Socio-ecological Challenges and Adaptation Strategies of Farmers Towards Changing Climate in Vindhyan highlands, India.

The Indian agriculture is highly vulnerable to climate change which adversely affects crop production and livelihood of farmers. The effect is more intensified in Vindhyan highlands, where prolong drought and high rate of poverty exist in depredation environment. In this context, present study conducted to explore farmers' perception, attitude about climate change and adaptive capabilities. We undertook an interview schedules survey through structured questionnaire in Duddhi block of Sonbhadra district. A total of 400 households were selected in which 347 (86.75%) male and 53 (13.25%) female respondents have participated. The perception of farmers on climate change is presented in SI (severity index) which varies from 36% to 68.63%. The statement 'rainy season decreases' ranked first with SI (68.63%) followed by 'temperature increases' SI (66.06%). This investigation identified 17 types of adaptive practices which are frequently performed in the Vindhyan highlands. Based on the WAI (Weighted Average Index) score, crop diversification (2.0), cultivation of drought-adapted crop varieties (1.99), changing plantation calendar (1.95) were the most adopted practices. Multiple regression analysis between the socio-economic status of farmers and the adaptation practices, recorded a significant positive relationship with age (P < 0.01), family size (P < 0.05), education (P < 0.01), caste categories (P < 0.05) and livestock ownership (P < 0.01) of farmer. This study will be helpful in developing drought resilience farming practices for sustaining the livelihood of farmers and inform policy making.

Hyperoxia reduces insulin release and induces mitochondrial dysfunction with possible implications for hyperoxic treatment of neonates.

We previously showed that hyperoxia in vitro negatively affects beta cells of the rat. Here, we tested for possible clinical significance as well as mitochondrial interactions by hyperoxia, using human islets (function and viability), INS-1 832/13 cells (mitochondrial metabolism), and mouse neonates (effects in vivo). Lastly, we assessed relevant parameters in a cohort of individuals born preterm and then exposed to hyperoxia. Human islets and INS-1 832/13 cells were exposed to 24 h of hyperoxia (90-92% oxygen). Mouse neonates were subjected to 5 days of continuous hyperoxia. Individuals born preterm were evaluated in terms of glucose homeostasis and beta cell function by HbA1c and the HOMA2 formula. In human islets, hyperoxia significantly reduced glucose-stimulated insulin secretion by 42.2 ± 5.3% and viability assessed by MTT by 22.5 ± 5.4%. Hyperoxia down-regulated mitochondrial complex II by 21 ± 5% and upregulated complex III by 26 ± 10.1% and complex IV by 37 ± 10.6%. Partly similar effects on mitochondrial complexes were found in hyperoxia-exposed INS-1 832/13 cells. Exposure to hyperoxia swiftly reduced oxygen consumption in these cells and increased mitochondrial uncoupling. Hyperoxia transiently but significantly reduced insulin release in mouse neonates. Individuals born preterm displayed higher HbA1c versus controls, as well as insulin resistance. Thus, hyperoxia exerts negative effects in vitro on human beta cells and results indicate inhibitory effects on insulin secretion in vivo in mouse neonates. Negative effects may be lessened by the demonstrated swift and profound mitochondrial adaptability. Our findings open the possibility that hyperoxia could negatively affect beta cells of preterm human neonates.

Culture at low glucose up-regulates mitochondrial function in pancreatic ß cells with accompanying effects on viability.

We tested whether exposure of ß cells at reduced glucose leads to mitochondrial adaptions and whether such adaptions modulate effects of hypoxia. Rat islets, human islets and INS-1 832/13 cells were pre-cultured short term at half standard glucose concentrations (5.5 mM for rat islets and cells, 2.75 mM for human islets) without overtly negative effects on subsequently measured function (insulin secretion and cellular insulin contents) or on viability. Culture at half standard glucose upregulated complex I and tended to upregulate complex II in islets and INS-1 cells alike. An increased release of lactate dehydrogenase that followed exposure to hypoxia was attenuated in rat islets which had been pre-cultured at half standard glucose. In INS-1 cells exposure to half standard glucose attenuated hypoxia-induced effects on several viability parameters (MTT, cell number and incremental apoptotic DNA). Thus culture at reduced glucose of pancreatic islets and clonal ß cells leads to mitochondrial adaptions which possibly lessen the negative impact of hypoxia on ß cell viability. These findings appear relevant in the search for optimization of pre-transplant conditions in a clinical setting.