Diagnosis, Differential ; Humans ; Medicine, Chinese Traditional ; Precancerous Conditions ; diagnosis ; Stomach Neoplasms ; diagnosis

Adolescent ; Female ; Humans ; Hypothyroidism ; etiology ; Lupus Erythematosus, Systemic ; complications

Objective To explore the role of tissue inhibitor of metalloproteinase-1(TIMP-1) during renal senescence by using human TIMP-1 transgenic mice.Methods Renal histological changes of wild type mice and transgenic mice at the age of 3,12,24 months were observed by periodic acid-schiff(PAS)staining of paraffin sections.The numbers of F4/80 positive cells were detected by immunofluoreseence.The protein expressions of TIMP-1,TIMP-2,matrix metalloproteinase(MMP)-9,MMP-2,intercellular adhesion molecule-1(ICAM-1),transforming growth factor?1(TGF-?1),collagenⅢand collagenⅣwere detected by Western blot.The activities of gelatinases and TIMP-1 were examined by gelatin zymography and reverse zymography respectively.Results Focal renal fibrosis was found in two genotypes with aging.At the age of 24 months,compared with wild type,in kidneys of transgenic type,the expressions and activities of gelatinases were dowregulated (MMP-2:2.08?0.20 vs.3.39?0.43;MMP-9:4.02?0.82 vs.6.72?1.40,all P＜0.05);the expressions of collagenⅢ,collagenⅣ,ICAM-1,and TGF-?1 were upragulated(0.72+0.11 vs.0.57?0.09;0.84?0.13 vs.0.6?0.11,0.72?0.12 vs.0.53?0.07; 0.69?0.12 vs.0.45?0.09,all P＜0.05),and the numbers of F4/80 positive cells were increased (18.8?4.4 vs.12.7?3.6,P＜0.05)with the upregulated expression and activity of TIMP-1(1.10?0.18 vs.0.62?0.09;50.75?7.25 vs.20.64?3.50,P＜0.05).Conclusions TIMP-1 could promote age-related renal fibrosis through enhancing inflammation reaction by ICAM-1 upregulation.

cDNA for Insulin-like growth factor binding protein 3 was cloned and constructed a prokaryotic expression vector--pET-DsBA-IGFBP3. The construct was transformed into E. coli BL21 (DE3)plysS. The induced fusion protein (D-IGFBP3) was expressed successfully in soluble form. We obtained D-IGFBP3 the purify of which is over 95% after purification by His affinity chromatography. The product was identified by Western-blot. The cell assay showed that the obtained fusion protein can inhibit the growth of MCF-7 and bind with IGF-I in vitro.
Blotting, Western ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Chromatography, Affinity ; Dose-Response Relationship, Drug ; Electrophoresis, Polyacrylamide Gel ; Enzyme-Linked Immunosorbent Assay ; Escherichia coli ; genetics ; Gene Expression ; Humans ; Insulin-Like Growth Factor Binding Protein 3 ; genetics ; metabolism ; pharmacology ; Insulin-Like Growth Factor I ; metabolism ; Protein Binding ; Recombinant Proteins ; isolation & purification ; metabolism ; pharmacology ; Solubility

AIMTo explore the relationship between the effects of curcumin on cerebral ischemic/reperfusion injury and immediately genic expressions of Fos, Jun and NF-kappaB in hippocampal CA1 area.

METHODSGerbils were randomly divided into sham group (SH), ischemia/reperfusion group (I/R), curcumin group (CU) and solvent control group (SC). Forebrain ischemia was induced by occlusion of bilateral common carotid arteries. Observations were carried out in each group 15 min, 1 h, 2 h, 6 h, 1 d, 3 d, 5 d and 7 d after ischemia: open field test was used to examine the behavioral change, the apoptosis neurons in hippocampal CA1 region was counted, the expression of Fos, Jun and NF-kappaB in hippocampal CA1 was detected by SABC immunocytochemical technique.

RESULTSThe behavioral mark and the number of apoptosis neurons in hippocampal (CA1 region was much less in CU group than in I/R group (P < 0.01) The expression of Fos was more and the expression of Jun and NF-kappaB was less in CA1 area in CU group than in I/R group (P < 0.01).

CONCLUSIONCurcumin can significantly protect neurons against cerebral ischemia, increasing the expression Fos and decreasing the expression of Jun and NF-kappaB may be the protective mechanisms.

