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71.
Darroudi Susan Saberi-Karimian Maryam Tayefi Maryam Tayefi Batool Khashyarmanesh Zahra Fereydouni Narges Haghighi Hamideh Moalemzadeh Mahmoudi Ali Asghar Kharazmi-Khorassani Jasmine Gonoodi Kayhan Esmaeili Habibolah Mohammadpour Amir Hooshang Ferns Gordon A. Ghayour-Mobarhan Majid 《Biological trace element research》2019,190(1):38-44
Biological Trace Element Research - The prevalence of hypertension (HTN) is increasing globally. It has been shown that there is an association between micronutrient deficiency and HTN. In the... 相似文献
72.
Amir Afkham Shadi Eghbal-Fard Hanieh Heydarlou Ramyar Azizi Leili Aghebati-Maleki Mehdi Yousefi 《Journal of cellular physiology》2019,234(3):2229-2240
Toll-like receptors (TLRs) are innate immune cells receptors. They are expressed on leukocytes, epithelial cells, and more particularly on placental immune cells and chorion trophoblast. Upregulation of innate immune response occurs during normal pregnancy, but its excessive activity is involved in the pathology of pregnancy complications including pregnancy-induced hypertension and pre-eclampsia (PE). The recent studies about the overmuch inflammatory responses and aberrant placentation are associated with increased expression of TLRs in PE patients. This review has tried to focus on the relationship between some activities of TLRs and the risk of preeclampsia development. 相似文献
73.
Reza Ranjbar Mojtaba Shafiee AmirReza Hesari Gordon A. Ferns Faezeh Ghasemi Amir Avan 《Journal of cellular physiology》2019,234(3):2277-2295
Inflammation is a normal part of the immune response to injury or infection but its dysregulation promotes the development of inflammatory diseases, which cause considerable human suffering. Nonsteroidal anti-inflammatory agents are the most commonly prescribed agents for the treatment of inflammatory diseases, but they are accompanied by a broad range of side effects, including gastrointestinal and cardiovascular events. The renin–angiotensin system (RAS) is traditionally known for its role in blood pressure regulation. However, there is increasing evidence that RAS signaling is also involved in the inflammatory response associated with several disease states. Angiotensin II increases blood pressure by binding to angiotensin type 1 (AT1) receptor, and direct renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors and AT1 receptor blockers (ARBs) are clinically used as antihypertensive agents. Recent data suggest that these drugs also have anti-inflammatory effects. Therefore, this review summarizes these recent findings for the efficacy of two of the most widely used antihypertensive drug classes, ACE inhibitors and ARBs, to reduce or treat inflammatory diseases such as atherosclerosis, arthritis, steatohepatitis, colitis, pancreatitis, and nephritis. 相似文献
74.
Mehran Pashirzad Mojtaba Shafiee Majid Khazaei Hamid Fiuji Mikhail Ryzhikov Saman Soleimanpour AmirReza Hesari Amir Avan Seyed Mahdi Hassanian 《Journal of cellular physiology》2019,234(2):1237-1247
Prostate cancer is a major cause of cancer-related death in males. Wnt/β-catenin signaling plays a critical role in the pathogenesis of this disease by regulating angiogenesis, drug resistance, cell proliferation, and apoptosis. Suppression of Wnt canonical or noncanonical signaling pathways via Wnt biological or pharmacological antagonists is a potentially novel therapeutic approach for patients with prostate cancer. This review summarizes the role of Wnt signaling inhibitors in the pathogenesis of prostate cancer for a better understanding and hence a better management of this disease. 相似文献
75.
Mohammad Khabbaz Shirazi Asaad Azarnezhad Mohammad Foad Abazari Mansour Poorebrahim Pegah Ghoraeian Nima Sanadgol Hanieh Bokharaie Sahar Heydari Amin Abbasi Sahra Kabiri Maryam Nouri Aleagha Seyed Ehsan Enderami Amir Savar Dashtaki Hassan Askari 《Journal of cellular physiology》2019,234(7):11411-11423
The interplay between H2S and nitric oxide (NO) is thought to contribute to renal functions. The current study was designed to assess the role of NO in mediating the renoprotective effects of hydrogen sulfide in the 5/6 nephrectomy (5/6 Nx) animal model. Forty rats were randomly assigned to 5 experimental groups: (a) Sham; (b) 5/6 Nx; (c) 5/6Nx+sodium hydrosulfide-a donor of H 2S, (5/6Nx+sodium hydrosulfide [NaHS]); (d) 5/6Nx+NaHS+ L -NAME (a nonspecific nitric oxide synthase [NOS] inhibitor); (e) 5/6Nx+NaHS+aminoguanidine (a selective inhibitor of inducible NOS [iNOS]). Twelve weeks after 5/6 Nx, we assessed the expressions of iNOS and endothelial NOS (eNOS), oxidative/antioxidant status, renal fibrosis, urine N-acetyl-b-glucosaminidase (NAG) activity as the markers of kidney injury and various markers of apoptosis, inflammation, remodeling, and autophagy. NaHS treatment protected the animals against chronic kidney injury as depicted by improved oxidative/antioxidant status, reduced apoptosis, and autophagy and attenuated messenger RNA (mRNA) expression of genes associated with inflammation, remodeling, and NAG activity. Eight weeks Nω-nitro-l-arginine methyl ester ( L -NAME) administration reduced the protective effects of hydrogen sulfide. In contrast, aminoguanidine augmented the beneficial effects of hydrogen sulfide. Our finding revealed some fascinating interactions between NO and H 2S in the kidney. Moreover, the study suggests that NO, in an isoform-dependent manner, can exert renoprotective effects in 5/6 Nx model of CKD. 相似文献
76.
