Experimental Characterisation of GLass Aluminum REinforced (GLARE™) laminates

Fibre metal laminates such as GLARE™ have found promising application in the aerospace industry. These laminates were developed at the structures and materials laboratory of Delft University of Technology, Netherlands. GLARE™ is a material belonging to the family of Fibre Metal Laminates consisting of thin aluminum layers bonded with unidirectional S2-Glass fibres with an adhesive. Aluminum and S2-Glass when combined as a hybrid material can provide best features of the both metals and composites. These materials have excellent fatigue, impact and damage tolerance characteristics and a lower density compared to aluminum. GLARE™ has found major application in front and aft upper fuselage, leading edges of empennages of advanced civil aircrafts like A380. This document looks into the evaluation of two configuration of GLARE™ for its mechanical and impact characteristics. The mechanical characterisation was carried out for tensile, compression, Flexure, ILSS, Open Hole Tension, Open Hole Compression and Shear (Iosipescu). The impact behaviour were characterised based on a low velocity drop weight impact carried on these laminates. The study shows that the basic properties evaluated were more dictated by the property of the S2-Glass used. The studies show that GLARE™ laminates posses’ high impact damage resistance compared to other composite material. All the test datas generated for this study will be brought out in this document

Development of 3D Angle-Interlock Woven Preforms for Composites

The advent of three dimensional (3D) reinforcements has been mainly to overcome the issue of delamination and improve upon the damage tolerance properties by introducing fibres in the thickness direction for advanced composite applications. 3D preforms can be developed using various techniques. Angle-interlock weaving is one of them. This paper details about the efforts being put at CSIR-NAL for developing angle-interlock woven preforms. Four types of angle-interlock structures viz., layer-to-layer and through thickness (both with and without stuffer yarns) were developed using 6K, 400 Tex TC-33 grade Carbon tows on a custom designed handloom. The preforms without stuffer yarns had 4 layers of warp and were of 1.5± 0.2 mm thick. Preforms with stuffer yarns had 6 layers of warp (including 2 stuffer yarn layers) and were of 2.3±0.1 mm thick. Thermoset composites were prepared from these preforms using EPOLAM 2063 (an epoxy based resin system) by RTM process. The fibre weight fraction for these composites ranged from 0.53 to 0.58 and they were subjected to mechanical tests such as tensile, flexural and interlaminar shear strength. Test results showed improved response (in the warp direction) with respect to shear properties while the tensile and flexural properties were equivalent to that of the plain woven composites

Conduction velocities in amphibian skeletal muscle fibres exposed to hyperosmotic extracellular solutions

Early quantitative analyses of conduction velocities in unmyelinated nerve studied in a constantly iso-osmotic volume conductor were extended to an analysis of the effects of varying extracellular osmolarities on conduction velocities of surface membrane action potentials in Rana esculenta skeletal muscle fibres. Previous papers had reported that skeletal muscle fibres exposed to a wide range of extracellular sucrose concentrations resemble perfect osmometers with increased extracellular osmolarity proportionally decreasing fibre volume and therefore diminishing fibre radius, a. However, classical electrolyte theory (Robinson and Stokes 1959, Electrolyte solutions 2nd edn. Butterworth & Co. pp 41–42) would then predict that the consequent increases in intracellular ionic strength would correspondingly decrease sarcoplasmic resistivity, Ri. An extension of the original cable analysis then demonstrated that the latter would precisely offset its expected effect of alterations in a on the fibre axial resistance, ri, and leave action potential conduction velocity constant. In contrast, other reports (Hodgkin and Nakajima J Physiol 221:105–120, 1972) had suggested that Riincreased with extracellular osmolarity, owing to alterations in cytosolic viscosity. This led to a prediction of a decreased conduction velocity. These opposing hypotheses were then tested in muscle fibres subject to just-suprathreshold stimulation at a Vaseline seal at one end and measuring action potentials and their first order derivatives, dV/dt, using 5–20 MΩ, 3 M KCl glass microelectrodes at defined distances away from the stimulus sites. Exposures to hyperosmotic, sucrose-containing, Ringer solutions then reversibly reduced both conduction velocity and maximum values of dV/dt. This was compatible with an increase in Ri in the event that conduction depended upon a discharge of membrane capacitance by propagating local circuit currents through initially passive electrical elements. Conduction velocity then showed graded decreases with increasing extracellular osmolarity from 250–750 mOsm. Action potential waveforms through these osmolarity changes remained similar, including both early surface and the late after-depolarisation events reflecting transverse tubular activation. Quantitative comparisons of reduced-χ 2 values derived from a comparison of these results and the differing predictions from the two hypotheses strongly favoured the hypothesis in which Riincreased rather than decreased with hyperosmolarity

