Combination of parent-child closeness and parent disapproval of teen sex predicts lower rates of sexual risk for offspring.

Effective parenting processes during offspring's adolescence can reduce sexual risk behavior for those offspring in emerging adulthood. Few studies consider how mothers' and fathers' parenting processes cluster together and predict emerging adults' risky sexual behavior. In this study, we used latent profile analysis (LPA) to identify patterns of teens' perceptions of their residential mothers' and fathers' closeness, disapproval of teen sex, monitoring/presence at home and communication. Using data from waves one and three of the National Longitudinal Study of Adolescent to Adult Health (Add Health), we identified four parenting classes: high disapproval/high closeness (54%), high disapproval/low closeness (7%), low disapproval/high closeness (15%) and moderate disapproval/high closeness (24%). Emerging adults within the high disapproval/high closeness class had lower rates of sexual risk behavior than other classes. These findings show benefits of authoritative parenting styles, and suggest parenting processes should be considered in combination, rather than as independent predictors of risk outcomes.

Parenting Practices and Emerging Adult Sexual Health: The Role of Residential Fathers.

Emerging adulthood is a developmental period with high rates of sexual risk behavior. Effective parenting practices can reduce the likelihood of this behavior, but most research on the protective effects of parenting focuses on mothers. Research is needed to assess the role of paternal parenting in regards to their children's sexual risk behavior, particularly for children of teen mothers, who show a greater likelihood of risky sexual behaviors than those with older mothers. We investigated associations between residential fathers' parenting processes-communication, disapproval of teen sexual behavior, parental presence, and closeness-during adolescence and sexual risk behaviors reported by their children in emerging adulthood. Using multiple group structural equation modeling with data from 7399 participants at Wave I and Wave III of the National Longitudinal Study of Adolescent to Adult Health (Add Health), we examined whether and how residential fathers' parenting relates to their children's sexual risk behavior independent of mothers' parenting processes, and whether these associations differ across children's sex and for children of teen and older mothers. We found that adolescents' perceptions of higher father disapproval of teen sexual behavior predicted lower levels of sexual risk behavior during emerging adulthood with no significant differences across emerging adults' sex or for children of teen relative to older mothers. Our findings suggest that teens' relationships with their fathers during adolescence are important for their future sexual health, despite a general understanding of emerging adulthood as a period characterized by independence and separation from parents. Additionally, our results suggest that even though children of teen mothers show greater likelihood of risky sexual behaviors than those of older parents, the processes through which fathers can support teens' sexual health may be similar.

CD3Z hypermethylation is associated with severe clinical manifestations in systemic lupus erythematosus and reduces CD3ζ-chain expression in T cells.

Objective: The importance of hypomethylation in SLE is well recognized; however, the significance of hypermethylation has not been well characterized. We screened hypermethylated marks in SLE and investigated their possible implications. Methods: DNA methylation marks were screened in SLE whole-blood DNA by microarray, and two marks ( CD3Z and VHL hypermethylations) were confirmed by a methylation single-base extension method in two independent ethnic cohorts consisting of 207 SLE patients and 151 controls. The correlation with clinical manifestations and the genetic influence on those epigenetic marks were analysed. Results: Two epigenetic marks, CD3Z and VHL hypermethylation, were significantly correlated with SLE: CD3Z hypermethylation (odds ratio = 7.76; P = 1.71 × 10 -13 ) and VHL hypermethylation (odds ratio = 3.77; P = 3.20 × 10 -8 ), and the increased CD3Z methylation was correlated with downregulation of the CD3ζ-chain in SLE T cells. In addition, less genetic influence on CD3Z methylation relative to VHL methylation was found in analyses of longitudinal and twin samples. Furthermore, a higher CD3Z methylation level was significantly correlated with a higher SLE disease activity index and more severe clinical manifestations, such as proteinuria, haemolytic anaemia and thrombocytopenia, whereas VHL hypermethylation was not. Conclusion: CD3Z hypermethylation is an SLE risk factor that can be modified by environmental factors and is associated with more severe SLE clinical manifestations, which are related to deranged T cell function by downregulating the CD3ζ-chain.

Decreased SMG7 expression associates with lupus-risk variants and elevated antinuclear antibody production.

