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61.
Leptin inhibition of insulin secretion from isolated human islets   总被引:10,自引:0,他引:10  
Leptin is a hormone produced and secreted from the adipose tissue. Its physiological actions include the regulation of satiety, food intake and energy balance. The production of leptin is increased by high insulin levels. Here, we demonstrate that leptin acts as an inhibitor of glucose-induced (20 mM) insulin secretion from isolated human islets. No effect was observed in the presence of lower glucose levels (2.8 and 10 mM glucose). The pancreatic β-cell might represent a target of a direct physiological action of leptin. We suggest the presence of an “adipo-insular axis” in which leptin mediates negative feedback from the adipose tissue to the endocrine pancreas. Received: 21 July 1997 / Accepted in revised form: 1 October 1997  相似文献   
62.
To determine whether the effects of the disaccharidase inhibitor Acarbose on glucose tolerance could be solely explained via an action on intestinal nutrient absorption, the effects of this agent and placebo (100 mg p.o.) on intravenous and postprandial glucose tolerance were compared in six normal subjects. Acarbose significantly diminished plasma glucose, insulin, and gastrointestinal inhibitory polypeptide responses following meal ingestion without affecting plasma glucagon and pancreatic polypeptide responses, but had no effect on plasma glucose and insulin responses following intravenous injection of glucose. These results suggest that the acute effects of Acarbose on glucose tolerance can be explained on the basis of its ability to alter intestinal nutrient absorption.  相似文献   
63.
It has been commonly recognized that circadian rhythm and sleep/wake cycle are causally involved in bipolar disorder. There has been a paucity of systematic research considering the relations between sleep and mood states in bipolar disorder. The current study examines the possible influences of sleep deprivation on mood states and endocrine functions among first-degree relatives of patients with bipolar disorder and healthy controls. Blood samples were taken at two time points in the consecutive mornings at predeprivation and postdeprivation periods. Participants simultaneously completed the Profiles of Mood States at two time points after giving blood samples. Plasma T3 and TSH levels increased after total sleep deprivation in both groups. Sleep deprivation induced TSH levels were reversely associated with depression–dejection among healthy controls. A paradoxical effect was detected for only the first-degree relatives of the patients that changes in plasma cortisol levels negatively linked to depression–dejection and anger–hostility scores after total sleep deprivation. Plasma DHEA levels became correlated with vigor-activity scores after sleep deprivation among first-degree relatives of bipolar patients. On the contrary, significant associations of depression–dejection, anger–hostility, and confusion–bewilderment with the baseline plasma DHEA levels became statistically trivial in the postdeprivation period. Findings suggested that first-degree relatives of patients with bipolar disorder had completely distinct characteristics with respect to sleep deprivation induced responses in terms of associations between endocrine functions and mood states as compared to individuals whose relatives had no psychiatric problems. Considering the relationships between endocrine functions and mood states among relatives of the patients, it appears like sleep deprivation changes the receptor sensitivity which probably plays a pivotal role on mood outcomes among the first-degree relatives of patients with bipolar disorder.  相似文献   
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Summary The possibility that the deterioration of glucose tolerance during pregnancy might be due to a change in the functional condition of the endocrine pancreas has been examined in normal pregnant women and in non-obese gestational diabetics. Three test-situations were applied to elucidate the problem: 1) an overnight fast; 2) a glucose tolerance test (OGTT); and 3) a protein-rich meal. After the overnight fast, hyperinsulinemia and hyperglucagonemia were found in late pregnancy in both groups. However, on a molar basis, basal insulin increased more than basal glucagon and the molar insulin: glucagon ratio was therefore increased. After oral administration of glucose, the insulin response was enhanced in the late stages of pregnancy both in normal women and in those with gestational diabetes while the depression of glucagon below fasting levels was exaggerated and sustained in both groups. In response to a protein-rich meal in normal late pregnancy, the glucagon response was significantly lower than post partum in the same subjects, whereas that of insulin was unchanged. Finally, in both groups the diminished glucose tolerance in pregnancy was not associated with an abnormally elevated proportion of total insulin immunoreactivity represented by the biologically almost inactive proinsulin. Based upon these findings and those reported in the literature, it is concluded that there is no evidence in support of the idea that the diabetogenicity of pregnancy can be explained by changes in the function of the endocrine pancreas in these patients.  相似文献   
67.
