Objective To analyze the clinical characteristics of autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) and AIH/PSC or/PBC overlap syndrome in order to further understand the autoimmune liver diseases (AILD). Methods One hundred and nine patients with AILDs confirmed pathologically were collected between Jan. 2004 and June 2006. Of 109 patients, AIH was found in 27 eases, PBC in 67 cases, PSC in 4 eases, AIH-PSC overlap syndrome in 1 case and AIH-PBC overlap syndrome in 10 cases. The clinical and laboratory data of all patients were assessed retrospectively. Results The AILD was predominantly found in middle-aged women (73.3% ,80/109), and the main clinical manifestations were jaundice, malaise, anorexia and pruritus. The age distribution of patients with AIH showed a single peak at 50 years. Elevated serum gamma globulin and IgG were found in patients with AIH, of whom 62.9% (17/27) were positive for anti-nuclear antibody (ANA) and 3 were positive for liver-kidney microsomes type 1 antibody. The main histological changes in severe AIH cases included interface hepatitis (77.7 %) and bridging necrosis. Most of the PBC patients were presented with elevated serum alkaline phosphatase, glutamyl transpeptidase and IgM. Fifty patients (74.6%) were positive for anti-mitochondrial antibody (AMA) and AMA-M2. The pathological examination showed that 28. 3% of the cases were in Ⅰ or Ⅱ stage and 71.7% in Ⅲ or Ⅳ stage in patients with PBC who received liver biopsy. The pathologic change of reduction or even disappearing of bile ducts was found in 62. 6% patients with PBC. The clinical and pathological manifestations in patients with AIH-PBC overlap syndrome had both characteristics of PBC and AIH. Three out of 10 patients with AIH-PBC overlap syndrome were positive for ANA and AMA/AMA-M2. Conclusion Since AILD is not rare in Chinese, its diagnosis should be based on the clinical presentation, biochemical, immunological and histologic changes.

Objective To investigate the protective effect and mechanism of serum containing Euonymus fortunei on the rat pancreatic islet cells. Methods Forty male SD rats were randomly divided into 5 groups (n=8 in each group), including the control group (normal rat islet cells were cultured with normal rat serum), ischemic preconditioning group (abdominal aorta was blocked first and then re-opened before the pancreas was obtained, and the pancreatic islet cells were cultured with normal rat serum), Euonymus fortunei treatment group (normal rat islet cells were cultured with rat serum containing Euonymus fortunei), Euonymus fortunei group and blank group (normal rats were administered orally with Euonymus fortunei extract or distilled water for the preparation of rat serum). Diphenylthiocarbazone (DTZ) staining was utilized to observe and calculate the quantity of islets. Acridine orange (AO)/propidium iodide (PI) staining was adopted to calculate the survival rate of islet cells. The insulin release experiment was performed to calculate the stimulation index (SI) and evaluate islet cell function. The concentration of glutathione (GSH) and nitric oxide (NO) in islet cells was detected using GSH and NO kits. The expression level of inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) was quantitatively measured by reverse transcription polymerase chain reaction (RT-PCR). Results Islet cells were observed in specifically scarlet color after DTZ staining. The quantity of islet cells did not significantly differ among different groups (all P>0.05). Along with the prolongation of culture time, the activity of islet cells in each group was gradually decreased. At 72 h after isolation and culture, compared with the control group, the survival rate of the cells was significantly higher in the Euonymus fortunei treatment group (P<0.05). The insulin release test results demonstrated that compared with the control group, the SI of the ischemic preconditioning and Euonymus fortunei treatment groups was significantly increased (both P<0.05). Compared with the control group, the GSH contents of pancreatic islet cells in the ischemic preconditioning and Euonymus fortunei treatment groups were considerably enhanced, the NO content was significantly decreased, and the expression level of iNOS mRNA was significantly down-regulated (all P<0.05). Conclusions Euonymus fortunei can increase the survival rate of islet cells and enhance the function of pancreatic islets by increasing the level of GSH, down-regulating the expression of iNOS and decreasing the NO production.

