全文获取类型
收费全文 | 1032篇 |
免费 | 0篇 |
专业分类
化学工业 | 4篇 |
机械仪表 | 1篇 |
无线电 | 5篇 |
一般工业技术 | 7篇 |
冶金工业 | 1015篇 |
出版年
2015年 | 1篇 |
2014年 | 1篇 |
2012年 | 2篇 |
2008年 | 1篇 |
2005年 | 2篇 |
2003年 | 5篇 |
2000年 | 1篇 |
1999年 | 22篇 |
1998年 | 314篇 |
1997年 | 152篇 |
1996年 | 117篇 |
1995年 | 62篇 |
1994年 | 68篇 |
1993年 | 68篇 |
1992年 | 7篇 |
1991年 | 21篇 |
1990年 | 15篇 |
1989年 | 16篇 |
1988年 | 18篇 |
1987年 | 12篇 |
1986年 | 9篇 |
1985年 | 11篇 |
1983年 | 1篇 |
1982年 | 7篇 |
1981年 | 5篇 |
1980年 | 12篇 |
1978年 | 4篇 |
1977年 | 26篇 |
1976年 | 48篇 |
1975年 | 2篇 |
1964年 | 1篇 |
1955年 | 1篇 |
排序方式: 共有1032条查询结果,搜索用时 0 毫秒
71.
72.
H Wakasaki D Koya FJ Schoen MR Jirousek DK Ways BD Hoit RA Walsh GL King 《Canadian Metallurgical Quarterly》1997,94(17):9320-9325
Increased cardiovascular mortality occurs in diabetic patients with or without coronary artery disease and is attributed to the presence of diabetic cardiomyopathy. One potential mechanism is hyperglycemia that has been reported to activate protein kinase C (PKC), preferentially the beta isoform, which has been associated with the development of micro- and macrovascular pathologies in diabetes mellitus. To establish that the activation of the PKCbeta isoform can cause cardiac dysfunctions, we have established lines of transgenic mice with the specific overexpression of PKCbeta2 isoform in the myocardium. These mice overexpressed the PKCbeta2 isoform transgene by 2- to 10-fold as measured by mRNA, and proteins exhibited left ventricular hypertrophy, cardiac myocyte necrosis, multifocal fibrosis, and decreased left ventricular performance without vascular lesions. The severity of the phenotypes exhibited gene dose-dependence. Up-regulation of mRNAs for fetal type myosin heavy chain, atrial natriuretic factor, c-fos, transforming growth factor, and collagens was also observed. Moreover, treatment with a PKCbeta-specific inhibitor resulted in functional and histological improvement. These findings have firmly established that the activation of the PKCbeta2 isoform can cause specific cardiac cellular and functional changes leading to cardiomyopathy of diabetic or nondiabetic etiology. 相似文献
73.
74.
75.
RH Kerman B Susskind J Ruth S Katz CT Van Buren BD Kahan 《Canadian Metallurgical Quarterly》1998,66(12):1833-1834
Performance of the pretransplant crossmatch requires 4 or more hours . Delays in the crossmatch might alter operating room availability and thereby increase donor organ cold ischemia time that might then result in increased risk of delayed graft function. To avoid these problems, recipients could be identified who would be expected to display negative donor crossmatches and who could be transplanted with a concurrent or retrospective rather than a pretransplant crossmatch. We, therefore, evaluated the percent reactive antibodies and donor IgG-antihuman globulin (AHG) crossmatch results of 1165 sera from 220 potential allograft recipients. Twenty-five (11%) of 220 recipients consistently displayed a 0% PRA and, with only one exception, their sera (n= 156) tested IgG-AHG crossmatch-negative against potential cadaveric donors (a 0.6% IgG-AHG positive crossmatch risk). These data suggest that the timing of the pretransplant serum crossmatch could be altered for a highly selected group of immunologically nonreactive recipients. 相似文献
76.
77.
The traditional understanding of knee kinematics holds that no single fixed axis of rotation exists in the knee. In contrast, a recent hypothesis suggests that knee kinematics are better described simply as two simultaneous rotations occurring about fixed axes. Knee flexion and extension occurs about an optimal flexion axis fixed in the femur, whereas tibial internal and external rotations occur about a longitudinal rotation axis fixed in the tibia. No other translations or rotations exist. This hypothesis has been tested. Tibiofemoral kinematics were measured for 15 cadaveric knees undergoing a realistic loadbearing activity (simulated squatting). An optimization technique was used to identify the locations of the optimal flexion and longitudinal rotation axes such that simultaneous rotations about them could best represent the measured kinematics. The optimal flexion axis was compared with the transepicondylar axis defined by bony landmarks. The longitudinal rotation axis was found to pass through the medial joint compartment. The optimal flexion axis passed through the centers of the posterior femoral condyles. No significant difference was found between the optimal flexion and transepicondylar axes. To an average accuracy of better than 3.4 mm in translation, and 2.9 degrees in orientation, knee kinematics were represented successfully by simple rotations about the optimal flexion and longitudinal rotation axes. The optimal flexion axis is fixed in the femur and can be considered the true flexion axis of the knee. The transepicondylar axis axis, which is identified easily by palpation, closely approximates the optimal flexion axis. 相似文献
78.
