Objective To examine the association between glycemia in COPD and pulmonary function. Methods 124 cases were divided as COPD and COPD with type 2 diabetes mellitus. COPD patients with diabetes were stratified according to the course of diabetes. The main pulmonary function measures included TLC,FVC, FEV_1, FEV_1/FVC%, FEF25%～75% and DLCO, DLCO/VA . Results DLCO and DLCO/VA in diabetic COPD were significantly lower than those of COPD ( P

Purpose:To study prognostic factors of younger women's eptihelial ovarian neoplasms.Methods: From Jan. 1980 to Dec. 1992, there were 86 cases of younger women's epithelial ovarian carcinoma in our hospital. We studied serveral prognostic factors retrospectively.Results:In this setting, 2 year survival rate were 79.07%, 5 year survival rate were 54.65%. There were 49 cases with stage Ⅰ and 41 cases with grade Ⅰ. No recurrence was found in 4 patients who preserved ovarian function. Cox model multifactor results showed that grade, residual tumor size and the method of surgery were prognostic factors( P 0 05). The pathological type, FIGO staging, grade, residual tumor size, the method of surgery were important factors according to unifactor analyze ( P

AIM: To study the protective effect of cardiomyopeptidin (CMP) attributed to polypeptide on cultured myocardial cells injured by anoxia-reoxygenation.METHODS: The anoxia-reoxygenation injury model were developed, anoxia for 60 min and reoxygenation for 30 min. The effect of CMP on myocardial ultrastructure was observed. ［Ca2＋］i was estimated with adherent cell analysis and sorting 570(ACAS 570) laser cytometer and measured with fluorescent dye Fura-2-AM, the lipid fluidity of cellular membrane was determined by fluorescence polarization technique. RESULTS: CMP could obviously improve the ultrastructure of myocardial cells and dose-dependently decrease ［Ca2＋］i and increase the lipid fluidity of cellular membrane, CMP also could markedly reduce the chromaticity value of pseudo-colour graphic model of Ca2＋. CONCLUSION: Cardiomyopeptidin has an obvious protective effect on cultured myocardial cells injured by anoxia-reoxygenation, this may be related to its effect of decreasing ［Ca2＋］i and increasing lipid fluidity of cellular membrane.

Objective To investigate the preventing and curative value of endoscopic injectim sclerotherapy underlying endoscopic variceal ligations in the treatment of the patients suffering form esophageal varix recurrence.Methods The endoscopic injection sclerotherapy was performed to the patients whose esophageal varix varnished or nearly varnished after the endoscopic variceal ligation.Results There were sinificant differences (P ＜ 0.05 ) between the group of the endoscopic variceal ligation combining more dose laurornacrogol and the group of the single endoscopic variceal ligation at the recurrence rate of bleeding.No severe complications were observed during the treatments.Conclusion The endoscopic injection clerotherapy of more amount doses lauromacrogol after the endoscopic variceal ligation can signiticantly reduce residual esophageal varix after the endoscopic variceal ligation and dday esophageal varix recurrrence.

The preventive effect of garlic against toxicity of dimethylnitrosamine (NDMA) in rats medicated with aminopyrine (AP) and NaNO2 was investigated. 28 rats were divided into three groups. The 6 rats of group C were set as control taking basal diet; the 10 rats of group B were given basal diet, AP, and NaNO2; the 12 rats of group A were given basal diet with an addition of 10% of garlic, AP and NaNO2. AP and NaNO2 in the dosage of 30 mg per kg of body weight were dissolved in 0.5% acetic acid and given by gavage to rats of groups A and B.During the experimental period of 35 days, 3 rats of group B died while all the rats of group A survived. At the end of the experiment, Hb, SGPT and SGOT were determined and all rats were killed for pathological studies. It was found Hb value of group A was higher than that of group B (P

AIM: To study the protective effect of cardiomyopeptidin (CMP) attributed to polypeptide on cultured myocardial cells injured by anoxia-reoxygenation.METHODS: The anoxia-reoxygenation injury model were developed, anoxia for 60 min and reoxygenation for 30 min. The effect of CMP on myocardial ultrastructure was observed. [Ca 2+ ] i was estimated with adherent cell analysis and sorting 570(ACAS 570) laser cytometer and measured with fluorescent dye Fura-2-AM, the lipid fluidity of cellular membrane was determined by fluorescence polarization technique. RESULTS: CMP could obviously improve the ultrastructure of myocardial cells and dose-dependently decrease [Ca 2+ ] i and increase the lipid fluidity of cellular membrane, CMP also could markedly reduce the chromaticity value of pseudo-colour graphic model of Ca 2+ . CONCLUSION: Cardiomyopeptidin has an obvious protective effect on cultured myocardial cells injured by anoxia-reoxygenation, this may be related to its effect of decreasing [Ca 2+ ] i and increasing lipid fluidity of cellular membrane. [

AIM:To check the physical interaction between GST-Na+-K+-ATPase domain and recombinant human augmenter of liver regeneration (rhALR) by GST pull down assay. METHODS: With PCR and genetic recombinant techniques, the coding region of ? subunit of Na+-K+-ATPase was cloned into expressing plasmid pGEX-4T and identified by endonuclease digestion and sequencing methods. Under the inducing of 0.1 mmol/L IPTG, the fusion protein GST-Na+-K+-ATPase domain was highly expressed by E.coli DH-5?. After hypersound quassating, the GST-Na+-K+-ATPase domain was purified by glutathione agarose beads and the physical interaction with rhALR was checked by GST pull down assay. RESULTS: Analysis by SDS-PAGE showed the rhALRs of monomer and dimmer in GST-Na+-K+-ATPase domain lane. The Western blotting of the GST-pull down assay showed the same results as well. CONCLUSION: The Na+-K+-ATPase domain is associated with rhALR specifically in vitro.

