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Seventy patients, aged 1–20 years, were seen at Jordan University Hospital with high blood pressure (BP) over a 3-year period. BP values ranged from 140 to 230 mmHg for systolic pressure and from 90 to 130 mmHg for diastolic pressure. Essential hypertension was seen in only 6 patients (8.6%); secondary hypertension (n=64 or 91.4%) was due to renal parenchymal diseases (RPD) in 46 patients (65.7%), reno-vascular lesions in 8 (11.4%), renal transplantation in 5 (7.2%), teenage pregnancy in 4 (5.7%), and phaeochromocytoma in 1 patient (1.4%). The aetiologies of RPD were as follows: end-stage renal disease requiring dialysis in 14 patients, acute glomerulonephritis in 14, idiopathic nephrotic syndrome in 10, chronic renal insufficiency in 5, and polycystic kidney in 3 patients. Surgical cure of hypertension was achieved in 5 of the children with reno-vascular lesions and in the patient with phaeochromocytoma.  相似文献   
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The alphavbeta6 integrin is an exclusively epithelial integrin that is highly expressed during fetal development. In adult tissue, alphavbeta6 integrin is expressed during inflammation, carcinogenesis, and in wound healing. We previously reported that alphavbeta6 integrin is highly expressed in poorly healing human wounds and its over-expression is associated with chronic wounds in a mouse model. The objective of this study was to investigate the role of alphavbeta6 integrin in compromised wound healing induced by hydrocortisone treatment or aging by using young and old mice deficient in or overexpressing the beta6 integrin subunit in the epidermis. Untreated aged beta6 integrin-deficient (beta6-/-) animals showed a significant delay in wound healing when compared to their age-matched controls or younger beta6-/- mice. The most significant delay was observed at the stages where granulation tissue deposition was occurring. Hydrocortisone treatment significantly delayed wound healing in wild-type and beta6 integrin-deficient mice in comparison with the untreated controls. However, hydrocortisone treatment in beta6 integrin overexpressing animals did not cause a significant delay in wound healing. The results of this study suggest that alphavbeta6 integrin plays an important role in wound healing in animals compromised by either age or stress mimicked by hydrocortisone.  相似文献   
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Purpose. To compare clinical advantages and hemodynamic and respiratory changes during one lung-collapsed ventilation (OLCV) using a double-lumen tube (DLT) or a single-lumen tube (SLT) with intrathoracic CO2 insufflation, in patients undergoing thoracic sympathectomy (TS) under general anesthesia. Methods. One hundred and twenty-five patients (94 men and 31 women) undergoing TS for the treatment of palmar hyperhidrosis (PH) were randomly allocated to two groups: group A (68 patients; age, 29 ± 6 years) in whom DLT was used, and group B (57 patients; age, 32 ± 3 years) in whom SLT with intrathoracic CO2 insufflation at a rate of 0.5–1 l·min−1 and sustained intrathoracic pressure at 6 mmHg insufflation were used. Anesthesia was maintained with 1 minimum alveolar concentration (MAC) isoflurane in 50% nitrous oxide in oxygen with incremental doses of sufentanil and atracurium when required. Arterial blood gases were measured in 10 patients in group B. Hemodynamic and respiratory parameters were obtained perioperatively. Results. There were no significant differences in hemodynamic and respiratory parameters between the two groups during the study phases, except for the arterial oxygen saturation (SpO2). The times required for anesthesia and surgery were significantly shorter in the SLT group than in the DLT group. SpO2 during OLCV was 95 ± 1% with DLT and 98 ± 1% with SLT, with a significant difference. Three patients had an SpO2 of less than 90% in the recovery room, where the chest tube position was readjusted, with no further sequelae. Conclusion. General anesthesia with SLT and intrathoracic CO2 insufflation provides optimal operating conditions, adequate oxygenation, and perfect hemodynamic stability during TS. Received: November 28, 2000 / Accepted: August 8, 2001  相似文献   
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BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited human kidney disease and is caused by germline mutations in PKD1 (85%) or PKD2 (15%). It has been estimated that around 1% of tubular cells give rise to cysts, and cell hyperproliferation has been noted to be a cardinal feature of cystic epithelium. Nevertheless, it is uncertain whether the increase in proliferative index observed is an early or late feature of the cystic ADPKD kidney. METHODS: Two Pkd2 mouse mutants (WS25 and WS183) have been recently generated as orthologous models of PKD2. To determine the effect of Pkd2 dosage on cell proliferation, cyst formation and renal fibrosis, we studied renal tissue from Pkd2(WS25/WS25) and Pkd2(+/-) mice by histological analysis. We also examined the proliferative index in archival nephrectomy tissue obtained from patients with ADPKD and normal controls. RESULTS: The proliferative index of non-cystic tubules in Pkd2 mutant mice as assessed by proliferating cell nuclear antigen and Ki67-positive nuclei was between 1-2%, values 5-10 times higher than control tissue. Similarly, the proliferative index of non-cystic tubules in human ADPKD kidneys was 40 times higher than corresponding controls. In Pkd2 mutant mice, significant correlations were found between the fibrosis score and the mean cyst area as well as with the proliferative index. Of significance, proliferating tubular cells were uniformly positive for polycystin-2 expression in Pkd2(+/-) kidney. CONCLUSION: These results suggest that an increase in cell proliferation is an early event preceding cyst formation and can result from haploinsufficiency at Pkd2. The possible pathogenic link between tubular cell proliferation, interstitial fibrosis and cyst formation is discussed.  相似文献   
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Introduction  

Cardiovascular disease (CVD) remains the main cause of morbidity and mortality in end stage renal disease (ESDR) patients. A common C–T mutation at nucleotide position 677 (C677T) has been identified in the gene coding for methylenetetrahydrofolate reductase (MTHFR), which is involved in the remethylation of homocysteine (Hcy). The C677T mutation decreases MTHFR activity, tends to increase Hcy concentrations in individuals who are homozygous for the T/T genotype, and may predispose to CVD. Recent reports suggested that the T/T genotype may predispose type 2 diabetic and hypertensive patients to the development of progressive renal insufficiency. The aim of this cross-sectional study is to analyze the prevalence of the MTHFR C677T gene polymorphism among a group of chronic dialysis patients in comparison to age- and gender-matched controls. We also examined the possible association between CVD and MTHFR gene mutation in this group of patients.  相似文献   
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