Changes in the demand for private medical insurance following a shift in tax incentives

The 1998 Spanish reform of the Personal Income Tax eliminated the 15% deduction for private medical expenditures including payments on private health insurance (PHI) policies. To avoid an undesired increase in the demand for publicly funded health care, tax incentives to buy PHI were not completely removed but basically shifted from individual to group employer-paid policies. In a unique fiscal experiment, at the same time that the tax relief for individually purchased policies was abolished, the government provided for tax allowances on policies taken out through employment. Using a bivariate probit model on data from National Health Surveys, we estimate the impact of said reform on the demand for PHI and the changes occurred within it. Our findings indicate that the total probability of buying PHI was not significantly affected by the reform. Indeed, the fall in the demand for individual policies (by 10% between 1997 and 2001) was offset by an increase in the demand for group employer-paid ones. We also briefly discuss the welfare effects on the state budget, the industry and society at large.     

Synthesis and Aqueous Solution Properties of Block Copolyethers with Latent Chemical Functionality

Three series of polyglycidol‐poly(allyl glycidyl ether)‐polyglycidol (PG‐PAGE‐PG) triblock copolymers with ranging PG contents and fixed molar masses of the middle PAGE block are prepared. The copolymers are analogous to the Pluronic, poly(ethylene oxide)‐poly(propylene oxide)‐poly(ethylene oxide) (PEO‐PPO‐PEO), block copolymers in which the chemically inert PEO and PPO are substituted by PG and PAGE, respectively, exhibiting latent chemical functionality. They are prepared by solvent‐free sequential anionic polymerization of allyl glycidyl ether and ethoxyethyl glycidyl ether followed by cleavage of the protective groups. In aqueous solution the block copolymers self‐associate. According to the thermodynamic data, the self‐association is enthalpically favored with a small entropy contribution, which is fundamentally different from that of Pluronic block copolymers. The nanostructures are parameterized by dynamic and static light scattering and visualized by transmission electron microscopy. Data indicate formation of relatively large particles that are identified as compound particles held together by strong hydrogen bonding promoted by the numerous hydroxyl groups from the PG moieties.

     

A gradient in the duration of the G1 phase in the murine neocortical proliferative epithelium

Neuronogenesis in the neocortical pseudostratified ventricular epithelium (PVE) is initiated rostrolaterally and progresses caudo- medially as development progresses. Here we have measured the cytokinetic parameters and the fractional neuronal output parameter, Q, of laterally located early-maturing regions over the principal embryonic days (E12-E15) of neocortical neuronogenesis in the mouse. These measures are compared with ones previously made of a medial, late- maturing portion of the PVE. Laterally, as medially, the duration of the neuronogenetic interval is 6 days and comprises 11 integer cell cycles. Also, in both lateral and medial areas the length of G1 phase (TG1) increases nearly 4-fold and is the only cell cycle parameter to change. Q progresses essentially identically laterally and medially with respect to the succession of integer cell cycles. Most importantly, from E12 to E13 there is a steeply declining lateral to medial gradient in TG1. The gradient is due both to the lateral to medial graded stage of neuronogenesis and to the stepwise increase in TG1 with each integer cycle during the neuronogenetic interval. To our knowledge this gradient in TG1 of the cerebral PVE is the first cell biological gradient to be demonstrated experimentally in such an extensive proliferative epithelial sheet. We suggest that this gradient in TG1 is the cellular mechanism for positionally encoding a protomap of the neocortex within the PVE.      

Autoantibodies against platelet membrane glycoproteins in children with acute and chronic immune thrombocytopenic purpura

The autoimmune nature of chronic immune thrombocytopenic purpura (ITP) in adults is widely accepted. In contrast, the pathogenetic mechanism in acute and chronic ITP in children is not known. In this report, we studied 39 children with destructive thrombocytopenia, 15 patients with acute ITP and 24 patients with chronic ITP. Platelet autoantibodies to platelet glycoprotein IIb/IIIa were detected in 14 of 24 patients (58.3%) in the chronic ITP group and in four of 15 (26.7%) with acute ITP. Binding ratios (+/- SD) of positive patients were significantly greater (P = .01) in chronic ITP (8.0 +/- 9.1) when compared with those of acute ITP where the binding ratios were only slightly above the normal range (1.9 +/- 0.4). The results show that autoantibodies against platelet glycoproteins are present in the majority of children with chronic ITP confirming the autoimmune nature of this disorder. The minimal elevation seen in the positive children with acute ITP suggests a different pathogenetic mechanism. These data suggest that this approach may be useful in differentiating acute from chronic ITP patients.     

