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991.
992.
Filippo Numeroso Mario Benatti Caterina Pizzigoni Elisabetta Sartori Giuseppe Lippi Gianfranco Cervellin 《世界急诊医学杂志(英文)》2015,6(2):111-117
BACKGROUND: A poor communication with immigrants can lead to inappropriate use of healthcare services, greater risk of misdiagnosis, and lower compliance with treatment. As precise information about communication between emergency physicians(EPs) and immigrants is lacking, we analyzed difficulties in communicating with immigrants in the emergency department(ED) and their possible associations with demographic data, geographical origin and clinical characteristics.METHODS: In an ED with approximately 85 000 visits per year, a multiple-choice questionnaire was given to the EPs 4 months after discharge of each immigrant in 2011.RESULTS: Linguistic comprehension was optimal or partial in the majority of patients. Signifi cant barriers were noted in nearly one fourth of patients, for only half of them compatriots who were able to translate. Linguistic barriers were mainly found in older and sicker patients; they were also frequently seen in patients coming from western Africa and southern Europe. Non-linguistic barriers were perceived by EPs in a minority of patients, more frequently in the elderly and frequent attenders. Factors independently associated with a poor f inal comprehension led to linguistic barriers, non-linguistic obstacles, the absence of intermediaries, and the presence of patient's fear and hostility. The latter probably is a consequence, not the cause, of a poor comprehension.CONCLUSION: Linguistic and non-linguistic barriers, although quite infrequent, are the main factors that compromise communication with immigrants in the ED, with negative effects especially on elderly and more seriously ill patients as well as on physician satisfaction and appropriateness in using services. 相似文献
993.
Inference on germline BAP1 mutations and asbestos exposure from the analysis of familial and sporadic mesothelioma in a high‐risk area 下载免费PDF全文
Marta Betti Elisabetta Casalone Daniela Ferrante Antonio Romanelli Federica Grosso Simonetta Guarrera Luisella Righi Simona Vatrano Giuseppe Pelosi Roberta Libener Dario Mirabelli Renzo Boldorini Caterina Casadio Mauro Papotti Giuseppe Matullo Irma Dianzani 《Genes, chromosomes & cancer》2015,54(1):51-62
Inherited loss‐of‐function mutations in the BAP1 oncosuppressor gene are responsible for an inherited syndrome with predisposition to malignant mesothelioma (MM), uveal and keratinocytic melanoma, and other malignancies. Germline mutations that were inherited in an autosomal dominant fashion were identified in nine families with multiplex MM cases and 25 families with multiple melanoma, renal cell carcinoma, and other tumors. Germline mutations were also identified in sporadic MM cases, suggesting that germline mutations in BAP1 occur frequently. In this article, we report the analysis of BAP1 in five multiplex MM families and in 103 sporadic cases of MM. One family carried a new truncating germline mutation. Using immunohistochemistry, we show that BAP1 is not expressed in tumor tissue, which is in accordance with Knudson's two hits hypothesis. Interestingly, whereas the three individuals who were possibly exposed to asbestos developed MM, the individual who was not exposed developed a different tumor type, that is, mucoepidermoid carcinoma. This finding suggests that the type of carcinogen exposure may be important for the cancer type that is developed by mutation carriers. On the contrary, the other families or the 103 sporadic patients did not show germline mutations in BAP1. Our data show that BAP1 mutations are very rare in patients with sporadic MM, and we report a new BAP1 mutation, extend the cancer types associated with these mutations, and suggest the existence of other yet unknown genes in the pathogenesis of familial MM. © 2014 Wiley Periodicals, Inc. 相似文献
994.
995.
