176 research outputs found

    Risk management in agriculture

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    This monograph was written to be part of the series of studies commissioned by the Ministry of Agriculture under the rubric of "State of Indian Farmer - A Millennium Study". On the basis of existing literature, this study documents the status of our knowledge on risks of agriculture and their management. Chapter 2 discusses the evidence on the nature, type and magnitude of agricultural risks. Chapter 3 discusses farmer strategies to combat risk. In addition to the mechanisms at the level of the farm household, the need to cope with risk can also affect community interactions and social customs. This is examined in Chapter 4. In chapter 5, we consider how production risks have been transformed by developments in the agricultural economy in the post-independence period. In chapter 6, we review the principal developments that have impacted on market risks.

    Price Performance of IPOS in Indian Stock Market

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    The present study   has been undertaken to gauge the underpricing in NSE in the short run periods, i.e., from the listing day to the six months after the listing and for the long period. The results depict that the presence of underpricing.   The study also tries to analyse the influence of factors on IPOs pricing performance. The results show that these factors viz. Subscription level, Issue size, Listing lead time and Age influence the initial returns, i.e., R_Ret. of the listing day of the company

    Dendritic Excitability and Protein Kinase C Activity Regulate Purkinje Neuron Dendrite Degeneration in Cerebellar Ataxia

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    Spinocerebellar ataxias (SCAs) are hereditary neurodegenerative disorders that are united by their autosomal dominant inheritance and their common clinical feature: cerebellar ataxia. Cerebellar ataxia is a disorder of impaired motor coordination, and in many SCAs the cause of degraded motor coordination is understood to be degeneration of cerebellar Purkinje neurons. The degeneration of Purkinje neurons in many SCAs is thought to progress from degeneration of the elaborate Purkinje neuron dendrite arbor to eventual cell death. Although it is likely that the early dendrite degeneration contributes substantially to motor impairment, the cellular processes which drive dendrite degeneration remain very poorly understood. It is known that synaptic inputs and intrinsic excitability shape Purkinje neuron dendrites during development, and several studies in different SCA models have suggested that altered synaptic input or action potential firing contributes to Purkinje neuron degeneration. Not yet explored in any of the SCA models is whether the physiology of the Purkinje neuron dendritic shaft are altered. In a mouse model of spinocerebellar ataxia type 1 (SCA1), we tested the hypothesis that SCA1 Purkinje neurons would show an increase in intrinsic dendritic excitability that promotes dendrite degeneration. Our studies identified an increase in intrinsic dendritic excitability throughout the course of dendritic degeneration, and we showed that this increased dendritic excitability was associated with changes in expression of several channels that regulate dendritic excitability. Subsequently, we demonstrated that normalizing dendritic excitability exerts a dendro-protective effect in SCA1 Purkinje neurons, supporting the hypothesis that increased intrinsic dendritic excitability drives SCA1 Purkinje neuron dendrite degeneration. In our attempts to uncover the pathway(s) by which increased dendritic excitability drives SCA1 Purkinje neuron dendrite degeneration, we uncovered a large increase in phosphorylation of protein kinase C (PKC) enzyme targets in SCA1 mice and SCA1 patient tissue. PKC activity is an important regulator of Purkinje neuron dendritic structure, and we hypothesized that increased PKC activity downstream of increased excitability promotes dendritic degeneration. Surprisingly, suppression of PKC activity in SCA1 mice resulted in accelerated dendritic degeneration, suggesting that the increased PKC activation is dendro-protective. A similar dendro-protective effect was observed in a model of a different cerebellar ataxia, Spinocerebellar ataxia type 2 (SCA2). Studies from the SCA1 mice suggest that PKC enzymes may be exerting their dendro-protective effect by counteracting (although incompletely) increases in dendritic excitability, further supporting the role that dendritic excitability plays as a driver of Purkinje neuron dendritic degeneration. This thesis establishes both intrinsic dendritic excitability and PKC activity as important regulators of Purkinje neuron dendrite degeneration in SCA1 and beyond. The results provide clinically-relevant therapeutic targets, and also provide a novel conceptual framework for understanding Purkinje neuron dendrite remodeling in health and disease. Together, these findings establish that Purkinje neuron dendrite degeneration is in fact a regulated process, with dendrite excitability and PKC activity specifically identified as two key regulators of that process.PHDNeuroscience PhDUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttps://deepblue.lib.umich.edu/bitstream/2027.42/155146/1/chopravi_1.pd

