A multi-dimensional perspective on the gender gap in health among older adults in India and China:Application of a new ageing measure

A continuous rise of female life expectancy above that of males among older adults in India and China may give the impression that the relative gender gap in health in these countries is decreasing. However, given the systemic gender bias against older females in these countries across multiple dimensions of health, a fuller understanding of the gender gap in health calls for a multi-dimensional perspective. We estimate a multi-dimensional old-age threshold (MOAT) that specifies different old-age thresholds for female and male populations which accommodates multiple dimensions related to physical, intellectual and general health. We use the MOAT to evaluate the multi-dimensional gender gap in India and China by differencing the MOAT for females with that of males. Females in both countries have a lower MOAT than their male counterparts, indicating an earlier advent of ‘old age’ for females. The multi-dimensional estimates of the gender gap are also higher than the estimates based on only one dimension of health. A considerable level of variation is also observed in the gender gap across provinces. The study illustrates the need to understand the gender gap in health in India and China from a multi-dimensional perspective and provides an innovative way to quantify such a gap. Province-specific as well as health dimension-specific interventions are vital in reducing the gender gap among older adults in these countries.<br/

Gender differentials in adult mortality in India - with notes on rural-urban contrasts

This paper is a preliminary exploration of the trends and spatial variation in gender differentials in adult mortality in India, as also of the related rural-urban differentials. We pay particular attention of female mortality in the two prime reproductive age groups 15-29 and 30-44. The data for the study are taken from the Sample Registration System, available on an annual basis since 1970.

Ranolazine Reduces Ca\u3csup\u3e2+\u3c/sup\u3e Overload and Oxidative Stress and Improves Mitochondrial Integrity to Protect Against Ischemia Reperfusion Injury in Isolated Hearts

Ranolazine is a clinically approved drug for treating cardiac ventricular dysrhythmias and angina. Its mechanism(s) of protection is not clearly understood but evidence points to blocking the late Na+ current that arises during ischemia, blocking mitochondrial complex I activity, or modulating mitochondrial metabolism. Here we tested the effect of ranolazine treatment before ischemia at the mitochondrial level in intact isolated hearts and in mitochondria isolated from hearts at different times of reperfusion. Left ventricular (LV) pressure (LVP), coronary flow (CF), and O2 metabolism were measured in guinea pig isolated hearts perfused with Krebs-Ringer’s solution; mitochondrial (m) O2 •−, Ca2+, NADH/FAD (redox state), and cytosolic (c) Ca2+ were assessed on-line in the LV free wall by fluorescence spectrophotometry. Ranolazine (5 μM), infused for 1min just before 30 min of global ischemia, itself did not change O2 •−, cCa2+, mCa2+ or redox state. During late ischemia and reperfusion (IR) O2 •− emission and m[Ca2+] increased less in the ranolazine group vs. the control group. Ranolazine decreased c [Ca2+] only during ischemia while NADH and FAD were not different during IR in the ranolazine vs. control groups. Throughout reperfusion LVP and CF were higher, and ventricular fibrillation was less frequent. Infarct size was smaller in the ranolazine group than the control group. Mitochondria isolated from ranolazinetreated hearts had mild resistance to permeability transition pore (mPTP) opening and less cytochrome c release than control hearts. Ranolazine may provide functional protection of the heart during IR injury by reducing cCa2+ and mCa2+ loading secondary to its effect to block the late Na+ current. Subsequently it indirectly reduces O2 •− emission, preserves bioenergetics, delays mPTP opening, and restricts loss of cytochrome c, thereby reducing necrosis and apoptosis

Enhanced Na\u3csup\u3e+\u3c/sup\u3e/H\u3csup\u3e+\u3c/sup\u3e Exchange During Ischemia and Reperfusion Impairs Mitochondrial Bioenergetics and Myocardial Function

