[Summary]_ Severe hypertriglyceridemia is the third common cause of acute pancreatitis following after alcohol abuse and cholelithiasis. Moreover, it is also an important risk factor of cardiovascular events. However, the cases of severe hypertriglyceridemia caused by autoimmune disease were rare in clinical, which would bring the difficulty for diagnosis and treatment. A better understanding of the clinical characteristics, possible pathogenesis, and corresponding therapy of the disease would be helpful, which would reduce the risk of complications, and finally improve both the survival rate as well as quality of life of these patients.

[Summary] In newly diagnosed diabetic patients, fasting plasma glucose, HbA1C , and plasma lipid profiles were measured to analyze the association between HbA1C and plasma lipid profiles. HbA1C might affect plasma lipid profiles in newly diagnosed diabetic patients. Higher HbA1C was associated with the worse plasma lipid profiles and more severe insulin resistance.

OBJECTIVE To clarify the long-term toxicity to the respiratory system in a rat model of acute lung injury (ALI) induced by a single low-dose of perfluoroisobutylene(PFIB) inhalation expo?sure,and observe the possible beneficial effect of early intervention via Qingkailing(QKL) injection. METHODS Totally 224 male Wistar rats were randomly divided into 4 groups:normal control group in which air exposure was followed by a saline 10 mL · kg-1(ip),QKL control group in which QKL 10 mL · kg-1 was ip given after air exposure,PFIB exposure group in which rats were exposed to PFIB 280 mg·m-3 for 5 min only,and QKL treatment group in which QKL 10 mL·kg-1 was given ip at 1 h after PFIB exposure. Lung functions of rats were measured at 24 h,3,6,12,24,36 and 48 weeks after exposure. The arterial blood gas,lung coefficient,protein content in bronchoalveolar lavage fluid(BALF),hydroxy?proline(HYP) content in lung tissue and plasma,and other indicators were detected or analyzed. RESULTS Within 24 h after PFIB exposure,the lung coefficient and protein content in BALF were increased significantly(P<0.01),whereas the PaO2(P<0.01) and SaO2(P<0.05) indices in arterial blood decreased significantly in PFIB group compared with normal control. The inhalation time , exhalation time,tidal volume(TV),expired volume(EV)and relaxed time were reduced significantly (P<0.01). However,all the above indicators returned to normal in 3 weeks,but TV,EV and peak expiratory flow were significantly lower than in normal group at 48 weeks(P<0.05). HYP contents in lung tissues,compared with normal control(P<0.05),were reduced significantly within 24 h after PFIB exposure,increased significantly in 6 weeks(P<0.05),then returned to normal in 12 weeks. HYP contents in plasma increased significantly compared with normal control(P<0.05) within 24 h after PFIB exposure but returned to normal in 3 weeks. The protein contents in BALF of QKL treatment group were significantly lower than those in PFIB group(P<0.01) within 24 h after PFIB exposure. From 24 h to 24 weeks after PFIB exposure,changes of pulmonary functions were similar to those in PFIB group. At 48 weeks,TV and EV in QKL treatment group were more significantly increased than those in PFIB group(P<0.05). CONCLUSION Rats with ALI induced by a single low dose of PFIB exposure undergo compensatory repair except for pulmonary capacity and pulmonary ventilation functions. Early treatment with QKL reduces protein content of BALF and alleviates pulmonary edema,and has some beneficial effect on lung function recovery later.

Objective To observe the abdominal ultrasonic manifestations of children with Langerhans cells histiocytosis (LCH).Methods Imaging features of histopathologically proved LCH in 28 children were retrospectively analyzed.Results Among 28 eases,multi system involvement was found in 25 cases,while only liver and bile duct involvement were detected in 3 cases.Different degrees of enlarged liver,inhomogeneous echo of liver parenchyma,scattered or diffuse hypoechoic regions were found in all 28 cases.Uneven thickening and echo enhancement of the bile duct wall,as well as local expansion or stricture of bile duct cavity were found in 13 cases.Splenomegaly was found in 17 cases,swelling of the pancreas was found in 5 cases,varying degrees of ascites were found in 13 cases,and hepatic hilar lymphadenectasis were found in 14 cases.Conclusion There are specific ultrasonographic manifestations of LCH in children,which may be helpful to improving diagnostic accuracy of LCH.

OBJECTIVETo investigate the effect of polyethylene oxide (PEO) on renal blood flow and its renoprotective effect in rabbits with endotoxin sepsis.

