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821.
822.
ABSTRACT Estimating the spatial position of birds in open habitats like intertidal mudflats is important for many studies, for example, detailed density estimates or linking predation pressure to resource availability. To date, several methods have been used to estimate the positions of birds, including density counts in predetermined plots, range finders, photography, and tracking individuals tagged with GPS‐equipped transmitters, and each method has advantages and shortcomings. Counts in premarked plots are possible over relatively long distances, but small‐scale information is lost due to within‐plot averaging. Other methods accurately determine the position of individuals, but can only be used at relatively short distances or involve capturing birds. We describe a simple and low‐cost method to estimate the spatial position of individual birds in open habitats using a telescope‐mounted instrument that measures the scope's viewing angle. Using this Telescope‐Mounted Angulator (TMA), the distance to focal birds can be calculated by simple trigonometry, requiring only the viewing angle and mounting height of the telescope. Laboratory tests revealed that the TMA was most accurate when calibrated for individual observers. Field experiments performed on a 4‐m high observation platform showed that the TMA can estimate the position of shorebirds with an accuracy of 18 to 36 m up to a distance of 500 m. By also including the direction, determined with a compass, the spatial position of birds can be reliably estimated. The TMA can be a valuable tool for estimating the spatial position of animals in various flat landscapes, providing detailed measurements in a relatively short period of time.  相似文献   
823.
The most common form of spinal muscular atrophy (SMA) is a recessive disorder caused by deleterious SMN1 mutations in 5q13, whereas the genetic etiologies of non-5q SMA are very heterogeneous and largely remain to be elucidated. In a Bulgarian family affected by autosomal-dominant proximal SMA, we performed genome-wide linkage analysis and whole-exome sequencing and found a heterozygous de novo c.320C>T (p.Ser107Leu) mutation in bicaudal D homolog 2 (Drosophila) (BICD2). Further analysis of BICD2 in a cohort of 119 individuals with non-5q SMA identified a second de novo BICD2 mutation, c.2321A>G (p.Glu774Gly), in a simplex case. Detailed clinical and electrophysiological investigations revealed that both families are affected by a very similar disease course, characterized by early childhood onset, predominant involvement of lower extremities, and very slow disease progression. The amino acid substitutions are located in two interaction domains of BICD2, an adaptor protein linking the dynein molecular motor with its cargo. Our immunoprecipitation and localization experiments in HeLa and SH-SY5Y cells and affected individuals’ lymphoblasts demonstrated that p.Ser107Leu causes increased dynein binding and thus leads to accumulation of BICD2 at the microtubule-organizing complex and Golgi fragmentation. In addition, the altered protein had a reduced colocalization with RAB6A, a regulator of vesicle trafficking between the Golgi and the endoplasmic reticulum. The interaction between p.Glu744Gly altered BICD2 and RAB6A was impaired, which also led to their reduced colocalization. Our study identifies BICD2 mutations as a cause of non-5q linked SMA and highlights the importance of dynein-mediated motility in motor neuron function in humans.  相似文献   
824.
Giving adequate diagnostic information is considered to be fundamental in dementia care. An important question is how the diagnostic disclosure in dementia actually takes place. The aim of this explorative ethnographic study was therefore to provide insight into the disclosure practice of medical specialists. For this study, 22 interviews performed by seven medical specialists were analyzed.The results of this study show that the observed doctors are direct and explicit in disclosing the diagnosis. Actual (medical) information about the diagnosis and the performed investigations is provided. The main areas for improvement are involving the patient in the conversation, align your language to the lifeworld of the patient and his/her significant other(s), avoiding the use of medical jargon, discussing the consequences of the diagnosis for daily life, and explicitly recognizing the emotional and existential challenges associated with the disclosure. In providing further information, doctors could discuss emotional and existential support more specifically.  相似文献   
825.
Field collections ofAmblyomma hebraeum Koch adults from six breeds of cattle were conducted on two farms in the Northern Transvaal. The density ofA. hebraeum adults was highest on Simmentaler cows, followed by Santa gertrudis, Africaner, Bonsmara, Brahman and Nguni. Indigenous breeds, namely Nguni, Bonsmara and Africaner, have the highest level of resistance toA. hebraeum. The relationship between tick abundance and the high level of resistance found in the indigenous breeds is discussed.  相似文献   
826.
Activation ofprotein kinase C with phorbol 12-myristate 13-acetate (PMA) causedcomplex transient perturbations of amiloride-sensitive short-circuitNa+ currents(INa) in A6epithelia and frog skins that were tissue and concentration dependent.A noninvasive channel blocker pulse method of noise analysis (18) wasused to investigate how PMA caused time-dependent changes of apicalmembrane epithelial Na+ channel(ENaC) single-channel currents, channel open probabilities (Po), andchannel densities(NT). In A6epithelia, 5 and 50 nM PMA caused within 7 min concentration-dependentsustained decreases ofPo (~55% belowcontrol, 50 nM) and rapid compensatory transient increases ofNT within 7 min(~220% above control, 50 nM), resulting in either small transientincreases of INaat 5 nM PMA or small biphasic decreases ofINa at 50 nM PMA.In contrast to A6 epithelia, 50 and 500 nM PMA in frog skin causedafter a delay of at least 10 min transient increases ofNT to~60-70% above control at 30-60 min. Unlike A6 epithelia,Po was increased~15% above control within 7 min and remained within±10-15% of control for the duration of the 2-h experiments.Despite differences in the time courses of secondary inhibition oftransport in A6 epithelia and frog skin, the delayed downregulation oftransport was due to time-dependent decreases ofNT from theirpreelevated levels in both tissues. WhereasPo is decreasedwithin minutes in A6 epithelia as measured by noise analysis or bypatch clamp (8), the discrepancy in regulation ofNT in A6epithelia as measured by noise analysis and patch clamp is most likelyexplained by the inability of on-cell patches formed before treatmentof tissues with PMA to respond to regulation of their channeldensities.

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