Objective This pre-DIC rat models were constructed by injecting LPS in order to reveal the relationship and significance among tissue factor pathway inhibitor (TFPI),platelet, fibrinogen, prothrombin time and activated partial thromboplastin time. Methods Enzyme-labeled immunosorbent assay was used to detect blood plasma TFPI in pre-DIC state rats(n=16),DIC state rats(n=8)and health rats(n=8).Platelet, fibrinogen, prothrombin time and activated partial thromboplastin time in the same rat were detected. Results TFPI increased first(pre-DIC state)and then decreased(DIC state)in the blood plasma of rata, but the levels of TFPI were always higher than that in the normal state. Conclusions TFPI is more sensitive and accurate to monitor the pro-DIC state than routine examination, which is very useful in the early diagnosis of pre-DIC state.

Action Potentials ; drug effects ; Animals ; Mice ; Mice, Inbred Strains ; Neurons ; drug effects ; physiology ; Plant Extracts ; pharmacology

Regeneration of axon was play an important role in the functional repair after spinal cord injury,and it was affected by vascular damage,absent availability nutrition transportation,urged to be solved.Inducing angiogenesis by electrical fields might be benefit to enhance anatomical plasticity and recovery of function after spinal cord injury.

Objective To investigate the protective effect of allicin on intestinal mucosal barrier of septic rats so as to explore the possible mechanism.Methods Twenty-four male SD rats were randomly (random number) divided into sham,septic model and allicin treatment group.Septic model was established by cecal ligation and puncture (CLP) in rats.Rats in the treatment group were administered with allicin (30 mg/kg,ip)at 6 h and 12 h after modeling,while those in the model and sham groups were treated with equal amount of saline instead.Rats were sacrificed at 24 h and the serum D-lactic acid,diamine oxidase (DAO) and fluorescence isothiocyanate-dextran (FITC-Dextran,FD-40) were determined to evaluate the intestinal mucosal barrier function.The levels of tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),malondialdehyde (MDA),and the activity of superoxide dismutase (SOD) in intestinal tissue were measured.Histopathological changes of intestinal mucosa injury were assessed by Hematoxylin-eosin staining.Results Compared with the sham group,levels of serum D-lactic acid,DAO and FD-40 increased significantly in the CLP group (D-lactic acid:599.4±101.1 vs.149.2±20.63 nmoL/mL,t=11.84,P＜0.01;DAO:302.1 ±64.5 vs.76.57±14.76 ng/mL,t=9.433,P＜0.01;FD-40:6664.0±1437.0vs.1446.0±205.0 ng/mL,t =9.704,P ＜0.01);intestinal morphology damage occurred in the CLP group;intestinal levels of TNF-α,IL-6 and MDA increased greatly (TNF-αt:186.35 ±20.43 vs.58.76 ±8.94 pg/mL,t=17.23,P＜0.01;IL-6:763.25±85.23vs.125.36±14.37 pg/mL,t=22.54,P＜0.01;MDA:29.36±3.27vs.7.24±0.85 nmol/mg prot,t=16.61,P＜0.01),while SOD activity reduced (35.75±6.53 vs.73.26 ±8.35 U/rmg prot,t =10.57,P ＜0.01) in the CLP group.Allicin treatment greatly inhibited the increase of D-lactic acid,DAO and FD-40 levels in rat plasma caused by CLP (D-lactic acid:330.1 ±81.77 vs.599.4±101.1 nmol/mL,t=7.086,P＜0.01;DAO:171.8±49.70vs.302.1±64.56ng/mL,t=5.45,P＜0.01;FD-40:3349.0±1167.0 vs.6664.0±1437.0 ng/mL,t=6.165,P＜0.01);intestinal morphology damage was improved in the allicin treatment group;allicin treatment greatly inhibited the intestinal levels of TNF-o,IL-6 and MDA and preserved the intestinal SOD activity compared with the CLP group (TNF-α:95.37 ±12.68 vs.186.35 ±20.43 pg/mL,t =12.29,P＜0.01;IL-6:354.27±46.27vs.763.25±85.23pg/mL,t=14.45,P＜0.01;MDA:16.27±3.14vs.29.36±3.27 nmol/mgprot,t=9.831,P＜0.01;SOD:55.35 ±6.23vs.35.75±6.53 U/mgprot,t=5.522,P ＜0.01).Conclusions Allicin could inhibit local inflammation and oxidative stress in the intestine and exerts protective effect on intestinal mucosal barrier of septic rats.

