> The Impact of Lipids on Lung Fibrosis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=G.%20Wojcik">G. Wojcik</a>, <a href="https://publications.waset.org/abstracts/search?q=J.%20Gindlhuber"> J. Gindlhuber</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20Syarif"> A. Syarif</a>, <a href="https://publications.waset.org/abstracts/search?q=K.%20Hoetzenecker"> K. Hoetzenecker</a>, <a href="https://publications.waset.org/abstracts/search?q=P.%20Bohm"> P. Bohm</a>, <a href="https://publications.waset.org/abstracts/search?q=P.%20Vesely"> P. Vesely</a>, <a href="https://publications.waset.org/abstracts/search?q=V.%20Biasin"> V. Biasin</a>, <a href="https://publications.waset.org/abstracts/search?q=G.%20Kwapiszewska"> G. Kwapiszewska</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Pulmonary fibrosis is a rare disease where uncontrolled wound healing processes damage the lung structure. Intensive changes within the extracellular matrix (ECM) and its interaction with fibroblasts have a major role in pulmonary fibrosis development. Among others, collagen is one of the main components of the ECM, and it is important for lung structure. In IPF, constant production of collagen by fibroblast, through TGFβ1-SMAD2/3 pathways, leads to an uncontrolled deposition of matrix and hence lung remodeling. Abnormal changes in lipid production, alterations in fatty acids (FAs) metabolism, enhanced oxidative stress, and lipid peroxidation in fibrotic lung and fibrotic fibroblasts have been reported; however, the interplay between the collagen and lipids is not yet established. One of the FAs influx regulators is Angiopoietin-like 4 (ANGPTL4), which inhibits lipoprotein lipase work, decreasing the availability of FAs. We hypothesized that altered lipid composition or availability could have the capability to influence the phenotype of different fibroblast populations in the lung and hence influence lung fibrosis. To prove our hypothesis, we aim to investigate lipids and their influence on human, animal, and in vitro levels. In the bleomycin model, treatment with the well-known metabolic drugs Rosiglitazone or Metformin significantly lower collagen production. Similar results were noticed in ANGPTL4 KO animals, where the KO of ANGPTL4 leads to an increase of FAs availability and lower collagen deposition after the bleomycin challenge. Currently, we study the treatment of different FAs on human lung para fibroblasts (hPF) isolated from donors. To understand the lipid composition, we are collecting human lung tissue from donors and pulmonary fibrosis patients for Liquid chromatography-mass spectrometry. In conclusion, our results suggest the lipid influence on collagen deposition during lung fibrosis, but further research needs to be conducted to understand the matter of this relationship. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=collagen" title="collagen">collagen</a>, <a href="https://publications.waset.org/abstracts/search?q=fibroblasts" title=" fibroblasts"> fibroblasts</a>, <a href="https://publications.waset.org/abstracts/search?q=lipidomics" title=" lipidomics"> lipidomics</a>, <a href="https://publications.waset.org/abstracts/search?q=lung" title=" lung"> lung</a>, <a href="https://publications.waset.org/abstracts/search?q=pulmonary%20fibrosis" title=" pulmonary fibrosis"> pulmonary fibrosis</a> </p> <a href="https://publications.waset.org/abstracts/167033/the-impact-of-lipids-on-lung-fibrosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/167033.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">84</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">108</span> Curcumin Reduces the Expression of Main Fibrogenic Genes and Phosphorylation of Smad3C Signaling Pathway in TGFB-Activated Human HSCs. A New Remedy for Liver Fibrosis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Elham%20Shakerian">Elham Shakerian</a>, <a href="https://publications.waset.org/abstracts/search?q=Reza%20Afarin"> Reza Afarin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The hepatic disease causes approximately 2 million deaths/year worldwide. Liver fibrosis is the last stage of numerous chronic liver diseases, and until now there is no definite cure or drug for it. Activation of hepatic stellate cells (HSCs) is the main reason for fibrosis. Transforming growth factor (TGF-β), as a main profibrogenic cytokine, if increased in these cells, leads to liver fibrosis through smad3 signaling pathways and increasing the expressions of Collagen type I and III, and actin-alpha smooth muscle (αSMA) genes. Curcumin (CUR) is a polyphenolic compound and an active ingredient derived from the rhizome of the turmeric plant that exerts effective antioxidant, anti-inflammatory, and antimicrobial activity. It has been shown that daily consumption of curcumin may have a protective effect on the liver against oxidative stress associated with alcohol consumption. In this study, we investigate the role of Curcumin in decreasing HSC activation and treating liver fibrosis. First, the human HSCs were treated with 2 ng/ml of (TGF-β) for 24 hours to become activated, then with Silibinin for 24 hours. Total RNAs were extracted, reversely transcribed into cDNA, Quantitative Real-time PCR, and western blot were performed. The mRNA expression levels of Collagen type I and III, αSMA genes, and the level of smad3 phosphorylation in TGF-β activated human HSCs treated with Curcumin were significantly reduced compared to human HSCs untreated with Curcumin. Curcumin is effective in reducing the expression of fibrogenic genes in the activated human HSCs treated with TGFB through downregulation of the TGF-β/smad3 signaling pathway. Therefore, Curcumin possesses significant antifibrotic properties in hepatic fibrosis <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hepatic%20fibrosis" title="hepatic fibrosis">hepatic fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=human%20HSCs" title=" human HSCs"> human HSCs</a>, <a href="https://publications.waset.org/abstracts/search?q=curcumin" title=" curcumin"> curcumin</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrogenic%20genes" title=" fibrogenic genes"> fibrogenic genes</a> </p> <a href="https://publications.waset.org/abstracts/146705/curcumin-reduces-the-expression-of-main-fibrogenic-genes-and-phosphorylation-of-smad3c-signaling-pathway-in-tgfb-activated-human-hscs-a-new-remedy-for-liver-fibrosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/146705.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">122</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">107</span> Rebamipide Retards CCL4 Induced Hepatic Fibrosis: A Role of PGE2 </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Alaa%20E.