Economic cost of tobacco use in India, 2004

ObjectiveTo estimate the tobacco-attributable costs of diseases separately for smoked and smokeless tobacco use in India.MethodsThe prevalence-based attributable-risk approach was used to estimate the economic cost of tobacco using healthcare expenditure data from the National Sample Survey, a nationally representative household sample survey conducted in India in 2004. Four major categories of tobacco-related disease-tuberculosis, respiratory diseases, cardiovascular diseases and neoplasms-were considered.ResultsDirect medical costs of treating tobacco related diseases in India amounted to $907 million for smoked tobacco and$285 million for smokeless tobacco. The indirect morbidity costs of tobacco use, which includes the cost of caregivers and value of work loss due to illness, amounted to $398 million for smoked tobacco and$104 million for smokeless tobacco. The total economic cost of tobacco use amounted to $1.7 billion. Tuberculosis accounted for 18$311 million) in India. Of the total cost of tobacco, 88% was attributed to men.ConclusionsThe cost of tobacco use was many times more than the expenditures on tobacco control by the government of India and about 16% more than the total tax revenue from tobacco. The tobacco-attributable cost of tuberculosis was three times higher than the expenditure on tuberculosis control in India. The economic costs estimated here do not include the costs of premature mortality from tobacco use, which is known to comprise roughly 50% to 80% of the total economic cost of tobacco in many countries

Programming DNA Tube Circumferences

Synthesizing molecular tubes with monodisperse, programmable circumferences is an important goal shared by nanotechnology, materials science, and supermolecular chemistry. We program molecular tube circumferences by specifying the complementarity relationships between modular domains in a 42-base single-stranded DNA motif. Single-step annealing results in the self-assembly of long tubes displaying monodisperse circumferences of 4, 5, 6, 7, 8, 10, or 20 DNA helices

Regional association of pCASL-MRI with FDG-PET and PiB-PET in people at risk for autosomal dominant Alzheimer's disease.

Autosomal dominant Alzheimer's disease (ADAD) is a small subset of Alzheimer's disease that is genetically determined with 100% penetrance. It provides a valuable window into studying the course of pathologic processes that leads to dementia. Arterial spin labeling (ASL) MRI is a potential AD imaging marker that non-invasively measures cerebral perfusion. In this study, we investigated the relationship of cerebral blood flow measured by pseudo-continuous ASL (pCASL) MRI with measures of cerebral metabolism (FDG PET) and amyloid deposition (Pittsburgh Compound B (PiB) PET). Thirty-one participants at risk for ADAD (age 39 ± 13 years, 19 females) were recruited into this study, and 21 of them received both MRI and FDG and PiB PET scans. Considerable variability was observed in regional correlations between ASL-CBF and FDG across subjects. Both regional hypo-perfusion and hypo-metabolism were associated with amyloid deposition. Cross-sectional analyses of each biomarker as a function of the estimated years to expected dementia diagnosis indicated an inverse relationship of both perfusion and glucose metabolism with amyloid deposition during AD development. These findings indicate that neurovascular dysfunction is associated with amyloid pathology, and also indicate that ASL CBF may serve as a sensitive early biomarker for AD. The direct comparison among the three biomarkers provides complementary information for understanding the pathophysiological process of AD

Validity of wearable physical activity monitors during activities of daily living