Using the field sampling and indoor soil cultivation methods, the dynamic of ginseng rhizosphere soil microbial activity and biomass with three cultivated ages was studied to provide a theory basis for illustrating mechanism of continuous cropping obstacles of ginseng. The results showed that ginseng rhizosphere soil microbial activity and biomass accumulation were inhibited observably by growing time. The soil respiration, soil cellulose decomposition and soil nitrification of ginseng rhizosphere soil microorganism were inhibited significantly (P <0.05), in contrast to the control soil uncultivated ginseng (R0). And the inhibition was gradual augmentation with the number of growing years. The soil microbial activity of 3a ginseng soil (R3) was the lowest, and its activity of soil respiration, soil cellulose decomposition, soil ammonification and soil nitrification was lower than that in R0 with 56.31%, 86.71% and 90. 53% , respectively. The soil ammonification of ginseng rhizosphere soil microbial was significantly promoted compared with R0. The promotion was improved during the early growing time, while the promotion was decreased with the number of growing years. The soil ammonification of R1, R2 and R3 were lower than that in R0 with 32.43%, 80.54% and 66.64% separately. The SMB-C and SMB-N in ginseng rhizosphere soil had a decreased tendency with the number of growing years. The SMB-C difference among 3 cultivated ages was significant, while the SMB-N was not. The SMB of R3 was the lowest. Compared with R0, the SMB-C and the SMB-N were significantly reduced 77.30% and 69.36%. It was considered by integrated analysis that the leading factor of continuous cropping obstacle in ginseng was the changes of the rhizosphere soil microbial species, number and activity as well as the micro-ecological imbalance of rhizosphere soil caused by the accumulation of ginseng rhizosphere secretions.
Agriculture ; Ammonium Compounds ; metabolism ; Bacteria ; growth & development ; Biomass ; Cellulose ; metabolism ; Nitrification ; Panax ; growth & development ; microbiology ; Plant Roots ; growth & development ; microbiology ; Rhizosphere ; Soil ; chemistry ; Soil Microbiology ; Time Factors

OBJECTIVETo compare the effect of citric acid stimulation on salivary alpha-amylase (sAA), total protein (TP), salivary flow rate, and pH value between Pi deficiency (PD) children and healthy children, thereby providing evidence for Pi controlling saliva theory.

METHODSTwenty PD children were recruited, and 29 healthy children were also recruited at the same time. Saliva samples from all subjects were collected before and after citric acid stimulation. The sAA activity and amount, TP contents, salivary flow rate, and pH value were determined and compared.

RESULTS(1) Citric acid stimulation was able to significantly increase salivary flow rate, pH value, sAA activities, sAA specific activity and sAA amount (including glycosylated and non-glycosylated sAA amount) in healthy children (P<0.05), while it could markedly increase salivary flow rate, pH value, and glycosylated sAA levels in PD children (P<0.05); (2) Although there was no statistical difference in determined salivary indices between the two groups (P>0.05), salivary indices except salivary flow rate and glycosylated sAA levels decreased more in PD children. There was statistical difference in sAA activity ratio, sAA specific activity ratio, and the ratio of glycosylated sAA levels between PD children and healthy children (P<0.05).

CONCLUSIONPD children had decreased response to citric acid stimulation.

Automobile Driving ; China ; Humans ; Seat Belts ; utilization

Objective To evaluate the effect of sufentanil on autophagy during myocardial ischemia-reperfusion (I/R) in rats.Methods Eighteen adult male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 3 groups (n =6 each) using a random number table:sham operation group (group SH),I/R group,and sufentanil group (group S).Myocardial I/R injury was produced by occlusion of the anterior descending branch of the left coronary artery for 30 min followed by 120 min reperfusion in the rats anesthetized with chloral hydrate in I/R and S groups.Sufentanil 3 μg/kg was injected via the caudal vein at 30 min prior to ischemia in group S.The equal volume of normal saline was given in SH and I/R groups.At 120 min of reperfusion,arterial blood samples were collected for determination of serum creatine kinase-MB (CK-MB) and lactic dehydrogenase (LDH) concentrations,and myocardial specimens were obtained for examination of the ultrastructure of myocardial cells (using transmission electron microscopy) and for determination of autophagy-related proteins microtubule-associated protein 1 light chain 3 Ⅱ (LC3Ⅱ),Beclin-1 and Bcl-2 expression (by Western blot).Results Compared with group SH,the serum CK-MB and LDH concentrations were significantly increased,the expression of LC3 Ⅱ and Beclin-1 was significantly up-regulated,and Bcl-2 expression was significantly down-regulated in group I/R,and the serum CK-MB concentration was significantly increased,the expression of Beclin-1 and Bcl-2 was significantly down-regulated in group S (P＜0.05).Compared with group I/R,the serum CK-MB concentrations were significantly decreased,the expression of LC3 Ⅱ and Beclin-1 was significantly down-regulated,Bcl-2 expression was significantly up-regulated (P＜ 0.05),no significant change was found in serum LDH concentrations (P＞0.05),and the pathological changes were reduced in group S.Conclusion The mechanism by which sufentanil reduces myocardial I/R injury may be related to decreased autophagy in rats.

Objective To investigate the effects and mechanisms of all-trans retinoic acid(ATRA)on the proliferation and cell cycle of lung carcinoma cell line A549.Methods The A549 cells were treated with ATRA at the dosages of 5,10,50 ?mol/L for 1-7 d.The proliferation of A549 was assessed by MTT method and cell cycle was analyzed by flow cytometry.The expressions of CDK4,Rb and p-ERK1/2 were assessed by Western blotting.CyclinD1 mRNA was analyzed by SYBR-PCR amplification.Results ATRA obviously inhibited the proliferation of A549 cells,and the cell cycle was arrested in G0/G1 phase.The expression of p-ERK1/2 protein and CyclinD1 mRNA on A549 cells were decreased.Conclusion ATRA might inhibit the proliferation of A549 cells through down-regulating p-ERK1/2 protein and CyclinD1 mRNA.