Risultati per: Lo stress può essere causa di infarto ed ictus

Il ricordo di Filippo Anelli, presidente della Fnomceo. Tre milioni italiani rinunciano a cure a causa del Ssn che arranca

Studio, individuati 5 casi, analogie con contagi in Svizzera

Studio Usa, essere fisicamente attivi ne diminuisce l’intensità

La sperimentazione condotta con successo dal Meyer

Background
It is well known that the COVID-19 pandemic has had a devastating impact on mental health, especially among individuals with long COVID. This systematic review and meta-analysis aims to investigate the prevalence of depression, stress and suicide tendencies among individuals with long COVID, as well as to explore the factors that contribute to these conditions.

Methods and analysis
A comprehensive review of literature will be conducted in various databases of including PubMed, including Medline, Embase, PsycINFO, CINAHL and Cochrane Library. The studies to be included in this review will be published in the English language, and the time frame of included studies will be from the date of inception of COVID-19 until 30 December 2023. Two independent reviewers will identify studies for inclusion based on a screening questionnaire, and the JBI standardised critical appraisal checklist for studies reporting prevalence data will be used to assess the methodological quality. The strength of the body of evidence will be assessed using the Grading of Recommendations Assessment, Development and Evaluation approach. To analyse the data, a robust Bayesian approach will be applied using the STATA software package (V.14; STATA) and JASP software. The findings of this systematic review and meta-analysis will provide valuable insights into the prevalence of depression, stress and suicide tendencies among individuals with long COVID, as well as the factors that contribute to these conditions.

Ethics and dissemination
There is no research ethics board approval required. The dissemination plan is to publish results in a peer-reviewed academic journal.

PROSPERO registration number
CRD42022346858.

La futura mamma può portare una persona cara in sala operatoria

‘Tecniche rimborsate da Ssn. Necessaria più informazione’

Aiom e ministero della Salute insieme per campagne di informazione

Stroke, Volume 55, Issue Suppl_1, Page ATP316-ATP316, February 1, 2024. Introduction:Tamoxifen (TAM), a selective estrogen receptor modulator, is a first-line treatment to prevent recurrence of hormone receptor positive breast cancer. Stroke risk is increased in women with low estrogen and doubles in women after the age of 55 (average age of menopause). Critically, women taking TAM as breast cancer therapy had increased risk of ischemic stroke (82%). We hypothesize treatment with TAM will increase stroke severity, which is associated with increased blood brain barrier (BBB) damage and worsened neuroinflammation. We investigated effects of TAM on mitochondrial stress and cellular function in astrocytes and microglia, key cells of the BBB and neuroimmune response, respectively.Methods:Cultured female human astrocytes and HMC3 microglia were treated with TAM (1uM), 17ß-estradiol (10nM, E2), 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. Mitochondrial function was assessed using a Seahorse XFe96 Analyzer. Microglial expression of mitochondrial proteins (Complex I & III and DRP1) was analyzed with western blot, and function was assessed with flow cytometry afterin vitrophagocytosis of pHrodo red zymosan.Results:TAM reduced maximal (p =0.0174) and basal respiration (p =0.0149) under OGD conditions in microglia compared with DMSO or E2 treatment. However, in astrocytes, maximal and basal respiration were increased in OGD (p =0.0003, p =0.0002). There was no significant difference in expression of mitochondrial proteins or phagocytic function in HMC3 microglia under either normoxic or OGD conditions after TAM treatment.Conclusions:TAM treatment resulted in a cell type-specific alteration in mitochondrial stress response. Since mitochondrial stress is a hallmark of stroke pathophysiology, and microglia and astrocytes are among the earliest cells to respond to ischemia, treatment with tamoxifen might alter the cellular environment, by its divergent actions on these two cell types, leading to worsened stroke outcomes. These data support the need forin vivoinvestigation to elucidate the mechanism by which TAM is altering cellular response. Support: RFAG042189 to FS, 1F30NS131053 to MEZ

