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We applied a decision tool for rationing choices, with a predetermined budget of about US$11 per household per year, to identify priorities of poor people regarding health insurance benefits in India in late 2005. A total of 302 individuals, organized in 24 groups, participated from a number of villages and neighborhoods of towns in Karnataka and Maharashtra. Many individuals were illiterate, innumerate and without insurance experience. Involving clients in insurance package design is based on an implied assumption that people can make judicious rationing decisions. Judiciousness was assessed by examining the association between the frequency of choosing a package and its perceived effectiveness. Perceived effectiveness was evaluated by comparing respondents' choices to the costs registered in 2049 illness episodes among a comparable cohort, using three criteria: 'reimbursement' (reimbursement regardless of the absolute level of expenditure), 'fairness' (higher reimbursement rate for higher expenses) and 'catastrophic coverage' (insurance for catastrophic exposure). The most frequently chosen packages scored highly on all three criteria: thus, rationing choices were confirmed as judicious. Fully 88.4% of the respondents selected at least three of the following benefits: outpatient, inpatient, drugs and tests, with a clear preference to cover high aggregate costs regardless of their probability. The results show that involving prospective clients in benefit package design can be done without compromising the judiciousness of rationing choices, even with people who have low education, low-income and no previous experience in similar exercises. Keywords: India: Benefit package design: Low-income population: Rationing choices: Access to healthcare; Health insurance

Abstract Background Most healthcare spending in developing countries is private out-of-pocket. One explanation for low penetration of health insurance is that poorer individuals doubt their ability to enforce insurance contracts. Community-based health insurance schemes (CBHI) are a solution, but launching CBHI requires obtaining accurate local data on morbidity, healthcare utilization and other details to inform package design and pricing. We developed the “Illness Mapping” method (IM) for data collection (faster and cheaper than household surveys). Methods IM is a modification of two non-interactive consensus group methods (Delphi and Nominal Group Technique) to operate as interactive methods. We elicited estimates from “Experts” in the target community on morbidity and healthcare utilization. Interaction between facilitator and experts became essential to bridge literacy constraints and to reach consensus. The study was conducted in Gaya District, Bihar (India) during April-June 2010. The intervention included the IM and a household survey (HHS). IM included 18 women’s and 17 men’s groups. The HHS was conducted in 50 villages with1,000 randomly selected households (6,656 individuals). Results We found good agreement between the two methods on overall prevalence of illness (IM: 25.9% ±3.6; HHS: 31.4%) and on prevalence of acute (IM: 76.9%; HHS: 69.2%) and chronic illnesses (IM: 20.1%; HHS: 16.6%). We also found good agreement on incidence of deliveries (IM: 3.9% ±0.4; HHS: 3.9%), and on hospital deliveries (IM: 61.0%. ± 5.4; HHS: 51.4%). For hospitalizations, we obtained a lower estimate from the IM (1.1%) than from the HHS (2.6%). The IM required less time and less person-power than a household survey, which translate into reduced costs. Conclusions We have shown that our Illness Mapping method can be carried out at lower financial and human cost for sourcing essential local data, at acceptably accurate levels. In view of the good fit of results obtained, we assume that the method could work elsewhere as well.

Abstract Background This study examines health-related "hardship financing" in order to get better insights on how poor households finance their out-of-pocket healthcare costs. We define hardship financing as having to borrow money with interest or to sell assets to pay out-of-pocket healthcare costs. Methods Using survey data of 5,383 low-income households in Orissa, one of the poorest states of India, we investigate factors influencing the risk of hardship financing with the use of a logistic regression. Results Overall, about 25% of the households (that had any healthcare cost) reported hardship financing during the year preceding the survey. Among households that experienced a hospitalization, this percentage was nearly 40%, but even among households with outpatient or maternity-related care around 25% experienced hardship financing. Hardship financing is explained not merely by the wealth of the household (measured by assets) or how much is spent out-of-pocket on healthcare costs, but also by when the payment occurs, its frequency and its duration (e.g. more severe in cases of chronic illnesses). The location where a household resides remains a major predictor of the likelihood to have hardship financing despite all other household features included in the model. Conclusions Rural poor households are subjected to considerable and protracted financial hardship due to the indirect and longer-term deleterious effects of how they cope with out-of-pocket healthcare costs. The social network that households can access influences exposure to hardship financing. Our findings point to the need to develop a policy solution that would limit that exposure both in quantum and in time. We therefore conclude that policy interventions aiming to ensure health-related financial protection would have to demonstrate that they have reduced the frequency and the volume of hardship financing.