PURPOSE: To evaluate the validity of wearable activity monitors in SPT and EE under free-living environment. PURPOSE: To evaluate the validity of wearable activity monitors in SPT and EEunder free-living environment. METHODS: Thirty-nine (24.9+5.4 years) healthymales (n=26) and females (n=11) participated in this study. Total SPT and EE weremeasured by eight monitors; Nike+Fuel Band SE (NFB), Garmin VivoFit (VF), MisfitShine (MF), Fitbit Flex (FF), Jawbone UP (JU), Basis B1 (BB1), Polar Loop (PL), andSense Wear Armband Mini (SWA). The monitors were worn for at least 23 hours to beincluded in final data analysis and no PA restriction was applied. The SWA and a sleeplog were used as a criterion measure for SPT and EE, respectively. RESULTS: Total 24hours of EE (Kcal) (means±SD) were 3234.51+977, 2352.2 ±423, 2291.4±567,2679.8±752, 1955.4±251, 2950.9±864, 2724.9 ±627, 2822.1±525 for SWA, VF, JU,PL, BB1, FB, NFB, and MF, respectively. Mean absolute percent errors (MAPE) werecalculated (means±SD) 23.4%±8.0, 24.2%±8.8, 14.0% ±9.7, 28.9% ±22.0,17.5%±12.1, 16.9%±12.8, and 17.7%±15.0 for the VF, JU, PL, BB1, FB, NFB, andMF, respectively. SPT in minutes (mean±SD) were 481±83.32, 370.1+86.9,432.9±93.2, 467.7 ±51.2, 440.6±85.7, 424.6±103.3, 480.3±128.6, 436.6±35.3, and436.2±78.2 for the log, SWA, SWA laying down, VF, JU, PL, BB1, FB, and NFB,respectively. MAPE were calculated for SPT (mean±SD) 22.77% ±13.6,12.96±11.510.58% ±25.1, 11.6%±9.3, 18.2%±16.4, 14.6%±7.7, 8.7%±9.3, and13.5%±9.9 for the SWA, SWA laying down, VF, JU, PL, BB1, FB, and MF,respectively. ANOVA and post-hoc analyses with LSD indicated no significantdifferences were found with the FB, NFB, and MF in EE estimates. Additional post-hocanalyses with LSD for SPT revealed no significant difference (P\u3e.05) in all monitorsexcept SWA. CONCLUSION: The present study indicates that the FF, MS, and NFBare the most accurate wearable activity monitors when estimating EE and all monitorsprovide reasonable estimates of sleep period time, except SWA

How accurate are the wrist-based heart rate monitors during walking and running activities? Are they accurate enough?

Background Heart rate (HR) monitors are valuable devices for fitness-orientated individuals. There has been a vast influx of optical sensing blood flow monitors claiming to provide accurate HR during physical activities. These monitors are worn on the arm and wrist to detect HR with photoplethysmography (PPG) techniques. Little is known about the validity of these wearable activity trackers. Aim Validate the Scosche Rhythm (SR), Mio Alpha (MA), Fitbit Charge HR (FH), Basis Peak (BP), Microsoft Band (MB), and TomTom Runner Cardio (TT) wireless HR monitors. Methods 50 volunteers (males: n=32, age 19–43 years; females: n=18, age 19–38 years) participated. All monitors were worn simultaneously in a randomised configuration. The Polar RS400 HR chest strap was the criterion measure. A treadmill protocol of one 30 min bout of continuous walking and running at 3.2, 4.8, 6.4, 8.0, and 9.6 km/h (5 min at each protocol speed) with HR manually recorded every minute was completed. Results For group comparisons, the mean absolute percentage error values were: 3.3%, 3.6%, 4.0%, 4.6%, 4.8% and 6.2% for TT, BP, RH, MA, MB and FH, respectively. Pearson product-moment correlation coefficient (r) was observed: r=0.959 (TT), r=0.956 (MB), r=0.954 (BP), r=0.933 (FH), r=0.930 (RH) and r=0.929 (MA). Results from 95% equivalency testing showed monitors were found to be equivalent to those of the criterion HR (±10% equivalence zone: 98.15–119.96). Conclusions The results demonstrate that the wearable activity trackers provide an accurate measurement of HR during walking and running activities