Inhibition of Na+/H+ exchange (NHE) during ischemia reduces cardiac injury due to reduced reverse mode Na+/Ca2+ exchange. We hypothesized that activating NHE-1 at buffer pH 8 during ischemia increases mitochondrial oxidation, Ca2+ overload, and reactive O2 species (ROS) levels and worsens functional recovery in isolated hearts and that NHE inhibition reverses these effects. Guinea pig hearts were perfused with buffer at pH 7.4 (control) or pH 8 +/- NHE inhibitor eniporide for 10 minutes before and for 10 minutes after 35- minute ischemia and then for 110 minutes with pH 7.4 buffer alone. Mitochondrial NADH and FAD, [Ca2+], and superoxide were measured by spectrophotofluorometry. NADH and FAD were more oxidized, and cardiac function was worse throughout reperfusion after pH 8 versus pH 7.4, Ca2+ overload was greater at 10-minute reperfusion, and superoxide generation was higher at 30-minute reperfusion. The pH 7.4 and eniporide groups exhibited similar mitochondrial function, and cardiac performance was most improved after pH 7.4+eniporide. Cardiac function on reperfusion after pH 8+eniporide was better than after pH 8. Percent infarction was largest after pH 8 and smallest after pH 7.4+eniporide. Activation of NHE with pH 8 buffer and the subsequent decline in redox state with greater ROS and Ca2+ loading underlie the poor functional recovery after ischemia and reperfusion

Adding ROS Scavengers to Cold K\u3csup\u3e+\u3c/sup\u3e Cardioplegia Reduces Superoxide Emission During 2 h Global Cold Cardiac Ischemia

We reported that the combination of reactive oxygen species (ROS) quenchers Mn(III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), catalase, and glutathione (MCG) given before 2 hours cold ischemia better protected cardiac mitochondria against cold ischemia and warm reperfusion (IR)-induced damage than MnTBAP alone. Here, we hypothesize that high K+ cardioplegia (CP) plus MCG would provide added protection of mitochondrial bioenergetics and cardiac function against IR injury. Using fluorescence spectrophotometry, we monitored redox balance, ie reduced nicotinamide adenine dinucleotide and flavin adenine dinucleotide (NADH/FAD), superoxide (O2 •−), and mitochondrial Ca2+ (m[Ca2+]) in the left ventricular free wall. Guinea pig isolated hearts were perfused with either Krebs Ringer’s (KR) solution, CP, or CP + MCG, before and during 27°C perfusion followed immediately by 2 hours of global ischemia at 27°C. Drugs were washed out with KR at the onset of 2 hours 37°C reperfusion. After 120 minutes warm reperfusion, myocardial infarction was lowest in the CP + MCG group and highest in the KR group. Developed left ventricular pressure recovery was similar in CP and CP + MCG and was better than in the KR group. O2 •−, m[Ca2+], and NADH/FAD were significantly different between the treatment and KR groups. O2 •− was lower in CP + MCG than in the CP group. This study suggests that CP and ROS quenchers act in parallel to improve mitochondrial function and to provide protection against IR injury at 27°C

Reversible Blockade of Complex I or Inhibition of PKCβ Reduces Activation and Mitochondria Translocation of p66\u3csup\u3eShc\u3c/sup\u3e to Preserve Cardiac Function after Ischemia

Aim Excess mitochondrial reactive oxygen species (mROS) play a vital role in cardiac ischemia reperfusion (IR) injury. P66Shc, a splice variant of the ShcA adaptor protein family, enhances mROS production by oxidizing reduced cytochrome c to yield H2O2. Ablation of p66Shc protects against IR injury, but it is unknown if and when p66Shc is activated during cardiac ischemia and/or reperfusion and if attenuating complex I electron transfer or deactivating PKCβ alters p66Shc activation during IR is associated with cardioprotection. Methods Isolated guinea pig hearts were perfused and subjected to increasing periods of ischemia and reperfusion with or without amobarbital, a complex I blocker, or hispidin, a PKCβ inhibitor. Phosphorylation of p66Shc at serine 36 and levels of p66Shc in mitochondria and cytosol were measured. Cardiac functional variables and redox states were monitored online before, during and after ischemia. Infarct size was assessed in some hearts after 120 min reperfusion. Results Phosphorylation of p66Shc and its translocation into mitochondria increased during reperfusion after 20 and 30 min ischemia, but not during ischemia only, or during 5 or 10 min ischemia followed by 20 min reperfusion. Correspondingly, cytosolic p66Shc levels decreased during these ischemia and reperfusion periods. Amobarbital or hispidin reduced phosphorylation of p66Shc and its mitochondrial translocation induced by 30 min ischemia and 20 min reperfusion. Decreased phosphorylation of p66Shc by amobarbital or hispidin led to better functional recovery and less infarction during reperfusion. Conclusion Our results show that IR activates p66Shc and that reversible blockade of electron transfer from complex I, or inhibition of PKCβ activation, decreases p66Shc activation and translocation and reduces IR damage. These observations support a novel potential therapeutic intervention against cardiac IR injury

