Cooling of Motorcycle Helment Using Phase Change Material

Human life is so precious and valuable, that it should not be compromised under any cost. In a latest survey, it is mentioned that nearly 62% of mortality in road accidents occur due to head injury, where the rider has not worn a helmet. It is not that people are very negligent about their lives on road, but that they experience dozens of discomforts by wearing helmets. But the most common discomfort is that, heavy sweat occurs due to excessive heat formation. This project mainly focuses on absorbing this heat produced inside the helmet. To achieve this, a suitable Phase change material (HS 22) is encapsulated inside an aluminium packet. Also 6 holes of 6mm diameter are drilled on the front and rear sides of helmet. This allows fresh air (reaction air coming opposite to riding direction) to continuously flow in and out of the helmet so that the heat produced in the helmet is instantaneously tapped out. During summer season, the inlet air itself will be hot which will be absorbed by the PCM. The PCM fuses taking its latent heat of fusion from the packet surface and cools it. Thus continuous cooling is achieved till the entire PCM fuses. After the ride, the PCM rejects the heat and again solidifies. Factors like position of PCM in the helmet, volume, latent heat of fusion, etc. are carefully adjusted to achieve effective forced convective heat transfer and thus cooling for a minimum drive of 1.5 hours at an utmost ambient temperature of 450C. This ventilation system is practically feasible, very economical and will surely promote the riders to wear helmets. This project has been successfully completed as our 3rd year project

On a continued fraction of order twelve

We present some new relations between a continued fraction U(q) of order 12 (established by M. S. M. Naika et al.) and U(q n) for n = 7, 9, 11, 13.Наведено деякі нові співвідношення між ланцюговим дробом U(q) дванадцятого порядку (який описано М. С. М. Найка та іншими авторами) і U(qn) для n=7,9,11та13

Security Enhancement in Surveillance Cloud Using Machine Learning Techniques

Most industries are now switching from traditional modes to cloud environments and cloud-based services. It is essential to create a secure environment for the cloud space in order to provide consumers with a safe and protected environment for cloud-based transactions. Here, we discuss the suggested approaches for creating a reliable and safe environment for a surveillance cloud. When assessing the security of vital locations, surveillance data is crucial. We are implementing machine learning methods to improve cloud security to more precisely classify image pixels, we make use of Support Vector Machines (SVM) and Fuzzy C-means Clustering (FCM). We also extend the conventional two-tiered design by adding a third level, the CloudSec module, to lower the risk of potential disclosure of surveillance data.In our work we  evaluates how well our proposed model (FCM-SVM) performed against contemporary models like ANN, KNN, SVD, and Naive Bayes. Comparing our model to other cutting-edge models, we found that it performed better, with an average accuracy of 94.4%

Acute fatty liver of pregnancy: an update on mechanisms

Acute fatty liver of pregnancy (AFLP), characterized by hepatic microvesicular steatosis, is a sudden catastrophic illness occurring almost exclusively in the third trimester of pregnancy. Defective fatty acid oxidation in the fetus has been shown to be associated with this disease. Since the placenta has the same genetic makeup as the fetus and as AFLP patients generally recover following delivery, we hypothesized that the placenta might be involved in pathogenesis of this disease. In an animal model of hepatic microvesicular steatosis (using sodium valproate), we found that microvesicular steatosis results in mitochondrial structural alterations and oxidative stress in subcellular organelles of the liver. In placentas from patients with AFLP, we observed placental mitochondrial dysfunction and oxidative stress in subcellular organelles. In addition, defective placental fatty acid oxidation results in accumulation of toxic mediators such as arachidonic acid. Escape of these mediators into the maternal circulation might affect the maternal liver resulting in microvesicular steatosis

