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fibrosis</title> <meta name="description" content="Search results for: interstitial fibrosis"> <meta name="keywords" content="interstitial 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 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action="https://publications.waset.org/abstracts/search"> <div 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="interstitial 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> 202</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: interstitial fibrosis</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">202</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">201</span> Plasma Levels of Collagen Triple Helix Repeat Containing 1 (CTHRC1) as a Potential Biomarker in Interstitial Lung Disease</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Rijnbout-St.James%20Willem">Rijnbout-St.James Willem</a>, <a href="https://publications.waset.org/abstracts/search?q=Lindner%20Volkhard"> Lindner Volkhard</a>, <a href="https://publications.waset.org/abstracts/search?q=Scholand%20Mary%20Beth"> Scholand Mary Beth</a>, <a href="https://publications.waset.org/abstracts/search?q=Ashton%20M.%20Tillett"> Ashton M. Tillett</a>, <a href="https://publications.waset.org/abstracts/search?q=Di%20Gennaro%20Michael%20Jude"> Di Gennaro Michael Jude</a>, <a href="https://publications.waset.org/abstracts/search?q=Smith%20Silvia%20Enrica"> Smith Silvia Enrica</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Fibrosing lung diseases are characterized by changes in the lung interstitium and are classified based on etiology: 1) environmental/exposure-related, 2) autoimmune-related, 3) sarcoidosis, 4) interstitial pneumonia, and 4) idiopathic. Among interstitial lung diseases (ILD) idiopathic forms, idiopathic pulmonary fibrosis (IPF) is the most severe. Pathogenesis of IPF is characterized by an increased presence of proinflammatory mediators, resulting in alveolar injury, where injury to alveolar epithelium precipitates an increase in collagen deposition, subsequently thickening the alveolar septum and decreasing gas exchange. Identifying biomarkers implicated in the pathogenesis of lung fibrosis is key to developing new therapies and improving the efficacy of existing therapies. The transforming growth factor-beta (TGF-B1), a mediator of tissue repair associated with WNT5A signaling, is partially responsible for fibroblast proliferation in ILD and is the target of Pirfenidone, one of the antifibrotic therapies used for patients with IPF. Canonical TGF-B signaling is mediated by the proteins SMAD 2/3, which are, in turn, indirectly regulated by Collagen Triple Helix Repeat Containing 1 (CTHRC1). In this study, we tested the following hypotheses: 1) CTHRC1 is more elevated in the ILD cohort compared to unaffected controls, and 2) CTHRC1 is differently expressed among ILD types. Material and Methods: CTHRC1 levels were measured by ELISA in 171 plasma samples from the deidentified University of Utah ILD cohort. Data represent a cohort of 131 ILD-affected participants and 40 unaffected controls. CTHRC1 samples were categorized by a pulmonologist based on affectation status and disease subtypes: IPF (n = 45), sarcoidosis (4), nonspecific interstitial pneumonia (16), hypersensitivity pneumonitis (n = 7), interstitial pneumonia (n=13), autoimmune (n = 15), other ILD - a category that includes undifferentiated ILD diagnoses (n = 31), and unaffected controls (n = 40). We conducted a single-factor ANOVA of plasma CTHRC1 levels to test whether CTHRC1 variance among affected and non-affected participants is statistically significantly different. In-silico analysis was performed with Ingenuity Pathway Analysis® to characterize the role of CTHRC1 in the pathway of lung fibrosis. Results: Statistical analyses of CTHRC1 in plasma samples indicate that the average CTHRC1 level is significantly higher in ILD-affected participants than controls, with the autoimmune ILD being higher than other ILD types, thus supporting our hypotheses. In-silico analyses show that CTHRC1 indirectly activates and phosphorylates SMAD3, which in turn cross-regulates TGF-B1. CTHRC1 also may regulate the expression and transcription of TGFB-1 via WNT5A and its regulatory relationship with CTNNB1. Conclusion: In-silico pathway analyses demonstrate that CTHRC1 may be an important biomarker in ILD. Analysis of plasma samples indicates that CTHRC1 expression is positively associated with ILD affectation, with autoimmune ILD having the highest average CTHRC1 values. While characterizing CTHRC1 levels in plasma can help to differentiate among ILD types and predict response to Pirfenidone, the extent to which plasma CTHRC1 level is a function of ILD severity or chronicity is unknown. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=interstitial%20lung%20disease" title="interstitial lung disease">interstitial lung disease</a>, <a href="https://publications.waset.org/abstracts/search?q=CTHRC1" title=" CTHRC1"> CTHRC1</a>, <a href="https://publications.waset.org/abstracts/search?q=idiopathic%20pulmonary%20fibrosis" title=" idiopathic pulmonary fibrosis"> idiopathic pulmonary fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=pathway%20analyses" title=" pathway analyses"> pathway analyses</a> </p> <a href="https://publications.waset.org/abstracts/142833/plasma-levels-of-collagen-triple-helix-repeat-containing-1-cthrc1-as-a-potential-biomarker-in-interstitial-lung-disease" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/142833.