M. Ejaz Hussain

Validity of the Pittsburgh Sleep Quality Index in Indian University Students

OBJECTIVES Despite the demonstrated utility of the Pittsburgh Sleep Quality Index (PSQI) in various demographic groups, it has never been validated in a sample of Indian subjects. To extend and confirm the PSQIs applicability for South Asian subjects, this preliminary study aimed to assess its psychometric and diagnostic validity in a sample of university students. METHODS Forty-seven male students were recruited from Jamia Millia Islamia, a public central university in New Delhi, India. The mean age of the students was 23.4±3.9 years, and they had a mean body mass index (BMI) of 23.3±3.3kg/m(2). The PSQI was administered to all subjects and overnight polysomnographic testing was carried out as a concurrent validation measure. RESULTS Cronbachs alpha for the questionnaire was found to be 0.736. Internal homogeneity was high, with the majority of correlations between questionnaire component scores and the summed global score being significant (p<0.010). Criterion validity-correlations between the PSQI global score and polysomnography (PSG) measures were low. However, the questionnaire component scores and the related polysomnographic measures did show some significant relationships. The optimal cut-off scores for distinguishing students with/without sleep problems was >6 and was generated using receiver operating characteristic curve analysis. The area under the curve, sensitivity, specificity, positive and negative likelihood ratios at the cut-off score were 0.838 (p<0.0001), 75.0%, 88.9%, 6.75, and 0.280, respectively. CONCLUSION The study found evidence that the PSQI had internal consistency, internal homogeneity, and diagnostic characteristics that compared well with PSG among a sample of young adult male students in India. This supports the applicability and certain aspects of the validity of the PSQI in the population.

Sleep-immune system interaction: advantages and challenges of human sleep loss model.

Sleep and its functional interaction with immune system is well recognized (Majde and Krueger, 2005; Krueger and Majde, 2011). Sleep synchronized changes in brain activity are implicated in direct rather than indirect immune function (Bryant et al., 2004). Sleep or at least its homeostatic component has been suggested to have an active auto-regulatory and/or auto-modulatory mechanism (Krueger et al., 2008; Kumar, 2010). This mechanism operates through adenosine and other sleep regulating substances (SRSs) like interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), growth-hormone-releasing hormone (GHRH), corticotropin-releasing hormone (CRH), nitric oxide (NO), prostaglandin D2 (PGD2), etc. These SRSs are most likely the connecting link between sleep and immune system (Krueger et al., 2008). The issue of peripheral cytokines affecting brain signaling in sleep has been reviewed comprehensively with three suggested routes for transfer of peripheral cytokines to the brain (Krueger and Majde, 2003). These routes may also be involved in transfer and hence in transmitting the signals from peripheral SRSs. Sleep–immune system co-relations has been investigated across a wide range of immune parameters out of which cytokines, immune cells, antibodies, and neuro-endocrine system constitute the focal group. Human sleep loss (SL) models have been of great help in mechanistic characterization of cytokines (IL-1β and TNF-α role) in sleep and neuroendocrine components (GHRH and CRH) in non-REM sleep, respectively (Majde and Krueger, 2005; Krueger and Majde, 2011). The paradigm has helped establish sleeps functional characterization because of practical simplicity (Reynolds and Banks, 2010) and often non-ambiguous results. However, there may be certain limitations with SL model in context of result translation pertaining to different parameter patterns. The comment has been surmised to highlight these challenges which may give direction to future research in minimizing the variable factors. It may also help to compare the results from available literature objectively.

Sleep in university students across years of university education and gender influences

Abstract Purpose: Assessment of the influence of gender and increasing years at university on sleep health of students. Methods: Four hundred and eighteen students from different streams across years of undergraduate to postgraduate courses participated. Descriptive statistics, test of differences, and correlation were used. The sleep health data comprised of subjective evaluation using a questionnaire and personal interviews. Results: Overall, 43.1% had sleep problems, females were more affected (51.67% vs. 48.33% in males) but were early bed goers. The prevalence of circadian rhythm sleep disorder (11.6% vs. 9.5%) and delayed sleep phase syndrome (4.5% vs. 2.7%) was slightly higher in males. The daytime dysfunction and hypnotic use significantly differed in students of the same class among gender. Bedtime got significantly delayed along years [H(2)=29.769, p<0.001], and hypnotic use [H(2)=8.807, p=0.012] differed significantly among them. The moderate-very strong correlational statistics among sleep health elements was very similar across gender and years of university education. However, more pronounced influence of years of university education than gender was seen in the significant differences for correlated correlation among sleep health parameters. Conclusion: Gender and years of university education influence sleep among university students both separately and concomitantly.

