全文获取类型
收费全文 | 3952篇 |
免费 | 323篇 |
专业分类
4275篇 |
出版年
2022年 | 23篇 |
2021年 | 48篇 |
2020年 | 34篇 |
2019年 | 36篇 |
2018年 | 62篇 |
2017年 | 47篇 |
2016年 | 94篇 |
2015年 | 161篇 |
2014年 | 187篇 |
2013年 | 205篇 |
2012年 | 297篇 |
2011年 | 271篇 |
2010年 | 180篇 |
2009年 | 164篇 |
2008年 | 213篇 |
2007年 | 197篇 |
2006年 | 202篇 |
2005年 | 211篇 |
2004年 | 190篇 |
2003年 | 189篇 |
2002年 | 199篇 |
2001年 | 28篇 |
2000年 | 30篇 |
1999年 | 47篇 |
1998年 | 56篇 |
1997年 | 30篇 |
1996年 | 37篇 |
1995年 | 28篇 |
1994年 | 41篇 |
1993年 | 35篇 |
1992年 | 29篇 |
1991年 | 25篇 |
1990年 | 20篇 |
1988年 | 23篇 |
1987年 | 22篇 |
1986年 | 20篇 |
1985年 | 29篇 |
1984年 | 45篇 |
1983年 | 18篇 |
1982年 | 39篇 |
1981年 | 28篇 |
1980年 | 30篇 |
1979年 | 21篇 |
1978年 | 21篇 |
1977年 | 28篇 |
1976年 | 27篇 |
1975年 | 22篇 |
1974年 | 21篇 |
1973年 | 27篇 |
1970年 | 18篇 |
排序方式: 共有4275条查询结果,搜索用时 0 毫秒
941.
LAUER, JOAN B., GEORGE W. REED, AND JAMES O. HILL. Effects of weight cycling induced by diet cycling in rats differing in susceptibility to dietary obesity. Obes Res. Objective Although the majority of evidence in rodents does not support the view that weight cycling (consisting of bouts of food restriction and refeeding) promotes obesity, the effects of weight cycling on body weight regulation remain controversial. We have previously demonstrated that some rats within a strain are more susceptible to develop obesity than others when given free access to a high-fat diet. In this study, we tested the hypothesis that rats most susceptible to weight gain on a high-fat diet would also be most susceptible to weight gain as a consequence of weight cycling. Research Methods and Procedures Rats were provided a low-fat diet (12% corn oil) for 2 weeks, then given a high-fat diet (45% corn oil) for 2 weeks to identify those most (obesity prone) and least (obesity resistant) susceptible to weight gain. Half of each group was then subjected to three 30-day cycles of food restriction (10 days) and refeeding (20 days) [weight cycler (WC) rats]. The other half were allowed free access to the high-fat diet [control (CO) rats]. All rats were then followed for an additional 10 weeks, with free access to the high-fat diet. Results When considering the entire 160 days of the study, we found no evidence that WC rats relative to CO rats had increased body weight, increased body fat content, or elevated energy efficiency. We found no evidence that rats most prone to dietary obesity were also prone to weight gain after weight cycling. During the weight cycling phase (days 1 to 90), weight cycled groups consumed less energy and gained less weight than controls. During the follow-up phase, WC and CO rats did not differ significantly in weight gain or energy intake. Discussion In this study, weight cycling did not exacerbate the obesity produced by high-fat diet feeding. 相似文献
942.
The objectives of this study were to (1) test a simple bioremediation treatment strategy in the Arctic and (2) examine the effect of fertilization on the degradation of aliphatic and aromatic hydrocarbons. The site is a coarse sand pad that once supported fuel storage tanks. Concentrations of diesel-range organics at the beginning of the study (July 1996) ranged from 250 to 860 mg/kg soil. Replicate field plots treated with fertilizer yielded final concentrations of 0, 50, 100, or 200 mg N/kg soil. Soil samples were collected three times during the thaw season and analyzed for physical and chemical properties, microbial populations and activities, and concentrations of semivolatile hydrocarbons. Soil pH and soil-water potentials declined as a result of fertilizer application. Addition of fertilizer significantly increased soil respiration potentials, but not the populations of microorganisms measured. Fertilizer addition also resulted in ∼50% loss of measured aliphatic and aromatic hydrocarbons in surface and subsurface soils. For fertilized plots, hydrocarbon loss was not related to the amount of fertilizer added. Losses of aliphatic hydrocarbons were attributed to biotic processes, whereas losses of aromatic hydrocarbons likely were a result of both biotic and abiotic processes. 相似文献
943.
