Alzheimer′s disease ( AD) , is a neurodegenerative disorder of the brain that is characterized by loss of memory and cognitive decline.At present, AD etiology remains unclear and there are no effective prevention and treatment measures in clinical practice.Peroxisome proliferator-activated receptorγ( PPARγ) is a ligand-regulated nuclear hormone receptor.Recent studies showed PPARγ-pathway played an important role in the pathogenesis of AD and some PPARγagonists have been proven to be neuroprotective in vitro and in vivo models.This paper reviews the roles of PPARγand related mechanisms in AD, summarizes affecting factors about PPARγpathway.Particularly, the effect of cyanidin-3-O-glucoside ( Cy3G) , one of the anthocyanidin glycoside forms, is a compound of naturally occurring phenolic compounds, suggesting the neuroprotective effect of Cy3G might be used as a potential natural PPARγagonist in the nervous system.

Objective To explore the clinical nursing of hip developmental dislocation in infants with Ferguson operation.Method The nursing strategy was performed including observation of the surgical incision,skin care,care of cast and instructions to their parents. Result No pressure sores occurred in all the 34 cases of hip developmental dislocation.1 case had delayed allergy reaction because of use of contrast media during operation,1 cast syndrome,and 19 edema of perineum of different degrees including 6 severe edemata,which were cured using wet compress with Adlerika.Conclusion It is of great importance for the reduced incurrence of operation complications and promising operative effect to observe the conditions and treat timely problems in postoperative nursing.

Objective To investigate the causes for death in rats after spinal cord injury.Methods A total of 120 adult Wister rats were selected for the study. The animal model with acute spinal injury at T10 was established by using Allen' s combat (25 g · cm). The dissection analysis was performed in death rats. Results Of all, 25 patients died, with mortality rate of 21%. Of death rats, five rats were died before awakening, with no abnormal anatomy; 12 rats died within three days after injury and three died of injuries 3-7days injury. Anatomy found pulmonary bleeding and edema, even hematocele bladder in some rats. There were three rats died within 1-2 weeks, one died of injury only after 2-3 weeks, with lung infection and urinary tract infection. There was no death after three weeks. Conclusions The early causes for death of rats with spinal cord injury is mainly due to lung congestion and pulmonary edema, whereas the leading cause of late death of rats is pulmonary and urinary tract infection.

Acquired Immunodeficiency Syndrome ; blood ; complications ; diagnosis ; Antibodies, Viral ; blood ; Child ; Cough ; complications ; Fatal Outcome ; Fever ; complications ; HIV-1 ; immunology ; Humans ; Male

0.05).Conclusions:There was no difference in terms of both effect and toxicity among the three regimens. All of them were effective and could be well tolerated by advanced colorectal cancer patients.

Objective To summarize the experience in pediatric nursing of children with congenital insensitivity to pain and anhidrosis (CIPA) combined with proximal femoral fracture.Methods Two CIPA children with proximal femoral fracture received good treatment of security,plaster casts/braces,body temperature and skin as well as guidance of function exercise and health care education.The nursing experience was summarized.Result After intensive nursing,all patients successfully tided over their perioperative period and discharged.Conclusions The security management,careful observation of skin and body temperature after plaster casts/braces fixation,are of great significance for the decreased complication.Function exercises are equally effective in CIPA children with proximal femoral fracture.

Objective To investigate alterations in epigenetic regulation in B cells in subacute cutaneous lupus erythematosus (SCLE).Methods Peripheral blood mononuclear cells (PBMC) were isolated from the peripheral venous blood of SCLE patients and healthy donors with density gradient centrifugation.B cells were isolated with CD19 micro beads and protocols provided by the manufacturer.Total RNAs were isolated with RNA kits.The expressions of silence information regulator 1 (Sirt1) mRNA were investigated with quantitative real time polymerase chain reaction (PCR).Results The levels of Sirt1 mRNA were significantly increased in SCLE B cells relative to healthy controls (P ＜ 0.01).Conclusions Histone modifications appear abnormal in B cells in SCLE.

Objective To determine if propofol can protect cultured rat hippocampal neurons from anoxia-induced injury and elucidate the underlying mechanism.Methods Neonatal Wistar rats were decapitated. Hippocampus was isolated, minced and digested with 0.125 % trypsin at 371 for 25 min, then centrifuged at 1000 r/min for 5 min. The supernatant was discartled and the precipitate was resuspended in growth medium. The cell suspension was incubated at 37 ℃ for 10 days. The cultured hippocampal neurons were randomly divided into 3 groups: control group(group C) ,anoxia group(group A), propofol + anoxia group (group PA) . Group PA was further divided into 3 subgroups of different end-propofol concentrations:3, 12,48 mg?L-1 . The cultured neurons were transferred to low glucose medium and incubated at 37 ℃ in closed incubator filled with anoxic atmosphere (95% N2-5% CO2) for 24 h in group A and group PA (following addition of propofol) . The cell survival rate in each group was measured by MIT colorimetry. The real-time changes in [Ca2+ ]i in cultured hippocampal neurons induced by anoxia or glutamate or KCL were measured by fluorescence and laser scan confocal microscopy ( LSCM) after staining with fluo-3/AM.Results The hippocampal neurons developed acute swelling and widespread degeneration following anoxia. Propofol attenuated the neuronal injury at 12 and 48 mg?L-1 in a dose-dependent manner and significantly increased the cell survival rate following anoxia (P

AIM To investigate the protective effects and mechanism of propofol on cultured rat hippocampal neurons subjected to anoxia injury METHODS Hippocampal neurons of neonatal rats, which had been cultured in vitro for 10 days, were allocated to control groups and propofol treating groups In propofol treated groups,the culture medium were loaded with propofol at the concentrations of 3, 6, 12, 24, 48 mg?L -1 respectively, and then the neurons were exposed to oxygen glucose deprivation for 24 h, to 40 ?mol?L -1 H 2O 2 for 24 h or to 100 ?mol?L -1 glutamate for 50 min The cell survival rate in each group was evaluated by MTT colorimetry. Using a laser scanning confocal microscope (LSCM), the effects of propofol on neuronal calcium overload and on the reduction of mitochondrial membrane potential (△?m) evoked by anoxia were observed with fluo 3 and rhodamine 123 for real time changes of [Ca 2+ ] i and △?m. The electron spin resonance (ESR) was used to measure the scavenging effects of propofol on hydroxyl radical and superoxide anion RESULTS Propofol at the concentrations of 6～48 mg?L -1 attenuated the anoxic injury ( P

ACEI,ACEII and Xyr1 are transcriptional factors that regulate cellulase gene expression in Trichoderma koningii.In vitro experiments have shown that ACEI and Xyr1 bind to the cbh1 promoter fragment(-304 to-18) and regulate the gene transcription.However,whether ACEII binds to this 287bp fragment is still unclear.To further elucidate the regulatory mechanism of ACEII for cellulase,DNA-binding domains of ACEII from T.Koningii were expressed in E.coli.It could not show binding to the cbh1 promoter fragment(-304 to-18) by electrophoresis mobility shift assays,suggesting that it is Xyr1 but not ACEII binds playing an essential role during induction of cbh1 gene transcription.