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Multiple studies indicate that post-traumatic stress disorder (PTSD) is a risk factor for cardiovascular disease (CVD), however the mechanisms behind this correlation is unknown. We hypothesize that PTSD stimulates recruitment of monocyte-derived macrophages to the heart, resulting in increased cardiac fibrosis and resetting cardiac homeostasis. To induce experimental PTSD, male C57BL/6 mice were given 5 different foot-shocks (IFS; 1.0 mA, 1 sec duration) in 6 min. Before each shock, a tone was played to act as the PTSD-associated trigger. Control mice were also placed in the IFS chambers for 6 min but did not receive foot shocks. Behavioral testing was performed to characterize mice into non-responders (NR; IFS mice that do not demonstrate PTSD-like behavioral characteristics) and PTSD-like mice. Terminal timepoints selected were 4-weeks (4.6±0.7 months old) and 13-weeks (8.2±0.0 months old) post-IFS. Doppler echocardiography was collected at the 4-week time point. Histological and immunoblot assessments were collected at 13-weeks post-IFS to determine chronic alterations in cardiac homeostasis. Doppler measurements revealed that 4-weeks post-IFS, PTSD-like mice had decreased aortic ejection time (p This work was supported by the National Institutes of Health T32GM123055; the American Heart Association Innovator Project IPA35260039; the Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development Award IK2BX003922; and South Carolina Translational Research Center UL1TR001450 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Objective: Post-traumatic stress disorder (PTSD) in patients is associated with hypertension, increased heart rate, and elevated plasma proinflammatory cytokines, which also are risk factors for the development of cardiovascular conditions, such as thoracic aortic aneurysm (TAA). Although the association between stress and aortic pathology has been suggested, the exact mechanism linking the two is unknown. Our hypothesis is that PTSD-induced changes in mechanical and inflammatory signaling alter thoracic aortic wall homeostasis, which can predispose to aortic disease. Methods: Adult male and female C57BL/6 mice (n=7) underwent PTSD induction consisting of inescapable foot shock (five x 1 sec, 1 mA foot shocks over 6 min paired with a 20 sec 80 db tone (conditioned stimulus)) followed by single prolonged stress events. Mice were subjected to behavioral testing at 4-week intervals over a 16-week paradigm to determine their PTSD-like phenotype. The behavioral tests were chosen to assess for each of the human criteria of PTSD based on the DSM-5. A composite t-score was generated for each mouse derived from their mean individual z-score for each parameter, of each behavioral test. Mice with a composite t-score above 1.96 were considered to have a PTSD-like phenotype. Blood pressure was measured (CODA, tail-cuff) at baseline and at 4-week intervals. At terminal study, thoracic aortic diameter was measured by digital microscopy. Plasma was collected to measure circulating cytokines and aortic tissue was harvested for biochemistry and histology. Aortic structure was examined for changes in elastic lamellae, collagen deposition, and cellular content. Control mice (n=8) underwent the same procedures except for PTSD induction. Results: Our protocol generated a PTSD-like phenotype in 71% (5 of 7) of the mice. PTSD mice had significantly higher systolic blood pressures following a conditioned stimulus (PTSD (n=5), 153 ± 8mmHg; control (n=8), 129 ± 7mmHg, p NIH-NCATS TL1 TR00145-08 & UL1TR001450-08 (HH) and VA Merit Award I01-BX000904-08A1 (JAJ) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

In light of the large swings in housing prices in the United States in recent years, there has been considerable interest in trying to understand the various factors which led to the boom and bust of the housing market. In this paper, we explore the impact of the legal environment from provisions for mortgage default across U.S. states. To do so, we develop a rigorous framework with microeconomic foundations for financial intermediaries. To be specific, we introduce a housing market and a residential mortgage market in the Diamond and Dybvig framework which emphasizes the role of depository institutions to help depositors manage idiosyncratic liquidity risk. Notably, we think of non-recourse provisions as a legal arrangement to protect risk-averse homeowners from the loss of housing value. While housing demand should be higher in markets where mortgage borrowers have full insurance, lenders also adjust the amount of mortgage credit provided to protect their risk-averse depositors. Thus, a priori, there is not an obvious connection between mortgage recourse provisions and housing prices. To draw further insights into the issue, we proceed to look at empirical evidence on housing prices at the MSA-level using the Case-Shiller Home Price Index. Once one controls for regional level unobservables, the evidence suggests that the demand side factors dominate in which prices are higher in non-recourse states, following the prediction from the model that the demand for mortgages would be higher. We next move to obtain more concrete predictions from our theoretical framework with calibration exercises to study the effects of mortgage recourse. Upon calibrating the model to match some stylized evidence on housing market conditions, the theoretical predictions are consistent with the regression analysis. In this manner, our work sheds numerous insights into the implications of the legal landscape regarding mortgage default for housing market activity.