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">191</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">200</span> Experimental and Finite Element Forming Limit Diagrams for Interstitial Free Steels</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Basavaraj%20Vadavadagi">Basavaraj Vadavadagi</a>, <a href="https://publications.waset.org/abstracts/search?q=Satishkumar%20Shekhawat"> Satishkumar Shekhawat</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Interstitial free steels posses better formability and have many applications in automotive industries. Forming limit diagrams (FLDs) indicate the formability of materials which can be determined by experimental and finite element (FE) simulations. FLDs were determined experimentally by LDH test, utilizing optical strain measurement system for measuring the strains in different width specimens and by FE simulations in Interstitial Free (IF) and Interstitial Free High Strength (IFHS) steels. In this study, the experimental and FE simulated FLDs are compared and also the stress based FLDs were investigated. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=forming%20limit%20diagram" title="forming limit diagram">forming limit diagram</a>, <a href="https://publications.waset.org/abstracts/search?q=limiting%20dome%20height" title=" limiting dome height"> limiting dome height</a>, <a href="https://publications.waset.org/abstracts/search?q=optical%20strain%20measurement" title=" optical strain measurement"> optical strain measurement</a>, <a href="https://publications.waset.org/abstracts/search?q=interstitial" title=" interstitial"> interstitial</a> </p> <a href="https://publications.waset.org/abstracts/3534/experimental-and-finite-element-forming-limit-diagrams-for-interstitial-free-steels" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/3534.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">231</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">199</span> Protection against Sodium Arsenate Induced Fetal Toxicity in Albino Mice by Vitamin C and E</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Fariha%20Qureshi">Fariha Qureshi</a>, <a href="https://publications.waset.org/abstracts/search?q=Mohammad%20Tahir"> Mohammad Tahir</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Epidemiological evidences indicated that arsenic contamination in drinking water increased the incidence of spontaneous abortion, stillbirth and premature babies in pregnant women. This study was designed to investigate the protective role of vitamin C&E against sodium arsenate induced fetal toxicity in albino mice. Twenty-four pregnant albino mice of BALB/c strain were randomly divided into 4 groups having 6 animals in each. Group A1 served as control and was injected with 0.1ml/kg/day distilled water I/P for 18 days. Groups A2,A3 & A4 received single I/P injection of sodium arsenate 35mg/kg on 8th gestational day, whereas groups A3 and A4 were also given Vitamin C and E by I/P injection, 9 mg/kg/day and 15 mg/kg/day respectively, starting from 8th GD and continued for the rest of the pregnancy period. The early implantation sites, fetal resorptions, weight of live fetuses and crown rump length were recorded. Gross morphological examination was carried out for malformations. Fetal kidneys were extracted for histological and micrometric analysis. Group A2 exhibited an increased incidence of abortion, fetal resorptions, significant decrease in number of litter and fetal weight; the difference of means was statistically significant among the groups (p<0.000). In group A2 fetal kidneys presented glomerulonephritis with acute tubular necrotic changes and interstitial fibrosis. Groups A3&A4 showed statistically significant improvement in these parameters. The results revealed the antioxidant potential of Vitamin C and E in protecting against arsenic induced fetal toxicity in mice. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=fetal%20toxicity" title="fetal toxicity">fetal toxicity</a>, <a href="https://publications.waset.org/abstracts/search?q=fetal%20resorptions" title=" fetal resorptions"> fetal resorptions</a>, <a href="https://publications.waset.org/abstracts/search?q=interstitial%20fibrosis" title=" interstitial fibrosis"> interstitial fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=tocopherol" title=" tocopherol"> tocopherol</a> </p> <a href="https://publications.waset.org/abstracts/12402/protection-against-sodium-arsenate-induced-fetal-toxicity-in-albino-mice-by-vitamin-c-and-e" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/12402.