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101.
BACKGROUND: Physical symptoms are an increasing problem among Japanese children and adolescents, and the symptoms seem to be related to their school situation. These symptoms are prevalent in Sweden, and a comparison with Japan is of interest due to the differences in the educational system and school climate. OBJECTIVE AND METHODS: To compare physical symptoms and psychiatric complaints in school pupils from Japan and Sweden, using a questionnaire that also addressed life satisfaction and stressful life events. The study population comprised 742 Japanese children and 1,120 Swedish children attending public compulsory schools, grades 4-9 (10-15 y). Physical symptom and psychiatric complaint scores were calculated for each pupil. RESULTS: The Japanese children had significantly higher physical symptom and psychiatric complaint scores than did the Swedish children. Both the physical symptom and psychiatric complaint scores were significantly higher in adolescents than in preadolescents in Japan; this trend was less apparent in Swedish children. In addition, Japanese children were found to have considerably lower life satisfaction. Loss of appetite was the only physical symptom more prevalent in the Swedish population compared to the Japanese population.CONCLUSION: We conclude that Japanese schoolchildren have more physical symptoms and psychiatric complaints and less life satisfaction than Swedish schoolchildren of corresponding ages.  相似文献   
102.
BACKGROUND: The behavior of host and graft cells during the healing process after autologous tendon graft has not been elucidated. HYPOTHESIS: Host cells will integrate into the bone-tendon interface and contribute to cellular repopulation of the graft. STUDY DESIGN: Controlled laboratory study. METHODS: Twelve-week-old, genetically identical, female green fluorescent protein transgenic rats (n = 20) and wild-type rats (n = 20) were used. The rats were divided into 2 experimental groups. In group A, the Achilles tendons of wild-type rats were harvested and transplanted into the transcondylar femoral bone tunnels of green fluorescent protein rats. In group B, the Achilles tendons of green fluorescent protein rats were transplanted into a transcondylar femoral bone tunnel of wild-type rats. Immediately after transplantation (time zero) and at 1, 2, and 4 weeks after the transplantation, distal femoral epiphyses were harvested and cut into 14-mum serial sagittal frozen sections. The sections were examined with a confocal laser-scanning microscope to quantify green fluorescent protein-positive cell survival. RESULTS: At time zero, only host cells in group A and only graft cells in group B demonstrated green fluorescent protein signals. At 1 week in group A, many green fluorescent protein-positive cells were found in the graft. In group B, a few green fluorescent protein-positive cells were found in the graft. At 2 and 4 weeks in group A, many green fluorescent protein-positive cells were detected in the graft, but green fluorescent protein-positive cells had disappeared completely in group B. CONCLUSION: Host cells, rather than graft cells, contribute to repair of the bone-tendon interface and the remodeling of grafts after simulated autologous tendon graft.  相似文献   
103.
Expression of dentin matrix protein 1 (DMP1) in nonmineralized tissues   总被引:2,自引:0,他引:2  
Dentin matrix protein 1 (DMP1) is an Arg-Gly-Asp-containing acidic phosphoprotein that was originally identified from a rat incisor cDNA library and was thought to be a dentin-specific protein. DMP1 was later shown to express in a number of hard tissue-forming cells, including osteoblasts, osteocytes, ameloblasts, and cementoblasts, and was considered to play important roles in mineralization. Further, DMP1 gene expression was also detected in fetal bovine brain and in newborn mouse brain. These findings indicate the possibility of DMP1 expression in other soft tissues. In the present study, to clarify the significance of DMP1 expression in nonmineralized tissues, we made a specific antibody to mouse DMP1 peptides and demonstrated that DMP1 protein was localized in mouse brain, pancreas, and kidney by immunohistochemistry. Further DMP1 mRNA was detected in nonmineralized mouse tissues including liver, muscle, brain, pancreas, and kidney by RT-PCR. Based on the evidence that the localization and the expression of DMP1 are not restricted to mineralized tissues, we assume that DMP1 may have functions other than the regulation of mineralization.  相似文献   
104.