Acute Ethanol-Induced Liver Injury is Prevented by Betaine Administration

Binge drinking is the most common form of excessive alcohol use. Repeated episodes of binge drinking cause multiple organ injuries, including liver damage. We previously demonstrated that chronic ethanol administration causes a decline in the intrahepatic ratio of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH). This decline causes impairments in essential methylation reactions that result in alcohol-induced fatty liver (steatosis) and other features of alcohol-associated liver disease (ALD). Co-treatment with betaine during chronic ethanol feeding, normalizes hepatocellular SAM:SAH ratio and alleviates many features of liver damage including steatosis. Here, we sought to examine whether betaine treatment similarly protects against liver injury in an alcohol binge-drinking model. We hypothesized that ethanol binge with prior or simultaneous betaine administration would prevent or attenuate acute alcohol-induced liver damage. Male C57Bl/6 mice were gavaged twice, 12 h apart, with either 6 g ethanol/kg BW or with an equal volume/kg BW of 0.9% NaCl. Two separate groups of mice (n = 5/group) were gavaged with 4 g betaine/kg BW, either 2 h before or simultaneously with the ethanol or saline gavages. All mice were sacrificed 8 h after the last gavage and serum and liver parameters were quantified. Ethanol binges caused a 50% decrease in hepatic SAM:SAH ratio and a \u3e3-fold rise in liver triglycerides (p ≤ 0.05). These latter changes were accompanied by elevated serum AST and ALT activities and blood alcohol concentrations (BAC) that were ∼three-times higher than the legal limit of intoxication in humans. Mice that were treated with betaine 2 h before or simultaneously with the ethanol binges exhibited similar BAC as in mice given ethanol-alone. Both betaine treatments significantly elevated hepatic SAM levels thereby normalizing the SAM:SAH ratio and attenuating hepatic steatosis and other injury parameters, compared with mice given ethanol alone. Simultaneous betaine co-administration with ethanol was more effective in preventing or attenuating liver injury than betaine given before ethanol gavage. Our findings confirm the potential therapeutic value of betaine administration in preventing liver injury after binge drinking in an animal model

Assessment of phytoplankton diversity, distribution, and environmental variables along the southeast coast of India

Coastal waters are dynamic because of anthropogenic activities that contribute nutrients and contaminants. These changes have the potential to alter patterns of primary production and thus pelagic food webs. Here, we investigated the spatial variation of the phytoplankton community and its response to changing environmental variables at 84 stations along the five coastal districts of Tamil Nadu (TN). During the present study, 85 phytoplankton species were recorded, such as diatoms (64), dinoflagellates (18), silicoflagellates (1), and Cyanophyceae (2). The maximum phytoplankton abundance was recorded on the Thanjavur coast and gradually decreased towards the south coast of Tamil Nadu. Among the phytoplankton community, 50% was dominated by pennate diatoms, attributed to higher NO3− concentrations in the coastal waters due to agricultural discharge. Cluster analysis revealed that Ramanathapuram and Tirunelveli formed a closed cluster, whereas Thanjavur and Pudukottai formed a separate closed cluster associated with higher nutrient and metal concentrations, highlighting the difference in physicochemical parameters between the northern and southern districts of the TN coast. Relatively high nutrient concentrations in the coastal waters of northern districts are of greater concern, which could impact the coastal ecosystem. Coastal eutrophication is becoming a widespread phenomenon, causing disruption in the food chain and ecosystem balances and hence requiring regular monitoring and management

Proline dehydrogenase is essential for proline protection against hydrogen peroxide induced cell death

Proline metabolism has an underlying role in apoptotic signaling that impacts tumorigenesis. Proline is oxidized to glutamate in the mitochondria with the rate limiting step catalyzed by proline dehydrogenase (PRODH). PRODH expression is inducible by p53 leading to increased proline oxidation, reactive oxygen species (ROS) formation, and induction of apoptosis. Paradoxical to its role in apoptosis, proline also protects cells against oxidative stress. Here we explore the mechanism of proline protection against hydrogen peroxide stress in melanoma WM35 cells. Treatment of WM35 cells with proline significantly increased cell viability, diminished oxidative damage of cellular lipids and proteins, and retained ATP and NADPH levels after exposure to hydrogen peroxide. Inhibition or siRNA-mediated knockdown of PRODH abolished proline protection against oxidative stress whereas knockdown of Δ1-pyrroline-5- carboxylate reductase, a key enzyme in proline biosynthesis, had no impact on proline protection. Potential linkages between proline metabolism and signaling pathways were explored. The combined inhibition of the mammalian target of rapamycin complex 1 (mTORC1) and mTORC2 eliminated proline protection. A significant increase in Akt activation was observed in proline treated cells after hydrogen peroxide stress along with a corresponding increase in the phosphorylation of the fork head transcription factor class O3a (FoxO3a). The role of PRODH in proline mediated protection was validated in the prostate carcinoma cell line, PC3. Knockdown of PRODH in PC3 cells attenuated phosphorylated levels of Akt and FoxO3a and decreased cell survival during hydrogen peroxide stress. The results provide evidence that PRODH is essential in proline protection against hydrogen peroxide mediated cell death and that proline/PRODH helps activate Akt in cancer cells

