A Study of the Advances in IoT Security

The Internet-of-things (IoT) holds a lot of benefits to our lives by removing menial tasks and improving efficiency of everyday objects. You are trusting your personal data and device control to the manufactures and you may not be aware of how much risk your putting your privacy at by sending your data over the internet. The internet-of-things may not be as secure as you think when the devices used are constrained by a lot of variables which attackers can exploit to gain access to your data / device and anything they connected to and as the internet-of-things is all about connecting devices together one weak point can be all it takes to gain full access. In this paper we have a look at the current advances in IoT security and the most efficient methods to protect IoT devices

A survey of emergency department use in patients with cyclic vomiting syndrome

<p>Abstract</p> <p>Background</p> <p>Cyclic vomiting syndrome (CVS), a chronic disorder characterized by recurrent episodes of vomiting, is frequently unrecognized and is associated with high utilization of emergency department (ED) services.</p> <p>Methods</p> <p>A web-based survey was posted on the Cyclic Vomiting Syndrome Association (CVSA) website to assess utilization of ED services in patients with CVS.</p> <p>Results</p> <p>Of 251 respondents, 104 (41.4%) were adult CVS patients and 147 (58.6%) were caregivers of pediatric and adult patients. In the adult group, the median number of ED visits for CVS symptoms was 15(range 1 - 200), with a median of 7 ED visits prior to a diagnosis of CVS (range 0 - 150). In the caregiver group, the median number of ED visits was 10 (range 1 - 175) and the median number of ED visits prior to a diagnosis of CVS was 5 (range 0 - 65). CVS was not diagnosed in the ED in 89/104 (93%) adults and 119/147 (93%) patients in the caregiver group. CVS was not recognized in the ED in 84/95 (88%) of adults and 97/122 (80%) of patients in the caregiver group, despite an established diagnosis of CVS.</p> <p>Conclusion</p> <p>There is a sub-group of adult and pediatric CVS patients who are high utilizers of ED services and CVS is not recognized in the ED in the majority of patients. Improved efforts to educate ED physicians are indicated to optimize treatment of patients with CVS and to decrease potential overuse of ED services.</p

Anaphylatoxin C3a receptors in asthma

The complement system forms the central core of innate immunity but also mediates a variety of inflammatory responses. Anaphylatoxin C3a, which is generated as a byproduct of complement activation, has long been known to activate mast cells, basophils and eosinophils and to cause smooth muscle contraction. However, the role of C3a in the pathogenesis of allergic asthma remains unclear. In this review, we examine the role of C3a in promoting asthma. Following allergen challenge, C3a is generated in the lung of subjects with asthma but not healthy subjects. Furthermore, deficiency in C3a generation or in G protein coupled receptor for C3a abrogates allergen-induced responses in murine models of pulmonary inflammation and airway hyperresponsiveness. In addition, inhibition of complement activation or administration of small molecule inhibitors of C3a receptor after sensitization but before allergen challenge inhibits airway responses. At a cellular level, C3a stimulates robust mast cell degranulation that is greatly enhanced following cell-cell contact with airway smooth muscle (ASM) cells. Therefore, C3a likely plays an important role in asthma primarily by regulating mast cell-ASM cell interaction

Genetic drivers of heterogeneity in type 2 diabetes pathophysiology.

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P < 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care

Genetic Drivers of Heterogeneity in Type 2 Diabetes Pathophysiology

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P \u3c 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care

Genetic drivers of heterogeneity in type 2 diabetes pathophysiology

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P &lt; 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care.</p

Novel method to synthesize and characterize Zinc Sulfide nanoparticles

Abstract: Zinc sulfide nanoparticles were fabricated by solvent evaporation method with and without using capping agent, Hexa decyltrimethyl ammonium bromide (CTAB) at room temperature. The product was received in powder form. The structure and composition of the resultant product was characterized by means of UV and FTIR spectrophotometric studies. FTIR analysis showed peaks at 352.02 cm-1 and 611.46 cm-1 for Zinc Sulfide with CTAB, corresponding to Zinc and Sulfide stretching. For Zinc Sulfide without CTAB, the same stretching frequencies were observed at 315.10 cm-1 and 615.32 cm-1. UV spectrophotometer study determined the band gap of nanocrystalline Zinc Sulfide (with and without CTAB) as 5.48 eV and 5.99 eV, respectively. The optical absorption edge exhibited a blue shift with respect to that of the bulk sample. The blue shift with the decrease in crystalline size was attributed to the quantum size effects. When ZnS was prepared without CTAB, there was decrease in the size of the nanoparticle than when it was prepared with CTAB. Even though no capping agent (CTAB) was used in preparing ZnS, the particle size was well reduced. It was achieved by stirring the solutions during preparation. No agglomeration of nanoparticles was detecte

Study of sulphonic acid functionalization of Vulcan XC-72 carbon black support of Pt/Vulcan XC-72 catalyst for methanol electrooxidation

704-707Sulphonic acid groups have been grafted onto the surface of Vulcan XC-72 carbon of the Pt/Vulcan XC-72 catalyst to improve platinum utilization in methanol electrooxidation studies. The sulphonic acid modification has been carried out by reacting the Pt/Vulcan XC-72 catalyst with formaldehyde and sodium sulfite. The resultant sulphonated catalysts are characterized by X-ray diffraction, Fourier transform infrared spectroscopy and cyclic voltammetry. FT-IR spectra confirm the incorporation of the sulphonic acid group on the carbon black support of the catalyst. XRD shows better dispersion of the Pt nanoparticles upon sulphonic acid modification. The electrochemical measurement using cyclic voltammetry shows enhanced activity for methanol electrooxidation for the sulphonic acid modified catalyst as compared to the unmodified one