OBJECTIVETo observe the efficacy of Xingnaojing Injection (XI) in treatment of sepsis-associated encephalopathy (SAE).

METHODSTotally 65 SAE patients were retrospectively analyzed at EICU from September 2010 to September 2013. They were assigned to the control group (32 cases) and the treatment group (33 cases) according to whether they received XI. Patients in the control group received anti-infection and symptomatic support, while those in the treatment group were intravenously injected with XI at 20 mL per day for additional 7-10 days. The fever clearance time, Glasgow coma scale (GCS), C-reactive protein (CRP), neuron-specific enolase (NSE), and improvement of electroen-cephalogram (EEG) were observed in the two groups.

RESULTSCompared with the control group, the fever clearance time was shortened, CRP levels decreased, GCS score and efficacy of EEG was alleviated in the treatment group after treatment with statistical difference (P < 0.05). No adverse reaction occurred during medication.

CONCLUSIONX1 was safe and effective in treatment of SAE.

C-Reactive Protein ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; therapeutic use ; Humans ; Injections ; Phosphopyruvate Hydratase ; metabolism ; Sepsis-Associated Encephalopathy ; drug therapy ; Treatment Outcome

OBJECTIVE To study the antibiotic resistance gene of qacE△1-sul1 in Acinetobacter baumannii isolated from inpatients in Urumqi and the distribution and difference of qacE△1-sul1 genotype in Xinjiang. METHODS Bacterial strains were identified by system of API and antibiotic susceptibility test was detected by K-B and microdilution methods according CLSI.PCR was used to determine the gene of qacE△1-sul1 and compared with the sequences in GenBank. RESULTS Antibiotic resistance phenotypes showed the resistance rate to cefataxime and tetracycline was the highest(100.0%),but that to cefoperazone/sulbactam was the lowest.The positive rate of qacE△1-sul1 gene in A.baumannii was 52.2%. CONCLUSIONS High resistance in A.baumannii is found in Xinjiang.The positive rate of qacE△1-sul1 is high.Strengthening epidemiology surveillance of resistance carried by integron-carrying gene is important.

Animals ; Area Postrema ; physiology ; Blood Pressure ; Electric Stimulation ; Electrocardiography ; Male ; Neurotransmitter Agents ; Peroneal Nerve ; physiology ; Rats ; Rats, Sprague-Dawley

Advance on chemical constituents and pharmacological activities of Stellera plants have been conducted. The chemical constituents include terpenes, coumarins, flavonoids, lignans, volatile oils, and other compounds. Pharmacological studies showed that diterpenoids and biflavones showed strong activities, such as antitumor, anti-HIV, and immune regulations. This review hopes to provide a scientific basis for further research and explorations of the medicinal values of the genus.
Animals ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; Humans ; Molecular Sequence Data ; Molecular Structure ; Thymelaeaceae ; chemistry ; classification

Adolescent ; Child ; Cord Blood Stem Cell Transplantation ; Female ; Flow Cytometry ; Humans ; Leukocyte Count ; Male ; Siblings ; Transplantation, Homologous ; immunology ; Treatment Outcome

Objective To investigate the changes in tumor necrosis factor-α(TNF-α) and plasminogen activator inhibitor(PAI) in the presence of obstructive sleep apnea syndrome(OSAS) in patients with type 2 diabetes mellitus,and to investigate if that 2 inflammatory factors is associated with hypoxemia during sleep.Methods Fiftyfour patients with type 2 diabetes mellitus hospitalized for glycemic control were subgrouped into 27 patients with OSAS (group O) and 27 patients without OSAS (group N).26 people without diabetes and OSAS were selected from a health check-up program to serve as control group (group C).Serum TNF-α and PAI levels were measured by commercial ELISA kits.Apnea hypopnea index (AHI),the lowest pulse oxygen saturation (LSpO2) at night were detected by portable sleep monitor.The relativity regarding TNF-α,PAI,homeostasis model assessment for insulin resistance (HOMA-IR),fasting blood glucose(FBG),AHI,LSpO2,and age was discussed.TNF-α and PAI were regard as dependent variables,and FBG,HOMA-IR,AHI,LSpO2,and age as independent variables in multivariate stepwise linear analysis.Results The levels of HOMA-IR,TNF-α,PAI in group O [2.69 ± 1.53,(1.97 ±0.13) ng/ml,and (2.27 ± 0.85) ng/ml] were higher than the those in other 2 groups,and those in group N [1.70 ± 0.88,(1.09 ±0.29) ng/ml,and (1.59 ± 0.13) ng/ml] were higher than group C [1.15 ± 0.67,(0.73 ± 0.19) ng/ml,and (0.89 ±0.25) ng/ml].The levels of FBG in the 2 diabetic groups were higher than those in group C.The level of AHI in group O was higher than that in group N and group C,while LSpO2 in group O was lower than that in group N and group C.Spearman univariate analysis showed that TNF-α and PAl both were associated positively with HOMA-IR,FBG,and AHI,while negatively with LSpO2.Multivariate stepwise linear analysis denoted that TNF-α was independently associated with AHI,FBG,while PAI was independently associated with AHI and HOMA-IR.Conclusions Patients with diabetes and OSAS manifest raised level of chronic inflammatory activity,and therefore,OSAS might be implicated in the pathogenesis of chronic complication of patients with type 2 diabetes.

