A long-term spatiotemporal analysis of vegetation greenness over the himalayan region using google earth engine

The Himalayas constitute one of the richest and most diverse ecosystems in the Indian sub-continent. Vegetation greenness driven by climate in the Himalayan region is often overlooked as field-based studies are challenging due to high altitude and complex topography. Although the basic information about vegetation cover and its interactions with different hydroclimatic factors is vital, limited attention has been given to understanding the response of vegetation to different climatic factors. The main aim of the present study is to analyse the relationship between the spatio-temporal variability of vegetation greenness and associated climatic and hydrological drivers within the Upper Khoh River (UKR) Basin of the Himalayas at annual and seasonal scales. We analysed two vegetation indices, namely, normalised difference vegetation index (NDVI) and enhanced vegetation index (EVI) time-series data, for the last 20 years (2001–2020) using Google Earth Engine. We found that both the NDVI and EVI showed increasing trends in the vegetation greening during the period under consideration, with the NDVI being consistently higher than the EVI. The mean NDVI and EVI increased from 0.54 and 0.31 (2001), respectively, to 0.65 and 0.36 (2020). Further, the EVI tends to correlate better with the different hydroclimatic factors in comparison to the NDVI. The EVI is strongly correlated with ET with R2 = 0.73 whereas the NDVI showed satisfactory performance with R2 = 0.45. On the other hand, the relationship between the EVI and precipitation yielded R2 = 0.34, whereas there was no relationship was observed between the NDVI and precipi-tation. These findings show that there exists a strong correlation between the EVI and hydroclimatic factors, which shows that changes in vegetation phenology can be better captured using the EVI than the NDVI

Aldose reductase deficiency in mice protects from ragweed pollen extract (RWE)-induced allergic asthma

<p>Abstract</p> <p>Background</p> <p>Childhood hospitalization related to asthma remains at historically high levels, and its incidence is on the rise world-wide. Previously, we have demonstrated that aldose reductase (AR), a regulatory enzyme of polyol pathway, is a major mediator of allergen-induced asthma pathogenesis in mouse models. Here, using AR null (AR^-/-) mice we have investigated the effect of AR deficiency on the pathogenesis of ragweed pollen extract (RWE)-induced allergic asthma in mice and also examined the efficacy of enteral administration of highly specific AR inhibitor, fidarestat.</p> <p>Methods</p> <p>The wild type (WT) and AR^-/-mice were sensitized and challenged with RWE to induce allergic asthma. AR inhibitor, fidarestat was administered orally. Airway hyper-responsiveness was measured in unrestrained animals using whole body plethysmography. Mucin levels and Th2 cytokine in broncho-alveolar lavage (BAL) were determined using mouse anti-Muc5A/C ELISA kit and multiplex cytokine array, respectively. Eosinophils infiltration and goblet cells were assessed by H&E and periodic acid Schiff (PAS)-staining of formalin-fixed, paraffin-embedded lung sections. T regulatory cells were assessed in spleen derived CD4⁺CD25⁺T cells population.</p> <p>Results</p> <p>Deficiency of AR in mice led to significantly decreased PENH, a marker of airway hyper-responsiveness, metaplasia of airway epithelial cells and mucus hyper-secretion following RWE-challenge. This was accompanied by a dramatic decrease in infiltration of eosinophils into sub-epithelium of lung as well as in BAL and release of Th2 cytokines in response to RWE-challenge of AR^-/-mice. Further, enteral administration of fidarestat significantly prevented eosinophils infiltration, airway hyper-responsiveness and also markedly increased population of T regulatory (CD4⁺CD25⁺FoxP3⁺) cells as compared to RWE-sensitized and challenged mice not treated with fidarestat.</p> <p>Conclusion</p> <p>Our results using AR^-/-mice strongly suggest the role of AR in allergic asthma pathogenesis and effectiveness of oral administration of AR inhibitor in RWE-induced asthma in mice supports the use of AR inhibitors in the treatment of allergic asthma.</p

Aldose Reductase Inhibition Prevents Metaplasia of Airway Epithelial Cells

BACKGROUND: Goblet cell metaplasia that causes mucus hypersecretion and obstruction in the airway lumen could be life threatening in asthma and chronic obstructive pulmonary disease patients. Inflammatory cytokines such as IL-13 mediate the transformation of airway ciliary epithelial cells to mucin-secreting goblet cells in acute as well as chronic airway inflammatory diseases. However, no effective and specific pharmacologic treatment is currently available. Here, we investigated the mechanisms by which aldose reductase (AR) regulates the mucus cell metaplasia in vitro and in vivo. METHODOLOGY/FINDINGS: Metaplasia in primary human small airway epithelial cells (SAEC) was induced by a Th2 cytokine, IL-13, without or with AR inhibitor, fidarestat. After 48 h of incubation with IL-13 a large number of SAEC were transformed into goblet cells as determined by periodic acid-schiff (PAS)-staining and immunohistochemistry using antibodies against Mucin5AC. Further, IL-13 significantly increased the expression of Mucin5AC at mRNA and protein levels. These changes were significantly prevented by treatment of the SAEC with AR inhibitor. AR inhibition also decreased IL-13-induced expression of Muc5AC, Muc5B, and SPDEF, and phosphorylation of JAK-1, ERK1/2 and STAT-6. In a mouse model of ragweed pollen extract (RWE)-induced allergic asthma treatment with fidarestat prevented the expression of IL-13, phosphorylation of STAT-6 and transformation of epithelial cells to goblet cells in the lung. Additionally, while the AR-null mice were resistant, wild-type mice showed goblet cell metaplasia after challenge with RWE. CONCLUSIONS: The results show that exposure of SAEC to IL-13 caused goblet cell metaplasia, which was significantly prevented by AR inhibition. Administration of fidarestat to mice prevented RWE-induced goblet cell metaplasia and AR null mice were largely resistant to allergen induced changes in the lung. Thus our results indicate that AR inhibitors such as fidarestat could be developed as therapeutic agents to prevent goblet cell metaplasia in asthma and related pathologies