77.
Saeed Noorolyai Ahad Mokhtarzadeh Elham Baghbani Milad Asadi Amir Baghbanzadeh Kojabad Mahsa Maleki Mogaddam Behzad Baradaran 《Journal of cellular physiology》2019,234(5):5664-5673
In recent decades, cancer has been one of the most important concerns of the human community, which affects human life from many different ways, such as breast, lung, colorectal, prostate, and other cancers. Colorectal cancer is one of the most commonly diagnosed cancers in the world that has recently been introduced as the third leading cause of cancer deaths in the world. microRNAs have a very crucial role in tumorgenesis and prevention of cancer, which plays a significant role with influencing various factors through different signaling pathways. Phosphoinositide 3 (PI3)-kinase/AKT is one of the most important signaling pathways involved in the control and growth of tumor in colorectal cancer, through important proteins of this pathway, such as PTEN and AKT, that they can perform specific influence on this process. Our effort in this study is to collect microRNAs that act as tumor suppressors and oncomirs in this cancer through PI3-kinase/AKT signaling pathway. 相似文献
78.
Atena Soleimani Mohammad Jalili-Nik Amir Avan Gordon A. Ferns Majid Khazaei Seyed Mahdi Hassanian 《Journal of cellular physiology》2019,234(6):8241-8248
Heat-shock protein 27 (HSP27) is a chaperone molecule that plays a critical role in the refolding and activity of several proteins responsible for cancer cell drug toxicity. Upregulation of HSP27 is associated with decreased drug sensitivity as well as poorer survival in gastrointestinal (GI) malignancies. It is, therefore, possible that HSP27 may be of value in the assessment of prognostic and therapeutic efficacy in the treatment of GI cancers. Pharmacological and biological inhibitors of HSP27 enhance tumor cell chemosensitivity. This review summarizes the potential role of HSP27 in chemotherapy drug resistance and the therapeutic potential of HSP27 inhibitors as a novel strategy in the treatment of GI cancers. 相似文献
79.
Zehsaz Farzad Safabakhsh Amir Hamzeh Farhangi Negin Keynezhad Narmin Monfaredan Amir Ghahramani Mehri 《Molecular biology reports》2019,46(2):1835-1843
Molecular Biology Reports - We studied to ascertain whether the ACE and/or CKMM genotypes independently influence the baseline level of some sport performances in 613 inactive male adolescents... 相似文献
80.
Azam Khedri Shahnaz Khaghani Alireza Kheirollah Hossein Babaahmadi-Rezaei Amir Shadboorestan Mohammad Zangooei Hajar Shokri Afra Reza Meshkani Mohammad Hossein Ghahremani 《Journal of cellular biochemistry》2019,120(6):9125-9137
Fragile histidine trail (FHIT) is a tumor suppressor in response to DNA damage which has been deleted in various tumors. However, the signaling mechanisms and interactions of FHIT with regard to apoptotic proteins including p53 and p38 in the DNA damage-induced apoptosis are not well described. In the present study, we used etoposide-induced DNA damage in MCF-7 as a model to address these crosstalks. The time course study showed that the expression of FHIT, p53, and p38MAPK started after 1 hour following etoposide treatment. FHIT overexpression led to increase p53 expression, p38 activation, and augmented apoptosis following etoposide-induced DNA damage compared to wild-type cells. However, FHIT knockdown blocked p53 expression, delayed p38 activation, and completely inhibited etoposide-induced apoptosis. Inhibition of p38 activity prevented induction of p53, FHIT, and apoptosis in this model. Thus, activation of p38 upon etoposide treatment leads to increase in FHIT and p53 expression. In p53 knockdown MCF-7, the FHIT induction was hampered but p38 activation was induced in lower doses of etoposide. In p53 knockdown cells, inhibition of p38 induced FHIT expression and apoptosis. Our data demonstrated that the exposure of MCF-7 cells to etoposide increases apoptosis through a mechanism involving the activation of the p38-FHIT-p53 pathway. Moreover, our findings suggest signaling interaction for these pathways may represent a promising therapy for breast cancer. 相似文献