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Several studies have proposed that brain glutamate signaling abnormalities and glial pathology have a role in the etiology of major depressive disorder (MDD). These conclusions were primarily drawn from post-mortem studies in which forebrain brain regions were examined. The locus coeruleus (LC) is the primary source of extensive noradrenergic innervation of the forebrain and as such exerts a powerful regulatory role over cognitive and affective functions, which are dysregulated in MDD. Furthermore, altered noradrenergic neurotransmission is associated with depressive symptoms and is thought to have a role in the pathophysiology of MDD. In the present study we used laser-capture microdissection (LCM) to selectively harvest LC tissue from post-mortem brains of MDD patients, patients with bipolar disorder (BPD) and from psychiatrically normal subjects. Using microarray technology we examined global patterns of gene expression. Differential mRNA expression of select candidate genes was then interrogated using quantitative real-time PCR (qPCR) and in situ hybridization (ISH). Our findings reveal multiple signaling pathway alterations in the LC of MDD but not BPD subjects. These include glutamate signaling genes, SLC1A2, SLC1A3 and GLUL, growth factor genes FGFR3 and TrkB, and several genes exclusively expressed in astroglia. Our data extend previous findings of altered glutamate, astroglial and growth factor functions in MDD for the first time to the brainstem. These findings indicate that such alterations: (1) are unique to MDD and distinguishable from BPD, and (2) affect multiple brain regions, suggesting a whole-brain dysregulation of such functions.

Somatosensory thalamus and cortex in rodents contain topological representations of the facial whisker pad. The thalamic representation of a single whisker ('barreloid') is presumed to project exclusively to the cortical representation ('barrel') of the same whisker; however, it was not known when this correspondence is established during early development, nor how precise the thalamocortical projection is at birth, before formation of barrels and barreloids. To answer these questions, we retrogradely labeled thalamocortical projection neurons in fixed brain slices from 0-8 d old (P0- P8) mice, by placing paired deposits of two fluorescent dyes in adjacent barrels or (before barrel formation) in adjacent loci in upper cortical layers. At all ages studied, a negligible fraction of the retrogradely labeled cells was double labeled, implying that branches of single thalamocortical axons never extended within layer IV over an area wider than a single barrel. In P0 preparations, 70% of paired dye deposits placed 75- 200 μm apart resulted in statistically significant segregation of labeled cell clusters in the thalamus. Quantitative analysis indicated that on P0 about 70% of thalamocortical axons were within 1.3 presumptive barrel diameters from their topologically precise target. In P4-P8 preparations, the great majority of thalamic cells retrogradely labeled from a single barrel were found in a single barreloid, implying a 1:1 projection of barreloids to barrels. The postnatal increase in topological precision was reproduced by a computer simulation, which assumed that many aberrant axons corrected their initial targeting error by extending terminal arborizations asymmetrically, towards the center of their appropriate barrel.

The purpose of this quasi-experimental, pre-post-test study was to test the effectiveness of the Deaf Heart Health Intervention (DHHI) in increasing self-efficacy for health-related behaviors among culturally deaf adults. The DHHI targets modifiable risk factors for cardiovascular disease. A sample of 84 participants completed time-1 and time-2 data collection. The sign language version of the Self-Rated Abilities Scale for Health Practices (SRAHP) was used to measure self-efficacy for nutrition, psychological well-being/stress management, physical activity/exercise, and responsible health practices. Total self-efficacy scores were significantly higher in the intervention group than in the comparison group at time-2, controlling for scores at baseline (F [1, 81] = 26.02, p < .001). Results support the development of interventions specifically tailored for culturally deaf adults to increase their self-efficacy for health behaviors. (c) 2007 Wiley Periodicals, Inc. Res Nurs Health 30: 185-192, 2007. [ABSTRACT FROM AUTHOR]

THE PRESENT ARTICLE describes the effectiveness of stress management classes in decreasing perceived stress among Deaf adults. Deaf adults may experience unique stressors, in addition to circumstances associated with increased stress in the general population. The Perceived Stress Scale (S. Cohen, Kamarck, and Mermelstein, 1983) was used as a pretest and posttest measure for participants in a study of the Deaf Heart Health Intervention. Results indicated that (a) some Deaf adults may have higher levels of perceived stress than the general population, and (b) culturally appropriate stress management interventions are promising as a means of assisting Deaf adults to decrease levels of perceived stress, and hence decrease risk for stress-related illnesses. Future research will focus on obtaining a larger, more diverse sample of Deaf adults and refining the intervention for maximum effectiveness. [ABSTRACT FROM AUTHOR]

PurposeTo present the pathophysiology, differential diagnoses, assessment techniques, and treatment options for hepatic hydrothorax.Data SourcesA case study is presented with supporting material from current medical literature.ConclusionsHepatic hydrothorax is a pleural effusion caused by the flow of ascitic fluid into the pleural space through an actual defect in the diaphragm. Successful outcomes depend on early detection and timely referral of oftensubtle lung involvement. [ABSTRACT FROM AUTHOR]

Two cDNAs M1, and M2, recently isolated by the differential display method from embryonic rat cerebral hemisphere were characterized and their patterns of spatiotemporal expression analysed in developing rat forebrain by in situ hybridization histochemistry and correlative immunocytochemistry. Neither gene bears any sequence homology to other known genes. Both genes are particularly expressed in medial regions of the cerebral hemisphere and M2 in the roof of the adjacent diencephalon. M1 expression is highly localized and confined to the neuroepithelium of the hippocampal rudiment from embryonic day (E) 12 onward. Its location corresponds to the fimbrial anlage, and immunocytochemical localization of M1 protein indicates its expression in radial glial cells. M2 expression at E12 is more extensive in the medial cerebral wall, extending into the preoptic region and beyond the hippocampus into dorsal hemisphere and into the dorsal diencephalon, with caudal extension along the dorsal midline and in the zona limitans intrathalamica. Later, M2 expression is found in association with the corpus callosum, hippocampal commissure, fimbria, optic neve, stria medullaris, mamillothalamic tract and habenulopenduncular tract. M1 and M2 expression domains corresponding to the locations of fiber tracts are present prior to the arrival of the earliest axons, as identified by neuron specific markers. These findings suggest M1 and/or M2 genes are involved in early regional specification of the hippocampus and related structures in paramedian regions of the forebrain, and that cell populations expressing these genes in advance of developing axonal pathways may be involved in the early specification of tract location. [ABSTRACT FROM AUTHOR]

Chronic focal epilepsy is associated with synaptic plasticity and growth of new connections. Brain-derived neurotrophic factor (BDNF) is associated with each of these processes in normal brain and shows acute up-regulation in models of generalized epilepsy. Here, using an experimental model of focal epilepsy, we show persistent up-regulation of BDNF mRNA, independent of that of other growth factors, in association with the development and persistence of chronic seizures. In situ hybridization histochemistry revealed that rats perfused within 2-3 days after seizure onset had widespread increases in BDNF mRNA levels i the neocortex. Rats perfused at later times, however, showed focal up-regulation of BDNF and mRNA at the injection site and down-regulation in a surrounding cortical zone. Nerve growth factor and neurotrophin-3 mRNAs were not significantly altered. These reciprocal changes in BDNF gene expression in the epileptic focus and the cortical surround may contribute to plastic changes in epileptic neuronal circuits that accompany the transition from acute to chronic epilepsy. BDNF down-regulation in the surround is likely to be associated with the inhibitory surround that hampers seizure spread, but facilitates the persistence of a chronic epileptic focus. [ABSTRACT FROM AUTHOR]