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941.
Herrmann-Storck C Brioudes A Quirin R Deloumeaux J Lamaury I Nicolas M Postic D Perez JM 《The West Indian medical journal》2005,54(1):42-46
Demographic, clinical, biological and personal data were obtained from patients hospitalized with symptoms of leptospirosis in the Hospital of Pointe a Pitre, Guadeloupe, French West Indies from 1994 to 2001. Of the 897 screened patients, 212 were acute cases, 607 were non-infected and 78 were undetermined cases. There was no predominant age group. Leptospirosis transmission followed the rainfall cycle and was greater in rural areas. Jaundice and conjunctival suffusion were significantly more frequent in cases than non-cases. Males, professions considered to be at risk and contact with swine or bovine were associated with infection. Serogroups Icterohaemorrhagiae, Cynopteri, Australis, Sejroe, Pomona and Ballum were serovars presumed responsible for acute cases. 相似文献
942.
Farmaki E Papachristou F Winn RM Karatzas N Sotiriou J Roilides E 《Pediatric nephrology (Berlin, Germany)》2005,20(2):180-183
Urinary tract infection (UTI) is a frequent cause of morbidity during the first years of life and may lead to renal insufficiency. Transforming growth factor-1 (TGF-) is both immunoregulatory and an important mediator of interstitial fibrosis. TGF- was detected in the urine of 52% of 48 children aged 1–24 months with a first episode of UTI (94% due to Escherichia coli) and no obstructive nephropathy compared with 0 of 20 healthy young children (P<0.001). TGF- was detected in the urine only during the early stage (<1 day) after initiation of treatment. It was detected more frequently (P=0.06) and in significantly higher concentrations (P=0.046) in children with a normal 99m Tc-dimercaptosuccinic acid scan compared with those with abnormal scans performed 3–14 days after the diagnosis of UTI, suggesting a regulatory role in fibrogenesis and outcome of pyelonephritis in childhood. 相似文献
943.
Circulating endothelial microparticles are associated with vascular dysfunction in patients with end-stage renal failure 总被引:13,自引:0,他引:13
Amabile N Guérin AP Leroyer A Mallat Z Nguyen C Boddaert J London GM Tedgui A Boulanger CM 《Journal of the American Society of Nephrology : JASN》2005,16(11):3381-3388
Endothelial dysfunction and arterial stiffness are major determinants of cardiovascular risk in patients with end-stage renal failure (ESRF). Microparticles are membrane fragments shed from damaged or activated cells. Because microparticles can affect endothelial cells, this study investigated the relationship between circulating microparticles and arterial dysfunction in patients with ESRF and identified the cellular origin of microparticles associated with these alterations. Flow cytometry analysis of platelet-free plasma from 44 patients with ESRF indicated that circulating levels of Annexin V+ microparticles were increased compared with 32 healthy subjects, as were levels of microparticles derived from endothelial cells (three-fold), platelets (16.5-fold), and erythrocytes (1.6-fold). However, when arterial function was evaluated noninvasively in patients with ESRF, only endothelial microparticle levels correlated highly with loss of flow-mediated dilation (r = -0.543; P = 0.004), increased aortic pulse wave velocity (r = 0.642, P < 0.0001), and increased common carotid artery augmentation index (r = 0.463, P = 0.0017), whereas platelet-derived, erythrocyte-derived, and Annexin V+ microparticle levels did not. In vitro, microparticles from patients with ESRF impaired endothelium-dependent relaxations and cyclic guanosine monophosphate generation, whereas microparticles from healthy subjects did not. Moreover, in vitro endothelial dysfunction correlated with endothelial-derived (r = 0.891; P = 0.003) but not platelet-derived microparticle concentrations. In fact, endothelial microparticles alone decreased endothelial nitric oxide release by 59 +/- 7% (P = 0.025). This study suggests that circulating microparticles of endothelial origin are tightly associated with endothelial dysfunction and arterial dysfunction in ESRF. 相似文献
944.