Modulation of Mitochondrial Bioenergetics in the Isolated Guinea Pig Beating Heart by Potassium and Lidocaine Cardioplegia: Implications for Cardioprotection

Mitochondria are damaged by cardiac ischemia/reperfusion (I/R) injury but can contribute to cardioprotection. We tested if hyperkalemic cardioplegia (CP) and lidocaine (LID) differently modulate mitochondrial (m) bioenergetics and protect hearts against I/R injury. Guinea pig hearts (n = 71) were perfused with Krebs Ringer\u27s solution before perfusion for 1 minute just before ischemia with either CP (16 mM K+) or LID (1 mM) or Krebs Ringer\u27s (control, 4 mM K+). The 1-minute perfusion period assured treatment during ischemia but not on reperfusion. Cardiac function, NADH, FAD, m[Ca2+], and superoxide (reactive oxygen species) were assessed at baseline, during the 1-minute perfusion, and continuously during I/R. During the brief perfusion before ischemia, CP and LID decreased reactive oxygen species and increased NADH without changing m[Ca2+]. Additionally, CP decreased FAD. During ischemia, NADH was higher and reactive oxygen species was lower after CP and LID, whereas m[Ca2+] was lower only after LID. On reperfusion, NADH and FAD were more normalized, and m[Ca2+] and reactive oxygen species remained lower after CP and LID. Better functional recovery and smaller infarct size after CP and LID were accompanied by better mitochondrial function. These results suggest that mitochondria may be implicated, directly or indirectly, in protection by CP and LID against I/R injury

Modeling the impact of fiscal decentralization on health outcomes : empirical evidence from India

Over the last two decades, many countries around the world have been enthusiastically embarking on the path of decentralization. Decentralization has been advocated as a powerful means to improve the provision of health care services and health outcomes in developing countries. However, due to a preconceived idea that decentralization will result in efficient allocation of public resources and lack of an analytical framework to systematically analyze its impact on health outcomes, very little empirical works have been done in this area. Scant attention has also been given to analyze factors enabling or constraining its outcomes. In this paper, we develop a theoretical model and use it to test empirically the impact of fiscal decentralization on rural infant mortality rates in India between 1990 and 1997. The random effect regression results show that fiscal decentralization plays a statistically significant role in reducing rural infant mortality rate in India and the results are robust to the way the decentralization variable is measured and to different model specifications. The results also show that the effectiveness of fiscal decentralization can be affected by other complementary factors such as the level of political decentralization. States who have good fiscal and political decentralization index are twice more effective in reducing infant mortality rates than states with high fiscal but low political decentralization index.Während der letzten beiden Jahrzehnte sind viele Länder mit Enthusiasmus den Weg der Dezentralisierung gegangen. Dezentralisierung wurde als ein wichtiges Instrument zur Verbesserung der Bereitstellung von Leistungen der Gesundheitsfürsorge angesehen. Da man jedoch von der Vorstellung ausging, dass Dezentralisierung automatisch zu effizienter Verteilung von öffentlichen Ressourcen führt, und da ein analytischer Rahmen zur Untersuchung der Auswirkungen von Dezentralisierung auf die Gesundheit fehlte, gab es bisher nur wenige empirische Untersuchungen auf diesem Gebiet. Ebenfalls nur wenig Aufmerksamkeit wurde der Analyse von Faktoren geschenkt, die sich positiv oder negativ auf das Ergebnis von Dezentralisierung auswirken können. In diesem Artikel entwickeln wir ein theoretisches Modell, um den Einfluss von fiskalischer Dezentralisierung auf die ländliche Kindersterblichkeit in Indien zwischen 1990 und 1997 empirisch zu bestimmen. Die Ergebnisse der Regression mit Zufallseffekten zeigen, dass fiskalische Dezentralisierung einen statistisch signifikanten Einfluss auf die Reduzierung der Kindersterblichkeitsrate in Indien hat. Die geschätzten Parameter sind sowohl gegenüber der Art der Messung von Dezentralisierung als auch gegenüber anderen Modellspezifikationen robust. Sie zeigen auch, dass die Effektivität fiskalischer Dezentralisierung beeinflusst werden kann durch andere, ergänzende Faktoren wie z.B. dem Grad der politischen Dezentralisierung. Staaten, die einen starken fiskalischen und politischen Dezentralisierungsgrad aufweisen, sind doppelt so effektiv bei der Reduzierung der Kindersterblichkeitsrate wie diejenigen, die zwar auch eine hohe fiskalische Dezentralisierung erreicht haben, aber politisch noch sehr zentralisiert sind

