BACKGROUND: Compared with single proprioceptive training and simple neuromuscular training in the trunk and hip, the integrative neuromuscular training possesses comprehensive effect, which not only prevents sport-induced knee injury, but also improves the athletes' sport ability.OBJECTIVE: To validate whether the integrative neuromuscular training can enhance sport quality of juvenile female athletes and improve biomechanical pattern of the lower limb when jumping.METHODS: Eighteen juvenile female tennis athletes were selected and randomized into experimental and control groups. The athletes in the experimental group received 8-week integrative neuromuscular training and technical training involving the strength of the lower limb, core stability, plyometrice training, dynamic equilibrium, agility and speed. Those controls were subjected to 8-week traditional physical training and technical training. The vertical jump dynamic equilibrium, agility and biomechanics of the lower limb were measured at 1 week before intervention and 7 weeks after intervention to quantize the effect of integrative neuromuscular training on the sport ability and prevention of knee injury.RESULTS AND CONCLUSION: The vertical jump, agility, overall stability index, the knee extension angle as well as knee adduction and abduction moment in the experimental group were significantly improved (P < 0.05). Integrative neuromuscular training cannot only enhance the explosive strength of the lower limb, dynamic equilibrium, and agility when juvenile female athletes exercising, but also improve the biomechanics of the lower limb when jumping, increase the knee extension angle, and reduce knee adduction and abduction moment

Objective To study investigate the dose accuracy that can be achieved with the method of bulk density assignment.Methods Sixteen cases of nasopharyngeal cancer patients and nineteen cases of esophageal cancer patients who accept radiotherapy in our department were selected.The planning CT images with bulk density assignment to different classes of tissues were applied to calculate the dose distributions,and then the resulting dose volume histograms (DVH) of the tumor and organs of risk were compared with the original treatment plan.The paired t-test was taken for dose comparison between two plans.Results The DVH comparison based on the planning CT and the bulk density assignment CT showed good agreements.With nasopharyngeal cancer patients,differences between the two plans about target and normal tissue were less than 1％.With esophageal cancer patients,the dose differences were less than 2％.Conclusion Preliminary results confirm that the bulk density assignment method can be applied to calculate the dose distributions.

Gallbladder cancer (GBC) is the most common cancer of the biliary tract,constituting 80％-95％ of malignant biliary tract tumors.Surgical resection is currently regarded as the sole curative treatment for GBC.Hepatopancreatoduodenectomy (HPD) has been adopted to remove the advanced gallbladder tumor together with the infiltrated parts within the liver,lower biliary tract and the peripancreatic region of GBC patients.However,patients who underwent HPD were reported to have a distinctly higher postoperative morbidity (71.4％,ranging from 30.8％ to 100％) and mortality (13.2％,ranging from 2.4％ to 46.9％) than those given pancreatoduodenectomy (PD) alone.We present two patients with advanced GBC who underwent a modified surgical approach ofHPD:PD with microwave ablation (MWA) of adjacent liver tissues and the technique of intraductal cooling of major bile ducts.No serious complications like bile leakage,pancreatic fistula,hemorrhage and organ dysfunction,etc.occurred in the two patients.They had a rapid recovery with postoperative hospital stay being 14 days.Application of this approach effectively eliminated tumor-infiltrated adjacent tissues,and maximally reduced the postoperative morbidity and mortality.This modified surgical method is secure and efficacious for the treatment of locally advanced GBC.

Objective　To study the effect of portal vein blocking on the permeability of the intestinal mucosa in pigs. Methods　Healthy Rongchang pigs were divided into 3 groups: ① sham operation group(SO), ② portal vein clamping for 45 min group (PVC-45'), ③ portal vein clamping for 60 min group (PVC-60'). Urine lactulose/mannitol(L/M) ratio was measured after portal vein blocking. Results　The L/M ratio was increased significantly (P<0.05) in PVC-45' and 60' groups than in SO group, with that of PVC-60' higher than that of PVC-45' group, but not significantly. Conclusion　The increase of intestinal mucosal permeability after portal vein blocking is an early and important index for the damage of the intestinal mucosa barrier.

