The nature of renal tubular cell injury in ischemic acute renal failure includes not only cell death (necrosis or apoptosis) but also sublethal injury causing cell dysfunction. The role of intracellu- lar calcium, calcium - dependent enzymes calpain, nitric oxide, phospholipase A2, loss of tubule cell polarity and tubular obstruction in the pathophysiology of the renal tubular cell injury during hypoxia/ischemia is described. The effects of vascular factors, infiltrating activited leukocytes, apoptosis and growth factors on renal tubular cell injury are discussed. Potential mechanisms that tubular injury leads to a profound fall in glomerular filtration rate are proposed.

BACKGROUND:The animal model of high fat diet-induced obesity is the first choice for the study of human obesity. Leptin and its receptor expression play an important role in the high fat diet-induced obesity and obesity resistant, but the exact mechanism and the role of swimming are not clear.
OBJECTIVE:To explore the effect of 7-week swimming on serum leptin and leptin receptor expression in hypothalamus in rats with high fat diets.
METHODS:A total of 60 Sprague-Dawley rats were fed with high fat diets for 8 weeks. Thediet-induced obeseand obese resistant rats were selected based on the body weight. 14 obese rats were equaly divided into two groups: obese group and obese-exercise group; and 14 obese resistant rats were equaly divided into two groups: obese resistantgroup and obese resistant-exercise group. Al the rats were continualy given high fat diets. Exercise groups accepted free swimming training for 7 weeks at the same time.
RESULTS AND CONCLUSION:Compared with the obese group, obese-exercise group had obviously decreased in body weight, fat pad weight, fat pad weight/body weight and serum leptin concentration. And obese-exercise group had obviously increased receptor mRNA expression in hypothalamus. There was no significant change in above indexes betweenthe obese resistant group and obese resistant-exercise group. Theresults showed that swimming exercise can increase energy consumption and improve metabolism, which decreased the concentration of leptin and effectively improved leptin receptor expressionin the hypothalamus to ease leptin resistance and improve the body’s metabolism.

Objective To investigate the serum neuron-specific enolase (NSE) and high sensitivity C-reactive protein (hs-CRP) on neonatal hypoxic-ischemic encephalopathy (HIE) in children with illness and prognosis of assessed value. Method The serum NSE, hs-CRP levels of 40 patients with HIE (HIE group) of the acute stage and convalescence, and 20 healthy neonates (control group ) were measured and the clinical sub-degree relationships were analyzed. Results The serum NSE, hs-CRP levels in HIE group of the acute stage [ (32.88 ± 12.61 ) μ g/L, (6.43 ± 2.07) mg/L] were significantly higher than those in control group [(8.62 ± 3.58) μ g/L, (2.61 ± 0.95) mg/L](P ＜ 0.01 ). The serum NSE, hs-CRP levels in HIE group of the severe acute stage were significantly higher than those of the mild and light acute stage (P＜0.01 ). The more severe disease, the more higher NSE, hs-CRP. Conclusion The serum NSE, hs-CRP reflect the brain neuronal damage or necrosis of the objective indicators that could be used as early objective indicators to judge the pathogenetic condition and prognosis of HIE.