%20El-sisi">Alaa E. El-sisi</a>, <a href="https://publications.waset.org/abstracts/search?q=Sherin%20Zakaria"> Sherin Zakaria </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Rebamipide is an antiulcer drug with unique properties such as anti-inflammatory action. It induces endogenous prostaglandin e2 (PGE2). PGE2 is considered as a potent physiological suppressor of liver fibrosis. Aim of study: This study investigated the effect of rebamipide on hepatic fibrosis. Material and Method: Hepatic fibrosis was induced by intraperitoneal injections (IP) injection of CCl4 (0.45 mL/kg) in corn oil 1:5 twice a week for 4 weeks. Rats were divided into four groups as follow: Group 1 treated with CCL4 only, group 2 and 3 treated with CCL4 and rebamipide 60 mg/kg/day (group2) or 100 mg/kg/day (group3), and the fourth group was considered as control group and treated with vehicles. ALT, AST, and Bilirubin were assayed in serum. Antioxidant markers such as malondialdhyde (MDA) and superoxide dismutase (SOD) and fibrotic markers such as hyaluronic acid (HA) and procollagen-III (procol-III) were evaluated in liver tissues. IL-10 as well as PGE2 were also assayed in liver tissues. Pathologic changes in the liver were detected by hematoxylin and eosin staining. Collagen precipitation in liver tissues was visualized using masson trichrom stain. Results: Rebamipide inhibit CCL4 induced increase in ALT and AST significantly (p < 0.05). Rebamipide exerted an antioxidant effect as it inhibits CCL4 induced increased MDA level and decreased SOD activity. Fibrotic markers assay revealed that repamipide (60 or 100 mg/kg/day) decreased the level of procol-III and HA compared to CCl4 (p < 0.05). Oral administration of Rebamipide was associated with a significant increase (p < 0.05) of PGE2 and IL-10. Rebamipide especially at the dose of (100 mg/kg/day) restores liver histology structure and abolish collagen precipitation in liver tissues. Conclusion: Rebamipide retards hepatic fibrosis induced by CCL4 may be through the induction of PGE2 level. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=fibrotic%20markers" title="fibrotic markers">fibrotic markers</a>, <a href="https://publications.waset.org/abstracts/search?q=hepatic%20fibrosis" title=" hepatic fibrosis"> hepatic fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=PGE2" title=" PGE2"> PGE2</a>, <a href="https://publications.waset.org/abstracts/search?q=rebamipide" title=" rebamipide "> rebamipide </a> </p> <a href="https://publications.waset.org/abstracts/23573/rebamipide-retards-ccl4-induced-hepatic-fibrosis-a-role-of-pge2" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/23573.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">484</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">106</span> Effects of Bone Marrow Derived Mesenchymal Stem Cells (MSC) in Acute Respiratory Distress Syndrome (ARDS) Lung Remodeling</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Diana%20Islam">Diana Islam</a>, <a href="https://publications.waset.org/abstracts/search?q=Juan%20Fang"> Juan Fang</a>, <a href="https://publications.waset.org/abstracts/search?q=Vito%20Fanelli"> Vito Fanelli</a>, <a href="https://publications.waset.org/abstracts/search?q=Bing%20Han"> Bing Han</a>, <a href="https://publications.waset.org/abstracts/search?q=Julie%20Khang"> Julie Khang</a>, <a href="https://publications.waset.org/abstracts/search?q=Jianfeng%20Wu"> Jianfeng Wu</a>, <a href="https://publications.waset.org/abstracts/search?q=Arthur%20S.%20Slutsky"> Arthur S. Slutsky</a>, <a href="https://publications.waset.org/abstracts/search?q=Haibo%20Zhang"> Haibo Zhang</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: MSC delivery in preclinical models of ARDS has demonstrated significant improvements in lung function and recovery from acute injury. However, the role of MSC delivery in ARDS associated pulmonary fibrosis is not well understood. Some animal studies using bleomycin, asbestos, and silica-induced pulmonary fibrosis show that MSC delivery can suppress fibrosis. While other animal studies using radiation induced pulmonary fibrosis, liver, and kidney fibrosis models show that MSC delivery can contribute to fibrosis. Hypothesis: The beneficial and deleterious effects of MSC in ARDS are modulated by the lung microenvironment at the time of MSC delivery. Methods: To induce ARDS a two-hit mouse model of Hydrochloric acid (HCl) aspiration (day 0) and mechanical ventilation (MV) (day 2) was used. HCl and injurious MV generated fibrosis within 14-28 days. 0.5x106 mouse MSCs were delivered (via both intratracheal and intravenous routes) either in the active inflammatory phase (day 2) or during the remodeling phase (day 14) of ARDS (mouse fibroblasts or PBS used as a control). Lung injury accessed using inflammation score and elastance measurement. Pulmonary fibrosis was accessed using histological score, tissue collagen level, and collagen expression. In addition alveolar epithelial (E) and mesenchymal (M) marker expression profile was also measured. All measurements were taken at day 2, 14, and 28. Results: MSC delivery 2 days after HCl exacerbated lung injury and fibrosis compared to HCl alone, while the day 14 delivery showed protective effects. However in the absence of HCl, MSC significantly reduced the injurious MV-induced fibrosis. HCl injury suppressed E markers and up-regulated M markers. MSC delivery 2 days after HCl further amplified M marker expression, indicating their role in myofibroblast proliferation/activation. While with 14-day delivery E marker up-regulation was observed indicating their role in epithelial restoration. Conclusions: Early MSC delivery can be protective of injurious MV. Late MSC delivery during repair phase may also aid in recovery. However, early MSC delivery during the exudative inflammatory phase of HCl-induced ARDS can result in pro-fibrotic profiles. It is critical to understand the interaction between MSC and the lung microenvironment before MSC-based therapies are utilized for ARDS. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=acute%20respiratory%20distress%20syndrome%20%28ARDS%29" title="acute respiratory distress syndrome (ARDS)">acute respiratory distress syndrome (ARDS)</a>, <a href="https://publications.waset.org/abstracts/search?q=mesenchymal%20stem%20cells%20%28MSC%29" title=" mesenchymal stem cells (MSC)"> mesenchymal stem cells (MSC)</a>, <a href="https://publications.waset.org/abstracts/search?q=hydrochloric%20acid%20%28HCl%29" title=" hydrochloric acid (HCl)"> hydrochloric acid (HCl)</a>, <a href="https://publications.waset.org/abstracts/search?q=mechanical%20ventilation%20%28MV%29" title=" mechanical ventilation (MV) "> mechanical ventilation (MV) </a> </p> <a href="https://publications.waset.org/abstracts/22549/effects-of-bone-marrow-derived-mesenchymal-stem-cells-msc-in-acute-respiratory-distress-syndrome-ards-lung-remodeling" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/22549.