Humidity and sleep: a review on thermal aspect

The peripheral humidity detector/detection is not clear though there are comprehensive reports of subjective perception. High relative humidity at ambient temperatures above thermo-neutral zone has deleterious effect on sleep. Humidity affects heat transfer rate by affecting evaporation and thereby disturbing the Tc and Ts dynamics. The effect is discernible across a host of sleep, body temperature, and microclimate indices. A number of hypotheses have been proposed to explain the sleep structure regulation of which circadian–homeostatic interaction model is the most accepted one. Humid heat may affect sleep through homeostatic pathway possibly interfering with adenosine accumulation in basal forebrain and thereby affecting non-rapid eye movement (NREM) sleep switch point. It may also have a circadian element by interfering with thermo-regulatory feedback loop and/or by affecting Ts change input to sleep regulation.

Factor scoring models of the Pittsburgh Sleep Quality Index: a comparative confirmatory factor analysis

Abstract The Pittsburgh Sleep Quality Index (PSQI) is a rigorously validated questionnaire with extensive use in sleep assessment. Findings from numerous factor analytic studies of the PSQI have been interpreted to support a heterogeneous factor structure model for the test. Nevertheless, the literature continues to lack a focused evaluation of whether this heterogeneous factor structure is justified. A consideration of this issue led to a conclusion that a closer analysis of the PSQI’s factor structure was merited. To address this need a comparative confirmatory factor analysis for assessing the performance of the accepted factors models of the PSQI was conducted. A sample of university students (n = 418), age = 20.92 ± 1.81 years, BMI = 23.30 ± 2.57 kg/m2 completed the multi-structured sleep survey at Jamia Millia Islamia, New Delhi, India. Seventeen putative factor structures (three 1-Factor, eight 2-Factor, and six 3-Factor) of the PSQI from the existing literature were selected for analysis. Fourteen models (82.35%) had almost similar values for model fit indices. Two models were misfits, and one model was a poor fit. The two misfit models incorporated gender and age as covariates. The third poor fit model was used to produce a unique path diagram, which made it distinct from the remaining 16 models. The overlapping values in the fit range of the model fit indices did not support the often projected heterogeneous factor structures of the PSQI for the vast majority of the models.

Exercise training and cardiac autonomic function in type 2 diabetes mellitus: A systematic review

Cardiac autonomic neuropathy (CAN) is a common complication of type 2 diabetes mellitus (T2DM). It has been found to independently predict all cause and cardiovascular disease (CVD) mortality. It remains unclear whether exercise training could improve autonomic control in T2DM patients. The purpose of this study was to systematically review the effects of exercise training on cardiac autonomic function in T2DM patients. Electronic databases (MEDLINE, CENTRAL, PEDro, Scopus and Web of science) were systematically searched to retrieve relevant evidence. Clinical trials administering exercise training for at least 4 weeks and examining either heart rate variability (HRV), baroreflex sensitivity (BRS), heart rate recovery (HRR) as outcome measures were eligible. Eighteen articles were found to be relevant and were then assessed for characteristics and quality. Fifteen studies out of 18 found that exercise training leads to positive improvements in autonomic function of T2DM patients. Exercise participation enhances cardiac autonomic function of type 2 diabetics and therefore should be implemented in their management programs.

Intracellular cAMP assay and Eu-GTP-γS binding studies of chimeric opioid peptide YFa