A multi-dimensional measure of population ageing accounting for Quantum and Quality in life years:An application of selected countries in Europe and Asia

Population ageing measured through a fixed old-age threshold like 60+ or 65+ ignores the other important dimensions of ageing. There has been changes among the older persons in multiple dimensions that corresponds to quantity of life years lived as well as the quality of life. The existing multi-dimensional measures also consider the characteristics within a fixed old-age threshold framework which does not account for significant improvements in life expectancy over the years. We propose a new Multidimensional Old Age Threshold (MOAT) measure that accommodates different dimensions of quantity and quality of older persons. We achieve this through a modified framework of the Characteristic Approach. Our measure incorporates a forward-looking approach to measure ageing and specifies an old-age threshold for different countries after accounting for different dimensions of life expectancy, health and human capital. This method is more suitable for comparison across countries with distinct demographic and health achievements. The empirical application of our method using selected countries from Europe and Asia shows that the relative performance of countries differs in terms of MOAT in comparison to estimates based on existing measures, primarily due to the inclusion of the quality dimensions. Countries that have better performance in life expectancy, health and human capital have higher values of MOAT and a lower ‘burden’ of older persons in a cross-country perspective in comparison to the existing measures

Abuse against elderly in India - The role of education

BACKGROUND: Abuse against the elderly is recognized as an important challenge to elderly health, but its determinants are not yet well understood. We present findings from a new dataset which covers a representative sample of the population aged 60 years and above from seven Indian states across India -- all of which have a higher proportion aged 60 plus compared to the national average. Earlier studies suggest that schooling levels can be relevant in determining the level of abuse against seniors. This study focuses on the role of education on the prevalence of elderly abuse in India. METHODS: We conduct an analysis of cross sectional primary data that contains information on elderly abuse. The households in the sample were randomly selected from the seven demographically oldest states in India. These states are Himachal Pradesh, Kerala, Maharashtra, Odisha, Punjab, Tamil Nadu and West Bengal. A total of 9852 elderly from 8329 households were interviewed. The statistical analysis is based on logistic regression to understand the independent relation of education with abuse against the elderly. RESULTS: Our findings reveal that 11% of 60+ year olds have experienced at least one type of elderly abuse (Physical 5.3%, Verbal 10.2%, Economic 5.4%, Disrespect 6%, Neglect 5.2%). The most common perpetrator is the son, who is reported to be responsible for the abuse among 41% of male victims and 43% of female victims. Formal education among elderly beyond a certain level (8 years) has a strong relation with reduced violence against elderly. CONCLUSIONS: Our findings suggest that level of schooling among elderly is strongly negatively related to abuse against them. More members in the household reduces the chance of abuse while having a greater number of children increases the chance of abuse (neglect and verbal abuse). We find that education even after controlling for wealth and other relevant variables is the factor that most consistently lowers elderly abuse. However, the relation of education to abuse is limited to those with more than 8 years of schooling. This suggests that the ongoing educational expansion beyond the basic schooling years in India may lead to a decline in the incidence of elderly abuse