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91.
进展期胃癌淋巴结转移与临床病理特征的关系 总被引:3,自引:1,他引:3
目的:探讨进展期胃癌淋巴结转移与临床病理特征的关系,为临床上进行合理的淋巴结清扫提供依据。方法:对55例进展期胃癌资料进行回顾性分析,术后常规解剖原发灶及各组淋巴结,并标记和计数,分析肿瘤部位、肿瘤大小、浸润深度、分化程度及Lauren分型与淋巴结转移率的关系。结果:进展期胃癌淋巴结转移率为74.5%;U、M、L区及全胃癌淋巴结转移率为85.7%、87.5%、67.6%和83.3%,各区和全胃癌淋巴结转移率差异无统计学意义(P〉0.05);浆膜受侵的胃癌淋巴结转移率为82.5%,明显高于浆膜未受侵者(53.3%)(P〈0.05);弥漫型胃癌淋巴结转移率为83.3%,明显高于肠型(64.0%)(P〈0.05);直径〉5cm癌灶淋巴结转移率为90.0%,明显高于直径≤5cm的胃癌患者(65.7%)(P〈0.05);浸润深度、Lauren分型和肿瘤大小是影响淋巴结转移率的主要因素,其中浸润深度为独立影响因素。结论:术中淋巴结清扫范围应结合肿瘤部位、肿瘤大小、浸润深度、分化程度及Lauren分型做出判断,并考虑患者的全身情况,合理选择淋巴结清扫范围。 相似文献
92.
BACKGROUND: The purpose of this study was to assess the feasibility of infrared (IR) spectroscopy for the simultaneous quantification of serum LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) concentrations. METHODS: Serum samples (n = 90) were obtained. Duplicate aliquots (5 microL) of the serum specimens were dried onto IR-transparent barium fluoride substrates, and transmission IR spectra were measured for the dry films. In parallel, the HDL-C and LDL-C concentrations were determined separately for each specimen by standard methods (the Friedewald formula for LDL-C and an automated homogeneous HDL-C assay). The proposed IR method was then developed with a partial least-squares (PLS) regression analysis to quantitatively correlate IR spectral features with the clinical analytical results for 60 randomly chosen specimens. The resulting quantification methods were then validated with the remaining 30 specimens. The PLS model for LDL-C used two spectral ranges (1700-1800 and 2800-3000 cm(-1)) and eight PLS factors, whereas the PLS model for HDL-C used three spectral ranges (800-1500, 1700-1800, and 2800-3500 cm(-1)) with six factors. RESULTS: For the 60 specimens used to train the IR-based method, the SE between IR-predicted values and the clinical laboratory assays was 0.22 mmol/L for LDL-C and 0.15 mmol/L for HDL-C (r = 0.98 for LDL-C; r = 0.91 for HDL-C). The corresponding SEs for the test spectra were 0.34 mmol/L (r = 0.96) and 0.26 mmol/L (r = 0.82) for LDL-C and HDL-C, respectively. The precision for the IR-based assays was estimated by the SD of duplicate measurements to be 0.11 mmol/L (LDL-C) and 0.09 mmol/L (HDL-C). CONCLUSIONS: IR spectroscopy has the potential to become the clinical method of choice for quick and simultaneous determinations of LDL-C and HDL-C. 相似文献
93.
