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411.
B I Posner 《Canadian journal of physiology and pharmacology》1975,53(5):689-703
Major developments in the area of polypeptide hormone receptors have been reviewed. Receptors are high affinity, high specificity binding sites which appear to be located largely, if not entirely, on the plasma membrane of cells. Receptors are proteins intimately associated with and influenced by lipids. Receptor sites and degrading sites appear to be readily distinguishable entities. The binding of hormone to receptor is distinct and has been dissociated from subsequent steps leading to hormonal response. There is no direct relationship between receptor occupancy and the magnitude of target response to hormone. So called 'spare' receptors can be viewed thermodynamically as enhancing target tissue sensitivity to hormone. The binding of hormone to receptor appears to be a point at which regulation of tissue sensitivity can be influenced either through altering the affinity for hormone or the number of receptors. One factor apparently involved in the regulation of receptor levels is the hormone itself. Receptors have been used to develop assay procedures which have significantly complemented the bioassay and radioimmunoassay. Finally, the measurement of receptor levels in disease has provided new insights into pathophysiology. 相似文献
412.
There is now abundant evidence that the intracellular concentration of the EGFR and many other receptors for peptide hormones and growth factors is important for the temporal and spatial regulation of cell signaling. Spatial control is achieved by the selective compartmentalization of signaling components into endosomes. However further control may be effected by sequestration into sub‐domains within a given organelle such as membrane rafts which are dynamic, nano scale structures rich in cholesterol and sphingolipids. Current data suggest the presence of EGFRs in non‐caveolae membrane rafts. High doses of EGF seem to promote the sorting of EGFR to late endosomes through a raft/cholesterol dependant mechanism, implicating them in EGFR degradation. However our work and that of others has led us to propose a model in which membrane rafts in late endosomes sequester highly active EGFR leading to the recruitment and activation of MAPK in this compartment. J. Cell. Biochem. 109: 1103–1108, 2010. © 2010 Wiley‐Liss, Inc. 相似文献
413.
Neubauer J. A.; Santiago T. V.; Posner M. A.; Edelman N. H. 《Journal of applied physiology》1985,58(5):1659-1668
The role of a sudden increase in brain perfusion on ventral medullary surface pH (Vm pH) and minute ventilation (VI) was assessed in anesthetized peripherally chemo denervated cats. Acute hypertension (AH), produced by rapid inflation of an aortic balloon, and hypoxemia, produced with either inhalation of 1% CO (COHx) or inhalation of a hypoxic gas (HHx), were used to increase brain blood flow. In the AH group, increasing arterial blood pressure (from 122 +/- 3 to 180 +/- 5 mmHg) caused a rapid (less than 5 s) increase in Vm pH in every trial (n = 18). Associated with the mean peak increases in Vm pH (0.003 +/- 0.0004 pH units) were significant decrease in tidal volume (7-9%). In the COHx group, 17% HbCO caused a significant increase in Vm pH (0.003 +/- 0.0005 pH unit) and diminution of VI (9%). Further increases in HbCO caused a progressive ventral medullary acidosis and greater reductions in VI. The results from the HHX group were qualitatively similar to the COHx group; there was a biphasic response of Vm pH, i.e., an initial increase in Vm pH (0.008 +/- 0.001) followed by a steady decrease in Vm pH, with reductions in VI associated with both phases. We conclude that hyperperfusion, per se, produces an increase in Vm pH and a reduction in VI equivalent in magnitude to that predicted from the CO2 stimulus-response curve; the alkalotic shift in Vm pH and concomitant diminution in VI associated with mild hypoxia is probably related to an increase in ventral medullary perfusion; and the ventilatory depression associated with the medullary acidosis of moderate brain hypoxia must be attributed to another mechanism. 相似文献
414.
415.
DCMU, in a sucrose supplemented medium, promoted short and longday flowering and inhibited long day frond production of wildtype Lemna perpusilla 6746, but not of mutant strain 1073. Resultssuggest a defect in the mutant that mimics DCMU poisoning.
