Depression,sleeping pattern,and suicidal ideation among medical students in Bangladesh: a cross-sectional pilot study

Journal of Public Health - Depression is a major morbidity and the most common mental disorder among the medical students in medical schools globally. Undergraduate students suffer stress more due...     

Study the Electrical Properties of Surface Mount Device Integrated Silver Coated Vectran Yarn

Smart textiles have attracted huge attention due to their potential applications for ease of life. Recently, smart textiles have been produced by means of incorporation of electronic components onto/into conductive metallic yarns. The development, characterizations, and electro-mechanical testing of surface mounted electronic device (SMD) integrated E-yarns is still limited. There is a vulnerability to short circuits as non-filament conductive yarns have protruding fibers. It is important to determine the best construction method and study the factors that influence the textile properties of the base yarn. This paper investigated the effects of different external factors, namely, strain, solder pad size, temperature, abrasion, and washing on the electrical resistance of SMD integrated silver-coated Vectran (SCV) yarn. For this, a Vectran E-yarn was fabricated by integrating the SMD resistor into a SCV yarn by applying a vapor phase reflow soldering method. The results showed that the conductive gauge length, strain, overlap solder pad size, temperature, abrasion, and washing had a significant effect on the electrical resistance property of the SCV E-yarn. In addition, based on the experiment, the E-yarn made from SCV conductive thread and 68 Ω SMD resistor had the maximum electrical resistance and power of 72.16 Ω and 0.29 W per 0.31 m length. Therefore, the structure of this E-yarn is also expected to bring great benefits to manufacturing wearable conductive tracks and sensors.     

Hearing aids versus ventilation tubes in persistent otitis media with effusion: a survey of clinical practice

A postal survey was carried out to determine the current clinical practice amongst consultant otolaryngologists in the UK, regarding re-insertion of ventilation tubes or recommendation of hearing aids in cases of recurrence of otitis media with effusion (OME) after ventilation tube extrusion. Amongst the 319 respondents, 15 (4.70 per cent) routinely, 146 (45.77 per cent) sometimes, and 158 (49.53 per cent) either never, or very rarely, recommend hearing aids. Hearing aids and ventilation tubes were both suggested to be equally good options by some consultants but they preferred surgery for a number of reasons. There were inconsistencies in practice and some of the reasons for re-inserting ventilation tubes are not evidence-based. A hearing aid is a non-invasive option and this survey shows a need for a randomized control trial of hearing aids and ventilation tubes in the management of persistent and recurrent OME.     

率的标准化与率差分解法在行为医学研究中的应用

目的 将率的标准化和率差分解法引入行为医学研究，调整因研究总体内部构成不同对率的影响。方法 应用重复抽自助法估计成分效尖的标准,并进行显著性检验。结果 美国北部某静脉吸毒人群血清HIV抗体阳性率资料分析表明，由年龄构成不同造成的效应贡献率为68．9％，有统计学意义；由种族构成不同造成的效应和年龄－种族别不同造成的率效应贡献率分别为－0．71％和31．65％，无统计学意义。结论 率的标准化和率差分解法可广泛应用于行为医学研究。     

Ca2+ signaling, TRP channels, and endothelial permeability

Increased endothelial permeability is the hallmark of inflammatory vascular edema. Inflammatory mediators that bind to heptahelical G protein-coupled receptors trigger increased endothelial permeability by increasing the intracellular Ca2+ concentration ([Ca2+]i). The rise in [Ca2+]i activates key signaling pathways that mediate cytoskeletal reorganization (through myosin-light-chain-dependent contraction) and the disassembly of VE-cadherin at the adherens junctions. The Ca2+-dependent protein kinase C (PKC) isoform PKCalpha plays a crucial role in initiating endothelial cell contraction and disassembly of VE-cadherin junctions. The increase in [Ca2+]i induced by inflammatory agonists such as thrombin and histamine is achieved by the generation of inositol 1,4,5-trisphosphate (IP3), activation of IP3-receptors, release of stored intracellular Ca2+, and Ca2+ entry through plasma membrane channels. IP3-sensitive Ca2+-store depletion activates plasma membrane cation channels (i.e., store-operated cation channels [SOCs] or Ca2+ release-activated channels [CRACs]) to cause Ca2+ influx into endothelial cells. Recent studies have identified members of Drosophila transient receptor potential (TRP) gene family of channels that encode functional SOCs in endothelial cells. These studies also suggest that the canonical TRPC homologue TRPC1 is the predominant isoform expressed in human vascular endothelial cells, and is the essential component of the SOC in this cell type. Further, evidence suggests that the inflammatory cytokine tumor necrosis factor-alpha can induce the expression of TRPC1 in human vascular endothelial cells signaling via the nuclear factor-kappaB pathway. Increased expression of TRPC1 augments Ca2+ influx via SOCs and potentiates the thrombin-induced increase in permeability in human vascular endothelial cells. Deletion of the canonical TRPC homologue in mouse, TRPC4, caused impairment in store-operated Ca2+ current and Ca2+-store release-activated Ca2+ influx in aortic and lung endothelial cells. In TRPC4 knockout (TRPC4-/-) mice, acetylcholine-induced endothelium-dependent smooth muscle relaxation was drastically reduced. In addition, TRPC4-/- mouse-lung endothelial cells exhibited lack of actin-stress fiber formation and cell retraction in response to thrombin activation of protease-activated receptor-1 (PAR-1) in endothelial cells. The increase in lung microvascular permeability in response to PAR-1 activation was inhibited in TRPC4-/- mice. These results indicate that endothelial TRP channels such as TRPC1 and TRPC4 play an important role in signaling agonist-induced increases in endothelial permeability.     

