Objective To study the methods of clinic diagnosis and treatment for chronic lumbar pain induced by lumbo-sacral compartment syndrome. Methods Thirty-three patients with chronic lumbar pain induced by lumbo-sacral compartment syndrome were diagnosed by physical, radiological examination and intra lumbo-sacral muscle compartmental pressure measurement. 33 patients consisted of 15 men and 18 women, with the mean age 42.3 years, and mean duration of chronic lumbar pain was 27 years. Lumbar erector spinae osteo-facial compartment was decompressed using mini-invasive surgery. Lumbar and abdomen muscles were rehabilitated extensively after operation. Results After operation, symptoms of low back pain were alleviated significantly, and walking distance were promoted as well. Post operative flexion and extension of lumbar spine were increased to (15??0.5?) and (7??0.7?) respectively. Intramuscular pressure in rest state, during movement and no more than 6 min after movement was (6.8?0.8), (162.3?12.35) and (7.1?0.6) mm Hg respectively [before operation was(10.4?0.9), (187.1?11.16) and (13.2?1.3) mm Hg respectively, P

A lactoferrin-containing PEGylated liposome system (Lf-PLS) was developed and tested in vitro as a hepatoma-targeting drug delivery system. PEGylated liposomes (PLS) were successfully prepared using the thin film hydration method with peglipid post insertion. Lf was covalently conjugated onto the carboxyl terminal of DSPE-PEG2000-COOH on liposomes. Coumarin-6 was used to trace Lf-PLS with fluorescence. The cellular uptake of this system was carried out in asialoglycoprotein receptor (ASGPR) positive HepG2 cells via confocal microscopy and flow cytometry. The Lf-PLS liposome was observed as spherical or oval vesicles with the particle size around 130 nm, zeta potential about -30 mV and encapsulation efficiency more than 80%. The confocal microscopy images and flow cytometry data demonstrated that Lf-PLS resulted in significantly higher cell association by ASGPR positive HepG2 cells compared to PLS. The association between Lf-PLS and cells were dependent on the concentration, time and temperature, which was inhibited by pre-incubation with excessive free Lf. The results suggest that Lf-PLS has a good targeting effect on HepG2 cells in vitro. The targeting mechanism may be related to the specific binding of Lf and ASGPR on HepG2 cells, which guides Lf-PLS to the cell surface to induce an active endocytosis process. All these results demonstrated that Lf-PLS might be a potential drug delivery system in targeting hepatocellular carcinoma, which deserves more research on its targeting ability, antitumor efficiency, and metabolism in vivo for treatment of hepatomacellular carcinoma.

BACKGROUND:Cdh1 has been shown to express in rat hippocampus and cortex in a large number. Moreover, in vitro test demonstrated that Cdh1 expression was higher in neurons than in neural stem cel s, which possibly associated with the differentiation of neural stem cel s into neurons. However, the effects of anaphase promoting complex Cdh1 on ischemic neuronal damage remain unclear.
OBJECTIVE:To investigate the expression of Cdh1 and its downstream substrate in primary cultured neurons with oxygen-glucose deprivation. METHODS:Primary neurons from cortex of postnatal 24-hour rat pups were cultured in vitro, and identified by immunofluorescence staining. The oxygen-and glucose-deprived models were established by three gas incubator fil ed with nitrogen in sugar-free Earle’s solution. After 1 hour of hypoxia, reoxygenation was conducted. Real-time fluorescent quantitative PCR was used to detect the mRNA expression of Cdh1 and its downstream substrates Skp2, Cyclin B1 before hypoxia, 6 hours, 1, 3, 7 days after oxygen glucose deprivation. RESULTS AND CONCLUSION:After oxygen glucose deprivation, the expression of Cdh1 and Cyclin B1 in primary neurons was increased (P<0.05), while Skp2 expression was decreased (P<0.05). Above data indicated that Cdh1 expression in neurons increased after oxygen-glucose deprivation. It may degrade Skp2 and participate in hypoxic neuronal apoptosis by ubiquitination.

Objective To establish a method to prepare anti-sodium estrone sulfate monoclonal antibody ( ESS-Mab) . Methods Balb/c mice were immunized by ESS. Immune methods were screened. The blood serum potencies were measured by indirect ELISA and the best consistence of antigen and the first antibody were confirmed with method of titration. Cell fusion was carried by using PEG method and McAb hybridoma was screened with the indirect ELISA. Results The best immunization method of mice was subcutaneously multi-point injection in mouse back with the dose of 200/100 μg ESS antigen five times. The fusion rate was 90. 2%. Hybridoma positive rate of ELISA screening was 4. 4%. Finally two cell lines 2C8 and 8A7 with good specificity and sensitivity were obtained. Conclusion The best immunization way is selected and indirect ELISA is set up effectively and reliably for screening and presenting ESS McAb. the hybridoma technique is able to prepare monoclonal antibody of anti-ESS successfully.