1 This work was supported by National Science Foundation GrantGB-12955. (Received December 11, 1972; ) 相似文献
416.
I Posner C S Wang W J McConathy 《Comparative biochemistry and physiology. B, Comparative biochemistry》1985,80(1):171-174
The kinetics of human and bovine milk lipoprotein lipase (HM-LPL and BM-LPL, respectively) were compared by varying apolipoprotein C-II (C-II) or triacylglycerol (TG) concentrations. The apparent Km (TG) and Km (C-II) for HM-LPL were 2.2 and 6.7-fold higher than for BM-LPL. Plots of 1/v vs 1/[TG] or 1/[C-II] intercepted the respective abscissas at the same points: C-II had no effect on Km (TG) and TG had no effect on Km (C-II). Replots of slope 1/s vs 1/[C-II] gave straight lines which yielded KA values identical to Km (C-II). It is concluded that the HM-LPL system follows a random, bireactant, rapid equilibrium mechanism as shown previously for BM-LPL. 相似文献
417.
A simple and specific method for assaying lipoprotein lipase activity is described. Postheparin plasma, heart homogenates, or extracts of acetone powder of adipose tissue were incubated with a triolein-coated Celite substrate, and enzyme activity was determined from the rate of free fatty acid (FFA) release in the incubation system. FFA release was linear for 30 min, and was proportional to protein concentration in the incubation system. FFA release was decreased by addition of deoxycholate or Triton X-100. Increasing the concentration of heparin in the incubation system caused a gradual decrease in FFA release by postheparin plasma and increases in activity of heart homogenates and adipose tissue lipoprotein lipase. The Celite substrate was found to be satisfactory for assaying pancreatic lipase activity as well. 相似文献
418.
419.
Neubauer J. A.; Posner M. A.; Santiago T. V.; Edelman N. H. 《Journal of applied physiology》1987,63(2):699-706
To assess whether endogenous opioids participate in respiratory depression due to brain hypoxia, we determined the ventilatory response to progressive carboxyhemoglobinemia (1% CO, 40% O2) before and after administration of naloxone (NLX, 0.1 mg/kg iv). Minute ventilation (VI) and ventral medullary surface pH (Vm pH) were measured in six anesthetized, peripherally chemodenervated cats. NLX consistently increased base-line hyperoxic VI from 618 +/- 99 to 729 +/- 126 ml/min (P less than 0.05). Although NLX did not alter the Vm pH response to CO [initial alkalosis, Vm pH +0.011 +/- 0.003 pH units, followed by acidosis, Vm pH -0.082 +/- 0.036 at carboxyhemoglobin (HbCO) 55%], NLX attenuated the amount of ventilatory depression; increasing HbCO to 55% decreased VI to 66 +/- 6% of base line before NLX and to 81 +/- 9% of base line after NLX (P less than 0.05). The difference in response after NLX was primarily the result of a linear increase in tidal volume (VT) with decreasing Vm pH (delta VT = 60.3 ml/-pH unit) which was absent before NLX. To assess whether the site of action of the endogenous opioid effect was the central chemosensors, the ventilatory and Vm pH response to progressive HbCO was determined in three additional cats before and after topical application of NLX (3 X 10(-4) M) to the ventral medullary surface. The effect of topical NLX was similar to systemic NLX; significant attenuation of the reduction in VI with increasing HbCO. We conclude that 1) endogenous opioids mediate a portion of the depression of ventilation due to acute brain hypoxia, and 2) this effect is probably at the central chemosensitive regions. 相似文献
420.
Sucrose inhibition of flowering in Lemna perpusilla 6746 wasat least partially reversed by 5'-AMP, cyclic 3',5'-AMP, 5'-ADP,5'-ATP and K2HPO4. These results are in contrast to those reportedfor L. gibba in which reversal was effected by cyclic AMP, butnot by other adenine derivatives.
1 This work was supported by National Science Foundation GrantGB-12955. (Received June 11, 1973; ) 相似文献