Objective To observe the changes of extracellular matrix(ECM) production and hypertrophy of glomerular mesangial cells(GMCs) induced by high glucose(HG),and the inhibitory role of myriocin(ISP-1).Methods GMC cultured with normal glucose(5.6 mmol/L D-Glucose,NG),HG(25.2 mmol/L D-Glucose) and HG plus ISP-1(100 mg/L) for different durations(0,24,48,(72 h)).The sizes of GMC were indicated by forward scatter intensity,measured by flow cytometery,and the levels of fibronection(FN),collagen Ⅳ(Col Ⅳ),laminin(LN),precollagen Ⅲ(Pcol Ⅲ) and hyaluronic acid(HA) in the supernatant of cultured GMC were detec-(ted) by ELISA.Results Compared with NG,HG could induce GMC hypertrophy(P

Animals ; Decompression ; Decompression Sickness ; physiopathology ; Electrocardiography ; Electroencephalography ; Electromyography ; Electrophysiology ; Male ; Rabbits

As the largest research-oriented specialty department in national traditional Chinese medicine hospitals, the Department of Critical Care Medicine in Guangdong Provincial Hospital of Chinese Medicine insists on the development mode combined with clinical medicine and scientific research. By taking clinical and basic researches for integrative medicine preventing and treating acute myocardial in-farction and sepsis as a breakthrough, authors explored key problems of Chinese medicine in improving the prognosis related diseases and patients' quality of life. In recent 3 years our department has successively become the principal unit of the national key specialties cooperative group of critical care medicine (awarded by State Administration of Traditional Chinese Medicine), the key clinical specialties (awarded by National Health and Family Planning Commission), and Guangzhou key laboratory construction unit, and achieved overall lap in clinical medical treatment, personnel training, scientific research, and social service.
Biomedical Research ; China ; Clinical Medicine ; Critical Care ; Hospital Departments ; organization & administration ; Humans ; Integrative Medicine ; Medicine, Chinese Traditional ; Quality of Life

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Female ; Fluorescence ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Mycobacterium tuberculosis ; isolation & purification ; Paraffin Embedding ; Polymerase Chain Reaction ; methods ; Retrospective Studies ; Tuberculosis, Pulmonary ; diagnosis ; microbiology ; Young Adult

Objective To explore the detection methods for cognitive dysfunction of the major depression in Elderly and analyze their clinical significance.Methods Using matched-pairs study,42 patients with seniie de- pressive disorders(experimental group)and 42 normal aged people(control group)were examined with auditory e- voked potential P300(event related potential,ERP-P300)and SECF,respectively.Results It was found that the scores with registration,span,recall,classification and total score of the subjects in the experimental group were sig- nificantly lower than those in the control group(P

OBJECTIVEMyriocin (ISP-1) is a new type of immune inhibitor extracted from cordyceps sinensis. This study was to observe the effects of ISP-1 on the expression of cell cycle regulatory protein D1 (cyclinD1) in high glucose-induced hypertrophy rat glomerular mesangial cells (GMCs).

METHODSRat GMCs were cultured in vitro and divided into three groups: high glucose (450 mg/dL D-glucose), normal glucose (100 mg/dL D-glucose, control) and ISP-1 (450 mg/dL D-glucose plus 100 μg/mL ISP-1). The protein expression of cyclinD1 was detected by flow cytometry.

RESULTSThe expression of cyclinD1 in GMCs in the high glucose group increased significantly in a time-dependent manner compared with that in the control group. ISP-1 treatment significantly inhibited the up-regulated expression of cyclinD1 induced by high concentration glucose, and the expression of cyclinD1 was restored to the level of the control group 48 and 72 hrs after ISP-1 treatment.

CONCLUSIONSHigh concentration of glucose can up-regulate the expression of cyclinD1 in GMCs. ISP-1 may inhibit the up-regulated expression of cyclinD1, which might contribute to the protective effect of ISP-1 against GMC hypertrophy induced by high glucose.

