Risultati per: Incontinenza urinaria da stress o mista

Concluso il progetto pilota messo a punto da Maior-Ama in collaborazione con l’Asl di Teramo per ridurre stress, ansia e burnout

Stroke, Ahead of Print. Background:Posttraumatic stress disorder (PTSD) can be triggered by life-threatening medical emergencies, such as stroke. Data suggest that up to 25% of stroke survivors will develop PTSD symptomatology, but little is known about predisposing factors. We sought to examine whether neuroimaging measures and coping styles are related to PTSD symptoms after stroke.Methods:Participants were survivors of first-ever, mild-moderate ischemic stroke, or transient ischemic attack from the TABASCO study (Tel Aviv Brain Acute Stroke Cohort). All participants underwent a 3T magnetic resonance imaging at baseline and were examined 6, 12, and 24 months thereafter, using neurological, neuropsychological, and functional evaluations. At baseline, coping styles were evaluated by a self-reported questionnaire. PTSD symptoms were assessed using the PTSD checklist. Data were available for 436 patients.Results:Forty-eight participants (11%) developed probable PTSD (PTSD checklist ≥44) during the first year after the stroke/transient ischemic attack. Stroke was more likely to cause PTSD than transient ischemic attack. Stroke severity, larger white matter lesion volume, and worse hippocampal connectivity were associated with PTSD severity, while infarct volume or location was not. In a multivariate analysis, high-anxious and defensive coping styles were associated with a 6.66-fold higher risk of developing poststroke PTSD ([95% CI, 2.08–21.34];P

Stroke, Volume 53, Issue Suppl_1, Page AWP252-AWP252, February 1, 2022. Introduction:Tamoxifen (TAM), a selective estrogen receptor modifier, is a first-line treatment option for hormone receptor positive breast cancer. TAM inhibits the downstream estrogen receptor signaling in tumor cells. Stroke risk is increased in women with low estrogen levels, such as early-onset menopause, and doubles in women after the age of 55, which corresponds with the average age of menopause. Women with breast cancer who were treated with tamoxifen had an increased risk for ischemic stroke (82%). Since stroke severity is associated with increased blood brain barrier (BBB) damage, we investigated the effects of tamoxifen on activation and mitochondrial stress in astrocytes, which is a cellular component of the BBB.Methods:Cultured female human astrocytes were treated with tamoxifen (1uM), 17ß-estradiol (10nM), or vehicle (DMSO) for 24 hours. Cells were separated into two groups: normoxic (21% O2, 25mM glucose) or oxygen and glucose deprivation (OGD) conditions 6 hours before analysis. ROS production was measured using the Cellular ROS Assay Kit (Red) and aquaporin-4 levels were visualized via immunocytochemistry. Mitochondrial function was assessed by using a Seahorse XFe96 Analyzer.Results:Tamoxifen treatment increased Aquaporin-4 protein levels (p

Stroke, Volume 53, Issue Suppl_1, Page AWP219-AWP219, February 1, 2022. Background:Stroke is a sudden-onset, unexpected life event over which individuals have little control. These features can make the experience of having a stroke extremely stressful, which may potentiate its debilitating effects. Yet the role of lifetime stress/trauma exposure (LSE) and post-stroke acute stress (AS) have received limited attention in research seeking to identify factors influencing stroke-related disability.Hypothesis:Higher lifetime trauma and AS symptoms are associated with poorer post-stroke modified Rankin (mRS) and Fugl-Meyer scores.Method:Multi-site national study of patients admitted for a new stroke. Interviews were conducted at 2-10 days (N=763) & 3 months (N=513) post-stroke. Assessments included admission Acute Stress Disorder Interview, day-90 mRS, day-90 upper extremity motor Fugl-Meyer scale (affected side), and LSE. Structural Equation Modeling examined relationships among LSE, AS, and outcomes, controlling for admission NIHSS score, IV TPA treatment, and demographics.Results:After controlling for key covariates, AS immediately post-stroke and LSE were both associated with poorer day-90 mRS scores (p

