Objective To investigate the relation between serum leptin/tumor necrosis factor-α (TNF-α)and malnutrition in patients with chronic obstructive pulmonary disease (COPD) and stable chronic cor pulmonale (CCP) at high altitude. Methods Totally 162 COPD and CCP patients and 40 normal controls (group C) were studied. COPD and CCP patients were divided into malnutrition group (group A, n = 104) and normal nutrition group (group B, n =58) according to the nutritional parameters. Levels of serum leptin and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA). Results Body mass index (BMI), percentage of normal body weight (NW%), triceps skinfold thickness (TSF), mid-upper arm circumference (MAC), serum albumin (ALB) ingroupA[(17.4±1.8) kg/m2, (82.3±4.3)%, (7.0±2.6) mm, (17.8±2.8) cm, (30.3±3.9)g/L, respectively] were significantly lower than those in group B and group C [(21.8 ± 2.0) kg/m2,(98.6±5.5)%, (9.3±2.6) mm, (21.5±2.9) cm, (36.2±3.8) g/L, and (23.1±2.3) kg/m2,(102.2±5.2)%, (9.7±3.8) mm, (22.1±2.8) cm, (36.8±3.9) g/L, respectively; all P＜0. 01].The levels of serum leptin and TNF-α in group A [(9.5 ±1. 8) ng/ml and (17.3 ±2. 2) ng/ml, respectively]were significantly higher than those in group A and group C [(7.3 ± 2. 0) ng/ml, (13.5 ± 2. 3) ng/ml; and (6. 7 ±2. 3) ng/ml, (12. 8 ±2. 1) ng/ml, respectively; all P ＜0.01). However, they were not significantly different between group A and group B (all P ＞ 0. 05). The level of leptin was negatively correlated with BMI (r=-0.745, P=0. 0005), NW% (r= -0.887, P=0. 0005), TSF (r= -0.725, P=0. 0005), MAC (r= -0. 761, P=0. 0005), serum albumin (r= -0. 558, P=0. 0005) in group A, and was positively correlated with TNF-α (r = 0. 527, P = 0. 0005). Conclusion Serum leptin and TNF-α correlate with malnutrition in patients with COPD and CCP at high altitude.

Objective: Our aim was to observe the protective effect of propofol in clinical relevant concentration on the peroxidative injured erythrocyte. Methods: Intravenous blood samples taken from 20 healthy adults were prepared for red blood cell (RBC) suspensions and divided equally into 5 groups: groupⅠfor control, group Ⅱ with hydrogen peroxide (H2O2, 100 mmol/L) -induced injury, and group Ⅲ, Ⅳ, Ⅴ with the same injury as the group Ⅱ but being pretreated with 3 different concentrations of propofol (25, 50, 75 μmol/L), respectively. The concentrations of potassium and malondialdehyde (MDA) in RBC suspensions and hemolytic degree after incubation were measured. Results: After 60-minute incubation, the extracellular potassium concentrations (0.16, 0.14, 0.14 mmol/L), MDA concentrations (5.66, 5.57, 6.20 nmol/L), and hemolytic degree (76.89%, 59.84%, 64.22%) decreased significantly in the groups that were pretreated with propofol as compared with the group Ⅱ (0.26 mmol/L, 9.19 nmol/L, and 100%), but no difference has been seen within the groups pretreated with 3 different concentrations of propofol and between the propofol-treated groups and the group Ⅰ(0.10 mmol/L, 4.13 nmol/L, 52.73%). Conclusion: Propofol in clinical relevant concentrations may decrease MDA production, hemolytic degree, and potassium exflux from erythrocyte in response to in vitro oxidative challenge with hydrogen peroxide and enhance erythrocyte antioxidant capacity. The protective effect is not related with concentrations.