Primary microgliopathy presenting as degenerative dementias: A case series of novel gene mutations from India

Introduction Microglia exert a crucial role in homeostasis of white matter integrity and several studies highlight the role of microglial dysfunctions in neurodegeneration. Primary microgliopathy are disorders where the pathogenic abnormality of the microglia causes white matter disorder and leads to a neuropsychiatric diseases. Triggering Receptor Expressed on Myeloid Cells (TREM2), TYRO protein tyrosine kinase binding protein (TYROBP), Colony-stimulating factor 1 receptor (CSF1R) are genes implicated in primary microgliopathy. Clinical manifestations of primary microgliopathy are myriad ranging from neuropsychiatric syndrome, motor disability, gait dysfunction, ataxia, pure dementia, frontotemporal dementia, Alzheimer dementia and so on. It becomes imperative to establish diagnosis of microgliopathy masquerading as degenerative dementia, especially with promising therapies on horizon for the same. We aim to describe a case series of subjects with dementia harboring novel genes of primary microgliopathy, along with their clinical, neuropsychological, and cognitive profile and radiological patterns. Methods: The prospective study was conducted in a university referral hospital in South India, as a part of an ongoing clinic-genetic research on Dementia subjects and was approved by the institutional ethics committee. All patients underwent detailed assessment including socio demographic profile, clinical and cognitive assessment, pedigree analysis and comprehensive neurological examination. Subjects consenting for blood sampling underwent genetic testing by Whole exome sequencing (WES). Results: 100 patients of dementia underwent genetic analysis using whole exome sequencing and three pathogenic variants, one each of TREM2, TYROBP and CSF1R and two variants of uncertain significance in CSF1R were identified as cause of primary microgliopathy .TREM 2 and TYROBP presented as frontotemporal syndrome whereas CSF1R presented as frontotemporal syndrome and Alzheimer dementia. Conclusion :WES has widened the spectrum of underlying neuropathology of degenerative dementias and diagnosing primary microglial dysfunction with emerging therapeutic options is of paramount importance. Cases of primary microgliopathy due to Novel mutations in TREM2, TYROBP and CSF1R with phenotype of degenerative dementia are being first time reported from Indian cohort. Our study enriches the spectrum of genetic variants implicated in degenerative dementia, and provides the basis for exploring complex molecular mechanisms like microglial dysfunction, as underlying cause for neurodegeneration

Resistance to ursodeoxycholic acid-induced growth arrest can also result in resistance to deoxycholic acid-induced apoptosis and increased tumorgenicity

BACKGROUND: There is a large body of evidence which suggests that bile acids increase the risk of colon cancer and act as tumor promoters, however, the mechanism(s) of bile acids mediated tumorigenesis is not clear. Previously we showed that deoxycholic acid (DCA), a tumorogenic bile acid, and ursodeoxycholic acid (UDCA), a putative chemopreventive agent, exhibited distinct biological effects, yet appeared to act on some of the same signaling molecules. The present study was carried out to determine whether there is overlap in signaling pathways activated by tumorogenic bile acid DCA and chemopreventive bile acid UDCA. METHODS: To determine whether there was an overlap in activation of signaling pathways by DCA and UDCA, we mutagenized HCT116 cells and then isolated cell lines resistant to UDCA induced growth arrest. These lines were then tested for their response to DCA induced apoptosis. RESULTS: We found that a majority of the cell lines resistant to UDCA-induced growth arrest were also resistant to DCA-induced apoptosis, implying an overlap in DCA and UDCA mediated signaling. Moreover, the cell lines which were the most resistant to DCA-induced apoptosis also exhibited a greater capacity for anchorage independent growth. CONCLUSION: We conclude that UDCA and DCA have overlapping signaling activities and that disregulation of these pathways can lead to a more advanced neoplastic phenotype

