A social learning approach to the examination of the temporal directionality between parenting behavior and early adolescents\u27 affect.

This study contributes to current literature by being the first to longitudinally examine the relation between early adolescents’ negative and positive affect and specific parenting behaviors. The five parenting behaviors examined in the current study are rooted within the social learning theory constructs of effective discipline (i.e., corporal punishment, inconsistent discipline), positive involvement (i.e., parental involvement), monitoring (i.e., poor monitoring and supervision), and social skills encouragement (i.e., positive parenting). Two research questions were addressed: (1) how are parenting behaviors at baseline associated with early adolescent-reported NA and PA at a later timepoint, and (2) how are early adolescents’ NA and PA at baseline associated with reports of parenting behaviors at a later timepoint? A representative sample of 331 early adolescents (M age at baseline = 12.62, SD = 0.99; 48.3% female; 76.1% European American, 11.2% African American, 1.8% Latina/o, 1.8% Asian/Pacific Islander, .9% Native American/Alaska Native, 7.9% other race/ethnicity) were recruited from public and private middle schools across urban and rural areas. Early adolescents completed the Positive and Negative Affect Scale for Children and the Alabama Parenting Questionnaire. After conducting seven multiple regressions, (a) PA and parental involvement were positively and bidirectionally related, (b) PA at baseline was positively and unidirectionally related with positive parenting at a later timepoint, (c) PA and adverse parenting behaviors (i.e., corporal punishment, inconsistent discipline, and poor monitoring and supervision) were not related, and (d) NA and parenting behaviors were not related. The findings were consistent with the claim that not all parent-child interactions are created equally. However, where previous literature found negative parent-child interactions (i.e., adverse parenting behavior in relation to externalizing behavior) to be particularly damaging, the current study found positive parent-child interactions (i.e., parental involvement and positive parenting in relation to PA) to be particularly helpful. Clinicians should intentionally promote parental involvement in parent-focused interventions while targeting an increase in positive affect in early adolescent-focused interventions like individual therapy

Genotype-phenotype correlation at codon 1740 ofSETD2

The SET domain containing 2, histone lysine methyltransferase encoded by SETD2 is a dual-function methyltransferase for histones and microtubules and plays an important role for transcriptional regulation, genomic stability, and cytoskeletal functions. Specifically, SETD2 is associated with trimethylation of histone H3 at lysine 36 (H3K36me3) and methylation of α-tubulin at lysine 40. Heterozygous loss of function and missense variants have previously been described with Luscan-Lumish syndrome (LLS), which is characterized by overgrowth, neurodevelopmental features, and absence of overt congenital anomalies. We have identified 15 individuals with de novo variants in codon 1740 of SETD2 whose features differ from those with LLS. Group 1 consists of 12 individuals with heterozygous variant c.5218C>T p.(Arg1740Trp) and Group 2 consists of 3 individuals with heterozygous variant c.5219G>A p.(Arg1740Gln). The phenotype of Group 1 includes microcephaly, profound intellectual disability, congenital anomalies affecting several organ systems, and similar facial features. Individuals in Group 2 had moderate to severe intellectual disability, low normal head circumference, and absence of additional major congenital anomalies. While LLS is likely due to loss of function of SETD2, the clinical features seen in individuals with variants affecting codon 1740 are more severe suggesting an alternative mechanism, such as gain of function, effects on epigenetic regulation, or posttranslational modification of the cytoskeleton. Our report is a prime example of different mutations in the same gene causing diverging phenotypes and the features observed in Group 1 suggest a new clinically recognizable syndrome uniquely associated with the heterozygous variant c.5218C>T p.(Arg1740Trp) in SETD2

Associations between Social Support from Family, Friends, and Teachers and depressive Symptoms in Adolescents

Approximately 20% of adolescents develop depressive symptoms. Family, friends, and teachers are crucial sources of social support for adolescents, but it is unclear whether social support impacts adolescents directly (principle-effect model) or by moderating the effect of stress (stress-buffer model) and whether each source of social support remains meaningful when their influence is studied simultaneously. To help fill this gap, we followed 1452 Australian students (average age at enrollment = 13.1, SD = 0.5; range: 11-16 years; 51.9% female) for 5 years. Based on our findings, each source of support is negatively related to depressive symptoms one year later when studied independently but when combined, only family and teacher support predicted depressive symptoms. Family support in all grades and teacher support in grade 8 to 10 but not in grade 11 directly impacted adolescent depressive symptoms 1 year later. Family support in grades 8 and 11 also buffered against the negative impact of stress on depressive symptoms one year later. Based on the unexpected findings, the most important limitations seem to be that the used instruments do not allow for a separation of different groups of friends (e.g., classmates, same-gender peers, romantic partners), types of social support, and stress. In addition, the high, nonrandom attrition rate with adolescents reporting less social support, more stressful events, a higher frequency of depressive symptoms, and/or being of Torres Strait Islander or Aboriginal background limits the generalizability of our findings. Summarized, our findings demonstrate that adolescents facing stress might benefit more from family support compared to their peers without stressful life events and that friends may have a weaker presence in adolescent lives than expected