BACKGROUND:Overweight and obesity can lead to a disorder of sex hormone in men. The increase in female hormone levels may inhibit the synthesis and secretion of male hormone, increase fat accumulation and form a vicious circle. Exercise can effectively reduce body fat. OBJECTIVE: To investigate the effects of different exercise loads on sex hormone and the quality of sperm in obese male mice. METHODS: Weanling male C57BL/6J mice were divided into normal control group and obesity group. Mice in the obesity group were given high fat diet for 10 weeks to establish mouse model of obesity. The amount of food and water was recorded daily. Body weight was weighed once every week. After model induction, models were assigned to obesity moderate load exercise group and obesity high load exercise group. These models did exercises for 8 weeks. Body length was measured. Body weight, abdominal fat, testis, epididymis and seminal vesicle were weighed. Sperm activity and motility were observed by the sperm counting method in the epididymis tail. Enzyme linked immunosorbent assay was used to measure serum progesterone, folicle stimulating hormone, testosterone and estradiol. RESULTS AND CONCLUSION:Compared with the normal control group, body weight, abdominal fat weight, and lee’s index were increased (P < 0.01); the coefficient of testis and seminal vesicle were significantly decreased (P < 0.01); serum levels of luteinizing hormone, folicle stimulating hormone and testosterone were significantly decreased and estradiol level was significantly increased (P< 0.05); sperm count and activity were significantly decreased in the obesity group (P < 0.01). Compared with the obesity group, body weight, abdominal fat weight and lee’s index were significantly decreased (P < 0.05 orP < 0.01); the coefficient of testis and seminal vesicle were significantly increased in the obesity moderate load exercise group and obesity high load exercise group (P < 0.05 orP < 0.01). Serum luteinizing hormone, folicle stimulating hormone and testosterone levels were significantly increased (P < 0.05 orP < 0.01); estradiol levels were significantly decreased (P < 0.05); sperm count and activity were significantly increased (P < 0.01,P < 0.05) in the obesity moderate load exercise group. Compared with the obesity moderate load exercise group, abdominal fat weight and lee’s index were significantly reduced (P < 0.05); serum luteinizing hormone, folicle stimulating hormone, testosterone, sperm count and activity were decreased in the obesity high load exercise group (P < 0.01). These results indicate that long-term high fat diet leads to early obesity in males, inhibits the development of the reproductive gland and reproductive organs, and causes the decrease of the level of male hormone and sperm quality. Long-term moderate load exercise effectively reduces body fat, improves the inhibitory effect on male reproductive organs and glands, and relieves the negative effect of obesity on reproductive function. The effect of long-term large load exercise on reducing body fat is better than medium load exercise, but it has little effect on improving the level of male hormone in obese mice or on relieving the negative effect of obesity on reproductive function, even has a tendency to aggravate.

Aim To study the effect of CSE ( cigarette smoke extract ) on the single-molecule interactional force between thrombomodulin and thrombin by live-cell single-molecule force spectroscopy. Methods CSE was prepared by a previously reported method. The plasmid of TM-GFP was constructed and transfect-ed in COS-7 cells. The expression of TM-GFP was de-tected by fluorescence microscopy and laser scanning confocal microscopy. The transfected COS-7 cells were grouped ( 1 ) GFP -thrombin group ( 2 ) TM-thrombin group ( 3 ) CSE-TM-thrombin group ( 4 ) CSE- GFP-thrombin group. Force measurements with the thrombin modified AFM tips on the living cell surface were car-ried out on PicoSPM II with a Pico-Scan 3000 control-ler and a larger scanner. The force curves measured in living cells were recorded by PicoScan 5 software and analyzed by MATLAB R2009aMetlab. Results The single-molecule binding force of thrombomodulin and thrombin ( TM-Thr ) was determined ( 60. 90 ± 0. 82 ) pN. The binding probability for TM-Thr was about (22. 58 ± 3. 95)%. Antibody blocking binding proba-bility for TM-Thr was ( 2. 58 ± 2. 0 )%. The binding probabilities for GFP-Thr group, CSE-TM-Thr group and CSE-GFP-Thr group were significantly decreased compared with TM-Thr group ( P<0. 05 ) . The mean value of the most probable single molecular interaction force of thrombin/TM-ECD was determined as ( 45. 30 ± 1. 37 ) pN, the binding probability of thrombin and TM-ECD was ( 23. 25 ± 7. 02 )%. When the binding was blocked with the TM-MAb solution, the binding probability decreased to ( 4. 64 ± 2. 31 )%. The bind-ing probability was ( 8. 31 ± 1. 06 )% in the CSE-TM-thr-S group. When further blocked with TM-MAb, the binding probability was ( 5. 17 ± 2. 96 )%. Conclusion CSE significantly decreases the binding probability for TM-Thr to induce intravascular thrombosis.

