105 research outputs found

    Screening of different rice varieties for the production of bioactive molecules by solid state fermentation of Monascus purpureus.

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    This Dissertation / Report is the outcome of investigation carried out by the creator(s) / author(s) at the department/division of Central Food Technological Research Institute (CFTRI), Mysore mentioned below in this page

    Self healing of cement based materials engineered through crystalline admixtures: results from a multinational university network

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    Self-healing cementitious composites are a broad category of smart construction materials to which strong and highly qualified research efforts are currently being devoted worldwide, with the aim of providing a sound scientific background to their consistent, and – design-wise – “consciously safe”, use in the engineering practice. Tailored additions can be employed to enhance the self-healing capacity, among which the so-called crystalline admixtures, play a prominent role. Crystalline admixtures consist of proprietary active chemicals, which, because of their hydrophilic nature, react with water and cement particles in the concrete to form calcium silicate hydrates, increasing the density of the CSH phase, and/or pore-blocking precipitates in the existing micro-cracks. The mechanism is analogous to the formation of CSH and the resulting crystalline deposits become integrally bound with the hydrated cement paste, thus contributing not only to a significantly increased resistance to water penetration but also to the healing of the existing damages and cracks. This paper summarizes the results of a wide experimental investigation jointly performed by Politecnico di Milano (Italy), Indian Institute of Technology Madras, Chennai (India) and Universitat Politecnica de Valencia (Spain) to assess the effectiveness of different commercially available crystalline admixtures on the self-healing capacity of cement based materials

    Cellular dysfunctions caused by dystrophin deficiency and the interaction of diet-induced insulin resistance

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    Duchenne muscular dystrophy (DMD), caused by the absence of a functional dystrophin protein, is a devastating degenerative muscle disease. The absence of dystrophin leaves the muscle vulnerable to injuries, especially during eccentric contractions, and causes metabolic dysfunctions and dysregulation of cellular processes including, but not limited to inflammation, mitochondrial dysfunction, impaired autophagy, and endoplasmic reticulum (ER) stress. The commonly used mouse model to study these cellular dysfunctions and pathophysiology is the mdx mouse model. However, this model has a mild disease phenotype compared to humans. Given this, an emerging mouse model, the D2-mdx mouse, was developed, which has a more severe pathology than mdx mice. Previously, we identified impaired autophagosomal degradation in mdx mice. Given the D2-mdx model’s expanding use, we evaluated how markers of autophagy are modified in skeletal muscles from 11-mo-old D2-mdx mice. We discovered that autophagosomal degradation was impaired in the diaphragm but not gastrocnemius. Further analysis in gastrocnemius muscles by evaluation of markers of autophagy in lysosomal and cytosolic fractions suggested increased lysosomal abundance so as to compensate for impaired lysosomal function. The findings from this study, together with the wide range of cellular dysfunctions identified in dystrophic muscles, point to an accumulation of unfolded proteins in the intracellular environment. This led us to the second research chapter, where we explored how the markers of ER stress and the unfolded protein response (UPR) are altered by dystrophin deficiency. In support of the findings from the first research chapter, we identified increased ER stress and activation of the UPR in diaphragm from D2-mdx mice. To add further clarity to these findings, we also considered how ER stress and the UPR may be impacted by DMD by probing a publicly available human Affymetrix data set. We discovered increased transcript abundance of ER stress and UPR-related transcripts and also predicted transcription factors that regulate the identified upregulation profile. Dystrophin deficiency results in a broad array of cellular dysfunctions, including discoveries made in the first two research chapters. DMD is also frequently accompanied by metabolic complications such as obesity, insulin resistance, hyperglycemia, hyperinsulinemia, and metabolic syndrome. Independent of dystrophin deficiency, these metabolic alterations can also cause a range of cellular dysfunctions raising the possibility of an additive or even synergistic interaction of DMD and obesity. In chapter three, we explored changes associated with a high-fat high sucrose diet (HFHSD) in mdx mice. We discovered diet-induced insulin resistance, glucose intolerance, hyperglycemia, and dyslipidemia in HFHSD-fed C57 (control) and, for the first time, in HFHSD-fed mdx mice. Interestingly, mdx mice on a control diet were inherently insulin resistant, raising the possibility that this may be a fundamental consequence of dystrophin deficiency. Metabolomic and lipidomic analyses suggested unique and common consequences of diet-induced insulin resistance with dystrophin deficiency. To further understand the molecular consequences of a HFHSD in dystrophic skeletal muscles, in the fourth research chapter, we performed and analyzed proteomics and phosphoproteomics on skeletal muscle from these mice. We discovered that the HFHSD resulted in some common changes in the muscle proteome and phosphoproteome in muscle from C57 and mdx mice, but importantly, dystrophin deficiency also caused some unique molecular consequences. Further, using these datasets we identified key transcription factors predicted to regulate these unique changes in the obese, dystrophic proteome. Data produced in support of this dissertation provide substantially new information regarding the fundamental consequences of dystrophin deficiency as well as new information regarding the complexities of obesity and insulin resistance

