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991.
文章介绍了在澳大利亚的中国人的“市场式”菜园子和房前屋后的花园。作者认为,这些园子反映了不可言表的中国传统。也许,正是这些园子以及建造园子的中国人,引起了我们认真地思考什么是传统、遗产等问题。这些园子在澳大利亚已经经历几代人,它们的变迁正好反映了中国人传统的生命力、创造力以及无限的适应能力。  相似文献   
992.
993.
The grain size dependence of the stress-strain behavior of annealed 70:30 brass was evaluated using room temperature tensile tests. The resulting data, which covered × 10-5 to 4 × 10-1, were analyzed in terms of the conventional Hall-Petch stress-grain size equation, σ = σO∈ +k∈l-1/2, and, also, in terms of the extended Hall-Petch equation previously proposed for 70:30 brass, σє = σ0y+ A Є p + β(є p /l 1/2 +kl −1/2 The lattice friction stress, σ0, increased linearly with plastic strain over nearly the full strain range. The lattice friction stress for the initiation of plastic flow, σ0y, was evaluated using two alternative double extrapolation procedures. Both extrapolation techniques, which involved the macrostrain behavior, gave the same σ0y value of 3.4 kg/mm2, which agreed with the σ0 value determined directly in the microstrain region (∈ <-10-3). Large grain size specimens, which yielded homogeneously, exhibited a kx2208; value of only 0.2 kg/mm3/2 at a plastic strain of 1 × 10-5; however this small kx2208; increased rapidly with increasing microstrain. For the small grain size specimens, which yielded via a Luders extension, was essentially constant at 0.8 kg/mm3/2 for all microstrains; however, kx03B5; did increase in the macrostrain region to a maximum value of 1.6 kg/mm3/2. When consideration was given to a grain size dependent increase in dislocation density, an intrinsic grain boundary resistance to plastic flow of approximately 0.7 kg/mm3/2 was obtained. This paper is based upon a thesis submitted by W. L. Phillips in partial fulfillment of the requirements of the degree of Doctor of Philosophy at University of Maryland.  相似文献   
994.
41 White and 37 Black psychotherapists with an average of 8.2 yrs' experience completed a 41-item questionnaire regarding psychotherapy with same- and opposite-race clients. White Ss did not experience racial issues in psychotherapy with the same salience that Black Ss did, yet they reported higher levels of subjective distress in cross-racial treatment. This distress focused on negative attitudes of clients, therapists' feelings of not being able to help or confront opposite race clients, or being oversolicitous or too distant with opposite-race clients. Both therapist groups reported equivalent abilities to empathize with opposite-race clients, but Blacks and Whites differed on a number of questions of racial attitudes and stereotyping. (9 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   
995.
Propionic acid is a cell nutrient but also a stimulus for cellular signaling. Free fatty acid receptor (FFAR)-3, also known as GPR41, is a Gi/o protein-coupled receptor (GPCR) that mediates some of the propionate’s actions in cells, such as inflammation, fibrosis, and increased firing/norepinephrine release from peripheral sympathetic neurons. The regulator of G-protein Signaling (RGS)-4 inactivates (terminates) both Gi/o- and Gq-protein signaling and, in the heart, protects against atrial fibrillation via calcium signaling attenuation. RGS4 activity is stimulated by β-adrenergic receptors (ARs) via protein kinase A (PKA)-dependent phosphorylation. Herein, we examined whether RGS4 modulates cardiac FFAR3 signaling/function. We report that RGS4 is essential for dampening of FFAR3 signaling in H9c2 cardiomyocytes, since siRNA-mediated RGS4 depletion significantly enhanced propionate-dependent cAMP lowering, Gi/o activation, p38 MAPK activation, pro-inflammatory interleukin (IL)-1β and IL-6 production, and pro-fibrotic transforming growth factor (TGF)-β synthesis. Additionally, catecholamine pretreatment blocked propionic acid/FFAR3 signaling via PKA-dependent activation of RGS4 in H9c2 cardiomyocytes. Finally, RGS4 opposes FFAR3-dependent norepinephrine release from sympathetic-like neurons (differentiated Neuro-2a cells) co-cultured with H9c2 cardiomyocytes, thereby preserving the functional βAR number of the cardiomyocytes. In conclusion, RGS4 appears essential for propionate/FFAR3 signaling attenuation in both cardiomyocytes and sympathetic neurons, leading to cardioprotection against inflammation/adverse remodeling and to sympatholysis, respectively.  相似文献   
996.
Statistical algorithm for nonuniformity correction in focal-plane arrays   总被引:11,自引:0,他引:11  
A statistical algorithm has been developed to compensate for the fixed-pattern noise associated with spatial nonuniformity and temporal drift in the response of focal-plane array infrared imaging systems. The algorithm uses initial scene data to generate initial estimates of the gain, the offset, and the variance of the additive electronic noise of each detector element. The algorithm then updates these parameters by use of subsequent frames and uses the updated parameters to restore the true image by use of a least-mean-square error finite-impulse-response filter. The algorithm is applied to infrared data, and the restored images compare favorably with those restored by use of a multiple-point calibration technique.  相似文献   
997.