Animals ; Cyclin D1 ; analysis ; Fatty Acids, Monounsaturated ; pharmacology ; G1 Phase ; Glucose ; toxicity ; Hypertrophy ; Mesangial Cells ; chemistry ; pathology ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To investigate the effects of subcutaneous administration of insulin on insulitis,beta cell apoptosis and diabetes in non-obese diabetic (NOD) mice, and to explore the mechanism of immune tolerance induced by insulin. METHODS: Sixty female NOD mice were randomly divided into insulin group (n=32) and phosphate buffered saline (PBS) group (PBS group, n=28). Insulin was subcutaneously injected with humulin N (60 microL, 6U)+IFA (60 microL) at 4, 12, 20, and 28 weeks respectively, while the PBS group received PBS (60 microL) + IFA (60 microL). Insulitis and beta cell apoptosis of islets were observed at 12 weeks. IL-4 and IFN-gamma in the sera were measured by enzyme linked immunosorbent assay (ELISA). The expression levels of I-Abeta(g7), IL-4, IFN-gamma, IL-1beta, and Fas mRNA of islets were measured by reverse transcription-polymerase chain reaction (RT-PCR) at 12 weeks. RESULTS: The incidences in the insulin group were significantly lower than those in the PBS group (21.4% vs 71.4% at 30 weeks, 28.6% vs 85.7% at 52 weeks, P<0.05). The insulitis scores in the insulin group were lower than those in the PBS group, but there was no statistical significance. Fas expression on islets and apoptotic beta cell rates in the insulin group were lower than those in the PBS group (P<0.05). In the insulin group, serum IL-4 levels were higher, but IFN-gamma levels were lower than those in the PBS group (P<0.05). The levels of I-Abeta g7, IFN-gamma, IL-1beta and Fas mRNA transcription in islets were lower in insulin group, but IL-4 mRNA levels were higher than those in the PBS group (P<0.05). CONCLUSION The specific autoantigen insulin may induce immune tolerance and prevent diabetes in NOD mice, but it can't block the progression of insulitis. Subcutaneous administration of insulin can induce the regulatory T cells, and make Th1 to Th2 cytokine shifts in system and islets, thus preventing the Fas-mediated beta-cell apoptosis and diabetes.
Animals ; Apoptosis ; drug effects ; Diabetes Mellitus, Experimental ; prevention & control ; Diabetes Mellitus, Type 1 ; prevention & control ; Female ; Injections, Subcutaneous ; Insulin ; administration & dosage ; pharmacology ; Islets of Langerhans ; immunology ; pathology ; Mice ; Mice, Inbred NOD ; Pancreatitis ; prevention & control ; Random Allocation

Objective To understand the mycoplasma pneumoniae(MP) infection degree in community children by testing specific IgM antibodies against MP in different age bracket group in Shanghai Meilong area. Methods Using random sampling method, blood specimens of 1 817 children from kindergartens and primary or junior high schools in Meilong area were obtained. Children were from 2 to 15 years old, 969 males, 848 females. The specimens were tested for IgM antibodies against MP using with gelatin particle agglutination test. The data were statistically analyzed using with ?2 test. Results Five hundred and fifty-nine (30.7%) IgM antibodies against MP were positive from 1 817 blood specimens. The positive percentages were 27.34% and 34.66% for males and females, which had significant difference(?2=11.383 P=0.001). The higher percentage was detected from kindergarten children than primary and junior high school children(P=0). The positive percentages of anti-mycoplasma IgM had no significant differences between different kindergartens and primary schools(P=0.526,0.232). On the contrary, between different junior high schools, there were siginificant differences (?2=9.825 P=0.002). Conclusions MP is an important pathogenic mycoplasma cause for respiratory tract infections in Meilong area. It is relative to childhood asthma. The prevention and cure of MP infection for children shall be paid more attention.

OBJECTIVEMast cells and eosinophil have been found to play important roles not only in the development of anaphylactic inflammation but also in the chronic progression of organ reconstruction. But their role in the pathogenesis of Henoch-Schonlein purpura nephritis (HSPN) has not been fully understood. The present study was conducted to observe the serum levels of eosinophil cationic protein (ECP) and renal infiltration of mast cells in HSPN in order to elucidate their role in the development and progression of HSPN in children.

