From SRI to ESG: The Changing World of Responsible Investing

The terms socially-responsible investing (SRI), mission-related investing, impact investing and environmental, social and governance (ESG) investing -- all frequently grouped under the heading of responsible investing -- have become a familiar part of the vocabulary of institutional and retail investors. Just what these terms mean in practice, however, and how their practitioners' claims can be impartially assessed, has been less clear. Responsible investing can be broken into three main categories: Socially-responsible investing (SRI) A portfolio construction process that attempts to avoid investments in certain stocks or industries through negative screening according to defined ethical guidelines. Impact investing Investing in projects, companies, fund or organizations with the express goal of generating and measuring effecting mission-related social, environmental or economic change alongside financial returns. Environmental, social and governance (ESG) investing Integrating the three ESG factors into fundamental investment analysis to the extent that they are material to investment performance. While these terms may all be gathered under the term responsible investing, these approaches serve very different purposes. SRI and impact investing use funding and investment activities to express institutional values or advance the institution's mission. In contrast, ESG investing aims to improve investment performance, thereby making additional resources available for mission support. For a long time, SRI was by far the most widely-used of the three approaches. In recent years, however, it has been argued that, although negative screening can be a useful tool for institutions desiring to express ethical, religious or moral values through their investment portfolio, for many it may prove too restrictive. ESG analysis, on the other hand, takes a broader view, examining whether environmental, social and governance issues may be material to a company's performance, and therefore to the investment performance of a long-term portfolio. Thus, while not every institution will choose to engage in SRI or impact investing, fiduciaries of long-term institutional investors should seek to develop a well-reasoned view on their institution's approach to ES

Rheumatoid Factor as a Potentiator of Anti–Citrullinated Protein Antibody–Mediated Inflammation in Rheumatoid Arthritis

Objective. The co-occurrence of rheumatoid factor (RF) and anti–citrullinated protein antibody (ACPA) positivity in rheumatoid arthritis (RA) is well described. However, the mechanisms underlying the potential interaction between these 2 distinct autoantibodies have not been well defined. The aim of this study was to evaluate the epidemiologic and molecular interaction of ACPAs and RF and its association with both disease activity and measures of RA-associated inflammation. Methods. In a cohort of 1,488 US veterans with RA, measures of disease activity and serum levels of cytokines and multiplex ACPAs were compared between the following groups of patients: double-negative (anti–cyclic citrullinated peptide [anti-CCP]-/RF-), anti-CCP+/RF-, anti-CCP-/RF+, or double-positive (anti-CCP+/RF+). Additional studies were performed using an in vitro immune complex (IC) stimulation assay in which macrophages were incubated with ACPA ICs in the presence or absence of monoclonal IgM-RF, and tumor necrosis factor α production measured as a readout of macrophage activation. Results. Compared with the double-negative subgroup (as well as each single-positive subgroup), the double-positive subgroup exhibited higher disease activity as well as higher levels of C-reactive protein and inflammatory cytokines (all P \u3c 0.001). In vitro stimulation of macrophages by ACPA ICs increased cytokine production, and the addition of monoclonal IgM-RF significantly increased macrophage tumor necrosis factor α production (P = 0.003 versus ACPA ICs alone). Conclusion. The combined presence of ACPAs and IgM-RF mediates increased proinflammatory cytokine production in vitro and is associated with increased systemic inflammation and disease activity in RA. Our data suggest that IgM-RF enhances the capacity of ACPA ICs to stimulate macrophage cytokine production, thereby providing a mechanistic link by which RF enhances the pathogenicity of ACPA ICs in RA

Psychotropic Medication Use by Children with Autism Served in Publicly Funded Mental Health Settings

