IoT based Driver Drowsiness and Pothole Detection Alert System

One of the common in progressing countries is the maintenance of roads. Well maintained roads contribute a major portion to the country’s economy. Identification of pavement distress such as potholes and humps not only help drivers to avoid accidents or vehicle damages, but also helps authorities to maintain roads. This paper discusses various pothole detection methods that have been developed and proposes a simple and cost-effective solution to identify the potholes and humps on roads and provide timely alerts to drivers to avoid accidents or vehicle damages. Not only Potholes and humps are the main cause of accidents other than over speeding and drowsiness of driver includes the issue of accidents. Drowsy state may be caused by lack of sleep, medication, tiredness, drugs or driving continuously for long period of time. So, here is the solution for detecting the potholes and humps and to alert the driver from drowsiness while driving. In this paper, the system is structured to detect potholes and to alert the drowsy driver by using the ultrasonic sensor, eyeblink sensor and IR sensor and microcontroller. Ultrasonic sensor senses the humps, IR sensor senses the potholes and eye blink sensor the blinking of eye and this sensing signals fed into the Arduino to alert the driver by buzzer sound

The Relationship of DNA Methylation with Age, Gender and Genotype in Twins and Healthy Controls

Cytosine-5 methylation within CpG dinucleotides is a potentially important mechanism of epigenetic influence on human traits and disease. In addition to influences of age and gender, genetic control of DNA methylation levels has recently been described. We used whole blood genomic DNA in a twin set (23 MZ twin-pairs and 23 DZ twin-pairs, N = 92) as well as healthy controls (N = 96) to investigate heritability and relationship with age and gender of selected DNA methylation profiles using readily commercially available GoldenGate bead array technology. Despite the inability to detect meaningful methylation differences in the majority of CpG loci due to tissue type and locus selection issues, we found replicable significant associations of DNA methylation with age and gender. We identified associations of genetically heritable single nucleotide polymorphisms with large differences in DNA methylation levels near the polymorphism (cis effects) as well as associations with much smaller differences in DNA methylation levels elsewhere in the human genome (trans effects). Our results demonstrate the feasibility of array-based approaches in studies of DNA methylation and highlight the vast differences between individual loci. The identification of CpG loci of which DNA methylation levels are under genetic control or are related to age or gender will facilitate further studies into the role of DNA methylation and disease

IL-1β Promotes TGF-β1 and IL-2 Dependent Foxp3 Expression in Regulatory T Cells

Earlier, we have shown that GM-CSF-exposed CD8α− DCs that express low levels of pro-inflammatory cytokines IL-12 and IL-1β can induce Foxp3+ Tregs leading to suppression of autoimmunity. Here, we examined the differential effects of IL-12 and IL-1β on Foxp3 expression in T cells when activated in the presence and absence of DCs. Exogenous IL-12 abolished, but IL-1β enhanced, the ability of GM-CSF-exposed tolerogenic DCs to promote Foxp3 expression. Pre-exposure of DCs to IL-1β and IL-12 had only a modest effect on Foxp3− expressing T cells; however, T cells activated in the absence of DCs but in the presence of IL-1β or IL-12 showed highly significant increase and decrease in Foxp3+ T cell frequencies respectively suggesting direct effects of these cytokines on T cells and a role for IL-1β in promoting Foxp3 expression. Importantly, purified CD4+CD25+ cells showed a significantly higher ability to maintain Foxp3 expression when activated in the presence of IL-1β. Further analyses showed that the ability of IL-1β to maintain Foxp3 expression in CD25+ T cells was dependent on TGF-β1 and IL-2 expression in Foxp3+Tregs and CD25− effectors T cells respectively. Exposure of CD4+CD25+ T cells to IL-1β enhanced their ability to suppress effector T cell response in vitro and ongoing experimental autoimmune thyroidits in vivo. These results show that IL-1β can help enhance/maintain Tregs, which may play an important role in maintaining peripheral tolerance during inflammation to prevent and/or suppress autoimmunity

Synergistic study of a Danshen (Salvia Miltiorrhizae Radix et Rhizoma) and Sanqi (Notoginseng Radix et Rhizoma) combination on cell survival in EA.hy926 cells

Background: This study investigated the protective effects of the Danshen (DS) and Sanqi (SQ) herb pair on cell survival in the human cardiovascular endothelial (EA.hy926) cell line exposed to injury. Methods: Nine combination ratios of Danshen-Sanqi extracts (DS-SQ) were screened for their protective effects in the EA.hy926 cell line against two different cellular impairments induced by DL-homocysteine (Hcy) – adenosine (Ado) – tumour necrosis factors (TNF) and oxidative stress (H2O2), respectively. The type of interaction (synergistic, antagonistic, additive) between DS and SQ was analysed using a combination index (CI) model. The effects of key bioactive compounds from DS and SQ were tested using the same models. The compound from each herb that demonstrated the most potent activity in cell viability was combined to evaluate their synergistic/antagonistic interaction using CI. Results: DS-SQ ratios of 6:4 (50–300 μg/mL) produced synergistic effects (CI < 1) in restoring cell viability, reducing lactate dehydrogenase (LDH) leakage and caspase-3 expressions against Hcy-Ado-TNF. Additionally, DS-SQ 6:4 (50–150 μg/mL) was found to synergistically protect endothelial cells from impaired cellular injury induced by oxidative damage (H2O2) by restoring reduced cell viability and inhibiting excessive expression of reactive oxygen species (ROS). In particular, the combination of salvianolic acid A (SA) and ginsenoside Rb1 (Rb1) at 4:6 (1–150 μM) showed synergistic effects in preventing cytotoxic effects caused by Hcy-Ado-TNF (CI < 1). This simplified combination also demonstrated synergistic effects on H2O2-induced oxidative damage on EA.hy926 cells. Conclusions: This study provides scientific evidence to support the traditional use of the DS-SQ combination on protecting endothelial cells through their synergistic interactions

The effects of ethanol on PPARS in MCF-7 human breast cancer cells

Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors involved in various metabolic diseases. In the liver, PPARα is involved in alcohol metabolism and may lead to the development of alcoholic fatty liver and other alcohol mediated liver injuries. PPARβ modulation by ethanol induces abnormal myelin production by oligodendrocytes. PPARα and PPARβ are PPAR isoforms expressed in the human breast cell lines. Epidemiological studies show a positive correlation between alcohol intake and breast cancer risk, however, the molecular mechanisms involved are unclear. We hypothesized that ethanol would affect the expression and transactivation of human PPAR isoforms in estrogen receptor (ER) positive and ER negative breast cancer cells. Using real time RT-PCR we looked at the transcription of PPAR isoforms in the presence of increasing concentrations of ethanol and saw isoform and time dependent specific effects. Gene reporter assays enabled us to ascertain the effects of ethanol on ligand-mediated activation of human PPARα and PPARβ at concentrations equivalent to both moderate and chronic alcohol consumption. Ethanol differentially blocked the ligand-mediated activation of both PPARα and PPARβ. Since PPARα and PPARβ are involved in the differentiation and proliferation of breast cancer cells, PPARs may be a possible mechanism involved in the effect of ethanol in breast cancer