OBJECTIVES: Following up the systemic lupus erythematosus (SLE) genome-wide association studies (GWAS) identification of NMNAT2 at rs2022013, we fine-mapped its 150 kb flanking regions containing NMNAT2 and SMG7 in a 15 292 case-control multi-ancestry population and tested functions of identified variants. METHODS: We performed genotyping using custom array, imputation by IMPUTE 2.1.2 and allele specific functions using quantitative real-time PCR and luciferase reporter transfections. SLE peripheral blood mononuclear cells (PBMCs) were cultured with small interfering RNAs to measure antinuclear antibody (ANA) and cyto/chemokine levels in supernatants using ELISA. RESULTS: We confirmed association at NMNAT2 in European American (EA) and Amerindian/Hispanic ancestries, and identified independent signal at SMG7 tagged by rs2702178 in EA only (p=2.4×10-8, OR=1.23 (95% CI 1.14 to 1.32)). In complete linkage disequilibrium with rs2702178, rs2275675 in the promoter region robustly associated with SMG7 mRNA levels in multiple expression quantitative trait locus (eQTL) datasets. Its risk allele was dose-dependently associated with decreased SMG7 mRNA levels in PBMCs of 86 patients with SLE and 119 controls (p=1.1×10-3 and 6.8×10-8, respectively) and conferred reduced transcription activity in transfected HEK-293 (human embryonic kidney cell line) and Raji cells (p=0.0035 and 0.0037, respectively). As a critical component in the nonsense-mediated mRNA decay pathway, SMG7 could regulate autoantigens including ribonucleoprotein (RNP) and Smith (Sm). We showed SMG7 mRNA levels in PBMCs correlated inversely with ANA titres of patients with SLE (r=-0.31, p=0.01), and SMG7 knockdown increased levels of ANA IgG and chemokine (C-C motif) ligand 19 in SLE PBMCs (p=2.0×10-5 and 2.0×10-4, respectively). CONCLUSION: We confirmed NMNAT2 and identified independent SMG7 association with SLE. The inverse relationship between levels of the risk allele-associated SMG7 mRNAs and ANA suggested the novel contribution of mRNA surveillance pathway to SLE pathogenesis.

Preferential binding to Elk-1 by SLE-associated IL10 risk allele upregulates IL10 expression.

Immunoregulatory cytokine interleukin-10 (IL-10) is elevated in sera from patients with systemic lupus erythematosus (SLE) correlating with disease activity. The established association of IL10 with SLE and other autoimmune diseases led us to fine map causal variant(s) and to explore underlying mechanisms. We assessed 19 tag SNPs, covering the IL10 gene cluster including IL19, IL20 and IL24, for association with SLE in 15,533 case and control subjects from four ancestries. The previously reported IL10 variant, rs3024505 located at 1 kb downstream of IL10, exhibited the strongest association signal and was confirmed for association with SLE in European American (EA) (P = 2.7×10⁻8, OR = 1.30), but not in non-EA ancestries. SNP imputation conducted in EA dataset identified three additional SLE-associated SNPs tagged by rs3024505 (rs3122605, rs3024493 and rs3024495 located at 9.2 kb upstream, intron 3 and 4 of IL10, respectively), and SLE-risk alleles of these SNPs were dose-dependently associated with elevated levels of IL10 mRNA in PBMCs and circulating IL-10 protein in SLE patients and controls. Using nuclear extracts of peripheral blood cells from SLE patients for electrophoretic mobility shift assays, we identified specific binding of transcription factor Elk-1 to oligodeoxynucleotides containing the risk (G) allele of rs3122605, suggesting rs3122605 as the most likely causal variant regulating IL10 expression. Elk-1 is known to be activated by phosphorylation and nuclear localization to induce transcription. Of interest, phosphorylated Elk-1 (p-Elk-1) detected only in nuclear extracts of SLE PBMCs appeared to increase with disease activity. Co-expression levels of p-Elk-1 and IL-10 were elevated in SLE T, B cells and monocytes, associated with increased disease activity in SLE B cells, and were best downregulated by ERK inhibitor. Taken together, our data suggest that preferential binding of activated Elk-1 to the IL10 rs3122605-G allele upregulates IL10 expression and confers increased risk for SLE in European Americans.

Genetic associations of leptin-related polymorphisms with systemic lupus erythematosus.

Leptin is abnormally elevated in the plasma of patients with systemic lupus erythematosus (SLE), where it is thought to promote and/or sustain pro-inflammatory responses. Whether this association could reflect an increased genetic susceptibility to develop SLE is not known, and studies of genetic associations with leptin-related polymorphisms in SLE patients have been so far inconclusive. Here we genotyped DNA samples from 15,706 SLE patients and healthy matched controls from four different ancestral groups, to correlate polymorphisms of genes of the leptin pathway to risk for SLE. It was found that although several SNPs showed weak associations, those associations did not remain significant after correction for multiple testing. These data do not support associations between defined leptin-related polymorphisms and increased susceptibility to develop SLE.