METHODSThe serum ECP levels were determined in 46 children with HSPN by fluoro-enzyme immunoassay (FEIA) using the Pharmacia CAP System. The distribution of mast cells infiltration was detected by immuno-enzyme-histological staining of tryptase (a marker for mast cell activation) and their relation with pathological changes was analyzed in 32 children with HSPN.

RESULTSThe serum ECP levels were 16.3 +/- 6.5 microg/L in the active stage of HSPN, significantly higher than that in remission stage (3.9 +/- 1.4 microg/L, P < 0.01) and that in control group (3.1 +/- 1.7 microg/L, P < 0.01). The number of mast cells in renal interstitium was 4.4 +/- 2.4 cells/mm2 in normal kidney, and significantly increased to 27.2 +/- 19.2 cells/mm2 in children with HSPN ISKDC grade II (P < 0.01) and 42.1 +/- 16.4 cells/mm2 in grade III (P < 0.05 when compared with grade II), 77.9 +/- 15.0 cells/mm2 in grade IV (P < 0.05 when compared with grade III).

CONCLUSIONThe serum ECP level could reflect disease activity of HSPN, and mast cell infiltration in kidney correlated significantly with renal histological severity in HSPN. Mast cells and eosinophil may play important roles in the development and progression of HSPN.

Biomarkers ; blood ; Child ; Disease Progression ; Eosinophil Cationic Protein ; blood ; Female ; Fluoroimmunoassay ; Humans ; Immunohistochemistry ; Kidney ; metabolism ; pathology ; Male ; Mast Cells ; metabolism ; pathology ; Nephritis ; blood ; metabolism ; pathology ; Purpura, Schoenlein-Henoch ; blood ; metabolism ; pathology ; Severity of Illness Index ; Tryptases ; metabolism

OBJECTIVEHepatitis B virus-associated glomerulonephritis (HBV-GN) is an immune complex-mediated glomerulonephritis. The present study was conducted to identify HBV S gene mutation in children with HBV-GN.

METHODSSerum HBV DNA was extracted in 53 children, including 30 with HBV-GN, 5 with HBV-carrying nephrosis (control group 1), and 18 HBV carriers (control group 2). HBV S gene sequence was amplified by polymerase chain reaction (PCR). The PCR products were sequenced directly and compared with AY167097.1, an epidemic HBV strain in China.

RESULTS(1) The adw serotype of HBV was found in all the 30 cases with HBV-GN, 5 cases with HBV-carrying nephrosis and 17 HBV carriers except for 1, in whom adr serotype was identified. (2) HBV genotype B was found in 29 children with HBV-GN, 5 cases with HBV-carrying nephrosis and 17 HBV carriers, genotype E was found in a child with HBV-GN, and genotype C in an HBV carrier. (3) A total of 17 kinds of different single nucleotide change in HBV S gene were identified in 21 of 30 (70%) HBV-GN patients. Among them, 16 of 21 (76.2%) nucleotide mutations resulted in amino acid substitution. It was interesting that most (11/16, 68.8%) amino acid substitutions involved threonine, serine and tyrosine, the potential phosphorylation sites of mitogen-activated protein kinase (MAPK) and protein tyrosine kinase (PTK) in HBV protein. Single nucleotide changes which didn not result in amino acid substitution were found in 2 HBV-carrying nephrosis patients, 2 HBV carriers and 5 cases with HBV-GN.

CONCLUSIONSingle nucleotide changes in HBV S gene were found in most children with HBV-GN. Most mutations in HBsAg resulted in amino acid substitutions involving threonine, serine and tyrosine, which may play a role in the pathogenesis of HBV-GN.

Amino Acid Substitution ; Carrier State ; Child ; DNA Mutational Analysis ; DNA, Viral ; genetics ; Genes ; Genotype ; Glomerulonephritis ; virology ; Hepatitis B virus ; genetics ; Humans ; Mutation ; Viral Envelope Proteins ; genetics