Animals ; Apoptosis ; Brain Ischemia ; metabolism ; pathology ; Curcumin ; pharmacology ; Gerbillinae ; Hippocampus ; drug effects ; metabolism ; Male ; NF-kappa B ; metabolism ; Proto-Oncogene Proteins c-fos ; metabolism ; Proto-Oncogene Proteins c-jun ; metabolism ; Reperfusion Injury ; metabolism ; pathology

BACKGROUNDMost of the studies on traditional Chinese medicine (TCM) 'spleen' deficiency syndrome in the recent 30 years were conducted only on the basis of single functional index, neglecting the study on the pathophysiologic internal relationship between spleen deficiency syndrome and gastric diseases in modern medicine. But it was at the subcellular molecular biological level that we explored the pathophysiologic basis of classification of spleen deficiency in chronic gastritis by detecting the bioactive substances in gastric mucosa nuclei and mitochondria.

METHODSBy means of optical microscope, scanning electron microscope (SEM), transmission electron microscopy (TEM) and histochemical staining, we conducted histopathological, subcellular ultrastructural analysis and nuclei and mitochondrial ultrastructural analysis of gastric mucosa of 188 spleen deficiency patients and of 42 voluntary blood donors. At the same time, bioactive substances were measured by means of X-ray energy dispersive analysis system (EDAX) image analysis system, radioimmunoassay method and chemiluminescence method.

RESULTSThe content of cAMP, superoxide dismutase (SOD), Zn and Cu in gastric mucosa, and the content of Zn and Cu in mitochondria decreased progressively in order of groups: healthy control (HC), spleen Qi deficiency without organic lesion (F-SQD), spleen Yang deficiency without organic lesion (F-SyangD), disease without symptoms group, spleen Qi deficiency with organic lesion (G-SQD), spleen Yang deficiency with organic lesion (G-SyangD), spleen Yin deficiency (SyinD) and spleen deficiency with Qi stagnation (SDQS), chronic spleen deficiency gastritis (CSG) and chronic atrophic gastritis (CAG); decreased in order of HC, intestinal metaplasia (IM)Ia, IMIb, IMIIa and IMIIb, P < 0.05. The content of DNA, Zn and Cu in nuclei progressively increased in order mentioned above, P < 0.05.

CONCLUSIONSThe quantitative changes of gastric mucosal cAMP, SOD, Zn, Cu, of mitochondrial Zn, Cu and of nuclear DNA, Zn and Cu are not only the substance base on which the lesion of gastric mucosa tissue structure occurs, but also the substance base on which spleen deficiency is classified. G-SQD and G-SyangD were more likely to be found in low-grade or middle-grade CSG and CAG, while SyinD and SDQS in middle-grade or high-grade CSG, CAG and IMIIb.

Adult ; Aged ; Chronic Disease ; Cyclic AMP ; analysis ; Female ; Gastric Mucosa ; pathology ; ultrastructure ; Gastritis ; metabolism ; pathology ; Humans ; Lipid Peroxides ; blood ; Male ; Medicine, Chinese Traditional ; Middle Aged ; Splenic Diseases ; classification ; Superoxide Dismutase ; analysis

To study the effects of glycosylation on survival of cold-storage human platelets by using rabbit model. (51)Cr-labeling platelets were used to detect the platelet storage survival. The human platelets (2.0 x 10(12)/L) treated with 5 g/L uridine diphosphate galactose (UDP-Gal) were stored in 4 degrees C refrigeratory up to 10 days. The survival of human platelets in rabbits whose reticuloendothelial system was inhibited by the administration of ethyl palmitate was monitored in blood drawn at various times after the platelet transfusion. The results showed that the survival rate of platelets was significantly increased in cold-storage human platelets by UDP-Gal treatment. The survival rates of platelets at 2 hours after transfusion into rabbits in groups of fresh platelets group, UDP-Gal + cold platelets group and cold platelets group were (68.9 +/- 8.5)%, (65.4 +/- 8.0)% and (5.0 +/- 2.6)%, respectively. Compared with cold platelets group, significant differences were seen among all groups (P < 0.01). UDP-Gal + cold platelets group had no significant differences compared with fresh platelets group (P > 0.05). It is concluded that UDG-Gal can provide the protective effect on cold-storage human platelets and prolong the survival time of refrigerated human platelets in rabbit model.
Animals ; Blood Platelets ; cytology ; metabolism ; Blood Preservation ; Cell Survival ; drug effects ; Cryopreservation ; methods ; Glycosylation ; drug effects ; Humans ; Models, Animal ; Platelet Transfusion ; Rabbits ; Uridine Diphosphate Galactose ; pharmacology