AIM: To study the effects of ?-amyloid protein (A?) on neural stem cells cultured in vitro. METHODS: Neural stem cells (NSC) were isolated from E13 SD rats and cultured in serum-free medium (DMEM/F12). After detected by nestin, the A? was added to the NSC medium to observe the viability and proliferation of NSC by MTT, cell count and flow-cytometric examination. The effects of A? on differentiated NSC were also observed. RESULTS: A? markedly inhibited the proliferation and the cell viability of NSC when its concentration was higher than 25 ?mol/L. The differentiatory ability of NSC was inhibited when A? was in very low concentration. CONCLUSION: A? significantly inhibits the proliferation and differentiation of NSC and this may be one of the reasons that Alzheimer's disease is induced. [

Objective: To study the protective effect of Xiaoyao Tablet(XYT)(Radix Bupleuri, Radix Angelicae Sinensis, Rhizoma Atractylodis Macrocephalae, Radix Paeoniae Alba, Poria, Radix Glycyrrhizae, Herba Menthae, Roasted ginger) on liver. Methods: Using the acute hepatic injury model induced by Tetrachloride and D-galactosamine (CD-GaIN) in rats or mice, we observed the influence of XYT on ALT and AST level in the serum, MDA level and glutathione-s-transferase(GST) activity in the liver homogenates. The pain-killing effect was tested by body twisting model induced by glacial acetic acid and by hot plate model in mice. Results: The XYT reduced the serum ALT level significantly in the acute hepatic injury model in rats and mice. In the CCl 4 reduced acute hepatic injury mice model, XYT decreased the MDA level and increased the GST activity in liver significantly, also it reduced the MDA level in the serum. The XYT reduced twisting number in mice induced by glacial acetic acid. In the hot plate test, the pain threshold was increased. Conclusion: The drug has the similar hepatoprotective function to Xiaoyao Pills.

ObjectiveTo investigate the expression of APC-Cdh1 protein after cerebral ischemia-reperfusion injury.Methods60 male Sprague-Dawley rats were randomly divided into Sham-operated group(SH) and ischemia-reperfusion group(IR). The rats of ischemia-reperfusion groups were induced by four-vessel occlusion (4-VO). At different times after injury, the expression of APC-Cdh1 of rat hippocampus was observed by Western blotting and immunohistochemistry.ResultsCompared with sham-operated group, the expression of Cdh1 protein significantly decreased 1 day and increased obviously 3 days, but decreased again 7 days after injury in ischemia-reperfusion group. The immuno-staining showed that APC-Cdh1 was highly cerebral cortex and hippocampus in ischemia-reperfusion group. ConclusionAPC-Cdh1 may be involved in the central nervous system injury.

Objective To evaluate the effect of sevoflurane postconditioning on autophagy during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Forty-five clean-grade healthy male SpragueDawley rats,weighing 280-350 g,were divided into 3 groups (n=15 each) using a random number table method:sham operation group (S group),cerebral I/R group (I/R group) and sevoflurane postconditioning group (SP group).Focal cerebral I/R injury model was established by Zea-Longa method in chloral hydrate-anesthetized rats.The animals in SP group inhaled 2.4％ sevoflurane for 30 min starting from onset of reperfusion.The expression of autophagy-related proteins LC3 and beclin-1 was detected by Western blot at 2 h of reperfusion.The cerebral cortex was removed for examination of the morphology and number of autophagosomes with an electron microscope.Neurological deficit was assessed and scored at 24 h of reperfusion.Rats were sacrificed at 72 h of reperfusion for determination of the cerebral infarct size.Results Compared with S group,the neurological deficit score was significantly increased,the percentage of cerebral infarct size was increased,LC3Ⅱ/LC3Ⅰ ratio in cerebral cortex was increased,the expression of beclin-1 was up-regulated,and the number of autophagosomes was increased in I/R and SP groups (P＜0.05).Compared with I/R group,the neurological deficit score was significantly decreased,the percentage of cerebral infarct size was decreased,LC3Ⅱ/LC3Ⅰ ratio in cerebral cortex was decreased,the expression of beclin-1 was down-regulated,and the number of autophagosomes was reduced in SP group (P＜0.05).Conclusion Sevoflurane postconditioning mitigates focal cerebral I/R injury through inhibiting autophagy in rats.

Objective Targeted temperature management (TTM) is often used in neuro-critical care to minimize secondary neurologic injury and improve outcomes. Evidence-based implementation guideline of TTM was generated from clinical questions relevant to TTM implementation for neuro-critical care by experts recruited by the American Neuro-critical Care Society. Interpretation of this guideline would help the readers to understand the implementation of TTM, bring benefits to standardization of TTM application, and contribute to the solving of specific issues related to TTM implementation.

OBJECTIVETo analyze the functions of differentially expressed genes between abdominal aortic aneurysm and normal aortic tissue by cDNA microarray.

METHODSTotal RNAs were respectively isolated from the normal aorta and aortic aneurysm, purified into mRNAs by oligotex. Subsequently they were reverse-transcribed into cDNAs incorporated with fluorescent dUTP to make hybridization probes, which were hybridized as the cDNA microarray for scanning of fluorescent signals and differentially expressed genes between the normal aortic and aortic aneurysm by using GenePix Pro 3.0 software.

RESULTSA total of 18 differentially expressed genes were detected, accounting for 0.44% of total genes. Among these genes, 11 were related to cell cycle and the remaining 7 to cell apoptosis. The number of upregulated genes in the aortic aneurysm was 9 (mean ratio: 3.860) and that of the downregulated 9 (mean Ratio: 0.294). Bio-informative analysis showed that these 18 genes might influence the growth and apoptosis of smooth muscle cells in abdominal aortic aneurysms.

CONCLUSIONSDuring the development of abdominal aortic aneurysms, modulations of multi-gene expression would undergo various changes. Cell cycle and apoptosis-related genes were related to the growth and apoptosis of smooth muscle cells in abdominal aortic aneurysms. Further research into these genes will clarify the mechanisms of abdominal aortic aneurysms.

Aortic Aneurysm, Abdominal ; genetics ; pathology ; Apoptosis ; physiology ; Cell Cycle ; genetics ; Cells, Cultured ; Gene Expression ; Gene Expression Profiling ; Humans ; Myocytes, Smooth Muscle ; metabolism ; pathology ; Oligonucleotide Array Sequence Analysis