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Coptis japonica root extract induces apoptosis through caspase3 activation in SNU-668 human gastric cancer cells 总被引:7,自引:0,他引:7
Park HJ Kim YJ Leem K Park SJ Seo JC Kim HK Chung JH 《Phytotherapy research : PTR》2005,19(3):189-192
Apoptosis-modulating approaches offer an attractive opportunity for therapeutic use for many tumors. We investigated the effects of the roots of Coptis japonica var. dissecta (Ranunculaceae) on human gastric cancer cells, SNU-668. The cytotoxicity of Coptis japonica at 100 microg/ml (methanol extract) by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was 13.89 +/- 1.91% of control value. Considering the features by 4,6-diamidino-2-phenylindole (DAPI) staining and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay, it was confirmed that the death of SNU-668 cells was due to apoptosis. In the apoptosis-regulating genes, BCL2 expression was diminished out, whereas BAX and CASP3 expressions were increased, compared with control. Furthermore, the activity of caspase3 was significantly increased by Coptis japonica treatment. These results suggest that Coptis japonica could induce apoptotic anticancer effect through caspase3 activation on SNU-668 human gastric cancer cells. 相似文献
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Spinal cord injury (SCI) often leads to central pain syndrome including hyperalgesia to mechanical stimulation. Since there is evidence that nerve growth factor (NGF) contributes to pain-related behaviors, we wished to determine if anti-NGF might inhibit abnormal somatosensory behaviors that develop following SCI in rats. SCI was performed in male Sprague-Dawley rats by T13 spinal hemisection. After spinal hemisection, animals were untreated or treated daily with anti-NGF or saline intraperitoneally for 10 days. In groups of both hemisection only and hemisection with saline treatment, mechanical hyperalgesia developed in both hindlimbs, as evidenced by a decrease in paw withdrawal thresholds. Mechanical responsiveness of wide dynamic range (WDR) neurons on both sides of spinal cord also increased. The anti-NGF treated group demonstrated significant suppression of both mechanical hyperalgesia and increased WDR neuronal responsiveness. These results indicate that anti-NGF prevents the development of abnormal somatosensory behavior and suggest a potential pre-emptive analgesic treatment for central pain. 相似文献
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We investigated the adrenergic sensitivity of afferent fibers in the L4 dorsal roots of rats with a unilateral ligation of the L5-L6 spinal nerves. About 12% of nociceptive fibers on the affected side were excited by sympathetic stimulation or by intra-arterial injection of norepinephrine which did not affect A beta-fiber activity. Sympathetic excitation of nociceptive fibers was suppressed by alpha 1-antagonist prazosin, while it was unaffected by alpha 2-antagonist yohimbine. Most of these fibers were excited by intra-arterial injection of alpha 1-agonist phenylephrine, without being affected by an injection of alpha 2-agonist clonidine. Sympathetic excitation was blocked by lidocaine applied near the receptive fields of recorded fibers. The results suggested that some nociceptors remaining intact after partial nerve injury become sensitive to sympathetic activity by the mediation of alpha 1-adrenoceptors in the peripheral endings. 相似文献
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Yea-Hyun Leem Jin-Sun Park Jung-Eun Park Do-Yeon Kim Hee-Sun Kim 《Biomolecules & therapeutics.》2021,29(3):295
Microglial priming is the process of microglial proliferation and activation in response to neurodegeneration and abnormal protein accumulation. Priming makes microglia susceptible to secondary inflammatory stimuli and causes exaggerated inflammatory responses. In the present study, we established a microglial priming model in mice by administering a single injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 20 mg/kg). MPTP induced microglial activation without dopaminergic degeneration; however, subsequent treatment with a sub-toxic dose of lipopolysaccharides (LPS) induced an amplified inflammatory response and caused nigrostriatal dopaminergic degeneration. These pathological and inflammatory changes, including microglial