Pollution, Health and Life Expectancy: How Environmental Policy Can Promote Growth

This article investigates the influence of environmental policy on growth assuming that the channel of transmission relies on the link between pollution, health and the survival probability, in an overlapping generations model à la Blanchard (1985) where growth is driven by a mechanism à la Romer (1986). We demonstrate that environmental policy has an ambiguous effect on growth in the steady-state when the detrimental impact of pollution on health and lifetime is taken into account: for low levels of taxation, environmental policy promotes growth while it is harmful to growth for high levels. Furthermore, we show that the environmental policy is more likely to promote growth (i.e. it stimulates growth for a wider range of environmental taxes) when public expenditures in health and/or the impact of pollution on health are important. Finally, using numerical simulations, we find that for the value of parameters chosen the environmental policy will be more likely to harm growth when agents smooth consumption over time

Income variation, endogenous population growth and health subsidy

This paper presents a fertility choice model in which the mortality rate is also endogenously determined and health expenditure provides utility to individuals as well as affects the mortality rate. The analysis shows that the model predictions agree with the empirical evidence on the relationship between demography trends and economic development. Public expenditure represents a large amount of total expenditure on health care in many countries. Thus, we also study the effects that introducing a subsidy to health expenditure has on economic and demographic variables. These effects are found to depend on the way the subsidy is financed.Este trabajo presenta un modelo de elección de la fertilidad en el que la tasa de mortalidad se determina endógenamente y el gasto sanitario proporciona utilidad al individuo además de influir sobre la tasa de mortalidad. El análisis muestra que las predicciones del modelo concuerdan con la evidencia empírica sobre la relación entre tendencias demográficas y desarrollo económico. El gasto público representa una gran proporción del gasto sanitario total en muchos países. Por ello, también se estudian los efectos de un subsidio al gasto sanitario sobre las variables económicas y demográficas, que dependerán de la fuente de financiación del subsidio

Attenuation of Age-Related Hearing Impairment in Senescence-Accelerated Mouse Prone 8 (SAMP8) Mice Treated with Fatty Acid Synthase Inhibitor CMS121

In the senescence-accelerated mouse prone 8 (SAMP8) mouse model, oxidative stress leads to premature senescence and age-related hearing impairment (ARHI). CMS121 inhibits oxytosis/ferroptosis by targeting fatty acid synthase. The aim of our study was to determine whether CMS121 is protective against ARHI in SAMP8 mice. Auditory brainstem responses (ABRs) were used to assess baseline hearing in sixteen 4-week-old female SAMP8 mice, which were divided into two cohorts. The control group was fed a vehicle diet, while the experimental group was fed a diet containing CMS121. ABRs were measured until 13 weeks of age. Cochlear immunohistochemistry was performed to analyze the number of paired ribbon-receptor synapses per inner hair cell (IHC). Descriptive statistics are provided with mean ± SEM. Two-sample t-tests were performed to compare hearing thresholds and paired synapse count across the two groups, with alpha = 0.05. Baseline hearing thresholds in the control group were statistically similar to those of the CMS121 group. At 13 weeks of age, the control group had significantly worse hearing thresholds at 12 kHz (56.5 vs. 39.8, p = 0.044) and 16 kHz (64.8 vs. 43.8, p = 0.040) compared to the CMS121 group. Immunohistochemistry showed a significantly lower synapse count per IHC in the control group (15.7) compared to the CMS121 group (18.4), p = 0.014. Our study shows a significant reduction in ABR threshold shifts and increased preservation of IHC ribbon synapses in the mid-range frequencies among mice treated with CMS121 compared to untreated mice