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">670</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">105</span> Electrospun Nanofibrous Scaffolds Modified with Collagen-I and Fibronectin with LX-2 Cells to Study Liver Fibrosis in vitro</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Prativa%20Das">Prativa Das</a>, <a href="https://publications.waset.org/abstracts/search?q=Lay%20Poh%20Tan"> Lay Poh Tan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Three-dimensional microenvironment is a need to study the event cascades of liver fibrosis in vitro. Electrospun nanofibers modified with essential extracellular matrix proteins can closely mimic the random fibrous structure of native liver extracellular matrix (ECM). In this study, we fabricate a series of 3D electrospun scaffolds by wet electrospinning process modified with different ratios of collagen-I to fibronectin to achieve optimized distribution of these two ECM proteins on the fiber surface. A ratio of 3:1 of collagen-I to fibronectin was found to be optimum for surface modification of electrospun poly(lactic-co-glycolic acid) (PLGA) fibers by chemisorption process. In 3:1 collagen-I to fibronectin modified scaffolds the total protein content increased by ~2 fold compared to collagen-I modified and ~1.5 fold compared to 1:1/9:1 collagen-I to fibronectin modified scaffolds. We have cultured LX-2 cells on this scaffold over 14 days and found that LX-2 cells acquired more quiescent phenotype throughout the culture period and shown significantly lower expression of alpha smooth muscle actin and collagen-I. Thus, this system can be used as a model to study liver fibrosis by using different fibrogenic mediators in vitro. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=electrospinning" title="electrospinning">electrospinning</a>, <a href="https://publications.waset.org/abstracts/search?q=collagen-I%20and%20fibronectin" title=" collagen-I and fibronectin"> collagen-I and fibronectin</a>, <a href="https://publications.waset.org/abstracts/search?q=surface%20modification%20of%20fiber" title=" surface modification of fiber"> surface modification of fiber</a>, <a href="https://publications.waset.org/abstracts/search?q=LX-2%20cells" title=" LX-2 cells"> LX-2 cells</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20fibrosis" title=" liver fibrosis"> liver fibrosis</a> </p> <a href="https://publications.waset.org/abstracts/104340/electrospun-nanofibrous-scaffolds-modified-with-collagen-i-and-fibronectin-with-lx-2-cells-to-study-liver-fibrosis-in-vitro" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/104340.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">127</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">104</span> Comparative Stem Cells Therapy for Regeneration of Liver Fibrosis </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=H.%20M.%20Imam">H. M. Imam</a>, <a href="https://publications.waset.org/abstracts/search?q=H.%20M.%20Rezk"> H. M. Rezk</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20F.%20Tohamy"> A. F. Tohamy </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Human umbilical cord blood (HUCB) is considered as a unique source for stem cells. HUCB contain different types of progenitor cells which could differentiate into hepatocytes. Aims: To investigate the potential of rat's liver damage repair using human umbilical cord mesenchymal stem cells (hUCMSCs). We investigated the feasibility for hUCMSCs in recovery from liver damage. Moreover, investigating fibrotic liver repair and using the CCl4-induced model for liver damage in the rat. Methods: Rats were injected with 0.5 ml/kg CCl4 to induce liver damage and progressive liver fibrosis. hUCMSCs were injected into the rats through the tail vein; Stem cells were transplanted at a dose of 1×106 cells/rat after 72 hours of CCl4 injection without receiving any immunosuppressant. After (6 and 8 weeks) of transplantation, blood samples were collected to assess liver functions (ALT, AST, GGT and ALB) and level of Procollagen III as a liver fibrosis marker. In addition, hepatic tissue regeneration was assessed histopathologically and immunohistochemically using antihuman monoclonal antibodies against CD34, CK19 and albumin. Results: Biochemical and histopathological analysis showed significantly increased recovery from liver damage in the transplanted group. In addition, HUCB stem cells transdifferentiated into functional hepatocytes in rats with hepatic injury which results in improving liver structure and function. Conclusion: Our findings suggest that transplantation of hUCMSCs may be a novel therapeutic approach for treating liver fibrosis. Therefore, hUCMSCs are a potential option for treatment of liver cirrhosis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=carbon%20tetra%20chloride" title="carbon tetra chloride">carbon tetra chloride</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20fibrosis" title=" liver fibrosis"> liver fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=mesenchymal%20stem%20cells" title=" mesenchymal stem cells"> mesenchymal stem cells</a>, <a href="https://publications.waset.org/abstracts/search?q=rat" title=" rat"> rat</a> </p> <a href="https://publications.waset.org/abstracts/27746/comparative-stem-cells-therapy-for-regeneration-of-liver-fibrosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/27746.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">342</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">103</span> The Type II Immune Response in Acute and Chronic Pancreatitis Mediated by STAT6 in Murine</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hager%20Elsheikh">Hager Elsheikh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Context: Pancreatitis is a condition characterized by inflammation in the pancreas, which can lead to serious complications if untreated. Both acute and chronic pancreatitis are associated with immune reactions and fibrosis, which further damage the pancreas. The type 2 immune response, primarily driven by alternative activated macrophages (AAMs), plays a significant role in the development of fibrosis. The IL-4/STAT6 pathway is a crucial signaling pathway for the activation of M2 macrophages. Pancreatic fibrosis is induced by dysregulated inflammatory responses and can result in the autodigestion and necrosis of pancreatic acinar cells. Research Aim: The aim of this study is to investigate the impact of STAT6, a crucial molecule in the IL-4/STAT6 pathway, on the severity and development of fibrosis during acute and chronic pancreatitis. The research also aims to understand the influence of the JAK/STAT6 signaling pathway on the balance between fibrosis and regeneration in the presence of