Adolescent ; Adult ; Female ; Humans ; Male ; Occupational Exposure ; Organotin Compounds ; poisoning ; Poisoning ; diagnosis ; therapy ; Retrospective Studies ; Young Adult

Objective To investigate the clinical characteristics and risk factors for healthcare-associated infection (HAI)in patients with severe chronic hepatitis B (CHB),and provide theoretical basis for preventing and controlling HAI.Methods Retrospective survey was used to investigate the occurrence of HAI in hospitalized patients with severe CHB in a hospital between January 2012 and January 2015,risk factors for HAI were analyzed. Results A total of 126 patients with severe CHB were investigated,49 patients developed 106 times of HAI, incidence of HAI was 38.89%.The main HAI site was respiratory tract (n=47,44.34%),the next was abdominal cavity (n=34,32.08%).A total of 76 isolates of pathogens were detected,gram-negative bacteria,gram-positive bacteria,and fungi accounted for 53.95%(n =41 ),43.42%(n =33),and 2.63%(n =2)respectively.Risk factors for HAI in patients with severe CHB were patients ’ age ≥ 60 years, length of hospital stay ≥ 30 days, complications,invasive operation,serum albumin < 35 g/L,and white blood cell count (WBC)< 4 × 109/L. Conclusion Incidence of HAI in patients with severe CHB is high,the majority are respiratory tract and abdominal cavity infection,risk factors are old age,long length of hospital stay,invasive operation,hypoalbuminemia,and low WBC count.

To investigate the influence of the difference enhancers on the transport mechanism of chlorogenic acid (CGA) across Caco-2 cells model, a RP-HPLC method was adopted to detect the concentrations of CGA. At the concentrations of 20 to 80 microg x mL(-1), the difference of absorption rate constants (K(a)) was not statistically significant. At the concentrations of 40 and 20 microg x mL(-1), the ratios of apparent permeability coefficients (P(app)) of the apical to basolateral and the basolateral to apical were 1.14 and 1.18, respectively. With the effect of enhancers K(a) and P(app) increased, the absorption half-life (T1/2) decreased. CGA passed through the Caco-2 cell membrane mainly by passive transport. It showed that monocarboxylic acid transporter (MCT) could be involved in the across membrane transport process of CGA. Borneol had no effect on the cell membrane transport processes. The order of increasing absorption of CGA caused by the enhancers was sodium lauryl sulphate > sodium taurocholate > carbomer.
Absorption ; Acrylic Resins ; pharmacology ; Caco-2 Cells ; Cell Membrane Permeability ; drug effects ; Chlorogenic Acid ; pharmacokinetics ; Humans ; Sodium Dodecyl Sulfate ; pharmacology ; Taurocholic Acid ; pharmacology

The purpose was to compare the difference between transgene expressions driven by homologous duplicated carbonic anhydrase (DCA) promoter and foreign CaMV35S promoter in the unicellular green alga, Dunaliella salina(D.salina).The CaMV35S promoter-bar construct and DCA promoter-bar construct into D.salina by a Backon 2000 electroporation system were introduced. After the repeated selections with the phosphinothricin (PPT) of 3mg/L, 3 PPT-resistant phenotype transformants were isolated from the CaMV-bar and DCA-bar pools of transformants of D. salina, respectively. The results of PCR and sequencing showed that bar genes were stably integrated into the genome of D.salina, and Southern bolts showed the number of transgene copy had no significant difference between both promoters. Semi-quantitive RT-PCR indicated that the mRNA levels of bar gene were higher in DCA-bar transformants than the CaMV-bar transformants, and could be increased under the induction of high salt in DCA-bar transformants but not in the CaMV-bar transformants. Analysis of growth rate of transformants showed DCA-bar transformants achieved the log stage faster than the CaMV-bar transformants. It is concluded that the homologous promoters have more advantages than the foreign promoters in the transgenic D.salina.

Carrier State ; virology ; Female ; Hepatitis B ; complications ; Humans ; Lymphoma, Large B-Cell, Diffuse ; virology ; Male ; Middle Aged