Objective To compare the clinical results of surgical and conservative treatment of acute patellar dislocations.Methods Retrospective analyzed the clinical data of 35 patients with acute patellar dislocations from June 2004 to October 2009,and divided the patients into 2 groups.One group with 18 patients underwent surgical treatments,and the other group with 17 patients underwent conservative treatments,record the number of relapses cases of both the two groups.A radiographic examination was performed in the evaluation of the patients,and the Kujala questionnaire was applied with the intention of analyzing the improvement of pain and quality of life.Results All patients were followed up for more than 12 months.(1) The conservative treatment group exhibited a higher number of recurrent dislocations (7 patients) (41.2％) than the surgical treatment group,which did not have any relapses (x2 =9.265,P =0.002).(2) The patellar tilt returned to normal in the surgical group,while 8 patients returned to normal in the conservative group,with statistical difference between groups (x2 =10.980,P =0.001).And the lateral shift ratio returned to normal in the surgical group,while 6 patients returned to normal in the conservative group,with statistical difference between groups(x2 =7.667,P =0.006).(3)The surgical treatment group obtained a significantly better mean score on the Kujala test than preoperative ((90 ± 5) vs.(58 ± 6),t =16.465,P ＜ 0.01) ; The conservative treatment group,compared with the preoperative,is not improved obviously ((72 ± 6) vs.(62 ± 8),t =0.943,P ＞ 0.05) ;Postoperative group comparison,surgical group was higher than that in conservative group,there was significant difference between two groups (t =12.256,P ＜ 0.01).Conclusion For acute patellar dislocation,surgical treatment can significantly restore patellar stability,improve the function of knee joint.

AIM To explore the effects of glycyrrhetinic acid on the gastric ulcer rats infected by Helicobacter pylori (Hp) and its action mechanism.METHODS Gastric ulcer rat models were induced by acetic acid stress and then followed by Hp infection.After treatment with low and high doses of glycyrrhetinic acid,the ulcer index,gastric acid and proteinase activities in gastric ulcer rats were analyzed.The effects of glycyrrhetinic acid on the expressions of BCL2 and Caspase-3,the GSK3β activity in gastric mucosa and gastric epithelial cells,and the cell apoptosis level were then detected.RESULTS Glycyrrhetinic acid reduced the ulcer index,gastric acid and proteinase activities in rats.Besides,the expression of BCL2 was significantly up-regulated by glycyrrhetinic acid in gastric mucosa and gastric epithelial cells,whereas the expression of Caspase-3,level of cell apoptosis,and GSK3β activity were significantly reduced.After the treatment with GSK3 β activator LY294002,the level of BCL2 was down-regulated,Caspase-3 expression was increased,and the level of cell apoptosis was enhanced.CONCLUSION Glycyrrhetinic acid promotes the healing of gastric ulcer infected by Hp via regulating GSK3β activity and inhibiting apoptosis of gastric epithelial cells.

[ ABSTRACT] AIM:To investigate the effect of artemisinin on lipopolysaccharide ( LPS)-induced intestinal epi-thelial barrier damage in IEC-6 cells and its molecular mechanism.METHODS:Cultured IEC-6 cells were divided to 5 groups:control group, LPS (100 mg/L) group and LPS +Artemisinin (30, 50 and 100μmol/L) groups.The cytotoxici-ty was detected by MTT assay.The releases of TNF-α, IL-1βand IL-6 in the IEC-6 cells were measured by ELISA.The transepithelial electrical resistance ( TER) was detected by electrical resistance tester, and the horseradish peroxidase (HRP) flux permeability were analyzed by a microplate reader.The expression of tight junction proteins, ZO-1, claudin-1 and occludin, and the expression of TLR4/MyD88/NF-κB at mRNA and protein levels were determined by RT-qPCR and Western blot.RESULTS:Artemisinin alone (up to 100 μmol/L) or in combination with LPS (100 mg/L) was not toxic to IEC-6 cells.Compared with control group, the releases of TNF-α, IL-1βand IL-6 in the culture supernatant of IEC-6 cells significantly increased after treatment with LPS.The expression of TLR4/MyD88/NF-κB was activated by LPS.LPS down-regulated the protein expression of ZO-1, claudin-1 and occludin.However, artemisinin treatment decreased the re-leases of TNF-α, IL-1βand IL-6 in the culture supernatant of IEC-6 cells.The expression of TLR4/MyD88/NF-κB at mR-NA and protein levels was gradually reduced after treatment with artemisinin.In addition, artemisinin upregulated the pro-tein expression of ZO-1, claudin-1 and occludin significantly (P<0.01) in a dose-dependent manner.CONCLUSION:Artemisinin attenuates LPS-induced intestinal epithelial barrier damage by inhibiting TLR4/MyD88/NF-κB activation in the IEC-6 cells.