different macrophage populations. Methodology: The research utilizes murine models of acute and chronic pancreatitis induced by cerulean injection. Animal models will be employed to study the effect of STAT6 knockout on disease severity and fibrosis. Isolation of acinar cells and cell culture techniques will be used to assess the impact of different macrophage populations on wound healing and regeneration. Various techniques such as PCR, histology, immunofluorescence, and transcriptomics will be employed to analyze the tissues and cells. Findings: The research aims to provide insights into the mechanisms underlying tissue fibrosis and wound healing during acute and chronic pancreatitis. By investigating the influence of the JAK/STAT6 signaling pathway and different macrophage populations, the study aims to understand their impact on tissue fibrosis, disease severity, and pancreatic regeneration. Theoretical Importance: This research contributes to our understanding of the role of specific signaling pathways, macrophage polarization, and the type 2 immune response in pancreatitis. It provides insights into the molecular mechanisms underlying tissue fibrosis and the potential for targeted therapies. Data Collection and Analysis Procedures: Data will be collected through the use of murine models, isolation and culture of acinar cells, and various experimental techniques such as PCR, histology, immunofluorescence, and transcriptomics. Data will be analyzed using appropriate statistical methods and techniques, and the findings will be interpreted in the context of the research objectives. Conclusion: By investigating the mechanisms of tissue fibrosis and wound healing during acute and chronic pancreatitis, this research aims to enhance our understanding of the disease progression and potential therapeutic targets. The findings have theoretical importance in expanding our knowledge of pancreatic fibrosis and the role of macrophage polarization in the context of the type 2 immune response. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=immunity%20in%20chronic%20diseases" title="immunity in chronic diseases">immunity in chronic diseases</a>, <a href="https://publications.waset.org/abstracts/search?q=pancreatitis" title=" pancreatitis"> pancreatitis</a>, <a href="https://publications.waset.org/abstracts/search?q=macrophages" title=" macrophages"> macrophages</a>, <a href="https://publications.waset.org/abstracts/search?q=immune%20response" title=" immune response"> immune response</a> </p> <a href="https://publications.waset.org/abstracts/186332/the-type-ii-immune-response-in-acute-and-chronic-pancreatitis-mediated-by-stat6-in-murine" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/186332.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">34</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">102</span> Phenotypical and Genotypical Diagnosis of Cystic Fibrosis in 26 Cases from East and South Algeria</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yahia%20Massinissa">Yahia Massinissa</a>, <a href="https://publications.waset.org/abstracts/search?q=Yahia%20Mouloud"> Yahia Mouloud</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Cystic fibrosis (CF), the most common lethal genetic disease in the Europe population, is caused by mutations in the transmembrane conductance regulator gene (CFTR). It affects most organs including an epithelial tissue, base of hydroelectrolytic transepithelial transport, notably that aerial ways, the pancreas, the biliary ways, the intestine, sweat glands and the genital tractus. The gene whose anomalies are responsible of the cystic fibrosis codes for a protein Cl channel named CFTR (cystic fibrosis transmembrane conductance regulator) that exercises multiple functions in the cell, one of the most important in control of sodium and chlorine through epithelia. The deficient function translates itself notably by an abnormal production of viscous secretion that obstructs the execrator channels of this target organ: one observes then a dilatation, an inflammation and an atrophy of these organs. It also translates itself by an increase of the concentration in sodium and in chloride in sweat, to the basis of the sweat test. In order to do a phenotypical and genotypical diagnosis at a part of the Algerian population, our survey has been carried on 16 patients with evocative symptoms of the cystic fibrosis at that the clinical context has been confirmed by a sweat test. However, anomalies of the CFTR gene have been determined by electrophoresis in gel of polyacrylamide of the PCR products (polymerase chain reaction), after enzymatic digestion, then visualized to the ultraviolet (UV) after action of the ethidium bromide. All mutations detected at the time of our survey have already been identified at patients attained by this pathology in other populations of the world. However, the important number of found mutation with regard to the one of the studied patients testifies that the origin of this big clinical variability that characterizes the illness in the consequences of an enormous diversity of molecular defects of the CFTR gene. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cystic%20fibrosis" title="cystic fibrosis">cystic fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=CFTR%20gene" title=" CFTR gene"> CFTR gene</a>, <a href="https://publications.waset.org/abstracts/search?q=polymorphism" title=" polymorphism"> polymorphism</a>, <a href="https://publications.waset.org/abstracts/search?q=algerian%20population" title=" algerian population"> algerian population</a>, <a href="https://publications.waset.org/abstracts/search?q=sweat%20test" title=" sweat test"> sweat test</a>, <a href="https://publications.waset.org/abstracts/search?q=genotypical%20diagnosis" title=" genotypical diagnosis"> genotypical diagnosis</a> </p> <a href="https://publications.waset.org/abstracts/10970/phenotypical-and-genotypical-diagnosis-of-cystic-fibrosis-in-26-cases-from-east-and-south-algeria" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/10970.