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排序方式: 共有117条查询结果,搜索用时 78 毫秒
1.
Mitani Genya Takagaki Tomonori Hamahashi Kosuke Serigano Kenji Nakamura Yutaka Sato Masato Mochida Joji 《Journal of orthopaedic surgery and research》2015,10(1):1-6
Growth factors such as nerve growth factor (NGF) and insulin-like growth factor-1 (IGF-1) have been shown to play a role in the healing process of nerve injury. Recent researches have also shown that oxytocin administration activates these growth factors of importance for the healing of nerve tissue. The objective of the present study was to evaluate the effects of oxytocin on peripheral nerve regeneration in rats. Twenty-four male Sprague-Dawley rats were underwent transection damage model on the right sciatic nerve and defective damage model on the left sciatic nerve. The animals were assigned to one of two groups: control group or treatment group (received 80 mg/kg oxytocin intraperitoneally for 12 weeks). The sciatic nerve was examined, both functionally (on the basis of climbing platform test) and histologically (on the basis of axon count), 3, 6, 9, and 12 weeks after the injury. Also, stereomicroscopic and electrophysiological evaluations were carried out. Significantly greater improvements in electrophysiological recordings and improved functional outcome measures were presented in the treatment group at 12-week follow-up. Stereomicroscopic examinations disclosed prominent increases in vascularization on proximal cut edges in the oxytocin group in comparison with the control group. Higher axon counts were also found in this group. Intraperitoneal oxytocin administration resulted in accelerated functional, histological, and electrophysiological recovery after different sciatic injury models in rats. 相似文献
2.
Case series of 17 patients with cholangiocarcinoma among young adult workers of a printing company in Japan
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Shoji Kubo Yasuni Nakanuma Shigekazu Takemura Chikaharu Sakata Yorihisa Urata Akinori Nozawa Takayoshi Nishioka Masahiko Kinoshita Genya Hamano Hiroaki Terajima Gorou Tachiyama Yuji Matsumura Terumasa Yamada Hiromu Tanaka Shoji Nakamori Akira Arimoto Norifumi Kawada Masahiro Fujikawa Hiromitsu Fujishima Yasuhiko Sugawara Shogo Tanaka Hideyoshi Toyokawa Yuko Kuwae Masahiko Ohsawa Shinichiro Uehara Kyoko Kogawa Sato Tomoshige Hayashi Ginji Endo 《Journal of hepato-biliary-pancreatic sciences》2014,21(7):479-488
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Genya Mitani Yutaka Nakamura Takashi Miura Yuhei Harada Masato Sato Masahiko Watanabe 《Journal of orthopaedic science》2018,23(6):1056-1062
Background
Locomotive syndrome (LS) includes disorders of the musculoskeletal system and is a high-risk condition that requires nursing care. We included an examination of locomotive function in specific health checkups to investigate the relationship between LS risk and the muscle strengths. The purpose of this study was to determine the distribution of LS and the relationship between LS and metabolic syndrome (MetS).Methods
Among 2695 participants who undertook a specific health checkup, 790 received a locomotive examination (302 men and 488 women; mean age, 65.9 years). Data for MetS components were measured in the specific health checkup. Data about the locomotive examination were obtained from five tests: the two-step test, stand-up test, 25-question Geriatric Locomotive Function Scale, and measurement of lower limb muscular strength and grip strength.Results
The MetS components did not differ according to LS risk level in men. In women, body weight, body mass index, and abdominal circumference were significantly lower in the non-LS group than in the LS risk level 1 or 2 groups. The ratio of lower limb muscular strength to body weight differed significantly between all risk groups in men and women. In women, lower limb muscular strength was significantly higher in those at risk of both LS and MetS (double-risk group) than in the LS-only group. In women, the ratio of lower limb muscular strength to body weight was significantly lower in the double-risk group than in the LS-only group.Conclusions
Adding a locomotive examination to the specific health checkup may be useful for identifying people at risk of LS or MetS. The prevalence rates of LS and MetS correlate positively in women. The ratio of lower limb muscular strength to body weight might be a better index of locomotor dysfunction than lower limb muscular strength alone. 相似文献6.
7.