BACKGROUND: The aim of this study was to investigate the potential of infrared (IR) spectroscopy as a fast and reagent-free adjunct tool in the diagnosis and screening of beta-thalassemia. METHODS: Blood was obtained from 56 patients with beta-thalassemia major, 1 patient with hemoglobin H disease, and 35 age-matched controls. Hemolysates of blood samples were centrifuged to remove stroma. IR absorption spectra were recorded for duplicate films dried from 5 microL of hemolysate. Differentiation between the two groups of hemoglobin spectra was by two statistical methods: an unsupervised cluster analysis and a supervised linear discriminant analysis (LDA). RESULTS: The IR spectra revealed changes in the secondary structure of hemoglobin from beta-thalassemia patients compared with that from controls, in particular, a decreased alpha-helix content, an increased content of parallel and antiparallel beta-sheets, and changes in the tyrosine ring absorption band. The hemoglobin from beta-thalassemia patients also showed an increase in the intensity of the IR bands from the cysteine -SH groups. The unsupervised cluster analysis, statistically separating spectra into different groups according to subtle IR spectral differences, allowed separation of control hemoglobin from beta-thalassemia hemoglobin spectra, based mainly on differences in protein secondary structure. The supervised LDA method provided 100% classification accuracy for the training set and 98% accuracy for the validation set in partitioning control and beta-thalassemia samples. CONCLUSION: IR spectroscopy holds promise in the clinical diagnosis and screening of beta-thalassemia. 相似文献
94.
建立测定复方红甲凝胶中乳糖酸红霉素的含量测定方法。方法:以一阶导数光谱的谷一零位值法测定乳糖酸红霉素的含量,测定波长λ谷=490±lnm。结果:回收率100.6%,RSD为3.1%,线性范围40~120μg/ml。结论:方法简便,结果准确,重现性好,适合于该制剂的含量测定。 相似文献
95.
Rationale: Ketoconazole (Keto) is an antifungal agent that also inhibits the synthesis of adrenocorticosteroids and has been reported
to act as a glucocorticoid receptor antagonist. Objective: The present experiments investigated the effects of Keto on the stressor-induced reinstatement of extinguished cocaine-seeking
behavior and on the generalization of a stressor-induced discriminative stimulus to cocaine in rats. Methods: In the first experiment, male Wistar rats were trained to self-administer cocaine (0.5 mg/kg per infusion, IV) under a fixed-ratio
4 schedule of reinforcement with a 90-s limited hold. Following ten consecutive extinction sessions, the effects of Keto (25
or 50 mg/kg, IP) or vehicle on the ability of EFS (electric footshock; 15 min) to reinstate extinguished cocaine-lever responding
were investigated. In the second experiment, rats were trained to discriminate cocaine (10 mg/kg, IP) from saline using a
two-lever, food-reinforced drug discrimination design. The effects of Keto (50 mg/kg, IP) or vehicle on the EFS-induced generalization
to cocaine were determined. Results: EFS reinstated extinguished cocaine- but not food-reinforced responding. Keto (25 and 50 mg/kg, IP) blocked the EFS-induced
reinstatement of cocaine-seeking behavior and significantly attenuated the plasma corticosterone response to EFS. These same
doses of Keto failed to affect responding in rats trained to self-administer food pellets under an FR4 schedule of reinforcement.
EFS also produced significant cocaine-appropriate responding in rats trained to discriminate the drug from saline. However,
Keto (50 mg/kg) failed to block the EFS-induced generalization to cocaine. Conclusions: Overall, these data suggest that corticosterone contributes to the stressor-induced reinstatement of extinguished cocaine-seeking
behavior.
Received: 5 June 1998 / Final version: 7 October 1998 相似文献
96.
97.
C Hastings T Rand H T Bergen J A Thliveris A R Shaw G A Lombaert H H Mantsch B L Giles S Dakshinamurti J E Scott 《Toxicological sciences》2005,84(1):186-194
Stachybotry chartarum, a fungal contaminant of water-damaged buildings commonly grows on damp cellulose-containing materials. It produces a complex array of mycotoxins. Their mechanisms of action on the pulmonary system are not entirely clear. Previous studies suggest spore products may depress formation of disaturated phosphatidylcholine (DSPC), the major surface-active component of pulmonary surfactant (PS). If S. chartarum can indeed affect formation of this phospholipid, then mold exposure may be a significant issue for pulmonary function in both mature lung and developing fetal lung. To address this possibility, fetal rat type II cells, the principal source of DSPC, were used to assess effects of S. chartarum extract on formation of DSPC. Isolated fetal rat lung type II cells prelabeled with 3H-choline and incubated with spore extract showed decreased incorporation of 3H-choline into DSPC. The activity of CTP:cholinephosphate cytidylyltransferase (CPCT), the rate-limiting enzyme in phosphatidylcholine synthesis was reduced by approximately 50% by a 1:10 dilution of spore extract. Two different S. chartarum extracts (isolates from S. chartarum (Cleveland) and S. chartarum (Hawaiian)) were used to compare activity of CPCT in the presence of phosphatidylglycerol (PG), a known activator. PG produced an approximate two-fold increase in CPCT activity. The spore isolate from Hawaii did not alter enzyme activity. S. chartarum (Cleveland) eliminated the PG-induced activation of CPCT. These results support previous observations that mold products alter PS metabolism and may pose a risk in developing lung, inhibiting surfactant synthesis. Different isolates of the same species of fungus are not equivalent in terms of potential exposure risks. 相似文献
98.
