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81.
Okazuka K Masuko M Seki Y Hama H Honma N Furukawa T Toba K Kishi K Aizawa Y 《International journal of hematology》2007,86(3):246-249
Acute promyelocytic leukemia (APL) is characterized by a reciprocal chromosomal translocation involving the gene for retinoic acid receptor alpha(RAR). Most APL patients have a t(15;17) translocation that generates the PML-RAR fusion gene, and such patients respond well to treatment with all-trans retinoic acid (ATRA). Some APL cases also involve rearrangements that fuse RAR to partner genes other than PML, including nucleophosmin (NPM), promyelocytic leukemia zinc finger (PLZF), nuclear mitotic apparatus (NUMA), and Stat5b, but the clinical characteristics of APL without PML-RAR have not been fully clarified. We describe a 64-year-old man with NPM-RAR-positive APL who was receiving hemodialysis therapy for chronic uremia. Complete remission was achieved with ATRA monotherapy and was maintained for 18 months with consolidation chemotherapy. These findings suggest that ATRA can be used to treat APL patients with NPM/RAR as well as APL with PML/RAR. 相似文献
82.
Coagulation factor XIII/13 (FXIII/13) stabilizes fibrin molecules by creating crosslinks with other fibrin molecules as well
as with α2-plasmin inhibitor (α2-PI). “Hemorrhagic acquired FXIII/13 deficiency” was formerly considered rare, but has been increasing recently in Japan.
During the 10 months of our nationwide campaign, we diagnosed five new patients with “acquired hemorrhaphilia due to anti-FXIII/13
autoantibodies,” after examining 20 newly suspected cases of “hemorrhagic acquired FXIII/13 deficiency.” When FXIII/13 activity
was reduced to less than 50% of normal, it was proportional to the difference in α2-PI levels between plasma and serum (plasma–serum α2-PI), likely due to its cross-linking to fibrin by activated FXIII/13. Accordingly, decreased amounts of the plasma–serum
α2-PI ex vivo may reflect reduced FXIII/13 activity in vivo. The plasma–serum α2-PI may thus also be a useful diagnostic marker for severe FXIII/13 deficiency. 相似文献
83.
Tonan T Fujimoto K Qayyum A Morita Y Nakashima O Ono N Kawahara A Kage M Hayabuchi N Ueno T 《Journal of gastroenterology and hepatology》2012,27(4):789-796
Background and Aim: Kupffer cell (KC) function and CD14 expression contributes to pathogenesis of non‐alcoholic steatohepatitis (NASH). However, these relationships remain unclear. We investigated the relationship of KC function with superparamagnetic iron oxide‐enhanced magnetic resonance imaging (SPIO‐MRI), histopathological severity of NASH, and number of CD14‐positive KCs in NASH. Methods: This retrospective study included 32 patients (24 with NASH and eight with simple steatosis) who had previously undergone SPIO‐MRI with T2‐weighted gradient‐recalled echo sequence. All subjects were diagnosed pathologically and were evaluated for necroinflammation grade, fibrosis stage, and number of CD14‐positive KCs. Patients with NASH and simple steatosis were compared by using the Mann–Whitney test to determine differences in percent reduction of liver‐to‐muscle signal intensity ratio (reduction‐%LMR), as a surrogate parameter of KC function, and number of CD14‐positive KCs. Kruskal–Wallis test and Pearson's correlation coefficient were used to analyze relation among reduction‐%LMR, histopathological severity and number of CD14‐positive KCs. Results: There were statistically significant differences in reduction‐%LMR and number of CD14‐positive KCs between NASH and simple steatosis patients (Mann–Whitney test, P < 0.001 for all comparisons). Reduction‐%LMR decreased with an increase in necroinflammation grade or fibrosis stage. The number of CD14‐positive KCs increased with an increase in necroinflammation grade and fibrosis stage (Kruskal–Wallis test, both, P < 0.001). A high correlation was seen between number of CD14‐positive KCs and reduction‐%LMR (Pearson r = 0.81; P < 0.001). Conclusions: KC phagocytic function evaluated with SPIO‐MRI correlated with histopathological severity and number of CD14‐positive KCs. These results support the concept that KC phagocytic dysfunction contributes to the pathogenesis of NASH. 相似文献
84.
Miura S Shirahama K Sakaguchi M Takao M Hirakawa T Nishihara M Shimada M Oka H Ishiguro S 《Nihon Shokakibyo Gakkai zasshi》2012,109(6):929-935
A 63-year-old woman who presented with chest and back pain underwent an upper gastrointestinal endoscopy which revealed elevated legion in the antrum mucosa. Histologic examinations of gastric biopsies were showing monoclonal proliferation plasma cells containing Russell bodies. Differential diagnosis from B-cell lymphoma and plasmacytoma is difficult, because of monoclonality. Molecular analyses of immunoglobulin heavy chain (IgH) gene demonstrated that gene rearrangement was negative. Thus, diagnosis of Russell body gastritis was made. The Giemsa stains were also showing infection of Helicobacter pylori (H.pylori). After eradication therapy for H.pylori, follow-up upper gastrointestinal endoscopy was performed. She then recovered. 相似文献
85.
