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121.
Endocrine surgeons have had an important role in the management of hyperthyroidism due to either Graves' disease or toxic nodule(s). Since alternative treatments such as antithyroid drugs or radioiodine are also available, the decision-making for management should be based on clear assessment of advantages and limitations of each of the treatment options. Surgery provides rapid resolution of these conditions, and cure rates are high, although it may be associated with perioperative complications and postoperative thyroid dysfunction. The authors' experience in the surgical treatment of hyperthyroidism and a review of the recent literature are outlined in this report.  相似文献   
122.
To improve low-pitched voices in cases with polypoid vocal cords, YAG laser irradiation combined with a mucosal suturing technique was attempted in 9 female cases with severe polypoid changes in their vocal cords. A YAG laser beam (5 to 10 W) was used to irradiate the upper surface of the polypoid vocal cord. The polypoid content of the cord was gradually coagulated, and the free edge of the cord appeared to slide up toward the burned area. The polypoid content was then removed and squeezed through an open wound made in the burned area using a conventional method. Bleeding was successfully controlled using the laser. After the excessive mucosal margin was trimmed and the contour of the vocal cord was adjusted, the wound was closed by 7-0 monofilament absorbable suture. Suturing was relatively easy because the mucosal edge was also coagulated. Postoperative evaluations of voice quality revealed an improvement in the GRBAS scale of voice quality as well as an elevation in voice pitch and an upwards shift in the voice range in all cases.  相似文献   
123.
Nicotine is known to improve cognitive performance such as attention, concentration and working memory in humans and animals. Previous research suggests that nicotine enhances visuospatial attention. But it could be hypothesized that nicotine intake alleviate a withdrawal-induced deficit in smokers. To evaluate the cognitive performance in smokers and never-smokers, we investigate eye movement while 4-points saccade task is performed. 5 smokers and 6 never-smokers are matched for age and education. Eye movement was investigated by using TKK2920 (Takei Co.) which determines the direction of gaze over a two-dimensional visual field without attachments to the eye. We found that a tendency which Mean Gazing Time is prolonged in smokers. These data suggest that impairment of visual attention in smokers is not significant.  相似文献   
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125.
BACKGROUND: Bleeding isolated gastric varices with a spontaneous portosplenorenal shunt are difficult to control. The urgent use of transjugular retrograde obliteration (TJO) to prevent early rebleeding and to improve early mortality has not yet been demonstrated. We report our experience with this technique in patients with isolated gastric varices after treatment of acute bleeding. METHODS: We reviewed our experience of 6 patients with isolated gastric varices with a spontaneous portosplenoral shunt treated with TJO after treatment of acute bleeding. We basically applied endoscopic glue embolization using cyanoacrylate monomer for treatment of acute bleeding. TJO was a method using an occlusive balloon catheter to control a spontaneous portosplenorenal shunt flow while injecting sclerosant retrograde into the gastric varices. RESULTS: Treatment of acute bleeding was achieved immediately by endoscopic glue embolization, endoscopic variceal ligation, and ligating the varices with sutures following anterior gastrotomy in 4, 1 and 1 patients, respectively, and then TJO was performed. Permanent hemostasis and variceal eradication was achieved in these 6, and they all survived. They were alive for 6-66 months without gastric variceal recurrence. CONCLUSIONS: We conclude that urgent TJO is effective in the prophylaxis of early and late rebleeding from isolated gastric varices in patients with a spontaneous portosplenorenal shunt.  相似文献   
126.
