Objective To create a model with simple expression of mechanical characteristics of the human chest for the development of a manikin. Methods A simplified Gruben-model was proposed based on the anatomical structure and physical characteristics of the materials, and perfect coefficients were computed. The model feasibility was proved by the coefficient of determination and residual analysis.Results The mathematic form of the model provided had three fewer terms than Gruben′s. The coefficient of determination approximated 1, the residue was small, and the perfect coefficients of "a typical human" were determined.Conclusion The hypothesis of the model makes the coefficients physically meaningful, which provides a new method to study the force-displacement relationship of the thorax. Also the simple form makes it easy to create the model and provide some guidance for the design of a manikin′s chest.

Objective To study the indications for extubation of percutaneous transhepatic gallbladder drainage(PTGD).Methods Between January 2009 and December 2013,PTGD were performed on 104 patients with acute cholecystitis.The clinical data were analyzed retrospectively.Results PTGD were performed on all 104 patients successfully.In all the patients,after drainage the abdominal pain was relieved within 0.5 to 8 hours and mean time was(2.3 ± 1.9) h.The temperature decreased to normal in 1 days after drainage.The time of drainage was from 7 to 49 days,(22.4 ± 10.3) days on average.Thirteen patients'tubes were accidentally off during 3 to 12 days,5 patients were performed PTGD again,and 8 patients were given anti-infection,fluid infusion and other symptomatic treatments and all these patients were back to normal in time.Re-intubation rate was 4.8％.In 78 patients laparoscopic cholecystectomy (LC) were performed 1 to 2 months after PTGD.Operation time was between 35 to 95 min and mean time was(52.7 ± 15.0) min.There were 6 patients done open operation and the conservation rate was 7.7％.A mount of blood during LC was 30 to 150 mL,(61.7 ± 31.0) mL on average.No operative deaths occurred during therapeutic session.Conclusions Patients who formed PTGD obey the indications can extubate in time and reduce retrograde infection and skin irritation,also shorten the time during hospital's,which will have a positive impact about LC.

Objective: To observe the changes of somatosensory evoked potential(SEP) and nitric oxide (NO) after subarachnoid hemorrhage(SAH), and the influence of Ginkgo biloba extract (EGb). Method: Rats in sham-operated group, SAH model group and EGb-treated group underwent measurement of dynamic changes of regional cerebral blood flow( rCBF),SEP and NO levels both in serum and in brain tissue within 24h after operation. Result: In SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24h. The latency of SEP delayed progressively from 1h to 24h after SAH. NO levels in serum and in brain tissue decreased and increased respectively from 1h to 24h after SAH. EGb effectively antagonized the changes of above parameters. Conclusion: SEP is helpful in the judgement on brain ischemic damage after SAH. Decrease of NO in serum and increase of that in brain tissue may lead to cerebral vasospasm and ischemic brain damage respectively after SAH. EGb relieves SAH-induced brain ischemic damage by reversing the pathological alterations of NO.

BACKGROUND: Vibrio vulnificus inside the body could activate the NF-κB signaling pathway and initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsis associated with acute lung injury. High mobility group protein B1 (HMGB1) is an important late-acting pro-inflammatory cytokine involving in the pathophysiology of sepsis. It is also involved in the injury process in the lung, liver and intestine. There has been no report on the involvement of HMGB1 in Vibrio vulnificus sepsis-induced lung injury. METHODS: Sixty rats were randomly divided into a normal control group (group A,n=10) and a Vibrio vulnificus sepsis group (group B,n=50). Sepsis was induced in the rats by subcutaneous injection of Vibrio vulnificus (concentration 6×108 cfu/mL, volume 0.1 mL/100g)) into the left lower limbs. The rats in group B were sacrificed separately 1, 6, 12, 24, and 48 hours after the infection. Their lungs were stored as specimens, lung water content was measured, and lung pathology was observed under a light microscope. The expressions of the HMGB1 gene and protein in the lungs were detected by RT-PCR and Western blot. Data were analyzed with one-way analysis of variance (ANOVA) and the LSD method for pair-wise comparison between the two groups.P<0.05 was considered statistically significant. RESULTS: Compared to group A (0.652±0.177), HMGB1 mRNA expression in the lungs of group B was significantly higher at 0 hour (1.161±0.358,P=0.013), 24 hours (1.679±0.235,P=0.000), and 48 hours (1.258±0.274,P=0.004) (P<0.05), and peaked at 24 hours. Compared to group A (0.594±0.190), HMGB1 protein expression at 6 hours (1.408±0.567,P=0.026) after infection was significantly increased (P<0. 05), and peaked at 24 hours (2.415±1.064,P=0.000) after infection. Compared to group A (0.699±0.054), lung water content was significantly increased at 6 hours (0.759±0.030,P=0.001),12 hours (0.767±0.023,P=0.000), 24 hours (0.771±0.043,P=0.000) and 48 hours (0.789±0.137,P=0.000) after infection (P<0.05). Compared to group A, pathological changes at 12 hours in group B indicate marked pulmonary vascular congestion, interstitial edema and inflammatory infiltration. Alveolar cavity collapse and boundaries of the alveolar septum could not be clearly identified. CONCLUSION:Vibrio vulnificus sepsis can lead to injury in rat lungs, and increased HMGB1 expression in lung tissue may be one of the mechanisms for injury from Vibrio vulnificus sepsis.

