IIT-H Students' Start-up: A 'Do-it-yourself' Model of Video Making

Ankit Mishra, Mudit Tanwani, Sanyam Kapoor and Chinmay Jindal have set up Storyxpress. A brand video which costs as less as five US dollars is what Storyxpress, a software application developed by them, offers. Started two years ago when Ankit and Mudit were in their third year and Sanyam Kapoor and Chinmay Jindal in the first year, Storyxpress evolved from a college startup idea to a full-fledged software application today. Storyxpress has won an award for student innovation among start-ups from the Hyderabad Software Enterprises Association (HYSEA

IIT-H Students' Start-up: A 'Do-it-yourself' Model of Video Making

Ankit Mishra, Mudit Tanwani, Sanyam Kapoor and Chinmay Jindal have set up Storyxpress. A brand\ud video which costs as less as five US dollars is what Storyxpress, a software application developed\ud by them, offers. Started two years ago when Ankit and Mudit were in their third year and Sanyam\ud Kapoor and Chinmay Jindal in the first year, Storyxpress evolved from a college startup idea to a\ud full-fledged software application today. Storyxpress has won an award for student innovation among\ud start-ups from the Hyderabad Software Enterprises Association (HYSEA

Technology Pipeline for Large Scale Cross-Lingual Dubbing of Lecture Videos into Multiple Indian Languages

Cross-lingual dubbing of lecture videos requires the transcription of the original audio, correction and removal of disfluencies, domain term discovery, text-to-text translation into the target language, chunking of text using target language rhythm, text-to-speech synthesis followed by isochronous lipsyncing to the original video. This task becomes challenging when the source and target languages belong to different language families, resulting in differences in generated audio duration. This is further compounded by the original speaker's rhythm, especially for extempore speech. This paper describes the challenges in regenerating English lecture videos in Indian languages semi-automatically. A prototype is developed for dubbing lectures into 9 Indian languages. A mean-opinion-score (MOS) is obtained for two languages, Hindi and Tamil, on two different courses. The output video is compared with the original video in terms of MOS (1-5) and lip synchronisation with scores of 4.09 and 3.74, respectively. The human effort also reduces by 75%

Reconstituted HDL (Milano) Treatment Efficaciously Reverses Heart Failure with Preserved Ejection Fraction in Mice

Heart failure with preserved ejection fraction (HFpEF) represents a major unmet therapeutic need. This study investigated whether feeding coconut oil (CC diet) for 26 weeks in female C57BL/6N mice induces HFpEF and evaluated the effect of reconstituted high-density lipoprotein (HDL)Milano (MDCO-216) administration on established HFpEF. Eight intraperitoneal injections of MDCO-216 (100 mg/kg protein concentration) or of an equivalent volume of control buffer were executed with a 48-h interval starting at 26 weeks after the initiation of the diet. Feeding the CC diet for 26 weeks induced pathological left ventricular hypertrophy characterized by a 17.1% (p < 0.0001) lower myocardial capillary density and markedly (p < 0.0001) increased interstitial fibrosis compared to standard chow (SC) diet mice. Parameters of systolic and diastolic function were significantly impaired in CC diet mice resulting in a reduced stroke volume, decreased cardiac output, and impaired ventriculo-arterial coupling. However, ejection fraction was preserved. Administration of MDCO-216 in CC diet mice reduced cardiac hypertrophy, increased capillary density (p < 0.01), and reduced interstitial fibrosis (p < 0.01). MDCO-216 treatment completely normalized cardiac function, lowered myocardial acetyl-coenzyme A carboxylase levels, and decreased myocardial transforming growth factor-β1 in CC diet mice. In conclusion, the CC diet induced HFpEF. Reconstituted HDLMilano reversed pathological remodeling and functional cardiac abnormalities

Role of Oxidative Stress in Diabetic Cardiomyopathy

Type 2 diabetes is a redox disease. Oxidative stress and chronic inflammation induce a switch of metabolic homeostatic set points, leading to glucose intolerance. Several diabetes-specific mechanisms contribute to prominent oxidative distress in the heart, resulting in the development of diabetic cardiomyopathy. Mitochondrial overproduction of reactive oxygen species in diabetic subjects is not only caused by intracellular hyperglycemia in the microvasculature but is also the result of increased fatty oxidation and lipotoxicity in cardiomyocytes. Mitochondrial overproduction of superoxide anion radicals induces, via inhibition of glyceraldehyde 3-phosphate dehydrogenase, an increased polyol pathway flux, increased formation of advanced glycation end-products (AGE) and activation of the receptor for AGE (RAGE), activation of protein kinase C isoforms, and an increased hexosamine pathway flux. These pathways not only directly contribute to diabetic cardiomyopathy but are themselves a source of additional reactive oxygen species. Reactive oxygen species and oxidative distress lead to cell dysfunction and cellular injury not only via protein oxidation, lipid peroxidation, DNA damage, and oxidative changes in microRNAs but also via activation of stress-sensitive pathways and redox regulation. Investigations in animal models of diabetic cardiomyopathy have consistently demonstrated that increased expression of the primary antioxidant enzymes attenuates myocardial pathology and improves cardiac function