Detaille D Guigas B Chauvin C Batandier C Fontaine E Wiernsperger N Leverve X 《Diabetes》2005,54(7):2179-2187
Hyperglycemia-induced oxidative stress is detrimental for endothelial cells, contributing to the vascular complications of diabetes. The mitochondrial permeability transition pore (PTP) is an oxidative stress-sensitive channel involved in cell death; therefore, we have examined its potential role in endothelial cells exposed to oxidative stress or high glucose level. Metformin, an antihyperglycemic agent used in type 2 diabetes, was also investigated because it inhibits PTP opening in transformed cell lines. Cyclosporin A (CsA), the reference PTP inhibitor, and a therapeutic dose of metformin (100 micromol/l) led to PTP inhibition in permeabilized human microvascular endothelial cells (HMEC-1). Furthermore, exposure of intact HMEC-1 or primary endothelial cells from either human umbilical vein or bovine aorta to the oxidizing agent tert-butylhydroperoxide or to 30 mmol/l glucose triggered PTP opening, cytochrome c decompartmentalization, and cell death. CsA or metformin prevented all of these effects. The antioxidant N-acetyl-l-cysteine also prevented hyperglycemia-induced apoptosis. We conclude that 1) elevated glucose concentration leads to an oxidative stress that favors PTP opening and subsequent cell death in several endothelial cell types and 2) metformin prevents this PTP opening-related cell death. We propose that metformin improves diabetes-associated vascular disease both by lowering blood glucose and by its effect on PTP regulation. 相似文献
945.
Accumulating evidence suggests that high concentrations of leptin observed in obesity and diabetes may contribute to their adverse effects on cardiovascular health. Metformin monotherapy is associated with reduced macrovascular complications in overweight patients with type 2 diabetes. It is uncertain whether such improvement in the cardiovascular outcome is related to specific vasculoprotective effects of this drug. In the present study, we determined the effect of leptin on human aortic smooth muscle cell (HASMC) proliferation and matrix metalloproteinase (MMP)-2 expression, the signaling pathways mediating these effects, and the modulatory effect of metformin on these parameters. Incubation of HASMCs with leptin enhanced the proliferation and MMP-2 expression in these cells and increased the generation of intracellular reactive oxygen species (ROS). These effects were abolished by vitamin E. Inhibition of NAD(P)H oxidase and protein kinase C (PKC) suppressed the effect of leptin on ROS production. In HASMCs, leptin induced PKC, extracellular signal-regulated kinase (ERK)1/2, and nuclear factor-kappaB (NF-kappaB) activation and inhibition of these signaling pathways abrogated HASMC proliferation and MMP-2 expression induced by this hormone. Treatment of HASMCs with metformin decreased leptin-induced ROS production and activation of PKC, ERK1/2, and NF-kappaB. Metformin also inhibited the effect of leptin on HASMC proliferation and MMP-2 expression. Overall, these results demonstrate that leptin induced HASMC proliferation and MMP-2 expression through a PKC-dependent activation of NAD(P)H oxidase with subsequent activation of the ERK1/2/NF-kappaB pathways and that therapeutic metformin concentrations effectively inhibit these biological effects. These results suggest a new mechanism by which metformin may improve cardiovascular outcome in patients with diabetes. 相似文献
946.
Poor intraoperative blood glucose control is associated with a worsened hospital outcome after cardiac surgery in diabetic patients 总被引:16,自引:0,他引:16
Ouattara A Lecomte P Le Manach Y Landi M Jacqueminet S Platonov I Bonnet N Riou B Coriat P 《Anesthesiology》2005,103(4):687-694
BACKGROUND: Tight perioperative control of blood glucose improves the outcome of diabetic patients undergoing cardiac surgery. Because stress response and cardiopulmonary bypass can induce profound hyperglycemia, intraoperative glycemic control may become difficult. The authors undertook a prospective cohort study to determine whether poor intraoperative glycemic control is associated with increased intrahospital morbidity. METHODS: Two hundred consecutive diabetic patients undergoing on-pump heart surgery were enrolled. A standard insulin protocol based on subcutaneous intermediary insulin was given the morning of the surgery. Intravenous insulin therapy was initiated intraoperatively from blood glucose concentrations of 180 mg/dl or greater and titrated according to a predefined protocol. Poor intraoperative glycemic control was defined as four consecutive blood glucose concentrations greater than 200 mg/dl without any decrease in despite insulin therapy. Postoperative blood glucose concentrations were maintained below 140 mg/dl by using aggressive insulin therapy. The main endpoints were severe cardiovascular, respiratory, infectious, neurologic, and renal in-hospital morbidity. RESULTS: Insulin therapy was required intraoperatively in 36% of patients, and poor intraoperative glycemic control was observed in 18% of patients. Poor intraoperative glycemic control was significantly more frequent in patients with severe postoperative morbidity (37% vs. 10%; P < 0.001). The adjusted odds ratio for severe postoperative morbidity among patients with a poor intraoperative glycemic control as compared with patients without was 7.2 (95% confidence interval, 2.7-19.0). CONCLUSION: Poor intraoperative control of blood glucose concentrations in diabetic patients undergoing cardiac surgery is associated with a worsened hospital outcome after surgery. 相似文献
947.
