Discharge Curve Backoff Sleep Protocol for Energy Efficient Coverage in Wireless Sensor Networks

AbstractIn energy constrained wireless sensor networks, maximizing network coverage lifetime while ensuring optimized coverage is important. The challenge is to determine an appropriate duty cycle for the nodes while maintaining sufficient count of active nodes for optimal network coverage. Most of the existing work, for coverage optimization based on duty cycle, does not consider the residual energy of the active nodes. This can result in suboptimal wake-up of sleeping nodes. RBSP considers the residual energy but ignores the active nodes’ battery discharge rate. In this paper, we propose DCBSP (Discharge Curve Backoff Sleep Protocol), which considers the battery discharge curve of the active nodes to determine the duty cycle of the inactive nodes. Thus in DCBSP, inactive nodes wake-up close to death of the active nodes which leads to lesser energy consumption and increased network lifetime. NS-2 simulations show the energy consumption of DCBSP is lesser than that of PEAS by 39% and lesser by 25% and 15% as compared to RBSP and PECAS respectively. Further, the coverage ratio of DCBSP is higher than PEAS by 32% and higher by 17% and 6% as compared to RBSP, PECAS respectively. Hence, DCBSP is effective in ensuring higher coverage while extending the network lifetime

A study on knowledge, awareness and preventive practice about tuberculosis among medical students in Udaipur, India

Background: Tuberculosis (TB) is a highly lethal infectious disease causing huge health burden worldwide, commonly involving the respiratory system. Medical students should also be empowered to impart awareness and reduce stigma related to TB. The objective of this study was to evaluate whether educational intervention would affect the level of TB awareness, knowledge, attitude and preventive practice of TB among medical students.Methods: The present study was carried out among the second year medical college students of Pacific Institute of Medical Sciences, Udaipur, India (n=142). A multiple-choice questionnaire of 45 questions was designed in English language, for pre- and post-tests. A 30-minute visual health education was given on TB and the assessment of knowledge, attitude and preventive practice of TB was done by a pre-test and post-test questionnaire.Results: Out of the total 150 student, 142 participated in the study making the response rate 94.66%. The total mean percentage of correct answers for TB knowledge was 48.59 (±20.44) which improved to 69.33 (±17.74) post-training. The total mean percentage of right attitude was 63.036 (±16.46) which improved to 77.06 (±15.58) post-training. The total mean percentage of correct answer for preventive practice were provided by 67.036 (±12.90) which changed to 79.50 (±12.01) post-training. There was significant difference in the knowledge, attitude and preventive practice of students in pre- and post-training tests (p=0.001).Conclusions: Our findings revealed that medical students had poor knowledge. A simple TB education session had a positive influence on knowledge, attitude and preventive practices about TB among them

Handwritten Devanagari Text Recognition using Single Classifier Approach with VSPCA Scheme

In this research paper we used individual classifier approach for Handwritten Devanagari text recognition. We experimented different categorical classifiers namely   Random Forest Classifier (RFC), Support Vector Machine (SVM), K Nearest Neighbor Classifier (KNN), Logistic Regression Classifier (LogRegr), Decision Tree Classifier (DTree). Seven different feature sets are used namely Eccentricity, Euler Number, Horizontal Histogram, Vertical Histogram, HOG Features, LBP Features, and Statistical Features. The experimentation is carried out on 9434 different characters whose features are extracted from 220 handwritten image documents from PHDIndic_11 dataset. We deduced and implemented a unique scheme namely VSPCA scheme. VSPCA is Vectorization, Scaling, and Principal Component Analysis carried out on all feature sets before being given for model training. We obtained varied accuracies using all these five classifiers on all these six feature sets in which 99.52% highest accuracy is observed

