全文获取类型
收费全文 | 436篇 |
免费 | 4篇 |
专业分类
儿科学 | 6篇 |
基础医学 | 61篇 |
临床医学 | 6篇 |
内科学 | 10篇 |
神经病学 | 296篇 |
特种医学 | 12篇 |
外科学 | 10篇 |
综合类 | 4篇 |
预防医学 | 5篇 |
眼科学 | 1篇 |
药学 | 20篇 |
中国医学 | 1篇 |
肿瘤学 | 8篇 |
出版年
2022年 | 3篇 |
2021年 | 6篇 |
2020年 | 14篇 |
2019年 | 7篇 |
2018年 | 11篇 |
2017年 | 16篇 |
2016年 | 6篇 |
2015年 | 10篇 |
2014年 | 16篇 |
2013年 | 18篇 |
2012年 | 14篇 |
2011年 | 12篇 |
2010年 | 11篇 |
2009年 | 12篇 |
2008年 | 19篇 |
2007年 | 15篇 |
2006年 | 9篇 |
2005年 | 10篇 |
2004年 | 16篇 |
2003年 | 8篇 |
2002年 | 3篇 |
2001年 | 9篇 |
2000年 | 14篇 |
1999年 | 9篇 |
1998年 | 8篇 |
1997年 | 9篇 |
1996年 | 14篇 |
1995年 | 8篇 |
1994年 | 9篇 |
1993年 | 21篇 |
1992年 | 11篇 |
1991年 | 9篇 |
1990年 | 10篇 |
1989年 | 10篇 |
1988年 | 3篇 |
1987年 | 2篇 |
1986年 | 2篇 |
1985年 | 7篇 |
1984年 | 6篇 |
1983年 | 4篇 |
1982年 | 9篇 |
1981年 | 7篇 |
1980年 | 3篇 |
1979年 | 5篇 |
1978年 | 2篇 |
1977年 | 3篇 |
1976年 | 2篇 |
1975年 | 1篇 |
1974年 | 3篇 |
1973年 | 4篇 |
排序方式: 共有440条查询结果,搜索用时 15 毫秒
1.
Generalized Convulsive Status Epilepticus in the Adult 总被引:10,自引:7,他引:3
David M. Treiman 《Epilepsia》1993,34(S1):S2-S11
Summary: Status epilepticus (SE) is denned as recurrent epileptic seizures without full recovery of consciousness before the next seizure begins, or more-or-less continuous clinical and/or electrical seizure activity lasting for more than 30 min whether or not consciousness is impaired. Three presentations of SE are now recognized: recurrent generalized tonic and/or clonic seizures without full recovery of consciousness between attacks, nonconvulsive status where the patient appears to be in a prolonged "epileptic twilight state," and continuous/repetitive focal seizure activity without alteration of consciousness. Generalized convulsive status epilepticus (GCSE) encompasses a broad spectrum of clinical presentations from repeated overt generalized tonic-clonic seizures to subtle convulsive movements in a profoundly comatose patient. Thus, GCSE is a dynamic state that is characterized by paroxysmal or continuous tonic and/or clonic motor activity, which may be symmetrical or asymmetrical and overt or subtle but which is associated with a marked impairment of consciousness and with bilateral (although frequently asymmetrical) ictal discharges on the EEG. Just as there is a progression from overt to increasingly subtle clinical manifestations of GCSE, there is also a predictable sequence of progressive EEG changes during untreated GCSE. A sequence of five patterns of ictal discharges has been observed: discrete electrographic seizures, waxing and waning, continuous, continuous with flat periods, and periodic epileptiform discharges on a relatively flat background. A patient actively having seizures or comatose who exhibits any of these patterns on EEG should be considered to be in GCSE and should be treated aggressively to stop all clinical and electrical seizure activity to prevent further neurological morbidity and mortality. 相似文献
2.
G. Lallement Didier Clarençon Catherine Masqueliez Dominique Baubichon Monique Galonnier Marie-France Burckhart Michel Peoc’h Jean Claude Mestries 《Archives of toxicology》1997,72(2):84-92
Organophosphorus nerve agents are still in use today in warfare and as terrorism compounds. Classical emergency treatment
of organophosphate poisoning includes the combined administration of a cholinesterase reactivator (an oxime), a muscarinic
cholinergic receptor antagonist (atropine) and a benzodiazepine anticonvulsant (diazepam). However, recent experiments with
primates have demonstrated that such treatment, even when administered immediately after organophosphate exposure, does not
rapidly restore normal electroencephalographic (EEG) activity and fails to totally prevent neuronal brain damage. The objective
of this study was to evaluate, in a realistic setting, the therapeutic benefit of administration of GK-11 (gacyclidine), an
antiglutamatergic compound, as a complement to the available emergency therapy against organophosphate poisoning. GK-11 was
injected at a dose of 0.1 mg/kg (i.v) after a 45-min latency period to heavily intoxicated (8 LD50) primates. Just after intoxication, man-equivalent doses of one autoinjector containing atropine/pralidoxime/diazepam were
administered. The effects of GK-11 were examined on survival, EEG activity, signs of toxicity, recovery after challenge and
central nervous system histology. The present data demonstrate that treatment with GK-11 prevents the mortality observed after
early administration of classical emergency medication alone. EEG recordings and clinical observations also revealed that
GK-11 prevented soman-induced seizures and motor convulsions. EEG analysis within the classical frequency bands (beta, theta,
alpha, delta) demonstrated that central activity was totally restored to normal after GK-11 treatment, but remained profoundly
altered in animals receiving atropine/pralidoxime/diazepam alone. GK-11 also markedly accelerated clinical recovery of soman-challenged
primates. Lastly, this drug totally prevented the neuropathology observed 3 weeks after soman exposure in animals treated
with classical emergency treatment alone. GK-11 represents a promising adjuvant therapy to the currently available emergency
polymedication to ensure optimal management of organophosphate poisoning in man. This drug is presently being evaluated in
a human clinical trial for a different neuroprotective indication.