In our previous studies chimeric peptide of Met-enkephalin and FMRFa, YGGFMKKKFMRFamide (YFa), demonstrated concentration dependent κ- and μ-opioid receptor mediated antinociception without tolerance development. To gain further insight of the observed behavior of YFa, the present study was undertaken. The effect of chimeric peptide on forskolin-stimulated cAMP formation under acute and chronic treatment and stimulation of Eu-GTP-γS binding in CHO cells stably expressing κ- and μ-opioid receptors was assessed. YFa showed concentration dependent inhibition of forskolin-stimulated cAMP in both hKOR and hMOR-CHO cells; however, the inhibition at 1nM was significantly higher in hKOR cells and comparable to DynA (1-13) than that shown at 20nM in hMOR cells. Chronic treatment of YFa, similar to DynA (1-13), did not show significant change in forskolin-stimulated cAMP level in both hKOR and hMOR cells. However, chronic treatment of morphine and DAMGO showed an increase in forskolin-stimulated cAMP level in hMOR-CHO cells indicating superactivation of adenylyl cyclase. Eu-GTP-γS binding studies of YFa showed a concentration dependent adherent binding with κ- and μ-opioid receptors; however, the latter demonstrated significant binding at higher concentration. Thus the study indicates the chimeric opioid peptide YFa as a potent κ- receptor specific antinociceptive moiety, showing no tolerance and hence may serve as a lead in understanding the mechanism of tolerance development, antinociception and its modulation.

Endothelium modulated vasorelaxant response of a polypharmaceutical herbal drug (lipotab) and its individual constituents.

The present study was undertaken to examine the endothelium modulated effects of polypharmaceutical drug lipotab and its individual ingredients in isolated aortic rings of rat. Endothelium intact and denuded aortic rings were precontracted with phenylephrine 10(-6) M and drugs were added in cumulative manner in concentration ranging from 1 to 50 microg/ml. The results demonstrated an endothelium-dependent vasorelaxant effect of lipotab and its individual ingredients, with the exception of nicotinic acid. The dose dependent relaxant response of nicotinic acid was not altered significantly in the endothelium-denuded rings, suggesting a direct effect of the drug on the vascular smooth muscle. Vasorelaxant effect of lipotab and its individual constituents suggests the therapeutic potential of these compounds in certain cardiovascular diseases.

Sleep and physiological systems: a functional perspective

The knowledge of sleep evaluation and its regulation processes has evolved dramatically over the last half-century. Sleep state and the preoccupied view of its obligation to perform positive function for the organism have kept enthusiastic research flourishing. The restoration of macromolecular synthesis and repair players, energy conservation, neural plasticity and synaptogenesis are cellular and biochemical-level functional implications of sleep. The demarcation between molecular, cellular and systemic strata is not mutually exclusive at organism level. Sleep functions have been researched with their focus at each of these strata. The review discusses the systemic-level functions of sleep in brief with special reference to respiration, reproduction, digestion, cardiovascular, endocrine, immune and integumentary systems. Sleep and physiological system relations are usually bidirectional and are operationally mediated by intercellular message transmitters like hormones, cytokines and/or continuum of direct anatomical connections with the neuroanatomy of sleep management.

Effects of a novel ACE inhibitor, 3-(3-thienyl)-l-alanyl-ornithyl-proline, on endothelial vasodilation and hepatotoxicity in l-NAME-induced hypertensive rats

Nitric oxide (NO) is a widespread biological mediator involved in many physiological and pathological processes, eg, in the regulation of vascular tone and hypertension. Chronic inhibition of NO synthase by NG-nitro-l-arginine methyl ester (l-NAME) hydrochloride results in the development of hypertension accompanied by an increase in vascular responsiveness to adrenergic stimuli. Recently, we developed a novel sulfur-containing angiotensin-converting enzyme inhibitor: 3-(3-thienyl)-l-alanyl-ornithyl-proline (TOP). Our previous studies indicated a superior nature of the molecule as an antihypertensive agent in spontaneously hypertensive rats (showing the involvement of renin–angiotensin–aldosterone system) in comparison to captopril. The aim of the present study was to investigate the effect of TOP on NO pathway in l-NAME-induced hypertensive rats, and captopril was included as the standard treatment group. Treatment with both TOP (20 mg/kg) and captopril (40 mg/kg) prevented the development of hypertension in l-NAME model, but TOP showed better restoration of NO and normal levels of angiotensin-converting enzyme. In addition, in vitro vasorelaxation assay showed an improvement in endothelium-dependent vasodilation in both the cases. Further, the biochemical (malondialdehyde, alanine aminotransferase, and aspartate aminotransferase) and the histopathological effects of TOP on rat liver tissues revealed a protective nature of TOP in comparison to captopril in the l-NAME model. In conclusion, TOP at 50% lesser dose than captopril was found to be better in the l-NAME model.