Health Promotion ; organization & administration ; Humans ; Occupational Health ; Occupational Health Services ; organization & administration ; Risk Assessment

Under the background of the new medical reform, a large variety of traditional Chinese medicine from complicated sources, Chinese traditional medicine of actor of true and false of the quality directly affect the drug safety and clinical efficacy, but also relate to the social and economic benefits of hospital. Along with the development of the modern management of medical institutions and drug circulation circulation system reform in our country, the hospital drug inventory, supply and management work is an important topic for the pharmaceutical trading. However, there is always contradiction, dispensary need to supple pharmacy, in order to satisfy the demands of hospital patients with normal diagnosis and treatment work. However, if the drug inventory is too much, not only increases the drug monitoring problem, at the same time, but also causes storage costs rise. Therefore, completing scientific and reasonable storage and management becomes urgent problems at present. Wherefore, our country administration of traditional Chinese medicine in 2007 promulgated the "Chinese traditional medicine yinpian management norms in hospital", aims to standardize management of Chinese traditional medicine quality and improve the safety of drugs. The author through looking up information and visiting survey, to understand the currently existing problems, and summarizes the literature inland and abroad in recent years Chinese medicine drug inventory management work experience, in view of status quo of Chinese medicine inventory management in China, put forward the solution. To guarantee TCM pharmacy management more standardized, more standard, to adapt to the new reform of Chinese traditional medicine industry, improve the management level of hospital, defend the hospital's reputation and the patient's interests.
Drugs, Chinese Herbal ; supply & distribution ; Humans ; Inventories, Hospital ; economics ; legislation & jurisprudence ; Medicine, Chinese Traditional ; economics ; standards ; Quality Control ; Safety

Objective To investigate the effect of tumor necrosis factor-α (TNF-α) on intracellular calcium concentration ([Ca2 +] i) and the contraction of glomerular mesangial cells (GMCs),and prove that hypercontractility of GMCs induced by TNF-α in hepatorenal syndrome(HRS) was connected with inositol 1,4,5-trisphophate receptors (IP3Rs).Methods GMCs were divided into TNF-α-treated 0 h,4h,and 24 h groups.Another 3 groups were blocked by 2-APB.The effect of TNF-α on [Ca2 +] i was identified and observed whether it could be blocked by 2-APB.Contraction of GMCs was determined by accessing the surface area of cells before and after contraction.Results TNF-α significantly increased ET-induced calcium release,in that we found higher [Ca2 +] i after stimulated by ET in TNF-α-treated 4 h group and 24 h group[4 h:(648.08 ±267.11) nmol/L; 24 h:(879.30 ±-260.29) nmol/L; 0 h:(619.93 ±258.94)nmol/L,F =5.486,4 h vs 0 h:P ＜ 0.05 ; 24 h vs 0 h:P ＜ 0.05 ;24 h vs 4 h:P ＞ 0.05].This phenomenon can be totally blocked by 2-APB in all groups.The change in planar surface area in response to ET was slightly in control cells but significantly enhanced in TNF-α-treated cells [4 h:(2198 ± 340)μm2; 24h:(2260±553)μm2; 0 h:(2436±474)μm2,F =4.001,4 h vs0 h:P ＜0.05; 24 h vs0 h:P ＜0.05;24 h vs 4 h:P ＞ 0.05].Conclusion TNF-α can enhance ET-induced sarcoplasmic reticulum Ca2 + release and increase the contractile responses of GMCs to ET,which is associated with IP3Rs.TNF-α is responsible for hyperconstractility of glomeruli in HRS.

Objective To study the effect of survivin gene expression on the lymphocyte’s proliferation and function in cultured K562 cells. Methods The constructed recombinant vector pEGFP-C1-survivin and the plasmid pTZU6+1-survivin encoding short hairpin RNA of survivin were transfected into K562 cells respectively to generate K562/survivin+ cells and K562/survivin-cells. K562/survivin+ cells were selected by G418. The survivin mRNA and protein levels in the 3 kinds of cells (K562/survivin+,K562 and K562/survivin-) were detected by semi-quantitative RT-PCR and immunohistochemistry methods. The peripheral blood mononuclear cells (PBMC) from healthy subjects were co-cultured with these 3 cells respectively in mixed lymphocyte-tumor cell culture (MLTC). Lymphocyte proliferation in the supernatant was evaluated by MTT assay. Nature killer activity was detected by flow cytometry and IFN-? level was measured by ELISA assay. Results Proliferation index in K562/survivin+ group was much lower than that in the other 2 groups (P