Received: 16 June 1997 / Accepted: 23 September 1997 相似文献
3.
Andrew S. Fix Jeffrey W. Horn Lewis L. Truex Ronald A. Smith Ernesto Gomez 《Acta neuropathologica》1994,88(6):511-519
Cytoplasmic vacuoles appear in neurons of the posterior cingulate/retrosplenial cortex (PC/RS) of rats after treatment with N-methyl-d-aspartate (NMDA) receptor antagonists. Prominent dilatation of mitochondria and endoplasmic reticulum has been described within 2 h; however, the ultrastructural features of vacuole formation are unknown. To investigate this, the present study examined the PC/RS cortex of male rats (age 60–70 days) at 15, 30, 45, 60, 90, and 120 min after subcutaneous treatment with 1 mg/kg of the noncompetitive NMDA antagonist MK-801 (dizocilpine maleate, 5-methyl-10, 11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine). Subtle mitochondrial dilatation was identified in a few neurons as early as 15 min postdose (MPD). By 30 MPD, dilatation was more pronounced in mitochondria and also involved the endoplasmic reticulum and perinuclear space. Ribosomal disaggregation and degranulation were also evident by 30 MPD. At all subsequent time points, dilatation of mitochondria and endoplasmic reticulum progressed in severity. Although the relative involvement of mitochondria and endoplasmic reticulum varied, glia were not involved. These ultrastructural data suggest that after treatment with MK-801, mitochondrial dilatation precedes involvement of endoplasmic reticulum in vacuolization of susceptible PC/RS cortical neurons. The early mitochondrial effects identified in this study suggest an initial metabolic insult that rapidly progresses to affect endoplasmic reticulum and ribosomes. This strengthens the relationship between the ability of certain NMDA antagonists to induce energy perturbations and neuronal vacuoles in the same region of the rat cerebral cortex. 相似文献
4.
Elisabetta Ciani Tiziana Guarnieri Antonio Contestabile 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1994,98(3):421-430
The excitotoxins kainic acid and N-methyl d-aspartate (NMDA) were unilaterally injected in the rat striatum. Kainic acid injections resulted in a widespread pattern of Fos protein induction, mainly involving cortical olfactory structures and hippocampus. Immunoreactive cells were observed in large number 2–24 h after injection and had almost completely disappeared by 48 h. NMDA injections elicited a shorter (2–8 h) expression of Fos protein, involving a lower number of cells in cortical olfactory structures, a much larger number of cells in the other cortical regions, and not involving the hippocampus at all. Characteristically none of the two excitotoxins stimulated Fos expression from striatal neurons, even in the close vicinity of the needle tract. In addition to striatal lesions almost equivalent in size, the two excitotoxins caused distant lesions of different extension: kainic acid resulted in extensive neuronal degeneration in the olfactory-entorhinal cortices and among pyramidal neurons of the hippocampus; NMDA caused a less widespread neurodegeneration, restricted to the olfactory cortex. Administration of the competitive NMDA antagonist CGP 39551 largely prevented the distant, but not the local, neuropathological changes caused by intrastriatal kainic acid or NMDA. The expression of Fos protein, however, was partially prevented only in NMDA cases. The present results show a good relationship between the spreading of circuit overexcitation caused by the two excitotoxins and the regional and temporal patterns of Fos expression. The relationship between Fos expression and neuropathological condition remains, however, elusive. 相似文献
5.
