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This study draws on an evolutionary model of exchange in relationships to examine the nature of perceived reciprocity in the context of kin and non-kin relationships among a sample of visually impaired older adults (age 63–99). Further, we examined the direct and moderating impact of functional impairment and adaptation to visual impairment on the nature of perceived reciprocity. Results showed that the greater the degree of genetic relatedness the more imbalanced the exchange. It was also found that degree of adaptation to visual impairment moderated the association between genetic relatedness and perceived exchange, such that the greater the degree of genetic relatedness the more people reported they gave rather than received except at very low levels of adaptation, when people received more than they gave the greater the degree of genetic relatedness. Thus, an evolutionary model was supported such that imbalanced exchange was found more with greater degrees of genetic relatedness, but the direction of exchange was different for high versus low levels of adaptation to vision impairment.  相似文献   
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A single session of exposure therapy can eliminate recalcitrant and disabling fear of phobogenic objects or situations. We studied neural mechanisms of this remarkable outcome by monitoring changes in brain activity as a result of successful 2-h treatment. Before treatment, phobogenic images excited activity in a network of regions, including amygdala, insula, and cingulate cortex, relative to neutral images. Successful therapy dampened responsiveness in this fear-sensitive network while concomitantly heightening prefrontal involvement. Six months later, dampened fear-network activity persisted but without prefrontal engagement. Additionally, individual differences in the magnitude of visual cortex activations recorded shortly after therapy predicted therapeutic outcomes 6 mo later, which involved persistently diminished visual responsiveness to phobogenic images. Successful therapy thus entailed stable reorganization of neural responses to initially feared stimuli. These effects were linked to fear-extinction mechanisms identified in animal models, thus opening new opportunities for the treatment and prevention of debilitating anxiety disorders.  相似文献   
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Purpose

The aims of this study were to evaluate the diagnostic accuracy of the dual imaging method combining cardiac iodine-123-metaiodobenzylguanidine single-photon emission computed tomography combined with low-dose chest computed tomography compared to routine cardiac scintigraphy, and assess regional differences in tracer distribution and the relationships between imaging and autonomic function in Parkinson’s disease and multiple system atrophy.

Methods

A prospective study including 19 Parkinson’s disease and 12 multiple system atrophy patients was performed. Patients underwent clinical evaluation, iodine-123-metaiodobenzylguanidine single-photon emission computed tomography combined with chest computed tomography, planar scintigraphy, and cardiovascular autonomic function tests.

Results

Co-registration of single-photon emission computed tomography and chest computed tomography resulted in three groups with distinct patterns of tracer uptake: homogeneous, non-homogeneously reduced and absent. There was a significant difference in group allocation among patients with multiple system atrophy and Parkinson’s disease (p?=?0.001). Most multiple system atrophy patients showed homogeneous uptake, and the majority of Parkinson’s disease patients showed absent cardiac tracer uptake. We identified a pattern of heterogeneous cardiac tracer uptake in both diseases with reductions in the apex and the lateral myocardial wall. Sympathetic dysfunction reflected by a missing blood pressure overshoot during Valsalva manoeuvre correlated with cardiac tracer distribution in Parkinson’s disease patients (p?<?0.001).

Conclusions

The diagnostic accuracy of the dual imaging method and routine cardiac scintigraphy were similar. Anatomical tracer allocation provided by the dual imaging method of cardiac iodine-123-metaiodobenzylguanidine single-photon emission computed tomography and chest computed tomography identified a heterogeneous subgroup of Parkinson’s disease and multiple system atrophy patients with reduced cardiac tracer uptake in the apex and the lateral wall. Sympathetic dysfunction correlated with cardiac imaging in Parkinson’s disease patients.

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Background

Temporary loop ileostomy is a routine procedure to reduce the morbidity of restorative proctocolectomy. However, morbidity of ileostomy closure could reduce the benefit of this concept. The objective of this systematic review was to assess the risks of ileostomy closure after restorative proctocolectomy for ulcerative colitis or familial adenomatous polyposis.

Materials and Methods

Publications in English or German language reporting morbidity of ileostomy closure after restorative proctocolectomy were identified by Medline search. Two hundred thirty-two publications were screened, 143 were assessed in full-text, and finally 26 studies (reporting 2146 ileostomy closures) fulfilled the eligibility criteria. Weighted means for overall morbidity and mortality of ileostomy closure, rate of redo operations, anastomotic dehiscence, bowel obstruction, wound infection, and late complications were calculated.