Objective: To investigate the distribution and related factors of birth weight of live births and full-term infants in Guangxi Zhuang Autonomous Region of China. Methods: Based on Guangxi women and children information system from 2016 to 2018, a large real-time database about maternal and live-birth information was established. It covered 1 712 midwifery institutions in Guangxi. A total of 2 394 240 cases of live births were collected and 2 243 129 cases of which were full-term infants. The multivariate logistic regression model was used to analyze the related factors of low birth weight. Results: The birth weight of 2 394 240 live births, (3 123.49±461.08) g, in Guangxi was approximately normal distribution with a peak distribution to the left. The incidence of low birth weight was 8.05%, and the incidence of macrosomia was 2.07%. The incidence of low birth weight was 10.92% for the puerpera with body mass index (BMI, kg/m²) <18.5, 16.82% for the puerpera with height <145 cm, 8.92% for the puerpera with age <20 years old, 7.67% for the puerpera with age ≥35 years old, and 54.65% for the puerpera with premature birth. The birth weight of 2 243 129 full-term infants, (3 176.01±400.78) g, was approximately normal distribution with a peak distribution to the right. The incidence of low birth weight was 2.97%, and the incidence of macrosomia was 2.19%. The incidence of low birth weight was 4.73% for puerpera with BMI<18.5, 8.17% for puerpera with height<145 cm, 4.83% for puerpera with age <20 years old, and 3.05% for puerpera with age ≥35 years old. The risks of low birth weight [OR (95%CI) value] of pregnant women aged <20, 25-29 and 30-34 years old were 1.31 (1.28-1.35), 0.88 (0.86-0.90) and 0.89 (0.87-0.91) times of those aged ≥35 years old. The risks of low birth weight [OR (95%CI) value] of pregnancy BMI <18.5 and 18.5-23.9 kg/m² group were 1.98 (1.94-2.03) and 1.20 (1.18-1.23) times of those pregnancy BMI ≥24 kg/m². The risks of low birth weight [OR (95%CI) value] of pregnant women′s height (cm)<145, 145-154, 155-159 and 160-164 cm were 4.67 (4.39-4.97), 2.36 (2.29-2.44), 1.58 (1.53-1.63) and 1.22 (1.18-1.26) times of those heights ≥165 cm group. The risks of low birth weight [OR (95%CI) value] of pregnant women′s gestational age <28, 28-31 and 32-36 years old were 136.65 (124.33-150.20), 1 704.37 (1 509.02-1 925.02) and 33.45 (32.98-33.94) times of those gestational age ≥37 years old. Conclusion The incidence of low birth weight of live births was higher in Guangxi from 2016 to 2018. There is a higher risk of low birth weight for younger, older, low height, low BMI and preterm women in Guangxi from 2016 to 2018.

Diabetic kidney disease (DKD) is the most common complication of diabetes mellitus (DM). Qianjin Wenwu decoction (QWD), a well-known traditional Korean medicine, has been used for the treatment of DKD, with satisfactory therapeutic effects. This study was designed to investigate the active components and mechanisms of action of QWD in the treatment of DKD. The results demonstrated that a total of 13 active components in five types were found in QWD, including flavonoids, flavonoid glycosides, phenylpropionic acids, saponins, coumarins, and lignins. Two key proteins, TGF-β1 and TIMP-1, were identified as the target proteins through molecular docking. Furthermore, QWD significantly suppressed Scr and BUN levels which increased after unilateral ureteral obstruction (UUO). Hematoxylin & eosin (H&E) and Masson staining results demonstrated that QWD significantly alleviated renal interstitial fibrosis in UUO mice. We also found that QWD promoted ECM degradation by regulating MMP-9/TIMP-1 homeostasis to improve renal tubulointerstitial fibrosis and interfere with the expression and activity of TGF- β1 in DKD treatment. These findings explain the underlying mechanism of QWD for the treatment of DKD, and also provide methodological reference for investigating the mechanism of traditional medicine in the treatment of DKD.
Rats ; Mice ; Animals ; Ureteral Obstruction/metabolism* ; Kidney/metabolism* ; Tissue Inhibitor of Metalloproteinase-1/metabolism* ; Molecular Docking Simulation ; Rats, Sprague-Dawley ; Kidney Diseases/drug therapy* ; Extracellular Matrix/metabolism* ; Flavonoids/metabolism* ; Fibrosis