ELECTROPHYSIOLOGICAL CHANGES IN LATENCY IN DIABETIC RETINOPATHY: AN OBSERVATIONAL STUDY

Purpose: Multifocal ERG is a useful indicator of diabetic retinopathy. The significant delay in local responses provides a chance for the detection and understanding of the various stages of diabetic retinopathy. Materials and Methods: This is a cross sectional study conducted in ERG clinic at M & J Western regional institute of ophthalmology, Ahmedabad from January 2013 to September 2015 who were more than 35yrs of age. Results: In our study, we studied 45 eyes of diabetic patients and 20 eyes of normal subjects. In our study the mean values of the various parameters was calculated in the control group with N1, P1 and N2 latency being 14.09ms. 29,76ms and 45.55ms respectively. The N1, P1 and N2 amplitude was found to be 31.52nV, 73.61nV and 90.38nV respectively. The maximum delay in N1, P1 and N2 latency was seen to be 3.24ms, 7.11ms and 8.40ms respectively from the normal value. We also found a decrease in amplitude of the ERG waveform with N1, P1 and N2 amplitude being 20.98nV, 61.48nV and 76.4nV respectively from the normal value. Also it is helpful in cases with clinically significant macular edema where responses are remarkably delayed suggesting local retinal dysfunction and macular pathology. It provides us information regarding the condition of the macula and some ideas about the extent of ischemia affecting this area. Conclusion: In conclusion, we can say that the delayed responses obtained indicate abnormal retinal function corresponding to local discrete retinal lesions. It provides a very sensitive and objective assessment of the local retinal condition in various stages of diabetic retinopathy. KEYWORDS: Diabetes mellitus; Diabetic retinopathy; Multifocal electroretinogram

ELECTROPHYSIOLOGICAL CHANGES IN LATENCY IN DIABETIC RETINOPATHY: AN OBSERVATIONAL STUDY

Purpose: Multifocal ERG is a useful indicator of diabetic retinopathy. The significant delay in local responses provides a chance for the detection and understanding of the various stages of diabetic retinopathy. Materials and Methods: This is a cross sectional study conducted in ERG clinic at M & J Western regional institute of ophthalmology, Ahmedabad from January 2013 to September 2015 who were more than 35yrs of age. Results: In our study, we studied 45 eyes of diabetic patients and 20 eyes of normal subjects. In our study the mean values of the various parameters was calculated in the control group with N1, P1 and N2 latency being 14.09ms. 29,76ms and 45.55ms respectively. The N1, P1 and N2 amplitude was found to be 31.52nV, 73.61nV and 90.38nV respectively. The maximum delay in N1, P1 and N2 latency was seen to be 3.24ms, 7.11ms and 8.40ms respectively from the normal value. We also found a decrease in amplitude of the ERG waveform with N1, P1 and N2 amplitude being 20.98nV, 61.48nV and 76.4nV respectively from the normal value. Also it is helpful in cases with clinically significant macular edema where responses are remarkably delayed suggesting local retinal dysfunction and macular pathology. It provides us information regarding the condition of the macula and some ideas about the extent of ischemia affecting this area. Conclusion: In conclusion, we can say that the delayed responses obtained indicate abnormal retinal function corresponding to local discrete retinal lesions. It provides a very sensitive and objective assessment of the local retinal condition in various stages of diabetic retinopathy. KEYWORDS: Diabetes mellitus; Diabetic retinopathy; Multifocal electroretinogram

Severe Diabetes and Leptin Resistance Cause Differential Hepatic and Renal Transporter Expression in Mice