Prevalence and risk factors for hypertension and association with ethnicity in Nigeria: results from a national survey

Hypertension is increasingly being recognised as an important public health problem in sub-Saharan Africa, with 26.9% of men and 28.4% of women in 2000 being estimated to have hypertension.1 Although lower than the prevalence in high-income countries (37.4% in men and 37.2% in women), in terms of numbers of people affected, the burden of hypertension in low- and middle-income countries is greater due to the large population.1Hypertension has been recognised as a strong independent risk factor for heart disease and stroke and a predictor of premature death and disability from cardiovascular complications.2 It has been reported that 13.5% of deaths and 6% of disability-adjusted life years (DALYs) were attributed to hypertension globally, and for low- and middle income people, these figures were 12.9 and 5.6%, respectively over the period 1990 to 2001.3 Although infectious diseases remain the leading cause of mortality and morbidity in sub-Saharan Africa, the prevalence of cardiovascular disease and hypertension is rising rapidly.4It has been emphasised that urbanisation is a key reason for the increasing rates of hypertension, as evidenced by the higher prevalence of hypertension in urban areas.4-6 Urban lifestyles, characterised by sedentary living, increased salt intake, obesity and stress contribute to these differences.5 With the urban population in sub-Saharan Africa projected to increase, a greater risk of hypertension is anticipated.Studies on the association between ethnicity and hypertension in high-income countries have documented a higher prevalence of hypertension in black ethnic groups compared to white ethnic groups.7-9 Reasons for this association are complex, unclear and much debated, reflecting genetic and biochemical mechanisms, and environmental and socio-economic factors.10,11 There is limited evidence regarding differences in the prevalence of hypertension between ethnic groups within the broader classification of black ethnicity.6,12,13Studies in Nigeria and sub-Saharan Africa have mainly involved specific geographical areas or have focused on sub-groups of the population.5,14 Surveys from Nigeria report prevalence estimates ranging from 20.2 to 36.6%, but all have involved participants with different age ranges.15-18 To plan services for hypertension in Nigeria, it is essential to have accurate prevalence estimates for the whole population and to identify populations at risk.Nigeria, which is the most populous country in sub-Saharan Africa, is home to over 250 different ethnic groups. Nigeria is experiencing rapid urbanisation of the population, which is likely to increase the population at risk for hypertension.19 The present study is one of the largest population-based surveys in the region and is able to provide a nationally representative estimate of hypertension for Nigeria.     

Time in hemodialysis modulates the levels of genetic damage in hemodialysis patients

It is assumed that hemodialysis treatment can diminish the levels of genetic damage in circulating lymphocytes by cleaning the blood of uremic toxins that cause oxidative stress. However, the hemodialysis process by itself may also induce genomic damage by producing reactive oxygen species (ROS). We conducted a follow‐up study in a group of 70 hemodialysis patients followed for a mean time of 15 months. We investigated the effect of exposure time in hemodialysis on the levels of genetic damage in peripheral blood lymphocytes using the micronucleus assay. In addition, genetic damage after in vitro irradiation with 0.5 Gy was also analyzed to evaluate changes in radiosensitivity. Our results showed that, at the end of the study, there was a decrease in both the basal levels of genetic damage (9.9 ± 1.0 vs. 7.6 ± 0.7) and radiosensitivity values (38.5 ± 3.0 vs. 27.6 ± 2.4). We conclude that hemodialysis procedures may act as an ameliorating factor reducing the genetic damage present in chronic kidney disease patients. Environ. Mol. Mutagen. 55:363–368, 2014. © 2014 Wiley Periodicals, Inc.     

Genomic damage as a biomarker of chronic kidney disease status

Patients suffering from chronic kidney disease (CKD) exhibit a high incidence of cancer and cardiovascular diseases, as well as high levels of genomic damage. To confirm the association of CKD with genomic damage we have carried out the largest study to date addressing this issue, using a total of 602 subjects (187 controls, 206 pre‐dialysis CKD patients and 209 CKD patients in hemodialysis). DNA oxidative damage was measured in all individuals using the comet assay. Our results indicate that CKD patients have significantly higher levels of DNA damage than controls, but no significant differences were observed between pre‐hemodialysis (pre‐HD) and hemodialysis (HD) patients. When oxidative damage was measured, no differences were observed between patients and controls, although HD patients showed significantly higher levels of oxidative damage than pre‐HD patients. In addition, a positive relationship was demonstrated between genomic damage and all‐cause mortality. Our study confirms that genomic damage can be predictive of prognosis in CKD patients, with high levels of DNA damage indicating a poor prognosis in HD patients. Environ. Mol. Mutagen. 56:301–312, 2015. © 2014 Wiley Periodicals, Inc.