The objective of this study was to assess the relationship of signaling molecules to monocyte/ macrophages as a precursor to venous valve and venous wall dysfunction in patients with varicose veins. One of the hallmarks of venous dysfunction is destruction of venous valves with subsequent reflux and elevation of distal venous pressure. We recently observed that monocytes/macrophages migrate into the venous walls and valves of patients with venous insufficiency. There, they may play a role in the pathogenesis of primary venous insufficiency. If so, an important element in their performance would be the interaction between the monocytes and the endothelium as a precursor of damage to venous valves and the venous wall. To explore this interaction, immunohistochemistry was carried out to detect adhesion molecules and cytokines in surgical specimens removed during surgical therapy. Twenty-four surgical specimens consisting of proximal saphenous vein and subterminal valve were obtained using minimally traumatic technique in 6 males and 18 females who ranged in age from 31 to 79 years. Reflux was confirmed preoperatively by duplex technique, and severity was classified by the CEAP classification of the American Venous Forum. Ten patient limbs were class 2, eight were class 3, four were class 4, and two were class 6. The venous specimens were labeled using monoclonal antibody against ICAM-1, E-selectin, IL-1alpha, and TNF-alpha. CD68 was used for detection of monocytes/macrophages. Our results indicate that not only luminal venous endothelium but also endothelium in the vasa vasora of refluxing saphenous veins is activated, as indicated by the up-regulation of ICAM-1. However, IL-1alpha and TNF-alpha were increased in only selected specimens and are mainly detected in the vein wall. The factors that serve as trigger mechanisms to activate cells in the pathogenesis of primary venous dysfunction remain to be explored.  相似文献   
127.
BACKGROUND: Infection of the gastric mucosa by helicobacter pylori is primarily responsible for gastritis, gastric ulcer, adenocarcinoma, and lymphoproliferative disorders. H. pylori appears to accelerate apoptosis and the proliferation of the gastric epithelium directly or indirectly. To precisely assess the proliferative and apoptotic profile of .H pylori-infected gastric mucosa, a quantitative imaging system is now required. METHODS: Fifty-two patients with H. pylori gastritis were the subjects of the study. Biopsy materials were taken from at least two sites (usually three to five sites) including the antrum and corpus. The grade of gastritis was evaluated by the updated Sydney System. The proliferative and apoptotic profile was examined by Ki-67 immunohistochemistry and by a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling method. In addition, Ki-67-positive cells were quantitated by an image processor for analytical pathology (IPAP) system. RESULTS: H. pylori density and polymorphonuclear neutrophil activity were significantly decreased after H. pylori eradication ( P< 0.0001). Chronic inflammation (P< 0.0001) and lymphoid follicle numbers ( P < 0.0005) were also significantly decreased after the eradication. Glandular atrophy and intestinal metaplasia were slightly decreased after eradication, but the decrease did not reach the significant level. the Ki-67 labeling index was significantly decreased after the eradication P< 0.0001). The apoptosis index was also decreased after the eradication, but this decrease did not reach the significant level ( P = 0.06). CONCLUSION: our data suggest that the activation of proliferative cells and induction of apoptosis in the gastric mucosa is a response to H. pylori-induced mucosal damage. Moreover, IPAP may be a useful technology for evaluating the results of immunohistochemistry, and it could provide quantitative and reliable data for studying H. pylori gastritis.  相似文献   
128.
