Family structure and children\u27s academic achievement : the role of income and parental control

The purpose of this quantitative study is to examine the relationship between family structure and children\u27s academic achievement, and to assess the roles of income and parental control in this relationship. The present study involves secondary analysis of data from the National Survey of Families and Households (Sweet & Bumpass, 1996) The National Survey of Families and Households (NSFH) is a national random sample survey conducted in two waves that covers a wide variety of issues on American family life. This study examines data gathered from the second wave of this data set. The total sample for the present research is 1056. The hypotheses guiding this study are derived from two theoretical perspectives which Bre based on the belief that children in intact, two-parent families exhibit higher levels of well-being than do children in single-parent families. First, economic-deprivation theory states that it is not family structure, per se, that has an effect on a child\u27s well-being; rather, it is the lack of resources, that often accompanies single-parent status (McLanahan, 1985). Second, father-absence theory suggests that income is not the key factor, but that the lack of motivation, supervision, attention, and role modeling that often occur in one-parent families are to blame for the lower wellbeing of children in single-parent families compared to those in intact, two-parent families (Amato & Keith, 1991). The objective of the present study was to compare these theories using a group which has been left out of prior analyses-the father-only family. The anticipated relationships between family structure and income were not found. However, results did indicate that parental control had significant effects on children\u27s academic achievement, regardless of family type. These findings have implications both for future research and for child custody arrangements

IL-17C-mediated innate inflammation decreases the response to PD-1 blockade in a model of Kras-driven lung cancer

Chronic obstructive pulmonary disease (COPD) is associated with neutrophilic lung infammation and CD8 T cell exhaustion and is an important risk factor for the development of non-small cell lung cancer (NSCLC). The clinical response to programmed cell death-1 (PD-1) blockade in NSCLC patients is variable and likely afected by a coexisting COPD. The pro-infammatory cytokine interleukin-17C (IL-17C) promotes lung infammation and is present in human lung tumors. Here, we used a Krasdriven lung cancer model to examine the function of IL-17C in infammation-promoted tumor growth. Genetic ablation of Il-17c resulted in a decreased recruitment of infammatory cells into the tumor microenvironment, a decreased expression of tumor-promoting cytokines (e.g. interleukin-6 (IL-6)), and a reduced tumor proliferation in the presence of Haemophilus infuenzae- (NTHi) induced COPD-like lung infammation. Chronic COPD-like infammation was associated with the expression of PD-1 in CD8 lymphocytes and the membrane expression of the programmed death ligand (PD-L1) independent of IL-17C. Tumor growth was decreased in Il-17c defcient mice but not in wildtype mice after anti-PD-1 treatment. Our results suggest that strategies targeting innate immune mechanisms, such as blocking of IL-17C, may improve the response to anti-PD-1 treatment in lung cancer patients

Examining the Effect of Genes on Depression as Mediated by Smoking and Modified by Sex.

Depression is heritable, differs by sex, and has environmental risk factors such as cigarette smoking. However, the effect of single nucleotide polymorphisms (SNPs) on depression through cigarette smoking and the role of sex is unclear. In order to examine the association of SNPs with depression and smoking in the UK Biobank with replication in the COPDGene study, we used counterfactual-based mediation analysis to test the indirect or mediated effect of SNPs on broad depression through the log of pack-years of cigarette smoking, adjusting for age, sex, current smoking status, and genetic ancestry (via principal components). In secondary analyses, we adjusted for age, sex, current smoking status, genetic ancestry (via principal components), income, education, and living status (urban vs. rural). In addition, we examined sex-stratified mediation models and sex-moderated mediation models. For both analyses, we adjusted for age, current smoking status, and genetic ancestry (via principal components). In the UK Biobank, rs6424532 [LOC105378800] had a statistically significant indirect effect on broad depression through the log of pack-years of cigarette smoking (p = 4.0 × 10−4) among all participants and a marginally significant indirect effect among females (p = 0.02) and males (p = 4.0 × 10−3). Moreover, rs10501696 [GRM5] had a marginally significant indirect effect on broad depression through the log of pack-years of cigarette smoking (p = 0.01) among all participants and a significant indirect effect among females (p = 2.2 × 10−3). In the secondary analyses, the sex-moderated indirect effect was marginally significant for rs10501696 [GRM5] on broad depression through the log of pack-years of cigarette smoking (p = 0.01). In the COPDGene study, the effect of an SNP (rs10501696) in GRM5 on depressive symptoms and medication was mediated by log of pack-years (p = 0.02); however, no SNPs had a sex-moderated mediated effect on depressive symptoms. In the UK Biobank, we found SNPs in two genes [LOC105378800, GRM5] with an indirect effect on broad depression through the log of pack-years of cigarette smoking. In addition, the indirect effect for GRM5 on broad depression through smoking may be moderated by sex. These results suggest that genetic regions associated with broad depression may be mediated by cigarette smoking and this relationship may be moderated by sex

The Mitochondrial Ca(2+) Uniporter: Structure, Function, and Pharmacology.

Mitochondrial Ca(2+) uptake is crucial for an array of cellular functions while an imbalance can elicit cell death. In this chapter, we briefly reviewed the various modes of mitochondrial Ca(2+) uptake and our current understanding of mitochondrial Ca(2+) homeostasis in regards to cell physiology and pathophysiology. Further, this chapter focuses on the molecular identities, intracellular regulators as well as the pharmacology of mitochondrial Ca(2+) uniporter complex