activation and dopaminergic cell loss in the substantia nigra (SN) area were reversed by papaverine (PAP) administration. In addition, MPTP/LPS enhanced interleukin-1β (IL-1β) expression and processing via nod-like receptor protein 3 (NLRP3) inflammasome activation in the SN region of mice. However, PAP treatment suppressed inflammasome activation and subsequent IL-1β maturation. Moreover, PAP inhibited nuclear factor-κB (NF-κB) and enhanced cAMP-response element binding protein (CREB) activity in the SN of MPTP/LPS mice. These results suggest that PAP inhibits the activation of NLRP3 inflammasome by modulating NF-κB and CREB signaling pathways, which results in reduced microglial activation and neuronal cell death. Thus, PAP may be a potential candidate for the treatment of Parkinsons’s disease, which is aggravated by systemic inflammation. 相似文献
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Hyun Hwang‐Bo Won Sup Lee Arulkumar Nagappan Hong Jae Kim Radha Panchanathan Cheol Park Seong‐Hwan Chang Nam Deuk Kim Sun‐Hee Leem Young‐Chae Chang Taeg Kyu Kwon Jae Hun Cheong Gon Sup Kim Jin‐Myung Jung Sung Chul Shin Soon Chan Hong Yung Hyun Choi 《Phytotherapy research : PTR》2019,33(5):1384-1393
Evidence suggests that auranofin (AF) exhibits anticancer activity by inhibiting thioredoxin reductase (TrxR). Here, in this study, we have investigated the synergistic effects of AF and morin and their mechanism for the anticancer effects focusing on apoptosis in Hep3B human hepatocellular carcinoma cells. We assessed the anticancer activities by annexin V/PI double staining, caspase, and TrxR activity assay. Morin enhances the inhibitory effects on TrxR activity of AF as well as reducing cell viability. Annexin V/PI double staining revealed that morin/AF cotreatment induced apoptotic cell death. Morin enhances AF‐induced mitochondrial membrane potential (ΔΨm) loss and cytochrome c release. Further, morin/AF cotreatment upregulated death receptor DR4/DR5, modulated Bcl‐2 family members (upregulation of Bax and downregulation of Bcl‐2), and activated caspase‐3, ‐8, and ‐9. Morin also enhances AF‐induced reactive oxygen species (ROS) generation. The anticancer effects results from caspase‐dependent apoptosis, which was triggered via extrinsic pathway by upregulating TRAIL receptors (DR4/DR5) and enhanced via intrinsic pathway by modulating Bcl‐2 and inhibitor of apoptosis protein family members. These are related to ROS generation. In conclusion, this study provides evidence that morin can enhance the anticancer activity of AF in Hep3B human hepatocellular carcinoma cells, indicating that its combination could be an alternative treatment strategy for the hepatocellular carcinoma. 相似文献
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Ju Yeon Ban Kyung Leem Yoon Su Kang Kim Sungwook Kang Joo-Ho Chung 《Pediatric cardiology》2009,30(3):331-335
Kawasaki disease (KD) is an acute febrile vasculitis that predominantly affects infants and young children. Tissue inhibitors
of matrix metalloproteinases (TIMPs) comprise a family of four members, of which TIMP4 is characterized by its restriction
to cardiovascular structures. In KD pathophysiology, TIMP4 is considered to be involved in the development of coronary artery
lesions (CALs). Therefore, this study investigated single-nucleotide polymorphisms (SNPs) of the TIMP4 gene as risk factors
for KD with CALs in Korean children. To observe this association, two SNPs (rs3755724, -55C/T, promoter; rs17035945, 3′-untranslated
region) were genotyped in TIMP4 using direct sequencing. There were no SNPs in the coding region of TIMP4, and two SNPs were
selected in the exon and promoter regions. This study recruited 250 control and 101 KD subjects. For data analysis, SNPStats,
SNPAnalyzer, and Helixtree programs were used. These SNPs were not associated with KD. However, in the recessive model, a
significant association was found between rs3755724 and the development of CALs in KD (P = 0.02; odds ratio, 0.31; 95% confidence interval, 0.11–0.85). The minor allele (C) of rs3755724 showed the susceptibility
of CALs to risk in KD patients. These results suggest that TIMP4 is related to the development of KD with CALs in Korean children.
Ju Yeon Ban and Kyung Leem Yoon—both authors contributed equally to this article. 相似文献
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