Stroke, Volume 55, Issue Suppl_1, Page AWMP1-AWMP1, February 1, 2024. Background:NBO has emerged as a promising neuroprotective strategy for ischemic stroke. Key to comprehending these effects is understanding its mechanisms. This study examines the pivotal roles of HIF-1α as an oxygen sensor, the protective emergence of stress granules (SGs) in response to various stimuli, and the inflammatory cell death process known as pyroptosis, triggered by inflammasomes. We elucidated the interplay between HIF-1α, SGs, inflammasomes in ischemia/reperfusion injury and in NBO-induced neuroprotection.Methods:A total of 132 adult male SD rats were subjected to 2 h middle cerebral artery occlusion (MCAO), followed by 2, 6, 24 or 48 h of reperfusion. At the onset of reperfusion, oxygen was inhaled for 2 h at concentration of 95% and flow rate of 2 L/min. YC-1 (HIF-1α inhibitor) was administered 2 h before MCAO. Brain damage was evaluated by infarct volumes (TTC), LDH and ROS levels (ELISA), apoptotic cell death (flow cytometry and TUNEL). Pyroptosis was evaluated by flow cytometry. mRNA and protein levels of HIF-1α and inflammasome related factors, including IL-18, IL-1β, ASC, NLRP3, TXNIP, N-GSDMD, cleaved-Caspase-1, as well as SGs proteins including DDX3X, G3BP1, TIA-1 were examined. Co-IP was used to detect the interaction between DDX3X and G3BP1, as well as DDX3X and NLRP3.Results:Infarct volumes, LDH and ROS levels, apoptotic and pyroptotic cell death, as well as HIF-1α expression were all increased after ischemia/reperfusion. All these increases were reversed by either NBO or YC-1. NBO or YC-1 further reversed the increase in expression of NLRP3 inflammasome related proteins and suppressed the interaction between DDX3X and NLRP3, thereby suppressing inflammasome activation. NBO or YC-1 stimulated the expressions of SGs proteins and facilitated the interaction between DDX3X and G3BP1, thereby promoting the formation of SGs, in association with cell protection.Conclusion:Our findings highlight the neuroprotective effects of NBO in ischemic stroke. This protection is attributed to its dual capacity to inhibit NLRP3 inflammasome activation while simultaneously promoting formation of SGs. Central to these processes, HIF-1α, as an instrumental modulator, sheds light on potential therapeutic targets for stroke intervention.

Stroke, Volume 55, Issue Suppl_1, Page AWP142-AWP142, February 1, 2024. Background:Intracranial atherosclerotic disease (ICAD) is associated with high recurrence rates of stroke despite aggressive medical management. Low wall shear stress (WSS) alters endothelial function and changes in WSS within the post-stenotic region of ICAD lesions is a potential driver of stroke recurrence.Methods:Using the SAMMPRIS imaging dataset, we identified medically managed patients with symptomatic middle cerebral artery (MCA) stenosis measured by CTA. WSS was calculated by creating a 3D volumetric mesh from CTA source imaging. Pulsatile flow profile reference standard boundary conditions were applied at pressure outlets to simulate normal hemodynamics. Arterial segments extending from the stenosis to the MCA bifurcation were captured and quantified. Contralateral arterial segments were matched by length and area. The ratio of area with low WSS (

Stroke, Volume 55, Issue Suppl_1, Page A18-A18, February 1, 2024. Background:Exposure to ambient air pollution causes neuroinflammation and white matter (WM) damage. In patients with preexisting cerebrovascular disease, pollution exposure can compound underlying pathology and may accelerate functional decline. Major mechanisms of this toxicity are microglial reactivity and oxidative stress. We therefore hypothesized that attenuation of the Toll-like receptor 4 (TLR4)-dependent microglial response would significantly decrease oxidative WM damage in a joint experimental model of pollutant exposure and chronic cerebral hypoperfusion modeled by surgical bilateral carotid artery stenosis (BCAS).Methods:Inducible microglial/macrophage-specific TLR4 deletion was achieved using a Tamoxifen-induced Cx3cr1CreER+/- mouse model. Male and female Cx3cr1CreER+/- mice treated with tamoxifen (i-mTLR4-ko) or corn oil (control) were exposed to 120 hours of filtered air (FA) or aerosolized diesel exhaust particulate (DEP), and 30 days of BCAS or sham surgery using a factorial design. The 8 experimental groups were: 1) control/FA (n=10), 2) control/DEP (n=10), 3) control/FA + BCAS (n=9), 4) control/DEP+BCAS (n=10), 5) i-mTLR4-ko/FA (n=9), 6) i-mTLR4-ko/DEP (n=8), 7) i-mTLR4-ko/FA + BCAS (n=8), and 8) i-mTLR4-ko/DEP+BCAS (n=10). Immunofluorescence was used to identify 4-HNE and 8-OHdG expression in the corpus callosum (CC).Results:While control mice showed elevations of 4-HNE in the CC after DEP (p

