Taxation reduces smoking but may not reduce smoking disparities in youth.

OBJECTIVE: This study examines the extent to which cigarette taxes affect smoking behaviour and disparities in smoking among adolescents by gender, socioeconomic status (SES) and race/ethnicity. METHODS: We used US nationally representative, repeated cross-sectional data from the 2005 to 2016 Monitoring the Future study to evaluate the relationship between state cigarette taxes and past 30-day current smoking, smoking intensity, and first cigarette and daily smoking initiation using modified Poisson and linear regression models, stratified by grade. We tested for interactions between tax and gender, SES and race/ethnicity on the additive scale using average marginal effects. RESULTS: We found that higher taxes were associated with lower smoking outcomes, with variation by grade. Across nearly all of our specifications, there were no statistically significant interactions between tax and gender, SES or race/ethnicity for any grades/outcomes. One exception is that among 12th graders, there was a statistically significant interaction between tax and college plans, with taxes being associated with a lower probability of 30-day smoking among students who definitely planned to attend college compared with those who did not. CONCLUSION: We conclude that higher taxes were associated with reduced smoking among adolescents, with little difference by gender, SES and racial/ethnicity groups. While effective at reducing adolescent smoking, taxes appear unlikely to reduce smoking disparities among youth.

The vexing relationship between socioeconomic status and health.

In a recent issue of this Journal, Politzer, Shmueli, and Avni estimate the economic costs of health disparities due to socioeconomic status (SES) in Israel (Politzer et al., Isr J Health Policy Res 8: 46, 2019). Using three measures of SES, the socioeconomic ranking of localities, individual income, and individual education, Politzer and colleagues estimate welfare loss due to higher mortality, productivity loss due to poorer health, excess health care treatment costs, and excess disability payments for individuals with below median SES relative to those with above median SES. They find the economic costs of health disparities are substantial, adding up to between 1.1 and 3.1 billion USD annually-between 0.7 and 1.6% of Israel's GDP.This paper is useful and informative. It is, to our knowledge, the first comprehensive quantification of the economic costs stemming from health disparities in Israel. In spite of many social policies designed to level economic opportunity and social welfare generally, by most measures, Israel is among the most unequal in the distribution of income among all OECD countries (Cornfeld and Danieli, Isr Econ Rev 12:51-95, 2015). Politzer and colleagues expose the magnitude and sources of health-related loss that Israel faces because of such inequality and shows how the costs of inequality are borne to some degree by all members of society. This short commentary discusses the complicated relationship between SES and health and puts the findings from Politzer and colleagues in the context of the international literature on the subject.

The Affordable Care Act Medicaid Expansion and Smoking Cessation Among Low-Income Smokers.

INTRODUCTION: This study sought to empirically evaluate whether the Medicaid expansion under the Affordable Care Act increased smoking cessation among low-income childless adult smokers. METHODS: The effects of the Medicaid expansion on smoking quit attempts and the probability of 30- and 90-day smoking cessation were evaluated using logistic regression and data from the 2010-2011 and 2014-2015 waves of the Tobacco Use Supplement to the Current Population Survey. Using boosted logistic regression, the Tobacco Use Supplement was restricted to an analytic sample composed of childless adults with high probability of being <138% of the federal poverty level. Propensity score weighting was used to compare changes in smoking cessation among a sample of current and past smokers in states that expanded Medicaid with a control sample of current and past smokers in states that did not expand Medicaid with similar sociodemographic characteristics and smoking histories. This study additionally controlled for state socioeconomic trends, welfare policies, and tobacco control policies. Analysis was conducted between January 2018 and June 2019. RESULTS: After weighting by propensity score and adjusting for state socioeconomic trends, welfare policies, and tobacco control policies, the Medicaid expansion was not associated with increases in smoking quit attempts or smoking cessation. CONCLUSIONS: The Medicaid expansion did not appear to improve smoking cessation, despite extending health insurance eligibility to 2.3 million low-income smokers. Greater commitments to reducing barriers to cessation benefits and increasing smoking cessation in state Medicaid programs are needed to reduce smoking in low-income populations.