OBJECTIVETo establish a reliable model for drug screening and therapy by culturing rat femoral head and inducing cartilage degeneration quickly in vitro.

METHODSThe femoral heads from the same SD rats of two-month old were divided into control group and experimental group respectively. They were cultured with DMEM medium plus 10% fetal bovine serum or DMEM medium plus 10% fetal bovine serum plus 50 ng/ml IL-1β for three days. Femoral heads were fixed in 4% paraformaldehyde, decalcified, dehydrated, embedded in paraffin and cut into slices. Specimens were stained with Toluidine blue and Safranine O-Fast Green FCF. The protein expression levels of type II collagen, MMP13, Sox9 and ADAMTS5 were analyzed by immunofluorescence.

RESULTSBoth the Toluidine blue and Safranine O staining were pale in the margin of femoral heads which were stimulated with IL-1β for three days compared to that in control group. The Fast Green FCF staining was positive at the edge of the femoral head in experimental group, which indicated that cartilage became degenerated. The expression levels of both type H collagen and Sox9 were decreased significantly while the expression levels of MMP13 and ADAMTS5 were increased in experimental group.

CONCLUSIONThe model of cartilage degeneration is established by culturing and inducing the degeneration of the femoral heads quickly in vitro.

Animals ; Cartilage Diseases ; genetics ; metabolism ; Collagen Type II ; genetics ; metabolism ; Disease Models, Animal ; Femur Head ; metabolism ; Humans ; In Vitro Techniques ; Interleukin-1beta ; genetics ; metabolism ; Male ; Matrix Metalloproteinase 13 ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; SOX9 Transcription Factor ; genetics ; metabolism

OBJECTIVETo investigate the effects of serum containing Gumibao (Chinese character: see text) on the proliferation and differentiation of osteoblast induced by dexamethasone.

METHODSOsteoblasts were extracted from skulls in newly born (within 24 hours) SD rats, and digested with collagenase. The first passage of cells were used for experiments. Cells were cultured in the medium containing different concentrations of dexamethasone (0, 10(-8), 10(-7), 10(-6), 10(-5) ,10(-4) mol/L). Alkaline phosphatase staining were carried out after 1 week and numbers of mineralized nodes with alizarin red staining were observed after 3 weeks. Accordingly, following the treatment of 10(-5) mol/L dexamethasone for 1 week, cells were cultured in the medium with serum containing Gumibao (Chinese character: see text). One week after Cumibao (Chinese character: see text) treatment, cells were stained with Alkaline phosphatase and collagen I and PCNA were examined by Western-blot. However, the observation of numbers of mineralized nodes with alizarin red stain required one more week.

RESULTSHigh concentration of dexamethasone could inhibit the expression of PCNA, collagen I, alkaline phosphatase and reduce the number of mineralized nodes of osteoblast, while serum containing Gumibao (Chinese character: see text) could reverse the inhibition.

CONCLUSIONHigh concentration of dexamethasone could inhibit the proliferation and differentiation of osteoblastic cells, while serum containing Gumibao (Chinese character: see text) could reverse the inhibition.

Animals ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Collagen Type I ; analysis ; Dexamethasone ; pharmacology ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; pharmacology ; Female ; Osteoblasts ; cytology ; drug effects ; physiology ; Proliferating Cell Nuclear Antigen ; analysis ; Rats ; Rats, Sprague-Dawley

