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Anatomical study of Rubens'flap in breast reconstruction
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作者 Ru Chen Lan Mu +4 位作者 Han Zhang Yan Zhang wen-yue liu Yi-Ping Yan Wei-Wei Chen 《Journal of Hainan Medical University》 2019年第18期1-4,共4页
Objective:To investigate the anatomical basis of Rubens'flap based on the deep circumflex iliac artery,and to apply more donor site tissue amount for big chest wall defect.Methods:Gross anatomical study was carrie... Objective:To investigate the anatomical basis of Rubens'flap based on the deep circumflex iliac artery,and to apply more donor site tissue amount for big chest wall defect.Methods:Gross anatomical study was carried on 8 sides of fresh specimens of 4 cases and data was measured by mean of the Vernier caliper.Besides,the surgical simulation was carried on 1 specimen(2 sides).Results:At the inguinal segment,the via artery gave off(9.16±6.22)branches;the diameter of the origin was(3.97±0.86)mm;the distance from starting point to the first branch was(15.87±9.24)mm;amount of osteomusculocutaneous branch was 3.12±1.34;the biggest diameter of perforator was(1.48±1.02)mm;pedicle length was(132.51±48.24)mm.In the surgical simulation,the layers of Ruben's flap from up to down ranged in skin,subcutaneous tissue,obliquus externus abdominis,oblique internal abdominis and transversus abdominis.Conclusion:Rubens'flap,with large tissue amount,based on the deep circumflex iliac artery,near to traditional abdominal flap,has a good clinical application prospect in breast reconstruction and repair of big chest wall defect,for its thin waist effect and slight donor site defect. 展开更多
关键词 Rubens's FLAP Deep circumflex ILIAC ARTERY BREAST reconstruction ANATOMY
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COVID-19 and Liver Dysfunction:Current Insights and Emergent Therapeutic Strategies 被引量:21
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作者 Gong Feng Kenneth I.Zheng +6 位作者 Qin-Qin Yan Rafael S.Rios Giovanni Targher Christopher D.Byrne Sven Van Poucke wen-yue liu Ming-Hua Zheng 《Journal of Clinical and Translational Hepatology》 SCIE 2020年第1期18-24,共7页
The outbreak of coronavirus disease 2019(COVID-19),caused by the severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),has attracted increasing worldwide attention.Cases of liver damage or dysfunction(mainly cha... The outbreak of coronavirus disease 2019(COVID-19),caused by the severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),has attracted increasing worldwide attention.Cases of liver damage or dysfunction(mainly characterized by moderately elevated serum aspartate aminotransferase lev-els)have been reported among patients with COVID-19.However,it is currently uncertain whether the COVID-19-related liver damage/dysfunction is due mainly to the viral infection per se or other coexisting conditions,such as the use of potentially hepatotoxic drugs and the coexistence of sys-temic inflammatory response,respiratory distress syndrome-induced hypoxia,and multiple organ dysfunction.Based on the current evidence from case reports and case series,this review article focuses on the demographic and clinical characteristics,potential mechanisms,and treatment options for COVID-19-related liver dysfunction.This review also describes the geo-graphical and demographic distribution of COVID-19-related liver dysfunction,as well as possible underlying mechanisms linking COVID-19 to liver dysfunction,in order to facilitate future drug development,prevention,and control measures for COVID-19. 展开更多
关键词 COVID-19 Liver dysfunction SARS-CoV-2
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Associations of Hydroxysteroid 17-beta Dehydrogenase 13 Variants with Liver Histology in Chinese Patients with Metabolicassociated Fatty Liver Disease 被引量:2
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作者 wen-yue liu Mohammed Eslam +11 位作者 Kenneth I.Zheng Hong-Lei Ma Rafael S.Rios Min-Zhi Lv Gang Li Liang-Jie Tang Pei-Wu Zhu Xiao-Dong Wang Christopher D.Byrne Giovanni Targher Jacob George Ming-Hua Zheng 《Journal of Clinical and Translational Hepatology》 SCIE 2021年第2期194-202,共9页
Background and Aims:In Europeans,variants in the hydroxysteroid 17-beta dehydrogenase 13(HSD17B13)gene impact liver histology in metabolic-associated fatty liver disease(MAFLD).The impact of these variants in ethnic C... Background and Aims:In Europeans,variants in the hydroxysteroid 17-beta dehydrogenase 13(HSD17B13)gene impact liver histology in metabolic-associated fatty liver disease(MAFLD).The impact of these variants in ethnic Chinese is unknown.The aim of this study was to investigate the potential associations in Chinese patients.Methods:In total,427 Han Chinese with biopsy-confirmed MAFLD were enrolled.Two single nucleotide polymorphisms in HSD17B13 were genotyped:rs72613567 and rs6531975.Logistic regression was used to test the association between the single nucleotide polymorphisms and liver histology.Results:In our cohort,the minor allele TA of the rs72613567 variant was related to an increased risk of fibrosis[odds ratio(OR):2.93(1.20–7.17),p=0.019 for the additive model;OR:3.32(1.39–7.91),p=0.007 for the recessive model],representing an inverse association as compared to the results from European cohorts.In contrast,we observed a protective effect on fibrosis for the minor A allele carriers of the HSD17B13 rs6531975 variant[OR:0.48(0.24–0.98),p=0.043 for the additive model;OR:0.62(0.40–0.94),p=0.025 for the dominant model].HSD17B13 variants were only associated with fibrosis but no other histological features.Furthermore,HSD17B13 rs6531975 modulated the effect of PNPLA3 rs738409 on hepatic steatosis.Conclusions:HSD17B13 rs72613567 is a risk variant for fibrosis in a Han Chinese MAFLD population but with a different direction for allelic association to that seen in Europeans.These data exemplify the need for studying diverse populations in genetic studies in order to fine map genome-wide association studies signals. 展开更多
