Unleashing The Growth Potential Of Indian MSME Sector

The MSME sector occupies a position of strategic significance in the Indian economic structure. This sector contributes nearly eight per cent to country’s GDP, employing over 80 million people in nearly 36 million widely-dispersed enterprises across the country; accounting for 45 per cent of manufactured output, 40 per cent of the country’s total export, and producing more than 8000 valueadded products ranging from traditional to high-tech. Furthermore, these enterprises are the nurseries for innovation and entrepreneurship, which will be key to the future growth of India. It is also an acknowledged fact that this sector can help realise the target of the proposed National Manufacturing Policy to enhance the share of manufacturing in GDP to 25 per cent and to create 100 million jobs by the end of 2022, as well as to foster growth and take India from its present two trillion dollar economy to a 20 trillion dollar economy. Despite the sector’s high enthusiasm and inherent capabilities to grow, its growth story still faces a number of challenges. In this light, the present paper examines the role of Indian MSMEs in India’s economic growth and explores various problems faced by the sector. The paper also attempts to discuss various policy measures undertaken by the Government to strengthen Indian MSMEs. Finally, the paper proposes strategies aimed at strengthening the sector to enable it to unleash its growth potential and help make India a 20 trillion dollar economy

FORMATION OF THE ETHER BRIDGE IN THE LOLINE ALKALOID BIOSYNTHETIC PATHWAY

Lolines are specialized metabolites produced by endophytic fungi, such as Neotyphodium and Epichloë species, that are in symbiotic relationships with cool-season grasses. Lolines are vital for the survival of the grasses because their insecticidal and antifeedant properties protect the plant from insect herbivory. Although lolines have various bioactivities, they do not have any concomitant antimammalian activities. Lolines have complex structures that are unique among naturally occurring pyrrolizidine alkaloids. Lolines have four contiguous stereocenters, and they contain an ether bridge connecting C(2) and C(7) of the pyrrolizidine ring. An ether bridge connecting bridgehead C atoms is unusual in natural products and leads to interesting questions about the biosynthesis of lolines in fungal endophytes. Dr. Pan, who was a graduate student in Dr. Schardl Lab at University of Kentucky, isolated a novel metabolite, 1-exo-acetamidopyrrolizidine (AcAP). She observed that AcAP was accumulating in naturally occurring and artificial lolO mutants. I synthesized an authentic sample of (±)-AcAP and compared it spectroscopically with AcAP isolated from a lolO mutant to determine the structure and stereochemistry of the natural product. I was also able to grow crystals of synthetic (±)-AcAP, X-ray analysis of which further supported our structure assignment. There were two possible explanations for the fact that a missing or nonfunctional LolO led to the accumulation of AcAP: that AcAP was the actual substrate of LolO, or that it was a shunt product derived from the real substrate of LolO, 1-exo-aminopyrrolizidine (AP), and that was produced only when LolO was not available to oxidize AP. To distinguish between the two hypotheses, I synthesized 2´,2´,2´,3-[2H4]-AcAP. Dr. Pan used this material to confirm that AcAP was an intermediate in loline alkaloid biosynthesis, not a shunt product. To determine the product of LolO acting on AcAP, Dr. Pan expressed LolO in yeast (Saccharomyces cerevisiae). When Dr. Pan fed AcAP (synthesized by me) to the modified organism, it produced NANL, suggesting that LolO catalyzed two C–H activations of AcAP and the formation of both C–O bonds of the ether bridge in NANL, a highly unusual transformation. Dr. Chang then cloned, expressed, and purified LolO and incubated it with (±)-AcAP, 2-oxoglutarate, and O2. He observed the production of NANL, further confirming the function of LolO. Dr. Chang also observed an intermediate, which we tentatively identified as 2-hydroxy-AcAP. In order to determine whether the initial hydroxylation of AcAP catalyzed by LolO occurred at C(2) or C(7), I prepared (±)-7,7-[2H2]- and (±)-2,2,8-[2H3]-AcAP. When Dr. Pan measured the rate of LolO-catalyzed hydroxylation of these substrates under conditions under which only one C–H activation would occur, she observed a very large kinetic isotope effect when C(2) was deuterated, but not when C(7) was deuterated, establishing that the initial hydroxylation of AcAP occurred at the C(2) position. In order to determine the stereochemical course of C–H bond oxidation by LolO at C(2) and C(7) of AcAP, I synthesized trans- and cis-3-[2H]-Pro and (2S,3R)-3-[2H]- and (2S,3S)-2,3-[2H2]-Asp. Feeding experiments with these substrates carried out by both Dr. Pan (Pro) and me (Asp) showed that at both the C(2) and C(7) positions of AcAP, LolO abstracted the endo H atoms during ether bridge formation. In summary, feeding experiments with deuterated (±)-AcAP derivatives and its amino acid precursors have shown that AcAP is an intermediate in loline biosynthesis. We have shown that LolO catalyzes the four-electron oxidation of AcAP at the endo C(2) position first and then the endo C(7) position to give NANL