Evolution of Streptozotocin–Pancreatic Damage in the Rat: Modulatory Effect of Endothelins on the Nitridergic and Prostanoid Pathway 总被引:2,自引:0,他引:2
Elida Gonzlez Alicia Jawerbaum Dbora Sinner Carolina Pustovrh Carme Xaus Carmen Peralta Gloria Gmez Joan Rosell-Catafau Emilio Gelpi Martha Gimeno 《Nitric oxide》1999,3(6):459-466
Many lines of evidence indicate that an increased pancreatic production of nitric oxide (NO) and prostaglandins (PGs) is found in the pancreas of streptozotocin-diabetic rats and that endothelins (ETs) are closely related to the nitridergic and prostanoid pathway in several tissues. In the present study the relationship between NO, ETs, and PGs has been explored in isolated pancreatic tissue from streptozotocin-diabetic rats. Pancreatic ET levels are higher in pancreatic tissues from diabetic (D) rats compared to control (C) animals. The addition of nitric oxide synthase (NOS) inhibitors (1 mM N(G)-nitro-l-arginine methyl ester, 600 microM N(G)-monomethyl-l-arginine) in the incubating medium reduces and NO donors (SIN-1, 300 microM spermine suppress, NONOate 100 microM) increases ET levels in pancreatic slices from C and D animals. PGE(2) (10(-7) M) increases and indomethacin (10(-6) M) decreases ET pancreatic production only in D but not in C tissues when added into the incubating bath. When tissues are incubated in the presence of endothelin 1 (ET-1) (10(-7) M), NOS activity is higher in C pancreas, while the ET-receptor antagonist bosentan (B) decreases NOS levels in D but not in C tissues. When pancreatic arachidonic acid (AA) conversion to prostaglandins was explored, ET-1 increased PGF(2alpha), PGE(2), and TXB(2) levels in C but not in D tissues. B abolishes TXB(2) increment due to the diabetic state, but failed in modulating AA conversion to 6-keto PGF(1alpha), PGF2(alpha) and PGE(2) in D pancreas. Our results show an alteration in AA metabolism, ET production, and NO increment associated with pancreatic damage due to streptozotocin. 相似文献
944.
945.
Margarida TerrnPuig Isabel HuberRuano Joan SabadellBasallote Miriam Ejarque Catalina NúezRoa Elsa MaymMasip Rosa Jorba Carolina Serena Joan Vendrell Sonia FernndezVeledo 《Aging cell》2022,21(8)
Dysfunctional adipocyte precursors have emerged as key determinants for obesity‐ and aging‐related inflammation, but the mechanistic basis remains poorly understood. Here, we explored the dysfunctional adipose tissue of elderly and obese individuals focusing on the metabolic and inflammatory state of human adipose‐derived mesenchymal stromal cells (hASCs), and on sirtuins, which link metabolism and inflammation. Both obesity and aging impaired the differentiation potential of hASCs but had a different impact on their proliferative capacity. hASCs from elderly individuals (≥65 years) showed an upregulation of glycolysis‐related genes, which was accompanied by increased lactate secretion and glycogen storage, a phenotype that was exaggerated by obesity. Multiplex protein profiling revealed that the metabolic switch to glycogenesis was associated with a pro‐inflammatory secretome concomitant with a decrease in the protein expression of SIRT1 and SIRT6. siRNA‐mediated knockdown of SIRT1 and SIRT6 in hASCs from lean adults increased the expression of pro‐inflammatory and glycolysis‐related markers, and enforced glycogen deposition by overexpression of protein targeting to glycogen (PTG) led to a downregulation of SIRT1/6 protein levels, mimicking the inflammatory state of hASCs from elderly subjects. Overall, our data point to a glycogen‐SIRT1/6 signaling axis as a driver of age‐related inflammation in adipocyte precursors. 相似文献
946.
