Objective To investigate the influence of dexmedetomidine on expressions of protein kinase c (PKC)γ, cal?cium/calmodulin-dependent protein kinase (CaMK)Ⅱαand pCaMKⅡαin spinal cord in rats with incisional pain (IP) and remifentanil-induced hyperalgesia. Methods Forty male Sprague-Dawley rats, aged 2-3 months, weighing 240-260 g, were randomly divided into 5 groups (n=8 each):blank control group (group C), remifentanil+incisional pain group (group R+I), dexmedetomidine + remifentanil + incisional pain group (group D+R+I), dexmedetomidine + remifentanil + incisional pain+phorbol myristate acetate+DMSO group (group D+R+I+P+DMSO) and dexmedetomidine+remifentanil+incisional pain+DMSO group (group D+R+I+DMSO). The incisional pain rat model was established by a plantar incision in left hind paw. Remifentanil was infused at a rate of 1.2μg·kg-1·min-1 for 90 min via the caudal vein. Dexmedetomidine was adminis?tered subcutaneously at a dose of 50μg/kg at 30 min before plantar incision. Phorbol myristate acetate and DMSO were intra?thecally injected at a dose of 10 μL. Paw withdrawal latency (PWL) to thermal stimulation and paw withdrawal threshold (PWT) to von Frey hair stimulation were measured 24 h before remifentanil infusion (T0) and at 2, 6, 24 and 48 h (T1-4) after intraveonus remifentanil injection. The rats were sacrificed after the last behavioral test and the L 4-6 segment of spinal cord was removed to determine the expressions of PKCγ, CaMKⅡαand pCaMKⅡαin spinal cord by Western blot analysis. Re? sults Compared with group C, the value of PWL was significantly shortened and PWT was significantly decreased except T0, and the expressions of PKCγ, CaMKⅡαand pCaMKⅡαwere up-regulated in other groups. Compared with group R+I, the value of PWL was significantly prolonged and PWT was significantly increased, the expressions of PKCγ, CaMKⅡαand pCaMKⅡαwere down-regulated in group D+R+I and group D+R+I+DMSO. Compared with group D+R+I, the value of PWL was significantly shortened and PWT was significantly decreased, the expressions of PKCγ, CaMKⅡαand pCaMKⅡαwere up-regulated in group D+R+I+P+DMSO. Compared with group D+R+I+P+DMSO, the value of PWL was significantly prolonged and PWT was significantly increased, the expressions of PKCγ, CaMKⅡαand pCaMKⅡαwere down-regulated in group D+R+I+DMSO. Conclusion Dexmedetomidine can reduce the expressions of PKCγ, CaMKⅡαand pCaMKⅡαin spinal cord in rats with IP and hyperalgesia induced by remifentanil.

One new dicyclopeptide cyclo-(L-N-methyl Glu-L-N-methyl Glu) (1), together with one new natural dicyclopeptide cyclo-(L-methyl Glu ester-L-methyl Glu ester) (2), and two known dicyclopeptides cyclo-(L-methyl Glu ester-L-Glu) (3), and cyclo-(L-Glu-L-Glu) (4), were isolated from the aerial parts of Dianthus chinensis L. Their structures were determined by spectroscopic analyses and chemical methods.
Dianthus ; chemistry ; Magnetic Resonance Spectroscopy ; Molecular Structure ; Plant Components, Aerial ; chemistry ; Plants, Medicinal ; chemistry

OBJECTIVETo evaluate efficacy of adjuvant chemotherapy after D2 dissection on survival for patients with gastric cancer.

METHODSRandomized clinical trials (RCT) that compared adjuvant chemotherapy after D2 dissection with D2 dissection alone for gastric cancer were searched with Pubmed, Cochrane, Embase and CBM databases. Eligible trials published between 1990 and 2012 were included in the study. The quality of RCTs was assessed by the Jadad scale. Data synthesis and statistical analysis were performed by RevMan 5.1 software.

RESULTEight RCTs with 3633 patients were included in this study. Among them, 1824 patients received adjuvant chemotherapy and 1809 patients didn't. Adjuvant chemotherapy was associated with a significant benefit in terms of overall survival (RR = 0.76, 95% CI: 0.69-0.84), disease free survival (RR = 0.72, 95%CI: 0.66-0.80) and recurrence rate (RR = 0.69, 95% CI: 0.62-0.77).

CONCLUSIONAdjuvant chemotherapy was associated with survival benefit for gastric cancer after D2 dissection.

Chemotherapy, Adjuvant ; Disease-Free Survival ; Female ; Gastrectomy ; Humans ; Male ; Neoplasm Recurrence, Local ; Prognosis ; Randomized Controlled Trials as Topic ; Stomach Neoplasms ; drug therapy ; mortality ; surgery ; Survival Rate

BACKGROUNDThe cholesterol-lowering statin drugs have some non-lipid-lowering effects, such as inhibiting myocardial remodeling. However, the underlying mechanism is still unclear.