ObjectiveThe aim of this study was to characterize patterns of and factors associated with psychotropic medication use in children with autism spectrum disorder (ASD) receiving publicly funded mental health services.MethodData were extracted from 202 children with ASD participating in a cluster randomized trial of An Individualized Mental Health Intervention for ASD conducted in 29 publicly funded mental health programs. Children with ASD were aged 5 to 13 years (M = 9.1 years, SD = 2.4), and were 84.2% male and 59.9% Latinx. Child ASD and cognitive functioning were determined by standardized assessment. Caregivers reported child psychotropic medication use, behavior problems, ASD symptom severity, mental health symptoms, family demographics, and caregiver strain at the baseline.ResultsNearly half (49.5%) of participants used psychotropic medication(s) within the past 6 months, with stimulants being most commonly reported. Child co-occurring attention-deficit/hyperactivity disorder (ADHD) (B = 1.55, p < 0.01; 95% confidence interval [CI]: 0.53-2.57), lower cognitive functioning (B = -0.03, p = 0.02; 95% CI: -0.05 to <0.00), and non-Hispanic White ethnicity (vs Hispanic/Latinx; B = 1.02, p = 02; 95% CI: -1.89 to -0.14) were associated with a greater likelihood of using any type of medication. Factors associated with medication use varied by class: stimulants-ADHD, lower ASD symptom severity, and more intensive behavior problems; SSRIs-higher ASD symptom severity; alpha-2 agonists-ADHD, higher ASD symptom severity, lower cognitive functioning, and higher caregiver strain; and antipsychotics-none.ConclusionThe findings highlight factors associated with psychotropic medication use for a clinically complex population, which may inform community care improvement efforts

Training Community Therapists in AIM HI: Individual Family and Neighborhood Factors and Child/Caregiver Outcomes.

OBJECTIVE: Publicly funded mental health services play an important role in caring for children with mental health needs, including children with autism spectrum disorder (ASD). This study assessed the associations between individual family- and neighborhood-level sociodemographic factors and baseline family functioning and long-term outcomes when community therapists were trained to deliver An Individualized Mental Health Intervention for ASD (AIM HI). METHOD: Participants included 144 children with ASD (ages 5 to 13 years; 58.3% Latinx) and their caregivers whose therapists received AIM HI training within a cluster-randomized effectiveness-implementation trial in publicly funded mental health services. Sociodemographic strain (e.g., low income, less education, single-parent status, minoritized status) was coded at the individual family and neighborhood level, and caregivers rated caregiver strain at baseline. Child interfering behaviors and caregiver sense of competence were assessed at baseline and 6-, 12- and 18-months after baseline. RESULTS: Higher caregiver strain was associated with higher intensity of child behaviors (B = 5.17, p < .001) and lower caregiver sense of competence (B = -6.59, p < 001) at baseline. Child and caregiver outcomes improved over time. Higher caregiver strain (B = 1.50, p < .001) and lower family sociodemographic strain (B = -0.58, p < .01) were associated with less improvements in child behaviors. Lower caregiver strain (B = -2.08, p < .001) and lower neighborhood sociodemographic strain (B = -0.51, p < .01) were associated with greater improvements in caregiver sense of competence. CONCLUSIONS: Findings corroborate the importance of considering both family and neighborhood context in the community delivery of child-focused EBIs. TRIAL REGISTRATION: Clinical Trials NCT02416323

MICAL2 is a novel human cancer gene controlling mesenchymal to epithelial transition involved in cancer growth and invasion

The MICAL (Molecules Interacting with CasL) proteins catalyze actin oxidation-reduction reactions destabilizing F-actin in cytoskeletal dynamics. Here we show for the first time that MICAL2 mRNA is significantly over-expressed in aggressive, poorly differentiated/undifferentiated, primary human epithelial cancers (gastric and renal). Immunohistochemistry showed MICAL2-positive cells on the cancer invasive front and in metastasizing cancer cells inside emboli, but not at sites of metastasis, suggesting MICAL2 expression was 'on' in a subpopulation of primary cancer cells seemingly detaching from the tissue of origin, enter emboli and travel to distant sites, and was turned 'off' upon homing at metastatic sites. In vitro, MICAL2 knock-down resulted in mesenchymal to epithelial transition, reduction of viability, and loss of motility and invasion properties of human cancer cells. Moreover, expression of MICAL2 cDNA in MICAL2-depleted cells induced epithelial to mesenchymal transition. Altogether our data indicate that MICAL2 over-expression is associated with cancer progression and metastatic disease. MICAL2 might be an important regulator of epithelial to mesenchymal transition and therefore a promising target for anti-metastatic therapy