Aged ; Aged, 80 and over ; Female ; Humans ; Hyponatremia ; chemically induced ; Iodipamide ; adverse effects

Abdominal Neoplasms ; genetics ; metabolism ; pathology ; Chromosomes, Human, Pair 20 ; genetics ; Chromosomes, Human, Pair 8 ; genetics ; Fibromatosis, Aggressive ; etiology ; genetics ; metabolism ; pathology ; Genes, APC ; Humans ; Mutation ; Trisomy ; beta Catenin ; genetics ; metabolism

Adenomatous Polyposis Coli Protein ; genetics ; Chromatography, High Pressure Liquid ; methods ; Codon ; genetics ; DNA Mutational Analysis ; Fibromatosis, Aggressive ; genetics ; pathology ; Humans ; Mutation ; Polymerase Chain Reaction ; beta Catenin ; genetics

0.05).There was significant difference between normal control group and group A and B(P0.05 ).Neuron counting was significantly higher in group B than that in group A 4 weeks after treatment(P

The gene of mutated TNF-?D4 gene was amplified by overlap PCR and cloned into the prokaryotic expressive vector pBV220.TNF-?D4 contains two changes:substitutions of Pro8Arg,Ser9Lys,Asp10Arg,Ile157Phe,Leu29Ser,Arg31Val and a deletion of the N terminal four amino acids.The recombinant vector pBV220-TNF-?D4 was transformated into E.coli strain DH5?,and the high expression strain was obtained by screening monoclones.The level of expression was about 45% of total cell protein.After purification,the purity of fusion protein was above 90% by HPLC and relative ability was 8 ?107.TNF-?D4 was modificated by mPEG-ButyrALD。After purification,the purity of mPEG-TNF-?D4 was above 85% and relative ability was 8.6?107.The in vivo systemic toxicity of mPEG-TNF-?D4,which is indicated by LD50,is lower than that of rhTNF-?.These results strongly supported for the further study and exploitation of TNF-antitumor drug.

Objective To explore the method of repairing wound defects with exposed tibia. Methods 32 patients with soft tissue defects with exposed tibia were treated with three kinds of flaps pedicled with interior,lateral and posterior vascular perforating branches in the leg,respectively.Re- suits One flap with distal part necrotic was treated with change of dressings and got one-stage healing. One case had delayed union for muscular infection under the flap.Other flaps all were successful and sur- vived.No ostemyelitis was found.Conclusion The flap pedicled with vascular perforating branches of leg has abundant blood supply and is a good method for repairing small or middle wound defect with ex- posed tibia.

OBJECTIVETo explore the role of abnormalities of chromosome 8, APC and beta-catenin genes in tumorigenesis of aggressive fibromatosis.

METHODSTrisomy 8 was detected by interphase fluorescence in situ hybridization (FISH). The APC gene and beta-catenin gene mutations were detected by denaturing high performance liquid chromatography (DHPLC) and direct sequence analysis after the PCR transition.

RESULTSThe rate of trisomy 8 in recurrent tumors (62.5%, 5/8) was significantly higher than that in the primary tumors (8.3%, 1/12). Somatic substitution of APC gene was found in 18 of 69 (26.1%) aggressive fibrometases. Somatic transition of beta-catenin gene was detected in 13 of 69 (18.8%) and mutation at codon 41 in exon 3 involving threonine residues implicated in the degradation of beta-catenin. The abnormal expression of beta-catenin had no significant correlation with the mutation of APC or beta-catenin gene. The group with positively expressed beta-catenin protein showed a significant higher c-myc protein expression than those without (P = 0.001). The Ki-67 index was extremely low in all the lesions. The apoptosis index (AI) of the groups with positively expressed c-myc and cyclin D1 showed significantly lower AI than those without.

CONCLUSIONTrisomy 8 may serve as a useful predictor of recurrence in aggressive fibromatosis. There are somatic mutations of the APC and beta-catenin genes in the aggressive fibromatosis, and there are abnormalities in the Wnt signaling pathway. These abnormalities may result in the aberrances of cell proliferation and apoptosis, which are likely to be import factors in the tumorigenesis.