Junji Kato Yoshihiro Mogi Yutaka Kohgo Rishu Takimoto Masayoshi Kobune Hiroyuki Hisai Tokiko Nakamura Kohichi Takada Yoshiro Niitsu 《Journal of gastroenterology》1998,33(6):855-859
Blood levels of inflammatory-related cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, are
elevated in patients with alcoholic liver diseases. We investigated the effects of these cytokines and ethanol on the expression
of hepatic asialoglycoprotein receptors (AGPRs) in a human hepatoblastoma cell line, HepG2. An [125I]-asialo-orosomucoid binding assay showed significant increases in surface AGPR numbers in HepG2 cells by treatment with
IL-1β, IL-6, and TNF-α, to levels which were approximately 130% of the values in untreated control cells. However, the enhanced
AGPR numbers induced by treatment with these cytokines were markedly suppressed, to 70%–80% of the number in the untreated
cells, by treatment with ethanol. Immunological detection of AGPR with a specific antibody demonstrated that the modulation
of surface AGPR numbers was correlated with the cellular expression levels of AGPR. These results suggest that, although IL-1β,
IL-6, and TNF-α stimulate the synthesis of hepatic AGPR, ethanol suppresses the expression of AGPR augmented by these cytokines.
This leads to an increase in serum asialo-orosomucoid levels caused by the disordered catabolism mediated by AGPR in patients
with alcoholic liver disease.
(Received Dec. 5, 1997; accepted May 22, 1998) 相似文献
86.
Yukiko Hasuike Naoto Kakita Makoto Aichi Satoko Masachika Mari Kantou Shoko Ikeda Takahashi Masayoshi Nanami Yasuyuki Nagasawa Takahiro Kuragano Takeshi Nakanishi 《Journal of vascular surgery》2019,69(1):174-180.e2
Objective
For patients with end-stage renal disease on hemodialysis, the durability of vascular access (VA) is still far from optimal, and access survival after intervention for access failure is an important aspect. Procoagulant status is a leading cause of access failure. Coagulation-fibrinolysis imbalance can occur in hemodialyzed patients, but the influence of the imbalance has not been fully elucidated.Methods
We prospectively examined coagulation-fibrinolysis balance to assess the risk of access failure after the intervention of revascularization in a cohort of 462 hemodialysis patients. Thrombin-antithrombin complex (TAT) and plasmin-α2-plasmin inhibitor complex (PIC) are markers for coagulation and fibrinolysis. Median follow-up was 243 days. The end point was clinical access failure: revascularization or access revision. The survival curve for VA patency was assessed using the Kaplan-Meier method and compared using the log-rank test. Cox proportional hazards regression models that allowed adjustment for baseline differences in age, sex, dialysis vintage, diabetes mellitus, and various factors (quantity of blood flow, prothrombin time-international normalized ratio, fibrin degradation products, C-reactive protein, interleukin-6, tumor necrosis factor-α, and pentraxin-3) were used.Results
The 162 patients who reached an end point had smaller access flow volume and smaller percentage of arteriovenous fistula and higher TAT/PIC ratio. Kaplan-Meier analysis indicated that the patients with elevated TAT/PIC ratio showed poorer outcome (P < .001). On Cox regression modeling, elevated TAT/PIC was an independent risk factor for access failure (hazard ratio, 1.58; P = .03).Conclusions
Our results suggest that coagulation-fibrinolysis imbalance is a significant risk factor for access failure and may predict VA failure in hemodialyzed patients after access intervention. 相似文献87.
Background
Nonalcoholic steatohepatitis (NASH) is a feature of metabolic syndrome. Advanced glycation end-products (AGEs) are formed by the Maillard reaction, which contributes to aging and to certain pathological complications of diabetes. A recent study has suggested that glyceraldehyde-derived AGEs (Glycer-AGEs) are elevated in the sera of patients with NASH. Furthermore, immunohistochemistry of Glycer-AGEs showed intense staining in the livers of patients with NASH. The present study aimed to examine the effect of intracellular Glycer-AGEs on hepatocellular carcinoma (Hep3B) cells. 相似文献88.
