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Using data from the 2001, 2004, and 2008 panels of the Survey of Income and Program Participation (SIPP), this research examines the characteristics of households that invested in rental real estate during the 2000s. Given the tumultuous real estate market during that decade, rental real estate investment was investigated during the early part of the housing market boom (2001), the height of the boom (2004), and after the market began to decline (2008). Results reveal relative stability with slight investment increases in rental real estate (4.57% in 2001 to 5.00% in 2004 to 5.08% in 2008), and several investor demographic and financial characteristics consistently associated with the investment decision. Evidence of potential over-reliance on real estate investment by some households indicates that financial planners should work to educate clients who invest, or are seeking to invest, in real estate. Education would emphasize that overweighting portfolios with real estate could be deleterious to client's wealth goals in times of slow rental or depreciating housing markets.

What is the impact of housing adequacy on recent home modification, controlling for demographics and housing characteristics? This study examined home modifications of households with a member aged 65 or older, focusing on relationships between selected demographic and housing variables and home modification. Binary logistic regression analysis was used on a sample of 6,627 homeowners from the newly released 2019 American Housing Survey (AHS) dataset. This analysis of the 2019 AHS data is important because of its pre-COVID pandemic era perspective in terms of home modifications and older adults aging in place. Results showed that recent housing modifications were significantly affected by select demographic and housing factors. [ABSTRACT FROM AUTHOR]

Large clinical trials indicated that CETP inhibitors increase HDL levels, but had unexpected side effects, such as hyperaldosteronism and hypertension. Some CETP inhibitors appear to accumulate in adipocytes, which are a source of aldosterone (Aldo). As such, we questioned whether CETP inhibitors influence Aldo production in adipocytes and assessed the role of reactive oxygen species (ROS) and STAT3 in this process. Human adipocytes (SW872), expressing CETP, were studied and compared to mouse adipocytes (3T3-L1), lacking CETP. Cells were treated with torcetrapib (TOR), dalcetrapib (DAL), or anacetrapib (ANA). To evaluate the role of ROS, cells were pre-treated with N-acetylcystein (NAC-ROS scavenger), ML171 and GKT136901 (Nox1/4 inhibitor, respectively), and Rotenone (Rot, mitochondrial ROS inhibitor). ROS were measured by lucigenin and amplex red. Aldo production, measured by ELISA, was induced by TOR (668pg/mL), DAL (348pg/mL) and ANA (434pg/mL) (p<0.05 vs control 196pg/mL); an effect blocked by NAC. TOR, DAL and ANA increased superoxide (2-fold) and H2O2 (1.5-fold) production, and STAT3 phosphorylation (p<0.05). TOR increased Nox1, 4 and 5 (2-fold); DAL increased Nox4 (2-fold) and, ANA increased Nox1 and 4 (3-fold). In TOR treated cells, Aldo production was inhibited by GKT (62%), ML171 (62%), Rot (45%), and S3I-201 (STAT3 inhibitor, 66%). DAL-induced Aldo production was blocked by ML171(62%) and S3I-201 (74%). In ANA treated cells, Aldo production was inhibited by GKT (94%), ML171 (83%), and Rot (66%). We also assessed effects of CETP inhibitors on chemerin production, a novel adipokine associated with hypertension. TOR, but not ANA or DAL stimulated chemerin production (331pg/mL vs control 154pg/mL p<0.05); an effect blocked by GKT (95%) and S3I-201 (100%). In mouse adipocytes, TOR, DAL, and ANA induced Aldo (453pg/mL, 375pg/mL, and 445pg/mL vs cont 253pg/mL, p<0.05) and ROS production (1.7-fold, p<0.05). In conclusion, CETP inbitors induced aldosterone production in human and mouse adipocytes through redox-related mechanisms involving STAT3, Noxs and mitochondria. These novel findings have important clinical significance and may explain, in part, the hyperaldosteronism and hypertension reported in CETP clinical trials. [ABSTRACT FROM AUTHOR]

Aldosterone (aldo) plays an important role in obesity-associated cardiovascular risk. We demonstrated that aldo is produced by adipocytes, an effect associated with increased generation of reactive oxygen species (ROS). These processes are exaggerated in obesity. The relationship between adipocyte aldosterone and ROS is unclear. We postulated that Nox4-derived ROS is important for aldo production in adipocytes and leads to a pro-inflammatory phenotype in obesity. Studies were performed in db/m (lean) and db/db (obese) mice, treated with low (20mg/kg/day) or high dose (60mg/kg/day) GKT137831 (GKT, Nox4 inhibitor, 16 weeks). Epididymal (EVAT) and perivascular (PVAT) fat were collected. Plasma and adipocyte aldo were measured by ELISA. Adipose tissue fibrosis was evaluated by picro Sirius red staining and inflammatory mediators by immunostudies. Body weight was increased in db/db mice (61.8g vs control 33.5g), with no effect of GKT. Epididymal adiposity was increased in db/db mice (0.098g vs. 0.067g, p<0.05). Plasma aldo levels in db/db (pg/mL: 518 vs. 272g) and aldo levels in culture media from db/db adipocytes were increased (pg/mL/μg RNA: 1964 vs. 388), p<0.05. All effects decreased by high dose GKT. In PVAT, CYP11B2 gene expression was increased in db/db (2.6±0.8 vs control 1.1±0.1, p<0.05), an effect blocked by Nox4 inhibition. Gene expression of adipocyte differentiation marker, AP2, was increased (3.5±1.1 vs control 1.4±0.4) while anti-inflammatory marker adiponectin was decreased (0.7±0.1 vs control 1.3±0.2, p<0.05)) in obese mice. GKT decreased AP2 levels. Adipocyte-derived TNFα was increased in db/db (4.9±1.8 vs control 1.6±0.6, p<0.05), an effect blocked by GKT. Pro-collagen I, marker of fibrosis, was increased in db/db mice (132±11 vs control 87±4, p<0.05). Sirius red staining was exaggerated in EVAT from db/db mice, and decreased by Nox4 inhibition. In conclusion, Nox4 plays a role in regulating adipocyte-derived aldosterone and promotes a pro-inflammatory and profibrotic adipose phenotype in obese db/db mice. These findings suggest that adipocyte Nox4 links hyperaldosteronism and inflammation/fibrosis in adiposity and as such may be a putative therapeutic target for obesity-associated cardiovascular damage. [ABSTRACT FROM AUTHOR]