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">310</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">101</span> STAT6 Mediates Local and Systemic Fibrosis and Type Ii Immune Response via Macrophage Polarization during Acute and Chronic Pancreatitis in Murine Model</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hager%20Elsheikh">Hager Elsheikh</a>, <a href="https://publications.waset.org/abstracts/search?q=Matthias%20Sendler"> Matthias Sendler</a>, <a href="https://publications.waset.org/abstracts/search?q=Juliana%20Glaubnitz"> Juliana Glaubnitz</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In pancreatitis, an inflammatory reaction occurs in the pancreatic secretory cells due to premature activation of proteases, leading to pancreatic self-digestion and necrotic cell death of acinar cells. Acute pancreatitis in patients is characterized by a severe immune reaction that could lead to serious complications, such as organ failure or septic shock, if left untreated. Chronic pancreatitis is a recurrence of episodes of acute pancreatitis resulting in a fibro-inflammatory immune response, in which the type 2 immune response is primarily driven by AAMs in the pancreas. One of the most important signaling pathways for M2 macrophage activation is the IL-4/STAT6 pathway. Pancreatic fibrosis is induced by the hyperactivation of pancreatic stellate cells by dysregulation in the inflammatory response, leading to further damage, autodigestion and possibly necrosis of pancreatic acinar cells. The aim of this research is to investigate the effect of STAT6 knockout in disease severity and development of fibrosis wound healing in the presence of different macrophage populations, regulated by the type 2 immune response, after inducing chronic and/or acute pancreatitis in mice models via cerulean injection. We further investigate the influence of the JAK/STAT6 signaling pathway on the balance of fibrosis and regeneration in STAT6 deficient and wild-type mice. The characterization of resident and recruited macrophages will provide insight into the influence of the JAK/STAT6 signaling pathway on infiltrating cells and, ultimately, tissue fibrosis and disease severity. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=acute%20and%20chronic%20pancreatitis" title="acute and chronic pancreatitis">acute and chronic pancreatitis</a>, <a href="https://publications.waset.org/abstracts/search?q=tissue%20regeneration" title=" tissue regeneration"> tissue regeneration</a>, <a href="https://publications.waset.org/abstracts/search?q=macrophage%20polarization" title=" macrophage polarization"> macrophage polarization</a>, <a href="https://publications.waset.org/abstracts/search?q=Gastroenterology" title=" Gastroenterology"> Gastroenterology</a> </p> <a href="https://publications.waset.org/abstracts/173320/stat6-mediates-local-and-systemic-fibrosis-and-type-ii-immune-response-via-macrophage-polarization-during-acute-and-chronic-pancreatitis-in-murine-model" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/173320.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">68</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">100</span> Repositioning Sodium Valproate for Amelioration of Bleomycin-induced Scleroderma: The Role of Oxidative Stress, Transforming Growth Factor Beta-1, and the Mammalian Target of Rapamycin</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ahmed%20M.%20Kabel">Ahmed M. Kabel</a>, <a href="https://publications.waset.org/abstracts/search?q=Maaly%20A.%20Abd%20Elmaaboud"> Maaly A. Abd Elmaaboud</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Scleroderma is one of the connective tissue disorders characterized by skin and systemic fibrosis. Its pathogenesis involves multiple interrelated processes of autoimmunity, vasculopathy, inflammation, and oxidative stress. This study was a trial to explore the possible ameliorative effects of sodium valproate on an experimental model of skin fibrosis induced by bleomycin. Forty male BALB/c mice were divided into four equal groups as follows: control group; bleomycin group; bleomycin + sodium valproate group, and sodium valproate group. Mice were assessed for their body weight every four days throughout the whole study. Skin tissues were used to evaluate the oxidative stress parameters, transforming growth factor beta 1 (TGF-β1), tumor necrosis factor alpha (TNF-α), interleukin 15, and mammalian target of rapamycin (mTOR). Skin fibrosis was evaluated by measuring dermal thickness and staining the skin tissues with Masson trichrome stain. Also, the skin tissues were immunostained with alpha smooth muscle actin (α-SMA). Administration of sodium valproate to bleomycin-treated mice resulted in the restoration of the body weight with a significant decrease in the dermal thickness, amelioration of oxidative stress, suppression of TGF-β1 and mTOR expression, and significant reduction of the percentage of α-SMA immunostaining and the proinflammatory cytokine levels compared to mice treated with bleomycin alone. In conclusion, sodium valproate has an antifibrotic effect on skin fibrosis which may represent a beneficial therapeutic modality for the management of scleroderma. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=scleroderma" title="scleroderma">scleroderma</a>, <a href="https://publications.waset.org/abstracts/search?q=bleomycin" title=" bleomycin"> bleomycin</a>, <a href="https://publications.waset.org/abstracts/search?q=sodium%20valproate" title=" sodium valproate"> sodium valproate</a>, <a href="https://publications.waset.org/abstracts/search?q=skin%20fibrosis" title=" skin fibrosis"> skin fibrosis</a> </p> <a href="https://publications.waset.org/abstracts/157892/repositioning-sodium-valproate-for-amelioration-of-bleomycin-induced-scleroderma-the-role-of-oxidative-stress-transforming-growth-factor-beta-1-and-the-mammalian-target-of-rapamycin" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/157892.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">82</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">99</span> Qualitative Modeling of Transforming Growth Factor Beta-Associated Biological Regulatory Network: Insight into Renal Fibrosis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ayesha%20Waqar%20Khan">Ayesha Waqar Khan</a>, <a href="https://publications.waset.org/abstracts/search?q=Mariam%20Altaf"> Mariam Altaf</a>, <a href="https://publications.waset.org/abstracts/search?q=Jamil%20Ahmad"> Jamil Ahmad</a>, <a href="https://publications.waset.org/abstracts/search?q=Shaheen%20Shahzad"> Shaheen Shahzad</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Kidney fibrosis is an anticipated outcome of possibly all types of progressive chronic kidney disease (CKD). Epithelial-mesenchymal transition (EMT) signaling pathway is responsible for production of matrix-producing fibroblasts and myofibroblasts in diseased kidney. In this study, a discrete model of TGF-beta (transforming growth factor) and CTGF (connective tissue growth factor) was constructed using Rene Thomas formalism to investigate renal fibrosis turn over. The kinetic logic proposed by Rene Thomas is a renowned approach for modeling of Biological Regulatory Networks (BRNs). This modeling approach uses a set of constraints which represents the dynamics of the BRN thus analyzing the pathway and predicting critical trajectories that lead to a normal or diseased state. The molecular connection between TGF-beta, Smad 2/3 (transcription factor) phosphorylation and CTGF is modeled using GenoTech. The