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991.
We use an unrestricted self-consistent Hartree-Fock approach to calculate the nature of doping states in the three-band Hubbard model. It turns out that for physically relevant parameter values one hole is localized within a small spin-polarized region where five Cu spins are aligned in the same direction. The spin polarization and binding energy between these spinpolaronic states are investigated as a function of different parameters including a Holstein-type electron-phonon coupling on the Cu sites. At higher doping concentration we observe the occurrence of afmon states where the holes are localized in a ring-shaped area. Inside this ring the antiferromagnetic order parameter has inverse sign with respect to the residual antifer-romagnetically ordered plane. 相似文献
992.
993.
994.
Rat liver microsomes and, to a lesser extent, nuclei were previously shown to produce reactive oxygen species at elevated rates after chronic ethanol treatment. The ability of intact rat liver mitochondria to interact with iron and either NADH or NADPH, and the effects of ethanol treatment, on production of reactive oxygen intermediates was determined. In the presence of ferric-ATP, NADH or NADPH catalyzed mitochondrial lipid peroxidation. Rates were elevated two- to threefold with mitochondria from ethanol-fed rats with both reductants. Mitochondrial lipid peroxidation was insensitive to superoxide dismutase, catalase, or hydroxyl radical scavengers but was sensitive to GSH and anti-oxidants such as trolox. Mitochondrial generation of hydroxyl radical-like species (assayed by oxidation of chemical scavengers) was increased after chronic ethanol treatment, as was H2O2 production. Modifiers of mitochondrial metabolism such as rotenone, cyanide, or an uncoupling agent, had no effect on mitochondrial production of reactive oxygen intermediates. The membrane-impermeable thiol reagent, p-chloromercuribenzoate, was complete inhibitory with both mitochondrial preparations. The activity of the rotenone-insensitive NADH-cytochrome c reductase, an enzyme of the outer mitochondrial membrane, was increased 40 to 60% by the ethanol treatment. These results suggest that NADH acting via the outer membrane NADH reductase can catalyze an iron-dependent production of oxygen radicals by rat liver mitochondria. The outer mitochondrial membrane fraction, prepared by digitonin fractionation, displayed increased rotenone-insensitive NADH-cytochrome c reductase activity after ethanol treatment and was more reactive in catalyzing scission of pBR322 DNA from the supercoiled form to the open circular forms. Rates of oxygen radical production by mitochondria and the extent of increase produced by chronic ethanol treatment are similar to those previously found with microsomes when NADH is the cofactor. Oxidation of ethanol by alcohol dehydrogenase generates NADH, and NADH-dependent production of reactive oxygen species by various organelles is increased after chronic ethanol treatment. These acute metabolic interactions coupled to induction by chronic ethanol treatment may play an important role in the development of a state of oxidative stress in the liver by ethanol. 相似文献
995.
Munro A. Guelen E. Deguine M. Melpignano G. Martinez A. 《Communications Magazine, IEEE》1998,36(2):118-126
The ACTS program is moving the results of the R&D of the parent RACE program nearer to realization through technology and user trials. Particularly in the mobile domain of ACTS, several projects have been investigating the user dimension in the context of the third-generation Universal Mobile Telecommunications Service. Results so far suggest many opportunities to broaden participation, exploit the inherent benefits of the mobile environment, and take advantage of the enormous improvements in wireless communications to realize the potential of global multimedia mobility. This article considers the needs of users for mobile multimedia applications and the consequences of those needs on the equipment, supporting services and teleservices, and communications bearers 相似文献
996.
The effect of spin fluctuations on the thermal properties of strongly correlated itinerant fermion systems is discussed based
on the self-consistent renormalized (SCR) spin fluctuation model. Specific heat and magnetic susceptibility in the normal
phase of liquid-3He and heavy electron compounds at finite temperatures are well described by the unified SCR picture including the mode-mode
coupling of spin fluctuations beyond the random phase approximation (RPA). 相似文献
997.