Objective To study the clinical efficacy of Akin combined Scarf osteotomies for moderate and severe hal?lux valgus. Methods Thirty-nine (58 feet) patients received Akin combined Scarf osteotomies, in which 12 patients (16 feet) with moderate hallux valgus received the single scarf osteotomy. Hallux valgus angle (HVA), intermetatarsal angle (IMA), tibial sesamoid position and American orthopedic foot and ankle society score (AOFAS) were measured and compared before and after operation respectively. Results All operations were successfully completed patients were followed up for 8-22 months. The mean operation time was (55.0±6.8) min. The amount of intraoperative bleeding was 3-20 mL with an aver?age of (11.0±5.4) mL. All patients were healed except for a delayed union of Akin on a severe hallux valgus patient. Two cas?es (2 feet) were found inflammation in surgical incision. Two cases (2 feet) were found numbness in dorsal medial side of hal?lux, which was considered nerve damage and improved in 3-5 months. There was no recurrence of hallux valgus in the peri?od of following up. After surgery, HVA (14.1°±5.3°), IMA (7.7°±3.8°) and tibial sesamoid position (2.58±0.61) were signifi?cantly decreased compared with those before operation (39.6° ± 6.8° , 18.7° ± 5.4° and 4.87 ± 0.59, P<0.05). AOFAS score (84.4±8.7) was significantly higher after surgery than that before surgery (37.3±9.5, P<0.05). Conclusion Akin combined Scarf osteotomies can achieve a excellent therapeutic effect for moderate and severe hallux valgus with very few complica?tions and recurrence, which is worth for clinical application.

Maintenance of skeletal integrity requires the coordinated activity of multinucleated bone-resorbing osteoclasts and bone-forming osteoblasts. Osteoclasts form resorption lacunae on bone surfaces in response to cytokines by fusion of precursor cells. Osteoblasts are derived from mesenchymal precursors and lay down new bone in resorption lacunae during bone remodeling. Nuclear factorkappa B (NF-κB) signaling regulates osteoclast and osteoblast formation and is activated in osteoclast precursors in response to the essential osteoclastogenic cytokine, receptor activator of NF-κB ligand (RANKL), which can also control osteoblast formation through RANK-RANKL reverse signaling in osteoblast precursors. RANKL and some pro-inflammatory cytokines, including tumor necrosis factor (TNF), activate NF-κB signaling to positively regulate osteoclast formation and functions. However, these cytokines also limit osteoclast and osteoblast formation through NF-κB signaling molecules, including TNF receptor-associated factors (TRAFs). TRAF6 mediates RANKL-induced osteoclast formation through canonical NF-κB signaling. In contrast, TRAF3 limits RANKL- and TNF-induced osteoclast formation, and it restricts transforming growth factor β (TGFβ)-induced inhibition of osteoblast formation in young and adult mice. During aging, neutrophils expressing TGFβ and C-C chemokine receptor type 5 (CCR5) increase in bone marrow of mice in response to increased NF-κB-induced CC motif chemokine ligand 5 (CCL5) expression by mesenchymal progenitor cells and injection of these neutrophils into young mice decreased bone mass. TGFβ causes degradation of TRAF3, resulting in decreased glycogen synthase kinase-3β/β-catenin-mediated osteoblast formation and age-related osteoporosis in mice. The CCR5 inhibitor, maraviroc, prevented accumulation of TGFβ+/CCR5+ neutrophils in bone marrow and increased bone mass by inhibiting bone resorption and increasing bone formation in aged mice. This paper updates current understanding of how NF-κB signaling is involved in the positive and negative regulation of cytokine-mediated osteoclast and osteoblast formation and activation with a focus on the role of TRAF3 signaling, which can be targeted therapeutically to enhance bone mass.

Osteoclasts are multinucleated cells formed mainly on bone surfaces in response to cytokines by fusion of bone marrow-derived myeloid lineage precursors that circulate in the blood. Major advances in understanding of the molecular mechanisms regulating osteoclast formation and functions have been made in the past 20 years since the discovery that their formation requires nuclear factor-kappa B (NF-kappaB) signaling and that this is activated in response to the essential osteoclastogenic cytokine, receptor activator of NF-kappaB ligand (RANKL), which also controls osteoclast activation to resorb (degrade) bone. These studies have revealed that RANKL and some pro-inflammatory cytokines, including tumor necrosis factor, activate NF-kappaB and downstream signaling, including c-Fos and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), and inhibition of repressors of NFATc1 signaling, to positively regulate osteoclast formation and functions. However, these cytokines also activate NF-kappaB signaling that can limit osteoclast formation through the NF-kappaB signaling proteins, TRAF3 and p100, and the suppressors of c-Fos/NFATc1 signaling, IRF8, and RBP-J. This paper reviews current understanding of how NF-kappaB signaling is involved in the positive and negative regulation of cytokine-mediated osteoclast formation and activation.
Cytokines ; NF-kappa B ; NFATC Transcription Factors ; Osteoclasts ; RANK Ligand ; Receptor Activator of Nuclear Factor-kappa B ; TNF Receptor-Associated Factor 3 ; Tumor Necrosis Factor-alpha