order of BRN is CTGF, TGF-B, and SMAD3 respectively. The predicted cycle depicts activation of TGF-B (TGF-β) via cleavage of its own pro-domain (0,1,0) and presentation to TGFR-II receptor phosphorylating SMAD3 (Smad2/3) in the state (0,1,1). Later TGF-B is turned off (0,0,1) thereby activating SMAD3 that further stimulates the expression of CTGF in the state (1,0,1) and itself turns off in (1,0,0). Elevated CTGF expression reactivates TGF-B (1,1,0) and the cycle continues. The predicted model has generated one cycle and two steady states. Cyclic behavior in this study represents the diseased state in which all three proteins contribute to renal fibrosis. The proposed model is in accordance with the experimental findings of the existing diseased state. Extended cycle results in enhanced CTGF expression through Smad2/3 and Smad4 translocation in the nucleus. The results suggest that the system converges towards organ fibrogenesis if CTGF remains constructively active along with Smad2/3 and Smad 4 that plays an important role in kidney fibrosis. Therefore, modeling regulatory pathways of kidney fibrosis will escort to the progress of therapeutic tools and real-world useful applications such as predictive and preventive medicine. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=CTGF" title="CTGF">CTGF</a>, <a href="https://publications.waset.org/abstracts/search?q=renal%20fibrosis%20signaling%20pathway" title=" renal fibrosis signaling pathway"> renal fibrosis signaling pathway</a>, <a href="https://publications.waset.org/abstracts/search?q=system%20biology" title=" system biology"> system biology</a>, <a href="https://publications.waset.org/abstracts/search?q=qualitative%20modeling" title=" qualitative modeling"> qualitative modeling</a> </p> <a href="https://publications.waset.org/abstracts/102386/qualitative-modeling-of-transforming-growth-factor-beta-associated-biological-regulatory-network-insight-into-renal-fibrosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/102386.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">179</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">98</span> Assessment of Hepatosteatosis Among Diabetic and Nondiabetic Patients Using Biochemical Parameters and Noninvasive Imaging Techniques</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Tugba%20Sevinc%20Gamsiz">Tugba Sevinc Gamsiz</a>, <a href="https://publications.waset.org/abstracts/search?q=Emine%20Koroglu"> Emine Koroglu</a>, <a href="https://publications.waset.org/abstracts/search?q=Ozcan%20Keskin"> Ozcan Keskin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aim: Nonalcoholic fatty liver disease (NAFLD) is considered the most common chronic liver disease in the general population. The higher mortality and morbidity among NAFLD patients and lack of symptoms makes early detection and management important. In our study, we aimed to evaluate the relationship between noninvasive imaging and biochemical markers in diabetic and nondiabetic patients diagnosed with NAFLD. Materials and Methods: The study was conducted from (September 2017) to (December 2017) on adults admitted to Internal Medicine and Gastroenterology outpatient clinics with hepatic steatosis reported on ultrasound or transient elastography within the last six months that exclude patients with other liver diseases or alcohol abuse. The data were collected and analyzed retrospectively. Number cruncher statistical system (NCSS) 2007 program was used for statistical analysis. Results: 116 patients were included in this study. Diabetic patients compared to nondiabetics had significantly higher Controlled Attenuation Parameter (CAP), Liver Stiffness Measurement (LSM) and fibrosis values. Also, hypertension, hepatomegaly, high BMI, hypertriglyceridemia, hyperglycemia, high A1c, and hyperuricemia were found to be risk factors for NAFLD progression to fibrosis. Advanced fibrosis (F3, F4) was present in 18,6 % of all our patients; 35,8 % of diabetic and 5,7 % of nondiabetic patients diagnosed with hepatic steatosis. Conclusion: Transient elastography is now used in daily clinical practice as an accurate noninvasive tool during follow-up of patients with fatty liver. Early diagnosis of the stage of liver fibrosis improves the monitoring and management of patients, especially in those with metabolic syndrome criteria. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=diabetes" title="diabetes">diabetes</a>, <a href="https://publications.waset.org/abstracts/search?q=elastography" title=" elastography"> elastography</a>, <a href="https://publications.waset.org/abstracts/search?q=fatty%20liver" title=" fatty liver"> fatty liver</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=metabolic%20syndrome" title=" metabolic syndrome"> metabolic syndrome</a> </p> <a href="https://publications.waset.org/abstracts/98077/assessment-of-hepatosteatosis-among-diabetic-and-nondiabetic-patients-using-biochemical-parameters-and-noninvasive-imaging-techniques" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/98077.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">152</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">97</span> Implementation of Cord- Blood Derived Stem Cells in the Regeneration of Two Experimental Models: Carbon Tetrachloride and S. Mansoni Induced Liver Fibrosis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Manal%20M.%20Kame">Manal M. Kame</a>, <a href="https://publications.waset.org/abstracts/search?q=Zeinab%20A.%20Demerdash"> Zeinab A. Demerdash</a>, <a href="https://publications.waset.org/abstracts/search?q=Hanan%20G.%20El-Baz"> Hanan G. El-Baz</a>, <a href="https://publications.waset.org/abstracts/search?q=Salwa%20M.%20Hassan"> Salwa M. Hassan</a>, <a href="https://publications.waset.org/abstracts/search?q=Faten%20M.%20Salah"> Faten M. Salah</a>, <a href="https://publications.waset.org/abstracts/search?q=Wafaa%20Mansour"> Wafaa Mansour</a>, <a href="https://publications.waset.org/abstracts/search?q=Olfat%20Hammam"> Olfat Hammam</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Cord blood (CB) derived Unrestricted Somatic Stem Cells (USSCs) with their multipotentiality hold great promise in liver regeneration. This work aims at evaluation of the therapeutic potentiality of USSCs in two experimental models of chronic liver injury induced either by S. mansoni infection in balb/c mice or CCL4 injection in hamsters. Isolation, propagation, and characterization of USSCs from CB samples were performed. USSCs were induced to differentiate into osteoblasts, adipocytes and hepatocyte-like cells. Cells of the third passage were transplanted in two models of liver fibrosis: (1) Twenty hamsters were induced to liver fibrosis by repeated i. p. injection of 100 μl CCl4 /hamster for 8 weeks. This model was designed as; 10 hamsters with liver