The role of extended family in diverse teens' sexual health.

Despite increasing extended family involvement in childrearing, particularly in minority families, few studies investigate their role in talking with teens about sex or how this relates to teens' sexual behavior. This mixed methods study assesses extended family sexuality communication through a survey of 1492 diverse middle school students and interviews with 32 students. Logistic regression shows that participants who report having had sex are more likely to report talking with extended family than those who report not having had sex. Interview themes explored reasons for and content of teen sexuality conversations with extended family. More sexually active teens' reporting communication with extended family is interpreted as extended family members gaining importance in sexuality communication as teens become sexually active.

Association of genetic variants in complement factor H and factor H-related genes with systemic lupus erythematosus susceptibility.

Systemic lupus erythematosus (SLE), a complex polygenic autoimmune disease, is associated with increased complement activation. Variants of genes encoding complement regulator factor H (CFH) and five CFH-related proteins (CFHR1-CFHR5) within the chromosome 1q32 locus linked to SLE, have been associated with multiple human diseases and may contribute to dysregulated complement activation predisposing to SLE. We assessed 60 SNPs covering the CFH-CFHRs region for association with SLE in 15,864 case-control subjects derived from four ethnic groups. Significant allelic associations with SLE were detected in European Americans (EA) and African Americans (AA), which could be attributed to an intronic CFH SNP (rs6677604, in intron 11, P(meta) = 6.6×10(-8), OR = 1.18) and an intergenic SNP between CFHR1 and CFHR4 (rs16840639, P(meta) = 2.9×10(-7), OR = 1.17) rather than to previously identified disease-associated CFH exonic SNPs, including I62V, Y402H, A474A, and D936E. In addition, allelic association of rs6677604 with SLE was subsequently confirmed in Asians (AS). Haplotype analysis revealed that the underlying causal variant, tagged by rs6677604 and rs16840639, was localized to a ~146 kb block extending from intron 9 of CFH to downstream of CFHR1. Within this block, the deletion of CFHR3 and CFHR1 (CFHR3-1Δ), a likely causal variant measured using multiplex ligation-dependent probe amplification, was tagged by rs6677604 in EA and AS and rs16840639 in AA, respectively. Deduced from genotypic associations of tag SNPs in EA, AA, and AS, homozygous deletion of CFHR3-1Δ (P(meta) = 3.2×10(-7), OR = 1.47) conferred a higher risk of SLE than heterozygous deletion (P(meta) = 3.5×10(-4), OR = 1.14). These results suggested that the CFHR3-1Δ deletion within the SLE-associated block, but not the previously described exonic SNPs of CFH, might contribute to the development of SLE in EA, AA, and AS, providing new insights into the role of complement regulators in the pathogenesis of SLE.

The "what" and "how" of father-teen talks about sex and relationships.

For adolescents who have a father in their lives, father-teen conversations about sex and relationships can protect teens from risky sexual behaviors. However, little is known about the content and process of these conversations. This study explored topics of and approaches to fathers' talk with their teens about sex and relationships in interviews with a diverse sample of 43 fathers of high school-aged adolescents from across the United States. Interview data were analyzed using content analysis. The results showed how fathers talked with their adolescent children about topics of sexual behavior, risks of sex, dating and relationships, as well as less studied areas of diverse sexual and gender identities and consent, and how these conversations differed with male and female teens. Findings also showed that fathers took multiple approaches to talk about sex, including personal talk, talk about friends and family, and use of media and other distal contexts to start conversations. These findings show how fathers contribute to the sexual socialization of their adolescent children and suggest points of access for fathers who are unsure how to approach talk with their teens about sex and relationships. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Fine mapping of Xq28: both MECP2 and IRAK1 contribute to risk for systemic lupus erythematosus in multiple ancestral groups.

