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1.
Preclinical and clinical studies show that gastrointestinal (GI) inflammation can evoke sensory changes occasionally far from the original inflammatory site. Animal models of colitis with either trinitrobenzenesulphonic acid (TNBS) or mustard oil (MO) produce distinct patterns of somatic and visceral sensory changes. We evaluated the effects of four doses of i.v. vincristine 150 μg kg?1 (total of 600 μg kg?1) treatment on the somatic (thermal nociceptive threshold) and colonic (morphological) changes induced by TNBS or MO in rats. TNBS and MO groups were further submitted to vincristine or saline pretreatments. TNBS induced somatic hypersensitivity, while MO induced somatic hyposensitivity (P < 0.05) when compared to the saline and ethanol control groups. Vincristine per se induced somatic hypersensitivity (P < 0.05). This effect was enhanced by TNBS and reversed by MO treatments. Although vincristine increased the colitis area (colonic weight length?1 ratio) and the Morris' score in TNBS‐treated rats, it did not alter the colitis area and even lowered the Morris' score in MO‐treated rats. Compared to the saline (control) group, vincristine did not alter the colonic microscopic pattern. However, such lesions scores are higher (P < 0.05) in colitis groups induced by TNBS and MO, pretreated or not with vincristine. In conclusion, the somatic changes induced by different models of experimental colitis are diverse and modulated differently by vincristine.  相似文献   
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Cell adhesion molecule cadherins play important roles in both development and maintenance of adult structures. Most studies on cadherin expression have been carried out in developing organisms, but information on cadherin distribution in adult vertebrate brains is limited. In this study we used in situ hybridization to examine mRNA expression of three cadherins, protocadherin‐19, protocadherin‐17, and cadherin‐6 in adult zebrafish brain. Each cadherin exhibits a distinct expression pattern in the fish brain, with protocadherin‐19 and protocadherin‐17 showing much wider and stronger expression than that of cadherin‐6. Both protocadherin‐19 and protocadherin‐17‐expressing cells occur throughout the brain, with strong expression in the ventromedial telencephalon, periventricular regions of the thalamus and anterior hypothalamus, stratum periventriculare of the optic tectum, dorsal tegmental nucleus, granular regions of the cerebellar body and valvula, and superficial layers of the facial and vagal lobes. Numerous sensory structures (e.g., auditory, gustatory, lateral line, olfactory, and visual nuclei) and motor nuclei (e.g., oculomotor, trochlear, trigeminal motor, abducens, and vagal motor nuclei) contain protocadherin‐19 and/or protocadherin‐17‐expressing cell. Expression of these two protocadherins is similar in the ventromedial telencephalon, thalamus, hypothalamus, facial, and vagal lobes, but substantially different in the dorsolateral telencephalon, intermediate layers of the optic tectum, and cerebellar valvula. In contrast to the two protocadherins, cadherin‐6 expression is much weaker and limited in the adult fish brain. J. Comp. Neurol. 523:1419–1442, 2015. © 2015 Wiley Periodicals, Inc.  相似文献   
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Background

Visual and hearing impairments are known to be related to functional disability, cognitive impairment, and depression in community-dwelling older people. The aim of this study was to examine the prevalence of sensory impairment in nursing home residents, and whether sensory impairment is related to other common clinical problems in nursing homes, mediated by functional disability, cognitive impairment, and depressive symptoms.

Methods

Cross-sectional data of 4007 nursing home residents in 59 facilities in 8 countries from the SHELTER study were analyzed. Visual and hearing impairments were assessed by trained staff using the interRAI instrument for Long-Term Care Facilities. Generalized linear mixed models adjusted for functional disability, cognitive impairment, and depressive symptoms were used to analyze associations of sensory impairments with prevalence of clinical problems, including behavioral symptoms, incontinence, fatigue, falls, problems with balance, sleep, nutrition, and communication.

Results

Of the participants, 32% had vision or hearing impairment (single impairment) and another 32% had both vision and hearing impairments (dual impairment). Residents with single impairment had significantly higher rates of communication problems, fatigue, balance problems, and sleep problems, as compared with residents without any sensory impairment. Those with dual impairment had significantly higher rates of all clinical problems assessed in this study as compared with those without sensory impairment. For each clinical problem, the magnitude of the odds ratio for specific clinical problems was higher for dual impairment than for single impairment.