fibrosis and treated with i.h. injection of 3x106 USSCs (USSCs transplanted group), 10 hamsters with liver fibrosis (pathological control group), and 10 hamsters with healthy livers (normal control group). (2) Murine chronics S.mansoni model: twenty mice were induced to liver fibrosis with S. mansoni ceracariae (60 cercariae/ mouse) using the tail immersion method and left for 12 weeks. This model was designed as; 10 mice with liver fibrosis were transplanted with i. v. injection of 1×106 USCCs (USSCs transplanted group). Other 2 groups were designed as in hamsters model. Animals were sacrificed 12 weeks after USSCs transplantation, and their liver sections were examined for detection of human hepatocyte-like cells by immunohistochemistry staining. Moreover, liver sections were examined for fibrosis level, and fibrotic indices were calculated. Sera of sacrificed animals were tested for liver functions. CB USSCs, with fibroblast-like morphology, expressed high levels of CD44, CD90, CD73 and CD105 and were negative for CD34, CD45, and HLA-DR. USSCs showed high expression of transcripts for Oct4 and Sox2 and were in vitro differentiated into osteoblasts, adipocytes. In both animal models, in vitro induced hepatocyte-like cells were confirmed by cytoplasmic expression of glycogen, alpha-fetoprotein, and cytokeratin18. Livers of USSCs transplanted group showed engraftment with human hepatocyte-like cells as proved by cytoplasmic expression of human alpha-fetoprotein, cytokeratin18, and OV6. In addition, livers of this group showed less fibrosis than the pathological control group. Liver functions in the form of serum AST & ALT level and serum total bilirubin level were significantly lowered in USSCs transplanted group than pathological control group (p < 0.001). Moreover, the fibrotic index was significantly lower (p< 0.001) in USSCs transplanted group than pathological control group. In addition liver sections, of i. v. injection of 1×106 USCCs of mice, stained with either H&E or sirius red showed diminished granuloma size and a relative decrease in hepatic fibrosis. Our experimental liver fibrosis models transplanted with CB-USSCs showed liver engraftment with human hepatocyte-like cells as well as signs of liver regeneration in the form of improvement in liver function assays and fibrosis level. These data provide hope that human CB- derived USSCs are introduced as multipotent stem cells with great potentiality in regenerative medicine & strengthens the concept of cellular therapy for the treatment of liver fibrosis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cord%20blood" title="cord blood">cord blood</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20fibrosis" title=" liver fibrosis"> liver fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=stem%20cells" title=" stem cells"> stem cells</a>, <a href="https://publications.waset.org/abstracts/search?q=transplantation" title=" transplantation"> transplantation</a> </p> <a href="https://publications.waset.org/abstracts/30937/implementation-of-cord-blood-derived-stem-cells-in-the-regeneration-of-two-experimental-models-carbon-tetrachloride-and-s-mansoni-induced-liver-fibrosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/30937.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">309</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">96</span> A Sub-Conjunctiva Injection of Rosiglitazone for Anti-Fibrosis Treatment after Glaucoma Filtration Surgery</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yang%20Zhao">Yang Zhao</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng%20Zhang"> Feng Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Xuanchu%20Duan"> Xuanchu Duan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Trans-differentiation of human Tenon fibroblasts (HTFs) to myo-fibroblasts and fibrosis of episcleral tissue are the most common reasons for the failure of glaucoma filtration surgery, with limited treatment options like antimetabolites which always have side-effects such as leakage of filter bulb, infection, hypotony, and endophthalmitis. Rosiglitazone, a specific thiazolidinedione is a synthetic high-affinity ligand for PPAR-r, which has been used in the treatment of type2 diabetes, and found to have pleiotropic functions against inflammatory response, cell proliferation and tissue fibrosis and to benefit to a variety of diseases in animal myocardium models, steatohepatitis models, etc. Here, in vitro we cultured primary HTFs and stimulated with TGF- β to induced myofibrogenic, then treated cells with Rosiglitazone to assess for fibrogenic response. In vivo, we used rabbit glaucoma model to establish the formation of post- trabeculectomy scarring. Then we administered subconjunctival injection with Rosiglitazone beside the ﬁltering bleb, later protein, mRNA and immunofluorescence of fibrogenic markers are checked, and filtering bleb condition was measured. In vitro, we found Rosiglitazone could suppressed proliferation and migration of fibroblasts through macroautophagy via TGF- β /Smad signaling pathway. In vivo, on postoperative day 28, the mean number of ﬁbroblasts in Rosiglitazone injection group was signiﬁcantly the lowest and had the least collagen content and connective tissue growth factor. Rosiglitazone effectively controlled human and rabbit fibroblasts in vivo and in vitro. Its subconjunctiiva application may represent an effective, new avenue for the prevention of scarring after glaucoma surgery. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title="fibrosis">fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=glaucoma" title=" glaucoma"> glaucoma</a>, <a href="https://publications.waset.org/abstracts/search?q=macroautophagy" title=" macroautophagy"> macroautophagy</a>, <a href="https://publications.waset.org/abstracts/search?q=rosiglitazone" title=" rosiglitazone"> rosiglitazone</a> </p> <a href="https://publications.waset.org/abstracts/73539/a-sub-conjunctiva-injection-of-rosiglitazone-for-anti-fibrosis-treatment-after-glaucoma-filtration-surgery" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/73539.