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">272</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">198</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">197</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">196</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">195</span> Effect of Rituximab Therapy Depending on the Age of Disease Onset in Systemic Sclerosis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Liudmila%20Garzanova">Liudmila Garzanova</a>, <a href="https://publications.waset.org/abstracts/search?q=Lidia%20Ananyeva"> Lidia Ananyeva</a>, <a href="https://publications.waset.org/abstracts/search?q=Olga%20Koneva"> Olga Koneva</a>, <a href="https://publications.waset.org/abstracts/search?q=Olga%20Ovsyannikova"> Olga Ovsyannikova</a>, <a href="https://publications.waset.org/abstracts/search?q=Oxana%20Desinova"> Oxana Desinova</a>, <a href="https://publications.waset.org/abstracts/search?q=Mayya%20Starovoytova"> Mayya Starovoytova</a>, <a href="https://publications.waset.org/abstracts/search?q=Rushana%20Shayahmetova"> Rushana Shayahmetova</a>, <a href="https://publications.waset.org/abstracts/search?q=Anna%20Khelkovskaya-Sergeeva"> Anna Khelkovskaya-Sergeeva</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objectives. The age of the disease onset could have an impact on the effect of therapy in systemic sclerosis(SSc). Late-age onset in SSc could have a more severe course of the disease and worse clinical effects on therapy. The aim of our study was to evaluate changes in skin fibrosis on rituximab(RTX) therapy in patients with SSc and different ages of the disease onset. Methods. 151 patients with SSc were included in this study. Patients were divided into groups depending on the age of the disease onset: group 1 - younger than 30 years (40 patients(26%), group 2 - 31-59 years (90 patients(60%) and group 3 – more than 60 years (21 patients(14%). The mean follow-up period was 13±2.3month. The mean age was 48±13years, female-83% of patients, and the diffuse cutaneous subset of the disease had 52% of patients. The mean disease duration was 6.4±5years. The cumulative mean dose of RTX was 1.5±0.6grams. Patients received RTX as a therapy for interstitial lung disease. All patients received prednisone at a dose of 11.6±4.8mg/day, immunosuppressants received 48% of them. The results at baseline and at the end of the follow-up are presented in the form of mean values. Results. There was a significant decrease of modified Rodnan skin score(mRss) in all groups: in group 1 - from 10.2±8 to 7.7±6.5(p=0.01); in group 2 - from 9±7.2 to 6.2±4.7(p=0.0001); in group 3 - from 20.5±14.1 to 10.8±9.4(p=0.001). There was a significant decrease of the activity index (EScSG-AI): in group 1 from 2.5±1.8 to 1.3±1.1; in group 2 – from 3.2±1.6 to 1.5±1.2; in group 3 – from 4.2±2.1 to 1.3±1. Conclusion. There was a significant improvement in skin fibrosis in a year after initiation of RTX therapy regardless of the age of the disease onset. The improvement was more pronounced in the group with late-age onset of the disease, but these data require further investigations. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=skin%20fibrosis" title="skin fibrosis">skin fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=systemic%20sclerosis" title=" systemic sclerosis"> systemic sclerosis</a>, <a href="https://publications.waset.org/abstracts/search?q=rituximab" title=" rituximab"> rituximab</a>, <a href="https://publications.waset.org/abstracts/search?q=disease%20onset" title=" disease onset"> disease onset</a> </p> <a href="https://publications.waset.org/abstracts/189249/effect-of-rituximab-therapy-depending-on-the-age-of-disease-onset-in-systemic-sclerosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/189249.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">31</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">194</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">193</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">192</span> Histopatological Analysis of Vital Organs in Cattle Infected with Lumpy Skin Disease in Rajasthan, India</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Manisha">Manisha</a>, <a href="https://publications.waset.org/abstracts/search?q=Manisha%20Mathur"> Manisha Mathur</a>, <a href="https://publications.waset.org/abstracts/search?q=Jay%20K.%20Desai"> Jay K. Desai</a>, <a href="https://publications.waset.org/abstracts/search?q=Shesh%20Asopa"> Shesh Asopa</a>, <a href="https://publications.waset.org/abstracts/search?q=Manisha%20Mehra"> Manisha Mehra</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The present study was carried out for the comprehensive analysis of lumpy skin disease (LSD) in cattle and to elucidate the histopathology of vital organs in natural outbreaks. Lumpy skin disease (LSD) is a viral infection that primarily affects cattle. It is caused by a Capri pox virus and is characterized by the formation of skin nodules or lesions. For this study, a postmortem of 20 cows who died of Lumpy skin disease in different regions of Rajasthan was conducted. This study aimed to examine a cow's external and internal organs to confirm if lumpy skin disease was the cause of death. Accurate diagnosis is essential for improving disease surveillance, understanding the disease's progression, and informing control measures. Pathological examinations reveal virus-induced changes across organs, while histopathological analyses provide crucial insights into the disease's pathogenesis, aiding in the development of advanced diagnostics and effective prevention strategies. Histopathological examination of nodular skin lesions revealed