METHODSThe left anterior descending coronary artery was ligated to establish a rat model of heart failure, and the rats were divided into a sham operation (SO) group, myocardial infarction model (MI) group, and MI-atorvastatin group. Changes in hemodynamic parameters were recorded after the final drug administration. Histological diagnosis was made by reviewing hematoxylin and eosin (HE) stained tissue. Real-time quantitative polymerase chain reaction (PCR) was performed to determine the expressions of type I and type III collagen, matrix metalloproteinase-2 (MMP-2), and tissue matrix metalloproteinase inhibitor-2 (TIMP-2). Further, primary rat cardiac fibroblasts were cultured and the MTT assay was performed to determine the effect of atorvastatin on cardiac fibroblast proliferation.

RESULTSThe model of heart failure was established and the results of HE staining and Masson's trichrome staining revealed that the rats in the heart failure group showed obvious hyperplasia of fibrotic tissue, which was significantly reduced in the atorvastatin group. Real-time quantitative PCR showed that the MI group showed a significantly increased expression of type I and type III collagen, MMP-2, and TIMP-2, but a significantly reduced MMP-2/TIMP-2 ratio. Compared with the MI group, the atorvastatin group showed significantly reduced expression of type I and III collagen, unchanged expression of MMP-2, significantly reduced expression of TIMP-2, and an increased MMP-2/TIMP-2 ratio. We further found that atorvastatin significantly inhibited the Ang II-induced fibroblast proliferation and the expression of type I and type III collagen in cardiac fibroblasts while increasing the MMP-2/TIMP-2 ratio.

CONCLUSIONSThese data suggest that atorvastatin can inhibit cardiac fibroblast proliferation and enhance collagen degradation by increasing the MMP-2/TIMP-2 ratio, thereby inhibiting the formation of myocardial fibrosis in rats with heart failure after myocardial infarction.

Animals ; Atorvastatin Calcium ; Collagen ; biosynthesis ; Disease Models, Animal ; Female ; Fibrosis ; Heart Failure ; drug therapy ; pathology ; Heptanoic Acids ; pharmacology ; therapeutic use ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; pharmacology ; Matrix Metalloproteinase 2 ; genetics ; Myocardial Infarction ; complications ; Myocardium ; pathology ; Pyrroles ; pharmacology ; therapeutic use ; Rats ; Rats, Wistar ; Tissue Inhibitor of Metalloproteinase-2 ; genetics ; Ventricular Remodeling ; drug effects

Adolescent ; Astrocytoma ; classification ; metabolism ; pathology ; surgery ; Brain Neoplasms ; metabolism ; pathology ; surgery ; Child ; Child, Preschool ; Female ; Follow-Up Studies ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; Male ; Neoplasm Recurrence, Local ; Retrospective Studies ; S100 Proteins ; metabolism ; Vimentin ; metabolism

Fertility ; Hematologic Diseases/therapy* ; Hematologic Neoplasms/therapy* ; Hematopoietic Stem Cell Transplantation ; Humans

Multidrug resistance (MDR) occurs frequently after long-term chemotherapy,resulting in refractory cancer and tumor recurrence.Therefore,combatting MDR is an important issue.Autophagy,a self-degradative system,universally arises during the treatment of sensitive and MDR cancer.Autophagy can be a double-edged sword for MDR tumors:it participates in the development of MDR and protects cancer cells from chemotherapeutics but can also kill MDR cancer cells in which apoptosis pathways are inactive.Autophagy induced by anticancer drugs could also activate apoptosis signaling pathways in MDR cells,facilitating MDR reversal.Therefore,research on the regulation of autophagy to combat MDR is expanding and is becoming increasingly important.We summarize advanced studies of autophagy in MDR tumors,including the variable role of autophagy in MDR cancer cells.

Acinetobacter Baumannii has become a common pathogen iso-lated in nosocomial infection, especially, the bacteria′s separation rate is higher and higher in Intensive Care Unit ( ICU) and respiratory depart-ment.Along with the application of antibiotics, multidrug -resistant Acinetobacter Baumannii followed and has drawn great global attention.The drug treatment for multidrug -resistant Acinetobacter Baumannii is reviewed in this paper.

Objective To investigate the effect of topiramate in the treatment of intractable epilepsy in children. Methods 120 cases with intractable epilepsy from May 2012 to May 2017 were randomly divided into 2 groups, the control group used antiepileptic drug treatment, study group combined application of anti epileptic drugs targeted nursing application. Results The clinical effect of the treatment group was better than that of the control group (P< 0.05). The frequency of epileptic seizure in the treatment group was significantly higher than that in the control group (P<0.05). Conclusion In the treatment of intractable epilepsy in children, the application of topiramate in the treatment of basic care is helpful to improve the effect of treatment, the effect is ideal, and should be further popularized in clinical practice.

Humans ; Hydrogen-Ion Concentration ; Malassezia ; growth & development ; physiology ; Staphylococcus epidermidis ; growth & development ; physiology