Objective To investigate the effect of bacillus Calmette-Guérin(BCG)on bladder cancer cells and their metabolites, and to preliminarily explore the possible mechanisms of BCG in the treatment of bladder cancer. Methods The rat model of bladder cancer was induced by intravesical instillation with N-methylnitrosourea(MNU). Bladder cancer cells and normal transitional epithelial cells were isolated and primarily cultured, and were divided into 5 groups according to the different components of the culture medium. The concentration of tumor necrosis factor-α(TNF-α) and interleukin-10(IL-10)in the supernatant of each group was detected by enzyme linked immunosorbent assay (ELISA). The concentration of BCG to inhibit the cancer cell growth was determined by MTT assay. Apoptosis of bladder cancer cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL). Results Among the 15 rats,2 rats died after 2 times of instillation, and 3 rats died after 3 times of instillation, without obvious tumors found at autopsy. The other 10 rats were killed after completion of the intravesically instillation of MNU, and obvious tumors were found in 8 of them after dissection. The results of MTT assay showed that BCG had an inhibitory effect on the growth of bladder cancer cells,and the inhibitory rate was positively correlated with the concentration of BCG. The results of ELISA showed that the concentrations of TNF-α in the supernatant of groups B and D were(160.654 ± 5.775) ng/L and(124.443 ± 4.972)ng/L, respectively, with significant differences from those of the other three groups. The concentrations of IL-10 in the groups B and E were(16.973 ± 3.428)ng/L and(20.327 ± 2.721)ng/L, significantly higher than those of the other three groups. Apoptosis of cancer cells was not found in all groups. HE staining of the primary bladder cancer cells showed that the volume of cell nucleus was increased, and the nucleo-cytoplasmic ratio was increased. The number of nucleoli in some cells was increased and some nuclei appeared like ink drops with prominent nucleoli. Conclusions BCG has an inhibitory effect on the growth of rat bladder cancer cells. IL-10 and TNF-α secreted by the tumor cells might be involved in this regulatory process. However,apoptosis does not show an obvious effect on this inhibitory process.

Objective To study the effect of curcumin on rat model of N-methylnitrosourea ( MNU) -induced bladder cancer and its mechanism. Methods One hundred SD rats were randomly divided into four groups:control group (n=10), model group (n=10), intervention group (n=40) and treatment group (n=40). Rats in the control group re-ceived intravesical infusion of distilled water. Rats in the other three groups were given MNU (1 mg/mL) in 2 mL saline at 2nd, 4th, 6th and 8th weeks to induce bladder cancer. In the model group, the rats were injected with distilled water in the bladder. The rats in the intervention group received 2 mL curcumin solution (400 μmol/L) at the 1st, 3rd, 5th, 7th and 9th weeks, and were sacrificed at the 11th week. In the model group, the rats were injected with distilled water in the bladder. In the treatment group, the rats had intravesical instillation of curcumin in the bladder (400 μmol/L, 2 mL) at 10, 12, 14, 16, and 18 weeks, and sacrificed at the 19th week. Bladder tissue samples were taken for pathological exami-nation using hematoxylin and eosin ( HE) staining. TUNEL staining assay was used to detect the apoptosis in tumor tissue. The expression of apoptosis-related proteins was detected by Western blot. Results The incidence of bladder cancer was 90% (9/10) in the model group, 12. 5% (5/40) in the intervention group and 92. 5% (37/40) in the treatment group at the 10th week, showing a significant difference between the intervention group and model group (P<0. 05), indicating an obvious interventional effect of curcumin on the bladder cancer. The incidence rate of bladder cancer in the treatment group was 78. 4% (30/37) at the 19th week, and compared with the 10th week before treatment, showing that curcumin can de-lay the recurrence of bladder cancer. TUNEL staining assay confirmed that curcumin significantly promoted the apoptosis in bladder cancer cells and inhibited their proliferation. The Western blot analysis showed that curcumin inhibited the activa-tion of NF-κB and effectively down-regulated the expression of NF-κB-regulated gene product. Conclusions Curcumin has a significant interventional effect on MNU-induced bladder cancer in the rat models. The mechanism may be through inhibi-tion of NF-κB activation and effective down-regulated NF-κB regulation of the gene products, and to regulate the expression of related proteins in bladder cancer, i. e. , inhibition of proliferation, induction of apoptosis, and further play a role of an-ti-cancer intervention and prevention of bladder cancer recurrence.