OBJECTIVES: The Xq28 region containing IRAK1 and MECP2 has been identified as a risk locus for systemic lupus erythematosus (SLE) in previous genetic association studies. However, due to the strong linkage disequilibrium between IRAK1 and MECP2, it remains unclear which gene is affected by the underlying causal variant(s) conferring risk of SLE. METHODS: We fine-mapped ≥136 SNPs in a ∼227 kb region on Xq28, containing IRAK1, MECP2 and seven adjacent genes (L1CAM, AVPR2, ARHGAP4, NAA10, RENBP, HCFC1 and TMEM187), for association with SLE in 15 783 case-control subjects derived from four different ancestral groups. RESULTS: Multiple SNPs showed strong association with SLE in European Americans, Asians and Hispanics at p<5×10(-8) with consistent association in subjects with African ancestry. Of these, six SNPs located in the TMEM187-IRAK1-MECP2 region captured the underlying causal variant(s) residing in a common risk haplotype shared by all four ancestral groups. Among them, rs1059702 best explained the Xq28 association signals in conditional testings and exhibited the strongest p value in transancestral meta-analysis (p(meta )= 1.3×10(-27), OR=1.43), and thus was considered to be the most likely causal variant. The risk allele of rs1059702 results in the amino acid substitution S196F in IRAK1 and had previously been shown to increase NF-κB activity in vitro. We also found that the homozygous risk genotype of rs1059702 was associated with lower mRNA levels of MECP2, but not IRAK1, in SLE patients (p=0.0012) and healthy controls (p=0.0064). CONCLUSIONS: These data suggest contributions of both IRAK1 and MECP2 to SLE susceptibility.

Sex-specific association of X-linked Toll-like receptor 7 (TLR7) with male systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a multisystem, autoimmune disease that predominantly affects women. Previous findings that duplicated Toll-like receptor 7 (Tlr7) promotes lupus-like disease in male BXSB mice prompted us to evaluate TLR7 in human SLE. By using a candidate gene approach, we identified and replicated association of a TLR7 3'UTR SNP, rs3853839 (G/C), with SLE in 9,274 Eastern Asians (P(combined) = 6.5 x 10(-10)), with a stronger effect in male than female subjects [odds ratio, male vs. female = 2.33 (95% CI = 1.64-3.30) vs. 1.24 (95% CI = 1.14-1.34); P = 4.1 x 10(-4)]. G-allele carriers had increased TLR7 transcripts and more pronounced IFN signature than C-allele carriers; heterozygotes had 2.7-fold higher transcripts of G-allele than C-allele. These data established a functional polymorphism in type I IFN pathway gene TLR7 predisposing to SLE, especially in Chinese and Japanese male subjects.

Adolescents' religious discordance with mothers: is there a connection to sexual risk behavior during emerging adulthood?

This study longitudinally investigates the relationship between adolescent/mother religious discordance and emerging adult sexual risk-taking 6-7 years later. We used Social Control Theory to examine the level and direction of concordance using data from Wave I and Wave III of the Add Health Study, focusing on constructs of religious importance, frequency of prayer, and attendance at religious services. We found that higher levels of adolescent/mother discordance in religious importance were related to increased emerging adult sexual risk-taking compared to those with similar levels adolescent/mother religiosity, but this occurred only when mothers reported higher levels of religious importance than their children. In contrast, adolescents reporting higher frequency of prayer than their mothers reported lower levels of sexual risk-taking than those with similar frequency of adolescent/mother prayer. These findings suggest that the protective effects of family religious socialization can be interrupted. However, this influence of religious difference on sexual risk-behavior operates differently depending on the direction and level of religious difference. Even in emerging adulthood, a period marked by distance from childhood values and institutions, religious difference with a parent remains a meaningful influence.

Association of a functional IRF7 variant with systemic lupus erythematosus.

OBJECTIVE: A previous genome-wide association study conducted in a population of European ancestry identified rs4963128, a KIAA1542 single-nucleotide polymorphism (SNP) 23 kb telomeric to IRF7 (the gene for interferon regulatory factor 7 [IRF-7]), to be strongly associated with systemic lupus erythematosus (SLE). This study was undertaken to investigate whether genetic polymorphism within IRF7 is a risk factor for the development of SLE. METHODS: We genotyped one KIAA1542 SNP (rs4963128) and one IRF7 SNP (rs1131665 [Q412R]) in an Asian population (1,302 cases, 1,479 controls), to assess their association with SLE. Subsequently, rs1131665 was further genotyped in independent panels of Chinese subjects (528 cases, 527 controls), European American subjects (446 cases, 461 controls), and African American subjects (159 cases, 115 controls) by TaqMan genotyping assay, to seek confirmation of association in various ethnic groups. A luciferase reporter assay was used to assess the effect of Q412R polymorphism on the activation of IRF-7. RESULTS: Consistent association of rs1131665 (Q412R) with SLE was identified in Asian, European American, and African American populations (total 2,435 cases and 2,582 controls) (P(meta) = 6.18 × 10(-6) , odds ratio 1.42 [95% confidence interval 1.22-1.65]). Expression of the IRF7 412Q risk allele resulted in a 2-fold increase in interferon-stimulated response element transcriptional activity compared with expression of IRF7 412R (P = 0.0003), suggesting that IRF7 412Q confers elevated IRF-7 activity and may therefore affect a downstream interferon pathway. CONCLUSION: These findings show that the major allele of a nonsynonymous SNP, rs1131665 (412Q) in IRF7, confers elevated activation of IRF-7 and predisposes to the development of SLE in multiple ethnic groups. This result provides direct genetic evidence that IRF7 may be a risk gene for human SLE.