This research compared the social and cognitive development of young mothers when they were children with the social and cognitive development of their offspring. Intergenerational development was investigated over a 17-year period for 57 women who had been studied longitudinally from childhood to adulthood and who became young mothers (R. B. Cairns & B. D. Cairns, 1994). The children of these women, in turn, were followed prospectively from 1 to 2 years old through the early school years. The academic competence of mothers when they were children was significantly linked to the academic competence of their children at school age. In contrast, the across-generation correlations between measures of aggressive behavior of the mothers when they were children and measures of aggressive behavior of their children in early school grades were modest and unreliable. Certain within-generation continuities were observed in both cognitive and aggressive development. 相似文献
79.
Y Sakata BD Hoit SB Liggett RA Walsh GW Dorn 《Canadian Metallurgical Quarterly》1998,97(15):1488-1495
BACKGROUND: Receptor-mediated activation of myocardial Gq signaling is postulated as a biochemical mechanism transducing pressure-overload hypertrophy. The specific effects of Gq activation on the functional and morphological adaptations to pressure overload are not known. METHODS AND RESULTS: To determine the effects of intrinsic myocyte G alpha q signaling on the left ventricular hypertrophic response to experimental pressure overload, transgenic mice overexpressing G alpha q specifically in the heart (G alpha q-25) and nontransgenic siblings underwent microsurgical creation of transverse aortic coarctation and the morphometric, functional, and molecular characteristics of these pressure-overloaded hearts were compared at increasing times after surgery. Before aortic banding, isolated G alpha q-25 ventricular myocytes exhibited contractile depression (depressed +dl/dt and -dl/dt) and G alpha q-25 hearts showed a pattern of fetal gene expression similar to the known characteristics of nontransgenic pressure-overloaded mice. Three weeks after transverse aortic banding, G alpha q-25 left ventricles hypertrophied to a similar extent (approximately 30% increase) as nontransgenic mice. However, whereas nontransgenic mice exhibited concentric left ventricular remodeling with maintained ejection performance (compensated hypertrophy), G alpha q-25 left ventricles developed eccentric hypertrophy and ejection performance deteriorated, ultimately resulting in left heart failure (decompensated hypertrophy). The signature hypertrophy-associated progress of fetal cardiac gene expression observed at baseline in G alpha q-25 developed after aortic banding of nontransgenic mice but did not significantly change in aortic-banded G alpha q-25 mice. CONCLUSIONS: Intrinsic cardiac myocyte G alpha q activation stimulates fetal gene expression and depresses cardiac myocyte contractility. Superimposition of the hemodynamic stress of pressure overload on G alpha q overexpression stimulates a maladaptive form of eccentric hypertrophy that leads to rapid functional decompensation. Therefore G alpha q-stimulated cardiac hypertrophy is functionally deleterious and compromises the ability of the heart to adapt to increased mechanical load. This finding supports a reevaluation of accepted concepts regarding the mechanisms for compensation and decompensation in pressure-overload hypertrophy. 相似文献
80.
DR DeSilva EA Jones MF Favata BD Jaffee RL Magolda JM Trzaskos PA Scherle 《Canadian Metallurgical Quarterly》1998,160(9):4175-4181
Three mitogen-activated protein kinase pathways are up-regulated during the activation of T lymphocytes, the extracellular signal-regulated kinase (ERK), Jun NH2-terminal kinase, and p38 mitogen-activated protein kinase pathways. To examine the effects of blocking the ERK pathway on T cell activation, we used the inhibitor U0126, which has been shown to specifically block mitogen-activated protein kinase/ERK kinase (MEK), the kinase upstream of ERK. This compound inhibited T cell proliferation in response to antigenic stimulation or cross-linked anti-CD3 plus anti-CD28 Abs, but had no effect on IL-2-induced proliferation. The block in T cell proliferation was mediated by down-regulating IL-2 mRNA levels. Blocking Ag-induced proliferation by inhibiting MEK did not induce anergy, unlike treatments that block entry into the cell cycle following antigenic stimulation. Surprisingly, induction of anergy in T cells exposed to TCR cross-linking in the absence of costimulation was also not affected by blocking MEK, unlike cyclosporin A treatment that blocks anergy induction. These results suggest that inhibition of MEK prevents T cell proliferation in the short term, but does not cause any long-term effects on either T cell activation or induction of anergy. These findings may help determine the viability of using mitogen-activated protein kinase inhibitors as immune suppressants. 相似文献