    Psychosocial Impact of Pandemic and State Imposed Lockdown on Caregivers of Patients Presenting with Respiratory Complaints Mimicking COVID-19: A Short-term Follow-up Study

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    Introduction: Pandemics and subsequent lockdowns affect mental health of different subgroups of populations. In Coronavirus Disease-2019 (COVID-19), caregivers of those patients who have respiratory complaints is one such subgroup which is more vulnerable to disturbances in mental health, because of the fear that their patient’s respiratory symptoms could be because of COVID-19. Aim: To assess the psychosocial impact of COVID-19 and subsequent state imposed lockdown on the caregivers of patients presenting with respiratory complaints and also to evaluate the effect of relaxation of lockdown after following-up them over a period of time. Materials and Methods: This prospective observational study was conducted in the Department of Pulmonary Medicine, Government Medical College, Patiala, Punjab, India (tertiary care institute), from April 2020 to June 2020. Baseline assessment was done using socio-demographic proforma, lockdown related questionnaire {3 domains, summed as total score (lockdown)}, COVID-19 related questionnaire {total score (COVID-19)} and General Health Questionnaire-12-Hindi version (GHQ-12). Reassessment was done twice i.e., at 11-15 days and 41-45 days after relaxation of lockdown. Quality Of Life (QOL) at first and second follow-up versus prelockdown times (score A and C) and first follow-up versus unlockdown (score B) was also noted. Analysis was conducted using Statistical Package for Social Sciences (IBM, SPSS)version 22.0. Results: Total 65 caregivers were enrolled in the study. Mean age of the participants was 40.2±11.812 years with maximum caregivers 25 (41.7%) aged between 31-40 years. Majority (83.3%) were men. Psychological distress was experienced in 50% of caregivers at baseline and 23.7% caregivers at first follow-up (p-value=0.001). Worry for COVID-19 (p-value=0.035), Domain 1 scores (p-value <0.001), Domain 2 scores (p-value=0.003), Domain 3 scores (p-value=0.001), and Total score lockdown (p-value <0.001) decreased significantly at first follow-up. Mean C score was significantly better than mean A score (p-value <0.001). Baseline psychological distress was significantly more in those with worry for COVID-19 (p-value=0.018), poorer scores of domains 1 (p-value=0.005), domains 2 (p-value <0.001), domains 3 (p-value <0.001), total score (lockdown) (p-value <0.001) and total score (COVID-19) (p-value=0.010). Follow-up psychological distress was more in those with “worry for COVID-19” (p-value <0.001), negative thoughts (p-value=0.001), poorer follow-up scores of three domains, total score (lockdown), mean A, B and C scores (p-value <0.001). Conclusion: Caregivers experienced extreme levels of psychological distress, which decreased, but persisted even after relaxation in lockdown

    Convalescent Plasma: An Evidence-Based Old Therapy to Treat Novel Coronavirus Patients

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    Novel Coronavirus (nCoV-2019) is a highly infectious viral outbreak that has so far infected more than 110 million people worldwide. Fast viral transmission and high infection rates have severely affected the entire population, especially the old aged and comorbid individuals leaving significantly less time to find some effective treatment strategy. In these challenging times, convalescent plasma (CP) therapy came as a ray of hope to save humankind. It is a form of passive immunization that has been used to treat various infectious diseases since 1890, including the 1918 Spanish flu, 2002/03 SARS-CoV, 2009 H1N1, 2012 MERS-CoV, and 2014 Ebola outbreak. The transfusion includes administration of CP containing a high value of neutralizing antibodies against the virus in hospitalized patients. This chapter summarizes the potential outcome of CP therapy in the treatment of nCoV-2019 patients

    Altered Capicua expression drives regional Purkinje neuron vulnerability through ion channel gene dysregulation in spinocerebellar ataxia type 1