目的 观察不同类型内分泌药物治疗对乳腺癌患者术后骨代谢水平的影响。方法 收集2013年5月至2019年1月南方医科大学附属小榄医院治疗的乳腺癌患者239例,按照内分泌治疗药物不同分为A组(采用他莫昔芬治疗,75例)、B组(采用氟维司群治疗,83例)和C组(采用依西美坦治疗,81例)。比较各组治疗前及治疗12个月降钙素(CT)、骨钙素(BGP)、骨碱性磷酸酶(BAP)和甲状旁腺素(PTH)水平,同时检测各组腰椎骨密度(BMP)并比较。结果 治疗前,三组CT、BGP、BAP、PTH和BMP值比较,差异均无统计学意义(P>0.05);治疗后,三组CT均不同程度升高,其中C组升幅最大,A组升幅最小,组间差值比较,差异有统计学意义(P=0.009);三组BGP均不同程度升高,其中A组升幅最大,B组升幅最小,组间差值比较,差异有统计学意义(P=0.005);三组BAP均不同程度降低,其中B组降幅最大,A组降幅最小,组间差值比较,差异有统计学意义(P=0.018);三组PTH均不同程度降低,其中C组降幅最大,A组降幅最小,组间差值比较,差异有统计学意义(P=0.025)。治疗后,A组腰椎BMP未见明显降低,但C组腰椎BMP下降较明显,三组间BMP治疗前后差值比较,差异有统计学意义(P=0.022)。结论 不同内分泌治疗药物均可导致乳腺癌患者BMP降低,但他莫昔芬对患者骨代谢水平影响程度较小。  相似文献   
68.
Nesfatin-1是一种厌食调节肽,在中枢和外周广泛表达.近年研究显示nesfatin-1在消化、内分泌、精神等多系统中发挥重要作用,但其作用机制尚未完全明确.本文就nesfatin-1的研究进展作一综述.  相似文献   
69.
《Pancreatology》2020,20(5):929-935
IntroductionThe majority of patients with pancreatic ductal adenocarcinoma (PC) display either impaired fasting glucose/glucose intolerance or overt diabetes. However, the pathophysiologic basis of this association remains largely unexplained.MethodsIn this case-control study we aimed to study the morphological changes in the islets of patients with PC, compared to control patients with and without type 2 diabetes mellitus (T2DM). T2DM controls and PC cases had a lower β-cell area and average islet size and density compared to non-T2DM controls (p < 0.05).ResultsCompared to both T2DM and non-T2DM controls, mean α-cell area was significantly lower and β/α-ratio was higher in PC cases (p < 0.05). Furthermore, whereas islets in T2DM controls were characterized by disrupted islet architecture and presence of islet amyloid aggregates, islet composition in PC islets was not significantly different compared to non-T2DM controls (p > 0.05 vs. Control).ConclusionsOur data shows that PC is associated with a unique pattern of islet pathology characterized by preserved architecture, absence of amyloid aggregates, and relative α-cell loss indicating that distinct mechanisms are likely involved in the pathophysiology of islet failure in PC-induced DM. Insights into the mechanisms mediating β-cell failure in PC can be important for our understanding of pathophysiology of PC.  相似文献   
70.
目的探讨多囊卵巢综合征(PCOS)患者卵巢的形态学改变与内分泌激素的相关性。方法选择94例PCOS患者作为研究组,按体质量指数(BMI)分为肥胖型PCOS组(OB-PCOS)和非肥胖型PCOS组(NOB-PCOS);同期选择69例有正常排卵的输卵管性不孕患者作为对照组,经阴道超声分别测量其卵巢总面积(A),同时检测其黄体生成素(LH)、卵泡刺激素(FSH)、睾酮(T)、雌二醇(E2)、人体催乳素(PRL)水平,并分析其与A值之间的相关性。结果 1.PCOS组卵巢总面积明显高于对照组(P〈0.001),LH、LH/FSH以及T水平较对照组明显升高,差异有统计学意义(P〈0.001),FSH水平明显降低,差异有统计学意义(P〈0.05);2.PCOS患者肥胖型组T水平较非肥胖型组升高,差异无统计学意义(P〉0.05);3.相关性分析显示,PCOS组A值与T值呈正相关,差异有统计学意义(P〈0.05)。结论 PCOS的发病过程中,卵巢总面积的改变受内分泌激素的影响。  相似文献   
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