Moving Past Assumptions: Recognizing Parents as Allies in Promoting the Sexual Literacies of Adolescents through a University-Community Collaboration

This article recounts how a university-community collaborative challenged prevailing assumptions about parents as barriers to the provision of gender and sexuality information to their children, allowing for the recognition of parents as critical stakeholders and partners in sexual literacy work with youth. We provide evidence that parents’ support for inclusive sexuality education uniquely situates them to educate and advocate for young people around these issues, and in so doing we hope to disrupt the rhetoric that casts parents in the United States as solely gatekeepers when it comes to young people’s access to information about the broad spectrum of human sexuality

Mitochondria Exert Age-Divergent Effects on Recovery from Spinal Cord Injury

The extent that age-dependent mitochondrial dysfunction drives neurodegeneration is not well understood. This study tested the hypothesis that mitochondria contribute to spinal cord injury (SCI)-induced neurodegeneration in an age-dependent manner by using 2,4-dinitrophenol (DNP) to uncouple electron transport, thereby increasing cellular respiration and reducing reactive oxygen species (ROS) production. We directly compared the effects of graded DNP doses in 4- and 14-month-old (MO) SCI-mice and found DNP to have increased efficacy in mitochondria isolated from 14-MO animals. In vivo, all DNP doses significantly exacerbated 4-MO SCI neurodegeneration coincident with worsened recovery. In contrast, low DNP doses (1.0-mg/kg/day) improved tissue sparing, reduced ROS-associated 3-nitrotyrosine (3-NT) accumulation, and improved anatomical and functional recovery in 14-MO SCI-mice. By directly comparing the effects of DNP between ages we demonstrate that mitochondrial contributions to neurodegeneration diverge with age after SCI. Collectively, our data indicate an essential role of mitochondria in age-associated neurodegeneration

Diasporas and secessionist conflicts : the mobilization of the Armenian, Albanian and Chechen diasporas

This article examines the impact of diasporas on secessionist conflicts, focusing on the Albanian, Armenian and Chechen diasporas and the conflicts in Kosovo, Karabakh and Chechnya during the 1990s. How do diasporas radicalize these conflicts? I argue that despite differences in diaspora communal characteristics and the types of the secessionist conflicts, a common pattern of mobilization develops. Large-scale diasporic support for secessionism emerges only after independence is proclaimed by the local elites. From that point onwards diasporas become engaged in a conflict spiral, and transnational coalitions are formed between local secessionist and diaspora groups. Depending on the organizational strength of the local strategic centre and the diasporic institutions, these coalitions endure or dissipate. Diasporas exert radicalization influences on the conflict spiral on two specific junctures – when grave violations of human rights occur in the homeland and when local moderate elites start losing credibility that they can achieve the secessionist goal

Large-eddy simulation of the tidal-cycle variations of an estuarine boundary layer

Author Posting. © American Geophysical Union, 2010. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research 115 (2010): C08003, doi:10.1029/2009JC005702.The estuarine boundary layer affected by a horizontal density gradient exhibits temporal evolution over a tidal cycle, in a manner similar to the diurnal cycle of the ocean surface mixed layer. A large eddy simulation (LES) model is developed to investigate the physics controlling the growth of the boundary layer during the flood tide and restratification during the ebb tide. Turbulent kinetic energy, momentum and salt fluxes, bottom stress, and energy dissipation rates calculated from the LES model all show a strong flood-ebb asymmetry. Analysis of the turbulent kinetic energy (TKE) budget shows a primary balance between shear production and dissipation in the well-mixed boundary layer over the tidal cycle. However, TKE transport term is found to be important across the edge of the boundary layer during the flood tide so turbulent energy generated in the bottom boundary layer can be transferred to the stratified pycnocline region. Tidal straining leads to a small and weakly convective region inside the boundary layer during the flood tide but the strain-induced buoyancy flux does not make a significant contribution to the turbulence generation. Additional LES runs are conducted by switching off the baroclinic pressure gradient term in the momentum equation and the tidal straining term in the salinity equation to show that the baroclinic pressure gradient is the main mechanism responsible for generating the flood-ebb mixing asymmetry.This work is supported by grants OCE-0451699 (M.L.), OCE-0452380 (U.P. and S.R.), and OCE-0451740 (W.R.G.) from the National Science Foundation