Differential regulation of NAB corepressor genes in Schwann cells

<p>Abstract</p> <p>Background</p> <p>Myelination of peripheral nerves by Schwann cells requires not only the Egr2/Krox-20 transactivator, but also the NGFI-A/Egr-binding (NAB) corepressors, which modulate activity of Egr2. Previous work has shown that axon-dependent expression of Egr2 is mediated by neuregulin stimulation, and NAB corepressors are co-regulated with Egr2 expression in peripheral nerve development. NAB corepressors have also been implicated in macrophage development, cardiac hypertrophy, prostate carcinogenesis, and feedback regulation involved in hindbrain development.</p> <p>Results</p> <p>To test the mechanism of NAB regulation in Schwann cells, transfection assays revealed that both <it>Nab1 </it>and <it>Nab2 </it>promoters are activated by Egr2 expression. Furthermore, direct binding of Egr2 at these promoters was demonstrated in vivo by chromatin immunoprecipitation analysis of myelinating sciatic nerve, and binding of Egr2 to the <it>Nab2 </it>promoter was stimulated by neuregulin in primary Schwann cells. Although Egr2 expression activates the <it>Nab2 </it>promoter more highly than <it>Nab1</it>, we surprisingly found that only <it>Nab1 </it>– but not <it>Nab2 </it>– expression levels were reduced in sciatic nerve from Egr2 null mice. Analysis of the <it>Nab2 </it>promoter showed that it is also activated by ETS proteins (Ets2 and Etv1/ER81) and is bound by Ets2 in vivo.</p> <p>Conclusion</p> <p>Overall, these results indicate that induction of <it>Nab2 </it>expression in Schwann cells involves not only Egr2, but also ETS proteins that are activated by neuregulin stimulation. Although <it>Nab1 </it>and <it>Nab2 </it>play partially redundant roles, regulation of <it>Nab2 </it>expression by ETS factors explains several observations regarding regulation of NAB genes. Finally, these data suggest that NAB proteins are not only feedback inhibitors of Egr2, but rather that co-induction of Egr2 and NAB genes is involved in forming an Egr2/NAB complex that is crucial for regulation of gene expression.</p

Pathophysiology, treatment, and animal and cellular models of human ischemic stroke

Stroke is the world's second leading cause of mortality, with a high incidence of severe morbidity in surviving victims. There are currently relatively few treatment options available to minimize tissue death following a stroke. As such, there is a pressing need to explore, at a molecular, cellular, tissue, and whole body level, the mechanisms leading to damage and death of CNS tissue following an ischemic brain event. This review explores the etiology and pathogenesis of ischemic stroke, and provides a general model of such. The pathophysiology of cerebral ischemic injury is explained, and experimental animal models of global and focal ischemic stroke, and in vitro cellular stroke models, are described in detail along with experimental strategies to analyze the injuries. In particular, the technical aspects of these stroke models are assessed and critically evaluated, along with detailed descriptions of the current best-practice murine models of ischemic stroke. Finally, we review preclinical studies using different strategies in experimental models, followed by an evaluation of results of recent, and failed attempts of neuroprotection in human clinical trials. We also explore new and emerging approaches for the prevention and treatment of stroke. In this regard, we note that single-target drug therapies for stroke therapy, have thus far universally failed in clinical trials. The need to investigate new targets for stroke treatments, which have pleiotropic therapeutic effects in the brain, is explored as an alternate strategy, and some such possible targets are elaborated. Developing therapeutic treatments for ischemic stroke is an intrinsically difficult endeavour. The heterogeneity of the causes, the anatomical complexity of the brain, and the practicalities of the victim receiving both timely and effective treatment, conspire against developing effective drug therapies. This should in no way be a disincentive to research, but instead, a clarion call to intensify efforts to ameliorate suffering and death from this common health catastrophe. This review aims to summarize both the present experimental and clinical state-of-the art, and to guide future research directions

Joint inversion for global isotropic and radially anisotropic mantle structure including crustal thickness perturbations

We present a new global whole‐mantle model of isotropic and radially anisotropic S velocity structure (SGLOBE‐rani) based on ~43,000,000 surface wave and ~420,000 body wave travel time measurements, which is expanded in spherical harmonic basis functions up to degree 35. We incorporate crustal thickness perturbations as model parameters in the inversions to properly consider crustal effects and suppress the leakage of crustal structure into mantle structure. This is possible since we utilize short‐period group‐velocity data with a period range down to 16 s, which are strongly sensitive to the crust. The isotropic S velocity model shares common features with previous global S velocity models and shows excellent consistency with several high‐resolution upper mantle models. Our anisotropic model also agrees well with previous regional studies. Anomalous features in our anisotropic model are faster SV velocity anomalies along subduction zones at transition zone depths and faster SH velocity beneath slabs in the lower mantle. The derived crustal thickness perturbations also bring potentially important information about the crustal thickness beneath oceanic crusts, which has been difficult to constrain due to poor access compared with continental crusts.Key PointsWe used a massive and varied data set to constrain radially anisotropic mantle structureWe include crustal thickness perturbations as model parametersWe observe faster SV velocity along subduction slabs in the transition zonePeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/112272/1/jgrb51168.pd