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From April 2017 to April 2018, three male patients aged 46-71 years with large area burns were treated in our hospital. Acute acalculous cholecystitis (AAC) symptoms of the patients began to appear 15-81 days after injury. AAC was diagnosed 24-81 days after injury. Ultrasound-guided percutaneous transhepatic cholecystostomy was performed 26-82 days after injury. The symptoms subsided in 2 patients, and cholecystectomy was performed in 1 patient with gallbladder perforation 94 days after injury. The patients were cured and discharged 41-118 days after injury. No recurrence of cholecystitis occurred during 8-9 months of follow-up after discharge.
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Objective To observe the efficacy of different degrees of portal vein ligation on portal pressure and liver regeneration of the unligated lobe in rats.Methods Seventy-two healthy male SpragueDawley rats were randomly divided into three groups:group A (sham,n =24);group B (n =24) undergoing 70％ portal vein ligation;group C (n =24) undergoing 90％ portal vein ligation.And then the portal pressure and liver regeneration rate (HRR) of the unligated lobe were detected immcdiately and postoperatively at each observation time point in each group.The serum alanine aminotransferase (ALT),aspartate aminotransferase (AST),hepatic proliferating cell nuclear antigen (PCNA) were compared at each observation time point,and the histological changes were observed by HE staining.Results The HRR of the unligated lobe in group B and group C increased obviously postoperatively at each time point,and the HRR in group C was significantly higher than that in group B [(220.1 ± 4.3) ％,(246.3 ± 5.6) ％,(261.4 ±2.3)％ vs (128.2 ±3.7)％,(143.4 ±8.7)％,(150.7 ±7.0)％,P＜0.05].The serum ALT and AST increased obviously on day 1 and then gradually declined,and the serum ALT and AST in group C was significantly higher than those in group B on day 1 [(821.7 ± 158.3) U/L,(1 372.0 ± 376.2) U/L vs (398.6 ± 80.4) U/L,(860.4 ± 80.0) U/L,P ＜ 0.05].The immediate portal pressure in both groups were obviously increased postoperatively and then gradually declined,and the portal pressure in group C was higher than that in group B at each observation time point [(23.5 ± 1.1)cmH2O,(18.8 ±0.9)cmH2O,(17.8±1.0)cmH2O,(16.6 ±1.0)cmH2O,(15.9±1.3)cmH2O vs (17.4 ±1.0)cmH2O,(16.5 ±1.2)cmH2O,(15.3±1.0)cmH2O,(10.2±1.2)cmH2O,(10.0±1.1)cmH2O,P＜0.05].ThePCNA index in group C was higher than that in group B on day 1 and3 [(21.5 ±1.1)％,(28.2±1.3)％ vs (12.8 ± 2.1) ％,(18.8 ± 1.9) ％,P ＜ 0.05].More foca1 necrosis of the unligated lobe were observed in group C on day 1,which were more than those in group B.Conclusion Higher degree of portal vein ligation could cause higher portal pressure,which leads to the greater regeneration of the unligated lobe.
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<p><b>OBJECTIVE</b>To investigate the changes in peripheral blood Th17 and CD4(+)CD25(+) regulatory T (Treg) cells and their significance among children with hand, foot and mouth disease (HFMD).</p><p><b>METHODS</b>Eighty-nine children with HFMD, including 55 cases of common HFMD and 34 cases of severe HFMD, were included in the study; and 30 healthy children were selected as the control group. The percentages of Th17 and CD4(+)CD25(+) Treg cells in CD4(+) T cells in peripheral blood were determined by flow cytometry. The expression levels of interleukin (IL)-10, transforming growth factor-β (TGF-β), and IL-17 were measured by enzyme-linked immunosorbent assay.</p><p><b>RESULTS</b>Compared with the control group, the cases of common HFMD and severe HFMD had significantly increased levels of Th17 cells and IL-17 (P<0.05) but significantly decreased levels of CD4(+)CD25(+) Treg cells, IL-10, and TGF-β (P<0.05). The severity of the HFMD was positively correlated with the levels of Th17 cells and IL-17 in peripheral blood but negatively correlated with the levels of CD4(+)CD25(+) Treg cells, IL-10, and TGF-β.</p><p><b>CONCLUSIONS</b>Children with HFMD have increased response of Th17 cells but decreased response of CD4(+)CD25(+) Treg cells in peripheral blood. Th17/CD4(+)CD25(+) Treg cell imbalance may play an important role in the pathogenesis of HFMD.</p>