Monitoring of Spatiotemporal Dynamics of Rabi Rice Fallows in South Asia Using Remote Sensing

Cereals and grain legumes are the most important part of human diet and nutrition. The expansion of grain legumes with improved productivity to cater the growing population’s nutritional security is of prime importance and need of the hour. Rice fallows are best niche areas with residual moisture to grow short-duration legumes, thereby achieving intensification. Identifying suitable areas for grain legumes and cereal grains is important in this region. In this context, the goal of this study was to map fallow lands followed by rainy season ( kharif ) rice cultivation or post-rainy ( rabi ) fallows in rice-growing environments between 2005 and 2015 using temporal moderate-resolution imaging spectroradiometer (MODIS) data applying spectral matching techniques. This study was conducted in South Asia where different rice ecosystems exist. MODIS 16 day normalized difference vegetation index (NDVI) at 250 m spatial resolution and season-wise-intensive ground survey data were used to map rice systems and the fallows thereafter ( rabi fallows) in South Asia. The rice maps were validated with independent ground survey data and compared with available subnational-level statistics. Overall accuracy and kappa coefficient estimated for rice classes were 81.5% and 0.79%, respectively, with ground survey data. The derived physical rice area and irrigated areas were highly correlated with the subnational statistics with R ^ 2 values of 94% at the district level for the years 2005–2006 and 2015–2016. Results clearly show that rice fallow areas increased from 2005 to 2015. The results show spatial distribution of rice fallows in South Asia, which are identified as target domains for sustainable intensification of short-duration grain legumes, fixing the soil nitrogen and increasing incomes of small-holder farmers

Preconditioning with Physiological Levels of Ethanol Protect Kidney against Ischemia/Reperfusion Injury by Modulating Oxidative Stress

Oxidative stress due to excessive production of reactive oxygen species (ROS) and subsequent lipid peroxidation plays a critical role in renal ischemia/reperfusion (IR) injury. The purpose of current study is to demonstrate the effect of antecedent ethanol exposure on IR-induced renal injury by modulation of oxidative stress.Bilateral renal warm IR was induced in male C57BL/6 mice after ethanol or saline administration. Blood ethanol concentration, kidney function, histological damage, inflammatory infiltration, cytokine production, oxidative stress, antioxidant capacity and Aldehyde dehydrogenase (ALDH) enzymatic activity were assessed to evaluate the impact of antecedent ethanol exposure on IR-induced renal injury.After bilateral kidney ischemia, mice preconditioned with physiological levels of ethanol displayed significantly preserved renal function along with less histological tubular damage as manifested by the reduced inflammatory infiltration and cytokine production. Mechanistic studies revealed that precondition of mice with physiological levels of ethanol 3 h before IR induction enhanced antioxidant capacity characterized by significantly higher superoxidase dismutase (SOD) activities. Our studies further demonstrated that ethanol pretreatment specifically increased ALDH2 activity, which then suppressed lipid peroxidation by promoting the detoxification of Malondialdehyde (MDA) and 4-hydroxynonenal (HNE).Our results provide first line of evidence indicating that antecedent ethanol exposure can provide protection for kidneys against IR-induced injury by enhancing antioxidant capacity and preventing lipid peroxidation. Therefore, ethanol precondition and ectopic ALDH2 activation could be potential therapeutic approaches to prevent renal IR injury relevant to various clinical conditions

Glucocortiocoid Treatment of MCMV Infected Newborn Mice Attenuates CNS Inflammation and Limits Deficits in Cerebellar Development

Infection of the developing fetus with human cytomegalovirus (HCMV) is a major cause of central nervous system disease in infants and children; however, mechanism(s) of disease associated with this intrauterine infection remain poorly understood. Utilizing a mouse model of HCMV infection of the developing CNS, we have shown that peripheral inoculation of newborn mice with murine CMV (MCMV) results in CNS infection and developmental abnormalities that recapitulate key features of the human infection. In this model, animals exhibit decreased granule neuron precursor cell (GNPC) proliferation and altered morphogenesis of the cerebellar cortex. Deficits in cerebellar cortical development are symmetric and global even though infection of the CNS results in a non-necrotizing encephalitis characterized by widely scattered foci of virus-infected cells with mononuclear cell infiltrates. These findings suggested that inflammation induced by MCMV infection could underlie deficits in CNS development. We investigated the contribution of host inflammatory responses to abnormal cerebellar development by modulating inflammatory responses in infected mice with glucocorticoids. Treatment of infected animals with glucocorticoids decreased activation of CNS mononuclear cells and expression of inflammatory cytokines (TNF-α, IFN-β and IFNγ) in the CNS while minimally impacting CNS virus replication. Glucocorticoid treatment also limited morphogenic abnormalities and normalized the expression of developmentally regulated genes within the cerebellum. Importantly, GNPC proliferation deficits were normalized in MCMV infected mice following glucocorticoid treatment. Our findings argue that host inflammatory responses to MCMV infection contribute to deficits in CNS development in MCMV infected mice and suggest that similar mechanisms of disease could be responsible for the abnormal CNS development in human infants infected in-utero with HCMV