Do Incarcerated Populations Serve as a Reservoir for Tuberculosis in South Africa?

Tuberculosis (TB) prevalence among incarcerated populations is as much as 1,000 times higher than in the general population. This study evaluates whether correctional facilities serve as a reservoir through which TB is transmitted to surrounding communities. Tuberculosis test data were extracted from the South African National Health Laboratory Service database for patients tested for TB between 2005 and 2011. We conducted graphical analysis to assess the relationship of TB rates between incarcerated and non-incarcerated populations over time. We performed generalized linear modeling with a log link function to assess TB risk in communities surrounding correctional facilities, net of confounders. We assessed linkages between incarcerated and non-incarcerated populations over time using Granger causality analysis. Tuberculosis prevalence among incarcerated populations was four times higher than in the general population. Tuberculosis incidence rates in incarcerated and non-incarcerated populations followed similar trends over time. The presence of a correctional facility in a municipality was associated with 34.9% more detected TB cases (confidence interval: 11.6-63.2; P < 0.01), controlling for potential confounders. Detected TB in incarcerated populations did not have predictive power in explaining detected TB rates in the non-incarcerated population after controlling for serial correlation in the time series data. Despite high TB prevalence, trends in correctional facilities do not appear to be driving temporal trends in the general population. However, correctional facilities still act as a TB reservoir that raises the overall TB risk in the vicinity. Intensified TB control policies for correctional facilities, formerly incarcerated individuals, and surrounding communities will reduce TB prevalence overall.

Key Factors Inhibiting Legislative Progress Toward Smoke-Free Coverage in Appalachia.

The Appalachian Region has among the highest rates of smoking and smoking-related illness in the United States. Strong smoke-free legislation could help protect nonsmoking residents from the harmful effects of secondhand smoke. However, there is a dearth of state, county, city, and subcounty smoke-free law coverage throughout Appalachia. As of July 2016, only 21% of Appalachian residents were covered by comprehensive smoke-free laws (i.e., 100% coverage for workplaces, restaurants, and bars). Only 46% of Appalachians lived in places with 100% smoke-free workplace laws, only 30% lived in places with 100% smoke-free restaurant laws, and only 29% lived in places with 100% smoke-free bar laws. Reasons for this lack of smoke-free law coverage include socioeconomic disadvantage, the historical importance of tobacco in Appalachian economies, and preemptive state legislation. By understanding the contextual issues that have inhibited smoke-free legislation, smoke-free advocates will be better prepared to lead efforts that expand smoke-free coverage in this region.

A diagnostic evaluation of real-time PCR, fluorescent antibody and microscopic agglutination tests in cases of equine leptospiral abortion.

REASONS FOR PERFORMING STUDY: A comprehensive evaluation of the real-time PCR assay for leptospirosis in comparison with other diagnostic assays on a large-scale basis is fundamental in validating the assay and determining the causes of equine abortions. OBJECTIVES: To compare and evaluate the diagnostic value of real-time PCR assay for leptospirosis with traditional methods in equine leptospiral abortions. STUDY DESIGN: Cross-sectional observational study. METHODS: A Leptospira spp. fluorescent antibody test (FAT), microscopic agglutination test (MAT) and real-time PCR (targeting the LipL32 gene) were compared and evaluated in equine fetal necropsy specimens (placenta, kidney, liver and heart blood) and maternal serum (when available) in 339 equine fetuses. RESULTS: From a total of 339 equine fetuses necropsied, 21 cases (6.19%) were diagnosed as leptospiral abortion. The majority of leptospiral abortions occurred in January (8 cases) and February (5 cases). Real-time PCR detected 21 of 21 cases, whereas MAT and FAT detected 19 and 18 (including 2 suspicious cases) cases, respectively. Comparing tissues, placenta yielded somewhat similar cycle of threshold values by real-time PCR compared with kidney, whereas kidney was the best specimen for the diagnosis of leptospirosis by the FAT test. In all MAT positive cases, the predominant titre in fetal heart blood was to serovar Pomona (ranging 1:100 to 1:204,800) with little or no cross-reaction to serovar Grippotyphosa. CONCLUSIONS: The results indicate that real-time PCR is an effective method for the diagnosis of leptospiral abortion in horses. However, MAT should continue to be used in clinical cases for serovar determination.