Stroke, Volume 55, Issue Suppl_1, Page ATMP114-ATMP114, February 1, 2024. Introduction:Iron is an essential element for vascular wall maintenance. However, iron deposition in the vascular wall may cause oxidative stress, which can attack DNA, proteins, and lipid membranes via the Fenton/Haber-Weiss reaction. Iron-induced oxidative stress triggers lipid oxidation, inflammation, endothelial cell activation and intracranial aneurysmal formation, growth, and rupture. Subarachnoid hemorrhage from intracranial aneurysm rupture results in significant morbidity and mortality. This study used a mouse model of intracranial aneurysm to evaluate the effect of dietary iron restriction on aneurysm formation and rupture.Methods:Intracranial aneurysms were induced using deoxycorticosterone acetate-salt-induced hypertension and a single injection of elastase into the cerebrospinal fluid of the basal cistern. Mice were fed an iron-restricted diet or a normal diet. Aneurysm rupture was detected by neurological symptoms, while the presence of intracranial aneurysm with subarachnoid hemorrhage was confirmed by post-mortem examination.Results:The aneurysmal rupture rate was significantly lower in iron-restricted diet mice (37%) compared with normal diet mice (76%;p< 0.05). Serum oxidative stress, iron accumulation, macrophage infiltration, and 8-hydroxy-2′-deoxyguanosine in the vascular wall were lower in iron-restricted diet mice (p< 0.01). The areas of iron positivity were similar to the areas of CD68 positivity and 8-hydroxy-2′-deoxyguanosine in both normal diet and iron-restricted diet mice aneurysms.Conclusions:Compared with a normal diet, an iron-restricted diet reduced the incidence of intracranial aneurysmal rupture in mice via inhibition of iron accumulation in the aneurysmal wall. Iron may be a potential therapeutic target to prevent intracranial aneurysm rupture. Long-term iron restriction may be required to affect aneurysm formationrupture.

Stroke, Volume 55, Issue Suppl_1, Page ATMP12-ATMP12, February 1, 2024. Background:Large-vessel vasculopathy (LVV), such as moyamoya syndrome, increases stroke risk with sickle cell disease (SCD). We hypothesized that tissue-based cerebral blood flow (CBF) and oxygen extraction fraction (OEF), as indicators of hemodynamic and metabolic stress, would differ in hemispheres with vs. without LVV.Methods:Patients underwent serial brain MRI and time-of-flight MRA to quantify voxel-wise CBF, OEF, and infarcts. LVV was defined as 75-99% stenosis of a major anterior circulation artery. Hemispheres with large vessel occlusion or revascularization surgery were excluded. Infarcted voxels were removed. Mean hemispheric (hemi-) CBF, OEF of the anterior circulation were extracted based on a vascular territory template. Hemi- OEF was normalized to whole brain OEF (nOEF). Hemi- cerebral metabolic rate of oxygen utilization (CMRO2) was calculated from arterial oxygen content, hemi- CBF, and hemi- OEF. Mann-WhitneyUwas used to compare hemispheres with vs. without LVV. Effects of age, hemoglobin, and repeated MRIs were adjusted for in linear mixed model.Results:Of 158 patients, 221 MRI and MRAs were performed. At baseline, LVV occurred in 5% of hemispheres. Median infarct volume was larger in hemispheres with vs. without LVV (6.5 vs. 0.04 mL,p

Stroke, Volume 55, Issue Suppl_1, Page A29-A29, February 1, 2024. Background:While Nitroglycerin (GTN) is predominantly recognized as a vasodilator for ischemic heart disease, its potential neuroprotective properties in acute ischemic stroke (AIS) remain under exploration. This investigation sought to discover the therapeutic advantages of GTN post-recanalization in AIS and underlying mechanisms.Methods:Adult male Sprague Dawley rats were categorized into sham, MCAO with or without GTN treatment, and MCAO treated with both GTN and KT5823, an inhibitor of cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG). AIS was induced by MCAO for 2 hours followed by 6 or 24 hours of reperfusion (tMCAO). A 28-hour MCAO without reperfusion was defined as the permanent MCAO group (pMCAO). The study assessed infarct volumes, neurological impairments, glucose metabolism metrics (lactate and ROS levels), nitric oxide (NO) and cGMP levels (via ELISA). mRNA and protein expressions of hyperglycolysis (GLUT1, GLUT3, PFK, LDH), gluconeogenesis (PCK1, PCK2), ER stress (BIP, PERK, EIF2α, ATF4, CHOP) as well as signaling molecules (PKG, AMPK), were measured with RT-PCR and Western blotting. Apoptotic cell death was evaluated using TUNEL.Results:GTN significantly reduced cerebral infarct volumes, neurological deficits, apoptotic cell death, lactate and ROS levels and decreased the expression of NO and cGMP levels and key glucose metabolism and ER stress-related genes and proteins, including GLUT1, GLUT3, PFK1, LDH, PCK1, PCK2, BIP, PERK, EIF2α, ATF4, CHOP and phosphorylated AMPK, while boosting PKG expression only in tMCAO. The coadministration of GTN and KT5823 reversed the observed GTN benefits.Conclusion:Our findings illuminate that GTN showcases neuroprotective properties in tMCAO (but not pMCAO) by enhancing glucose metabolism (hyperglycolysis and gluconeogenesis), controlling ER stress, and working through the NO-CGMP-PKG signaling cascade to inhibit AMPK phosphorylation.