Electrochemical energy storage device for securing future renewable energy

An electrochemical cell comprising molten sodium and molten sulphur as the anode and cathode, respectively, with beta alumina electrolyte has never found extensive use. An approach to develop large energy storage device based on aqueous sodium electrolyte at low temperature is described. An electrochemical cell with low cost, safe and utilizing sustainable manganese dioxide (MnO2) cathode coupled with zinc (Zn) anode in aqueous sodium hydroxide (NaOH) electrolyte is reported. The cyclic voltammetric (CV) profiles are found to be quite different in terms of peak position and current response depending on concentration of NaOH electrolyte. Among the concentrations of NaOH studied (2, 5, 7 and 10 M) the best performance was found to be between 5 and 7 M. The CV curves exhibits a pair of reversible redox peaks (within 1e- region) corresponding to sodium ion insertion and extraction but while extending the potential window to second electron reduction resulted in irreversible nature. This is explained to the formation of inhomogeneous reduction reaction due to slow electron diffusion. CV experiments at various scan rates revealed that the MnO2 material may not be suitable enough for higher scan rates indicating a sluggish kinetics occurring in the bulk material. Our study highlights the MnO2 cathode in NaOH electrolyte features a flat discharge voltage of 1.3 V vs. Zn with discharge capacity of 220 mAh/g

Lipid peroxidation as an alternative pathway for bilirubin metabolism

A standard hepatic microsomal model for the peroxidation of membrane phospholipids was found to degrade bilirubin to colourless diazo-negative products. Lipid peroxidation (LPO) and bilirubin degradation (BRD) activities were strongly correlated and both showed identical requirements for cofactors and oxygen, regardless of whether peroxidation was initiated enzymatically or non- enzymatically. Bilirubin did not appear to have an antioxidant effect on LPO in the system tested. Superoxide anions, hydroxyl radicals and hydrogen peroxide were not found to have a significant role in microsomal BRD activity and are probably not the oxidants involved in the enzymatically driven, NADPH-dependent LPO studied. Lipid radicals arising during LPO are most likely the oxidising species involved in BRD. In order to examine the possible role of LPO in maintaining bilirubin homeostasis in the bilirubin UDP-glucuronyl transferase deficient Gunn rat, plasma bilirubin was modulated by altering the diet. A lipid free diet caused a significant rise in plasma bilirubin (BR), together with marked decreases in microsomal LPO and BRD activities, compared to a high lipid diet which resulted in a decrease in hyperbilirubinaemia and increased LPO and BRD activities. Neither of these diets influenced the microsomal ethoxyresorufin deethylase activity, suggesting that cytochrome P448 was not involved in the dietary effect. However, the high lipid diet resulted in a higher proportion of unsaturation in the fatty acid chains of the microsomal phpspholipid compared with normal or lipid free diets, which could account for the increased LPO. In vivo injection studies with two antioxidants were performed. Vitamin E, abolished LPO and BRD but did not alter plasma bilirubin concentration over 3 days. Vitamin C, had no effect on LPO and BRD and a variable effect on plasma bilirubin concentration. Both in vitro and dietary studies suggest that the oxidation of bilirubin by LPO might provide an alternative pathway for bilirubin disposal in Gunn rats

An Epidemiological Study of Hepatitis Outbreak in Cuttack City, Odisha

Hepatitis is a highly infectious disease caused by a number of viruses. A study was undertaken in a ward of Cuttack City, where suddenly a number of cases of Jaundice reported. A team from the departments of Community Medicine visited the ward and collected the data by door to door survey. A total of 281 houses were surveyed and data was obtained. There were a total number of 55 jaundice cases. The cases reported with symptoms of fever, anorexia, yellow sclera and yellow urine. 64.3% of cases used Municipality source of water. 7.3% used the water for drinking purpose after boiling and filtration. 28% of houses did not have sanitary latrine, 85.5% from all the jaundice cases used the water for drinking purposes. The young adults were mostly affected. The cause of jaundice could be due to contamination of water supply by Municipality because of leakage and the causative agent was Hepatitis E Virus