D.F. Wozniak G. Brosnan-Watters A. Nardi M. McEwen T.D. Corso J.W. Olney A.S. Fix 《Brain research》1996,707(2):165
Several histological and behavioral experiments were conducted to investigate the neurotoxic effects of MK-801 in male mice. Moderate subcutaneous (s.c.) doses of MK-801 (0.5 and 1.0 mg/kg) induced the formation of intracytoplasmic vacuoles in pyramidal neurons in layers III and IV of the posterior cingulate/retrosplenial (PC/RS) cortex in 50% and 100% of the mice from the two respective treatment groups. Electron microscopic analysis of the vacuoles indicated that mitochondria and endoplasmic reticulum are the cellular organelles most prominently involved in this pathomorphological change. Treating mice with a high systemic dose of MK-801 (10 mg/kg s.c. or intraperitoneal (i.p.)) caused selective, irreversible degeneration of a small number of PC/RS cortical neurons. Compared to saline controls, the acquisition performance of mice treated i.p. with 10 mg/kg MK-801 was chronically impaired on a spatial learning task (modified hole board food search task) when tested at several posttreatment intervals (up to at least 5 months), although the groups did not differ on activity or sensorimotor tests conducted 2 weeks posttreatment. In summary, MK-801 caused histopathological changes in the mouse brain similar to those observed in the rat. Furthermore, high dose MK-801 treatment that killed a small number of mouse PC/RS cortical neurons resulted in a chronic acquisition impairment in spatial learning, an effect not previously demonstrated in any species. 相似文献
6.
Clinicopathological study of familial late infantile Hallervorden-Spatz disease: a particular form of neuroacanthocytosis 总被引:1,自引:0,他引:1
Alessandro Malandrini Gian Maria Fabrizi Paola Bartalucci Claudio Salvadori Gianna Berti Gian Carlo Guazzi Claudio Sabò 《Child's nervous system》1996,12(3):155-160
The cases of two sisters with late infantile Hallervorden-Spatz disease are reported, one of whom has died. Autopsy of the deceased patient showed typical pallidal lesions, such as axonal spheroids and iron deposits, without involvement of the substantia nigra. Ultrastructural examination revealed that pallidal axonal enlargements consisted of collecition of mitochondria, dense bodies, vesicles and amorphous material. In the living patient, brain MRI showed the classical tiger's eye appearance of the globus pallidus. Retinitis pigmentosa, acanthocytosis and slight neuromuscular involvement with an increase in serum creatine kinase were observed in both subjects. The appearance of the globus pallidus on MRI was in line with the pathological abnormalities. Ultrastructural differences between the principal disorders characterized by neuroaxonal dystrophy are compared and the clinical spectrum and similarities of the different forms of neuroacanthocytosis analysed. 相似文献
7.
癫痫患者突然意外死亡(sudden unexpected death in epilepsy,SUDEP)是指检证明没有解剖和毒理学原因的癫痫患者的突然死亡,它是慢性癫痫患者抽搐相关死亡最常见的原因. 相似文献
8.
《Biochemical pharmacology》2014,89(4):652-660
Dementia research over the last 50 years has expanded enormously and has greater international interest now than at any time in history. A variety of scientific approaches have been brought to bear on this complex disorder in which the syndrome of clinical features is its defining importance in societal terms. Little has emerged in terms of tangible benefits for people with dementia to date other than a hugely increased awareness at societal and governmental levels. One of the drivers for the increase in focus has been epidemiological evidence, which has provided background numbers for the justification of resources for dementia research. However it can be argued that this justification did not take into account the true meaning of the population evidence, drawing instead on preconceptions which were, at the time, the widely accepted interpretations of earlier evidence. Current evidence, along with the lack of single therapeutic successes, suggests that a clearer analysis is required which not only examines the value and applicability of existing knowledge, most particularly its generation and generalizability, but also where future investment should go for most likely benefit of populations. This includes a hard look at the pre-occupation of societies with single therapies, their place in the context of prevention more generally, particularly within aging populations, and how evidence is generated on likely impacts and their timeframes. 相似文献
9.
Almost one-third of the participants in a neuropsychological study signed the consent form below the given line. The relationship between a signature position on or below the line and participants’ cognitive function was investigated. Fifty drug-dependent individuals, 50 of their siblings, and 50 unrelated control participants completed a battery of neuropsychological tests using the Cambridge Neuropsychological Test Automated Battery (CANTAB). Individuals signing below, rather than on, the line performed more poorly on tests of visuospatial memory, but no differently on other cognitive tests. Signature positioning may be a soft sign for impairment of the mechanisms involved in visuospatial memory. 相似文献
10.
Inflammation involving the helper T cell 17 (Th17) subset of lymphocytes has been implicated in a number of diseases that affect the nervous system. As the canonical cytokine of Th17 cells, interleukin 17A (IL-17A) is thought to contribute to these neuroimmune interactions. The main receptor for IL-17A is expressed in many neural tissues. IL-17A has direct effects on neurons but can also impact neural function via signaling to satellite cells and immune cells. In the central nervous system, IL-17A has been associated with neuropathology in multiple sclerosis, epilepsy syndromes and ischemic brain injury. Effects of IL-17A at the level of dorsal root ganglia and the spinal cord may contribute to enhanced nociception during neuropathic and inflammatory pain. Finally, IL-17A plays a role in sympathetic axon growth and regeneration of damaged axons that innervate the cornea. Given the widespread effects of IL-17A on neural tissues, it will be important to determine whether selectively mitigating the damaging effects of this cytokine while augmenting its beneficial effects is a possible strategy to treat inflammatory damage to the nervous system. 相似文献