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61.
BACKGROUND: Athletes consume arginine and/or aspartate as potential nutritional ergogenics. Their metabolic effects are controversial and there is some evidence that ingestion of large doses of single amino acids can adversely affect the nitrogen balance or induce an amino acid imbalance. Nevertheless, the general metabolic influence of an arginine aspartate supplementation during a prolonged exercise bout has not yet been investigated. AIM OF THE STUDY: The aim of this study was, therefore, to investigate the general metabolic impact of a chronic supplementation with arginine aspartate in endurance-trained athletes at rest and during a marathon run. METHODS: Fourteen endurance-trained runners participated in this field study which was carried out according to a double-blind crossover design. 15 g of arginine aspartate or a carbohydrate-based placebo were supplemented daily for 14 days before a marathon run. Blood samples for analysis of metabolites and hormones were collected shortly before the run, after 31 km, at the end of the run, and after a recovery period of two hours. Additionally, the respiratory exchange ratio was determined during the run. RESULTS: The plasma level of carbohydrate (glucose, lactate, pyruvate) and fat metabolites (fatty acids, glycerol, beta-hydroxybutyrate), cortisol, insulin, ammonia, lactate dehydrogenase, and creatine kinase as well as the respiratory exchange ratio were unaffected by the supplementation. In contrast, the plasma level of somatotropic hormone, glucagon, urea, and arginine were significantly increased, and the level of most of the remaining plasma amino acids as well as their sum was significantly reduced. CONCLUSIONS: There was no obvious metabolic benefit derived from the chronic supplementation with arginine aspartate. And since furthermore the consequences of a reduction of the total plasma amino acid level are not known, the practice of using single amino acid supplements as potential ergogenics should be critically reevaluated.  相似文献   
62.
The detection of pancreatic cancer or the discrimination between pancreatic cancer and chronic pancreatitis remains an important diagnostic problem. The increased glucose metabolism in malignant tumours formed the basis for this investigation, which focused on the role of positron emission tomography (PET) with 2[18F]-fluoro-2-deoxy-D-glucose (FDG) in the detection of pancreatic cancer and its differentiation from chronic pancreatitis. Eighty patients admitted for elective pancreatic surgery received preoperatively 250-350 mBq FDG intravenously and emission scans were recorded 45 minutes later. Intense focal activity in the pancreatic region was taken at the time of scanning as showing the presence of pancreatic cancer. The presence of cancer was later confirmed by histological examination of the surgical specimens and histological findings were compared with the preoperative PET results. Forty one patients with pancreatic cancer (group I: n = 42) had a focally increased FDG uptake in the pancreatic region. Two patients with a periampullary carcinoma (group II: n = 6) failed to develop FDG accumulation. In 28 patients with chronic pancreatitis (group III: n = 32) no FDG accumulation occurred. Overall sensitivity and specificity of PET for malignancy (group I + II) were 94% (45 of 48) and 88% (28 of 32), respectively. The standard uptake value of the patients with pancreatic carcinoma was significantly higher than in patients with chronic pancreatitis (3.09 (2.18) v 0.87 (0.56); p < 0.001; median (interquartile range)). These findings show that FDG-PET represents a new and non-invasive diagnostic procedure for the diagnosis of pancreatic cancer and to differentiate pancreatic cancer from chronic pancreatitis. However, the diagnostic potential of this technique requires further evaluation.  相似文献   
63.
BACKGROUND: Cutaneous T-cell lymphoma (CTCL) is a slowly progressive malignancy for which there is no cure. Therefore, accurate prediction of prognosis is important for the conduct of clinical trials and for counselling of individuals. OBJECTIVES: To improve prediction of survival in patients with CTCL. METHODS: Prognostic factors including tumour-node-metastasis (TNM) criteria and the CTCL Severity Index (CTCL-SI) were analysed using a Weibull model for multivariate analysis in a sample of 62 patients with classical CTCL (mycosis fungoides and Sézary syndrome). The Brier score was used to quantify the quality of individual prediction. RESULTS: Estimated 5-year survival rate (SR5) differed according to TNM stage: stage IA, 100% (95% confidence interval 70-100%); IB-III, 86% (73-100%); IVA, 54% (32-91%); IVB, 0% (0-52%). In a multivariate analysis, two independent prognostic factors were identified: lymph node (P = 0.036) and blood involvement (P = 0.015). A probability of survival model showed correlation of CTCL-SI with survival in patients with CTCL-SI > 20 according to the following formula: SR5 = 124-2 x (CTCL-SI)%. Calibration of SR5 against CTCL-SI-independent CTCL subsets revealed underestimation of Sézary syndrome. When CTCL-SI parameters were adjusted accordingly, the probability of survival model did not change significantly, while SR5 values became adequate. In addition, CTCL-SI was shown to be superior to TNM by 30% regarding individual predictive power. CONCLUSIONS: Probability of survival in CTCL can be accurately predicted by a CTCL-SI-based survival rate formula. Careful monitoring of lymph node and blood compartments and quantification by CTCL-SI are reliable tools for follow-up of patients with CTCL and allow progression-adjusted prediction of prognosis.  相似文献   
64.