The purpose of study was to investigate the feasibility of the application of cationic propyl gallate (C-PG) as inducer of platelet aggregation for evaluating the platelet function of single-donor plateletpheresis and identifying the incidence of defective platelet function among donors. Experiments were as follows: 3 healthy volunteers' platelet aggregation induced by 100-300 micromol/L C-PG was determined by LG-PABER analyzer to observe the effect of C-PG concentration on platelet aggregation; 30 healthy volunteers' platelet aggregation before and 24 hours after administration of 200-400 mg acetylsalicylic acid (ASA) was examined after induction by 200 micromol/L C-PG for determining the cut-off value to discriminate platelet dysfunction donors; the platelet aggregation of 483 platelet donors was detected and the activated plasma clotting time (APCT) of donors who have deficiency in platelet aggregation was examined for investigating the incidence of defective platelet function among donors. The results showed that platelets were activated by C-PG induction in a dose dependent manner, when concentration of C-PG reached 200 micromol/L, the percentage of platelet aggregation was highest. It significantly decreased after 24 hours with ASA than that before the administration (P < 0.001), especially in 180 seconds induced by C-PG. If cut-off point was fixed on the platelet aggregation < 20% in 180 seconds, donors of platelet dysfunction can be selected effectively. 25 of defective platelet aggregation function among 483 donors were detected, and 11 out of 25 platelet dysfunction donors had the deficiency in procoagulant activity with prolonged APCT. It is concluded that C-PG as inducer of platelet aggregation is feasible to screen the platelet function of donors. Five percent of platelet donors has function defect examined by C-PG as inducer of platelet aggregation.
Antioxidants ; chemistry ; pharmacology ; Aspirin ; administration & dosage ; Blood Donors ; Blood Platelets ; cytology ; drug effects ; physiology ; Cations ; chemistry ; Humans ; Platelet Activation ; drug effects ; Platelet Aggregation ; drug effects ; Platelet Aggregation Inhibitors ; administration & dosage ; Platelet Function Tests ; Platelet Transfusion ; Propyl Gallate ; administration & dosage ; chemistry ; Whole Blood Coagulation Time

Child, Preschool ; Humans ; Lymphohistiocytosis, Hemophagocytic ; diagnosis ; genetics ; therapy ; Male

This study was purposed to investigate the serum levels of soluble intracellular adhesion molecule (sVCAM-1), interleukin 18 (IL-18) and vascular endothelial growth factor (VEGF) in patients with aplastic anemia (AA) and their clinical significance. Enzyme linked immunosorbent assay (ELISA) was used to detect sVCAM-1, IL-18 and VEGF in serums of 30 patients with AA and 25 normal controls. The results showed that the serum levels of sVCAM-1 and IL-18 in patients with AA [(839.08 +/- 173.97) ng/ml, (380.35 +/- 47.76) pg/ml] were significantly higher than those in normal controls [(538.16 +/- 91.21) ng/ml, (256.39 +/- 59.52) pg/ml] (p < 0.01; p < 0.01). The levels of sVCAM-1 and IL-18 in severe AA patients [(969.94 +/- 182.54) ng/ml, (388.96 +/- 46.06) pg/ml] were higher than those in chronic AA patients [(709.26 +/- 165.32) ng/ml, IL-18 (352.21 +/- 47.08) pg/ml] (p < 0.01; p < 0.05), but the level of VEGF in AA patients [(69.63 +/- 27.42) pg/ml] was lower than that in the normal controls [(125.62 +/- 32.15) pg/ml] (p < 0.01)]. The level of VEGF in severe AA patients [(51.30 +/- 29.86) pg/ml] was significantly lower than that in chronic AA patients [(80.02 +/- 25.14) pg/ml] (p < 0.01). The levels of sVCAM-1 and IL-18 in AA patients after treatment were lower than those before treatment (p < 0.01; p < 0.05), but the level of VEGF after treatment was significantly higher than that before treatment (p < 0.05). It is concluded that the high levels of sVCAM-1, IL-18 and low level of VEGF in serum may be involved in the pathogenesis and progress of AA.
Adolescent ; Adult ; Aged ; Anemia, Aplastic ; blood ; Case-Control Studies ; Female ; Humans ; Interleukin-18 ; blood ; Male ; Middle Aged ; Vascular Cell Adhesion Molecule-1 ; blood ; Vascular Endothelial Growth Factor A ; blood ; Young Adult