edema, hyperemia, acanthosis, severe hydropic degeneration/ballooning degeneration, and hyperkeratosis in the epidermis. In the lungs, congestion, oedema, emphysema, and atelectasis were observed grossly. Microscopically changes were suggestive of interstitial pneumonia, suppurative pneumonia, bronchopneumonia post pneumonic fibrosis, and stage of resolution. Grossely liver showed congestion and necrotic foci microscopically in most of the cases, and the liver showed acute viral hepatitis. Microscopically in kidneys, multifocal interstitial nephritis was observed. There was marked interstitial inflammation and zonal fibrosis with cystically dilated tubules and bowman's capsules. Microscopically, most of the heart tissue section showed normal histology with few sarcocysts in between cardiac muscles. In some cases, loss of cross striation, sarcoplasmic vacuolation, fregmentation, and disintegration of cardiac fibres were observed. The present study revealed the characteristic gross and histopathological changes in different organs in natural cases of lumpy skin disease. Further, the disease was confirmed based on the molecular diagnosis and transmission electron microscopy of capripox infection in the affected cattle in the study area. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Capripoxvirus" title="Capripoxvirus">Capripoxvirus</a>, <a href="https://publications.waset.org/abstracts/search?q=lumpy%20skin%20disease" title=" lumpy skin disease"> lumpy skin disease</a>, <a href="https://publications.waset.org/abstracts/search?q=polymerage%20chain%20reaction" title=" polymerage chain reaction"> polymerage chain reaction</a>, <a href="https://publications.waset.org/abstracts/search?q=transmission%20electron%20microscopy" title=" transmission electron microscopy"> transmission electron microscopy</a> </p> <a href="https://publications.waset.org/abstracts/189333/histopatological-analysis-of-vital-organs-in-cattle-infected-with-lumpy-skin-disease-in-rajasthan-india" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/189333.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">25</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">191</span> Sudden Death of a Cocaine Body Packer: An Autopsy Examination Findings</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Parthasarathi%20Pramanik">Parthasarathi Pramanik</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Body packing is a way of transfer drugs across the international border or any drug prohibited area. The drugs are usually hidden in body packets inside the anatomical body cavities like mouth, intestines, rectum, ear, vagina etc. Cocaine is a very common drug for body packing across the world. A 48 year old male was reported dead in his hotel after complaining of chest pain and vomiting. At autopsy, there were eighty-two white cylindrical body packs in the stomach, small and large intestines. Seals of few of the packets were opened. Toxicological examination revealed presence of cocaine in the stomach, liver, kidney and hair samples. Microscopically, presence of myocardial necrosis with interstitial oedema along with hypertrophy and fibrosis of the myocardial fibre suggested heart failure due to cocaine cardio toxicity. However, focal lymphocyte infiltration and perivascular fibrosis in the myocardium also indicated chronic cocaine toxicity of the deceased. After careful autopsy examination it was considered the victim was died due congestive heart failure secondary to acute and chronic cocaine poisoning. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cardiac%20failure" title="cardiac failure">cardiac failure</a>, <a href="https://publications.waset.org/abstracts/search?q=cocaine" title=" cocaine"> cocaine</a>, <a href="https://publications.waset.org/abstracts/search?q=body%20packer" title=" body packer"> body packer</a>, <a href="https://publications.waset.org/abstracts/search?q=sudden%20death" title=" sudden death"> sudden death</a> </p> <a href="https://publications.waset.org/abstracts/54469/sudden-death-of-a-cocaine-body-packer-an-autopsy-examination-findings" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/54469.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">319</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">190</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">20</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">189</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">188</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">187</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">186</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">185</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">184</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">183</span> The Microstructure of Aging ZnO, AZO, and GZO Films</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Zue%20Chin%20Chang">Zue Chin Chang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shih-Chang%20Liang"> Shih-Chang Liang</a> </p> <p class="card-text"><strong>Abstract:</strong></p> RF magnetron sputtering is used on the ceramic targets, each of which contains zinc oxide (ZnO), zinc oxide doped with aluminum (AZO) and zinc oxide doped with gallium (GZO). The electric conduction mechanism of the AZO and GZO films came mainly from the Al and Ga, the oxygen vacancies, Zn interstitial atoms, and Al and/or Ga interstitial atoms. AZO and GZO films achieved higher conduction than did ZnO film, it being ion vacant and nonstoichiometric. The XRD analysis showed a preferred orientation along the (002) plane for ZnO, AZO, and GZO films. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ZnO" title="ZnO">ZnO</a>, <a href="https://publications.waset.org/abstracts/search?q=AZO" title=" AZO"> AZO</a>, <a href="https://publications.waset.org/abstracts/search?q=GZO" title=" GZO"> GZO</a>, <a href="https://publications.waset.org/abstracts/search?q=doped" title=" doped"> doped</a>, <a href="https://publications.waset.org/abstracts/search?q=sputtering" title=" sputtering"> sputtering</a> </p> <a href="https://publications.waset.org/abstracts/4918/the-microstructure-of-aging-zno-azo-and-gzo-films" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/4918.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">396</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">182</span> Detection of Leptospira interrogans in Kidney and Urine of water Buffalo and its Relationship with Histopathological and Serological Findings</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=M.%20R.%20Haji%20Hajikolaei">M. R. Haji Hajikolaei</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20A.%20Nikvand"> A. A. Nikvand</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20R.%20Ghadrdan"> A. R. Ghadrdan</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20Ghorbanpoor"> M. Ghorbanpoor</a>, <a href="https://publications.waset.org/abstracts/search?q=B.%20Mohammadian"> B. Mohammadian</a> </p> <p class="card-text"><strong>Abstract:</strong></p> This study was carried out on water buffalo for detection of Leptospira interrogans in kidney and urine and its relationship with serological findings. Blood, urine and kidney samples were taken immediately after slaughter from 353 water buffalos at Ahvaz abattoir in Khouzestan province, Iran. Sera were initially screened at serum dilution of 1:100 against seven live antigens of Leptospira interrogans: pomona, hardjo, ballum, icterohemorrhagiae, tarasovi, australis and grippotyphosa using the microscopic agglutination test (MAT) and sera with positive results were titrated against reacting antigens in serial twofold dilution from 1:100 to 1:800. The samples of kidney were embedded in paraffin wax and 5µm thick sections were stained routinely with Haematoxylin and Eosin (H&E). Polymerase chain reaction (PCR) examination was done on urine and kidney by using LipL32 gene primers. Antibodies against one or more serovars at dilution >:100 were detected in sera. The most frequent reactor was hardjo (56.2%), followed by pomona (52.3%), australis (9.8%), tarassovi (5.9%), grippotyphosa (4.5%) and icterohaemorrhagiae (3.9%). The L. interrogans were detected in 43 (12.2%) of examined buffaloes, so that 26 (8.2%) of kidney tissues, 14 (4.8%) of urine samples separately and 3 (0.84%) of both kidney and urine samples were positive in PCR. From 153 (43.3%) buffaloes with positive MAT, 24 cases were positive by PCR of kidney and/or urine samples, synchronously. Renal lesions such as interstitial nephritis, acute tubular necrosis (ATN), pyelonephritis, glomerolonephritis, renal fibrosis and hydronephrosis were found in 128 (36.3%) cases. Statistical analysis indicated that there was no significant association between results of MAT, PCR and interstitial nephritis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=leptospiral%20infection" title="leptospiral infection">leptospiral infection</a>, <a href="https://publications.waset.org/abstracts/search?q=PCR" title=" PCR"> PCR</a>, <a href="https://publications.waset.org/abstracts/search?q=MAT" title=" MAT"> MAT</a>, <a href="https://publications.waset.org/abstracts/search?q=histopathology" title=" histopathology"> histopathology</a>, <a href="https://publications.waset.org/abstracts/search?q=river%20buffalo" title=" river buffalo"> river buffalo</a> </p> <a href="https://publications.waset.org/abstracts/39412/detection-of-leptospira-interrogans-in-kidney-and-urine-of-water-buffalo-and-its-relationship-with-histopathological-and-serological-findings" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/39412.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">332</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">181</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">180</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">179</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">178</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">177</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">176</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">126</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">175</span> Overview and Pathophysiology of Radiation-Induced Breast Changes as a Consequence of Radiotherapy Toxicity</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Monika%20Rezacova">Monika Rezacova</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Radiation-induced breast changes are a consequence of radiotherapy toxicity over the breast tissues either related to targeted breast cancer treatment or other thoracic malignancies (eg. lung cancer). This study has created an overview of different changes and their pathophysiology. The main conditions included were skin thickening, interstitial oedema, fat necrosis, dystrophic calcifications, skin retractions, glandular atrophy, breast fibrosis and radiation induced breast cancer. This study has performed focused literature search through multiple databases including pubmed, medline and embase. The study has reviewed English as well as non English publications. As a result of the literature the study provides comprehensive overview of radiation-induced breast changes and their pathophysiology with small focus on new development and prevention. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=radiotherapy%20toxicity" title="radiotherapy toxicity">radiotherapy toxicity</a>, <a href="https://publications.waset.org/abstracts/search?q=breast%20tissue%20changes" title=" breast tissue changes"> breast tissue changes</a>, <a href="https://publications.waset.org/abstracts/search?q=breast%20cancer%20treatment" title=" breast cancer treatment"> breast cancer treatment</a>, <a href="https://publications.waset.org/abstracts/search?q=radiation-induced%20breast%20changes" title=" radiation-induced breast changes"> radiation-induced breast changes</a> </p> <a href="https://publications.waset.org/abstracts/137891/overview-and-pathophysiology-of-radiation-induced-breast-changes-as-a-consequence-of-radiotherapy-toxicity" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/137891.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">159</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">174</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">173</span> Hydrogeological Factors of the Ore Genesis in the Sedimentary Basins</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=O.%20Abramova">O. Abramova</a>, <a href="https://publications.waset.org/abstracts/search?q=L.%20Abukova"> L. Abukova</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20Goreva"> A. Goreva</a>, <a href="https://publications.waset.org/abstracts/search?q=G.%20Isaeva"> G. Isaeva</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The present work was made for the purpose of evaluating the interstitial water’s role in the mobilization of metal elements of clay deposits and occurrences in sedimentary formation in the hydro-geological basins. The experiments were performed by using a special facility, which allows adjusting the pressure, temperature, and the frequency of the acoustic vibrations. The dates for study were samples of the oil shales (Baltic career, O<sub>2</sub>kk) and clay rocks, mainly montmorillonite composition (Borehole SG-12000, the depth of selection 1000–3600 m, the Azov-Kuban trough, N<sub>1</sub>). After interstitial water squeezing from the rock samples, decrease in the original content of the rock forming components including trace metals V, Cr, Co, Ni, Cu, Zn, Zr, Mo, Pb, W, Ti, and others was recorded. The experiments made it possible to evaluate the ore elements output and organic matters with the interstitial waters. Calculations have shown that, in standard conditions, from each ton of the oil shales, 5-6 kg of ore elements and 9-10 kg of organic matter can be escaped. A quantity of matter, migrating from clays in the process of solidification, is changed depending on the lithogenesis stage: more recent unrealized deposits lose more ore and organic materials than the clay rocks, selected from depth over 3000 m. Each ton of clays in the depth interval 1000-1500 m is able to generate 3-5 kg of the ore elements and 6-8 kg of the organic matters. The interstitial waters are a freight forwarder over transferring these matters in the reservoir beds. It was concluded that the interstitial waters which escaped from the study samples are solutions with abnormal high concentrations of the metals and organic matters. In the discharge zones of the sediment basins, such fluids can create paragenetic associations of the sedimentary-catagenetic ore and hydrocarbon mineral resources accumulations. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hydrocarbons" title="hydrocarbons">hydrocarbons</a>, <a href="https://publications.waset.org/abstracts/search?q=ore%20genesis" title=" ore genesis"> ore genesis</a>, <a href="https://publications.waset.org/abstracts/search?q=paragenesis" title=" paragenesis"> paragenesis</a>, <a href="https://publications.waset.org/abstracts/search?q=pore%20water" title=" pore water"> pore water</a> </p> <a href="https://publications.waset.org/abstracts/49058/hydrogeological-factors-of-the-ore-genesis-in-the-sedimentary-basins" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/49058.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">258</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=interstitial%20fibrosis&page=2">2</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=interstitial%20fibrosis&page=3">3</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=interstitial%20fibrosis&page=4">4</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=interstitial%20fibrosis&page=5">5</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=interstitial%20fibrosis&page=6">6</a></li> <li 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