Neurofibromatosis 1 (NF1) heterozygosity results in a cell-autonomous growth advantage for astrocytes.

Individuals with neurofibromatosis 1 (NF1) develop low-grade astrocytomas at an increased frequency. To gain insight into the function of the Nf1 gene product as a growth regulator for astrocytes, we examined mice heterozygous for a targeted Nf1 mutation. In our previous studies, we demonstrated increased numbers of proliferating astrocytes in Nf1 heterozygote (Nf1+/-) mice in vivo. We now show that cultured Nf1+/- astrocytes exhibit a cell-autonomous growth advantage in vitro associated with increased p21-ras pathway activation. Furthermore, we demonstrate that Nf1+/-;wild-type N-ras mice have a similar astrocyte growth advantage in vitro and in vivo as either oncogenic N-ras or Nf1+/-; oncogenic N-ras mice. Lastly, mice heterozygous for targeted defects in both Nf1 and p53 as well as Nf1 and Rb exhibit 3- and 2.5-fold increases in astrocyte proliferation in vivo, respectively, suggesting that abnormalities in Nf1- and p53/Rb-regulated pathways cooperate in the heterozygous state to confer a growth advantage for brain astrocytes. Collectively, these results provide evidence for a cell-autonomous growth advantage in Nf1+/- astrocytes and suggest that some of the brain pathology in individuals with NF1 might result from reduced, but not absent, NF1 gene function.

Loss of neurofibromatosis 1 (NF1) gene expression in NF1-associated pilocytic astrocytomas.

The critical role of the neurofibromatosis 1 (NF1) gene as a tumour suppressor has been clearly demonstrated for malignancies arising in NF1 patients. However, little is known about the more common benign tumours, such as the pilocytic astrocytoma. Most NF1-associated astrocytomas are benign and clinically non-progressive, though aggressive tumours are occasionally encountered. In this study, eight pilocytic astrocytomas from six individuals affected with NF1 were analysed for NF1 expression. All eight tumours demonstrated loss of neurofibromin expression by immunohistochemistry, which was confirmed in one case using Western blot analysis. Microsatellite analysis showed loss of a single NF1 allele (LOH) in two of four NF1-associated tumours. These results demonstrate that, in contrast to sporadic astrocytomas, loss of NF1 expression is an important primary genetic event in the pathogenesis of NF1-associated pilocytic astrocytomas.

Loss of DAL-1, a protein 4.1-related tumor suppressor, is an important early event in the pathogenesis of meningiomas.

Meningiomas are common nervous system tumors, whose molecular pathogenesis is poorly understood. To date, the most frequent genetic alteration detected in these tumors is loss of heterozygosity (LOH) on chromosome 22q. This finding led to the identification of the neurofibromatosis 2 (NF2) tumor suppressor gene on 22q12, which is inactivated in 40% of sporadic meningiomas. The NF2 gene product, merlin (or schwannomin), is a member of the protein 4.1 family of membrane-associated proteins, which also includes ezrin, radixin and moesin. Recently, we identified another protein 4.1 gene, DAL-1 (differentially expressed in adenocarcinoma of the lung) located on chromosome 18p11.3, which is lost in approximately 60% of non-small cell lung carcinomas, and exhibits growth-suppressing properties in lung cancer cell lines. Given the homology between DAL-1 and NF2 and the identification of significant LOH in the region of DAL-1 in lung, breast and brain tumors, we investigated the possibility that loss of expression of DAL-1 was important for meningioma development. In this report, we demonstrate DAL-1 loss in 60% of sporadic meningiomas using LOH, RT-PCR, western blot and immunohistochemistry analyses. Analogous to merlin, we show that DAL-1 loss is an early event in meningioma tumorigenesis, suggesting that these two protein 4.1 family members are critical growth regulators in the pathogenesis of meningiomas. Furthermore, our work supports the emerging notion that membrane-associated alterations are important in the early stages of neoplastic transformation and the study of such alterations may elucidate the mechanism of tumorigenesis shared by other tumor types.