关键词 Metabolic-associated fatty liver disease(MAFLD) Nonalcoholic fatty liver disease(NAFLD) Hydroxysteroid 17-beta dehydrogenase 13(HSD17B13) Single nucleotide polymorphism(SNP)
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Metabolic Acidosis in Critically Ill Cirrhotic Patients with Acute Kidney Injury 被引量:1
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作者 Dan-Qin Sun Lai Zhang +5 位作者 Chen-Fei Zheng wen-yue liu Kenneth I.Zheng Xiao-Ming Chen Ming-Hua Zheng Wei-Jie Yuan 《Journal of Clinical and Translational Hepatology》 SCIE 2019年第2期112-121,共10页
Background and Aims:The metabolic acid-base disorders have a high incidence of acute kidney injury(AKI)in critically ill cirrhotic patients(CICPs).The aims of our study were to ascertain the composition of metabolic a... Background and Aims:The metabolic acid-base disorders have a high incidence of acute kidney injury(AKI)in critically ill cirrhotic patients(CICPs).The aims of our study were to ascertain the composition of metabolic acidosis of CICPs with AKI and explore its relationship with hospital mortality.Methods:Three-hundred and eighty consecutive CICPs with AKI were eligible for the cohort study.Demographic,clinical and laboratory parameters were recorded and arterial acid-base state was analyzed by the Stewart and Gilfix methodology.Results:Net metabolic acidosis,lactic acidosis,acidosis owing to unmeasured anions,acidemia,and dilutional acidosis were less frequent in the non-survival group compared to the survival group of CICPs.The presence of acidemia,acidosis owing to unmeasured anions,and lactic acidosis were independently associated with increased risk of intensive care unit 30-day mortality,with hazard ratios of 2.11(95%confidence interval(CI):1.43–3.12),3.38(95%CI:2.36–4.84),and 2.16(95%CI:1.47–3.35),respectively.After full adjustment for confounders,the relationship between acidosis owing to unmeasured anions with hospital mortality was still significant,with hazard ratio of 2.29(95%CI:1.22–4.30).Furthermore,arterial lactate concentration in combination with chronic liver failure-sequential organ failure assessment and BEUMA had the strongest ability to differentiate 30-day mortality(area under the receiver operating characteristic curve:0.79,95%CI:0.74–0.83). 展开更多
关键词 Metabolic acidosis Critically ill cirrhotic patients Acute kidney injury Hospital morality
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Interaction of SAMM50-rs738491,PARVB-rs5764455 and PNPLA3-rs738409 Increases Susceptibility to Nonalcoholic Steatohepatitis
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作者 Ke Xu Kenneth IZheng +10 位作者 Pei-Wu Zhu wen-yue liu Hong-Lei Ma Gang Li Liang-Jie Tang Rafael SRios Giovanni Targher Christopher DByrne Xiao-Dong Wang Yong-Ping Chen Ming-Hua Zheng 《Journal of Clinical and Translational Hepatology》 SCIE 2022年第2期219-229,共11页
Background and Aims:Previous studies have reported that the single nucleotide polymorphisms(SNPs)of SAMM50-rs738491,PARVB-rs5764455 and PNPLA3-rs738409 are associated with nonalcoholic fatty liver disease(NAFLD).Howev... Background and Aims:Previous studies have reported that the single nucleotide polymorphisms(SNPs)of SAMM50-rs738491,PARVB-rs5764455 and PNPLA3-rs738409 are associated with nonalcoholic fatty liver disease(NAFLD).However,no studies have examined the effect of interactions between these three genotypes to affect liver disease severity.We assessed the effect of these three SNPs on nonalcoholic steatohepatitis(NASH)and also examined the gene-gene interactions in a Chinese population with biopsy-confirmed NAFLD.Methods:We enrolled 415 consecutive adult individuals with biopsy-proven NAFLD.Multivariable logistic regres-sion analysis was undertaken to test associations between NASH and SNPs in SAMM50-rs738491,PARVB-rs5764455 and PNPLA3-rs738409.Gene-gene interactions were ana-lyzed by performing a generalized multifactor dimensionality reduction(GMDR)analysis.Results:The mean±standard deviation age of these 415 patients was 41.3±12.5 years,and 75.9%were men.Patients with SAMM50-rs738491 TT,PARVB-rs5764455 AA or PNPLA3-rs738409 GG genotypes had a higher risk of NASH,even after adjustment for age,sex and body mass index.GMDR analysis showed that the combination of all three SNPs was the best model for predicting NASH.Additionally,the odds ratio of the haplotype T-A-G for predicting the risk of NASH was nearly three times higher than that of the haplotype G-C-C.Conclusions:NAFLD patients carrying the SAMM50-rs738491 TT,PARVB-rs5764455 AA or PNPLA3-rs738409 GG genotypes are at greater risk of NASH.These three SNPs may synergistically interact to increase susceptibility to NASH. 展开更多
关键词 Gene polymorphisms Gene-gene interaction SAMM50 PARVB PNPLA3 NASH
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