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排序方式: 共有5022条查询结果,搜索用时 15 毫秒
91.
92.
The elevated gene expression level of the A2B adenosine receptor is associated with hyperglycemia in women with gestational diabetes mellitus 下载免费PDF全文
93.
Anna Szumera‐Ciekiewicz Grzegorz Rymkiewicz Kamil Sok Ewa Paszkiewicz‐Kozik Anita Borysiuk Jan Poleszczuk Katarzyna Bachnio Zbigniew Bystydzienski Renata Woroniecka Beata Grygalewicz Martyna Kotarska Monika Staczak Daria Owczarek Beata Pytlak Monika Prochorec‐Sobieszek Jan Walewski 《International journal of laboratory hematology》2020,42(4):453-463
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95.
Katarzyna Szkudelska Leszek Nogowski Tomasz Szkudelski 《International journal of experimental pathology》2014,95(2):86-94
Administration of streptozotocin (STZ) and nicotinamide (NA) to adult rats allows for the induction of mild diabetes. However, this experimental model has not been fully characterized. This study was undertaken to determine the metabolic and secretory activity of adipose tissue in rats with STZ‐NA‐induced diabetes. Experiments were performed using epididymal adipocytes isolated from control and mildly diabetic rats. Lipogenesis, glucose transport as well as glucose and alanine oxidation, lipolysis, anti‐lipolysis, cAMP levels and adipokine secretion were compared in cells isolated from the control and diabetic rats. Lipogenesis, glucose transport and oxidation were diminished in the adipocytes of diabetic rats compared with the fat cells of control animals. However, alanine oxidation appeared to be similar in the cells of non‐diabetic and diabetic animals. Lipolytic response to low epinephrine concentrations was slightly increased in the adipocytes of diabetic rats; however, at higher concentrations of the hormone, lipolysis was similar in both groups of cells. The epinephrine‐induced rise in cAMP levels was higher in the adipocytes of STZ‐NA‐induced diabetic rats, even in the presence of insulin. Lipolysis stimulated by dibutyryl‐cAMP did not significantly differ, whereas anti‐lipolytic effects of insulin were mildly decreased in the cells of diabetic rats. Secretion of adiponectin and leptin was substantially diminished in the adipocytes of diabetic rats compared with the cells of control animals. Our studies demonstrated that the balance between lipogenesis and lipolysis in the adipose tissue of rats with mild diabetes induced by STZ and NA is slightly shifted towards reduced lipid accumulation. Simultaneously, adiponectin and leptin secretion is significantly impaired. 相似文献
96.
Katarzyna Kościelska-Kasprzak Dorota Bartoszek Marta Myszka Marcelina Żabińska Marian Klinger 《Archivum immunologiae et therapiae experimentalis》2014,62(1):47-57
Serum complement cascade, a part of innate immunity required for host protection against invading pathogens, is also a mediator of various forms of disease and injury. It is activated by classical, lectin, and alternative pathways that lead to activation of C3 component by C3 convertases, release of C3b opsonin, C5 conversion and eventually membrane attack complex formation. The tightly regulated activation process yields also C3a and C5a anaphylatoxins, which target a broad spectrum of immune and non-immune cells. The review discusses the involvement of the complement cascade in kidney disease pathogenesis and injury. The role of the complement pathways in autoantibody-mediated forms of glomerulonephritis (lupus nephritis, anti-glomerular basement membrane disease, anti-neutrophil cytoplasmic autoantibody-induced or membranoproliferative glomerulonephritis, membranous nephropathy), C3 glomerulopathy, atypical forms of hemolytic uremic syndrome, ischemic-reperfusion injury of transplanted kidney, and antibody-mediated renal allograft rejection are discussed. The disturbances in complement activation and regulation with underlying genetics are presented and related to observed pathology. Also promising strategies targeting the complement system in complement-related disorders are mentioned. 相似文献
97.