Karen A. Nunley Caterina Rosano Christopher M. Ryan J. Richard Jennings Howard J. Aizenstein Janice C. Zgibor Tina Costacou Robert M. Boudreau Rachel Miller Trevor J. Orchard Judith A. Saxton 《Diabetes care》2015,38(9):1768-1776
OBJECTIVE
The aim of this study was to investigate the presence and correlates of clinically relevant cognitive impairment in middle-aged adults with childhood-onset type 1 diabetes (T1D).RESEARCH DESIGN AND METHODS
During 2010–2013, 97 adults diagnosed with T1D and aged <18 years (age and duration 49 ± 7 and 41 ± 6 years, respectively; 51% female) and 138 similarly aged adults without T1D (age 49 ± 7 years; 55% female) completed extensive neuropsychological testing. Biomedical data on participants with T1D were collected periodically since 1986–1988. Cognitive impairment status was based on the number of test scores ≥1.5 SD worse than demographically appropriate published norms: none, mild (only one test), or clinically relevant (two or more tests).RESULTS
The prevalence of clinically relevant cognitive impairment was five times higher among participants with than without T1D (28% vs. 5%; P < 0.0001), independent of education, age, or blood pressure. Effect sizes were large (Cohen d 0.6–0.9; P < 0.0001) for psychomotor speed and visuoconstruction tasks and were modest (d 0.3–0.6; P < 0.05) for measures of executive function. Among participants with T1D, prevalent cognitive impairment was related to 14-year average A1c >7.5% (58 mmol/mol) (odds ratio [OR] 3.0; P = 0.009), proliferative retinopathy (OR 2.8; P = 0.01), and distal symmetric polyneuropathy (OR 2.6; P = 0.03) measured 5 years earlier; higher BMI (OR 1.1; P = 0.03); and ankle-brachial index ≥1.3 (OR 4.2; P = 0.01) measured 20 years earlier, independent of education.CONCLUSIONS
Clinically relevant cognitive impairment is highly prevalent among these middle-aged adults with childhood-onset T1D. In this aging cohort, chronic hyperglycemia and prevalent microvascular disease were associated with cognitive impairment, relationships shown previously in younger populations with T1D. Two additional potentially modifiable risk factors for T1D-related cognitive impairment, vascular health and BMI, deserve further study. 相似文献996.
Low birth weight and later development of insulin resistance and biochemical/clinical features of polycystic ovary syndrome 总被引:1,自引:0,他引:1
Pandolfi C Zugaro A Lattanzio F Necozione S Barbonetti A Colangeli MS Francavilla S Francavilla F 《Metabolism: clinical and experimental》2008,57(7):999-1004
Reduced insulin sensitivity in adult life has been reported in subjects born at term small for gestational age (SGA) and in those born prematurely with very low birth weight (LBW) (<1,500 g). We assessed whether LBW (<2,500 g) young women, irrespective of whether they were born SGA or adequate for gestational age (premature AGA), exhibited a reduction in insulin sensitivity through a prospective historical design. The risk of developing biochemical and clinical features of polycystic ovary syndrome was also investigated. The study population included 35 LBW women (19 SGA [BW range, 1,000-2,400 g] and 16 premature AGA [BW range, 1,700-2,440 g]) aged 21.8 +/- 1.8 years and 35 term AGA controls, of similar age, recruited from a neonatal registry. All women underwent clinical, ultrasonographic, hormonal, and metabolic evaluations, including the composite insulin sensitivity index. Women under hormonal contraception (21.4%) were excluded from hormonal and metabolic analyses. Composite insulin sensitivity index was significantly lower in LBW women even when the 2 LBW subgroups, SGA and premature AGA, were analyzed separately (4.4 +/- 2.2 and 4.0 +/- 1.7, respectively) than in controls (6.9 +/- 4.4). The LBW women showed a significantly higher incidence proportion of irregular menses (14/35 [40%] vs 2/35 [5.7%]) and a significantly higher free androgen index (5.8 +/- 3.5 vs 3.9 +/- 3.2). They also showed a nonsignificantly higher proportion of hirsutism, acne, and polycystic ovaries. In conclusion, LBW (<2,500 g) young women, irrespective of whether they were SGA and premature AGA, exhibited a reduction in insulin sensitivity as compared with born at term AGA women. Furthermore, they exhibited an increased risk of developing clinical and biochemical features of polycystic ovary syndrome. 相似文献
997.
998.