Proline dehydrogenase is essential for proline protection against hydrogen peroxide induced cell death

Proline metabolism has an underlying role in apoptotic signaling that impacts tumorigenesis. Proline is oxidized to glutamate in the mitochondria with the rate limiting step catalyzed by proline dehydrogenase (PRODH). PRODH expression is inducible by p53 leading to increased proline oxidation, reactive oxygen species (ROS) formation, and induction of apoptosis. Paradoxical to its role in apoptosis, proline also protects cells against oxidative stress. Here we explore the mechanism of proline protection against hydrogen peroxide stress in melanoma WM35 cells. Treatment of WM35 cells with proline significantly increased cell viability, diminished oxidative damage of cellular lipids and proteins, and retained ATP and NADPH levels after exposure to hydrogen peroxide. Inhibition or siRNA-mediated knockdown of PRODH abolished proline protection against oxidative stress whereas knockdown of Δ1-pyrroline-5- carboxylate reductase, a key enzyme in proline biosynthesis, had no impact on proline protection. Potential linkages between proline metabolism and signaling pathways were explored. The combined inhibition of the mammalian target of rapamycin complex 1 (mTORC1) and mTORC2 eliminated proline protection. A significant increase in Akt activation was observed in proline treated cells after hydrogen peroxide stress along with a corresponding increase in the phosphorylation of the fork head transcription factor class O3a (FoxO3a). The role of PRODH in proline mediated protection was validated in the prostate carcinoma cell line, PC3. Knockdown of PRODH in PC3 cells attenuated phosphorylated levels of Akt and FoxO3a and decreased cell survival during hydrogen peroxide stress. The results provide evidence that PRODH is essential in proline protection against hydrogen peroxide mediated cell death and that proline/PRODH helps activate Akt in cancer cells

Purification and characterization of prophenoloxidase from cotton bollworm, Helicoverpa armigera

Phenoloxidases are oxidative enzymes, which play an important role in both cell mediated and humoral immunity. Purification and biochemical characterization of prophenoloxidase from cotton bollworm, Helicoverpa armigera (Hübner) were carried out to study its biochemical properties. Prophenoloxidase consists of a single polypeptide chain with a relative molecular weight of 85 kDa as determined by SDS–PAGE, MALDI–TOF MS and LC–ESI MS. After the final step, the enzyme showed 71.7 fold of purification with a recovery of 49.2%. Purified prophenoloxidase showed high specific activity and homology with phenoloxidase subunit-1 of Bombyx mori and the conserved regions of copper binding (B) site of phenoloxidase. Purified prophenoloxidase has pH optima of 6.8 and has high catalytic efficiency towards the dopamine as a substrate in comparison to catechol and L-Dopa. The PO activity was strongly inhibited by phenylthiourea, thiourea, dithiothreitol and kojic acid

Liver Injury in Acute Fatty Liver of Pregnancy: Possible Link to Placental Mitochondrial Dysfunction and Oxidative Stress

Acute fatty liver of pregnancy (AFLP) is a rare disorder which is fatal if not recognized and treated early. Delivery of the feto-placental unit results in dramatic improvement in maternal liver function, suggesting a role for the placenta. However, the mechanisms by which defects in the fetus or placenta lead to maternal liver damage are not well understood and form the focus of this study. Placenta and serum were obtained at delivery from patients with AFLP, and placental mitochondria and peroxisomes were isolated. Placental mitochondrial function, oxidative stress, and fatty acid composition as well asserumantioxidants, oxidativeandnitrosative stress markers,andfatty acid analysis were carried out. Hepatocytes in culture were used to evaluate cell death, mitochondrial function, and lipid accumulation on exposure to fatty acids. Oxidative stress was evident in placental mitochondria and peroxisomes of patients with AFLP, accompanied by compromised mitochondrial function. Increased levels of arachidonic acid were also seen inAFLPplacenta when compared to control. Patients with AFLP also had a significant increase in oxidative and nitrosative stress markers in serum, along with decreased antioxidant levels and elevated levels of arachidonic acid. These levels of arachidonic acid were capable of inducing oxidative stress in hepatocyte mitochondria accompanied by induction of apoptosis. Exposure to arachidonic acid also resulted in increased lipid deposition in hepatocytes. Conclusion: Oxidative stress in placental mitochondria and peroxisomes is accompanied by accumulation of toxic mediators such as arachidonic acid, which may play a causative role in maternal liver damage seen in AFLP