Neurodegenerative disorders are a major public health issue. Despite decades of research efforts, we are still seeking an efficient cure for these pathologies. The initial paradigm of large aggregates of amyloid proteins (amyloid plaques, Lewis bodies) as the root cause of Alzheimer’s and Parkinson’s diseases has been mostly dismissed. Instead, membrane-bound oligomers forming Ca2+-permeable amyloid pores are now considered appropriate targets for these diseases. Over the last 20 years, our group deciphered the molecular mechanisms of amyloid pore formation, which appeared to involve a common pathway for all amyloid proteins, including Aβ (Alzheimer) and α-synuclein (Parkinson). We then designed a short peptide (AmyP53), which prevents amyloid pore formation by targeting gangliosides, the plasma membrane receptors of amyloid proteins. Herein, we show that aqueous solutions of AmyP53 are remarkably stable upon storage at temperatures up to 45 °C for several months. AmyP53 appeared to be more stable in whole blood than in plasma. Pharmacokinetics studies in rats demonstrated that the peptide can rapidly and safely reach the brain after intranasal administration. The data suggest both the direct transport of AmyP53 via the olfactory bulb (and/or the trigeminal nerve) and an indirect transport via the circulation and the blood–brain barrier. In vitro experiments confirmed that AmyP53 is as active as cargo peptides in crossing the blood–brain barrier, consistent with its amino acid sequence specificities and physicochemical properties. Overall, these data open a route for the use of a nasal spray formulation of AmyP53 for the prevention and/or treatment of Alzheimer’s and Parkinson’s diseases in future clinical trials in humans.  相似文献   
998.
Current methods for diagnosis and treatment of small cell lung cancer (SCLC) have only a modest efficacy. In this pilot study, we analyzed circulating tumor cells (CTCs) and cancer stem cells (CSCs) in patients with SCLC to search for new diagnostic and prognostic markers and novel approaches to improve the treatment of the disease. In other forms of lung cancer, we showed a heterogeneity of blood CTCs and CSCs populations, as well as changes in other cell populations (ALDH+, CD87+CD276+, and EGF+Axl+) in smokers. A number of CTCs and CSCs in patients with SCLC have been shown to be resistant to chemotherapy (CT). High cytotoxic activity and resistance to apoptosis of reprogrammed CD3+CD8+ T-lymphocytes (rTcells) in relation to naive CD3+CD8+ T-lymphocytes was demonstrated in a smoking patient with SCLC (Patient G) in vitro. The target for rTcells was patient G’s blood CSCs. Reprogramming of CD3+CD8+ T-lymphocytes was carried out with the MEK1/2 inhibitor and PD-1/PD-L1 pathway blocker nivolumab. The training procedure was performed with a suspension of dead CTCs and CSCs obtained from patient’s G blood. The presented data show a new avenue for personalized SCLC diagnosis and targeted improvement of chemotherapy based on the use of both CTCs and CSCs.  相似文献   
999.
In the ruminant placenta, glucose uptake and transfer are mediated by facilitative glucose transporters SLC2A1 (GLUT1) and SLC2A3 (GLUT3). SLC2A1 is located on the basolateral trophoblast membrane, whereas SLC2A3 is located solely on the maternal-facing, apical trophoblast membrane. While SLC2A3 is less abundant than SLC2A1, SLC2A3 has a five-fold greater affinity and transport capacity. Based on its location, SLC2A3 likely plays a significant role in the uptake of glucose into the trophoblast. Fetal hypoglycemia is a hallmark of fetal growth restriction (FGR), and as such, any deficiency in SLC2A3 could impact trophoblast glucose uptake and transfer to the fetus, thus potentially setting the stage for FGR. By utilizing in vivo placenta-specific lentiviral-mediated RNA interference (RNAi) in sheep, we were able to significantly diminish (p ≤ 0.05) placental SLC2A3 concentration, and determine the impact at mid-gestation (75 dGA). In response to SLC2A3 RNAi (n = 6), the fetuses were hypoglycemic (p ≤ 0.05), exhibited reduced fetal growth, including reduced fetal pancreas weight (p ≤ 0.05), which was associated with reduced umbilical artery insulin and glucagon concentrations, when compared to the non-targeting sequence (NTS) RNAi controls (n = 6). By contrast, fetal liver weights were not impacted, nor were umbilical artery concentrations of IGF1, possibly resulting from a 70% increase (p ≤ 0.05) in umbilical vein chorionic somatomammotropin (CSH) concentrations. Thus, during the first half of gestation, a deficiency in SLC2A3 results in fetal hypoglycemia, reduced fetal development, and altered metabolic hormone concentrations. These results suggest that SLC2A3 may be the rate-limiting placental glucose transporter during the first-half of gestation in sheep.  相似文献   
1000.
The presence of insoluble aggregates of amyloid β (Aβ) in the form of neuritic plaques (NPs) is one of the main features that define Alzheimer’s disease. Studies have suggested that the accumulation of these peptides in the brain significantly contributes to extensive neuronal loss. Furthermore, the content and distribution of cholesterol in the membrane have been shown to have an important effect on the production and subsequent accumulation of Aβ peptides in the plasma membrane, contributing to dysfunction and neuronal death. The monomeric forms of these membrane-bound peptides undergo several conformational changes, ranging from oligomeric forms to beta-sheet structures, each presenting different levels of toxicity. Aβ peptides can be internalized by particular receptors and trigger changes from Tau phosphorylation to alterations in cognitive function, through dysfunction of the cholinergic system. The goal of this review is to summarize the current knowledge on the role of lipids in Alzheimer’s disease and their relationship with the basal cholinergic system, as well as potential disease-modifying therapies.  相似文献   
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