Clonal Hematopoiesis and Blood-Cancer Risk Inferred from Blood DNA Sequence

Background Cancers arise from multiple acquired mutations, which presumably occur over many years. Early stages in cancer development might be present years before cancers become clinically apparent. Methods We analyzed data from whole-exome sequencing of DNA in peripheral-blood cells from 12,380 persons, unselected for cancer or hematologic phenotypes. We identified somatic mutations on the basis of unusual allelic fractions. We used data from Swedish national patient registers to follow health outcomes for 2 to 7 years after DNA sampling. Results Clonal hematopoiesis with somatic mutations was observed in 10% of persons older than 65 years of age but in only 1% of those younger than 50 years of age. Detectable clonal expansions most frequently involved somatic mutations in three genes (DNMT3A, ASXL1, and TET2) that have previously been implicated in hematologic cancers. Clonal hematopoiesis was a strong risk factor for subsequent hematologic cancer (hazard ratio, 12.9; 95% confidence interval, 5.8 to 28.7). Approximately 42% of hematologic cancers in this cohort arose in persons who had clonality at the time of DNA sampling, more than 6 months before a first diagnosis of cancer. Analysis of bone marrow–biopsy specimens obtained from two patients at the time of diagnosis of acute myeloid leukemia revealed that their cancers arose from the earlier clones. Conclusions Clonal hematopoiesis with somatic mutations is readily detected by means of DNA sequencing, is increasingly common as people age, and is associated with increased risks of hematologic cancer and death. A subset of the genes that are mutated in patients with myeloid cancers is frequently mutated in apparently healthy persons; these mutations may represent characteristic early events in the development of hematologic cancers. (Funded by the National Human Genome Research Institute and others.)National Human Genome Research Institute (U.S.) (Grant U54 HG003067)National Human Genome Research Institute (U.S.) (Grant R01 HG006855)Stanley Center for Psychiatric ResearchAlexander and Margaret Stewart TrustNational Institute of Mental Health (U.S.) (Grant R01 MH 077139)National Institute of Mental Health (U.S.) (Grant RC2 MH089905)Sylvan C. Herman Foundatio

Responsiveness of sphingosine phosphate lyase insufficiency syndrome to vitamin B6 cofactor supplementation

Sphingosine- 1- phosphate (S1P) lyase is a vitamin B6- dependent enzyme that degrades sphingosine- 1- phosphate in the final step of sphingolipid metabolism. In 2017, a new inherited disorder was described caused by mutations in SGPL1, which encodes sphingosine phosphate lyase (SPL). This condition is referred to as SPL insufficiency syndrome (SPLIS) or alternatively as nephrotic syndrome type 14 (NPHS14). Patients with SPLIS exhibit lymphopenia, nephrosis, adrenal insufficiency, and/or neurological defects. No targeted therapy for SPLIS has been reported. Vitamin B6 supplementation has therapeutic activity in some genetic diseases involving B6- dependent enzymes, a finding ascribed largely to the vitamin’s chaperone function. We investigated whether B6 supplementation might have activity in SPLIS patients. We retrospectively monitored responses of disease biomarkers in patients supplemented with B6 and measured SPL activity and sphingolipids in B6- treated patient- derived fibroblasts. In two patients, disease biomarkers responded to B6 supplementation. S1P abundance and activity levels increased and sphingolipids decreased in response to B6. One responsive patient is homozygous for an SPL R222Q variant present in almost 30% of SPLIS patients. Molecular modeling suggests the variant distorts the dimer interface which could be overcome by cofactor supplementation. We demonstrate the first potential targeted therapy for SPLIS and suggest that 30% of SPLIS patients might respond to cofactor supplementation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162713/2/jimd12238.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162713/1/jimd12238_am.pd