65.
IDH1/2 mutations occur at high frequency in diffusely infiltrating gliomas of the WHO grades II and III and were identified as a strong prognostic marker in all WHO grades of gliomas. Mutated IDH1 or IDH2 protein leads to the generation of excessive amounts of the metabolite 2-hydroxyglutarate (2HG) in tumor cells. Here, we evaluated whether 2HG levels in preoperative serum samples from patients with gliomas correlate with the IDH1/2 mutation status and whether there is an association between 2HG levels and glioma size. In contrast to the strong accumulation of 2HG in the serum of patients with IDH1/2 mutated acute myeloid leukaemia, no accumulation was observed in this series of IDH1/2 mutated gliomas. Furthermore, we found no association between glioma size measured by magnetic resonance imaging and 2HG levels. We conclude that 2HG levels in preoperative sera from patients with diffusely infiltrating gliomas of the WHO grades II and III cannot be used as a marker to differentiate between tumors with versus without IDH1/2 mutation. Furthermore, the observation that there is no correlation between 2HG levels and tumor volume may indicate that 2HG cannot be utilized as marker to monitor tumor growth in gliomas.  相似文献   
66.
We recently reported that brief, remotely controlled intrameal hepatic‐portal vein infusions of glucagon‐like peptide‐1 (GLP‐1) reduced spontaneous meal size in rats. To investigate the neurobehavioural correlates of this effect, we equipped male Sprague‐Dawley rats with hepatic‐portal vein catheters and assessed (i) the effect on eating of remotely triggered infusions of GLP‐1 (1 nmol/kg, 5 min) or vehicle during the first nocturnal meal after 3 h of food deprivation and (ii) the effect of identical infusions performed at dark onset on c‐Fos expression in several brain areas involved in the control of eating. GLP‐1 reduced (P < 0.05) the size of the first nocturnal meal and increased its satiety ratio. Also, GLP‐1 increased (P < 0.05) the number of c‐Fos‐expressing cells in the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala, but not in the arcuate or paraventricular hypothalamic nuclei. These data suggest that the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala play a role in the eating‐inhibitory actions of GLP‐1 infused into the hepatic‐portal vein; it remains to be established whether activation of these brain nuclei reflect satiation, aversion, or both.  相似文献   
67.
The arcuate nucleus (Arc) and the lateral hypothalamic area (LHA), two key hypothalamic nuclei regulating feeding behavior, express c-Fos, a marker of neuronal activation in fasted animals. This is reversed by refeeding. In the present study we tested whether an anorectic dose of lipopolysaccharide (LPS), the cell wall component of Gram-negative bacteria, also inhibits fasting-induced c-Fos expression in these hypothalamic nuclei. This would suggest that they are involved in anorexia during bacterial infections as well. We also studied whether LPS modulates the activity of orexin-A positive (OX+) LHA neurons. Food deprived BALB/c mice were injected with LPS or saline and were sacrificed 4 or 6h later. Four hours after injection, LPS reduced the number of c-Fos positive cells in the Arc and in the LHA, but had no effect on c-Fos in OX+ neurons. Six hours after injection, LPS reduced c-Fos expression in the LHA, both in the OX- and OX+ neurons, but not in the Arc. These results show that LPS modulates neuronal activity in the Arc and LHA similar to feeding-related stimuli, suggesting that the observed effects might contribute to the anorectic effect of LPS. Thus, physiological satiety signals released during refeeding and anorexia during bacterial infection seem to engage similar neuronal substrates.  相似文献   
68.