Association of PPP2CA polymorphisms with systemic lupus erythematosus susceptibility in multiple ethnic groups.

OBJECTIVE: T cells from patients with systemic lupus erythematosus (SLE) express increased amounts of PP2Ac, which contributes to decreased production of interleukin-2 (IL-2). Because IL-2 is important in the regulation of several aspects of the immune response, it has been proposed that PP2Ac contributes to the expression of SLE. This study was designed to determine whether genetic variants of PPP2AC are linked to the expression of SLE and specific clinical manifestations and account for the increased expression of PP2Ac. METHODS: We conducted a trans-ethnic study of 8,695 SLE cases and 7,308 controls of 4 different ancestries. Eighteen single-nucleotide polymorphisms (SNPs) across PPP2CA were genotyped using an Illumina custom array. PPP2CA expression in SLE and control T cells was analyzed by real-time polymerase chain reaction. RESULTS: A 32-kb haplotype comprising multiple SNPs of PPP2CA showed significant association with SLE in Hispanic Americans, European Americans, and Asians, but not in African Americans. Conditional analyses revealed that SNP rs7704116 in intron 1 showed consistently strong association with SLE across Asian, European American, and Hispanic American populations (odds ratio 1.3 [95% confidence interval 1.14-1.31], meta-analysis P=3.8×10(-7)). In European Americans, the largest ethnic data set studied, the risk A allele of rs7704116 was associated with the presence of renal disease, anti-double-stranded DNA, and anti-RNP antibodies. PPP2CA expression was ∼2-fold higher in SLE patients carrying the rs7704116 AG genotype than those carrying the GG genotype (P=0.007). CONCLUSION: Our data provide the first evidence of an association between PPP2CA polymorphisms and elevated PP2Ac transcript levels in T cells, which implicates a new molecular pathway for SLE susceptibility in European Americans, Hispanic Americans, and Asians.

Constructing Profiles of Religious Agreement and Disagreement Between Adolescents and Mothers: A Research Note.

This research note describes the use of latent class analysis to examine how three dimensions of religiosity-the importance of religion (religious salience), attendance at religious services, and frequency of prayer-cluster together to form unique profiles. Building upon recent research identifying different profiles of religiosity at the level of the individual, we used data from the National Longitudinal Study of Adolescent Health to identify dyadic profiles of religious concordance or discordance between 14,202 adolescents and their mothers. We identified five profiles: one concordant (27% of sample), two discordant (25% of sample), and two of mixed concordance/discordance (49%). The profiles distinguish between various levels of adolescent/mother relations, suggesting that they may represent distinct family dynamics. They also distinguish between several variables (race, adolescent age, geographical region) in predictable ways, providing additional demonstration of the categories' meaningfulness.

Associations of early social media initiation on digital behaviors and the moderating role of limiting use.

Little is known about the effects of social media initiation on digital behaviors from middle childhood to early adolescence, a critical developmental period marked by peer influence and inaugural access to mobile devices. Participants from middle schools in the Northeast U.S. (N=773; 11-15 years, Mean = 12.6) completed a cross-sectional survey about social media initiation, digital behaviors, and parental restrictions on digital use. Descriptive results demonstrated that overall early adolescents more frequently engaged in positive digital behaviors compared to negative ones. Results from structural equation models showed that initiating social media platforms, namely Instagram or Snapchat, in later childhood (10 years or younger) was significantly associated with problematic digital behavior outcomes compared to either tween (11-12) and/or teen (13+) initiation, including having online friends or joining social media sites parents would disapprove of, more problematic digital technology behaviors, more unsympathetic online behaviors, and greater likelihood of online harassment and sexual harassment victimization. Additionally, there is evidence to show that childhood initiators demonstrated a greater tendency to engage in supportive or civically-engaged online community behaviors compared to older initiator counterparts. Parental restriction of mobile phone use and a less frequent checking of social media ameliorated some of the negative effects.

