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61.
Hamid S Lim KP Zain RB Ismail SM Lau SH Mustafa WM Abraham MT Nam NA Teo SH Cheong SC 《International journal of molecular medicine》2007,19(3):453-460
We have established 3 cell lines ORL-48, -115 and -136 from surgically resected specimens obtained from untreated primary human oral squamous cell carcinomas of the oral cavity. The in vitro growth characteristics, epithelial origin, in vitro anchorage independency, human papilloma-virus (HPV) infection, microsatellite instability status, karyotype and the status of various cell cycle regulators and gatekeepers of these cell lines were investigated. All 3 cell lines grew as monolayers with doubling times ranging between 26.4 and 40.8 h and were immortal. Karyotyping confirmed that these cell lines were of human origin with multiple random losses and gains of entire chromosomes and regions of chromosomes. Immunohistochemistry staining of cytokeratins confirmed the epithelial origin of these cell lines, and the low degree of anchorage independency expressed by these cell lines suggests non-transformed phenotypes. Genetic analysis identified mutations in the p53 gene in all cell lines and hypermethylation of p16INK4a in ORL-48 and -136. Analysis of MDM2 and EGFR expression indicated MDM2 overexpression in ORL-48 and EGFR overexpression in ORL-136 in comparison to the protein levels in normal oral keratinocytes. Analysis of the BAT-26 polyadenine repeat sequence and MLH-1 and MSH-2 repair enzymes demonstrated that all 3 cell lines were microsatellite stable. The role of HPV in driving carcinogenesis in these tumours was negated by the absence of HPV. Finally, analysis of the tissues from which these cell lines were derived indicated that the cell lines were genetically representative of the tumours, and, therefore, are useful tools in the understanding of the molecular changes associated with oral cancers. 相似文献
62.
Malik Nauman Geraghty Benjamin Dasgupta Archya Maralani Pejman Jabehdar Sandhu Michael Detsky Jay Tseng Chia-Lin Soliman Hany Myrehaug Sten Husain Zain Perry James Lau Angus Sahgal Arjun Czarnota Gregory J. 《Journal of neuro-oncology》2021,151(2):181-191
Journal of Neuro-Oncology - Primary malignant spinal astrocytomas present rare oncological entities with limited median survival and rapid neurological deterioration. Evidence on surgical therapy,... 相似文献
63.
James Stewart Arjun Sahgal Young Lee Hany Soliman Chia-Lin Tseng Jay Detsky Zain Husain Ling Ho Sunit Das Pejman Jabehdar Maralani Nir Lipsman Greg Stanisz James Perry Hanbo Chen Eshetu G. Atenafu Mikki Campbell Angus Z. Lau Mark Ruschin Sten Myrehaug 《International journal of radiation oncology, biology, physics》2021,109(3):736-746
64.
65.
Oleg Butovsky PhD Mark P. Jedrychowski PhD Ron Cialic PhD MD Susanne Krasemann PhD Gopal Murugaiyan PhD Zain Fanek BSc David J. Greco BSc Pauline M. Wu BSc Camille E. Doykan BSc Olga Kiner MSc Robert J. Lawson BSc Matthew P. Frosch MD Nathalie Pochet PhD Rachid El Fatimy PhD Anna M. Krichevsky PhD Steven P. Gygi PhD Hans Lassmann MD James Berry MD Merit E. Cudkowicz MD Howard L. Weiner MD 《Annals of neurology》2015,77(1):75-99
66.
Jeyanthi Suppiah Rozainanee Mohd Zain Norazlah Bahari Salbiah Haji Nawi Zainah Saat 《Hepatitis monthly》2015,15(10)
Background:
Precore stop codon (G1896A) mutation is one of the commonest mutations found in patients with chronic hepatitis B. However, over the years, this mutation was not reported much in Malaysia.Objectives:
We therefore investigated the presence of G1896A mutation in Malaysian population and its association with HBeAg status, clinical stage, hepatitis B virus (HBV) genotype and e-seroconversion rate.Patients and Methods:
Serum samples from 93 patients confirmed as hepatitis B carriers were collected for molecular assay. The whole genome of HBV was amplified by polymerase chain reaction and directly sequenced. The precore and basal core promoter regions were analyzed for presence of mutations.Results:
The most commonly observed mutation in the precore region was C1858T with 64.5% prevalence. The precore mutation of interest (G1896A) was identified in 25.8% of isolates. The basal core promoter mutations detected were A1762T-G1764A (26.9%), C1653T (8.6%), A1752G (10.8%) and C1766T (2.2%). No significant association was observed between G1896A mutation and HBeAg-negativity. Nonetheless, G1896A was highly prevalent among HBV genotype B. Clinical association revealed that subjects with G1896A mutations were mainly detected in asymptomatic chronic hepatitis B (58.3%) and liver cirrhosis (41.7%). One subject was diagnosed with fulminant hepatitis (4.2%) and 8.3% had hepatocellular carcinoma (HCC).Conclusions:
Our data suggested an intermediate prevalence of G1896A mutation among Malaysian hepatitis B carriers. The stop codon mutation has a significant association with genotype B and patients with chronic hepatitis B and liver cirrhosis. 相似文献67.