Report of the Committee on foreign relations together with the views of the minority upon the general arbitration treaties with Great Britain and France, signed on August 3, 1911, and the proposed committee amendments. With appendices

"Views of a minority," by S. M. Cullom and Elihu Root; "Supplemental view of Mr. Burton"; "Views" by Isidor Rayner; and "Proposed resolution of ratification": p. 9-25. The two latter papers were also pub. separately, 1912, as pt. 2 and pt. 3 of Senate doc. 98, 62d Cong., 2d [i.e. 1st] sessPresented by Mr. Lodge. Ordered printed Aug. 15, 1911. Ordered reprinted with additional matter Aug. 21, 1911Mode of access: Internet

Neutralizing antibody affords comparable protection against vaginal and rectal simian/human immunodeficiency virus challenge in macaques

ObjectivePassive administration of broadly neutralizing antibodies has been shown to protect against both vaginal and rectal challenge in the simian/human immunodeficiency virus (SHIV)/macaque model of HIV transmission. However, the relative efficacy of antibody against the two modes of exposure is unknown and, given differences in the composition and immunology of the two tissue compartments, this is an important gap in knowledge. To investigate the significance of the challenge route for antibody-mediated protection, we performed a comparative protection study in macaques using the highly potent human monoclonal antibody, PGT126.DesignAnimals were administered PGT126 at three different doses before challenged either vaginally or rectally with a single dose of SHIVSF163P3.MethodsViral loads, PGT126 serum concentrations, and serum neutralizing titers were monitored.ResultsIn vaginally challenged animals, sterilizing immunity was achieved in all animals administered 10 mg/kg, in two of five animals administered 2 mg/kg and in one of five animals administered 0.4 mg/kg PGT126. Comparable protection was observed for the corresponding groups challenged rectally as sterilizing immunity was achieved in three of four animals administered 10 mg/kg, in two of four animals administered 2 mg/kg and in none of four animals administered 0.4 mg/kg PGT126. Serological analysis showed similar serum concentrations of PGT126 and serum neutralization titers in animals administered the same antibody dose.ConclusionOur data suggest that broadly neutralizing antibody-mediated protection is not strongly dependent on the mucosal route of challenge, which indicates that a vaccine aimed to induce a neutralizing antibody response would have broadly similar efficacy against both primary transmission routes for HIV

Genotype–phenotype correlation at codon 1740 of SETD2

The SET domain containing 2, histone lysine methyltransferase encoded by SETD2 is a dual-function methyltransferase for histones and microtubules and plays an important role for transcriptional regulation, genomic stability, and cytoskeletal functions. Specifically, SETD2 is associated with trimethylation of histone H3 at lysine 36 (H3K36me3) and methylation of α-tubulin at lysine 40. Heterozygous loss of function and missense variants have previously been described with Luscan-Lumish syndrome (LLS), which is characterized by overgrowth, neurodevelopmental features, and absence of overt congenital anomalies. We have identified 15 individuals with de novo variants in codon 1740 of SETD2 whose features differ from those with LLS. Group 1 consists of 12 individuals with heterozygous variant c.5218C>T p.(Arg1740Trp) and Group 2 consists of 3 individuals with heterozygous variant c.5219G>A p.(Arg1740Gln). The phenotype of Group 1 includes microcephaly, profound intellectual disability, congenital anomalies affecting several organ systems, and similar facial features. Individuals in Group 2 had moderate to severe intellectual disability, low normal head circumference, and absence of additional major congenital anomalies. While LLS is likely due to loss of function of SETD2, the clinical features seen in individuals with variants affecting codon 1740 are more severe suggesting an alternative mechanism, such as gain of function, effects on epigenetic regulation, or posttranslational modification of the cytoskeleton. Our report is a prime example of different mutations in the same gene causing diverging phenotypes and the features observed in Group 1 suggest a new clinically recognizable syndrome uniquely associated with the heterozygous variant c.5218C>T p.(Arg1740Trp) in SETD2