Objective　To investigate the effects of glucagon-like peptide 2 (GLP-2) on recovery of small intestinal epithelia from radiation injury in mice. Methods　Mice received a single 8 Gy dose of total body irradiation from 60Co gamma ray followed by treatment with GLP-2 or vehicle. DNA and protein content in small intestinal mucosa were measured, and small intestine was processed for histological examination with light microscope and scanning electron microscope. Results　Small intestinal mucosal DNA and protein content, villus height, and villus number significantly decreased in irradiated mice, partial villus tips were ulcerated. GLP-2 administration caused increase in DNA and protein content, villus height, and villus number as compared with irradiated control group. Meanwhile, the villus tips were lack of ulceration. Conclusion　GLP-2 can promote recovery of small intestinal epithelia from radiation injury in mice.

Objective　To study the effect of glucagon-like peptide 2 (GLP-2) on mitogen-activated protein kinase (MAPK) activity in small intestinal epithelia in mice after radiation injury and its relation with the change of small intestinal epithelial proliferation. Methods　Mice were given a single dose of 8 Gy of total body 60Co gamma irradiation and then divided into GLP-2 and control groups. The activity of MAPK and proliferation rate in small intestinal epithelia were measured. Results　The activity of MAPK in small intestinal epithelia was higher in GLP-2-treated mice than in irradiated mice, and the proliferation rate in small intestinal epithelia significantly increased in GLP-2-treated mice. These two indices were of significantly positive correlated. Conclusion　GLP-2 can promote small intestinal epithelial proliferation in irradiated mice, and this may be related to activation of MAPK in small intestinal epithelia.

Aim To explore the changes of Apelin/APJ system in LPS-induced injury of rat pulmonary mi-crovascular endothelial cells( PMVECs) , and the effect and mechanism of Apelin. Methods PMVECs were cultured with the explant technique, and the identifica-tion of rat PMVECs was carried out by immunocyto-chemical staining of factorⅧrelated antigen. MTT as-say was used to evaluate the viability of PMVECs. The mRNA expression of Apelin and APJ was detected by RT-PCR. The protein expression of PCNA and the phosphorylation of Akt was analyzed by Western blot. Results The mRNA expression of Apelin and APJ showed a compensatory increase after LPS treatment for a short period of time ( P<0. 01 ) , but with the exten-sion of time, which was significantly inhibited, even lower than the control group ( P<0. 05 or P<0. 01 ) , suggesting that Apelin/ APJ system might be involved in LPS-induced PMVECs injury. MTT results showed that 10 -6 ~10 -9 mol · L-1 Apelin obviously promoted the proliferation of rat PMVECs ( P <0. 05 or P <0. 01 ) , and with certain concentration and time de-pendence. Moreover, Apelin also improved the LPS-induced PMVECs injury in different degrees ( P<0. 05 or P < 0. 01 ) . In addition, Western blot analysis showed that Apelin significantly reversed the decrease of the protein expression of PCNA and the Akt phos-phorylation level induced by LPS ( P <0. 05 or P <0. 01 ) . Conclusions The Apelin/APJ system is in-volved in LPS-induced PMVECs injury. Apelin plays an important role in protecting the pulmonary microvas-cular endothelial function and reversing the LPS-in-duced PMVECs injury, which might be related to the activation of Akt phosphorylation pathway.

Objective To investigate the effect of a novel lymphotoxin with selectively binding to p55 tumor necrosis factor receptor (p55TNFR) on myocardial ischemia-reperfusion injury in rats in order to explore the mechanism.Methods A total of 40 SD rats were randomly (random number) assigned into four groups (n =10 in each),namely sham operation group (group A),I/R group (group B),wild type rhLTα treatment group (group C),and p55TNFR selective rhLTα (rhLTα-Q107E) treatment group (group D).After I/R model rats were established,various therapeutic agents or saline were given by continuous intravenous infusion for 24 h via a micropump.After 24 hours of treatment,serum myocardial zymogram,such as aspartate aminotransferase (AST),lactate dehydrogenase (LDH) and creatine kinase (CK),as well as superoxide dismutase (SOD),malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) activities were determined.Myocardial infarction size (MIS) was measured by nitro blue tetrazolium chloride (NBT) staining.Results Compared to sham operation group,MIS,AST,LDH,CK,MDA were increased,while the activities of SOD and GSH-Px were decreased.However,all the effects were significantly reversed by treatment with rhLTα-Q107E (P ＜ 0.05) but not rhLTα (P ＞ 0.05).Conclusions The rhLTα-Q107E plays a role in the protection against myocardial ischemia-reperfusion injury in rats by the mechanism of scavenging oxygen free radicals and increasing the activity of endogenous antioxidant system.