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21.
Acne is known to be one of the features of hyperandrogenism. The aim of the present work was to study women with persistent acne and without other evidence of hyperandrogenism, such as hirsutism, alopecia, or irregular menses. Among 87 female patients with acne and/or hirsutism, we defined three groups: group 1 (n = 29), patients having treatment-resistant acne without menstrual disturbance, alopecia, or hirsutism; group 2 (n = 27), patients with acne and hirsutism; and group 3 (n = 31), patients with hirsutism alone. Clinical chemistry criteria for hyperandrogenism were based on elevated values of one or more of the following parameters: plasma testosterone, delta-4-androstenedione, dehydroepiandrosterone, urinary 5 alpha-androstane 3 alpha-17 beta-diol, and 17-ketosteroids (with chromatography). Plasma and urine samples were drawn between the 18th and 25th days of the cycle. Among group 1 patients, we found 25 subjects (86%) with hyperandrogenism, according to these laboratory criteria. The etiologies were: polycystic ovary syndrome (36%), adrenal hypersecretion (40%, of which 12% showed secondary polycystic ovaries), isolated increase in 5 alpha-androstane 3 alpha-17 beta-diol (20%), and hyperandrogenism without diagnosis (4%). The parameters were found to be more elevated in these patients than in a control group of 30 normal volunteer women. In groups 2 and 3, the findings were essentially the same as in group 1, except for increased levels of testosterone and the testosterone/SHBG ratio. Furthermore, it was evident that persistent acne may be an isolated sign of hyperandrogenism.  相似文献   
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J. Gony    P. Vexiau    C. Lhomme    A. Marcelli    J. C. Poirier    V. Bochu    G. Cathelineau    R. Assan    I. Deschamps  J. Hors 《Tissue antigens》1988,31(5):229-234
Seventy IDDM patients (insulin-dependent diabetics), 48 females and 22 males, most of them adults at the onset of diabetes, and suffering from at least one other associated autoimmune manifestation (AAM) were studied for HLA A,B,C, DR markers and Bf, C4 complement components. Comparisons were made with 108 normal controls and a series of 287 IDDM patients with juvenile onset (under 25 years) and no patent other autoimmune disease. The increase in frequency of HLA-B8 among IDDM patients with AAM was confirmed (36% versus 20% in controls) (p less than 0.04). The frequency of DR4 among diabetics with AAM (33%) was not significantly different from the normal frequency (27%), and the allelic combination DR3/4 was found in only 13% of IDDM with AAM. Corresponding frequencies in patients with IDDM alone were 66% for DR4 and 34% for DR3/4 (p less than 10(-6) and 10(-3) respectively). These results confirm the heterogeneity of IDDM and support, by genetic arguments, the concept of overlapping entities. The hypothesis of a common background of autoimmunity associated with B8 DR3 can be postulated, while the organ specific target process should be associated with various DR alleles.  相似文献   
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INTRODUCTION: Treatment failures with isotretinoin in female patients are frequently related to endocrinological dysfunctions. Such a concept has never been discussed in male patients. CASE REPORTS: An extensive endocrinological work-up has been performed in nine male patients who presented with an acne refractory to conventional treatment and to isotretinoin. Adrenal dysfunction was found in four patients and isolated 5-alpha reductase hyperactivity in 2 cases. Three work-ups were normal. A suppressive treatment in three patients with adrenal dysfunction provided immediate efficacy. COMMENTS: These results would provide insight into the mechanism of refractory acne in men.  相似文献   
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We determined the prevalence and indicators of infection in intensive care unit (ICU) patients with diabetic ketoacidosis (DKA) by performing a retrospective analysis of 123 episodes of DKA (in 113 patients) managed in a medical ICU between 1990 and 1997. In univariate analysis, features associated with infection were female sex, neurological symptoms at admission, fever during the week before admission, a need for colloids, a high blood lactate level at admission, and lack of complete clearance of ketonuria within 12 h. Multivariate analysis identified 3 independent predictors of infection: female sex (odds ratio [OR], 2.31; confidence interval [CI], 1.05-5.35), neurological symptoms at admission (OR, 2.83; CI, 1.18-6.8), and lack of complete clearance of ketonuria within 12 h (OR, 3.73; CI, 1.58-9.09). Infection is the leading trigger of DKA in ICU patients. Neurological symptoms at admission and lack of complete clearance of ketonuria within 12 h are useful warning signals of infection.  相似文献   