OBJECTIVE: We have observed that, in cases of smell loss, patients often complain of taste loss as well even though they actually have normal gustatory acuity according to gustatory tests; we have defined such symptoms as "flavor disturbance". The clinical features of flavor disturbance are reported in this paper. MATERIAL AND METHODS: A total of 297 patients (99 males, 198 females; mean age 55.5 years) were treated for olfactory disturbance at the hospital of Hyogo College of Medicine between July 1995 and August 2001. Sixty-six out of 297 patients (22.5%) also experienced taste disturbance, and 49 of these 66 cases were evaluated by means of smell and taste tests. These 49 patients who complained of taste and smell loss were classified into two groups according to the results of their smell and taste tests. Patients who only complained of olfactory disturbance were also reviewed. RESULTS: There was no relationship between the severity of olfactory disturbance and the degree of flavor disturbance. The incidence of flavor disturbance was high in patients with sudden olfactory disturbance after upper respiratory tract infection or head trauma and low in those with slowly progressive olfactory disturbance. The symptoms of flavor disturbance improved regardless of whether smell was improved or not. CONCLUSIONS: The patients with flavor disturbance tended to misrecognize that they had taste loss because of sudden smell loss, and there were more of these cases than we expected. When patients with smell and taste loss are treated, flavor disturbance should also be considered.  相似文献   
105.
Zinc is a vital metal that is a structural and functional component of many proteins. The precise mechanism of zinc transport in the placenta remains unclear. In this study, we investigated the expression of zinc transporters (ZnTs) in the mouse placenta and in two rat trophoblast cell lines, TR-TBT cells, which are syncytiotrophoblast cells of the labyrinth zone, and Rcho-1 cells, which retain trophoblast cell features and differentiate into trophoblast giant cells of the junctional zone. All of the ZnTs that have been identified in mice (ZnT1-7) were detected in the mouse placenta by RT-PCR. The expression profiles of ZnTs in the placenta during pregnancy were different. The mRNA levels of ZnTs, with the exception of ZnT7, did not change during pregnancy. The ZnT7 mRNA level in placenta was elevated during pregnancy. In TR-TBT cells, ZnT1, ZnT3 and ZnT4 were detected by RT-PCR analysis. In Rcho-1 cells, all of the ZnTs that have been identified in rats (ZnT1-4) were detected by RT-PCR analysis. There were no differences between the mRNA expression levels of ZnT family members in undifferentiated Rcho-1 cells and differentiated Rcho-1 cells. This is the first report of expression profiles of ZnTs during differentiation of the placenta in the mouse placenta and rat placental cell models.  相似文献   
106.
Some antitumor agents, including tumor necrosis factor-alpha (TNF-alpha) and camptothecin (CPT), often cause resistance of tumor cells to antitumor agents through activation of the nuclear factor-kappa B (NF-kappa B) pathway that leads to up-regulation of anti-apoptotic proteins. Therefore, co-treatment of an inhibitor of the NF-kappa B pathway with antitumor agents is a useful strategy for chemotherapy. Here we report that ent-11 alpha-hydroxy-16-kauren-15-one (KD) selectively inhibits NF-kappa B-dependent gene expression due to treatment with TNF-alpha. KD in combination with TNF-alpha caused a dramatic increase in apoptosis in human leukemia cells accompanied by activation of caspases. A broad-spectrum inhibitor of caspases decreased the apoptosis induced by treatment with KD and TNF-alpha. KD in combination with CPT also caused an increase in apoptosis. These results suggest that the apoptotic potency of co-treatment of KD with TNF-alpha or CPT is elicited through selective inhibition of NF-kappa B-dependent anti-apoptotic proteins and thus may provide a basis for the development of useful approaches to the treatment of leukemia.  相似文献   
107.
One of the serious problems that occurs after cardiopulmonary resuscitation is brain posthypoxic/ischemic deoxygenation. However, there has been no report concerning the effect of isoflurane (ISO) on the brain oxygenation during hypoxia-reoxygenation in relation to cell adhesion molecules (CD11b) in polymorphonuclear leukocyte. Rats were anesthetized with a low concentration of ISO (0.5 MAC: low ISO) or high concentration of ISO (1.5 MAC: high ISO) and brain oxygenation was detected by near infrared spectroscopy during 10-min hypoxia (5% O(2)) and a subsequent 120-min reoxygenation period. Hypoxia induced a decrease in oxyhemoglobin (HbO(2)) and an increase in deoxyhemoglobin (Hb). Reoxygenation induced a significant decrease in total hemoglobin (tHb) and HbO(2) with low ISO, but not with high ISO. The changes in Hb were minimal during reoxygenation in both groups. CD11b increased during reoxygenation with low ISO anesthetization, but not with high ISO. A significant negative correlation was observed between CD11b and two of the measured oxyparameters, HbO(2) and tHb, during reoxygenation at low ISO, but not at high ISO. These findings suggest that brain deoxygenation during hypoxia-reoxygenation is partly related to the expression of CD11b. We conclude that ISO modifies the brain circulation at least in part through attenuating the expression of CD11b during hypoxia-reoxygenation.  相似文献   
108.