Stroke, Volume 53, Issue Suppl_1, Page ATP1-ATP1, February 1, 2022. Background:Excess reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) promotes apoptotic cell death following ischemic/reperfusion injury. Effect of chlorpromazine and promethazine (C+P) on brain activity was reported to induce neuroprotection. The current study was designed to evaluate the inhibitory function of C+P on oxidative injury after stroke.Methods:Adult male Sprague-Dawley rats were subjected to 2 h middle cerebral artery occlusion (MCAO) followed by 6 or 24 h of reperfusion. At the onset of reperfusion, rats received C+P, or apocynin (NOX inhibitor), or rottlerin [protein kinase C (PKC) δ inhibitor]. Brain damage was evaluated using infarct volumes and neurological deficits as well as apoptotic cell death (TUNEL). The enzymatic activity of NOX and ROS production as well as protein expressions of NOX subunits (gp91phox, p67phox, p47phox, and p22phox), phosphorylation of PKC δ (p-PKC δ)/PKC δ and manganese superoxide dismutase (MnSOD) was examined. Neural SHSY5Y cells were used under 2 h of oxygen-glucose deprivation (OGD) followed by reoxygenation for 6 and 24 h with or without C+P treatment. ROS and protein levels of NOX subunits, p-PKC δ/PKC δ and MnSOD were detected. Moreover, measurement of PKC δ membrane translocation and detection of the interaction of p47phoxand PKC δ through co-immunoprecipitation were performed.Results:C+P reduced cerebral infarct volumes, neurological deficits, and apoptotic cell death in the ischemic rats, as well observed in the presence of NOX and PKC δ inhibitors. ROS production, NOX activity, expression of NOX subunits, p-PKC δ/PKC δ and MnSOD were significantly reduced by C+P. In ischemic rats administered with NOX and PKC δ inhibitors, ROS, activity of NOX and the NOX subunits protein levels were all decreased. In the OGD/R model, C+P decreased ROS and protein levels of NOX subunits, p-PKC δ/PKC δ and MnSOD. Furthermore, C+P reduced the PKC δ membrane translocation and the interaction of p47phoxand PKC δ.Conclusion:C+P treatments confers neuroprotection in severe stroke by suppressing oxidative stress and ROS production. PKC δ/NOX/MnSOD may be the vital regulators and the potential targets for an efficacious therapy following ischemic stroke.

Stroke, Volume 53, Issue Suppl_1, Page AWP217-AWP217, February 1, 2022. Introduction:Ischemic stroke is the leading cause of death and disability worldwide. It was recently reported that mental stress could aggravate stroke damage. However, the causal relationship between mental stress and stroke outcomes remained unclear. In current study, we determined whether mitochondria dysfunction was induced by mental stress and thus enhanced brain damage after ischemic stroke. The translocator protein (TSPO) is a transmembrane protein located on the outer mitochondria membrane (OMM) and induced mitochondrial dysfunction. This study focused on the key role of TSPO in stress aggravated ischemia/reperfusion injury.Methods:Six-week-old male C57BL/6J mice were divided into four groups: control, chronic restraint stress (CRS), TSPO antagonist (PK11195, 3mg/kg, i.p.) and TSPO antagonist+CRS. Mice in CRS were placed in ventilated 50mL tubes 6 hours/day for 28 days. On the day 29th, behavioral tests were conducted to measure the depressive-like levels. Mice then were subjected to middle cerebral artery occlusion (MCAO). At 6/24 hours after MCAO, TTC staining and modified scoring systems were applied to analyze infarct volume and neurological deficits, and the expression of TSPO was detected using immunofluorescence. Apoptotic cell death and apoptotic proteins (Bcl-2, Bax and caspase-3/9) were measured by TUNEL and Western blot. Effects of TSPO on mitochondrial membrane potential (MMP) and mito-ROS were measured by JC-1 staining and live cell imaging dyes (mitoSOX and DCFDA)in vitro.Results:As depressive model, CRS aggravated infarct volume and neurological deficits after MCAO, with increased levels of apoptosis (cell death and protein expressions), in association with increased TSPO levels. TSPO antagonist could decrease stress-aggravated stroke injury and apoptotic cell death, indicating TSPO was involved in stress related stroke outcomes.In vitro, MMP was increased and mito-ROS was decreased after TSPO siRNA transfection, suggesting TSPO may induce mitochondria deficits through producing more mito-ROS.Conclusions:Mental stress by CRS exacerbated ischemic injury after stroke. Importantly, the results showed that TSPO may play a key role in inducing mitochondrial dysfunction in stress-aggravated stroke damage.

Stroke, Volume 53, Issue Suppl_1, Page ATMP116-ATMP116, February 1, 2022. Background:The endoplasmic reticulum (ER) is responsible for cellular protein synthesis and folding. Cellular stimuli that perturb ER homeostasis create an imbalance between the protein-folding load and capacity of ER, causing unfolded or misfolded proteins to accumulate in the ER lumen, known as ER stress. Recent studies suggested that ER stress plays significant roles in the pathogenesis of inflammatory vascular diseases. Since inflammation is emerging as a vital component of the pathophysiology of intracranial aneurysms, we hypothesized that ER stress promotes the development of aneurysm rupture by inducing sustained vascular wall inflammation. We tested this hypothesis utilizing pharmacological approaches in mice.Methods:We used 10-week-old male C57BL/6J mice and induced intracranial aneurysms by combining an elastase injection and hypertension. We tested the effects of an ER stress activator (Tunicamycin) and inhibitor (4-phenylbutyric acid, 4-PBA) on the development of aneurysmal rupture. In addition, we assessed the roles of ER stress induced via deactivation of epidermal growth factor receptor (EGFR) by Erlotinib on aneurysm rupture.Results:The pharmacological inhibition of ER stress significantly decreased the rupture rate (P