METHODSTwenty normal New Zealand white rabbits were randomly divided into normal saline (NS) group and PEO group (n=10), and endotoxin shock was induced by an intravenous injection of 0.6 mg/kg lipopolysaccharide. Resuscitation was performed when the blood pressure of the rabbits showed a 30% decline, using NS (in NS group) or the mixture of equal volumes of NS and 20 ng/g PEO (in PEO group) perfused at the rate of 5 ml/kg per hour. Before and during shock and at 1 h after resuscitation, the renal hemodynamics was monitored by ultrasound and the venous blood was extracted to examine the renal functions. The heart rate and arterial blood pressure were monitored throughout the experiment.

RESULTSThe rabbits in both groups showed a significantly lower renal artery blood flow velocity during the shock (P<0.05) with significantly increased pulsatility index (PI) and resistance index (RI) compared with those before the shock. One hour after resuscitation, the blood flow velocity in the renal arteries at all levels and the tertiary veins were reduced in NS group without obvious reduction of the PI and RI; in PEO group, the blood flow velocities in the renal arteries increased significantly compared to those before shock (P<0.05), and the PI and RI of the tertiary arteries were significantly lower than those in NS group (P<0.05). In both groups, BUN and Cr increased during endotoxin shock stage, and 1 h after resuscitation, PEO group showed significantly lower BUN and Cr levels than NS group (P<0.05).

CONCLUSIONA small dose of PEO can significantly promote renal perfusion in rabbits with septic shock, thus offering renoprotective effect against early damage in septicopyemia and septic shock.

Animals ; Hemodynamics ; Polyethylene Glycols ; pharmacology ; therapeutic use ; Rabbits ; Renal Circulation ; Shock, Septic ; drug therapy ; physiopathology

Objective To investigate the effect of nucleotide-binding oligomerization domaincontaining protein 1 (NOD1) on pyroptosis in hepatic ischemia-reperfusion injury.Methods An animal model of ischemia-reperfusion injury was established.Thirty healthy,male,and clean C57 BL mice were randomly divided into sham operation group (sham group) and ischemia-reperfusion group (IR,including 2 h,6 h,12 h,24 h subgroups),6 per group.Serum ALT and AST levels in each group were measured by blood biochemistry.HE staining and TUNEL were used to observe the pathological changes of liver and hepatocyte apoptosis.Immunohistochemistry was used to detect the expression and distribution of NOD1 in each group.Western blotting was used to detect NOD1,MM2,pro-Caspase-1 and active-Caspase-1 expression.NOD1 siRNA and empty control siRNA were transfected into AML12 cells,then the hypoxia/reoxygenation model was established and cells were collected to detect the expression of NOD1,AIM2 and active-Caspase-1.Results The ALT and AST levels in IR group were significantly higher than those in sham group,and peaked at IR 12-h subgroup (P＜0.05).HE staining showed that hepatic injury was the most severe at 12 h after reperfusion.TUNEL results showed that the number of apoptotic cells was the greated at 12 h after reperfusion.Western blotting showed that NOD1 protein expression was highest at 12 h after reperfusion.With the prolongation of reperfusion time,the expression of AIM2 and active-Caspase-1 gradually increased,and that of pro-Caspase-1 gradually decreased.The expression of NOD1,AIM2 and activeCaspase-1 decreased after transfection of NOD1 siRNA into AML12 cells.Conclusions NOD1 promotes liver ischemia-reperfusion injury,which may be related to NOD1 promoting liver injury by activating pyroptosis.