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AIMS: We aimed to characterize a cohort of 'atypical' diabetic patients of sub-Saharan African origin and to analyse possible determinants of long-term remission. METHODS: Over 6 years, we studied the clinical and therapeutic profile of 42 consecutive patients undiagnosed or untreated prior to inclusion presenting with cardinal features of diabetes mellitus. We measured insulin secretion and sensitivity at inclusion. Immunogenetic (anti-GAD, anti-ICA and HLA class II) markers of Type 1 diabetes were compared with a 90-non-diabetic unrelated adult African population. RESULTS: Twenty-one ketonuric patients (age 42 +/- 9 (sd) years; body mass index (BMI) 26 +/- 3 kg/m2) were initially insulin-treated (IT), and 21 non-ketonuric patients (age 38 +/- 8 years; BMI 26 +/- 5 kg/m2) had oral and/or diet therapy (NIT). Insulin could be discontinued in 47.6% (10/21) IT with adequate glycaemic control (HbA1c 6.7 +/- 1.3%), while insulin was secondarily started in 38.1% (8/21) NIT in expectation of better control. The initial basal (odds ratio (OR) 9.1, 95% confidence interval (CI) 1.3-64.4) and stimulated C-peptide (OR 8.17, 95% CI 1.5-44.1) were independently associated with remission. Insulin resistance was present in all the groups, more marked in the insulin-treated NIT. Anti-GAD antibodies and ICA were rare, but 38.1% IT vs. 1.1% controls had Type 1 diabetes HLA susceptibility haplotypes (P < 0.001) without significant difference between the subgroups. CONCLUSION: Prolonged discontinuation of insulin is frequent in African diabetic patients initially presenting with signs of insulinopenia. In our patients, long-term insulin therapy was not associated with immunogenetic markers of Type 1 diabetes. The initial measure of insulin secretion seemed a good predictor of long-term remission.  相似文献   
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CONTEXT: Ketosis-prone diabetes (KPD) is mostly observed in males of West African descent and is characterized by phasic or permanent insulin dependence without apparent autoimmune process. OBJECTIVE: KPD subjects display a propensity to hyperglycemia-induced acute insulin deficiency, suggesting that they exhibit a propensity to oxidative stress in beta-cells. The enzyme glucose-6-phosphate dehydrogenase (G6PD) is a defense mechanism against oxidative stress, and G6PD deficiency, an X-linked genetic disorder with male predominance, is frequent in West Africans. We hypothesized that mutations in the G6PD gene could predispose to KPD. DESIGN: We studied G6PD erythrocyte enzyme activity and the insulin secretory reserve (glucagon-stimulated C peptide) in a cohort of hospitalized West Africans with KPD (n = 59) or type 2 diabetes (T2DM; n = 59) and in normoglycemic controls (n = 55). We also studied the G6PD gene in an extended population of KPD patients (n = 100), T2DM patients (n = 59), and controls (n = 85). RESULTS: The prevalence of G6PD deficiency was higher in KPD than in T2DM and controls (42.3%; 16.9%; 16.4%; P = 0.01). In KPD, but not in T2DM, insulin deficiency was proportional to the decreased G6PD activity (r = 0.33; P = 0.04). We found no increase in the prevalence of G6PD gene mutations in KPD compared with T2DM and controls. Rather, we found a 20.3% prevalence of G6PD deficiency in KPD without gene mutation. CONCLUSIONS: This study suggests that 1) G6PD deficiency alone is not causative of KPD; and 2) alterations in genes controlling both insulin secretion and G6PD-mediated antioxidant defenses may contribute to the predisposition to KPD in West Africans.  相似文献   
28.
The prevalence of diabetes in African communities is increasing with ageing of the population and lifestyle changes associated with rapid urbanisation and westernisation. Traditional rural communities still have very low prevalence, at most 1-2%, except in some specific high-risk groups, whereas 1-13% or more adults in urban communities have diabetes. Type 2 diabetes is the predominant form (70-90%), the rest being represented by typical type 1 patients and patients with atypical presentations that require more pathophysiological insight. Due to the high urban growth rate, dietary changes, reduction in physical activity, and increasing obesity, it is estimated that the prevalence of diabetes is due to triple within the next 25 years. In addition, long-term complications occur early in the course of diabetes and concern a high proportion of patients, probably higher than in other ethnic groups, and that could be partly explained by uncontrolled hypertension, poor metabolic control and possible ethnic predisposition. The combination of the rising prevalence of diabetes and the high rate of long-term complications in Africans will lead to a drastic increase of the burden of diabetes on health systems of African countries. The design and implementation of appropriate strategy for early diagnosis and treatment, and population-based primary prevention of diabetes in these high-risk populations is therefore a public health priority.  相似文献   
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OBJECTIVE