Impact of High-Density Lipoproteins on Sepsis

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Here, we review the impact of high-density lipoproteins (HDL) on sepsis from the perspective of biochemistry and pathophysiology, epidemiological research, and intervention studies in animals. Pathogen lipid moieties are major ligands for innate immunity receptors, such as toll-like receptors. The binding of pathogen-associated lipids to lipoproteins leads to sequestration, neutralization, and inactivation of their pro-inflammatory effects. Lipoproteins constitute an arm of the innate immune system. Pathogen-associated lipids can be removed from the body via the reverse lipopolysaccharide transport pathway in which HDL play a key role. Independent of the capacity for sequestration, the direct anti-inflammatory effects of HDL may counteract the development of sepsis. Mendelian randomization research using genetic variants associated with HDL cholesterol as an instrumental variable was consistent with a probable causal relationship between increased HDL cholesterol levels and decreased risk of infectious hospitalizations. Low HDL cholesterol independently predicts an adverse prognosis in sepsis both in observational epidemiology and in Mendelian randomization studies. Several HDL-associated enzymes, including phospholipid transfer protein (PLTP) and cholesterol ester transfer protein (CETP), undergo profound changes during sepsis. Potential HDL-directed interventions for treatment of sepsis include apolipoprotein A-I-based therapies, recombinant PLTP, and CETP inhibition

Role of Oxidative Stress in Diabetic Cardiomyopathy

Type 2 diabetes is a redox disease. Oxidative stress and chronic inflammation induce a switch of metabolic homeostatic set points, leading to glucose intolerance. Several diabetes-specific mechanisms contribute to prominent oxidative distress in the heart, resulting in the development of diabetic cardiomyopathy. Mitochondrial overproduction of reactive oxygen species in diabetic subjects is not only caused by intracellular hyperglycemia in the microvasculature but is also the result of increased fatty oxidation and lipotoxicity in cardiomyocytes. Mitochondrial overproduction of superoxide anion radicals induces, via inhibition of glyceraldehyde 3-phosphate dehydrogenase, an increased polyol pathway flux, increased formation of advanced glycation end-products (AGE) and activation of the receptor for AGE (RAGE), activation of protein kinase C isoforms, and an increased hexosamine pathway flux. These pathways not only directly contribute to diabetic cardiomyopathy but are themselves a source of additional reactive oxygen species. Reactive oxygen species and oxidative distress lead to cell dysfunction and cellular injury not only via protein oxidation, lipid peroxidation, DNA damage, and oxidative changes in microRNAs but also via activation of stress-sensitive pathways and redox regulation. Investigations in animal models of diabetic cardiomyopathy have consistently demonstrated that increased expression of the primary antioxidant enzymes attenuates myocardial pathology and improves cardiac function

The Role of Sodium-Glucose Cotransporter-2 Inhibitors in Heart Failure Management: The Continuing Challenge of Clinical Outcome Endpoints in Heart Failure Trials

The introduction of sodium-glucose cotransporter-2 (SGLT2) inhibitors in the management of heart failure with preserved ejection fraction (HFpEF) may be regarded as the first effective treatment in these patients. However, this proposition must be evaluated from the perspective of the complexity of clinical outcome endpoints in heart failure. The major goals of heart failure treatment have been categorized as: (1) reduction in (cardiovascular) mortality, (2) prevention of recurrent hospitalizations due to worsening heart failure, and (3) improvement in clinical status, functional capacity, and quality of life. The use of the composite primary endpoint of cardiovascular death and hospitalization for heart failure in SGLT2 inhibitor HFpEF trials flowed from the assumption that hospitalization for heart failure is a proxy for subsequent cardiovascular death. The use of this composite endpoint was not justified since the effect of the intervention on both components was clearly distinct. Moreover, the lack of convincing and clinically meaningful effects of SGLT2 inhibitors on metrics of heart failure-related health status indicates that the effect of this class of drugs in HFpEF patients is essentially restricted to an effect on hospitalization for heart failure. In conclusion, SGLT2 inhibitors do not represent a substantial breakthrough in the management of HFpEF

Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure

Murine coronary arteries are very resistant to the development of atherosclerosis, which may be related to their intramyocardial course. Blood pressure promotes atherosclerotic plaque formation by acting as a physical force that potentiates the migration of pro-atherogenic lipoproteins across the endothelium. C57BL/6N apolipoprotein (apo) E deficient mice have increased remnant lipoproteins that are a risk factor for coronary atherosclerosis. In this study, our aim was to quantify coronary atherosclerosis and artery remodeling following transverse aortic constriction (TAC) in C57BL/6N apo E−/− mice and to evaluate the impact of increased remnant lipoproteins on the development of pressure overload-induced cardiac hypertrophy and heart failure. Advanced atherosclerotic lesions were observed in the left coronary artery of C57BL/6N apo E−/− TAC mice but not in C57BL/6N TAC mice. Pressure overload resulted in markedly increased cardiac hypertrophy and more pronounced heart failure in C57BL/6N apo E−/− TAC mice in comparison to C57BL/6N TAC mice. Pathological hypertrophy, as evidenced by increased myocardial fibrosis and capillary rarefaction, was more prominent in C57BL/6N TAC apo E−/− than in C57BL/6N TAC mice and led to more marked cardiac dysfunction. In conclusion, TAC in apo E deficient mice induces coronary atherosclerosis and aggravates the development of pathological cardiac hypertrophy and heart failure

Selective binding of benzoquinone with a Pt^II-cyclophane constructed on the skeleton of<i style=""> N,N'</i>-bis(salicylidene)-<i style="">p</i>-phenylenediamine: Synthesis and spectroscopic studies

1644-1651The Schiff base N,N'-bis(salicylidene)-p-phenylenediamine has been complexed with Pt(en)Cl2 and the resulting PtII-cyclophane, [Pt(en)L]2·4PF6, reacted with phenol, resorcinol, hydroquinone or benzoquinone in DMSO solution. Their binding has been monitored by the variation in the corresponding UV-visible and emission spectral patterns. The binding properties are compared with the earlier reported ZnII-cyclophane [Zn(bpy)L]2 (bpy = 2,2'-bipyridine). A few solid adducts of phenol and benzoquinone with the PtII-cyclophane complex and hydroquinone as well as that of resorcinol with the Zn-cyclophane have also been synthesized and characterized