Gender Transformative Philanthropy

As foundations and other philanthropic institutions assess where they can maximize the social return on their charitable investments, many are looking at issues of gender norms and gender equity. One program officer put it this way: "Our grantees and staff get race and class; some are even starting to get sexual orientation. What I want to know is -- what happened to gender? Where is the gender analysis?" Over two decades of research has now shown that challenging harmful codes of masculinity and femininity is a major key to improving outcomes in reproductive health and gender-based violence. Yet the field continues to mostly overlook gender norms. As the same time, studies have shown conclusively that having a strong gender analysis of the disparate impacts on women and men is crucial to increasing the effectiveness of civic engagement organizing. However, many non-profits in this space either ignore gender equity, or marginalize it as a "women's issue." As one experienced program officer put it, "Grantees need to see gender and race together. Gender impacts every issue they work on. But grantees are not being challenged to do innovative work around gender [in a way that parallels their work on race or class concerns]. This accessible overview will help program officers who want to integrate a stronger gender focus into their giving and their grantees' work and analysis

Factors Associated with Revision Surgery after Internal Fixation of Hip Fractures

Background: Femoral neck fractures are associated with high rates of revision surgery after management with internal fixation. Using data from the Fixation using Alternative Implants for the Treatment of Hip fractures (FAITH) trial evaluating methods of internal fixation in patients with femoral neck fractures, we investigated associations between baseline and surgical factors and the need for revision surgery to promote healing, relieve pain, treat infection or improve function over 24 months postsurgery. Additionally, we investigated factors associated with (1) hardware removal and (2) implant exchange from cancellous screws (CS) or sliding hip screw (SHS) to total hip arthroplasty, hemiarthroplasty, or another internal fixation device. Methods: We identified 15 potential factors a priori that may be associated with revision surgery, 7 with hardware removal, and 14 with implant exchange. We used multivariable Cox proportional hazards analyses in our investigation. Results: Factors associated with increased risk of revision surgery included: female sex, [hazard ratio (HR) 1.79, 95% confidence interval (CI) 1.25-2.50; P = 0.001], higher body mass index (fo

Premature expression of a muscle fibrosis axis in chronic HIV infection

Abstract Background Despite the success of highly active antiretroviral therapy (HAART), HIV infected individuals remain at increased risk for frailty and declines in physical function that are more often observed in older uninfected individuals. This may reflect premature or accelerated muscle aging. Methods Skeletal muscle gene expression profiles were evaluated in three uninfected independent microarray datasets including young (19 to 29 years old), middle aged (40 to 45 years old) and older (65 to 85 years old) subjects, and a muscle dataset from HIV infected subjects (36 to 51 years old). Using Bayesian analysis, a ten gene muscle aging signature was identified that distinguished young from old uninfected muscle and included the senescence and cell cycle arrest gene p21/Cip1 (CDKN1A). This ten gene signature was then evaluated in muscle specimens from a cohort of middle aged (30 to 55 years old) HIV infected individuals. Expression of p21/Cip1 and related pathways were validated and further analyzed in a rodent model for HIV infection. Results We identify and replicate the expression of a set of muscle aging genes that were prematurely expressed in HIV infected, but not uninfected, middle aged subjects. We validated select genes in a rodent model of chronic HIV infection. Because the signature included p21/Cip1, a cell cycle arrest gene previously associated with muscle aging and fibrosis, we explored pathways related to senescence and fibrosis. In addition to p21/Cip1, we observed HIV associated upregulation of the senescence factor p16INK4a (CDKN2A) and fibrosis associated TGFβ1, CTGF, COL1A1 and COL1A2. Fibrosis in muscle tissue was quantified based on collagen deposition and confirmed to be elevated in association with infection status. Fiber type composition was also measured and displayed a significant increase in slow twitch fibers associated with infection. Conclusions The expression of genes associated with a muscle aging signature is prematurely upregulated in HIV infection, with a prominent role for fibrotic pathways. Based on these data, therapeutic interventions that promote muscle function and attenuate pro-fibrotic gene expression should be considered in future studies.</p

Top Ten Tips Palliative Care Clinicians Should Know About Psychosocial and Family Support.