68.
Activation of microglia by retroviral infection correlates with transient clearance of prions from the brain but does not change incubation time 下载免费PDF全文
Christiane Muth Katharina Schröck Charlotte Madore Kristin Hartmann Zain Fanek Oleg Butovsky Markus Glatzel Susanne Krasemann 《Brain pathology (Zurich, Switzerland)》2017,27(5):590-602
Prion diseases are fatal transmissible diseases, where conversion of the endogenous prion protein (PrPC) into a misfolded isoform (PrPSc) leads to neurodegeneration. Microglia, the immune cells of the brain, are activated in neurodegenerative disorders including prion diseases; however, their impact on prion disease pathophysiology is unclear with both beneficial PrPSc‐clearing and detrimental potentially neurotoxic effects. Moreover, monocytes entering the brain from the periphery during disease course might add to disease pathophysiology. Here, the degree of microglia activation in the brain of prion infected mice with and without an additional intraperitoneal retrovirus infection was studied. Peripheral murine retrovirus infection leads to activation of parenchymal microglia without recruitment of monocytes. This activation correlated with transient clearance or delay in accumulation of infectious prions specifically from the brain at early time points in the diseases course. Microglia expression profiling showed upregulation of genes involved in protein degradation coinciding with prion clearance. This enforces a concept where microglia act beneficial in prion disease if adequately activated. Once microglia activation has ceased, prion disease reemerges leading to disease kinetics undistinguishable from the situation in prion‐only infected mice. This might be caused by the loss of microglial homeostatic function at clinical prion disease. 相似文献
69.
Romidepsin in peripheral and cutaneous T‐cell lymphoma: mechanistic implications from clinical and correlative data 下载免费PDF全文
Susan E. Bates Robin Eisch Alexander Ling Douglas Rosing Maria Turner Stefania Pittaluga H. Miles Prince Mark H. Kirschbaum Steven L. Allen Jasmine Zain Larisa J. Geskin David Joske Leslie Popplewell Edward W. Cowen Elaine S. Jaffe Jean Nichols Sally Kennedy Seth M. Steinberg David J. Liewehr Louise C. Showe Caryn Steakley John Wright Tito Fojo Thomas Litman Richard L. Piekarz 《British journal of haematology》2015,170(1):96-109
Romidepsin is an epigenetic agent approved for the treatment of patients with cutaneous or peripheral T‐cell lymphoma (CTCL and PTCL). Here we report data in all patients treated on the National Cancer Institute 1312 trial, demonstrating long‐term disease control and the ability to retreat patients relapsing off‐therapy. In all, 84 patients with CTCL and 47 with PTCL were enrolled. Responses occurred early, were clinically meaningful and of very long duration in some cases. Notably, patients with PTCL receiving romidepsin as third‐line therapy or later had a comparable response rate (32%) of similar duration as the total population (38%). Eight patients had treatment breaks of 3·5 months to 10 years; in four of six patients, re‐initiation of treatment led to clear benefit. Safety data show slightly greater haematological and constitutional toxicity in PTCL. cDNA microarray studies show unique individual gene expression profiles, minimal overlap between patients, and both induction and repression of gene expression that reversed within 24 h. These data argue against cell death occurring as a result of an epigenetics‐mediated gene induction programme. Together this work supports the safety and activity of romidepsin in T‐cell lymphoma, but suggests a complex mechanism of action. 相似文献
70.
Ryan M. Mizumoto Faris Z. Jamjoom Burak Yilmaz 《The Journal of prosthetic dentistry》2018,119(4):552-559