Adenomatous Polyposis Coli Protein ; genetics ; metabolism ; Apoptosis ; Chromosomes, Human, Pair 8 ; Cyclin D1 ; metabolism ; Fibromatosis, Aggressive ; genetics ; metabolism ; pathology ; Genes, APC ; Humans ; Ki-67 Antigen ; metabolism ; Neoplasm Recurrence, Local ; Point Mutation ; Proto-Oncogene Proteins c-myc ; metabolism ; Signal Transduction ; Trisomy ; Wnt Proteins ; metabolism ; beta Catenin ; genetics ; metabolism

Atrial Fibrillation ; etiology ; Humans ; Recurrence ; Sleep Apnea, Obstructive ; complications

OBJECTIVETo investigate the influence of persistent rapid atrial pacing on the levels of connexin 43 (Cx43) and type III collagen in pulmonary vein and atrium in a canine model.

METHODSSixteen mongrel dogs were divided into rapid atrial pacing (RAP) group (n = 8) and normal control group (n = 8) randomly. In the RAP group, atrial pacing was performed with a rate of 400 bpm for 10 weeks to establish atrial fibrillation model. The tissues of left superior pulmonary vein (LSPV), left atrial free wall (LAFW) and right atrial appendage (RAA) were collected from each dogs. The levels of Cx43 and type III collagen were measured in each tissue.

RESULTSTen weeks later, persistent atrial fibrillation was induced in all dogs in RAP group. The level of Cx43 in RAP group was higher than that in normal control group (LSPV: 3370.91 +/- 275.11 vs 1405.82 +/- 90.38, P < 0.05; LAFW: 2448.68 +/- 272.10 vs 1467.12 +/- 147.93, P < 0.05, RAA: 2331.96 +/- 199.61 vs 1288.27 +/- 216.22, P < 0.05). The level of Cx43 in LSPV was higher than that in LAFW and RAA in RAP group, whereas the difference between LAFW and RAA was not significant in RAP group. The quantities of type III collagen in RAP group were higher than those in normal control group (LSPV: 3301.97 +/- 309.70 vs 1404.56 +/- 178.02, P < 0.05; LAFW: 2477.86 +/- 190.43 vs 1479.20 +/- 187.17, P < 0.05; RAA: 2045.92 +/- 139.43 vs 1417.07 +/- 139.43, P < 0.05). The quantities of type III collagen in LSPV was higher than those in LAFW and RAA in RAP group.

CONCLUSIONSPersistent rapid atrial pacing could increase the levels of Cx43 and type III collagen in pulmonary vein and atrium in a canine model of atrial fibrillation. The levels of Cx43 and type III collagen in pulmonary vein were higher than those in atrium. This findings indicated that pulmonary vein may be a crucial regions in maintaining atrial fibrillation.

Animals ; Atrial Fibrillation ; metabolism ; physiopathology ; Cardiac Pacing, Artificial ; methods ; Collagen Type III ; blood ; Connexin 43 ; blood ; Disease Models, Animal ; Dogs ; Female ; Male ; Pulmonary Veins ; metabolism ; physiopathology

OBJECTIVETo investigate the changes in angiotensinogen (AGT), angiotensin II type 1 receptor (AT(1)R), endothelial nitric oxide synthase (eNOS) mRNA and protein expressions and nitric oxide (NO) content in the rat glomeruli in response to leptin stimulation.

METHODSThe glomeruli isolated from male SD rats were stimulated with 3 nmol/L leptin for 2 h. Real-time PCR and Western blotting were performed to analyze the mRNA and protein expressions of AGT, AT(1)R and eNOS in the glomeruli, and nitrite concentration in the glomeruli was measured by nitrate reductase assay.

RESULTSIn comparison with the control group, exposure to leptin increased the mRNA levels of AGT, ATR(1) and eNOS in the isolated glomeruli by 2.69-/+0.17, 3.77-/+0.16 and 2.56-/+0.29 folds (P=0.024, 0.018 and 0.044), and their protein levels by 2.06-/+0.10, 2.67-/+0.08 and 1.61-/+0.13 folds (P=0.021, 0.015 and 0.032), respectively. The NO production in the glomeruli was also increased by 2.77-/+0.14 folds (P=0.000) following leptin exposure.

CONCLUSIONLeptin exposure of isolated rat glomeruli directly causes activation of the internal renal renin-angiotensin system and enhanced NO production, suggesting that leptin plays a role in the pathogenesis of maladaptation in renal hemodynamics in obesity.

Animals ; Gene Expression Regulation ; drug effects ; Kidney Glomerulus ; drug effects ; metabolism ; Leptin ; pharmacology ; Male ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase Type III ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1 ; genetics ; metabolism ; Renin-Angiotensin System ; drug effects