Objective To analyze the expression and role of ubiquitin specific peptidase 18 (USP18) in gastric cancer cells,and to investigate the relationship between the development of gastric cancer and USP18.Methods The levels of USP18 protein and mRNA expression in immortalized gastric mucosa epithelial GSE cell lines and gastric cancer cell lines (AGS,MKN45,MKN25,BGC823,BGC803,SGC7901) were detected by using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot,respectively.The role of USP18 in the invasion and proliferation of gastric cancer cells was analyzed by using CCK8 and Transwell assays.Results The mRNA level of USP18 was lower in GSE cell lines than that in gastric cancer cells (F =794.052,P ＜ 0.000 1).In six gastric cancer cell lines,mRNA level of USP18 was relatively high in BGC823 (17.62±0.55) and BGC803 (13.52±0.50) cell lines,and low in MKN28 (1.40±0.17) and MKN45 cell lines (4.23±0.26).As for the protein level,the expression of USP18 was lowest in GSE cell line.In six gastric cancer cell lines,the expression of USP18 was the highest in more aggressive SGC7901 and BGC803 cell lines and the lowest in AGS and MKN45 cells.Compared with the control group,interference of USP18 decreased the invasion and proliferation abilities of SGC7901 and BGC803 cell lines (P ＜ 0.01).Conclusion USP18 is highly expressed in more invasive gastric cancer cells,and the downregulation of USP18 can suppress the invasion and proliferation of gastric cancer cells.

Objective To observe the efficacy of mesalazine combined with probiotics in the treatment of ulcerative colitis. Methods 60 patients with ulcerative colitis who were admitted to our hospital from May 2015 to May 2017 were selected randomly. These patients were divided into two groups according to the treatment method: mesalamine com bined with probiotic group(combination therapy group, n=30) and mesalamine alone treatment group (n=30). The clinical symptom score, endoscopic score, serum CRPlevel, clinical efficacy, incidence of adverse reactions and recurrence in both groups were statistically analyzed. Results Compared with those before treatment, the clinical symptom score, en doscopic score and serum CRPlevel were significantly lower in both groups after treatment(P＜0. 05); After treatment, clinical symptom score, endoscopic score and serum CRPlevel were significantly lower in the combination therapy group than those in the treatment alone group(P＜0. 05). The total effective rate in the combination therapy group was 93. 3％(28/30), significantly higher than 63. 3％(19/30) in the treatment alone group(P＜0. 05). The recurrence rate was 13. 3％ (4/30), significantly lower than that of 33. 3％(10/30) in the treatment alone group(P＜0. 05). However, the incidence rates of adverse reactions in the two groups was 6. 7％(2/30) and 10. 0％(3/30) respectively, which were not significantly different(P＞0. 05). Conclusion The efficacy of mesalazine combined with probiotics in the treatment of ulcerative colitis is more significant than that of mesalazine alone. At the same time, it is also more effective in improving the clinical symptoms, reducing the serum CRPlevel and recurrence rate in the patients, and will not increase the patients' adverse reactions to a great extent, so it is worthy of promotion and application in clinical settings.

SOCS3, a feedback inhibitor of the JAK/STAT signal pathway, negatively regulates axonal regrowth and inflammation in the central nervous system (CNS). Here, we demonstrated a distinct role of SOCS3 in the injured spinal cord of the gecko following tail amputation. Severing the gecko spinal cord did not evoke an inflammatory cascade except for an injury-stimulated elevation of the granulocyte/macrophage colony-stimulating factor (GM-CSF) and interferon gamma (IFN-γ) cytokines. Simultaneously, the expression of SOCS3 was upregulated in microglia, and unexpectedly not in neurons. Enforced expression of SOCS3 was sufficient to suppress the GM-CSF/IFN-γ-driven inflammatory responses through its KIR domain by attenuating the activities of JAK1 and JAK2. SOCS3 was also linked to GM-CSF/IFN-γ-induced cross-tolerance. Transfection of adenovirus overexpressing SOCS3 in the injured cord resulted in a significant decrease of inflammatory cytokines. These results reveal a distinct role of SOCS3 in the regenerating spinal cord, and provide new hints for CNS repair in mammals.