Background: Type-2 Diabetes is a major health concern in the United States and other Westernized countries, with prevalence increasing yearly. There is a need to better model and predict adverse drug reactions, drug-induced liver injury, and drug efficacy in this population. Because transporters significantly contribute to drug clearance and disposition, it is highly significant to determine whether a severe diabetes phenotype alters drug transporter expression, and whether diabetic mouse models have altered disposition of acetaminophen (APAP) metabolites. Results: Transporter mRNA and protein expression were quantified in livers and kidneys of adult C57BKS and db/db mice, which have a severe diabetes phenotype due to a lack of a functional leptin receptor. The urinary excretion of acetaminophen-glucuronide, a substrate for multidrug resistance-associated proteins transporters was also determined. The mRNA expression of major uptake transporters, such as organic anion transporting polypeptide Slco1a1 in liver and kidney, 1a4 in liver, and Slc22a7 in kidney was decreased in db/db mice. In contrast, Abcc3 and 4 mRNA and protein expression was more than 2 fold higher in db/db male mouse livers as compared to C57BKS controls. Urine levels of APAP-glucuronide, -sulfate, and N-acetyl cysteine metabolites were higher in db/db mice. Conclusion: A severe diabetes phenotype/presentation significantly altered drug transporter expression in liver and kidney, which corresponded with urinary APAP metabolite levels

Enhanced Nrf2 Activity Worsens Insulin Resistance, Impairs Lipid Accumulation in Adipose Tissue, and Increases Hepatic Steatosis in Leptin-Deficient Mice

The study herein determined the role of nuclear factor erythoid 2–related factor 2 (Nrf2) in the pathogenesis of hepatic steatosis, insulin resistance, obesity, and type 2 diabetes. Lepob/ob-Keap1-knockdown (KD) mice, which have increased Nrf2 activity, were generated. Markers of obesity and type 2 diabetes were measured in C57Bl/6J, Keap1-KD, Lepob/ob, and Lepob/ob-Keap1-KD mice. Lepob/ob-Keap1-KD mice exhibited less lipid accumulation, smaller adipocytes, decreased food intake, and reduced lipogenic gene expression. Enhanced Nrf2 activity impaired insulin signaling, prolonged hyperglycemia in response to glucose challenge, and induced insulin resistance in Lepob/ob background. Nrf2 augmented hepatic steatosis and increased lipid deposition in liver. Next, C57Bl/6J and Keap1-KD mice were fed a high-fat diet (HFD) to determine whether Keap1 and Nrf2 impact HFD-induced obesity. HFD-induced obesity and lipid accumulation in white adipose tissue was decreased in Keap1-KD mice. Nrf2 activation via Keap1-KD or sulforaphane suppressed hormone-induced differentiation and decreased peroxisome proliferator–activated receptor-γ, CCAAT/enhancer–binding protein α, and fatty acid–binding protein 4 expression in mouse embryonic fibroblasts. Constitutive Nrf2 activation inhibited lipid accumulation in white adipose tissue, suppressed adipogenesis, induced insulin resistance and glucose intolerance, and increased hepatic steatosis in Lepob/ob mice

Keap1 knockdown increases markers of metabolic syndrome after long-term high fat diet feeding

The nuclear factor E2-related factor 2 (Nrf2)–Kelch-like ECH-associated protein 1 (Keap1) pathway upregulates antioxidant and biotransformation enzyme expression to counter cellular oxidative stress. The contributions of Nrf2 to other cellular functions, such as lipid homeostasis, are emerging. This study was conducted to determine how enhanced Nrf2 activity influences the progression of metabolic syndrome with long-term high-fat diet (HFD) feeding. C57BL/6 and Keap1-knockdown (Keap1-KD) mice, which exhibit enhanced Nrf2 activity, were fed a HFD for 24 weeks. Keap1-KD mice had higher body weight and white adipose tissue mass compared to C57BL/6 mice on HFD, along with increased inflammation and lipogenic gene expression. HFD feeding increased hepatic steatosis and inflammation to a greater extent in Keap1-KD mice compared to C57BL/6 mice, which was associated with increased liver Cd36, fatty acid-binding protein 4, and monocyte chemoattractant protein 1 mRNA expression, as well as increased acetyl-CoA carboxylase 1 and stearoyl-CoA desaturase-1 protein expression. The HFD altered short-term glucose homeostasis to a greater degree in Keap-KD mice compared to C57BL/6 mice, which was accompanied by downregulation of insulin receptor substrate 1 mRNA expression in skeletal muscle. Together, the results indicate that Keap1 knockdown, on treatment with HFD, increases certain markers of metabolic syndrome