Soluble E-selectin, leptin, triglycerides, and insulin resistance in nonobese Japanese type 2 diabetic patients 总被引:2,自引:0,他引:2
Taniguchi A Fukushima M Nakai Y Kuroe A Yamano G Yanagawa T Ohgushi M Ohya M Yoshii S Taki Y Seino Y 《Metabolism: clinical and experimental》2005,54(3):376-380
The aim of the present study was to investigate the relationships between insulin resistance and soluble E-selectin, body mass index (BMI), leptin, and serum lipid profile including triglycerides in nonobese Japanese type 2 diabetic patients. A total of 97 nonobese Japanese type 2 diabetic patients aged 43 to 84 years were examined. The duration of diabetes was 11.2 +/- 0.8 years. In conjunction with BMI and fasting concentrations of plasma glucose, serum lipids (triglycerides, total cholesterol, and high-density lipoprotein cholesterol) and serum insulin, soluble E-selectin, and leptin were also measured. The low-density lipoprotein (LDL) cholesterol level was calculated using the Friedewald formula. Insulin resistance was estimated by the homeostasis model assessment. The subjects were divided into 2 groups according to the value of insulin resistance estimated by the homeostasis model assessment. Values greater than 2.5 were indicative of the insulin-resistant state, and values less than 2.5 were indicative of the insulin-sensitive state. The insulin-resistant group had significantly higher levels of E-selectin, leptin, triglycerides, total and LDL cholesterol, and diastolic blood pressure as compared with the insulin-sensitive group. There was, however, no significant difference in age, sex, diabetes duration, BMI, systolic blood pressure, HbA1c, and high-density lipoprotein cholesterol between the 2 groups. Univariate regression analysis showed that insulin resistance was positively correlated to E-selectin (r = 0.305, P = .003), BMI (r = 0.283, P = .006), leptin (r = 0.296, P = .004), HbA1c (r = 0.241, P = .018), serum triglycerides (r = 0.385, P < .001), serum total (r = 0.240, P = .019) and LDL cholesterol (r = 0.254, P = .013) levels, and systolic (r = 0.247, P = .024) and diastolic (r = 0.305, P = .006) blood pressure. Multiple regression analyses showed that insulin resistance was independently predicted by serum E-selectin (F = 18.4), serum leptin (F = 14.0) and serum triglycerides (F = 20.0) levels, which explained 45.0% of the variability of insulin resistance. From these results, it can be concluded that in conjunction with serum triglycerides and serum leptin, serum E-selectin is another important independent factor associated with insulin resistance in nonobese Japanese type 2 diabetic patients. 相似文献
89.
Kunio Okuda Toshiro Nakashima Masahiko Okudaira Masayoshi Kage Yoshibumi Aida Masao Omata Hirotaka Musha Shunji Futagawa Mitsuo Sugiura Haruo Kameda 《Liver international》1981,1(4):255-263
ABSTRACT— Hepatic venograms made in 40 authentic cases of idiopathic portal hypertension (Banti's syndrome) were compared with 13 normal venograms and venograms obtained in 88 cases of cirrhosis, and analyzed in the light of the pathological changes seen in 16 postmortem liver specimens. There were frequent anastomoses between hepatic vein radicles, approximation of middle-size branches to the liver surface, reduction in the angles between the main hepatic vein and its tributaries, and difficulty in opacifying portal vein branches in wedged retrograde portography. These angiographic alterations were corroborated by gross pathological findings which comprised displacement of middle-size hepatic vein branches closer to the liver surface and their approximation among themselves, and seem to be accounted for by the disappearance of liver parenchyma secondary to the peripheral portal circulatory failure. 相似文献
90.
We assessed the effects of angiotensin-converting enzyme (ACE) inhibition on changes in the myocardial intracellular creatine kinase (CK) system in relation to left ventricular (LV) remodeling and function in heart failure after myocardial infarction (MI) in rats. We compared the findings at 4 weeks after MI to those at 12 weeks after MI. LV weight and chamber size were significantly increased and percent fractional shortening (%FS) was decreased in untreated MI rats compared with normal control animals both at 4 and 12 weeks after MI. Animals with MI and treated with the ACE inhibitor temocapril showed significantly reduced LV weight and chamber size and increased %FS compared with untreated MI rats at 12 weeks after MI, but not at 4 weeks after MI. At 4 weeks after MI, no significant changes were found in the total creatine and relative distribution of each CK isoenzyme in either the temocapril-treated or untreated animals with MI compared with the normal controls. In contrast, at 12 weeks after MI, untreated MI rats showed significant reductions in the total creatine and mitochondrial and MM-CK fractions and increases in the MB- and BB-CK fractions compared with the controls. The alterations in the mitochondrial and MB-CK fractions were significantly attenuated after 12 weeks of ACE inhibition. Thus, LV myocardial energy metabolism is progressively impaired and its alteration is not related to the magnitude of geometric changes and LV dysfunction after MI. Most of the beneficial effects of ACE inhibition were observed at 12 weeks after MI. Our results may provide an insight into the therapeutic strategy of ACE inhibition in chronic heart failure after MI. 相似文献