The active metabolite of vitamin D calcitriol and its analogs are well-known for their anti-inflammatory action in the skin, while their main side effect associated with topical treatment of inflammatory disorders is irritant contact dermatitis. Prostaglandin E2 (PGE2) is proinflammatory at the onset of inflammation and anti-inflammatory at its resolution. We hypothesized that induction of PGE2 synthesis by calcitriol in epidermal keratinocytes may contribute both to its pro-inflammatory and anti-inflammatory effects on the skin. Treatment of human immortalized HaCaT keratinocytes with calcitriol (3-100 nM, 2-24 h) increased PGE2 production due to increased mRNA and protein expression of COX-2, but not to increase of COX-1 or release of arachidonic acid. The effect of calcitriol on COX-2 mRNA was observed also in primary human keratinocytes. The increase in COX-2 mRNA is associated with COX-2 transcript stabilization. Calcitriol exerts this effect by a rapid (2 h) and protein synthesis independent mode of action that is dependent on PKC and Src kinase activities. Treatment with a COX-2 inhibitor partially prevented the attenuation of the keratinocyte inflammatory response by calcitriol. We conclude that upregulation of COX-2 expression with the consequent increase in PGE2 synthesis may be one of the mechanisms explaining the Janus face of calcitriol as both a promoter and attenuator of cutaneous inflammation. [ABSTRACT FROM AUTHOR]

Introduction: This study deals with consensus by poor persons in the informal sector in rural India on the benefit-package of their community-based health insurance (CBHI). In this article we describe the process of involving rural poor in benefit-package design and assess the underlying reasons for choices they made and their ability to reach group consensus. Methods: The benefit-package selection process entailed four steps: narrowing down the options by community representatives, plus three Choosing Healthplans All Together (CHAT) rounds conducted among female members of self-help groups. We use mixed-methods and four sources of data: baseline study, CHAT exercises, in-depth interviews, and evaluation questionnaires. We define consensus as a community resolution reached by discussion, considering all opinions, and to which everyone agrees. We use the coefficient of unalikeability to express consensus quantitatively (as variability of categorical variables) rather than just categorically (as a binomial Yes/No). Findings: The coefficient of unalikeability decreased consistently over consecutive CHAT rounds, reaching zero (ie, 100% consensus) in two locations, and confirmed gradual adoption of consensus. Evaluation interviews revealed that the wish to be part of a consensus was dominant in all locations. The in-depth interviews indicated that people enjoyed the participatory deliberations, were satisfied with the selection, and that group decisions reflected a consensus rather than majority. Moreover, evidence suggests that pre-selectors and communities aimed to enhance the likelihood that many households would benefit from CBHI. Conclusion: The voluntary and contributory CBHI relies on an engaging experience with others to validate perceived priorities of the target group. The strongest motive for choice was the wish to join a consensus (more than price or package-composition) and the intention that many members should benefit. The degree of consensus improved with iterative CHAT rounds. Harnessing group consensus requires catalytic intervention, as the process is not spontaneous. [ABSTRACT FROM AUTHOR]

Abstract: The anti-cancer activity of calcitriol, the active metabolite of Vitamin D, in the colon is usually attributed to its anti-proliferative and pro-differentiative actions. The levels of reactive oxygen species (ROS) are high in colon carcinomas due to increased aerobic metabolism and exposure to various anti-cancer modalities. We examined whether calcitriol modulates the response of colon cancer cells to the cytotoxic action of the common mediator of ROS injury, H2O2. Pretreatment with calcitriol (100nM, 48h) sensitized HT-29 colon cancer cells to cell death induced by acute exposure to H2O2 or chronic exposure to the H2O2 generating system, glucose/glucose-oxidase. Although the morphological features of H2O2-induced HT-29 cell death are consistent with apoptosis, we detected no executioner caspase activation in response to cytotoxic concentrations of H2O2 and treatment with a pan-caspase inhibitor did not affect H2O2-induced cytotoxicity nor its enhancement by calcitriol. Conversely, exposure of HT-29 cells to sub-toxic concentrations of H2O2 resulted in low executioner caspase activation that was inhibited by pretreatment with calcitriol. The sensitization of colon cancer cells to ROS-induced cytotoxicity may contribute to its assumed action as a chemopreventive agent and to its therapeutic potential alone or in combination with other anti-cancer modalities. [Copyright &y& Elsevier]

