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991.
992.
Tanaka S Tanabe Y Tamura H Ishii S Shuto Y Kamegai J Sugihara H Kobayashi M Wakabayashi I Murano T Shirai K Oikawa S 《Internal medicine (Tokyo, Japan)》2002,41(4):300-303
A 39-year-old man with lipoprotein lipase (LPL) deficiency (height 177.7 cm, body weight 67 kg, and body mass index 21.2 kg/m2) showed severe hypertriglyceridemia (2,032 mg/dl). LPL activity and concentration were markedly low in postheparin plasma. LPL gene analysis revealed a homozygous mutation, Asp204 --> Glu in exon 5. Fasting plasma glucose (81 mg/dl) and insulin (2.7 microU/ml) levels were normal. Plasma glucose pattern during oral glucose (75 g) tolerance test was normal, however 30 minutes after glucose-loading the insulin secretion unexpectedly increased to 89.4 microU/ml. These data suggested that chylomicronemia might be related to a hyper-response of insulin secretion to glucose without obesity. 相似文献
993.
Uncoupling protein 2 plays an important role in nitric oxide production of lipopolysaccharide-stimulated macrophages 总被引:6,自引:0,他引:6
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994.
Quinapril prevents restenosis after coronary stenting in patients with angiotensin-converting enzyme D allele. 总被引:3,自引:0,他引:3
Kenji Okumura Takahito Sone Junichiro Kondo Hideyuki Tsuboi Hiroaki Mukawa Michitaka Tsuzuki Hajime Imai Hiroki Kamiya Yukio Mabuchi Hideo Matsui Tetsuo Hayakawa 《Circulation journal》2002,66(4):311-316
Restenosis after coronary artery stent implantation is attributed chiefly to intimal hyperplasia, which is prevented experimentally by angiotensin-converting enzyme (ACE) inhibitors. Therefore, the present study investigated whether the effect of quinapril, a tissue-specific ACE inhibitor, on the prevention of coronary restenosis differs according to ACE polymorphism. One hundred consecutive patients with successful stent implantation were randomly assigned to quinapril and control groups. Both follow-up angiography and ACE polymorphism analysis were obtained from 92 patients (control, 46; quinapril treatment, 46). The prevalence of risk factors did not differ statistically according to quinapril treatment or ACE genotypes. There was no statistically significant difference in the occurrence of restenosis 6 months after stenting between the groups. Quantitative coronary angiography revealed that quinapril treatment resulted in significantly higher minimal lumen diameter and significantly lower percent diameter stenosis (22.9 +/- 22.6 vs 37.1 +/- 19.7% in the control group, p < 0.05) in patients with the D allele although there was no difference in those with the II genotype. In addition, intravascular ultrasound revealed that quinapril treatment significantly prevented the loss of minimal lumen cross-sectional area and the increase in percent area stenosis (34.5 +/- 14.0 vs 53.3 +/- 16.4% in the control group, p < 0.05) in patients with the D allele compared to those with the II genotype. These results suggest that the administration of ACE inhibitors for the attenuation of lumen loss after coronary stent implantation is best for subjects with the D allele of the ACE genotype. 相似文献
995.
Nakamura Y Arai Y Nakamura F Maki K Aoyagi A Saito K Mitani K 《[Rinshō ketsueki] The Japanese journal of clinical hematology》2002,43(3):204-206
A 69-year-old man was diagnosed as having idiopathic thrombocytopenic purpura (ITP) in April 2000, and treated with prednisolone (PSL) without effect. Splenectomy performed in June 2000 had only a transient and marginal influence on his platelet count. Two months later, he developed autoimmune hemolytic anemia (AIHA) without Coombs test positivity, and his diagnosis was changed to Coombs-negative Evans syndrome. Treatment with PSL led to recovery of his hemoglobin level, but not his platelet count. Although the mechanism responsible for development of AIHA after splenectomy in this patient with ITP remains unknown, close observation is required for any association with other autoimmune diseases such as SLE. 相似文献
996.
997.
Niro Okimoto Takashi Kibayashi Kimihiro Mimura Kenji Yamato Takeyuki Kurihara Yoshihiro Honda Kohichi Osaki Naoko Asaoka Hideo Ohba 《Nihon Kokyūki Gakkai zasshi》2006,44(6):431-435
We studied the clinical effect of continuous infusion over 24 hours of meropenem (MEPM) on bacterial pneumonia in the elderly (over 65). The subjects were 26 patients (community-acquired pneumonia: moderate, n = 9; severe, n= 4; hospital-acquired pneumonia: group III, n = 13) whose performance status was 3 or 4. MEPM 1.0g/day was infused continuously for 7-14 days, and its clinical efficacy, bacteriological efficacy, and side effects were examined prospectively. It was effective in 23 of the 26 patients (community-acquired pneumonia: moderate, 8/9; severe, 3/4; hospital-acquired pneumonia: group III, 12/13; efficacy rate: 88.5%). Bactericidal effects were obtained in 3 strains of Klebsiella pneumoniae, 2 strains of Streptococcus pneumoniae, 2 strains of methicillin-sensitive Staphlococcus aureus, 1 strain of Streptococcus agalactiae and 1 strain of Proteus mirabilis, but not in 2 strains of methicillin-resistant S. aureus, 1 strain of Pseudomonas aeruginosa and 1 strain of Serratia marcescens. Mild abnormal laboratory findings were observed in 2 patients: elevation of GPT, gamma-GTP, BUN and elevation of ALP. Based on the above, continuous infusion of MEPM on bacterial pneumonia in the elderly obtained excellent clinical effects. Further study is needed to compare the efficacy of continuous versus intermittent administration of MEPM. 相似文献
998.