BACKGROUND: Dysregulation of apoptosis is one of the likely underlying mechanisms of mesangial proliferative glomerulonephritis (GN), a disease in which proinflammatory cytokines exhibit a wide range of biological activities. Among them, tumor necrosis factor-alpha (TNF-alpha) induces two conflicting pathways, one leading to activation of the nuclear factor-kappa B (NF-kappa B), and the other leading to caspase-mediated apoptosis. We investigated whether or not specific inhibition of NF-kappa B affects TNF-alpha-induced apoptosis in rat mesangial cells (MCs). METHODS: To specifically inhibit NF-kappa B activation, we constructed a recombinant adenovirus vector expressing a truncated form of I kappa B alpha (AdexI kappa B delta N) that lacks the phosphorylation sites essential for the activation of NF-kappa B. Electrophoretic mobility shift assay was performed to evaluate NF-kappa B activity. Nuclear morphology was observed by staining with Hoechst-33258. DNA fragmentation was detected using an ELISA kit with an antihistone antibody. To investigate the regulation of apoptosis, we measured caspase-3 and caspase-8 activity by ELISA, and examined the Bcl-2 and Bax protein level by Western blot. RESULTS: TNF-alpha-induced NF-kappa B activation was blocked by overexpression of I kappa B delta N. Overexpression of I kappa B delta N potentiated TNF-alpha-induced apoptosis compared to mock transfection, and the potentiation was abolished by treatment with a caspase-3 inhibitor, Z-DEVD-FMK. Overexpression of I kappa B delta N augmented TNF-alpha-induced caspase-3 and caspase-8 activity, but did not affect Bcl-2 or Bax protein expression. CONCLUSION: Overexpression of I kappa B delta N potentiates TNF-alpha-induced apoptosis and augments caspase-8 and caspase-3 activity in rat MCs without changing Bcl-2 or Bax protein expression. These results suggest the potential usefulness of AdexI kappa B delta N to induce apoptosis in MCs under inflammatory conditions.  相似文献   
129.
Hori Y  Takeyama Y  Ueda T  Shinkai M  Takase K  Kuroda Y 《Surgery》2000,127(6):641-649
BACKGROUND: The mechanism of acute pancreatitis-induced hepatocellular injury is unclear. We have observed hepatocyte apoptosis in rat acute necrotizing pancreatitis. These studies were designed to determine the mediator(s) responsible for hepatocyte apoptosis and to clarify the significance of macrophages as its source. METHODS: A rat sodium deoxycholate-induced pancreatitis model was used. Immunohistochemical studies for apoptosis-inducing mediators on hepatocytes were examined in the liver and on the peritoneal macrophages. The levels of transforming growth factor-beta1 (TGF-beta1) were also evaluated quantitatively with an enzyme-linked immunosorbent assay. Induction of apoptosis on the hepatocytes was evaluated by in situ nick-end labeling and tissue DNA fragmentation enzyme-linked immunosorbent assay. Finally, the effects of TGF-beta1 neutralization and macrophage depletion were examined. RESULTS: In the liver and the peritoneal macrophages, strong expression of TGF-beta1 was detected early in the course of pancreatitis. In sodium deoxycholate-induced pancreatitis, the levels of TGF-beta1 were also elevated in the plasma (9.2 +/- 0.8 ng/mL), in the pancreatitis-associated ascitic fluid (11.5 +/- 0.6 ng/mL), and in the liver homogenate (2.8 +/- 0.3 ng/g of liver tissue). Moreover, the amount of fragmented DNA of the liver with pancreatitis was 290% +/- 20% of that with a sham operation and serum alanine aminotransferase levels elevated to 248.2 +/- 67.0 IU/L. TGF-beta1 neutralization partly blocked the positive labeling on the nuclei of the hepatocytes, the elevation of the amounts of fragmented DNA (205% +/- 10% of sham operation), and the serum alanine aminotransferase level (144.2 +/- 14.9 IU/L). On the other hand, the macrophage depletion caused a marked decrease in the TGF-beta1 protein level in the plasma (4.8 +/- 1.2 ng/mL) or in the pancreatitis-associated ascitic fluid (8.0 +/- 1.0 ng/mL). Moreover, the macrophage depletion completely inhibited the elevation of the TGF-beta1 protein level in the liver homogenate (1.5 +/- 0.4 ng/g of liver tissue), and thereafter decreased the amounts of the positive labeling on the nuclei of the hepatocytes and decreased the amount of fragmented DNA (120% +/- 18% of sham operation) and the serum alanine aminotransferase elevation (119.2 +/- 24.2 IU/L). CONCLUSIONS: In a model of sodium deoxycholate-induced pancreatitis, macrophages are responsible for pancreatitis-induced hepatocellular injury by means of apoptosis, and macrophage-derived TGF-beta1 is one of the major factors inducing the hepatocyte apoptosis.  相似文献   
130.
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