This study was purposed to investigate the inhibitory effect of bactericidal permeability-increasing protein (BPI) on lipopolysaccharide (LPS)-mediated activation of platelets. Venous blood samples were obtained from 10 healthy volunteers and were prepared into platelet-rich plasma (PRP, 1 × 10(8)/ml). Experiments were divided into four groups: normal platelet group (untreated group); LPS group, BPI group and BPI+LPS group. PRP were stimulated by LPS (10 µg/ml) in the presence and absence of BPI (100 µg/ml) or BPI alone. Then platelets were harvested and determined for Toll-like receptor-4 (TLR-4) with flow cytometry (FCM), the supernatant was used for detection of cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) with enzyme-linked immunosorbent assay (ELISA). The results showed that as compared with normal platelet group, TLR-4 expression on platelets was significantly increased under LPS stimulation (P < 0.001); the levels of TNF-α and IL-6 in the supernatant were also remarkably elevated (P < 0.001). However, either TLR-4 expression or the cytokine levels significantly decreased in the presence of BPI when platelets underwent LPS-challenge (P < 0.05), but still were higher than that in normal platelet group. Stimulating the platelets with BPI alone could not enhance the TLR-4 expression and cytokine levels. It is concluded that BPI has the ability to inhibit the LPS-induced platelet activation.
Antimicrobial Cationic Peptides ; pharmacology ; Blood Proteins ; pharmacology ; Humans ; Inflammation ; Lipopolysaccharides ; adverse effects ; Platelet Activation ; drug effects ; Platelet-Rich Plasma ; metabolism ; Toll-Like Receptor 4 ; metabolism

Objective To investigating knowledge,attitudes,current behavior among primary school students on nutrition and food safety in two State-level poverty-stricken counties,and to explore the best educational model on nutrition and food safety.Methods 478 pupils at 4-6 grades were selected,using the method of stratified cluster sampling and questionnairs.Results The average score on knowledge was 18.66 ± 3.75,with the qualified rate as 61.09％ (the highest was 60.6％).The average score in the section of attitude was 5.82 ± 1.50.More than 97％ of the students agreed that it was necessary to receive knowledge on nutrition and food safety.The average score of behavior was 8.52 ± 2.56.Conclusion Rate of awareness on knowledge of nutrition and food safety had greatly improved among the students under study.Their habit tended to be more regular.However,we also noticed the gap between knowledge and behavior on this issue.

OBJECTIVETo detect the changes in the expression of apoptosis signals: Fas, FasL and NF-kappa B in the process of osteoclast-like cell (OLC) apoptosis effected by sodium fluoride.

METHODSAfter co-culture of osteoclast-like cells with 0, 5, 10 and 15 mg/L sodium fluoride, Fas, FasL and NF-kappa B antibody expressions were detected by immune-histochemistry.

RESULTSThe expression of Fas and FasL increased with the concentration of the sodium fluoride, however the expression of NF-kappa B decreased with the concentration of sodium fluoride.

CONCLUSIONIn the process of OLC apoptosis induced by sodium fluoride, the expression of Fas and FasL increased, and that of NF-kappa B decreased with the concentration of sodium fluoride respectively, and the changes of the expression present a dose-dependent pattern.

Animals ; Apoptosis ; Fas Ligand Protein ; Female ; Fluorides ; pharmacology ; Ligands ; Membrane Glycoproteins ; metabolism ; Mice ; Mice, Inbred C57BL ; NF-kappa B ; metabolism ; Osteoclasts ; cytology ; metabolism ; fas Receptor ; metabolism

OBJECTIVEIn this study, the authors investigated inhibition of coxsackievirus B (CVB) gene expression using antisense oligonucleotides complementary to the 5' NCR, translation initiation codon and structural protein coding sequences and also observed the dose-response of the sequence specific inhibition of CVB plaque formation by antisense oligonucleotides.

METHODSAntiviral activities of these oligonucleotides were evaluated by using plaque reduction assay, yield reduction assay, cytopathic effect (CPE) and Western blot analysis. The cells were treated with random oligonucleotides as a specificity control.

RESULTSAt a screening concentration of 5 micromole, 6 of the phosphorothioate oligonucleotide demonstrated some reduction of virus replication relative to untreated cells. 70%-90% inhibition of virus at 0.1 MOI (multiplicity of infection), 50% inhibition of virus infection at 10 MOI. The levels of the VP1 were reduced in CVB-infected cells treated with Scb561 and Scb733. VP1 was significantly reduced after treatment with 0.625 micromole Scb561 and almost undetectable in cells treated with 2.5 micromole Scb561. Dose response experiments implied that sequence specific oligonucleotide doses were related to effect on inhibition of CVB3 infection. When oligonucleotide doses were increased from 1.25 to 5 micromole, 75% to 90% inhibition were observed with Scb561 and 65% to 80% inhibition with Scb733, whereas random control failed to inhibit CVB replication (8% inhibition for each). CONCLUSION The present studies showed that antisense oligonucleotides against internal ribosome entry site (IRES) and translation initiation codon were capable of specifically inhibiting the synthesis of viral protein and subsequent productive CVB replication.The selective inhibition using antisense oligonucleotide might lead to development of an effective antiviral agent for future clinical evaluation.

5' Untranslated Regions ; genetics ; Dose-Response Relationship, Drug ; Enterovirus B, Human ; drug effects ; genetics ; Gene Expression ; drug effects ; HeLa Cells ; Humans ; Oligonucleotides, Antisense ; pharmacology ; Ribosomes ; metabolism ; Viral Structural Proteins ; biosynthesis ; genetics ; Virus Replication ; drug effects