Objective:To analyze the relationship between aquaporin 1 (AQP1) level and vascular calcification in patients with diabetes nephropathy.Methods:A total of 125 diabetic nephropathy patients admitted to Suzhou Hospital of Nanjing Medical University from March 2020 to March 2023 were retrospectively selected as case group. The case group was divided into group A (diabetes nephropathy stage Ⅰ and Ⅱ) with 31 cases, group B (diabetes nephropathy stage Ⅲ) with 32 cases, group C (diabetes nephropathy stage Ⅳ) with 39 cases, and group D (diabetes nephropathy stage V) with 23 cases. In these patients, 51 cases had vascular calcification, taken as the calcification group, and 74 cases had no vascular calcification, taken as the non calcification group. Sixty volunteers who underwent health examinations in the same hospital were selected as the control group. Receiver operating characteristic curve was used to analyze the predictive value of AQP1 on vascular calcification in diabetes nephropathy patients and to explore the related factors of vascular calcification in diabetes nephropathy patients.Results:Compared with the control group, AQP1 level and calcification rate in groups A, B, C and D were higher: 6.41 ± 1.04, 7.93 ± 1.23, 9.50 ± 1.52 and 11.37 ± 2.01 vs. 3.83 ± 0.56 ng/L, 6.45% (2/31), 28.13% (9/32), 51.28% (20/29) and 86.96% (20/23) vs. 0 ( P<0.05). Compared with group A, the level of AQP1 and calcification rate in groups B, C and D were higher ( P<0.05); compared with group B, the AQP1 level and calcification rate in groups C and D were higher ( P<0.05); compared with group C, the level of AQP1 and calcification rate in group D were higher ( P<0.05). Compared to the non calcification group, the levels of uric acid, homocysteine and cystatin C in calcification group were higher: (313.82 ± 38.72) μmol/L vs. (253.42 ± 30.14) μmol/L, (20.03 ± 3.01) μmol/L vs. (15.01 ± 2.71) μmol/L, (1.73 ± 0.26) mg/L vs. (1.30 ± 0.17) mg/L ( P<0.05). AQP1 was positively correlated with uric acid, homocysteine, and cystatin C ( P<0.05). The area under the curve of AQP1, uric acid, homocysteine and cystatin C in predicting vascular calcification in patients with diabetes nephropathy were 0.892, 0.803, 0.738 and 0.763, respectively. Taking whether vascular calcification occurs in patients with diabetes nephropathy as the dependent variable (no = 0, yes = 1), the variables of P<0.05 in the single factor analysis were selected for multivariate Logistic regression analysis. The results showed that uric acid, homocysteine, cystatin C and AQP1 were the main factors affecting vascular calcification in patients with diabetes nephropathy ( P<0.05). Conclusions:Serum AQP1 has a high predictive value for vascular calcification in diabetes nephropathy patients, and is expected to be used as a biomarker for early diagnosis of vascular calcification in diabetes nephropathy patients.

