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排序方式: 共有679条查询结果,搜索用时 15 毫秒
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G.P.H. LUCKER P.C.M. Van De KERKHOF M.R. Van DÏJK P.M. STEIJLEN 《The British journal of dermatology》1994,131(4):546-550
We investigated the clinical efficacy of topically applied calcipotriol in six patients with congenital ichthyosis, using a double-blind, bilaterally paired, comparative approach. Unilateral improvement, in favour of the calcipotriol-treated side, was observed in three patients with lamellar ichthyosis. A beneficial response was also observed in a patient with bullous ichthyotic erythroderma of Brocq. No clinical side-effects or laboratory anomalies were observed. This study indicates that calcipotriol constitutes a new and promising approach in alleviating disorders of keratinization characterized by hyperproliferation, other than psoriasis. 相似文献
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Bégin S Burgoyne B Mercier V Villeneuve A Vallée R Côté D 《Biomedical optics express》2011,2(5):1296-1306
We present a wavelength-swept coherent anti-Stokes Raman scattering (WS-CARS) spectroscopy system for hyperspectral imaging in thick tissue. We use a strategy where the Raman lines are excited sequentially, circumventing the need for a spectrometer. This fibre laser system, consisting of a pump laser synchronized with a rapidly tunable programmable laser (PL), can access Raman lines over a significant fraction of the high wavenumber region (2700-2950 cm(-1)) at rates of up to 10,000 spectral points per second. To demonstrate its capabilities, we have acquired WS-CARS spectra of several samples as well as images and hyperspectral images (HSI) of thick tissue both in forward and epi-detection. This instrument should be especially useful in providing local biochemical information with surrounding context supplied by imaging. 相似文献
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Calcium signalling plays a crucial role in the control of neuronal function and plasticity. Changes in neuronal Ca2+ concentration are detected by Ca2+-binding proteins that can interact with and regulate target proteins to modify their function. Members of the neuronal calcium sensor (NCS) protein family have multiple non-redundant roles in the nervous system. Here we review recent advances in the understanding of the physiological roles of the NCS proteins and the molecular basis for their specificity. 相似文献
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Advances in highly active antiretroviral therapy (HAART) options for people living with HIV/AIDS have resulted in decreased morbidity and mortality. To some extent, the role of disease progression in eroding quality of life (QOL) erosion in the pre-HAART age is now supplanted by drug toxicities, one of the Achilles' heels of HAART. This article reviews research findings on treatment and QOL outcomes a decade into the HAART era. 相似文献
679.
Isles AR Davies W Burrmann D Burgoyne PS Wilkinson LS 《Human molecular genetics》2004,13(17):1849-1855
Recent work has indicated altered emotional functioning in Turner's syndrome (TS) subjects (45,XO). We examined the role of X-chromosome deficiency on fear reactivity in X-monosomic mice (39,XO), and found that they exhibited anxiogenic behaviour relative to normal females (40,XX). A molecular candidate for this effect is Steroid sulfatase (Sts) as this is located in the pseudoautosomal region (PAR) of the X-chromosome and consequently is normally biallelically expressed. In addition, the steroid sulfatase enzyme (STS) is putatively linked to fear reactivity by an effect on GABAA receptors via the action of neurosteroids. Real-time PCR demonstrated that levels of Sts mRNA were reduced by half in the brains of 39,XO mice compared with 40,XX, and that expression levels of a number of GABAA subunits previously shown to be important components of fear processing (Gabra3, Gabra1 and Gabrg2) were also altered. However, 40,XY*X mice, in which the Y*X is a small chromosome comprising of a complete PAR and a small non-PAR segment of the X-chromosome, exhibited the same pattern of fear reactivity behaviour as 39,XO animals, but equivalent expression levels of Sts, Gabra1, Gabra3 and Gabrg2 to 40,XX females. This showed that although Sts may cause alterations in GABAA subunit expression, these changes do not result in increased fear reactivity. This suggests an alternative X-chromosome gene, that escapes inactivation, is responsible for the differences in fear reactivity between 39,XO and 40,XX mice. These findings inform the TS data, and point to novel genetic mechanisms that may be of general significance to the neurobiology of fear. 相似文献