Regulation of Cancer Cell Survival Mediated by Endogenous Tumor Suppression: A Dissertation

Cancer is the second leading cause of death among men and women after heart disease. Though our knowledge associated with the complexities of the cancer network has significantly improved over the past several decades, we have only recently started to get a more complete molecular understanding of the disease. To better comprehend signaling pathways that prevent disease development, we focused our efforts on investigating endogenous tumor suppression networks in controlling effectors of cancer cell survival and proliferation. Survivin is one such effector molecule that controls both cell proliferation and survival. In order to identify how this protein is overexpressed in cancer cells as opposed to normal cells, we looked at signaling molecules that negatively regulate this inhibitor of apoptosis protein. PTEN and caspase 2 are two of the identified proteins that utilize their enzymatic activity to suppress tumor growth by inhibiting downstream cell survival effectors, namely survivin. PTEN uses its phosphatase activity to suppress the PI3K/AKT pathway and maintain cellular homeostasis. In the absence of AKT activity, FOXO transcription factors are able to target downstream gene expression and regulate cell proliferation and survival. Here we have identified survivin as a novel gene target of FOXO, which binds to a specific promoter region of survivin and suppresses its transcription. Alternatively, caspase 2 uses its catalytic activity to suppress survivin gene expression by targeting the NFκB pathway. Caspase 2 acts by cleaving a novel substrate known as RIP1 that prevents NFκB from entering the nucleus, thus inhibiting target gene transcription. Interestingly, survivin is known to be a direct gene target of NFκB that controls cancer cell survival. In our investigation, we found that survivin is downregulated upon caspase 2 activation via the NFκB pathway, resulting in decreased cell cycle kinetics, increased apoptotic threshold and suppressed tumor growth in mice. These studies conclude that survivin is a common effector molecule that is regulated by tumor suppressors to maintain cellular homeostasis. However, upon deactivation of the tumor suppressor pathway, survivin is deregulated and contributes significantly to disease progression. These observations may lead to potential therapeutic implications and novel targeting strategies that will help eradicate harmful cancer cells and spare surrounding healthy cells; often the most persistent problem of most conventional chemotherapy

Investigating the Relationship Between Goal- Oriented Strivings and Motives for Engaging in Physical Activity

Chronic psychological stress has been shown to increase risk for conditions such as obesity and cardiovascular disease. Social Action Theory (SAT) says that an individual\u27s patterns of goal-oriented strivings influence his or her ability to manage stress responses as well as his or her overall exposure to stress. According to SAT, self-regulatory skills, which involve the ability to plan and maintain behavior with the intent of achieving goals, and goal motives influence an individual’s exposure and vulnerability to certain stressors. Using SAT as a framework, the present study explores the negative consequences of implicit motives on health via the body’s response to stress. This study examines the relationships between goal-oriented striving patterns and motivations to perform exercise. More specifically, the focus is on how different goals may motivate engagement in physical activity and exercise; hypothesized motives for performing exercise include the desire to attain physical attractiveness and the drive to maximize physical fitness. One hundred and three healthy undergraduate students completed questionnaires related to demographic information, exercise and dietary habits. A trained undergraduate student administered the Social Competence Interview (SCI), a brief interview that evaluates an individual\u27s goal-oriented strivings in response to a self-reported interpersonal stressor. Analyses investigated the influence of goal striving patterns on motivation to exercise, evaluating whether individuals exhibiting a particular goal striving pattern are more likely to exercise due to a particular motivation (such as attractiveness, healthy lifestyle habits, or respect from others). It was found that individuals who exercised to seek approval did not exercise because of interest, to gain competence in an activity, or to improve their fitness level, and individuals who exercised to improve themselves did not exercise for any social benefits. Another interesting finding was that individuals exercising to seek approval tended to report not knowing why they were exercising in the first place, suggesting that individuals who do not exercise to improve themselves might be less likely to continue an exercise plan. Understanding these relationships may help researchers gain further insights about the underlying mechanisms for stress management interventions aimed at young adults. Such programs require a better understanding of how motivational interventions may be designed so that health professionals can tailor how they encourage physical activity to promote a healthy lifestyle