Adolescent ; Exercise Tolerance ; physiology ; Female ; Humans ; Male ; Oxygen Consumption ; physiology ; Swimming ; physiology ; Young Adult

Objective To clarify the effect of Fogarty balloon catheter thrombectomy on venous wall integraty when performed on different time phases.MethodsA murine model of inferior vena caval thrombosis was established. Collagen of venous wall was measured by Van Gieson staining and this was used as the criteria of venous wall injury. The thrombus residue was determined after Fogarty balloon catheter thrombectomy in each individual time phase. Results Collagen deposit in the adventitia of venous wall increased every day,to an amount of (5 902?399) ?m2 on the third day which was significantly different from that of controls (5 333?454) ?m2(P

20% improvement in 4/7 primary indices.Sharp declines in several parameters were noticed during 3 to 6 months.Pain in 9 patients disappeared.There was also a statistically significant decrease in TNF ? transcripts in the PBMC.Conclusion Thalidomide is a reasonably promising drug for treating resistant ankylosing spondylitis and its biological mechanism is related to the gene expression suppression of proinflammatory cytokine TNF ?.

Forest musk deer (Moschus berezovskii), a rare wild medicinal animal, is listed under the category of the state key protected wildlife list of China. Musk, secreted by the musk glands, is with high economic and medicinal value and used as precious traditional medicine in China. In order to meet the needs of musk in Chinese traditional medicine, forest musk deer farming was conducted in 1950s, but the research progress on musk secretion mechanism was slow. Therefore, by reviewing the histological and anatomical structure of forest musk deer musk gland, the relationship between sex hormones and the musk secretion process, and the molecular mechanism of the musk secretion, the existing problems in investigating the musk secretion mechanism were analyzed and the development trends in this field were also discussed, in order to provide a reference for further studies on the musk secretion mechanism and improve musk production of forest musk deer.
Animals ; Deer ; metabolism ; Exocrine Glands ; anatomy & histology ; chemistry ; secretion ; Fatty Acids, Monounsaturated ; chemistry ; metabolism ; Male

70% to 80% of people with diabetes died from cardiovascular complications, which had become the leading cause of death in diabetic patients. Cardiovascular complications in diabetic patients are mainly associated with vascular endothelial dysfunction and poor neovascularization. Its important influencing factors are changes in the number of endothelial progenitor cells and dysfunction. Hyperglycemia in diabetic patients can cause endothelial progenitor cell dysfunction, inhibit its proliferation ability, angiogenesis ability and paracrine effect. In order to provide research ideas for the prevention and treatment of cardiovascular complications in diabetic patients, this article aims to review the relevant mechanism of the effect of hyperglycemia on the number and function of endothelial progenitor cells in patients with diabetes, and the application of endothelial progenitor cells in the treatment of diabetic cardiovascular disease.

OBJECTIVETo study the role and mechanisms of STAT3 signaling pathway in hypoxic-ischemic brain damage (HIBD) of neonatal rats.

METHODSEighty 7-day-old Sprague-Dawley rats were randomly divided into two groups: HI and sham-operated (n=40 each). The rats in the HI group were subjected to right carotid artery ligation and subsequent hypoxia exposure (8% O2) for 2.5 hours, and the rats in the sham-operated group underwent the right carotid artery dissection without subsequent ligation or hypoxia treatment. Brain tissue samples were collected at 4, 6, 8, 12 and 24 hours after operation and hypoxic exposure. Immunohistochemistry and Western blot were used to detect the expression of STAT3, phosphorylated STAT3 (p-STAT3) and vascular endothelial growth factor (VEGF) proteins. TUNEL staining was used to detect apoptotic cells.

RESULTSNo significant difference in STAT3 expression was observed at all time points between the HI and sham-operated groups (P>0.05). Compared with the sham-operated group, the expression of p-STAT3 protein in the HI group was significantly upregulated at 4, 6, 8, 12 hours after operation and hypoxic exposure, and peaked at 6 hours (P<0.01). The VEGF expression in the HI group was higher than that in the sham-operated group at all time points, which peaked at 8 hours (P<0.05). TUNEL staining showed that the apoptotic cells increased significantly in a time-dependent manner compared with the sham-operated group (P<0.01).

CONCLUSIONSHI may lead to phosphorylation of STAT3 which probably induces the VEGF expression in the brain of neonatal rats. The activated STAT3 signaling pathway may be involved in the apoptosis regulation of nerve cells, and related to apoptosis inhibition of nerve cells.

Animals ; Animals, Newborn ; Female ; Hypoxia-Ischemia, Brain ; metabolism ; Male ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; STAT3 Transcription Factor ; physiology ; Signal Transduction ; physiology ; Vascular Endothelial Growth Factor A ; analysis

OBJECTIVETo study the effect of endotoxin on the expression of peroxisome proliferator-activated receptor alpha (PPARa) in the development of nonalcoholic steatohepatitis in rats.

METHODSA model of nonalcoholic steatohepatitis (NASH) was developed with Wistar rats fed a chow containing 20% maize oil for 14 weeks. The endotoxin group rats were intraperitoneally injected with lipopolysaccharide (LPS, 1 g/L, 3.0 ml/kg) once 4 hours before the end of the experiment. The concentrations of lipids, endotoxin, tumor necrosis factor-a, malondialdehyde, free fatty acid in plasma and hepatic tissues were determined and the degree of hepatocytic steatosis was studied. The expression of PPARa mRNA in hepatic tissues was measured using reverse transcriptase-polymerase chain reaction (RT-PCR).

RESULTSThe expression of PPARa mRNA in the hepatic tissue of the LPS group was downregulated markedly in comparison to that of the control group. The level of free fatty acid and endotoxin by secreting tumor necrosis factor-a increased and triglyceride accumulated in the liver caused malondialdehyde content to increase, then lipid peroxidation process enhanced and ALT activity increased. Thus, hepatic injury and inflammatory reaction could be accelerated.

CONCLUSIONEndotoxemia can enhance hepatocellular steatosis and lead to NASH due to its downregulating the expression of PPARa mRNA.

Animals ; Down-Regulation ; Endotoxins ; pharmacology ; Fatty Liver ; metabolism ; Liver ; metabolism ; Male ; PPAR alpha ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction

Animals ; Endotoxemia ; complications ; Fatty Liver ; etiology ; Hepatitis ; etiology ; Male ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; metabolism

Adolescent ; Adult ; Cytokines ; blood ; Endotoxemia ; complications ; Female ; Hepatitis B, Chronic ; complications ; immunology ; Humans ; Male ; Middle Aged ; Th1 Cells ; immunology ; Th2 Cells ; immunology