In animal studies, hyperglycemia during fetal development reduces nephron numbers. We tested whether this observation translates into renal dysfunction in humans by studying renal functional reserve in adult offspring exposed in utero to maternal type 1 diabetes.

RESEARCH DESIGN AND METHODS

We compared 19 nondiabetic offspring of type 1 diabetic mothers with 18 offspring of type 1 diabetic fathers (control subjects). Glomerular filtration rate (51Cr-EDTA clearance), effective renal plasma flow (123I-hippurate clearance), mean arterial pressure, and renal vascular resistances were measured at baseline and during amino acid infusion, which mobilizes renal functional reserve.

RESULTS

Offspring of type 1 diabetic mothers were similar to control subjects for age (median 27, range 18–41, years), sex, BMI (23.1 ± 3.7 kg/m2), and birth weight (3,288 ± 550 vs. 3,440 ± 489 g). During amino acid infusion, glomerular filtration rate and effective renal plasma flow increased less in offspring of type 1 diabetic mothers than in control subjects: from 103 ± 14 to 111 ± 17 ml/min (8 ± 13%) vs. from 108 ± 17 to 128 ± 23 ml/min (19 ± 7%, P = 0.009) and from 509 ± 58 to 536 ± 80 ml/min (5 ± 9%) vs. from 536 ± 114 to 620 ± 140 ml/min (16 ± 11%, P = 0.0035). Mean arterial pressure and renal vascular resistances declined less than in control subjects: 2 ± 5 vs. −2 ± 3% (P = 0.019) and 3 ± 9 vs. −14 ± 8% (P = 0.001).

CONCLUSIONS

Reduced functional reserve may reflect a reduced number of nephrons undergoing individual hyperfiltration. If so, offspring of type 1 diabetic mothers may be predisposed to glomerular and vascular diseases.A reduced number of nephrons may cause hypertension and favor renal and cardiovascular risks in humans (1). Autopsy findings support this assumption (2). In addition, birth weight is a determinant of nephron numbers in humans (3). In animal models, moderate hyperglycemia during pregnancy affects birth weight and nephron numbers in offspring (4), and favors the development of hypertension in adulthood (5). In addition, angiogenesis affects kidney development (6,7). In this respect, moderate hyperglycemia induces a defect in angiogenesis as reported in experimental conditions (8).We hypothesized that the effects of moderate hyperglycemia on kidney development reported in animal studies might have clinical relevance in humans. Thus, we studied kidney function in subjects who had been exposed to hyperglycemia during their fetal development. For this purpose, we investigated, as previously (9), adults whose mothers had type 1 diabetes at the time of their conception and used the offspring of type 1 diabetic fathers as control subjects to minimize potential genetic heterogenicity between groups. Type 1 diabetes as a source of hyperglycemia during fetal development also minimizes confounding factors associated with type 2 diabetes such as hypertension. Counting nephron numbers and/or visualizing glomerular size by noninvasive methods is not currently feasible in humans. Thus, we measured global kidney function at baseline and during vasodilatation produced by amino acid infusion, i.e., renal functional reserve. Reduction in renal functional reserve can be interpreted as reflecting a reduced surface available for filtration, suggesting that the number of functional nephrons is reduced. As a result, the global hemodynamic load provokes hyperfiltration at the single nephron level (1). This disturbance in renal hemodynamics was associated with renal and vascular diseases, both in experimental models (1,4,5) and clinical settings (1013). We report here that renal functional reserve is reduced in offspring of type 1 diabetic mothers.  相似文献   
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