It is unanimously accepted that stroke is a highly heterogeneous disorder.Different subtypes of ischemic stroke may have different risk factors,clinical features,and prognoses.The aim of this study was to evaluate the risk factors,clinical characteristics,and prognoses of different subtypes of ischemic stroke defined by the Trial of ORG10172 in Acute Stroke Treatment (TOAST) criteria.We prospectively analyzed the data from 530 consecutive patients who were admitted to our hospital with acute ischemic stroke within 7 days of stroke onset during the study period.Standardized data assessment was used and the cause of ischemic stroke was classified according to the TOAST criteria.Patients were followed up till 30 and 90 days after stroke onset.It was found that large-artery atherosclerosis was the most frequent etiology of stroke (37.4％),and showed the highest male preponderance,the highest prevalence of previous transient ischemic attack,and the longest hospital stay among all subtypes.Small artery disease (36.4％) was associated with higher body mass index,higher plasma triglycerides,and lower plasma high-density lipoprotein cholesterol than cardioembolism.Cardioembolism (7.7％),which was particularly common in the elderly (i.e.,individuals aged 65 years and older),showed the highest female preponderance,the highest prevalence of atrial fibrillation,the earliest presentation to hospital after stroke onset,the most severe symptoms on admission,the maximum complications associated with an adverse outcome,and the highest rate of stroke recurrence and mortality.Our results suggest that ischemic stroke should be regarded as a highly heterogeneous disorder.Studies involving risk factors,clinical features,and prognoses of ischemic stroke should differentiate between etiologic stroke subtypes.

Objective: To investigate the effects of tumor necrosis factor-α (TNF-α) monoclonal anti-body on nuclear factor-κB (NF-κB) activation and inducible nitric oxide synthase (iNOS) expression in rats with pulmonary fibrosis induced by silica dust. Methods: A total of 48 male Wistar rats were randomly divided into intervention group, silica dust exposure group, and control group, with 16 rats in each group. The rats in the intervention group were given intratracheal injection of 50 mg silicon dioxide dust once to establish a rat model and then treated with subcutaneously injected TNF-α monoclonal antibody 15 mg/kg for 5 consecutive days at 2-6 days after the establishment of the model. The rats in the silica dust exposure group were treated with the same method to establish the model and then given subcutaneous injection of the same volume of normal saline. The rats in the control group were given intratracheal and subcutaneous injection of normal saline. In both groups, 8 rats each were sacrificed at 7 and 14 days after the establishment of the model. Hematoxylin-eosin staining or Masson staining was used to observe morphological changes in lung tissue, ELISA was used to measure the serum level of TNF-α, IHC was used to measure the expression of NF-κBp65 in lung tissue, Western blot was used to measure the protein expression of I-κB in lung tissue, and RT-qPCR was used to measure the transcriptional level of iNOS mRNA in lung tissue. Results: Compared with the control group, the silica dust exposure group had significant increases in the lung inflammation score (3.375±1.061 and 2.500±0.535) , serum TNF-α level (86.405±20.494 and 77.064±11.829) , absorbance of cells with positive NF-κBp65 in lung tissue (0.297±0.05 and 0.287±0.039) , and mRNA expression of iNOS (12.906±0.590 and 12.600±0.517) at 7 and 14 days after dust exposure, a significant increase in pulmonary fibrosis score at 14 days (3.250±0.707) , and significant reductions in the protein expression of I-κB at 7 and 14 days (0.579±0.141 and 0.748±0.081) (P<0.05) . Compared with the silica dust exposure group, the intervention group had significant reductions in the lung inflammation score at 7 days (2.375±1.061) , pulmonary fibrosis score at 14 days (2.375±1.061) , serum level of TNF-α at 7 and 14 days (66.565±19.850 and 58.734±16.335) , absorbance of cells with positive NF-κBp65 in lung tissue at 7 and 14 days (0.248±0.028 and 0.238±0.027) , and mRNA expression of iNOS at 7 and 14 days (11.656±0.405 and 12.025±0.618) , as well as significant increases in the protein expression of I-κB at 7 and 14 days (0.802±0.165 and 0.888±0.144) (P<0.05) . Conclusion TNF-α monoclonal antibody can inhibit the activation of the NF-κB signaling pathway and down-regulate the expression of iNOS, and thus exerts a certain protective effect on lung tissue in rats with pulmonary fibrosis induced by silica dust.