Objective:To explore the effect of miR-223-3p regulating FOXO3a-mediated autophagy in hepatic injury-reperfusion injury (LIRI).Methods:The model of hepatic ischemia-reperfusion injury (IR) was established in C57BL6 mice. According to different reperfusion timepoints, mice were randomly divided into 2 h, 6 h, 12 h and 24 h group. For sham group, there was no intraoperative clamping of hepatic pedicle. Murine hepatic AML12 cells were treated with miR-223-3p mimics, miR-223-3p inhibitor and FOXO3a interfering RNA. A hypoxic 1 h reoxygenation 6 h model was established. And miRNA-NC, miR-223-3p mimics, miR-223-3p inhibitor and siRNA-NC and FOXO3a siRNA groups were assigned. Hepatic injury and apoptosis were detected by hematoxylin eosin or TdT-mediated nick end labeling (HE/TUNEL) at different timepoints. The changes of proliferating cell nuclear antigen (PCNA) and Caspase-3 in hepatocytes were detected by immunohistochemistry. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were employed for detecting the expressions of miR-223-3p, FOXO3a, LC3, p62 and Caspase-3 in hepatocytes.Results:The results of HE/TUNEL indicated that reperfusion injury and apoptosis of hepatic tissue were most severe in 12 h group. In hepatic ischemia-reperfusion model, RT-PCR results showed that the expressions of miR-223-3p and FOXO3a were higher in IR group than those in sham group (1.00±0), the expression level of miR-223-3p mRNA peaked at 12 h (9.13±2.12) after reperfusion and FOXO3a was the highest at 6 h (5.23±0.90, P<0.05). Western blot showed that the expression of FOXO3a peaked at 6 h post-reperfusion and the expressions of LC3 and caspase-3 were the highest at 12 h. ( P<0.05). In the model of cell hypoxia and reoxygenation, RT-PCR indicated that the expression of FOXO3a mRNA decreased in miR-223-3p mimics group (0.45±0.21) as compared with miRNA-NC group (1.00±0). In contrast, miR-223-3p inhibitor group increased (2.73±0.53, P<0.05). Western blot indicated that FOXO3a protein expression was highest in miR-223-3p inhibitor and miR-223-3p mimics groups whereas LC3 and Caspase-3 were the highest in miR-223-3p mimics group ( P<0.05). The expression of FOXO3a was higher in siRNA-NC group than that in FOXO3a siRNA group while the expressions of Caspase-3 and LC3 were the higher in FOXO3a siRNA group. Conclusions:FOXO3a has protective effect on hepatic ischemia-reperfusion injury. It may be related to its inhibition of autophagy and apoptosis and miR-223-3p promotes injury through a down-regulation of FOXO3a-mediated autophagy. It suggests that miR-223-3p and FOXO3a are negatively correlated and may be potential gene therapeutic targets for hepatic injury.

Objective To investigate the mRNA expression of liver receptor homolog 1 (LRH-1) gene in patients with cholesterol gallstone disease so that to elucidate the biomolecular pathogenesis of gallstone for- mation.Methods Twenty-seven patients with cholesterol gallstone (CGS) and 14 controls were included in this study.Biliary composition was assayed and mRNA expression of hepatic LRH 1 gene was determined by real time polymorphism chain reaction.Results In CGS patients,expression of LRH-1 was significantly higher than that in controls (14.18?9.37 vs 7.86?6.19,P＜0.05),and cholesterol of bile was oversaturated (1.17?0.27).Conclusion The formation of CGS may be related to increased expression of hepatic LRH-1 gene.

Objective To investigate the role of miRNA-30a-3p on inhibiting the proliferation,invasion and metastasis of HCC cells by targeting Caspase 1 involved in pyroptosis.Methods The qRT-PCR and immunohistochemical staining were used to detect the expressions of miRNA-30a-3p and Caspase 1 in HCC cells.SMMC-7721 cells were transfected with miR-30a-3p agonists,inhibitors and Caspase 1-specific inhibitors.Western blot was obtained to detect the expression of EMT-related proteins (N-cadherin,vimentin,snail,MMP-2) and Caspase 1,IL-18 and IL-1β.Plate clone assay,CCK-8 kit and Transwell were carried out to detect the proliferation and immigration of HCC cells.Results Caspase 1 was highly expressed (t =17.54,P ＜ 0.05) in HCC tissues.Overexpression of miR-30a-3p inhibited HCC cells proliferation and metastasis,while miR-30a-3p inhibition increased the proliferation and metastasis of HCC cells.Overexpression of miR-30a-3p decreased the expression of Caspase 1 (t =12.73,P ＜ 0.05) and inhibited the induction of pyroptosis,inhibiting the expression of IL-18 (t =7.32,P ＜ 0.05) and IL-1 β (t =7.32,P ＜0.05).When miRNA-30a-3p was inhibited,the cell viability of HCC was increased (F1 =9.57,P ＜0.05).When miRNA-30a-3p and Caspase 1 were inhibited together,the cell viability of HCC decreased (F2 =10.66,P ＜ 0.05).Conclusion MiRNA-30a-3p regulate cell pyroptosis through Caspase 1 pathway,inhibiting the proliferation,invasion and metastasis of HCC cells.

In order to cultivate talents who fuel and lead medical innovation, it is critical to implement medical English writing "Golden Course" in the substantial development of English teaching in medical universities. Based on the guidelines issued by the Ministry of Education, this paper proposes five principles in the construction of medical English writing "Golden Course", suggests the integration of big data technology, and explores approaches to construct "Golden Course" in terms of teaching objectives, curriculum design, models of instruction, curriculum evaluation and teaching staff.