Conclusion

Visual and hearing impairments are associated with higher rates of common clinical problems among nursing home residents, independent of functional disability, cognitive impairment, and depressive symptoms.  相似文献   
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The Dystonin gene (Dst) is responsible for dystonia musculorum (dt), an inherited mouse model of hereditary neuropathy accompanied by progressive motor symptoms such as dystonia and cerebellar ataxia. Dst‐a isoforms, which contain actin‐binding domains, are predominantly expressed in the nervous system. Although sensory neuron degeneration in the peripheral nervous system during the early postnatal stage is a well‐recognised phenotype in dt, the histological characteristics and neuronal circuits in the central nervous system responsible for motor symptoms remain unclear. To analyse the causative neuronal networks and roles of Dst isoforms, we generated novel multipurpose Dst gene trap mice, in which actin‐binding domain‐containing isoforms are disrupted. Homozygous mice showed typical dt phenotypes with sensory degeneration and progressive motor symptoms. The gene trap allele (DstGt) encodes a mutant Dystonin‐LacZ fusion protein, which is detectable by X‐gal (5‐bromo‐4‐chloro‐3‐indolyl‐β‐D‐galactoside) staining. We observed wide expression of the actin‐binding domain‐containing Dystonin isoforms in the central nervous system (CNS) and peripheral nervous system. This raised the possibility that not only secondary neuronal defects in the CNS subsequent to peripheral sensory degeneration but also cell‐autonomous defects in the CNS contribute to the motor symptoms. Expression analysis of immediate early genes revealed decreased neuronal activity in the cerebellar‐thalamo‐striatal pathway in the homozygous brain, implying the involvement of this pathway in the dt phenotype. These novel DstGt mice showed that a loss‐of‐function mutation in the actin‐binding domain‐containing Dystonin isoforms led to typical dt phenotypes. Furthermore, this novel multipurpose DstGt allele offers a unique tool for analysing the causative neuronal networks involved in the dt phenotype.  相似文献   
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Although exercise therapy is considered part of the treatment of neuropathic patients, and somatosensory input is essential for motor learning, performance and neural plasticity, rehabilitation of patients with sensory ataxia has received little attention so far. The aim of this prospective pilot study was to explore the short‐ and medium‐term efficacy of a 3‐week intensive balance and treadmill exercise program in chronic ataxic neuropathy patients; 20 consecutive patients with leg overall disability sum score (ODSS‐leg) ≥2, absent/mild motor signs, clinical and therapeutic stability ≥4 months were enrolled. Evaluations were done at baseline, at the end of treatment and at 3‐ and 6‐month follow‐up. Outcome measurements included: ODSS‐leg, Berg balance scale, 6‐min walk distance, and the functional independence measure (FIM) scale. The short‐form‐36 health status scale (SF‐36) was used to measure health‐related quality of life (HRQoL). ODSS‐leg improved significantly compared with baseline, 3 weeks, 3 months (primary outcome), and 6 months follow‐up. A significant improvement in all functional secondary outcome measurements and in some SF‐36 subscales was also observed. This pilot study suggests that balance exercise is safe and well tolerated and might be effective in ameliorating disability and HRQoL in patients with chronic peripheral sensory ataxia.  相似文献   
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To identify novel mutations causing hereditary motor and sensory neuropathy (HMSN) with pyramidal signs, a variant of Charcot‐Marie‐Tooth disease (CMT), we screened 28 CMT and related genes in four members of an affected Japanese family. Clinical features included weakness of distal lower limb muscles, foot deformity, and mild sensory loss, then late onset of progressive spasticity. Electrophysiological studies revealed widespread neuropathy. Electron microscopic analysis showed abnormal mitochondria and mitochondrial accumulation in the neurons and Schwann cells. Brain magnetic resonance imaging (MRI) revealed an abnormally thin corpus callosum. In all four, microarrays detected a novel heterozygous missense mutation c.1166A>G (p.Y389C) in the gene encoding the light‐chain neurofilament protein (NEFL), indicating that NEFL mutations can result in a HMSN with pyramidal signs phenotype.  相似文献   
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