Objective To investigate the signal mechanism of protein kinase C alpha(PKC-α)participated in enhanced expression of type Ⅰ inositol 1,4,5-trisphophate receptors (IP3 RI) induced by tumor necrosis factor alpha(TNFα),in order to delineate the mechanisms of decreased glomerular filtration rate (GFR) in hepatorenal syndrome caused by TNFα.Methods The glomerular mesangial cells (GMCs)line from rats was chosen as experimental material.GMCs were divided into control (D),TNFα-2 h,TNFα-4 h,TNFα-8 h,and TNFα-24 h groups.Moreover,another two groups were sanflngol-8h (S),TNFα + Sanfingol-8h(TS)groups.The effect of TNFα on the expression of IP3RI was detected by immunocytochemical staining,Western blotting,teal time-polymerase chain reaction (PCR) assays.Results Immunocytochemical staining demonstrated that IP3 RI was mainly distributed in cytoplasm of GMCs.Enhanced positive staining was determined in all TNFα-treated groups,especially in TNFα-8 h group.Western blotting demonstrated that the expression of IP3RI protein was significantly higher in TNFα-4 h,TNFα-8h and TNFα-24 h groups than control group(4 h:1.82 ± 0.63 ; 8 h:2.95 ± 0.66 ; 24 h:2.48 ± 0.72 ; D:1 ±0.02 ; F =9.24,P ＜ 0.05).The expression of IP3 RI protein was the highest in TNFα-8 h and TNFα-24 h groups(P ＜0.05).No difference was found among S,TS,and control groups(S:1.39 ±0.65; TS:1.35± 0.37 ; P ＞ 0.05).Real time-PCR found the expression of IP3 RImRNA was significantly higher in all TNFα-treated groups than control group(2 h:3.35 ± 1.97; 4 h:3.16 ± 1.35; 8 h:3.70 ± 1.76; 24 h:4.49±1.70; D:1 ±0.01; F =6.167,P ＜0.05).No difference was found among all TNFα-treated groups(P ＞0.05).No difference was found among S,TS,and control groups(S:1.53 ±0.79; TS:1.32 ± 0.38 ; P ＞ 0.05).Conclusions IP3 RI was mainly distributed in cytoplasm of GMCs.TNFa could enhance the expression of IP3 RI protein and IP3 RI mRNA,which could be blocked by sanfingol,a PKCα inhibitor.It might be an important signal in the mechanisms of GFR decrease caused by TNFα in hepatorenal syndrome.

Heart Failure ; diagnosis ; therapy ; Humans ; Phonocardiography ; methods

OBJECTIVETo investigate the effect of Actinidia chinensis Planch polysaccharide (ACPS) on the growth and apoptosis of human gastric cancer SGC-7901 cells, and to explore the effect of SGC-7901 cells on p-p38 expression.

METHODSThe inhibition rates at different concentrations of ACPS on SGC-7901 cells at 24, 48, and 72 h were detected using CCK-8 method. Apoptosis ratios in SGC-7901 were determined by flow cytometry after 48-h treatment of different concentrations of ACPS. The expression of pro-caspase-9, PARP, and p-p38 in SGC-7901 cells after treated by different concentrations of ACPS was detected using Western blot. The expression of pro-caspase-9, PARP, and p-p38 was detected after SGC-7901 cells were pre-treated by p38 specific inhibitor.

RESULTSCompared with the control group, the optical density of SGC-7901 cells decreased after treated by 1, 2.5, 5, and 10 mg/mL ACPS (P < 0.05). Meanwhile, the longer the acting time, the lower the optic density (P < 0.01). IC50 was 7.43 mg/mL at 24 h; 3.88 mg/mL at 48 h, and 1.32 mg/mL at 72 h respectively. ACPS suppressed the protein expression of pro-caspase-9 (P < 0.01) and up-regulated the expression of PARP (89KD) (both P < 0.01). Further study showed that the protein expression of p-p38 was up-regulated in SGC-7901 cells treated by ACPS of different concentrations at 24 h (P < 0.05). The expression of phosphorylation p38 and the ACPS induced apoptosis of SGC-7901 cells could be inhibited after treated by specific inhibitor for 2 h.