Shih CD  Chuang YC 《Neuroscience》2007,149(3):625-635
The present study investigated the cardiovascular effects of orexin (OX)-A and OX-B in the nucleus tractus solitarii (NTS) and delineated the engagement of nitric oxide (NO) and GABA in OX-induced cardiovascular responses. In adult male Sprague-Dawley rats maintained under propofol anesthesia, microinjection bilaterally into the NTS of OX-A or OX-B evoked bi-directional cardiovascular effects in a dose-dependent manner. At a lower dose (5 pmol), OX-A or OX-B decreased systemic arterial pressure (SAP), heart rate (HR), and power density of the vasomotor components of SAP signals, our experimental index for sympathetic neurogenic vasomotor tone. At higher doses (>20 pmol), these two compounds elicited cardiovascular excitatory responses. These bi-directional cardiovascular effects of OX were abolished by co-injection of an OX(1) receptor antagonist, 1-(2-methylbenzoxazol-6-yl)-3-[1,5]naphthyridin-4-yl-urea hydrochloride (SB-334867, 0.75 nmol) or the OX(2) receptor antiserum (1:20). In addition, the vasodepressor effects of low dose (5 pmol) OX-A or OX-B in the NTS were attenuated by a nitric oxide synthase (NOS) inhibitor, N(G)-nitro-l-arginine methyl ester (l-NAME, 5 nmol), a neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (2.5 pmol) or the soluble guanylate cyclase (sGC) inhibitor, 1H-[1,2,4]oxadiazole[4,3-alpha]quinoxalin-1-one (250 pmol). The vasopressor effects of high dose (200 pmol) OX were reversed by co-administration with GABA(A) or GABA(B) receptor antagonist, bicuculline methiodine (10 pmol) or 2-hydroxy saclofen (100 pmol), or l-NAME (5 nmol). Our results indicate that OX-A or OX-B elicited bi-directional cardiovascular effects via OX receptor-dependent mechanisms. The vasodepressor effects of OX were induced by the nNOS-derived NO and activation of sGC-associated signaling pathway, whereas the vasopressor effects were mediated by interaction with GABAergic or nitrergic neurotransmission in the NTS.  相似文献   
69.
The feeding behavior of 11 calves fed milk ad lib was characterized and analyzed at the age of 5 weeks, and the short-term changes in the plasma concentrations of various metabolites (glucose, lactate, free fatty acids, triglycerides, beta-hydroxybutyrate) and insulin in relation to a representative spontaneous milk meal were measured during the following week. In a 6-day period, the calves consumed 287 (=86%) of a total of 335 milk meals during the light phase from 0500-2200 [on average, 4.4 +/- 0.5 (mean +/- SEM) meals]. The meal size and duration during light were 2.0 +/- 0.3 kg and 5.3 +/- 0.3 min, respectively. However, only 0.7 +/- 0.1 milk meals of similar size and duration were consumed during the dark phase. The plasma concentrations of insulin and glucose increased in response to the spontaneous milk meal and remained elevated for at least 2 h after meal end. The plasma concentrations of triglycerides, free fatty acids, and beta-hydroxybutyrate also increased after meal termination, and remained elevated until 40 min (triglycerides, free fatty acids) and 60 min (beta-hydroxybutyrate) after meal end, respectively. The observed spontaneous milk intake patterns were similar to the natural suckling behavior described for calves, suggesting that the conditions of the present experiment did not disrupt the animals' natural feeding behavior. Some of the profound metabolic changes in relation to a spontaneous milk meal might contribute to the control of milk intake in calves, but further experiments are necessary to test this idea.  相似文献   
70.
Since it has to be expected that individuals exposed to oxidative stress who take supplements of beta-carotene are simultaneously exposed to both beta-carotene cleavage products (CPs) and oxidative stress, and both exposures have been demonstrated to cause genotoxic effects in primary rat hepatocytes, cyto- and genotoxic effects on primary rat hepatocytes after supplementation of the medium with increasing concentrations of a CP mixture during exposure to oxidative stress by treatment with either DMNQ (2,3-dimethoxy-1,4-naphthoquinone) or hypoxia/reoxygenation (Hy/Reox) was investigated. The cytological endpoints analysed were the mitotic indices, the percentages of apoptotic and necrotic cells, the percentages of micronucleated (MN) cells and the number of chromosomal aberrations (CAs) and sister chromatid exchanges (SCE). The results obtained clearly demonstrate that the CP mixture enhances the genotoxic effects of oxidative stress exposure, whereas it had no effect at all on the endpoints of cytotoxicity studied. These results further support the hypothesis that CP might be responsible for the reported carcinogenic response in the beta-CArotene and Retinol Efficacy Trial (CARET) and Alpha-Tocopherol Beta-carotene Cancer prevention (ATBC) chemoprevention trials.  相似文献   
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