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BackgroundStroke incidence among young adults of working age (under 65 years of age) has significantly increased in the past decade, with major individual, social, and economic implications. There is a paucity of research exploring the needs of this patient population. This study assessed: (1) young adult stroke patients' physical, psychological, and occupational functioning and health-related quality of life (HRQoL); and (2) post-stroke care preferences using patient-reported outcome measures (PROMs), with attention to gender differences.MethodsA cross-sectional pilot study was conducted. Sociodemographic and clinical characteristics were collected through chart review and data on occupational function, physical, psychological, and social wellbeing >90 days post-stroke through a self-reported survey. Descriptive statistics, gender-based, and regression analyses were conducted.ResultsThe sample included 85 participants. Participants reported impairments in both, occupational functioning, with 58.7% not returned to work (RTW), and HRQoL, specifically with social activities (37%), anxiety (34%), and cognitive function (34%). Women had significantly (p < 0.05) worse physical symptoms (sleep disturbance and fatigue), emotional health (depression, stigma, emotional dyscontrol) scores, and sense of self-identify post-stroke. Over 70% of participants preferred in-person post-stroke care led by health care providers and felt they would have benefited from receiving information on physical health (71.4%), emotional and psychological health (56.0%), RTW (38.1%), and self-identity (26.2%) post-stroke. Women preferred cognitive behavioral therapy (p = 0.018) and mindfulness-based stress reduction therapy (p = 0.016), while men preferred pharmacotherapy (p = 0.02) for psychological symptoms.ConclusionThis is the first study to report impaired HRQoL, psychological and occupational functioning using PROMs, with significant gender differences and preferences for post-stroke care delivery among young adult stroke patients at >90 days after stroke. The findings highlight the importance of needs, gender, and age-specific post-stroke education and interventions.

Background: The influence of prenatal exposure to per- and poly- fluoroalkyl substances (PFAS) on birth size and offspring adiposity is unclear, especially for the newer, shorter-chained replacement PFAS. Methods: In the GUSTO multi-ethnic Singaporean mother-offspring cohort, 12 PFAS were measured in 783 cord plasma samples using ultra-performance-liquid chromatography-tandem-mass-spectrometer (UPLC-MS/MS). Outcomes included offspring anthropometry, other indicators of body composition/metabolic health, and MRI-derived abdominal adiposity (subset) at birth and 6 years of age. PFAS were modeled individually, in categories of long-chain and short-chain PFAS, and as scores of three principal components (PC) derived using PC analysis (PC1, PC2, and PC3 reflect predominant exposure patterns to “very-long-PFAS”, “long-PFAS”, and “short-PFAS”, respectively). Associations with outcomes were assessed using multivariable linear regressions, adjusted for important covariates such as maternal sociodemographic and lifestyle factors. Results: Overall, cord PFAS levels showed either no or positive associations (mostly for long-chain PFAS) with birth weight, length and head circumference. In general, PFAS were associated with higher neonatal abdominal adiposity, driven by shorter-chain PFAS. Perfluoroheptanoic acid (PFHpA) was associated with higher volumes of superficial subcutaneous adipose tissue (sSAT) (3.75 [1.13, 6.37] mL per SD increase in PFAS) and internal adipose tissue (IAT) (1.39 [0.41, 2.38] mL). Higher levels of perfluorobutanesulfonic acid (PFBS), short-chain PFAS, and PC3 were associated with higher IAT volume (β range 1.22–1.41 mL/SD, all P

When postmenopausal women are under stress conditions, this exacerbates mood disorders and issues with neuroimmune systems. The porcine placenta is known to relieve menopausal depression in clinical trials, but its underlying mechanisms for depression and anti-inflammatory functions remain poorly defined. The present study was designed to examine the anti-inflammatory effects of enzymatic porcine placenta hydrolysate (EPPH) on LPS-induced levels of nitric oxide (NO), prostaglandin E2 (PGE2), corticosterone (CORT), and pro-inflammatory cytokine interleukin-1 beta (IL-1β) in RAW 264.7 macrophage cells. In addition, the neurite outgrowth of PC12 cells was evaluated to examine the effects of EPPH on neurite growth. To mimic the symptoms of women with menopause-related depression, a stressed ovariectomized (OVX) female mouse model was used to evaluate the antidepressant effects of EPPH. The female mice were randomly divided into five groups: (1) the sham-operated (Sham) group, (2) the OVX + repeated stress + saline-treated (OVX + ST) group, (3) the OVX + repeated stress + estradiol (0.2 mg/kg)-treated (positive control) group, (4) the OVX + repeated stress + EPPH (300 mg/kg)-treated (300) group, and (5) the OVX + repeated stress + EPPH (1500 mg/kg)-treated (1500) group. Female mice were OVX and repeatedly immobilization-stressed for 2 weeks (2 h/day). A tail suspension test was conducted on the 13th day, followed by the forced swimming test on the 14th day to assess the antidepressant effects of EPPH. After the behavioral tests, the levels of CORT, PGE2, and IL-1β were evaluated. In addition, c-Fos expression in the paraventricular nucleus (PVN) was evaluated using immunohistochemistry. The concentrations of NO, PGE2, and IL-1β stimulated by LPS were significantly reduced via the addition of EPPH to RAW 264.7 cells. EPPH significantly promoted neurite outgrowth in PC12 cells compared to that of the controls. In the tail suspension test, the duration of immobility was reduced in mice treated with EPPH 1500 compared to the OVX + ST group. The EPPH 1500 group had significantly decreased levels of c-Fos-positive neurons in the PVN and reduced levels of CORT and IL-1β in the serum of the Sham group. These results suggested that the high dose of EPPH administration induced the antidepressant-like effect in the ovariectomized mice with repeated stress via downregulating the levels of CORT, IL-1β, and PGE2 in the serum through reducing the expression of c-Fos in the PVN regions.