Abstract: Calcitriol, the hormonal form of vitamin D3, sensitizes breast cancer cells to reactive oxygen species (ROS)-dependent cytotoxicity induced by various anticancer modalities. This effect could be due to increased generation of ROS and/ or to increased sensitivity of the target cells to ROS. This work examined the effect of calcitriol on the damage inflicted on breast cancer cells by the direct action of ROS represented by H2O2. Treatment of MCF-7 cells with H2O2 resulted in activation of caspase 7 as well as induction of caspase-independent cell death. Both were enhanced by 48–72 h of pretreatment with calcitriol. This effect was not due to modulation of H2O2 degradation or to a specific effect on OH-mediated cytotoxicity. The H2O2-induced drop in mitochondrial membrane potential and release of cytochrome c were enhanced by calcitriol. These findings indicate that calcitriol sensitizes breast cancer cells to ROS-induced death by affecting event(s) common to both caspase-dependent and -independent modes of cell death upstream to mitochondrial damage. [Copyright &y& Elsevier]

Calcitriol, the hormonal form of vitamin D, inhibited caspase-3-like activation in HaCaT keratinocytes exposed to hyperosmotic and oxidative stresses, heat shock, and the inflammatory cytokine TNF. The hormone also protected the cells from caspase-independent cell death induced by hyperosmotic and oxidative stresses. The protection against hyperosmotic stress is not affected by inhibitors of the EGF receptor, ERK or PI13 kinase pathways, neither is it due to reduced activity of the proapoptotic p38 MAP kinase. These results are in accordance with previous in vivo findings that vitamin D protects epidermal keratinocytes from apoptosis due to UV radiation or chemotherapy. [ABSTRACT FROM AUTHOR]

Calpain is a ubiquitous neutral calcium-activated thiol protease that is implicated in various cellular functions including exocytosis, cell fusion, apoptosis and proliferation. The calpain system is composed of the enzymes μ-calpain and m-calpain and their endogenous inhibitor, calpastatin. We employed the spontaneously immortalized human HaCaT keratinocytes, which retain their ability to differentiate in vitro and in vivo, to study the modulation of the calpain system during keratinocyte differentiation. The cellular levels of keratinocyte differentiation markers and of the components of the calpain system were monitored by immunoblotting. Three established differentiation stimuli: increase in cell density as a function of time in culture, elevation of extracellular calcium concentration and exposure to 1,25-dihydroxyvitamin D3 enhanced the expression of the three keratinocyte differentiation markers keratin 10, involucrin and transglutaminase. The differentiation of HaCaT cells was accompanied by elevation of the components of the calpain system, although the pattern of increase varied according to the specific differentiation stimulus. A higher increase in calpains as compared with the increase in calpastatin suggests an increase in net calpain activity during differentiation. Such an increase may play a part in the differentiation process itself and/or in the regulation of key events in differentiating keratinocyte metabolism. [ABSTRACT FROM AUTHOR]

Agents that increase intracellular cAMP (cAMP elevating agents) and 1,25(OH)2D3 inhibit the proliferation of many cell types. We investigated the combined effect of 1,25(OH)2D3 and cAMP elevating agents on exponentially growing mouse 3T3 fibroblasts. The following cAMP elevating agents were used: theophylline and pentoxyfilline, which inhibit cAMP-dependent phosphodiesterase; prostaglandin E2 which activates adenylate cyclase by a receptor-mediated mechanism; forskolin, which directly stimulates adenylate cyclase; and the cell permeable cAMP analogs 8-bromo cAMP and N6 benzoyl cAMP. 1,25(OH)2D3 and cAMP elevating agents were added to exponentially growing fibroblasts cultured in 96-well microtiter plates and cell number was monitored 3–7 d later. 1,25(OH)2D3 and the cAMP elevating agents as single agents inhibited the growth of the 3T3 cells. The combined treatment of the fibroblasts with 1,25(OH)2D3 and the cAMP elevating agents resulted in an antiproliferative effect that was more than additive. The synergistic interaction depended on the dose of 1,25(OH)2D3 and was apparent already at 10−8 M of the hormone. The specificity of the effect of 1,25(OH)2D3 was demonstrated by the finding that 24,25-dihydroxyvitamin D3, a vitamin D metabolite with low affinity for the vitamin D receptor, did not affect the antiproliferative effect of cAMP elevating agents. From the synergistic interaction between 1,25(OH)2D3 and the cell permeable cAMP analogs, we infer that the site of interaction between the two signaling pathways is distal to the cAMP generating and degrading machinery. [ABSTRACT FROM AUTHOR]