Stroke, Volume 53, Issue Suppl_1, Page ATP17-ATP17, February 1, 2022. Background:Major depressive disorder (MDD) is one of the fastest-growing disability disorders in the US and worldwide. Extensive clinical data suggest that MDD is associated with an increased risk of hypertension, coronary heart disease, and other cardiovascular diseases. A close relation between cardiovascular and cerebrovascular diseases and clinical evidence presents a potential link between depression and stroke. MDD when combined with other comorbidities, makes the prognosis worse. Dysregulation of the sympathetic nervous system, impaired hypothalamic-pituitary-adrenal axis, and increased inflammatory response are plausible mechanisms that have been linked to depression-induced cardio- and cerebrovascular complications. In the current study, we investigated cardiac structural and functional alterations in a mouse model of chronic mild stress (CMS) exhibiting depression-like behavior.Methods and Results:The mice were divided into control (CT) and CMS groups. The CMS mice were subjected to various mild, unpredictable stressors for 7 weeks. Depression-like traits were confirmed in the CMS group by analyses of behavioral changes using open field and forced swim tests and a decrease in hippocampal brain-derived neurotrophic factor (BDNF) protein level. To evaluate depression-associated neuronal damage and neuronal plasticity, Fluoro-Jade C staining and expression of microtubule-associated protein 2 were examined. However, we did not observe neuronal damage in the CMS mice as compared to the CT mice. We also observed a decrease in cardiac BDNF expression and upregulation of IL-6 in the CMS mice compared to the CT group. Echocardiographic and histological analyses showed an increase in ventricular wall thickness with increased cardiomyocyte size in the CMS group. However, we did not find changes in fetal gene expression or fibrosis markers. Investigation of underlying mechanisms showed a significant upregulation in ERK1/2 signaling in the left ventricles of the CMS mice as compared to the control group, with no changes in phospho-p38, NFATc3, or JNK levels.Conclusion:In conclusion, these data suggest that ERK1/2 signaling might have an important role in cardiac hypertrophic response during the CMS-induced depression in mice.

Stroke, Ahead of Print. Background and Purpose:Chronic hypoxia-ischemia is a putative mechanism underlying the development of white matter hyperintensities (WMH) and microstructural disruption in cerebral small vessel disease. WMH fall primarily within deep white matter (WM) watershed regions. We hypothesized that elevated oxygen extraction fraction (OEF), a signature of hypoxia-ischemia, would be detected in the watershed where WMH density is highest. We further hypothesized that OEF would be elevated in regions immediately surrounding WMH, at the leading edge of growth.Methods:In this cross-sectional study conducted from 2016 to 2019 at an academic medical center in St Louis, MO, participants (age >50) with a range of cerebrovascular risk factors underwent brain magnetic resonance imaging using pseudocontinuous arterial spin labeling, asymmetric spin echo, fluid-attenuated inversion recovery and diffusion tensor imaging to measure cerebral blood flow (CBF), OEF, WMH, and WM integrity, respectively. We defined the physiologic watershed as a region where CBF was below the 10th percentile of mean WM CBF in a young healthy cohort. We conducted linear regression to evaluate the relationship between CBF and OEF with structural and microstructural WM injury defined by fluid-attenuated inversion recovery WMH and diffusion tensor imaging, respectively. We conducted ANOVA to determine if OEF was increased in proximity to WMH lesions.Results:In a cohort of 42 participants (age 50–80), the physiologic watershed region spatially overlapped with regions of highest WMH lesion density. As CBF decreased and OEF increased, WMH density increased. Elevated watershed OEF was associated with greater WMH burden and microstructural disruption, after adjusting for vascular risk factors. In contrast, WM and watershed CBF were not associated with WMH burden or microstructural disruption. Moreover, OEF progressively increased while CBF decreased, in concentric contours approaching WMH lesions.Conclusions:Chronic hypoxia-ischemia in the watershed region may contribute to cerebral small vessel disease pathogenesis and development of WMH. Watershed OEF may hold promise as an imaging biomarker to identify individuals at risk for cerebral small vessel disease progression.

L’impatto psicologico della pandemia sugli operatori sanitari è stato considerevole. Al prolungarsi della pandemia il rischio è che lo stress cronicizzi, determinando sindromi da burn-out. Azioni di tutela sono essenziali per prevenire queste problematiche.