A spiral high-resolution coronary artery imaging sequence (SH) interfaced with real-time localization system (RT) has been developed. A clinical study of 40 patients suspected of coronary artery disease (CAD) was conducted.Segmented k-space acquisition techniques have dominated magnetic resonance coronary angiography (MRCA) over the last decade. Although a recent multicenter trial using this technique demonstrated encouraging results, the technique was hampered by low specificity. Spiral k-space acquisition had demonstrated several advantages for MRCA. Therefore, a first clinical trial implementing spiral high-resolution coronary imaging sequence with real-time localization (SH-RT) was performed.A clinical study of 40 patients suspected of CAD undergoing X-ray angiography was conducted to analyze the clinical reliability of this novel imaging system. The SH-RT had been designed to exploit the unique capability of two imaging sequences. The RT allowed a rapid localization of the coronary arteries. Then SH achieved multislice acquisition during a short breath-hold with submillimeter resolution. The MRCA data were analyzed for scan time, anatomic coverage, image quality, and accuracy in detecting CAD.In 40 subjects, SH achieved 0.7 to 0.9 mm resolution with 14-heartbeat breath-holds. Excellent or good image quality was achieved in 78% (263/337) of the coronary segments. Blinded consensus reading among three observers generated sensitivity of 76% and specificity of 91% in the detection of CAD compared with X-ray angiography.The MRCA imaging sequence implementing a novel spiral k-space acquisition technique enabled rapid and reliable imaging of the CAD in submillimeter resolution with short breath-holds.  相似文献   
109.
We describe a case of myotonic dystrophy presenting with a disturbed circadian rhythm of the serum cortisol and an isolated thyrotropin deficiency. The diagnosis of myotonic dystrophy was based on clinical characteristics, positive electromyographic findings, and increased number of CTG repeats in the dystrophia myotonica protein kinase (DMPK) gene. The patient presented with a variable circadian rhythm of the serum cortisol, increased excretion of urinary free cortisol, and a high adrenocorticotropin hormone responses to corticotropin-releasing hormone. The basal serum thyrotropin concentration was low and did not increase after thyrotropin-releasing hormone stimulation. The protein encoded by the DMPK gene may act as a second messenger in signal transduction, like a protein kinase. The present patient had a diverse pattern of disturbances in the hypothalamus-pituitary-endocrine organ axis, probably mediated by differences in the action or expression of the gene products in each endocrine cell.  相似文献   
110.
Platelet-derived growth factor (PDGF) plays an important role in the pathogenic course of atherosclerosis, pulmonary fibrosis, and glomerulonephritis, and increased activity of the PDGF signaling pathway has been implicated as a contributing factor in the progression of the diseases. Taurine may be a prophylactic amino acid for atherosclerosis not only by decreasing plasma cholesterol level, but also by inhibiting the cell proliferation-signaling pathway. To elucidate how taurine affects the signaling pathway, we investigated the effect of taurine on the expression of immediate-early genes and activation of mitogen-activated protein kinases (MAPKs) in NIH/3T3 cells as standard mesenchymal cells. Taurine inhibited PDGF-BB-induced c-fos and c-jun mRNA expressions dose-dependently, although structural analogues of taurine did not. Taurine decreased the PDGF-induced p44/p42 ERK (extracellular signal-regulated kinase) phosphorylation state dose-dependently, although no phosphorylation was observed on JNK/SAPK (c-Jun N-terminal kinase/stress-activated protein kinase) and p38 MAPK. Further, PDGF-BB-induced tyrosine phosphorylation of the PDGF-beta receptor was not influenced by treatment with taurine, indicating that taurine never affects ligand-receptor interaction, and may act downstream of the PDGF receptor. Thus, the inhibitory mechanism of taurine on PDGF-induced c-fos and c-jun mRNA expressions may depend on the p44/p42 ERK pathway, but not on PDGF-beta receptor tyrosine phosphorylation, JNK/SAPK or p38 MAPK pathway. These results suggest that taurine may suppress the cell proliferation-signaling pathway through the inhibition of ERK activity and immediate-early gene expression.  相似文献   
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