Mental Health Care Transitions from Incarceration

The scope of the problem of mental health and incarceration Case & Consideration 1: Severe Mental Illness ○ Brief history of de institutionalization and re institutionalization ○ Philadelphia’s jails at a glance Case & Consideration 2: Violence and trauma Consideration & Consideration 3: Addiction and substance use Models of transitions of care for reentry Community teams and resources Next steps for a Family Medicine physicia

Medical Stereotypes: Assessing the Use of Race as a Risk Factor

Discussion Objectives: Introduction to issues of race as a risk factor (VBAC Calculator) Race is a social construct, not genetic Unclear causality of observed disparities Possible medical consequences for patients Patient and community trust/mistrust Evaluating the VBAC Calculator Theory/Research into Causes of Health Disparities Ecosocial Theory Racism as opposed to race Evaluating race use in eGFR algorithms Evidence Causal mechanism Effect on health equity/patients Next step

C. Stratton Hill, Jr., MD, Oral History Interview, February 20, 2012

Major Topics Covered: Developing the Ambulatory Care Clinichttps://openworks.mdanderson.org/mchv_interviewsessions/1209/thumbnail.jp

C. Stratton Hill, Jr., MD, Oral History Interview, February 17, 2012

Major Topics Covered: MD Anderson history and culture: research innovation Pain management: development of field; first book on; cultural and social factors influencing use of opioidshttps://openworks.mdanderson.org/mchv_interviewsessions/1208/thumbnail.jp

C. Stratton Hill, Jr., MD, Oral History Interview, February 14, 2012

Major Topics Covered: Personal and educational background; faith Research: thyroid cancer; pain management and policyhttps://openworks.mdanderson.org/mchv_interviewsessions/1207/thumbnail.jp

C. Stratton Hill, Jr., MD, Oral History Interview, February 28, 2012

Major Topics Covered: Hospice and MD Anderson The Texas Cancer Council; Texas Cancer Pain Initiativehttps://openworks.mdanderson.org/mchv_interviewsessions/1210/thumbnail.jp

Team-based Outreach to Improve Colorectal Cancer Screening Rates in an Urban Family Medicine Practice

Aims for Improvement Aim to increase CRCS rates for our resident team patients by 5% by May, 2021 Target Population (n=99): Age 50-74, due for CRCS, office visit within last 2 years, team resident listed as PCP, active on MyChart, and speak Englis

Improving Blood Pressure Control Through Blood Pressure Measurement in an Ambulatory Urban Family Medicine Clinic

Aim Statement: To increase the percentage of patients over the age of 18 with BP controlled to a goal of \u3c140/90 from a baseline of 58% to 68% by April 2020

A Role of Myocardin Related Transcription Factor-A (MRTF-A) in Scleroderma Related Fibrosis.

In scleroderma (systemic sclerosis, SSc), persistent activation of myofibroblast leads to severe skin and organ fibrosis resistant to therapy. Increased mechanical stiffness in the involved fibrotic tissues is a hallmark clinical feature and a cause of disabling symptoms. Myocardin Related Transcription Factor-A (MRTF-A) is a transcriptional co-activator that is sequestered in the cytoplasm and translocates to the nucleus under mechanical stress or growth factor stimulation. Our objective was to determine if MRTF-A is activated in the disease microenvironment to produce more extracellular matrix in progressive SSc. Immunohistochemistry studies demonstrate that nuclear translocation of MRTF-A in scleroderma tissues occurs in keratinocytes, endothelial cells, infiltrating inflammatory cells, and dermal fibroblasts, consistent with enhanced signaling in multiple cell lineages exposed to the stiff extracellular matrix. Inhibition of MRTF-A nuclear translocation or knockdown of MRTF-A synthesis abolishes the SSc myofibroblast enhanced basal contractility and synthesis of type I collagen and inhibits the matricellular profibrotic protein, connective tissue growth factor (CCN2/CTGF). In MRTF-A null mice, basal skin and lung stiffness was abnormally reduced and associated with altered fibrillar collagen. MRTF-A has a role in SSc fibrosis acting as a central regulator linking mechanical cues to adverse remodeling of the extracellular matrix

Inhibition of Overactive Transforming Growth Factor–β Signaling by Prostacyclin Analogs in Pulmonary Arterial Hypertension

YesHeterozygous loss of function mutations in the type II bone morphogenetic protein receptor (BMPR-II), a member of the transforming growth factor (TGF-β) receptor family, underlie the majority of familial cases of pulmonary arterial hypertension (PAH). The TGF-β1 pathway is activated in PAH and inhibitors of TGF-β1 signaling prevent the development and progression of PAH in experimental models. However, the effect of currently utilized therapies on the TGF-β pathway is not known. Prostacyclin analogues remain the first line of treatment for clinical PAH. We hypothesized that these agents effectively decrease the activity of the TGF-β1 pathway. Beraprost sodium (BPS), a prostacyclin analogue selectively inhibits proliferation in a dose-dependent manner in mouse primary pulmonary arterial smooth muscle cells (PASMCs) harbouring a pathogenic BMPR2 nonsense mutation in both the presence and absence of TGF-β1 stimulation. This study demonstrates that this agent inhibits TGF-β1–induced SMAD-dependent and -independent signaling via a PKA dependent pathway by reducing the phosphorylation of SMADs 2 and 3 and p38MAPK proteins. Finally, in a monocrotaline (MCT)-induced rat model of PAH, which is associated with increased TGF-β signaling, this study confirms that treprostinil (TPS), a stable prostacyclin analogue, inhibits the TGF-β pathway by reducing SMAD3 phosphorylation. Taken together, these data suggest that prostacyclin analogues inhibit dysregulated TGF-β signaling in vitro and in vivo and reduce BMPR-II-mediated proliferation defects in mutant mice PASMCs.The authors acknowledge financial support from the British Heart Foundation, United Kingdom (Programme Grant 1-2004-357 to R.C.T. and N.W.M.), a Heptagon Life Science Proof of Concept Fund (grants KCL24 and KCL25 to M.T.N. and R.C.T., respectively), and the Great Britain Sasakawa Foundation (grant B70 to M.T.N.