Nightingale KP Baumann M Eberharter A Mamais A Becker PB Boyes J 《Nucleic acids research》2007,35(18):6311-6321
Targeted chromatin remodelling is essential for many nuclear processes, including the regulation of V(D)J recombination. ATP-dependent nucleosome remodelling complexes are important players in this process whose activity must be tightly regulated. We show here that histone acetylation regulates nucleosome remodelling complex activity to boost RAG cutting during the initiation of V(D)J recombination. RAG cutting requires nucleosome mobilization from recombination signal sequences. Histone acetylation does not stimulate nucleosome mobilization per se by CHRAC, ACF or their catalytic subunit, ISWI. Instead, we find the more open structure of acetylated chromatin regulates the ability of nucleosome remodelling complexes to access their nucleosome templates. We also find that bromodomain/acetylated histone tail interactions can contribute to this targeting at limited concentrations of remodelling complex. We therefore propose that the changes in higher order chromatin structure associated with histone acetylation contribute to the correct targeting of nucleosome remodelling complexes and this is a novel way in which histone acetylation can modulate remodelling complex activity. 相似文献
947.
948.
Joan Orpella M. Florencia Assaneo Pablo Ripolls Laura Noejovich Diana Lpez-Barroso Ruth de Diego-Balaguer David Poeppel 《PLoS biology》2022,20(7)
People of all ages display the ability to detect and learn from patterns in seemingly random stimuli. Referred to as statistical learning (SL), this process is particularly critical when learning a spoken language, helping in the identification of discrete words within a spoken phrase. Here, by considering individual differences in speech auditory–motor synchronization, we demonstrate that recruitment of a specific neural network supports behavioral differences in SL from speech. While independent component analysis (ICA) of fMRI data revealed that a network of auditory and superior pre/motor regions is universally activated in the process of learning, a frontoparietal network is additionally and selectively engaged by only some individuals (high auditory–motor synchronizers). Importantly, activation of this frontoparietal network is related to a boost in learning performance, and interference with this network via articulatory suppression (AS; i.e., producing irrelevant speech during learning) normalizes performance across the entire sample. Our work provides novel insights on SL from speech and reconciles previous contrasting findings. These findings also highlight a more general need to factor in fundamental individual differences for a precise characterization of cognitive phenomena.In the context of speech, statistical learning is thought to be an important mechanism for language acquisition. This study shows that language statistical learning is boosted by the recruitment of a fronto-parietal brain network related to auditory-motor synchronization and its interplay with a mandatory auditory-motor learning system. 相似文献
949.
Deem TL Abdala-Valencia H Cook-Mills JM 《Journal of immunology (Baltimore, Md. : 1950)》2007,178(6):3865-3873
Lymphocytes migrate from the blood into tissue by binding to and migrating across endothelial cells. One of the endothelial cell adhesion molecules that mediate lymphocyte binding is VCAM-1. We have reported that binding to VCAM-1 activates endothelial cell NADPH oxidase for the generation of reactive oxygen species (ROS). The ROS oxidize and stimulate an increase in protein kinase C (PKC)alpha activity. Furthermore, these signals are required for VCAM-1-dependent lymphocyte migration. In this report, we identify a role for protein tyrosine phosphatase 1B (PTP1B) in the VCAM-1 signaling pathway. In primary cultures of endothelial cells and endothelial cell lines, Ab cross-linking of VCAM-1 stimulated an increase in serine phosphorylation of PTP1B, the active form of PTP1B. Ab cross-linking of VCAM-1 also increased activity of PTP1B. This activation of PTP1B was downstream of NADPH oxidase and PKCalpha in the VCAM-1 signaling pathway as determined with pharmacological inhibitors and antisense approaches. In addition, during VCAM-1 signaling, ROS did not oxidize endothelial cell PTP1B. Instead PTP1B was activated by serine phosphorylation. Importantly, inhibition of PTP1B activity blocked VCAM-1-dependent lymphocyte migration across endothelial cells. In summary, VCAM-1 activates endothelial cell NADPH oxidase to generate ROS, resulting in oxidative activation of PKCalpha and then serine phosphorylation of PTP1B. This PTP1B activity is necessary for VCAM-1-dependent transendothelial lymphocyte migration. These data show, for the first time, a function for PTP1B in VCAM-1-dependent lymphocyte migration. 相似文献
950.
A new phenoxo-bridged binuclear manganese(III) Schiff base complex, [Mn(L)(N3)]2 (1) where L = N,N′-bis(salicylidene)-1,2-propanediamine has been synthesized and characterized by IR, elemental analysis, crystal structure analysis and variable temperature magnetic susceptibility measurements. The single crystal X-ray diffraction reveals that the structure is dimeric with each phenolate oxygen atom acting as a bridge between two symmetry equivalent Mn atoms. Low temperature magnetic study shows that the complex exhibits intra-dimer ferromagnetic exchange and single-molecule-magnet (SMM) behavior as well. 相似文献