99.
Altered metabolism of familial Alzheimer's disease-linked amyloid precursor protein variants in yeast artificial chromosome transgenic mice 总被引:4,自引:3,他引:4
Lamb BT; Call LM; Slunt HH; Bardel KA; Lawler AM; Eckman CB; Younkin SG; Holtz G; Wagner SL; Price DL; Sisodia SS; Gearhart JD 《Human molecular genetics》1997,6(9):1535-1541
Missense mutations in the beta-amyloid precursor protein gene (APP) co-
segregate with a small subset of autosomal dominant familial Alzheimer's
disease (FAD) cases wherein deposition of the 39-43 amino acid beta-amyloid
(A beta) peptide and neurodegeneration are principal neuropathological
hallmarks. To accurately examine the effect of missense mutations on APP
metabolism and A beta production in vivo, we have introduced yeast
artificial chromosomes (YACs) containing the entire approximately 400 kbp
human APP gene encoding APP harboring either the asparagine for lysine and
leucine for methionine FAD substitution at codons 670 and 671
(APP(K670N/M671L)), the isoleucine for valine FAD substitution at codon 717
(APP(V7171)) or a combination of both substitutions into transgenic mice.
We demonstrate that, relative to YAC transgenic mice expressing wild-type
APP, high levels of A beta peptides are detected in the brains of YAC
transgenic mice expressing human APP(K670N/M671L) that is associated with a
concomitant diminution in the levels of apha-secretase-generated soluble
APP derivatives. Moreover, the levels of longer A beta peptides (species
terminating at amino acids 42/43) are elevated in YAC transgenic mice
expressing human APP(V7171). These mice should prove valuable for detailed
analysis of the in vivo effects of the APP FAD mutations in a variety of
tissues and throughout aging and for testing therapeutic agents that
specifically alter APP metabolism and A beta production.
相似文献
100.
Cloning and characterization of DXS6673E, a candidate gene for X-linked mental retardation in Xq13.1 总被引:3,自引:0,他引:3
van der Maarel SM; Scholten IH; Huber I; Philippe C; Suijkerbuijk RF; Gilgenkrantz S; Kere J; Cremers FP; Ropers HH 《Human molecular genetics》1996,5(7):887-897
In several families with non-specific X-linked mental retardation (XLMR)
linkage analyses have assigned the underlying gene defect to the
pericentromeric region of the X chromosome, but none of these genes have
been isolated so far. Here, we report on the cloning and characterization
of a novel gene, DXS6673E, that maps to Xq13.1, is subject to
X-inactivation and is disrupted in the 5' untranslated region by a balanced
X;13 translocation in a mentally retarded female. The DXS6673E gene is
highly conserved among vertebrates and its expression is most abundant in
brain. It encodes a hydrophilic protein of 1358 amino acids (aa) that does
not show sequence homology to other known proteins. A segment of this
protein consisting of neutral and hydrophobic aa with a proline residue in
every second position may represent a transmembrane domain. Almost complete
sequence identity was found between the 3' end of the DXS6673E gene and two
expressed sequence tags (ESTs) and between the 5' end of the DXS6673E gene
and a third EST. Moreover, weaker sequence similarity was observed between
coding regions and two other ESTs.
相似文献