Results

Overall morbidity of ileostomy closure was 16.5 %, there was no mortality. Redo operations for complications were necessary in 3.0 %. Anastomotic dehiscence occurred in 2.0 %. Postoperative bowel obstruction developed in 7.6 %, with 2.9 % of patients requiring laparotomy for this complication. Wound infection rate was 4.0 %. Hernia or bowel obstruction as late complications developed in 1.9 and 9.4 %, respectively.

Conclusion

The considerable morbidity of ileostomy reversal reduces the overall benefit of temporary fecal diversion. However, ileostomy creation is still recommended, as it effectively reduces the risk of pouch-related septic complications.  相似文献   
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The main purposes of the study were: (I) in vivo comparison of accumulation of live tumorigenic cells (LTC) in macroscopcally normal lungs of animals bearing 6 s.c. Syrian hamster sarcomas differing in spontaneous metastasizing activity (SMA); (2) in vitro examination of the sensitivity of these cell strains to the growth-regulating signals of normal fibroblasts. Cell strains used differed in SMA from very weak (WM) to extremely high (HM). The numbers of LTC doses in “normal” lung tissue of tumorbearing animals were determined in s.c. transplantation tests by titrating single-cell suspensions prepared from the lung tissues of 5 tumor-bearing animals, for each cell strain, every 5 days during 30 days of s.c. tumor growth, until the appearance of the first spontaneous lung metastases. The sensitivity of WM and HM cells to growth-regulating signals of normal hamster embryo fibroblasts (HEFs) was examined by in vitro co-culturing during 6 days with daily determination of 3H-TdR incorporation in the WM and HM cells grown with or without contact with HEFs. The data presented demonstrate (I) the surprisingly similar efficiency in the occupation of macroscopically normal lung tissues by live tumorigenic cells of WM and HM strains, disseminating spontaneously from the s.c. tumors; (2) the significantly lower sensitivity of HM cells, in contrast to WM, to growth inhibition by contact with HEFs and especially their marked ability to usurp the growth-stimulating signals of normal HEFs. © 1994 Wiley-Liss, Inc.  相似文献   
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This report presents findings supporting the hypothesis of a clinically relevant subtype of childhood speech sound disorder, provisionally titled speech delay-developmental psychosocial involvement (SD-DPI). Conversational speech samples from 29 children who met inclusionary criteria for SD-DPI were selected from a case record archive at a university speech clinic for children. Participants with SD-DPI had been characterized by speech clinicians and caregivers as having speech delay with psychosocial issues that required attention in the course of at least 1 semester of speech treatment. The 29 participants were divided into 2 subgroups, based on clinicians' and parents' records indicating either approach-related negative affect (n = 23) or withdrawal-related negative affect (n = 6). Each participant with SD-DPI was matched by age, gender, and type of speech involvement to 3 comparison speakers with speech delay of unknown origin (n = 87). Analyses of the conversational speech samples indicated that in comparison with participants in the control group, those with SD-DPI had significantly more severe speech delay, averaging approximately 7% to 10% lowered speech competence in conversation. The clinical prevalence of SD-DPI was estimated at approximately 12% of children referred to the university speech clinic in the present study. The authors interpret the present findings to indicate that approach-related or withdrawal-related negative affect, negative emotionality or mood, and decreased task persistence or attention are risk factors for increased severity of expression of speech delay.  相似文献   
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Smith-Magenis syndrome (SMS) is a multiple congenital anomaly/mental retardation syndrome associated with del(17)(p11.2p11.2). The phenotype is variable even in patients with deletions of the same size. RAI1 has been recently suggested as a major gene for majority of the SMS phenotypes, but its role in the full spectrum of the phenotype remains unclear. Df(11)17/+ mice contain a heterozygous deletion in the mouse region syntenic to the SMS common deletion, and exhibit craniofacial abnormalities, seizures and marked obesity, partially reproducing the SMS phenotype. To further study the genetic basis for the phenotype, we constructed three lines of mice with smaller deletions [Df(11)17-1, Df(11)17-2 and Df(11)17-3] using retrovirus-mediated chromosome engineering to create nested deletions. Both craniofacial abnormalities and obesity have been observed, but the penetrance of the craniofacial phenotype was markedly reduced when compared with Df(11)17/+ mice. Overt seizures were not observed. Phenotypic variation has been observed in mice with the same deletion size in the same and in different genetic backgrounds, which may reflect the variation documented in the patients. These results indicate that the smaller deletions contain the gene(s), most likely Rai1, causing craniofacial abnormalities and obesity. However, genes or regulatory elements in the larger deletion, which are not located in the smaller deletions, as well as genes located elsewhere, also influence penetrance and expressivity of the phenotype. Our mouse models refined the genomic region important for a portion of the SMS phenotype and provided a basis for further molecular analysis of genes associated with SMS.  相似文献   
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