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101.
Mina Cho Jeonghyun Kang Im-kyung Kim Kang Young Lee Seung-Kook Sohn 《Yonsei medical journal》2014,55(6):1611-1616
Purpose
Analyses of risk factors associated with surgical site infections (SSIs) after laparoscopic appendectomy (LA) have been limited. Especially, the association of an underweight body mass index (BMI) with SSIs has not been clearly defined. This study aimed to identify the impact of underweight BMI in predicting SSIs after LA.Materials and Methods
The records of a total of 101 consecutive patients aged ≥16 years who underwent LA by a single surgeon between March 2011 and December 2012 were retrieved from a prospectively collected database. The rate of SSIs was compared among the underweight, normal and overweight and obese groups. Also, univariate and multivariate analyses were performed to identify the factors associated with SSIs.Results
The overall rate of SSIs was 12.8%. The superficial incisional SSI rate was highest in the underweight group (44.4% in the underweight group, 11.0% in the normal group, and 0% in the overweight and obese group, p=0.006). In univariate analysis, open conversion and being underweight were determined to be risk factors for SSIs. Underweight BMI was also found to be a significant predictor for SSIs in multivariate analysis (odds ratio, 10.0; 95% confidence interval, 2.0-49.5; p=0.005).Conclusion
This study demonstrated underweight BMI as being associated with SSIs after LA. Surgeons should be more cautious to prevent SSIs in patients that are underweight when performing LA. 相似文献102.
M. J. Mina R. M. Burke K. P. Klugman 《European journal of clinical microbiology & infectious diseases》2014,33(9):1585-1589
Coinfections with common bacterial respiratory pathogens and influenza viruses are well-known causes of disease, often via synergistic interactions between the influenza virus, the bacteria, and the human host. However, relatively little is known about interactions between atypical bacteria and influenza viruses. A recent report by Reinton et al. explored this issue by analyzing data from 3,661 patients seeking medical assistance for the presence of Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Bordetella pertussis, as well as influenza A or B virus in nasal swab specimens. The report, however, did not accurately assess the epidemiologic interactions of these pathogens. We aimed to describe the interactions between these bacterial species and influenza infections. Strong and highly statistically significant antagonistic interspecies interactions were detected between C. pneumoniae and influenza virus [odds ratio (OR): 0.09; p?0.0001) and M. pneumoniae and influenza virus infections (OR: 0.29; p?=?0.003). No association was detected between B. pertussis and influenza infection (p?=?0.34), contrary to the initial report, and coinfection was not detected at a higher-than-by-chance frequency within the population. Further support of these results is supplied by the analysis of two earlier investigations reporting data on influenza virus and these atypical bacteria. Our results supplement the large body of literature regarding interactions between influenza virus and typical respiratory pathogens, providing a fuller picture of the spectrum of interactions between influenza viruses and respiratory bacteria. Further, we demonstrate the importance of choosing the most appropriate reference populations for the analysis being performed and describe the pitfalls that may occur when care is not taken in this regard. 相似文献
103.
This study aimed to analyze trends in the 10 leading causes of death in Korea from 1983 to 2012. Death rates were derived from the Korean Statistics Information Service database and age-adjusted to the 2010 population. Joinpoint regression analysis was used to identify the points when statistically significant changes occurred in the trends. Between 1983 and 2012, the age-standardized death rate (ASR) from all causes decreased by 61.6% for men and 51.2% for women. ASRs from malignant neoplasms, diabetes mellitus, and transport accidents increased initially before decreasing. ASRs from hypertensive diseases, heart diseases, cerebrovascular diseases and diseases of the liver showed favorable trends (ASR % change: -94.4%, -53.8%, -76.0%, and -78.9% for men, and -77.1%, -36.5%, -67.8%, and -79.9% for women, respectively). ASRs from pneumonia decreased until the mid-1990s and thereafter increased. ASRs from intentional self-harm increased persistently since around 1990 (ASR % change: 122.0% for men and 217.4% for women). In conclusion, death rates from all causes in Korea decreased significantly in the last three decades except in the late 1990s. Despite the great strides made in the overall mortality, temporal trends varied widely by cause. Mortality trends for malignant neoplasms, diabetes mellitus, pneumonia and intentional self-harm were unfavorable.