    ゼブラフィッシュ網膜においてBanpはDNA損傷応答と染色体分離を制御することで、細胞周期の進行と細胞生存を促進する。

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    Okinawa Institute of Science and Technology Graduate UniversityDoctor of PhilosophyBtg3 associated nuclear protein (Banp) was initially identified as a nuclear matrix associated protein and is a tumor suppressor. Recently it was reported that Banp binds to the CGCG element containing motif enriched near the transcription initiation site of CpG island promoters, namely Banp motif, promotes the transcription in a DNA methylation dependent manner, and controls metabolic genes in pluripotent stem and differentiated neuronal cells. However, cellular roles of Banp in embryonic development remains to be elucidated. Here we report a novel role of Banp in cell-cycle progression and cell survival of zebrafish retinal progenitor cells (RPCs). In zebrafish banprw337 mutants, retinal progenitor cells showed mitotic cell accumulation and subsequent apoptosis. DNA replication stress and tp53-dependent DNA damage response were activated in banprw337 mutants. Inhibition of Tp53 significantly rescued apoptosis but not mitotic defect and DNA double strand break accumulation, suggesting that Banp is required for maintaining integrity of DNA during segregation and replication. Furthermore, live imaging of mitosis in banp morphant retinas revealed that chromosome segregation was not smoothly processed from prometaphase to anaphase, leading to prolonged M-phase. Bulk RNA-seq analysis show that mRNA expression of two chromosomal segregation regulators, cenpt and ncapg, were decreased in banprw337 mutants. Furthermore, ATAC-seq analysis showed that chromatin near their transcription start site was closed in banprw337 mutants and indeed Banp motif was found in this chromatin-closed region, suggesting that Banp directly regulates cenpt and ncapg transcription via Banp motif to promote chromosome segregation during mitosis. Our findings reveal that Banp is required for cell-cycle progression and cell survival by regulating replicative DNA damage response and mitotic chromosome segregation

    A Study on Impact of Maternal Obesity on Pregnancy Outcome

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    AIMS AND OBJECTIVES: The aim of the study was to analyse whether obese women have an increased risk of pregnancy complications and adverse foetal outcome. MATERIALS AND METHODS: Pregnant mothers attending antenatal out- patient department at Raja Mirasudhar Hospital, Thanjavur medical college hospital were selected based on inclusion and exclusion creiteria. Hundred non- obese pregnant women and hundred obese pregnant women were allotted to the control and study group respectively. In the study group, women were allotted according to the class of obesity: CLASS I - BMI 30 to 34.9 Kg/m2, CLASS II - BMI 35 to 39.9 Kg/m2, CLASS III - BMI > 40 Kg/m2. In all women a detailed history followed by complete general and physical examination was done. Relevant haematological, biochemical investigations, USG were done. They were followed up to delivery and postpartum until discharge and outcome studied. RESULTS: In our study obese pregnant woman belonged to older age group and were with increased parity. The incidence of gestational diabetes and gestational hypertension were 13% and 28%. Our study showed increased induction and caesarean section rate in the obese group (control- 10% obese – 48% with p<0.001) compared to control group. In our study 22% of babies born to obese mothers required NICU admissions compared to 7% in the control group with p < 0.001.Early neonatal death constituted 2% in the obese group. CONCLUSION: Our study showed an increased incidence in the morbidities in both obese women and fetus compared to normal BMI pregnant woman. This indicates the importance of pre - conceptional counselling which is the appropriate time for creating awareness regarding the hazards of obesity in pregnancy and ideal time for the interventional measures to be sought. Greater significance and awareness needs to be placed on the importance of normal weight before pregnancy

    Ayurvedic Management of Non-Productive Cough in SSC- Interstitial Lung Disease

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    Interstitial lung diseases (ILDs) encompass a diverse group of disorders that affect the lung parenchyma or interstitium, leading to inflammation and progressive scarring of lung tissue. This process results in thickening and stiffening of the lung tissue, impairing the lungs\u27 ability to expand and fill with air. As occupational disorders rise in society, particularly conditions like ILD, there is an increasing need for preventive healthcare approaches. While current invasive diagnostic methods and therapeutic interventions offer certain benefits, they often come with drawbacks such as side effects and high costs. Ayurvedic medicine, with its holistic focus on prevention and individualized treatment, offers a promising alternative. By addressing underlying imbalances and promoting overall wellness, Ayurvedic remedies could provide a feasible and effective solution for managing symptoms of ILD and preventing its progression, aligning with modern healthcare\u27s push towards more natural and sustainable care practices

    A Study on Zero-Day Attacks

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