Palliative care (PC) is perhaps the most inherently interdisciplinary specialty within health care. Comprehensive PC is delivered by a core team of physicians, nurses, social workers, spiritual care providers, pharmacists, and others who address the broad range of medical, psychosocial, and spiritual needs of those living with serious illness. While PC clinicians are typically skilled in screening for distress, the best path to follow when patients screen positive for psychosocial distress or exhibit mental health challenges may not always be clear. This article brings together the perspectives of experienced social workers practicing across PC and hospice settings. It seeks to identify opportunities and rationale for the integration of palliative social work (PSW) in the provision of quality, person-centered, family-focused, and culturally congruent care for the seriously ill. Increasing recognition of the impact of social determinants of health highlights the critical importance of including PSW if we are to better understand and ultimately address the broad range of factors that influence people\u27s quality of life

Induction of heme oxygenase I (HMOX1) by HPP-4382: a novel modulator of Bach1 activity.

Oxidative stress is generated by reactive oxygen species (ROS) produced in response to metabolic activity and environmental factors. Increased oxidative stress is associated with the pathophysiology of a broad spectrum of inflammatory diseases. Cellular response to excess ROS involves the induction of antioxidant response element (ARE) genes under control of the transcriptional activator Nrf2 and the transcriptional repressor Bach1. The development of synthetic small molecules that activate the protective anti-oxidant response network is of major therapeutic interest. Traditional small molecules targeting ARE-regulated gene activation (e.g., bardoxolone, dimethyl fumarate) function by alkylating numerous proteins including Keap1, the controlling protein of Nrf2. An alternative is to target the repressor Bach1. Bach1 has an endogenous ligand, heme, that inhibits Bach1 binding to ARE, thus allowing Nrf2-mediated gene expression including that of heme-oxygenase-1 (HMOX1), a well described target of Bach1 repression. In this report, normal human lung fibroblasts were used to screen a collection of synthetic small molecules for their ability to induce HMOX1. A class of HMOX1-inducing compounds, represented by HPP-4382, was discovered. These compounds are not reactive electrophiles, are not suppressed by N-acetyl cysteine, and do not perturb either ROS or cellular glutathione. Using RNAi, we further demonstrate that HPP-4382 induces HMOX1 in an Nrf2-dependent manner. Chromatin immunoprecipitation verified that HPP-4382 treatment of NHLF cells reciprocally coordinated a decrease in binding of Bach1 and an increase of Nrf2 binding to the HMOX1 E2 enhancer. Finally we show that HPP-4382 can inhibit Bach1 activity in a reporter assay that measures transcription driven by the human HMOX1 E2 enhancer. Our results suggest that HPP-4382 is a novel activator of the antioxidant response through the modulation of Bach1 binding to the ARE binding site of target genes

American Society of Clinical Oncology Strategic Plan for Increasing Racial and Ethnic Diversity in the Oncology Workforce

In December 2016, the American Society of Clinical Oncology (ASCO) Board of Directors approved the ASCO Strategic Plan to Increase Racial and Ethnic Diversity in the Oncology Workforce. Developed through a multistakeholder effort led by the ASCO Health Disparities Committee, the purpose of the plan is to guide the formal efforts of ASCO in this area over the next three years (2017 to 2020). There are three primary goals: (1) to establish a longitudinal pathway for increasing workforce diversity, (2) to enhance ASCO leadership diversity, and (3) to integrate a focus on diversity across ASCO programs and policies. Improving quality cancer care in the United States requires the recruitment of oncology professionals from diverse backgrounds. The ASCO Strategic Plan to Increase Racial and Ethnic Diversity in the Oncology Workforce is designed to enhance existing programs and create new opportunities that will move us closer to the vision of achieving an oncology workforce that reflects the demographics of the US population it serves. (C) 2017 by American Society of Clinical Oncology6 month embargo; Published Online: 1 May 2017This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

HPP-4382 increases cellular glutathione levels: NHLF cells grown in 96-well Optilux plates were treated with compounds for 4 hours (BSO, 200 µM; Sulphorafane, 10 µM; CDDO-Me, 0.1 µM; HPP-1014, 10 µM; CoPP, 10 µM; HPP-4382 3 µM) and glutathione levels were determined using the GSH/GSSG-Glo Assay Kit (Promega).

<p>Positive values show pairs of means that are significantly different. All samples in duplicate, error bars represent standard deviation compared to DMSO. *, <i>p</i><0.05; **, <i>p</i><0.01, ***; <i>p</i><0.001.</p