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1.
Dr. Hasan Horoz MD Dr. Hansan H. Erbil MD Varol Sen MD Esma Duru MD Dr. Hale Aral MD 《Annals of Ophthalmology》2005,37(4):267-271
We investigated the effects of activated protein C resistance (APCR), Factor V Leiden (FVL) mutation, and high lipoprotein
(a) levels in 32 young patients with branch retinal vein occlusion (BRVO) vs 30 controls. No difference between patients with
BRVO and controls was found with regard to APCR, FVL mutation, or lipoprotein (a) levels. These factors do not seem important
in the etiology of BRVO.
The authors have stated that they do not have a significant financial interest or other relationship with any product manufacturer
or provider of services discussed in this article. The authors also do not discuss the use of off-label products, which includes
unlabeled, unapproved, or investigative products or devices. 相似文献
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Pupose
Obstructive sleep apnea (OSA) is associated with various metabolic disorders, and oxidative stress was suggested to play an important role. In the present study, we aimed to investigate serum adiponectin and oxidative stress markers, especially protein carbonyls, and to evaluate the correlation between these parameters and lipid, insulin and fasting glucose concentrations in OSA patients and controls. 相似文献5.
Nesrin Saitogullari Ugurcan Sayili Esma Altunoglu Hafize Uzun 《Annales d'endocrinologie》2021,82(1):1-7
BackgroundThis study aimed to investigate the relationship between lipopolysaccharide (LPS) and zonulin levels and also to show the effect of acute hyperglycemic stress induced by oral glucose tolerance testing (OGTT) on zonulin levels in pre-diabetic patients.MethodsFour groups were constituted according to the criteria of the American Diabetes Association (ADA), based on OGTT results: control group (n:40); prediabetic group (n:56), divided into two subgroups: impaired fasting glucose group (IFG) (n:36), and impaired glucose tolerance (IGT) + IFG group (n:20) and type-2 diabetes mellitus (T2DM) group (n:45).ResultsZonulin and LPS did not significantly differ between the prediabetes and control groups, but were significantly higher in the T2DM group compared to both the prediabetic and the control group (P < 0.001). After OGTT, zonulin and LPS were significantly higher in the prediabetes group compared to the control group (P < 0.01 and P < 0.05, respectively), and significantly lower in the IFG and IFG + IGT groups compared to the T2DM group (P < 0.001, P < 0.001 and P < 0.001, P < 0.001, respectively). A positive correlation was detected between fasting zonulin and 2-hour zonulin (r = 0.727, P < 0.001) and between fasting LPS (r = 0.555, P < 0.001) and 2-hour LPS (r = 0.567, P < 0.001) in the prediabetic group. Increased zonulin and LPS levels and the positive correlation between these levels during the prediabetic period although non significant suggests onset of intestinal permeability.ConclusionsDuring acute hyperglycemia in prediabetic patients, up-regulation of zonulin and LPS may affect intestinal function. The intestines may play a key role in up-regulation of glucose and the pathogenesis of diabetes. 相似文献
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Clinical and Radiographic Evaluation of Marginal Bone Changes around Platform‐Switching Implants Placed in Crestal or Subcrestal Positions: A Randomized Controlled Clinical Trial 下载免费PDF全文
7.
Popović M Smiljanić K Dobutović B Syrovets T Simmet T Isenović ER 《Journal of thrombosis and thrombolysis》2012,33(2):160-172
Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits
thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates
a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites, and at the same time promotes
coagulation, thrombin generation, and fibrin deposition in an attempt to close the wound. Life-long persistent infection with
human cytomegalovirus (HCMV) has been associated with atherosclerosis. In vivo studies have revealed that HCMV infection of
the vessel wall affects various cells including monocytes/macrophages, smooth muscle cells (SMCs) and endothelial cells (ECs).
HCMV-infected SMCs within vascular lesions display enhanced proliferation and impaired apoptosis, which contribute to intima-media thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas
ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following
the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving
nuclear factor κB, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth
factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the
intima of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection
induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages.
As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between
infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation
linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the
molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein
complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production
of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombin-dependent
proinflammatory cell activation. This review summarizes the existing evidence on the role of HCMV in vascular inflammation. 相似文献
8.
Activation induced cell death (AICD) via Fas/FasL is the primary homeostatic molecular mechanism employed by the immune system to control activated T-cell responses and promote tolerance to self-antigens. We herein investigated the ability of a novel multimeric form of FasL chimeric with streptavidin (SA-FasL) having potent apoptotic activity to induce apoptosis in diabetogenic T cells and modulate insulin-dependent type 1 diabetes (IDDM) in an adoptive transfer model. Diabetogenic splenocytes from NOD/Lt females were co-cultured in vitro with SA-FasL, SA control protein, or alone without protein, and adoptively transferred into NOD/Lt-Rag1(null) recipients for diabetes development. All animals receiving control (Alone: n=16 or SA: n=17) cells developed diabetes on average by 6 weeks, whereas animals receiving SA-FasL-treated (n=25) cells exhibited significantly delayed progression (p<.001) and decreased incidence (70%). This effect was associated with an increase in CD4(+)CD25(+) T cells and correlated with FoxP3 expression in pancreatic lymph nodes. Extracorporeal treatment of peripheral blood lymphocytes using SA-FasL during disease onset represents a novel approach that may alter the ability of pathogenic T cells to mediate diabetes and have therapeutic utility in clinical management of IDDM. 相似文献
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Kyle B. Woodward Hong Zhao Pradeep Shrestha Lalit Batra Min Tan Orlando Grimany‐Nuno Laura Bandura‐Morgan Nadir Askenasy Haval Shirwan Esma S. Yolcu 《American journal of transplantation》2020,20(5):1285-1295
We have previously shown that pancreatic islets engineered to transiently display a modified form of FasL protein (SA‐FasL) on their surface survive indefinitely in allogeneic recipients without a need for chronic immunosuppression. Mechanisms that confer long‐term protection to allograft are yet to be elucidated. We herein demonstrated that immune protection evolves in two distinct phases; induction and maintenance. SA‐FasL‐engineered allogeneic islets survived indefinitely and conferred protection to a second set of donor‐matched, but not third‐party, unmanipulated islet grafts simultaneously transplanted under the contralateral kidney capsule. Protection at the induction phase involved a reduction in the frequency of proliferating alloreactive T cells in the graft‐draining lymph nodes, and required phagocytes and TGF‐β. At the maintenance phase, immune protection evolved into graft site‐restricted immune privilege as the destruction of long‐surviving SA‐FasL‐islet grafts by streptozotocin followed by the transplantation of a second set of unmanipulated islet grafts into the same site from the donor, but not third party, resulted in indefinite survival. The induced immune privilege required both CD4+CD25+Foxp3+ Treg cells and persistent presence of donor antigens. Engineering cell and tissue surfaces with SA‐FasL protein provides a practical, efficient, and safe means of localized immunomodulation with important implications for autoimmunity and transplantation. 相似文献
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