Behavior analysis and revaluation.

Revaluation refers to phenomena in which the strength of an operant is altered by reinforcer-related manipulations that take place outside the conditioning situation in which the operant was selected. As an example, if lever pressing is acquired using food as a reinforcer and food is later paired with an aversive stimulus, the frequency of lever pressing decreases when subsequently tested. Associationist psychology infers from such findings that conditioning produces a response-outcome (i.e., reinforcer) association and that the operant decreased in strength because pairing the reinforcer with the aversive stimulus changed the value of the outcome. Here, we present an approach to the interpretation of these and related findings that employs neural network simulations grounded in the experimental analysis of behavior and neuroscience. In so doing, we address some general issues regarding the relations among behavior analysis, neuroscience, and associationism.

The S-R issue: its status in behavior analysis and in Donahoe and Palmer's learning and complex behavior.

The central focus of this essay is whether the effect of reinforcement is best viewed as the strengthenng of responding or the strengthening of the environmental control of responding. We make the argument that adherence to Skinner's goal of achieving a moment-to-moment analysis of behavior compels acceptance of the latter view. Moreover, a thoroughgoing commitment to a moment-to-moment analysis undermines the fundamental distinction between the conditioning process instantiated by operant and respondent contingencies while buttressing the crucially important differences in their cumulative outcomes. Computer simulations informed by experimental analyses of behavior and neuroscience are used to illustrate these points.

Prevalence and serovars of leptospira involved in equine abortions in central Kentucky during the 1991-1993 foaling seasons.

In this study, the prevalence of leptospira-induced abortions/stillbirths for the past 3 foaling seasons (1991-1993) was determined, and fetal tissues and/or the mare's urine from positive cases were cultured in an attempt to isolate and identify the leptospira serovars responsible for the abortions. The sensitivity and specificity of the primary diagnostic tests, the fluorescent antibody test (FAT) and the microscopic agglutination test (MAT), used for the diagnosis of leptospirosis were also determined. For the 3 years, 74 (3.3%) of 2,264 abortion/stillborn submissions were diagnosed as leptospirosis. Twelve cases occurred in the 1991, 19 in the 1992, and 43 in the 1993 foaling seasons. Leptospires were isolated from 45 (60.8%) of the 74 cases, and they were identified as serovar kennewicki (43 cases), serovar grippotyphosa (1 case), and a serovar similar to pomona (1 case). Of the 29 culture-negative cases, serologic results indicated that leptospires in the Pomona serogroup (kennewicki is a member of this serogroup) were responsible for 25 abortions, leptospires in the Grippotyphosa serogroup for 1 abortion, and leptospires in the Sejroe serogroup for 1 abortion. The specificities of the FAT on fetal tissues and mare's placenta and of the MAT on fetal fluid were 100%. The sensitivity of the FAT was 98.7%, and that of the MAT was 81.3%.

A selectionist approach to reinforcement.

We describe a principle of reinforcement that draws upon experimental analyses of both behavior and the neurosciences. Some of the implications of this principle for the interpretation of behavior are explored using computer simulations of adaptive neural networks. The simulations indicate that a single reinforcement principle, implemented in a biologically plausible neural network, is competent to produce as its cumulative product networks that can mediate a substantial number of the phenomena generated by respondent and operant contingencies. These include acquisition, extinction, reacquisition, conditioned reinforcement, and stimulus-control phenomena such as blocking and stimulus discrimination. The characteristics of the environment-behavior relations selected by the action of reinforcement on the connectivity of the network are consistent with behavior-analytic formulations: Operants are not elicited but, instead, the network permits them to be guided by the environment. Moreover, the guidance of behavior is context dependent, with the pathways activated by a stimulus determined in part by what other stimuli are acting on the network at that moment. In keeping with a selectionist approach to complexity, the cumulative effects of relatively simple reinforcement processes give promise of simulating the complex behavior of living organisms when acting upon adaptive neural networks.