Objective To explore the effect of FBXW7 on ferroptosis in head and neck squamous cell carcinoma.Methods Head and neck squamous cell lines HN4 and HN6 were cultured in vitro.FBXW7 and SOX2 overexpression plasmids were constructed,and the plasmids were stably transfected into cell lines.The overexpression transfection efficiency was verified at the transcription level and protein level by qRT-PCR and Western blot experiments,respectively.The lipid peroxidation levels of head and neck squamous cell carcinoma cells with overexpressing FBXW7 were verified by measuring malondialdehyde(MDA),glutathione(GSH),and reactive ox-ygen species(ROS)levels.After treating cells with ferroptosis inhibitor Fer-1,the changes in cell viability were further detected to ver-ify the effect of FBXW7 on ferroptosis.The effect of transfection of the overexpressed plasmid on cellular pathways was detected by Western blot.Results HN4 and HN6 cell lines showed increased levels of lipid peroxidation after overexpression of FBXW7,and the ferroptosis inhibitor Fer-1 was able to effectively reverse the ferroptosis induced by overexpression of FBXW7.Western blot assay results showed that overexpression of FBXW7 reduced the expression of c-Myc,SOX2 and SLC7A11.Conclusion FBXW7 regulates the ex-pression of SOX2-SLC7A11 by degrading c-Myc,thereby effectively regulating ferroptosis in HNSCC.

Objective To explore the impact of knocking down Sec31A on the malignant phenotype of head and neck squamous cell carcinoma(HNSCC)and its possible mechanisms.Methods Transcriptome sequencing data of HNSCC tissues and adjacent tissues were obtained from the TCGA database,and the expression levels of Sec31A were compared.Immunohistochemical staining was used to analyze the expression of Sec31A in HNSCC tissues.Kaplan-Meier survival analysis was used to compare the relationship between Sec31A and the prognosis of HNSCC patients.Small interfering plasmids si-Sec31A and si-NC were transfected into HNSCC cell lines HN6 and HN4,and the impact of knocking down Sec31A on the biological behavior of HNSCC cells was detected through CCK-8 exper-iments,plate cloning experiments,scratch healing experiments,and Transwell experiments.Changes in the expression levels of PI3K/AKT/mTOR pathway related proteins in cells were detected after knocking down Sec31A with HN6 and HN4 through Western Blot(WB)experiments.Stable transfected cell lines of HN6 siSec31A and HN6 siNC were constructed and inoculated subcutaneously in nude mice to further verify the tumorigenic effect of Sec31A in vivo.Results TCGA data showed that Sec31A was higher in HNSCC tissues than in adjacent normal tissues(P＜0.01),and high expression of Sec31A was significantly correlated with poor prognosis in pa-tients(P＜0.05).Immunohistochemical staining showed that Sec31A was expressed stronger in HNSCC tissues than in normal tissues.In HN6 and HN4 cells,knocking down Sec31A resulted in significantly weaker proliferation,migration,and invasion abilities compared to the control group.Through WB experiments,it was found that transfection of si-Sec31A with HN6 and HN4 significantly reduced the expression levels of p-PI3K,p-AKT,and p-mTOR proteins.After knocking down Sec31A with HN6,the transplanted tumor volume in nude mice was significantly smaller than that in the control group.Conclusion Knocking down Sec31A can inhibit the proliferation,migration and invasion of HNSCC cells,possibly through the PI3K/AKT/mTOR pathway.

The historical evolution， fermentation technology and key links of Sojae Semen Praeparatum （SSP） were sorted out by consulting ancient books and modern literature， and the influencing factors and control methods of quality were analyzed and summarized in order to provide reference for the quality control of SSP. After analysis， it was found that in the fermentation process of SSP， fermentation strains， miscellaneous bacteria， temperature and humidity were all important factors affecting the quality of SSP. The condition control of "post fermentation" process has been paid more attention to in the past dynasties. In addition， the delicious SSP recognized in ancient times should be made from mold fermentation， and the breeding and application of fermented mold may be the key point to solve the quality problem of SSP. Therefore， based on the evaluation indexes of SSP in the past dynasties， it is of great significance to study and optimize the technological conditions such as strain， temperature and humidity in depth to improve the quality of SSP.