Significative enhancement of free radical formation (FRO) in vivo is an important feature of hypertensive disorders of pregnancy (HDP), namely preeclampsia (PIH). The latest investigations about the pathology of HDP, showed the contribution of placental circulation to the development and evolution of such disease. The placental bed can be a potential source of FRO or activation of cells that can produce FRO. Glutathione, is an important molecule for cellular protection against damage, is a cofactor of many enzymes, in particular, for the glutathione peroxidase of the placental tissue; this enzyme in the placenta bed prevent the production of thromboxan and lipoperoxides; the latter are potentially damaging to the endothelium cells and can cause vasoconstriction, the most important feature of PIH. The activity of that enzyme is deficient in PIH. We studied, by fluorometric assay, the concentrations of the two states of glutathione in placental homogenates (PLH) from pregnant women without pathology (PWN) and from pregnant women with PIH (PWPIH). The data showed significant low concentrations in the PLH of the two states of glutathione in the PWN against high concentrations of this molecule in the PLH from PWPIH. This feature can result from a deficient user of the glutathione by the cellular mechanism for prevention against oxidative factors. In addition, our study shows a biochemical marker that is suggestive that the placental bed is a potential source of FRO production in PIH. 相似文献
998.
Apoptosis in the failing human heart 总被引:1,自引:0,他引:1
G Olivetti R Abbi F Quaini J Kajstura W Cheng JA Nitahara E Quaini C Di Loreto CA Beltrami S Krajewski JC Reed P Anversa 《Canadian Metallurgical Quarterly》1997,336(16):1131-1141
BACKGROUND: Loss of myocytes is an important mechanism in the development of cardiac failure of either ischemic or nonischemic origin. However, whether programmed cell death (apoptosis) is implicated in the terminal stages of heart failure is not known. We therefore studied the magnitude of myocyte apoptosis in patients with intractable congestive heart failure. METHODS: Myocardial samples were obtained from the hearts of 36 patients who underwent cardiac transplantation and from the hearts of 3 patients who died soon after myocardial infarction. Samples from 11 normal hearts were used as controls. Apoptosis was evaluated histochemically, biochemically, and by a combination of histochemical analysis and confocal microscopy. The expression of two proto-oncogenes that influence apoptosis, BCL2 and BAX, was also determined. RESULTS: Heart failure was characterized morphologically by a 232-fold increase in myocyte apoptosis and biochemically by DNA laddering (an indicator of apoptosis). The histochemical demonstration of DNA-strand breaks in myocyte nuclei was coupled with the documentation of chromatin condensation and fragmentation by confocal microscopy. All these findings reflect apoptosis of myocytes. The percentage of myocytes labeled with BCL2 (which protects cells against apoptosis) was 1.8 times as high in the hearts of patients with cardiac failure as in the normal hearts, whereas labeling with BAX (which promotes apoptosis) remained constant. The near doubling of the expression of BCL2 in the cardiac tissue of patients with heart failure was confirmed by Western blotting. CONCLUSIONS: Programmed death of myocytes occurs in the decompensated human heart in spite of the enhanced expression of BCL2; this phenomenon may contribute to the progression of cardiac dysfunction. 相似文献
999.
Hagness S.C. Taflove A. Bridges J.E. 《IEEE transactions on bio-medical engineering》1998,45(12):1470-1479
A novel focused active microwave system is investigated for detecting tumors in the breast. In contrast to X-ray and ultrasound modalities, the method reviewed here exploits the breast-tissue physical properties unique to the microwave spectrum, namely, the translucent nature of normal breast tissues and the high dielectric contrast between malignant tumors and surrounding lesion-free normal breast tissues. The system uses a pulsed confocal technique and time-gating to enhance the detection of tumors while suppressing the effects of tissue heterogeneity and absorption. Using published data for the dielectric properties of normal breast tissues and malignant tumors, the authors have conducted a two-dimensional (2-D) finite-difference time-domain (FDTD) computational electromagnetics analysis of the system. The FDTD simulations showed that tumors as small as 2 mm in diameter could be robustly detected in the presence of the background clutter generated by the heterogeneity of the surrounding normal tissue. Lateral spatial resolution of the tumor location was found to be about 0.5 cm 相似文献
1000.
V. S. -Kh. Kim V. A. Samoilov E. M. Sherysheva Chen Yun 《Chemical and Petroleum Engineering》1993,29(8):355-358
Translated from Khimicheskoe i Neftyanoe Mashinostroenie, No. 8, pp. 9–11, August, 1993. 相似文献