Simoncini T De Caterina R Genazzani AR 《The Journal of clinical endocrinology and metabolism》1999,84(2):815-818
Selective estrogen receptors modulators (SERMs) are a series of new compounds exerting estrogenic or anti-estrogenic effects in different tissues. 17Beta-estradiol is known to inhibit endothelial vascular cell adhesion molecule (VCAM)-1 expression. We studied the relative effects of the raloxifene analogue LY117018 and of tamoxifen on lipopolysaccharide (LPS)-induced VCAM-1 expression in cultured human saphenous vein endothelial cells (HSVEC) and on HSVEC adhesiveness towards U937 monocytoid cells. We here demonstrate a concentration-dependent inhibitory action on VCAM-1 protein expression both for 17beta-estradiol and LY117018. The action of both compounds was blocked by the pure anti-estrogen ICI 182,780. LY117018 did not antagonize 17beta-estradiol activity. On the contrary, tamoxifen had no effects of his own. Both 17beta-estradiol and LY117018 inhibited HSVEC VCAM-1 expression at the mRNA level, while tamoxifen was ineffective. Finally, 17beta-estradiol and LY117018, but not tamoxifen, inhibited HSVEC adhesiveness towards U937 monocytoid cells induced by LPS stimulation. Therefore, only some SERMs have potential anti-atherogenic actions exerted directly at the vascular level through the regulation of endothelial cell adhesion molecules expression and of endothelial-leukocyte interactions. 相似文献
999.
Petronio AS Amoroso G Limbruno U Baglini R Paterni G Pinori E Ferdeghini M Balbarini A De Caterina R Mariani M 《The American journal of cardiology》1999,84(9):1085-8, A9
To assess the effects of percutaneous transluminal coronary angioplasty on endothelin-1 (ET-1) release, we assessed ET-1 concentrations at different sites of the coronary circulation in patients submitted to elective procedures. ET-1 levels immediately downstream from the plaque and ET-1 aortocoronary gradient increased significantly after the procedure, which was related to mechanical wall stress in patients only receiving balloons, but not in those undergoing stent percutaneous transluminal coronary angioplasty. No changes were found in the coronary sinus; these results suggest ET-1 release from the plaque rather than an ischemia/reperfusion-related production from the distal myocardium. 相似文献
1000.
Aims/hypothesis Although hyperinsulinaemia in Type 2 diabetes in states of insulin resistance is a risk factor for atherosclerotic vascular disease, underlying mechanisms are poorly understood. We tested the hypothesis that insulin increases monocyte-endothelial interactions, which are implicated in atherosclerosis.Methods We treated human umbilical vein endothelial cells with insulin (10–10 to 10–7 mol/l) for 0 to 24 h. To dissect potentially implicated signal transduction pathways, we treated endothelial cells with known pharmacological inhibitors of two distinct insulin signalling pathways: the phosphatidylinositol-3-kinase (PI3-kinase) inhibitor wortmannin (3×10–8 to 10–6 mol/l), involved in insulin-induced endothelial nitric oxide synthase stimulation, and the p38 mitogen-activated protein (p38MAP) kinase inhibitor SB-203580 (10–7 to 2×10–6 mol/l). We measured adhesion molecule expression by cell surface enzyme immunoassays and U937 monocytoid cell adhesion in rotational adhesion assays.Results At pathophysiological concentrations (10–9 to 10–7 mol/l), insulin concentration-dependently induced vascular cell adhesion molecule (VCAM)-1 (average increase: 1.8-fold) peaking at 16 h. By contrast, the expression of intercellular adhesion molecule-1 and E-selectin were unchanged. The effect on VCAM-1 was paralleled by increased U937 cell adhesion. In the absence of cytotoxicity, wortmannin significantly potentiated the effect of insulin alone on VCAM-1 surface expression and monocytoid cell adhesion, whereas SB-203580 (10–6 mol/l) completely abolished such effects.Conclusions/interpretation These observations indicate that insulin promotes VCAM-1 expression in endothelial cells through a p38MAP-kinase pathway, amplified by the PI3-kinase blockage. This could contribute to explaining the increased atherosclerosis occurring in subjects with hyperinsulinaemia, or in states of insulin resistance, which feature a defective PI3-kinase pathway.Abbreviations VCAM-1
vascular cell adhesion molecule-1
- ICAM-1
intercellular adhesion molecule-1
- PI3-kinase
phosphatidylinositol 3-kinase
- MAP
mitogen-activated protein
- NO
nitric oxide
- EIA
enzyme immunoassays 相似文献