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">274</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">95</span> Application of Deep Learning and Ensemble Methods for Biomarker Discovery in Diabetic Nephropathy through Fibrosis and Propionate Metabolism Pathways</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Oluwafunmibi%20Omotayo%20Fasanya">Oluwafunmibi Omotayo Fasanya</a>, <a href="https://publications.waset.org/abstracts/search?q=Augustine%20Kena%20Adjei"> Augustine Kena Adjei</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Diabetic nephropathy (DN) is a major complication of diabetes, with fibrosis and propionate metabolism playing critical roles in its progression. Identifying biomarkers linked to these pathways may provide novel insights into DN diagnosis and treatment. This study aims to identify biomarkers associated with fibrosis and propionate metabolism in DN. Analyze the biological pathways and regulatory mechanisms of these biomarkers. Develop a machine learning model to predict DN-related biomarkers and validate their functional roles. Publicly available transcriptome datasets related to DN (GSE96804 and GSE104948) were obtained from the GEO database (https://www.ncbi.nlm.nih.gov/gds), and 924 propionate metabolism-related genes (PMRGs) and 656 fibrosis-related genes (FRGs) were identified. The analysis began with the extraction of DN-differentially expressed genes (DN-DEGs) and propionate metabolism-related DEGs (PM-DEGs), followed by the intersection of these with fibrosis-related genes to identify key intersected genes. Instead of relying on traditional models, we employed a combination of deep neural networks (DNNs) and ensemble methods such as Gradient Boosting Machines (GBM) and XGBoost to enhance feature selection and biomarker discovery. Recursive feature elimination (RFE) was coupled with these advanced algorithms to refine the selection of the most critical biomarkers. Functional validation was conducted using convolutional neural networks (CNN) for gene set enrichment and immunoinfiltration analysis, revealing seven significant biomarkers—SLC37A4, ACOX2, GPD1, ACE2, SLC9A3, AGT, and PLG. These biomarkers are involved in critical biological processes such as fatty acid metabolism and glomerular development, providing a mechanistic link to DN progression. Furthermore, a TF–miRNA–mRNA regulatory network was constructed using natural language processing models to identify 8 transcription factors and 60 miRNAs that regulate these biomarkers, while a drug–gene interaction network revealed potential therapeutic targets such as UROKINASE–PLG and ATENOLOL–AGT. This integrative approach, leveraging deep learning and ensemble models, not only enhances the accuracy of biomarker discovery but also offers new perspectives on DN diagnosis and treatment, specifically targeting fibrosis and propionate metabolism pathways. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=diabetic%20nephropathy" title="diabetic nephropathy">diabetic nephropathy</a>, <a href="https://publications.waset.org/abstracts/search?q=deep%20neural%20networks" title=" deep neural networks"> deep neural networks</a>, <a href="https://publications.waset.org/abstracts/search?q=gradient%20boosting%20machines%20%28GBM%29" title=" gradient boosting machines (GBM)"> gradient boosting machines (GBM)</a>, <a href="https://publications.waset.org/abstracts/search?q=XGBoost" title=" XGBoost"> XGBoost</a> </p> <a href="https://publications.waset.org/abstracts/194139/application-of-deep-learning-and-ensemble-methods-for-biomarker-discovery-in-diabetic-nephropathy-through-fibrosis-and-propionate-metabolism-pathways" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/194139.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">9</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">94</span> Insulin Resistance in Patients with Chronic Hepatitis C Virus Infection: Upper Egypt Experience</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ali%20Kassem">Ali Kassem</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: In the last few years, factors such as insulin resistance (IR) and hepatic steatosis have been linked to progression of hepatic fibrosis.Patients with chronic liver disease, and cirrhosis in particular, are known to be prone to IR. However, chronic HCV (hepatitis C) infection may induce IR, regardless of the presence of liver cirrhosis. Our aims are to study insulin resistance (IR) assessed by HOMA-IR (Homeostatic Model Assessment Insulin Resistance) as a possible risk factor in disease progression in cirrhotic patients and to evaluate the role of IR in hepatic fibrosis progression. The correlations of HOMA-IR values to laboratory, virological and histopathological parameters of chronic HCV are also examined. Methods: The study included 50 people divided into 30 adult chronic hepatitis C patients diagnosed by PCR (polymerase chain reaction) within previous 6 months and 20 healthy controls. The functional and morphological status of the liver were evaluated by ultrasonography and laboratory investigations including liver function tests and by liver biopsy. Fasting blood glucose and fasting insulin levels were measured and body mass index and insulin resistance were calculated. Patients having HOMA-IR >2.5 were labeled as insulin resistant. Results: Chronic hepatitis C patients with IR showed significantly higher mean values of BMI (body mass index) and fasting insulin than those without IR (P < 0.000). Patients with IR were more likely to have steatosis (p = 0.006), higher necroinflammatory activity (p = 0.05). No significant differences were found between the two groups regarding hepatic fibrosis. Conclusion: HOMA-IR measurement could represent a novel marker to identify the cirrhotic patients at greater risk for the progression of liver disease. As IR is a potentially modifiable risk factor, these findings may have important prognostic and therapeutic implications. Assessment of IR by HOMA-IR and improving insulin sensitivity are recommended in patients with HCV and related chronic liver disease. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hepatic%20fibrosis" title="hepatic fibrosis">hepatic fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=hepatitis%20C%20virus%20infection" title=" hepatitis C virus infection"> hepatitis C virus infection</a>, <a href="https://publications.waset.org/abstracts/search?q=hepatic%20steatosis" title=" hepatic steatosis"> hepatic steatosis</a>, <a href="https://publications.waset.org/abstracts/search?q=insulin%20resistance" title=" insulin resistance"> insulin resistance</a> </p> <a href="https://publications.waset.org/abstracts/94698/insulin-resistance-in-patients-with-chronic-hepatitis-c-virus-infection-upper-egypt-experience" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/94698.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">154</span> </span> </div> </div> <ul class="pagination"> <li class="page-item disabled"><span class="page-link">&lsaquo;</span></li> <li class="page-item active"><span class="page-link">1</span></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=fibrosis&page=2">2</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=fibrosis&page=3">3</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=fibrosis&page=4">4</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=fibrosis&page=5">5</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=fibrosis&page=2" 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