CONCLUSIONSACPS could inhibit the growth of SGC-7901 cells and induce apoptosis. The underlying mechanism of inducing apoptosis was partially due to activating the p38MAPK path and further activating Caspase9 and PARP, finally leading to cell death.

Actinidia ; chemistry ; Apoptosis ; drug effects ; Caspase 9 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Poly (ADP-Ribose) Polymerase-1 ; Poly(ADP-ribose) Polymerases ; metabolism ; Polysaccharides ; pharmacology ; Stomach Neoplasms ; metabolism ; pathology ; p38 Mitogen-Activated Protein Kinases ; metabolism

Objective To evaluate the effect of dexmedetomidine on noise-induced hearing loss in guinea pigs.Methods Twenty-four adult male guinea pigs,aged 3 months,weighing 400-500 g,were randomly divided into 3 groups (n =8 each) using a random number table:dexmedetomdine group (group D),noise-induced hearing loss group (group N) and dexmedetomidine + noise-induced hearing loss group (group DN).A loading dose of dexmedetomidine 5 μg/kg was infused over 5 min,followed by 135 min of infusion at a rate of 10 μg· kg-1 · h-1.The equal volume of normal saline was infused in group N.Groups N and DN were exposed to noise of 4 kHz center frequency and 118-122 dB SPL for 120 min starting from 20 min of administration.Mean arterial pressure (MAP) and cochlear blood flow (COBF) were recorded before administration and every 5 min during drug administration.The changing rate of COBF was calculated.Arterial blood samples were collected for determination of plasma concentration of noradrenaline (NE) by high performance liquid chromatography at 20 and 140 min of administration.Auditory brainstem response (ABR) threshold was recorded before administration and at 1 and 72 h and 10 days after the end of administration.Results Compared with group N,MAP was significantly decreased,the changing rate of COBF was increased at 5-10 min and 30-140 min of administration,ABR threshold was decreased at 1 and 72 h and 10 days after the end of administration,and the plasma concentration of NE was decreased at 140 min of administration in D + N group (P ＜ 0.05).Conclusion Dexmedetomidine can attenuate noise-induced hearing loss in guinea pigs possibly through inhibiting activation of sympathetic nerves and increasing COBF.

Objective To assess the safety and the efficacy of endoscopic ultrasound (EUS)-guided transmural drainage of pancreatic pseudocysts (PPC).Methods A total of 17 patients with PPC who underwent EUS to detect the optimal site and depth of puncture.The needle was punctured into the PPC cavity through endoscopic biopsy hole,cyst fluid was drained with a syringe.The guide wire was inserted along the pinhole under X-ray,and then the needle-knife was sent along the guide wire to cut the gastric wall and pseudocysts wall,followed by balloon dilation.The way of drainage was selected according to the cyst fluid properties.The technical success rate,treatment success rate,complication occurring rate and the skills were evaluated.Results Four patients were with nasalcystic catheter drainage,9 patients with double pigtail stents internal drainage,and 4 patients with nasal-cystic catheter and double pigtail stents combination drainage.The treatment success rates were 3/4,7/9,and 4/4 respectively.Only 1 patient subsequently developed bleeding from puncture site after stent successively placed,and was turned to surgery because of ineffective endoscopic treatment.Infection occurred in 4 patients during drainage,two of those were switched to surgical resection due to poor medical treatment response,and the other 2 were cured with intravenous infusion of antibiotics sensitive to cyst fluid bacteria and metronidazole rinse PPC.The median follow-up duration was 28.5months,and there was none of recurrence.Conclusions EUS-guided transmural drainage of PPC is safe.Stent placement and nasal-cystic catheter play an important role in PPC treatment.

Aim To express hepatitis C virus glycoprotein E (gE) deleting carboxy-terminal 31 amino acids, and detect anti-E antibody in HCV patients using expressed gE. Methods E gene derived from HCV H strain was inserted into baculovirus transfer vector containing a polyhedrin promotor. The recombinant plasmid was cotransfected into insect cell sf9 with a viral expression vector. The expression of gE was analyzed with Western blot, and the cells were used for dectecting antibodies against E1 and E2 in 35 hepatitis C patients by indirect immunofluorescence. Results A series of proteins with different relative molecular masses(Mr) could be detected by Western blot. Results from indirect immunofluorescence staining showed and only 4 patients were anti-E antibody positive gE was located in cytoplasm. Conclusion HCV gE is expressed successfully in insect cells, the study lay the foundation for further developing HCV vaccine.