Avian influenza viruses (AIV) can cause serious economic losses and threaten to human health. The laboratory methods for rapid and accurate detecting AIV ensure timely implementation of intervention strategies so that it plays a key role in avian influenza prevention and control. The laboratory technologies for detecting AIV are topic subject and developed quickly those days. This paper reviews the advances of laboratory diagnosis technologies for AIV at 3 aspects of virus isolation, immunoassay and molecular diagnostics.

Cannabinoid Receptor Modulators ; Endocannabinoids ; Humans ; Metabolic Syndrome ; metabolism

Humans ; Osteotomy ; adverse effects ; methods ; Scoliosis ; surgery

Dust ; analysis ; Environmental Monitoring ; methods ; Silicon Dioxide ; analysis

This article has elaborated the present situations and the existing problems,mentioned basic contents and methods and finally discussed thoughts in details on how to improve the teaching work supervision in vocational colleges and colleges.

Objective To analyze the karyotypes of 11 cases of Turner syndrome with marker chromosome,and study the phenotypic effects resulting from the abnormal karyotype.Methods Eleven Turner syndrome patients had a mosaic karyotype and carried a marker chromosome,and 6 marker chromosomes were ring chromosomes.Their karyotypes were showed as mos.45,X/46,X,+mar or mos. 45,X/46,X,+r.Fluorescence in situ hybridization(FISH)technique with X/Y centromere probes was performed to determine the origin of the marker chromosome.Reverse chromosome painting technique was used to identify the breakpoints of two largest markers.Phenotype effects with different chromosome breakpoints were compared.Results All the 11 marker chromosomes were ring X chromosomes.The breakpoints of the r(X)were involved in Xp22,Xq22,Xq24 and Xq26,etc.Conclusions The marker chromosomes in Turner syndrome mainly originate from X chromosome and form ring chromosome X.Each r (X)in our patients was mosaic,indicating it was originated from mitosis error during early embryo development.To analyze the origin of the marker chromosome and the breakpoint of r(X)will provide guidance for the therapy and prognosis of the Turner syndrome patient.

Human sTNFR1 (soluble tumor necrosis factor receptor 1) gene was amplified by RT-PCR from Hela cells. A recombinant expression vector of sTNFR1-MBP was constructed in pMAL-c2x, and transformed into E. Coli JM109.It was sequenced and confirmed to be identifical to the sTNFR1 gene in data bank. Recombinant protein sTNFR1-MBP was induced by IPTG and purified by Amylose resin Affinity Chromatography. sTNFR1-MBP was binded to sTNFR1's antibody in Western-blotting. From MTT assays, the results showed that sTNFR1-MBP could effectively block the cytotoxicity mediated by TNF?on QSG7701 cells. Annexin V-FITC staining and flowcytometry were used to observe the recombinant protein's anti-apoptosis capacity and the recombinant protein has marked anti-apoptosis effect in vitro.sTNFR1-MBP had good biological activity and it will be employed in further study.

Insulin hypersensitivity reactions are rare, but cause significant complexity in the care of patients with diabetes mellitus. A 54-year-old Filipino male with type 2 diabetes mellitus and multiple co-morbidities developed delayed-type hypersensitivity reactions to biphasic isophane human insulin and glargine. Despite good glycemic control on oral hypoglycemic agents, his endocrinologist foresaw the need for future insulin therapy, particularly one basal and one short-acting insulin. Targeted skin tests demonstrated protamine allergy and negative reactions to regular insulin and detemir. Close coordination of care among endocrinologists, allergists, patients and patients' family is needed to optimize glucose control, prevent complications, and minimize the risk of future hypersensitivity reactions.

Key Words: drug hypersensitivity, insulin, diabetes mellitus

Objective:To observe the change of periphery and centra lymphocyte subsets at the crest-time of MOG_(35-55) induced EAE disease in mice,and to explore the alteration of cellular immunity and humoral immunity in the invasion process in EAE.Methods:MOG_(35-55) was used to establish EAE model in femina C57BL/6 mice.The behavioral changes and the histological scores were recorded after the mice were immuned .The changes of CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ on periphery and centra lymphocytes in spleen,brain and spinal cord were analyzed by flow cytometry.Results:The CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ lymphocytes were detected in the brain and spinal cord of EAE group mice,but they were not detected in CFA control group.The CD3~+CD4~+ and CD3+CD8+lymphocytes in the spleen of EAE crest-time group were lower than those in CFA control group(P＜0.05).The B220~+ lymphocytes were obviously higher than in the CFA control group (P＜0.01).And CD4~+CD25~+ lymphocytes were slight higher than the CFA control group.Conclusion:At the crest-time during EAE,the CD3~+CD4~+,CD3~+CD8~+lymphocytes of spleen reduced obviously,B220~+ lymphocytes increased markedly,and the CD4~+CD25~+ lymphocytes just have the increasing trend.It indicates that cellular immunity and humoral immunity coregulated the patho-process at the crest-time of EAE,T lymphocytes and B lymphocytes all played important roles in the pathogenesy of EAE.

Aging ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Glutathione Peroxidase ; metabolism ; Male ; Malondialdehyde ; metabolism ; Rats ; Rats, Wistar ; Superoxide Dismutase ; metabolism ; Testis ; drug effects ; metabolism