SMARTphone-based, early cardiac REHABilitation in patients with acute coronary syndromes [SMART-REHAB Trial]: A randomized controlled trial protocol

© 2016 The Author(s). Background: There are well-documented treatment gaps in secondary prevention of coronary heart disease and no clear guidelines to assist early physical activity after acute coronary syndromes (ACS). Smartphone technology may provide an innovative platform to close these gaps. This paper describes the study design of a randomized controlled trial assessing whether a smartphone-based secondary prevention program can facilitate early physical activity and improve cardiovascular health in patients with ACS. Methods: We have developed a multi-faceted, patient-centred smartphone-based secondary prevention program emphasizing early physical activity with a graduated walking program initiated on discharge from ACS admission. The program incorporates; physical activity tracking through the smartphone's accelerometer with interactive feedback and goal setting; a dynamic dashboard to review and optimize cardiovascular risk factors; educational messages delivered twice weekly; a photographic food diary; pharmacotherapy review; and support through a short message service. The primary endpoint of the trial is change in exercise capacity, as measured by the change in six-minute walk test distance at 8-weeks when compared to baseline. Secondary endpoints include improvements in cardiovascular risk factor status, psychological well-being and quality of life, medication adherence, uptake of cardiac rehabilitation and re-hospitalizations. Discussion: This randomized controlled trial will use a smartphone-phone based secondary prevention program to emphasize early physical activity post-ACS. It will provide evidence regarding the feasibility and utility of this innovative platform in closing the treatment gaps in secondary prevention. Trial registration: The trial was retrospectively registered in the Australian New Zealand Clinical Trials Registry (ANZCTR) on April 4, 2016. The registration number is ACTRN12616000426482

Aberrant Mitochondrial Homeostasis in the Skeletal Muscle of Sedentary Older Adults

The role of mitochondrial dysfunction and oxidative stress has been extensively characterized in the aetiology of sarcopenia (aging-associated loss of muscle mass) and muscle wasting as a result of muscle disuse. What remains less clear is whether the decline in skeletal muscle mitochondrial oxidative capacity is purely a function of the aging process or if the sedentary lifestyle of older adult subjects has confounded previous reports. The objective of the present study was to investigate if a recreationally active lifestyle in older adults can conserve skeletal muscle strength and functionality, chronic systemic inflammation, mitochondrial biogenesis and oxidative capacity, and cellular antioxidant capacity. To that end, muscle biopsies were taken from the vastus lateralis of young and age-matched recreationally active older and sedentary older men and women (N = 10/group; ♀  =  ♂). We show that a physically active lifestyle is associated with the partial compensatory preservation of mitochondrial biogenesis, and cellular oxidative and antioxidant capacity in skeletal muscle of older adults. Conversely a sedentary lifestyle, associated with osteoarthritis-mediated physical inactivity, is associated with reduced mitochondrial function, dysregulation of cellular redox status and chronic systemic inflammation that renders the skeletal muscle intracellular environment prone to reactive oxygen species-mediated toxicity. We propose that an active lifestyle is an important determinant of quality of life and molecular progression of aging in skeletal muscle of the elderly, and is a viable therapy for attenuating and/or reversing skeletal muscle strength declines and mitochondrial abnormalities associated with aging

Comparative Performance of Private and Public Healthcare Systems in Low- and Middle-Income Countries: A Systematic Review

A systematic review conducted by Sanjay Basu and colleagues reevaluates the evidence relating to comparative performance of public versus private sector healthcare delivery in low- and middle-income countries

Measurement of the inclusive and differential Higgs boson production cross sections in the decay mode to a pair of τ Leptons in pp collisions at sqrt[s]=13 TeV

Measurements of the inclusive and differential fiducial cross sections of the Higgs boson are presented, using the τ lepton decay channel. The differential cross sections are measured as functions of the Higgs boson transverse momentum, jet multiplicity, and transverse momentum of the leading jet in the event, if any. The analysis is performed using proton-proton collision data collected with the CMS detector at the LHC at a center-of-mass energy of 13  TeV and corresponding to an integrated luminosity of 138  fb^{-1}. These are the first differential measurements of the Higgs boson cross section in the final state of two τ leptons. In final states with a large jet multiplicity or with a Lorentz-boosted Higgs boson, these measurements constitute a significant improvement over measurements performed in other final states