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.

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

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.

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 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 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 study the MRI findings of HE and the pathological mechanism and to improve the diagnosis and differential diagnosis of HE. Methods Five patients of HE diagnosed by clinical and laboratory examination were examined with conventional MRI scan. Additional DWI, MRA and enhancement MRI scan were performed on 3 patients in which abnormal findings was detected on the conventional MRI. The distribution of lesions and signal characteristics were analyzed. The ADC values of the lesions and of the contralateral non-lesion area were measured. Moreover, the possible pathological mechanisms of HE were discussed on the basis of changes of clinical and imaging manifestations in the two cases with serial clinical and MRI data. Results Of 5 patients, brain abnormalities were found in 3 cases,which showed scattered spotted supratentorial white matter lesions of isointensity on T1 WI and DWI, and high signal intensity on T2WI and fluid-attenuated inversion recovery (FLAIR). Meanwhile, multiple plaque-like lesions involving both white matter and gray matter were found, mainly located at the basal ganglia nuclei, hippocampus and cingulate cortex. The lesions demonstrated iso-or hypo-intensity on T1 WI,and iso-or hyper-intensity on T2 WI, FIAIR and DWI at the initial stage. No enhancement was found in these lesions and MRA disclosed no remarkable findings. The ADC value of the lesions [ (0. 449 ± 0. 092) ×10-3 mm2/s] was decreased significantly compared with the contralateral noninvolved area [ (0. 838 ±0. 062) × 10-3 mm2/s] at the early onset. In 2 cases with glucocorticoid therapy, together with symptom relief, MRI follow-up scan demonstrated the reduction of lesion volume, the signal change to hyperintensity on T1 WI and hypo-intensity on DWL The ADC of the lesions increased significantly. Conclusion The MRI could be one of the effective tools for diagnosis, differential diagnosis, and judging the prognosis and therapeutic results of HE. Meanwhile, it may be a non-invasive method to study the pathological mechanism of HE.

Objective:To establish a multidrug resistant human salivary gland adenoid cystic carcinoma cell line.Methods:Human salivary gland adenoid cystic carcinoma cell line ACC-2 was treated by 24-hour-exposure to high dose of Bleomycin(BLM)(20 ?g/ml).Drug sensitivity was evaluated by MTT assay.Cell counting was employed to make the growth curve and to calculate the cell doubling time.Flow cytometry(FCM) was used to study the cell cycle distribution and apoptosis.The colony formation ability was also observed.Results:Multidrug resistant cell line of human salivary gland adenoid cystic carcinoma was established and named ACC-2/BLM.After 10 times repeated exposure to BLM,the resistance index(RI) to BLM,5-Fluorouracil(5-FU),Cisplatin(CDDP),Cyclophosphamide(CTX),Vincristine(VCR) were 7.299,1.03,2.15,1.114 and 5.96 respectively.Compared with ACC-2,the proliferation potential of ACC-2/BLM cells was decreased.The ACC-2 apoptosis cells were much more than ACC-2/BLM cells after 9-day-treatment by BLM at 60 ?g/ml.Conclusion:ACC-2/BLM cell line has multidrug resistant characteristics.

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.