Employers’ Perception on the Antecedents of Graduate Employability for the Information Technology Sector

This chapter aims to analyze the perceptions of the employers in the Information Technology (IT) sector in India on the antecedents of graduate employability. With an increased emphasis on Organizational flexibility in today’s volatile and complex Business environment, the employability of the workforce has gained crucial significance. Flexibility has been acknowledged as a predictor of Organizational performance (Sushil, Global J Flex Syst Manag 16(4):309–311, 2015) and its Strategic driver (Sharma et al., Global J Flex Syst Manag 11(3):51–68, 2010). Flexible strategies and business plan often demand the need to scale up the quality of manpower or shift the required skill set to swiftly adapt to the Market changes accordingly. This Flexibility is not confined to the quantity of manpower only but also encompasses the quality of skills deployed by the manpower (Srivastava, Global J Flex Syst Manag 17(1):105–108, 2016). Therefore, it is imperative for the potential Job seeker to understand and continuously adapt to the changing knowledge and skill requirements of the employers to develop and maintain their employability. The employers in this dynamic sector demand a range of knowledge, skills, and other attributes from potential job seekers. However, the graduates passing out of Higher Education Institutions fail to meet these expectations of the employers. Therefore, the sector is struggling with the challenges of talent crunch and qualitative demand–Demand–supply mismatch of manpower. The identification of factors that influence graduate employability is based on literature review. This chapter is empirical and examines the perceptions of the employers on the factors that impact employability and validates the association between the research constructs. Opinion surveys are used to elicit responses from a sample of 236 respondents, i.e., Technical/HR personnel at the middle-level/upper middle-level management positions spanning across 71 reputed IT companies in India. These respondents are actively involved in the staffing of graduates seeking Technical jobs in IT sector. The perception of these employers has been investigated using bivariate and multivariate analysis techniques. The key insights drawn in this chapter enable potential job seekers to clearly understand the employer demands in the IT sector and equip themselves with the required knowledge and skills. This also contributes to enhancing the manpower Flexibility in organizations. The chapter has significant implications for the policy-makers and key stakeholders to bridge the Employability gap in this sector

Inhibition of Aldose Reductase Prevents Experimental Allergic Airway Inflammation in Mice

The bronchial asthma, a clinical complication of persistent inflammation of the airway and subsequent airway hyper-responsiveness, is a leading cause of morbidity and mortality in critically ill patients. Several studies have shown that oxidative stress plays a key role in initiation as well as amplification of inflammation in airways. However, still there are no good anti-oxidant strategies available for therapeutic intervention in asthma pathogenesis. Most recent studies suggest that polyol pathway enzyme, aldose reductase (AR), contributes to the pathogenesis of oxidative stress-induced inflammation by affecting the NF-kappaB-dependent expression of cytokines and chemokines and therefore inhibitors of AR could be anti-inflammatory. Since inhibitors of AR have already gone through phase-III clinical studies for diabetic complications and found to be safe, our hypothesis is that AR inhibitors could be novel therapeutic drugs for the prevention and treatment of asthma. Hence, we investigated the efficacy of AR inhibition in the prevention of allergic responses to a common natural airborne allergen, ragweed pollen that leads to airway inflammation and hyper-responsiveness in a murine model of asthma.Primary Human Small Airway Epithelial Cells (SAEC) were used to investigate the in vitro effects of AR inhibition on ragweed pollen extract (RWE)-induced cytotoxic and inflammatory signals. Our results indicate that inhibition of AR prevents RWE -induced apoptotic cell death as measured by annexin-v staining, increase in the activation of NF-kappaB and expression of inflammatory markers such as inducible nitric oxide synthase (iNOS), cycloxygenase (COX)-2, Prostaglandin (PG) E(2), IL-6 and IL-8. Further, BALB/c mice were sensitized with endotoxin-free RWE in the absence and presence of AR inhibitor and followed by evaluation of perivascular and peribronchial inflammation, mucin production, eosinophils infiltration and airway hyperresponsiveness. Our results indicate that inhibition of AR prevents airway inflammation and production of inflammatory cytokines, accumulation of eosinophils in airways and sub-epithelial regions, mucin production in the bronchoalveolar lavage fluid and airway hyperresponsiveness in mice.These results suggest that airway inflammation due to allergic response to RWE, which subsequently activates oxidative stress-induced expression of inflammatory cytokines via NF-kappaB-dependent mechanism, could be prevented by AR inhibitors. Therefore, inhibition of AR could have clinical implications, especially for the treatment of airway inflammation, a major cause of asthma pathogenesis

Regulation of inflammation in Japanese encephalitis

Uncontrolled inflammatory response of the central nervous system is a hallmark of severe Japanese encephalitis (JE). Although inflammation is necessary to mount an efficient immune response against virus infections, exacerbated inflammatory response is often detrimental. In this context, cells of the monocytic lineage appear to be important forces driving JE pathogenesis