Moving from Needs Assessment to Intervention: Fathers' Perspectives on Their Needs and Support for Talk with Teens about Sex.

Talk with fathers about sex and relationships can support teens' health, but its impact is limited as few fathers talk with their teens about sexual issues. Needs assessment and fathers' input on intervention content and structure can guide the development of programs that support fathers' health-promoting talk with their teen children about sex and relationships. In the present study, we explored fathers' goals in their talk with teens about sex and relationships and barriers they perceive to these conversations, as well as what they would look for in an intervention program. Content analysis was conducted using interviews in the U.S. with 43 fathers of high school-aged teens (age 14-18). Themes explored fathers' roles in talk with teens, key messages to teens, and approaches and barriers to conversations, in addition to attitudes toward an intervention, and feedback on intervention structure, content, and process. The findings suggest that fathers see talk with teens about sex as part of their roles, but face challenges in accomplishing this goal. Fathers' feedback highlights their openness to an intervention and can guide the development of a peer-based and interactive program that addresses how to talk with teens about sex in addition to the content of these conversations.

Osteoporosis prevention.

PURPOSE OF REVIEW: Patients with osteoporosis suffer from the morbidity and mortality associated with resultant fractures. The number of persons at risk for fractures is increasing as the US population ages. This review addresses preventive strategies that can be used to decrease the risk of minimal trauma fractures. RECENT FINDINGS: Dietary and lifestyle modifications and screening to identify individuals most likely to benefit from pharmacologic interventions, important components of osteoporosis prevention, will be discussed. Currently available osteoporosis therapies and fall prevention, which should be utilized in those at increased risk of fracture, will be reviewed. SUMMARY: The ultimate goal of implementing a multipronged osteoporosis preventive program is to improve function and quality of life in later life.

Novel autoantibodies against the activated coagulation factor IX (FIXa) in the antiphospholipid syndrome that interpose the FIXa regulation by antithrombin.

We previously reported that some human antiphospholipid Abs (aPL) in patients with the antiphospholipid syndrome (APS) bind to the homologous enzymatic domains of thrombin and the activated coagulation factor X (FXa). Moreover, some of the reactive Abs are prothrombotic and interfere with inactivation of thrombin and FXa by antithrombin (AT). Considering the enzymatic domain of activated coagulation factor IX (FIXa) is homologous to those of thrombin and FXa, we hypothesized that some aPLs in APS bind to FIXa and hinder AT inactivation of FIXa. To test this hypothesis, we searched for IgG anti-FIXa Abs in APS patients. Once the concerned Abs were found, we studied the effects of the Ab on FIXa inactivation by AT. We found that 10 of 12 patient-derived monoclonal IgG aPLs bound to FIXa and that IgG anti-FIXa Abs in APS patients were significantly higher than those in normal controls (p < 0.0001). Using the mean + 3 SD of 30 normal controls as the cutoff, the IgG anti-FIXa Abs were present in 11 of 38 (28.9%) APS patients. Importantly, 4 of 10 FIXa-reactive monoclonal aPLs (including the B2 mAb generated against beta(2)-glycoprotein I significantly hindered AT inactivation of FIXa. More importantly, IgG from two positive plasma samples were found to interfere with AT inactivation of FIXa. In conclusion, IgG anti-FIXa Ab occurred in approximately 30% of APS patients and could interfere with AT inactivation of FIXa. Because FIXa is an upstream procoagulant factor, impaired AT regulation of FIXa might contribute more toward thrombosis than the dysregulation of the downstream FXa and thrombin.

Same-Sex Attraction Disclosure and Sexual Communication Topics within Families.

Few studies compare family communication about sex and relationships for sexual minority youth versus hetero-sexual teenagers. Further, existing studies often focus on mothers, overlooking fathers and extended family. Our survey of 952 adolescents aged 14-21 included 115 adolescents disclosing non-heterosexual attraction. Mothers offered more sexual protection methods messages to their non-SM teens, whereas fathers talked less with SM teens about risks of sex and relational sex. Most participants identified mothers, sisters, and female cousins, with male SMs having the highest number of disclosures to family members, whereas female and non-binary SMs confided in fewer family members or no one.