Diagnostic approaches for pancreatic tuberculosis

To the Editor:Pancreatic tuberculosis refers to tuberculosis of pancreas and peripancreatic lymph nodes due to both conditions having similar clinical manifestations and therapeutic regimens[1,2].It is a rare entity worldwide,which is often shown as mass and treated by the unnecessary surgery due to misdiagnosis as pancreatic malignancy[1,2].

Ubiquitin-conjugating enzyme E2T knockdown suppresses hepatocellular tumorigenesis via inducing cell cycle arrest and apoptosis

BACKGROUND Hepatocellular carcinoma(HCC)is now the most common primary liver malignancy worldwide,and multiple risk factors attribute to the occurrence and development of HCC.Recently,increasing studies suggest that ubiquitinconjugating enzyme E2T(UBE2T)serves as a promising prognostic factor in human cancers,although the molecular mechanism of UBE2T in HCC remains unclear.AIM To investigate the clinical relevance and role of UBE2T in HCC development.METHODS UBE2T expression in HCC tissues from the TCGA database and its association with patient survival were analyzed.A lentivirus-mediated strategy was used to knock down UBE2T in HCC cells.qRT-PCR and Western blot assays were performed to check the effect of UBE2T silencing in HCC cells.Cell growth in vitro and in vivo was analyzed by multiparametric high-content screening and the xenograft tumorigenicity assay,respectively.Cell cycle distribution and apoptosis were determined by flow cytometry.The genes regulated by UBE2T were profiled by microarray assay.RESULTS UBE2T was overexpressed in HCC tissues compared with paired and non-paired normal tissues.High expression of UBE2T predicted a poor overall survival in HCC patients.In vitro,lentivirus-mediated UBE2T knockdown significantly reduced the viability of both SMMC-7721 and BEL-7404 cells.In vivo,the xenograft tumorigenesis of SMMC-7721 cells was largely attenuated by UBE2T silencing.The cell cycle was arrested at G1/S phase in SMMC-7721 and BEL-7404 cells with UBE2T knockdown.Furthermore,apoptosis was increased by UBE2T knockdown.At the molecular level,numerous genes were dysregulated after UBE2T silencing,including IL-1B,FOSL1,PTGS2,and BMP6.CONCLUSION UBE2T plays an important role in cell cycle progression,apoptosis,and HCC development.

Progressive liver injury and increased mortality risk in COVID-19 patients:A retrospective cohort study in China

BACKGROUND Liver injury is common and also can be fatal,particularly in severe or critical patients with coronavirus disease 2019(COVID-19).AIM To conduct an in-depth investigation into the risk factors for liver injury and into the effective measures to prevent subsequent mortality risk.METHODS A retrospective cohort study was performed on 440 consecutive patients with relatively severe COVID-19 between January 28 and March 9,2020 at Tongji Hospital,Wuhan,China.Data on clinical features,laboratory parameters,medications,and prognosis were collected.RESULTS COVID-19-associated liver injury more frequently occurred in patients aged≥65 years,female patients,or those with other comorbidities,decreased lymphocyte count,or elevated D-dimer or serum ferritin(P<0.05).The disease severity of COVID-19 was an independent risk factor for liver injury(severe patients:Odds ratio[OR]=2.86,95%confidence interval[CI]:1.78-4.59;critical patients:OR=13.44,95%CI:7.21-25.97).The elevated levels of on-admission aspartate aminotransferase and total bilirubin indicated an increased mortality risk(P<0.001).Using intravenous nutrition or antibiotics increased the risk of COVID-19-associated liver injury.Hepatoprotective drugs tended to be of assistance to treat the liver injury and improve the prognosis of patients with COVID-19-associated liver injury.CONCLUSION More intensive monitoring of aspartate aminotransferase or total bilirubin is recommended for COVID-19 patients,especially patients aged≥65 years,female patients,or those with other comorbidities.Drug hepatotoxicity of antibiotics and intravenous nutrition should be alert for COVID-19 patients.

Effect of paraoxonase1 gene polymorphism on carotid plaque and cerebral infarction in Hainan population

Objective:To investigate the effect of paraoxonase 1 gene polymorphism on carotid plaque stability with cerebral infarction in Hainan population.Methods:277 patients of caroticl plaque With cerebral infarction who underwent physical examination in a hospital in Hainan from 2015 to another awarding 2018 were selected as the experimental group and the 363 people who no cerebral infarction as the Analytical methods:control group.The clinical data analyzed.DNA was collected from peripheral blood of two groups of patients and genotyped by flight mass analytical methods.''AG and GG could be detected by rs3917538.The distribution frequencies of The three genotypes in The control group accorded with Hardy-Weinberg equilibrium.Results:The distribution frequencies of AA,AG and GG in the control group were 97(26.7%),175(48.2%)and 91(25.1%)respectively.In the experimental group,the distribution frequencies were 76(27.4%),136(49.1%)and 65(23.5%).There were no statistical differences among the three detection methods of co-dominant model,Dominant model and recessive model.There was no difference in the frequency of allele A and G between groups.Conclusion:Polymorphism of paraoxonase 1 gene rs3917538 has No significant effect on carotid plaque formation and cerebral infarction in Hainan population.The Supplementary sample size to add more SNP research sites for further study,It is expected to further Revral the relationship between PON1and carotial piaque complicatecl with cerebral infarction in Hainan.