Ma?gorzata ?awniczak Alicja Gawin Halina Jaroszewicz-Heigelmann Wies?awa Rogoza-Mateja Joanna Raszeja-Wyszomirska Andrzej Bia?ek Katarzyna Karpińska-Kaczmarczyk Teresa Starzyńska 《World journal of gastroenterology : WJG》2014,20(23):7480-7487
AIM: To determine the prevalence and characteristics of additional primary malignancies in gastric cancer (GC) patients.METHODS: GC patients (862 total; 570 men, 292 women; mean age 59.8 ± 12.8 years) diagnosed at the Department of Gastroenterology at Pomeranian Medical University over a period of 23 years were included in this retrospective analysis of a prospectively maintained database. Mean follow-up time was 31.3 ± 38.6 mo (range 1-241 mo). The following clinicopathological features of patients with synchronous tumors were compared to those with metachronous tumors: age, sex, symptom duration, family history of cancer, tumor site, stage (early vs advanced), histology, and blood group. GC patients with and without a second tumor were compared in terms of the same clinicopathological features.RESULTS: Of 862 GC patients, 58 (6.7%) developed a total of 62 multiple primary tumors, of which 39 (63%) were metachronous and 23 (37%) synchronous. Four (6.9%) of the 58 multiple GC patients developed two or more neoplasms. The predominant tumor type of the secondary neoplasms was colorectal (n = 17), followed by lung (n = 9), breast (n = 8), and prostate (n = 7). Age was the only clinicopathological feature that differed between GC patients with synchronous vs metachronous malignancies; GC patients with synchronous neoplasms were older than those with metachronous neoplasms (68.0 ± 10.3 years vs 59.9 ± 11.1 years, respectively, P = 0.008). Comparisons between patients with and without a second primary cancer revealed that the only statistically significant differences were in age and blood group. The mean age of the patients with multiple GC was higher than that of those without a second primary tumor (63.4 ± 11.4 years vs 59.5 ± 13.0 years, respectively, P = 0.026). GC patients with a second primary tumor were more commonly blood group O than those without (56.2% vs 31.6%, respectively, P = 0.002).CONCLUSION: GC patients may develop other primary cancers; appropriate preoperative and postoperative diagnostic modalities are thus required, particularly if patients are older and blood group O. 相似文献
98.
Maternal insulin sensitivity is associated with oral glucose-induced changes in fetal brain activity
Katarzyna Linder Franziska Schleger Caroline Ketterer Louise Fritsche Isabelle Kiefer-Schmidt Anita Hennige Hans-Ulrich Häring Hubert Preissl Andreas Fritsche 《Diabetologia》2014,57(6):1192-1198
Aims/hypothesis
Fetal programming plays an important role in the pathogenesis of type 2 diabetes. The aim of the present study was to investigate whether maternal metabolic changes during OGTT influence fetal brain activity.Methods
Thirteen healthy pregnant women underwent an OGTT (75 g). Insulin sensitivity was determined by glucose and insulin measurements at 0, 60 and 120 min. At each time point, fetal auditory evoked fields were recorded with a fetal magnetoencephalographic device and response latencies were determined.Results
Maternal insulin increased from a fasting level of 67?±?25 pmol/l (mean ± SD) to 918?±?492 pmol/l 60 min after glucose ingestion and glucose levels increased from 4.4?±?0.3 to 7.4?±?1.1 mmol/l. Over the same time period, fetal response latencies decreased from 297?±?99 to 235?±?84 ms (p?=?0.01) and then remained stable until 120 min (235?±?84 vs 251?±?91 ms, p?=?0.39). There was a negative correlation between maternal insulin sensitivity and fetal response latencies 60 min after glucose ingestion (r?=?0.68, p?=?0.02). After a median split of the group based on maternal insulin sensitivity, fetuses of insulin-resistant mothers showed a slower response to auditory stimuli (283?±?79 ms) than those of insulin-sensitive mothers (178?±?46 ms, p?=?0.03).Conclusions/interpretation
Lower maternal insulin sensitivity is associated with slower fetal brain responses. These findings provide the first evidence of a direct effect of maternal metabolism on fetal brain activity and suggest that central insulin resistance may be programmed during fetal development. 相似文献99.
100.
DB Foster AS Ho J Rucker AO Garlid L Chen A Sidor KD Garlid B O'Rourke 《Circulation research》2012,111(4):446-454
Rationale: Activation of the mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) has been implicated in the mechanism of cardiac ischemic preconditioning, yet its molecular composition is unknown. Objective: To use an unbiased proteomic analysis of the mitochondrial inner membrane to identify the mitochondrial K(+) channel underlying mitoK(ATP). Methods and Results: Mass spectrometric analysis was used to identify KCNJ1(ROMK) in purified bovine heart mitochondrial inner membrane and ROMK mRNA was confirmed to be present in neonatal rat ventricular myocytes and adult hearts. ROMK2, a short form of the channel, is shown to contain an N-terminal mitochondrial targeting signal, and a full-length epitope-tagged ROMK2 colocalizes with mitochondrial ATP synthase β. The high-affinity ROMK toxin, tertiapin Q, inhibits mitoK(ATP) activity in isolated mitochondria and in digitonin-permeabilized cells. Moreover, short hairpin RNA-mediated knockdown of ROMK inhibits the ATP-sensitive, diazoxide-activated component of mitochondrial thallium uptake. Finally, the heart-derived cell line, H9C2, is protected from cell death stimuli by stable ROMK2 overexpression, whereas knockdown of the native ROMK exacerbates cell death. Conclusions: The findings support ROMK as the pore-forming subunit of the cytoprotective mitoK(ATP) channel. 相似文献