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    Selective neuronal vulnerability in neurodegenerative disease is poorly understood. Using the ATXN1[82Q] model of spinocerebellar ataxia type 1 (SCA1), we explored the hypothesis that regional differences in Purkinje neuron degeneration could provide novel insights into selective vulnerability. ATXN1[82Q] Purkinje neurons from the anterior cerebellum were found to degenerate earlier than those from the nodular zone, and this early degeneration was associated with selective dysregulation of ion channel transcripts and altered Purkinje neuron spiking. Efforts to understand the basis for selective dysregulation of channel transcripts revealed modestly increased expression of the ATXN1 co-repressor Capicua (Cic) in anterior cerebellar Purkinje neurons. Importantly, disrupting the association between ATXN1 and Cic rescued the levels of these ion channel transcripts, and lentiviral overexpression of Cic in the nodular zone accelerated both aberrant Purkinje neuron spiking and neurodegeneration. These findings reinforce the central role for Cic in SCA1 cerebellar pathophysiology and suggest that only modest reductions in Cic are needed to have profound therapeutic impact in SCA1

    Effect of Smartphone Use on Sleep in Undergraduate Medical Students: A Cross-Sectional Study

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    Smartphone use, particularly at night, has been shown to provoke various circadian sleep–wake rhythm disorders such as insomnia and excessive daytime tiredness. This relationship has been mainly scrutinized among patient groups with higher rates of smartphone usage, particularly adolescents and children. However, it remains obscure how smartphone usage impacts sleep parameters in adults, especially undergraduate college students. This study sought to (1) investigate the association between smartphone use (actual screen time) and four sleep parameters: Pittsburgh sleep quality score (PSQI), self-reported screen time, bedtime, and rise time; (2) compare the seven PSQI components between good and poor sleep quality subjects. In total, 264 undergraduate medical students (aged 17 to 25 years) were recruited from the Government Doon Medical College, Dehradun, India. All participants completed a sleep questionnaire, which was electronically shared via a WhatsApp invitation link. Hierarchical and multinomial regression analyses were performed in relation to (1) and (2). The average PSQI score was 5.03 ± 0.86, with approximately one in two respondents (48.3%) having a poor sleep index. Smartphone use significantly predicted respondents’ PSQI score (β = 0.142, p = 0.040, R2 = 0.027), perceived screen time (β = 0.113, p = 0.043, R2 = 343), bedtime (β = 0.106, p = 0.042, R2 = 045), and rise time (β = 0.174, p = 0.015, R2 = 0.028). When comparing poor-quality sleep (PSQI ≥ 5) to good-quality sleep (PSQI 0.05), five PSQI components declined significantly: subjective sleep quality (β = −0.096, p < 0.001); sleep latency (β = −0.034, p < 0.001); sleep duration (β = −0.038, p < 0.001); sleep disturbances (β = 1.234, p < 0.001); and sleep dysfunction (β = −0.077, p < 0.001). Consequently, public health policymakers should take this evidence into account when developing guidelines around smartphone use—i.e., the when, where, and how much smartphone use—to promote improved sleep behaviour and reduce the rate of sleep–wake rhythm disorders

    MTSS1/Src family kinase Dysregulation Underlies Multiple Inherited Ataxias

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    The genetically heterogeneous spinocerebellar ataxias (SCAs) are caused by Purkinje neuron dysfunction and degeneration, but their underlying pathological mechanisms remain elusive. The Src family of nonreceptor tyrosine kinases (SFK) are essential for nervous system homeostasis and are increasingly implicated in degenerative disease. Here we reveal that the SFK suppressor Missing-in-metastasis (MTSS1) is an ataxia locus that links multiple SCAs. MTSS1 loss results in increased SFK activity, reduced Purkinje neuron arborization, and low basal firing rates, followed by cell death. Surprisingly, mouse models for SCA1, SCA2, and SCA5 show elevated SFK activity, with SCA1 and SCA2 displaying dramatically reduced MTSS1 protein levels through reduced gene expression and protein translation, respectively. Treatment of each SCA model with a clinically approved Src inhibitor corrects Purkinje neuron basal firing and delays ataxia progression in MTSS1 mutants. Our results identify a common SCA therapeutic target and demonstrate a key role for MTSS1/SFK in Purkinje neuron survival and ataxia progression
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