Nitric oxide within periaqueductal gray modulates glutamatergic neurotransmission and cardiovascular responses during mechanical and thermal stimuli

We have previously reported that nitric oxide (NO) within the rostral ventrolateral medulla (RVLM) attenuates cardiovascular responses and extracellular concentrations of glutamate during thermal, but not during mechanical nociceptive stimulation (Ishide. T., Maher, T.J., Ally, A. 2003. Role of nitric oxide in the ventrolateral medulla on cardiovascular responses and glutamate neurotransmission during mechanical and thermal stimuli. Pharmacol. Res. 47, 59-68). In this study, we examined the role of nitric oxide within the dorsolateral periaqueductal gray matter (PAG), a higher center integrating nociceptive reflexes, on cardiovascular responses and glutamate release during both mechanical and thermal nociception using anesthetized Sprague-Dawley rats. Two types of stimuli were studied, both activating peripheral A(delta) and C fiber polymodal nociceptors. Noxious mechanical stimulus was given by applying a bilateral hindpaw pinch for 5 s. Mechanical stimulation of a hindlimb increased mean arterial pressure (MAP), heart rate (HR), and extracellular fluid glutamate within PAG by 20+/-3 mmHg, 37+/-6 bpm, and 1.7+/-0.3 ng/5 microl, respectively (n=10). Bilateral microdialysis of L-arginine (1.0 microM), a NO precursor, into the PAG significantly attenuated MAP, HR, and glutamate increases during a mechanical stimulation. Subsequent administration of N(G)-methyl-L-arginine (L-NMMA) (1.0 microM), a NO synthase inhibitor, into the PAG blocked the ability of NO within PAG to modulate the cardiovascular responses to mechanical stimulus. The noxious thermal stimulus was generated by immersing the metatarsus of a hindpaw in water-bath at a temperature of 52 degrees C for 5 s. Similar increases were observed following thermal stimulation: 35+/-5 mmHg, 40+/-6 bpm, and 1.14+/-0.4 ng/5 microl (n=10). L-Arginine attenuated both cardiovascular responses and glutamate increase during thermal nociception. These results demonstrate that NO within the dorsolateral PAG plays a role in modulating cardiovascular responses by altering glutamate concentrations during both thermal and mechanical nociception.     

Contralateral suppression of otoacoustic emissions in children with specific language impairment

OBJECTIVE: The purpose of the investigation was to determine whether a group of children with specific language impairments (SLI) have reduced peripheral auditory processes thought to be associated with speech-in-noise intelligibility. DESIGN: Transient evoked otoacoustic emissions (TEOAE) and their suppression by the efferent activity of the medial olivocochlear system (MOCS) in response to contralateral acoustic stimulation were used to compare these processes in 18 children with SLI and 21 controls. RESULTS: The results revealed no group difference in TEOAE suppression effect or left/right asymmetry of TEOAE suppression effect. CONCLUSIONS: These results suggest that children with SLI do not have auditory processing problems at this peripheral level casting doubt on a hypothesized relationship between strength of MOCS activity and language impairment.     

Cardiovascular effects of central administration of clonidine in conscious cats

The effects on arterial blood pressure and heart rate after an intracerebroventricular (i.c.v.) administration of clonidine were investigated using conscious normotensive cats. Injection of clonidine (5–10 μg; 5 μl; i.c.v.) elicited a decrease in mean arterial pressure (MAP) and heart rate (HR) in a dose-dependent manner. The highest dose of 10 μg of clonidine decreased MAP and HR by 39 ± 3 mmHg and 74 ± 5 b.p.m., respectively (n = 7). Pretreatment with yohimbine, the α₂-adrenoceptor antagonist (8 μg; 5 μl; i.c.v.) blocked the cardiovascular responses to a subsequent i.c.v. injection of 10 μg clonidine (n = 7). Furthermore, preadministration of cimetidine (100 μg; 5 μl; i.c.v.), the H₂ histamine receptor antagonist with imidazoline receptor activating properties, prevented the decreases in MAP and HR to a subsequent i.c.v. injection of 10 μg clonidine (n = 7). By contrast, pretreatment with the specific I₁ imidazoline receptor blocker, efaroxan (100–500 μg; 5 μl; i.c.v.), failed to inhibit the cardiovascular effects of an i.c.v. administration of 10 μg clonidine (n = 7). These results suggest that the effects of centrally administered clonidine on MAP and HR are probably not mediated through activation of the I₁ subtype of imidazoline receptors in conscious cats. However, the cardiovascular effects elicited by i.c.v. administration of clonidine appear to result from stimulation of central α₂-adrenergic or the H₂ histaminergic-like receptors.