Yamamori T White AR Mattagajasingh I Khanday FA Haile A Qi B Jeon BH Bugayenko A Kasuno K Berkowitz DE Irani K 《Journal of molecular and cellular cardiology》2005,39(6):101-995
The p66shc adaptor protein mediates age-associated oxidative stress. We examined the role of p66shc in endothelial nitric oxide synthase (eNOS) signaling. Overexpression of p66shc inhibited eNOS-dependent NO production. RNAi-mediated down-regulation of endogenous p66shc led to activation of the proto-oncogene ras, and Akt kinase, with a corresponding increase in phosphorylation of eNOS at S1177 (S1179 on bovine eNOS). In rat aortic rings, down-regulation of p66shc suppressed the vasoconstrictor response to phenyephrine that was abrogated by treatment with the NOS inhibitor l-NAME, and enhanced vasodilation induced by sub-maximal doses of acetylcholine. These findings highlight a pivotal role for p66shc in inhibiting endothelial NO production, and endothelium-dependent vasorelaxation, that may provide important mechanistic information about endothelial dysfunction seen with aging. 相似文献
999.
Koichi Aiura Ryo Ohshima Kenji Matsumoto Seiichiro Ishii Yoshito Arisawa Motohito Nakagawa Katsuhiko Noga 《Journal of hepato-biliary-pancreatic sciences》1996,3(3):308-312
We report a case of spontaneous rupture of a giant cavernous hemangioma of the liver arising from the caudate lobe, with extrahepatic growth, in a 67-year-old man. At emergency laparotomy, partial resection of the caudate lobe was performed and the hemangioma was found to measure 13 ×12×8 cm. The patient had a 10-year history of severe asthma requiring steroid therapy. To investigate the risk factors for spontaneous rupture of hepatic hemangioma, we compared the characteristics of patients with ruptured and non-ruptured lesions showing extrahepatic growth reported in the Japanese literature. Lesions with a diameter ≥4 cm located on the surface of the liver or showing extrahepatic growth appear to have a high risk of spontaneous rupture if the patient receives steroid therapy for a coexisting disorder. Even in patients who have not received steroid therapy, hemangiomas≥7–8 cm in diameter located in the left lobe with extrahepatic growth may also have a high risk of rupture. The treatment of hepatic hemangioma should be decided on the basis of the size and the location, and on the requirement for steroid therapy. 相似文献
1000.
Dr. Kenji Fujiward MD PhD Satoshi Mochida MD Akihiko Ohno MD Masahiro Arai MD Atsushi Matsui MD Naohiko Masaki MD Keiichi Hirata MD Tomoaki Tomiya MD Miho Yamaoka MD Sumiko Nagoshi MD Yasuhiko Ohta MD Itsuro Ogata MD Antonio Francavilla MD David H. Van Thiel MD Thomas E. Starzl MD PhD 《Digestive diseases and sciences》1995,40(1):41-47
Endothelial cell damage causes massive hepatic necrosis as a result of fibrin deposition in the hepatic sinusoids. When a stable analog of prostaglandin I2, beraprost sodium, was administered to rats given either dimethylnitrosamine, carbon tetrachloride, or endotoxin followingCorynebacterium parvum administration, the hepatic necrosis produced in each was attenuated, but to a greater extent in the dimethylnitrosamine and endotoxin/Corynebacterium parvum models, where fibrin deposition in the hepatic sinusoids occurs, as compared to the carbon tetrachloride model, where such fibrin deposition does not occur. Beraprost sodium reduced the expected increase of portal venous pressure in the endotoxin/Corynebacterium parvum model without affecting plasma thrombin-antithrombin III complex levels. Beraprost sodium also significantly reduced cell killing of both isolated rat hepatocytes and hepatic sinusoidal endothelial cells exposed totert-butyl hydroperoxide when compared to controls. Beraprost sodium could prove to be a therapeutic candidate for the treatment of hepatic necrosis, particularly in cases associated with fibrin deposition in the hepatic sinusoids because of its fibrin clot-clearning action. 相似文献