948.
Fatty liver in the intensive care unit 总被引:2,自引:0,他引:2
PURPOSE OF REVIEW: Non-alcoholic steatohepatitis is a liver disease characterized by steatosis and steatohepatitis in subjects whose alcohol consumption is negligible. The primary form is associated with insulin resistance whereas secondary non-alcoholic steatohepatitis occurs notably during total parenteral nutrition or in patients in the intensive care unit. This review is mainly focused on recent developments in the understanding of the pathogenesis of this disease. RECENT FINDING: Pathogenesis involves the direct role of fatty acids in liver injury, oxidative stress, cytokines, genetic susceptibility or mitochondrial dysfunction. An increased delivery of free fatty acids to the liver contributes to the first hit, originating liver steatosis. The process may undergo a second hit, characterized by inflammation and hepatocellular degeneration. Mitochondrial dysfunction plays a key role by leading to abnormal generation of reactive oxygen species, which cause lipid peroxidation. The peroxidation products and cytokines favor progression from steatohepatitis to fibrosis. Fatty liver disease may also be encountered in the intensive care unit in patients receiving parenteral nutrition. However, an adapted glucose-lipid ratio as source of non-protein calories prevents the development of fatty liver. Moreover, recent evidence suggests the importance of the type of lipid infused (structured lipid emulsion or fish oils). The acute phase response associated with severe disease can also lead to the development of fatty liver in spite of adequate nutritional support. SUMMARY: The pathogenesis of non-alcoholic steatohepatitis is multifactorial, but there is growing evidence that mitochondrial dysfunction always plays a key role. Adapted nutrition may prevent in part fatty liver in the intensive care unit. 相似文献
949.
Most published data on myelodysplastic syndromes (MDS) are derived from Western countries, which report MDS as a disease of the elderly. However, it was observed that Asian MDS patients were younger than subjects in Western reports. With this in mind, the study was conducted prospectively on 52 Indian patients to define chromosomal abnormalities and to understand ethno-geographical differences, if any, underlying the pathogenesis of MDS among this Asian population. Cytogenetic analysis was performed using GTG banding and karyotyped according to the International System for Human Cytogenetic Nomenclature (ISCN). The incidence of MDS was predominant in the age group of 41–60 years (44.23%), with a median age at diagnosis of 55 years. The disease was more frequent in males (33 patients, 63.46%) than females (19 patients, 36.53%). Of 48 patients successfully karyotyped, 17 had normal karyotype (35.4%) and 31 patients (64.5%) had a chromosomal abnormality. The most frequent chromosome abnormalities were del 5q/–5 in 13 patients (42%), –7/7q– in 10 patients (32.2%), +8 and del 20q– in 6 cases each (19.3%) and i(17)(q10) in 1 patient (3.2%). In addition to these non-random chromosomal abnormalities, some rare abnormalities were also encountered. A higher rate of transformation to acute myeloid leukaemia (AML) was observed in the Chinese population compared to other Asian countries. The incidence of chromosomal abnormalities varied considerably across the different Asian populations. The overall frequency of chromosomal abnormalities in our study was comparable to most Western reports. Further prospective studies are warranted to elucidate precisely the ethnic differences in the pathogenesis of MDS in the Indian population. 相似文献
950.
The follow-up of patients with asthma should focus on asthma control (disease course over a number of weeks). 相似文献