Graphical Abstract
相似文献104.
Khezrian Mina McNeil Christopher J. Myint Phyo K. Murray Alison D. 《International journal of clinical pharmacy》2019,41(1):251-257
International Journal of Clinical Pharmacy - Background Polypharmacy is a growing health concern for older adults and is associated with poorer clinical outcome. Objective This study aim is to... 相似文献
105.
Mandana Veiseh Daniel H. Kwon Alexander D. Borowsky Cornelia Tolg Hon S. Leong John D. Lewis Eva A. Turley Mina J. Bissell 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(17):E1731-E1739
Tumor heterogeneity confounds cancer diagnosis and the outcome of therapy, necessitating analysis of tumor cell subsets within the tumor mass. Elevated expression of hyaluronan (HA) and HA receptors, receptor for HA-mediated motility (RHAMM)/HA-mediated motility receptor and cluster designation 44 (CD44), in breast tumors correlates with poor outcome. We hypothesized that a probe for detecting HA–HA receptor interactions may reveal breast cancer (BCa) cell heterogeneity relevant to tumor progression. A fluorescent HA (F-HA) probe containing a mixture of polymer sizes typical of tumor microenvironments (10–480 kDa), multiplexed profiling, and flow cytometry were used to monitor HA binding to BCa cell lines of different molecular subtypes. Formulae were developed to quantify binding heterogeneity and to measure invasion in vivo. Two subsets exhibiting differential binding (HA−/low vs. HAhigh) were isolated and characterized for morphology, growth, and invasion in culture and as xenografts in vivo. F-HA–binding amounts and degree of heterogeneity varied with BCa subtype, were highest in the malignant basal-like cell lines, and decreased upon reversion to a nonmalignant phenotype. Binding amounts correlated with CD44 and RHAMM displayed but binding heterogeneity appeared to arise from a differential ability of HA receptor-positive subpopulations to interact with F-HA. HAhigh subpopulations exhibited significantly higher local invasion and lung micrometastases but, unexpectedly, lower proliferation than either unsorted parental cells or the HA−/low subpopulation. Querying F-HA binding to aggressive tumor cells reveals a previously undetected form of heterogeneity that predicts invasive/metastatic behavior and that may aid both early identification of cancer patients susceptible to metastasis, and detection/therapy of invasive BCa subpopulations.Breast tumors display substantial heterogeneity driven by genetic and epigenetic mechanisms (1–3). These processes select and support tumor cell subpopulations with distinct phenotypes in proliferation, metastatic/invasive proclivity, and treatment susceptibility that contribute to clinical outcomes. Currently, there is a paucity of biomarkers to identify these subpopulations (3–12). Although detection of genetic heterogeneity may itself be a breast cancer (BCa) prognostic marker (3, 13–15), the phenotypes manifested from this diversity are context-dependent. Therefore, phenotypic markers provide additional powerful tools for biological information required to design diagnostics and therapeutics. Glycomic approaches have enormous potential for revealing tumor cell phenotypic heterogeneity because glycans are themselves highly heterogeneous and their complexity reflects the nutritional, microenvironmental, and genetic dynamics of the tumors (16–18).We used hyaluronan (HA) as a model carbohydrate ligand for probing heterogeneity in glycosaminoglycan–BCa cell receptor interactions. We reasoned this approach would reveal previously undetected cellular and functional heterogeneity linked to malignant progression because the diversity of cell glycosylation patterns, which can occur as covalent and noncovalent modifications of proteins and lipids as well as different sizes of such polysaccharides as HA, is unrivaled (16, 17, 19). In particular, tumor and wound microenvironments contain different sizes of HA polymers that bind differentially to cell receptors to activate signaling pathways regulating cell migration, invasion, survival, and proliferation (19–22).More than other related glycosaminoglycans, HA accumulation within BCa tumor cells and peritumor stroma is a predictor of poor outcome (23) and of the conversion of the preinvasive form of BCa, ductal carcinoma in situ, to an early invasive form of BCa (24). HA is a nonantigenic and large, relatively simple, unbranched polymer, but the manner in which it is