The brain's intrinsic immune system consists of glial cells that produce cytokines and chemokines in response to stimulation with cytomegalovirus (CMV). The present experiments were undertaken to determine whether this intrinsic glial cell response alone is sufficient to control CMV infection of the central nervous system (CNS) or whether effector cells from the somatic immune system are also required. Following stereotactic, intracerebroventricular (icv), injection of murine cytomegalovirus (MCMV) into immunocompetent (C.B-17) mice, viral spread in the brain was limited to the cells of the ventricular walls and the infection was resolved by 10 days post infection (p.i.). In contrast, icv infection of immunodeficient (C.B-17 SCID/bg) mice resulted in viral spread from the ventricles throughout the brain parenchyma and these mice succumbed to lethal disease. Adoptive transfer of total splenocytes from major histocompatibility complex (MHC)-matched, MCMV-primed animals restricted intracerebral viral infection to the periventricular cells and reduced levels of reporter gene expression from the viral genome. Peripheral immune cell transfer also protected immunodeficient animals from lethal disease. Depletion of Thy 1.2(+) cells from MCMV-primed splenocytes abolished the protective effect of adoptive transfer. Viral expression was found to be fourfold greater in the brains of animals given Thy 1.2-depleted splenocytes than from those receiving total undepleted cells. As MCMV infection proceeded in the brains of immunodeficient mice, levels of the T-cell chemoattractants CXCL10 and CCL2 remained elevated, whereas CXCL10 levels waned in the brains of animals receiving transferred splenocytes. Taken together, these results demonstrate the ability of T lymphocytes to restrict intracerebral viral spread and indicate that intrinsic glial cell responses alone are insufficient to control MCMV brain infection. 相似文献
8.
Diazepam inhibits HIV-1 Tat-induced migration of human microglia 总被引:1,自引:0,他引:1
Lokensgard JR Hu S Hegg CC Thayer SA Gekker G Peterson PK 《Journal of neurovirology》2001,7(5):481-486
During HIV-1 encephalitis, the chemotaxis-inducing activity of Tat may enhance the viral life cycle through recruitment of additional susceptible microglial cells to foci of infection. Benzodiazepines (BDZs) readily penetrate the blood-brain barrier and are known to possess anti-inflammatory properties. Pretreatment of human microglial cells with peripheral (Ro5-4864) and mixed (diazepam), but not central (clonazepam), benzodiazepine receptor ligands was found to potently suppress HIV-1 Tat-induced chemotaxis. Application of Tat to microglial cells evokes an increase in intracellular calcium concentration ([Ca(2+)]i) that rapidly desensitizes the cells. Diazepam's inhibitory effect was associated with its ability to block Tat-induced [Ca(2+)]i mobilization. These data support the notion that through their effects on microglia, peripheral BDZ receptor ligands could alter the neuropathogenesis of HIV-1. 相似文献
9.
The pathogenesis of human immunodeficiency virus type 1 (HIV-1) encephalopathy has been associated with multiple factors including the neurotoxin quinolinate (an endogenous N-methyl-D-aspartate [NMDA] receptor ligand) and viral proteins. The kappa opioid receptor (KOR) agonist U50,488 recently has been shown to inhibit HIV-1 p24 antigen production in acutely infected microglial cell cultures. Using primary human brain cell cultures in the present study, we found that U50,488 also suppressed in a dose-dependent manner the neurotoxicity mediated by supernatants derived from HIV-1-infected microglia. This neuroprotective effect of U50,488 was blocked by the KOR selective antagonist nor-binaltorphimine. The neurotoxic activity of the supernatants from HIV-1-infected microglia was blocked by the NMDA receptor antagonists 2-amino-5-phosphonovalerate and MK-801. HIV-1 infection of microglial cell cultures induced the release of quinolinate, and U50,488 dose-dependently suppressed quinolinate release by infected microglial cell cultures with a corresponding inhibition of HIV-1 p24 antigen levels. These findings suggest that the kappa opioid ligand U50,488 may have therapeutic potential in HIV-1 encephalopathy by attenuating microglial cell production of the neurotoxin quinolinate and viral proteins. 相似文献
10.
Opioid-mediated suppression of interferon-gamma production by cultured peripheral blood mononuclear cells 总被引:7,自引:0,他引:7
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P K Peterson B Sharp G Gekker C Brummitt W F Keane 《The Journal of clinical investigation》1987,80(3):824-831
Mounting evidence suggests that opiate addiction and stress are associated with impaired cell-mediated immunity. We tested the hypothesis that morphine and the endogenous opioid beta-endorphin (beta-END), a pituitary peptide released in increased concentrations during stress, can suppress the production of the key macrophage-activating lymphokine interferon-gamma (IFN-gamma) by cultured human peripheral blood mononuclear cells (PBMNC). Using a radioimmunoassay to measure IFN-gamma, we found that exposure of PBMNC to biologically relevant concentrations of both opioids significantly inhibited IFN-gamma generation by cells stimulated with concanavalin A and varicella zoster virus. Studies of the mechanism of suppression revealed (a) a classical opioid receptor is involved (suppression was antagonized by naloxone and was specific for the NH2 terminus of beta-END), (b) monocytes are the primary target cell for opioids (monocyte-depleted lymphocyte preparations showed little suppression), and (c) reactive oxygen intermediates (ROI) and prostaglandin E2 are important mediators (scavengers of ROI and indomethacin eliminated the suppression). Based on these findings we suggest that opioid-triggered release of inhibitory monocyte metabolites may play a role in the immunodeficiency associated with narcotic addiction and stress. 相似文献