BACKGROUNDNF-kappaB p65 was shown to inhibit transcription of phosphoenolpyruvate carboxykinase (PEPCK), a rate-limiting enzyme in gluconeogenesis in the liver. To understand the mechanism of action of NF-kappaB p65, we investigated the nuclear receptor corepressor in the regulation of PEPCK transcription.

METHODSRat H4IIE cells, human hepatoma HepG2 cells and human embryo kidney (HEK) 293 cells were used in this study. The transcriptional activity of a rat PEPCK gene promoter (-490/+100) was analyzed in HepG2 cells, a HepG2 super suppressor IkBalpha (ssIkBalpha) stable cell line, and HEK 293 cells. The effects of p65 and ssIkBalpha on a rat PEPCK gene promoter were observed using the PEPCK luciferase reporter system. The interaction of the cAMP-response- element-binding (CREB) protein, histone deacetylase 3 (HDAC3) and silencing mediator for retinoic and thyroid hormone receptors (SMRT) with the PEPCK gene promoter were investigated using the chromatin immunoprecipitation (ChIP) assay. p65 cotransfection and RNAi-mediated gene knockdown were used to determine the corepressor involved in the inhibition of PEPCK by NF-kappaB p65 and the transcriptional regulation of CREB by NF-kappaB p65.

RESULTSNF-kappaB p65 inhibited PEPCK expression and the inhibition was blocked by ssIkBalpha. The inhibitory effect of p65 was completely blocked in a HepG2 stable cell line in which ssIkBalpha was expressed. HDAC3 or SMRT knockdown led to a significant up-regulation of PEPCK reporter activity in the presence of p65 cotransfection. In the ChIP assay the interaction of HDAC3 and SMRT with the PEPCK gene promoter was induced by p65 activation, but the CREB signal was reduced. Transcriptional activity of CREB was inhibited by NF-kappaB p65 cotransfection. The inhibitory effect of NF-kappaB p65 was blocked by HDAC3 RNAi or SMRT RNAi.

CONCLUSIONSThe study showed that the inhibition of PEPCK by NF-kappaB p65 was dependent on HDAC3 and SMRT, which form a nuclear corepressor complex for transcriptional inhibition. The transcription factors NF-kappaB p65 and CREB share the same corepressor HDAC3-SMRT, and the corepressor exchange leads to inhibition of PEPCK gene transcription by NF-kappaB p65.

Animals ; Blotting, Western ; Cell Line ; Chromatin Immunoprecipitation ; Cyclic AMP Response Element-Binding Protein ; genetics ; metabolism ; Hep G2 Cells ; Histone Deacetylases ; genetics ; metabolism ; Humans ; NF-kappa B ; genetics ; metabolism ; Nuclear Receptor Co-Repressor 2 ; genetics ; metabolism ; Phosphoenolpyruvate Carboxykinase (ATP) ; genetics ; Promoter Regions, Genetic ; genetics ; Protein Binding ; genetics ; physiology ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factor RelA ; genetics ; metabolism

Objective To explore the relationship between maternal passive smoking during early pregnancy and the risk of neural tube defects (NTDs). Methods Data was derived from a populationbased case-control study on birth defects in Shanxi province. The study subjects included 515 NTDs defects cases (236 cases of anencephaly, 237 spina bifida and 42 encephalocele) ascertained during January 2003 and June 2007 in the study areas and 682 normal controls randomly selected in the same residence during the same period as cases. Results The risk of NTDs in their offspring was 1.84 (95 % CI : 1.39-2.44) for mothers with passive smoking history during peri-conceptional period. There was a marked dose-response relation between maternal passive smoking and the risk of NTDs in offspring. Compared to the women without passive smoking, the NTDs risk in offspring was 1.51 for women with occasional passive smoking and 2.44 for women with passive smoking for almost everyday during the peri-conceptional period.Conclusion Maternal passive smoking during peri-conceptional period increased the risk of NTDs in offspring.