metabolized is highly complex (19, 25). There are literally thousands of different HA sizes in remodeling microenvironments, including tumors. HA polymers bind to cells via at least six known receptors (16, 19, 20, 26–32). Two of these, cluster designation 44 (CD44) and receptor for HA-mediated motility/HA-mediated motility receptor (RHAMM/HMMR), form multivalent complexes with different ranges of HA sizes (19, 29, 33), and both receptors are implicated in BCa progression (19–21, 23, 29, 30, 33–36). Elevated CD44 expression in the peritumor stroma is associated with increased relapse (37), and in primary BCa cell subsets may contribute to tumor initiation and progression (38–40). Elevated RHAMM expression in BCa tumor subsets is a prognostic indicator of poor outcome and increased metastasis (22, 33, 41). RHAMM polymorphisms may also be a factor in BCa susceptibility (42, 43).We postulated that multivalent interactions resulting from mixture of a polydisperse population of fluorescent HA (F-HA) sizes, typical of those found in remodeling microenvironments of wounds and tumors (19, 20, 29), with cellular HA receptors would uncover a heterogeneous binding pattern useful for sorting tumor cells into distinct subsets. We interrogated the binding of F-HA to BCa lines of different molecular subtypes, and related binding/uptake patterns to CD44 and RHAMM display, and to tumor cell growth, invasion, and metastasis. 相似文献
106.
107.
108.
Kim J Villadsen R Sørlie T Fogh L Grønlund SZ Fridriksdottir AJ Kuhn I Rank F Wielenga VT Solvang H Edwards PA Børresen-Dale AL Rønnov-Jessen L Bissell MJ Petersen OW 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(16):6124-6129
The majority of human breast cancers exhibit luminal epithelial differentiation. However, most aggressive behavior, including invasion and purported cancer stem cell activity, are considered characteristics of basal-like cells. We asked the following questions: Must luminal-like breast cancer cells become basal-like to initiate tumors or to invade? Could luminally differentiated cells within a basally initiated hierarchy also be tumorigenic? To answer these questions, we used rare and mutually exclusive lineage markers to isolate subsets of luminal-like and basal-like cells from human breast tumors. We enriched for populations with or without prominent basal-like traits from individual tumors or single cell cloning from cell lines and recovered cells with a luminal-like phenotype. Tumor cells with basal-like traits mimicked phenotypic and functional behavior associated with stem cells assessed by gene expression, mammosphere formation and lineage markers. Luminal-like cells without basal-like traits, surprisingly, were fully capable of initiating invasive tumors in NOD SCID gamma (NSG) mice. In fact, these phenotypically pure luminal-like cells generated larger and more invasive tumors than their basal-like counterparts. The tumorigenicity and invasive potential of the luminal-like cancer cells relied strongly on the expression of the gene GCNT1, which encodes a key glycosyltransferase controlling O-glycan branching. These findings demonstrate that basal-like cells, as defined currently, are not a requirement for breast tumor aggressiveness, and that within a single tumor there are multiple “stem-like” cells with tumorigenic potential casting some doubt on the hypothesis of hierarchical or differentiative loss of tumorigenicity. 相似文献
109.
Children and adolescents who are forcibly displaced represent almost half the world's internally displaced and refugee populations. We undertook a two-part systematic search and review of the evidence-base for individual, family, community, and societal risk and protective factors for the mental health outcomes of children and adolescents. Here we review data for displacement to low-income and middle-income settings. We draw together the main findings from reports to identify important issues and establish recommendations for future work. We draw attention to exposure to violence as a well established risk factor for poor mental health. We note the paucity of research into predictor variables other than those in the individual domain and the neglect of other variables for the assessment of causal associations, including potential mediators and moderators identifiable in longitudinal work. We conclude with research and policy recommendations to guide the development and assessment of effective interventions. 相似文献