Objective To investigate the effect of emulsified isoflurane anesthesia on the expression of hippocampal amyloid-beta protein (Aβ) and phosphorylation of Tau protein in rats.Methods Seventy-two healthy Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly divided into 3 groups:normal control group (group C,n =12),fat emulsion group (group E,n =12),and 8％ emulsified isoflurane group (group EI,n =48).30％ fat emulsion and 8％ emulsified isoflurane 0.15 ml/100 g were slowly injected via the tail vein in groups E and EI,respectively.Morris water maze test was performed 6 days before anesthesia.Twelve animals in each group were chosen at 2 h after administration (T1) in E group,at the corresponding time points in C group,or at T1 and 1,7 and 14 days after administration (T2-4) in EI group and underwent spatial probe tests,and the escape latency was measured.The rats were anesthetized with intraperitoneal 1％ pentobarbital sodium 4 g/100 g after the end of Morris water maze test.Blood samples were taken for determination of the plasma S100 protein concentration.The rats were then sacrificed and brains were removed for determination of the expression of hippocampal Aβ and phosphorylated Tau (p-Tau) protein by immunohistochemistry.Results The escape latency and swimming distance were significantly shorter on 3rd,4th and 5th days than those on 1st day of place navigation test before anethesia (P ＜ 0.01).Compared with group C,the escape latency and swimming distance were significantly prolonged and the time of staying at the original platform quadrant was shortened at T1,and the plasma S100 protein concentration was decreased at T4 in group EI (P ＜ 0.05),and no significant change was found in the each parameter of Morris water maze test,plasma S100 protein concentration,and expression of Aβ and p-Tau protein in group E (P ＞ 0.05).The escape latency and swimming distance were significantly shorter and the time of staying at the original platform quadrant was longer at T2-T4 than at T1 in group EI (P ＜ 0.05).Conclusion Emulsified isoflurane anesthesia exerts no effect on the expression of hippocampal Aβ and phosphorylation of Tau protein,indicating that hippocampal Aβ and Tau protein are not involved in emulsified isoflurane anesthesia-induced cognitive dysfunction in rats.

Objective To study the anti-tumor effect of anti-HER-2 engineering antibodies chA21 and Herceptin on nude mice xenografts of human ovarian cancer SKOV3 cells and explore its mechanism.Methods An animal model with human ovarian cancer SKOV3 cells involved in nude mice was established and the mice were randomized into 3 groups: normal saline(NS),chA21 and Herceptin.The mice were respectively administrated with Herceptin(30mg/kg) and chA21(30mg/kg) via caudal vein injection twice a week for consecutive 6 weeks,and then were killed after 44 days adminstration of the drugs.The volumes of the xenografts were measured twice a week.The tumor weight and inhibition ratio were measured after mice were killed.Ki67 and NF?B expression in the three groups was quantificationally analyzed by immunohistochemistry on tissue microarray sections combined with a micro-image analysing system.Results The growth of xenografts of human ovarian cancer SKOV3 cells in nude mice was significantly inhibited by either Herceptin or chA21. Both Ki-67 labeling indices and NF?B levels in chA21 and Herceptin groups were lower than those in the control(P

0.05).The serum PICP of tubercular meningitis children after 4 neeks glucocorticoid therapy (108.85?46.13) ?g/L was significantly lower than that in control group((154.38)?47.98) ?g/L and glucocorticoid- pretreatment (152.99?44.78) ?g/L (P

Aim To explore the effects of anti-HER-2 chimeric antibody chA 21 on proliferation and apoptosis of SKBR3 cells.Methods MTT colorometric assay,HE staining,transmission electron microscopy,flow cytometry,and TUNEL were used to study the proliferation inhibition and apoptosis induction of SKBR3 cells by chA 21 in vitro.Results Proliferative inhibition rates and apoptotic index of SKBR3 cells were increased in a dose and time dependent manner after exposure to chA21(0.2～5.4 mg?L~(-1)).Conclusion chA 21 could remarkably inhibit proliferation of SKBR3 cells in vitro and apoptosis induction may be one of its main mechanisms.

Objective To evaluate ketamine-induced cerebral protection in mice with traumatic brain injury (TBI) by magnetic resonance imaging (MRI).Methods Thirty-two pathogen-free healthy male C57BL/6 mice,aged 8 weeks,weighing 26-30 g,were divided into 4 groups using a random number table:control group (group C,n=7),ketanine group (group K,n=7),TBI group (n=9) and TBI plus ketamine group (group TBI+K,n =9).TBI was produced with a pneumatically driven controlled cortical impact device.Ketamine 150 mg/kg was intraperitoneally injected at l h after operation in TBI+K and K groups,while the equal volume of normal saline was given instead in TBI and C groups.Open field test was conducted at 24 h,72 h and 7 days after operation.The animals in TBI and TBI+K groups were scanned by T1-weighted MRI at 6,24 and 72 h after operation,the animals in C and K groups were scanned by MRI at 24 h after operation,and the development of cerebral edema was observed.Results MRI scan showed no cerebral edema in C and K groups,and different degrees of cerebral edema were found in TBI and TBI+K groups.Compared with group C,the locomotor distance was significantly shortened at 24 and 72 h after operation in group TBI (P＜0.05).Compared with group TBI,the size of cerebral edema was significantly decreased,and the locomotor distance was prolonged at 24 and 72 h after operation in group TBI+K (P＜0.05 or 0.01).Conclusion MRI method further clarifies that ketamine can produce cerebral protection to some extent in mice with TBI.