Hepatic Lipid Accumulation and Nrf2 Expression following Perinatal and Peripubertal Exposure to Bisphenol A in a Mouse Model of Nonalcoholic Liver Disease

Background: Exposure to chemicals during critical windows of development may re-program liver for increased risk of nonalcoholic fatty liver disease (NAFLD). Bisphenol A (BPA), a plastics component, has been described to impart adverse effects during gestational and lactational exposure. Our work has pointed to nuclear factor E2-related factor 2 (Nrf2) being a modulator of hepatic lipid accumulation in models of NAFLD. Objectives: To determine if chemical exposure can prime liver for steatosis via modulation of NRF2 and epigenetic mechanisms. Methods: Utilizing BPA as a model exposure, pregnant CD-1 mice were administered 25μg/kg/day role= presentation \u3e25μg/kg/day BPA via osmotic minipumps from gestational day 8 through postnatal day (PND)16. The offspring were weaned on PND21 and exposed to same dose of BPA via their drinking water through PND35. Tissues were collected from pups at week 5 (W5), and their littermates at week 39 (W39). Results: BPA increased hepatic lipid content concomitant with increased Nrf2 and pro-lipogenic enzyme expression at W5 and W39 in female offspring. BPA exposure increased Nrf2 binding to a putative antioxidant response element consensus sequence in the sterol regulatory-element binding protein-1c (Srebp-1c) promoter. Known Nrf2 activators increased SREBP-1C promoter reporter activity in HepG2 cells. Methylated DNA immunoprecipitation-PCR and pyrosequencing revealed that developmental BPA exposure induced hypomethylation of the Nrf2 and Srebp-1c promoters in livers of W5 mice, which was more prominent in W39 mice than in others. Conclusion: Exposure to a xenobiotic during early development induced persistent fat accumulation via hypomethylation of lipogenic genes. Moreover, increased Nrf2 recruitment to the Srebp-1c promoter in livers of BPA-exposed mice was observed. Overall, the underlying mechanisms described a broader impact beyond BPA exposure and can be applied to understand other models of NAFLD

Deficiency in Nrf2 transcription factor decreases adipose tissue mass and hepatic lipid accumulation in leptin‐deficient mice

Objective: To evaluate whether Nrf2 deficiency impacts insulin resistance and lipid accumulation in liver and white adipose tissue. Methods: Lepob/ob mice (OB) with targeted Nrf2 deletion (OB‐Nrf2KO) were generated. Pathogenesis of obesity and type 2 diabetes was measured in C57BL/6J, Nrf2KO, OB, and OB‐Nrf2KO mice. Hepatic lipid content, lipid clearance, and very low‐density lipoprotein (VLDL) secretion were determined between OB and OB‐Nrf2KO mice. Results: OB‐Nrf2KO mice exhibited decreased white adipose tissue mass and decreased adipogenic and lipogenic gene expression compared with OB mice. Nrf2 deficiency prolonged hyperglycemia in response to glucose challenge, which was paralleled by reduced insulin‐stimulated Akt phosphorylation. In OB mice, Nrf2 deficiency decreased hepatic lipid accumulation, decreased peroxisome proliferator‐activated receptor γ expression and nicotinamide adenine dinucleotide phosphate (NADPH) content, and enhanced VLDL secretion. However, this observation was opposite in lean mice. Additionally, OB‐Nrf2KO mice exhibited increased plasma triglyceride content, decreased HDL‐cholesterol content, and enhanced apolipoprotein B expression, suggesting Nrf2 deficiency caused dyslipidemia in these mice. Conclusions: Nrf2 deficiency in Lepob/ob mice reduced white adipose tissue mass and prevented hepatic lipid accumulation but induced insulin resistance and dyslipidemia. This study indicates a dual role of Nrf2 during metabolic dysregulation—increasing lipid accumulation in liver and white adipose tissue but preventing lipid accumulation in obese mice