Search Results for: Le cause della polmonite nei bambini

Introduction
Stroke is a leading cause of death and disability worldwide. Stroke survivors and their caregivers often face profound social isolation and various participation restrictions, resulting in frustration and adverse health outcomes. Dyad-focused interventions, which address both survivor and caregiver needs, are essential during the transition process. However, few interventions equally prioritise the outcomes of both survivors and caregivers. This study aims to evaluate the efficacy of a newly developed dyad-focused strategy training intervention in enhancing participation among stroke survivors and their caregivers.

Methods and analysis
This study employs a single-blind, parallel-group randomised controlled trial with allocation concealment and assessor blinding. We aim to enrol 138 stroke survivor-caregiver dyads, randomly assigned in a 1:1 ratio to either the experimental intervention group or the control group. Both groups will receive their usual rehabilitation plus 45–60 min sessions of the intervention twice weekly for a total of 12 sessions. Outcome measures, including the Participation Measure-3 Domains, 4 Dimensions, General Self-Efficacy Scale and Activity Measure for Post-Acute Care, will be collected at baseline, post-intervention and at 3-month, 6-month and 12-month follow-ups. Data will be analysed using multiple linear regression and mixed-effects regression models. Qualitative indepth interviews with participants, caregivers and therapists will be conducted post intervention, transcribed and thematically analysed.

Ethics and dissemination
Ethics approval was obtained from the Ethics Committee of Taipei Medical University (approval number: N202203083), National Taiwan University Hospital (approval number: 202207096RINA) and Taipei Tzu Chi Hospital (approval number: 11 M-107). Findings will be disseminated through presentations at scientific conferences and publications in peer-reviewed journals.

Trial registration number
NCT05571150; Preresults.

Objective
The study investigated the association between the triglyceride–glucose (TyG) index (a surrogate measure for insulin resistance) and all-cause and cardiovascular disease (CVD) mortality among individuals with cardiovascular–kidney–metabolic syndrome.

Design
Population-based cohort study.

Setting
US National Health and Nutrition Examination Survey, 1999–2018.

Participants
A total of 13 585 participants who had valid data were included in this analysis.

Outcome measures
Data from the participants were linked to death certificates to obtain follow-up mortality information from the National Death Index. Cox proportional hazards models were used to assess the associations between the TyG index and all-cause and CVD mortality. Non-linear associations and threshold effects were investigated using restricted cubic spline regression and a two-piecewise Cox proportional hazards model.

Results
During a median follow-up of 99 months, a total of 2876 (16.24%) deaths occurred, of which 961 were attributed to CVD. Each one-unit increase in the TyG index was associated with an 8.9% relative increase in the hazard of all-cause mortality (HR 1.089, 95% CI 1.013 to 1.171) and a 19.5% relative increase in the hazard of CVD mortality (HR 1.195, 95% CI 1.027 to 1.390). Non-linear relationships were identified between the TyG index and all-cause and CVD mortality, with threshold values of 8.97 and 8.81 for all-cause and CVD mortality, respectively. A significant interaction effect was found between age and the TyG index.

Conclusion
There was a U-shaped relationship between the TyG index and both all-cause and CVD mortality. The thresholds of the TyG index may serve as potential tools for managing populations with cardiovascular–kidney–metabolic syndrome to reduce mortality risk.

Systematic review shows that use of prescribed testosterone and SGLT-2 inhibitors is associated with erythrocytosis; but whether these drugs cause thrombosis remains unclear.

Stroke, Ahead of Print. Stroke remains a leading cause of death and disability worldwide. While well-established risk factors play a major role, genetic predisposition is a crucial determinant of stroke susceptibility, with heritability estimates up to 39% for ischemic stroke and 29% for intracerebral hemorrhage. Advances in next-generation sequencing and genome-wide association studies have identified numerous genetic loci associated with stroke risk, paving the way for the development of genetic risk scores. These scores aggregate information from multiple genetic variants to estimate an individual’s stroke risk, offering a promising tool for personalized risk stratification that complements traditional clinical models. While GRSs have demonstrated strong predictive potential for primary stroke events in population-based settings, their integration into clinical practice remains limited. Emerging evidence suggests that GRSs could add value in clinical decision-making, for instance, for stratifying ischemic stroke risk in patients with atrial fibrillation, assessing intracerebral hemorrhage risk in anticoagulant users, and predicting vascular risk factor control in stroke survivors. The incorporation of GRSs with multiomics data and machine learning may further refine risk assessment, driving personalized prevention strategies for both primary and secondary stroke preventions. A major challenge is the limited applicability of GRS across diverse populations, as most genome-wide association studies have been conducted in individuals of European ancestry. Addressing this limitation is critical for ensuring equitable and effective implementation of GRSs in clinical settings. As methodologies continue to evolve, integrating GRS into stroke research could significantly enhance risk assessment and support precision medicine approaches tailored to individual patients.

Circulation, Ahead of Print. BACKGROUND:Myocardial ischemia/reperfusion (I/R) injury is a substantial challenge to the management of ischemic heart disease, the leading cause of mortality worldwide. Arachidonic acid (AA) is a prominent polyunsaturated fatty acid in the human body and plays an important role in various physiological and pathological conditions. AA metabolic enzymes determine AA levels; however, currently there is no comprehensive analysis of AA enzymes in cardiac I/R injury.METHODS:The profiling of AA metabolic enzymes was analyzed with the RNA sequencing transcriptome data from the mouse heart tissues with I/R injury. Cultured neonatal and adult rat ventricular myocytes, human embryonic stem cell–derived cardiomyocytes, and in vivo mouse I/R models were used to confirm the role of L-PGDS (lipocalin-type prostaglandin D2 synthase)/15d-PGJ2 in I/R injury. A biotin-tagged 15d-PGJ2 analog combined with liquid chromatography–tandem mass spectrometry was used to identify the downstream signaling of L-PGDS/15d-PGJ2.RESULTS:Based on the transcriptome data and experimental validations, L-PGDS, together with its downstream metabolite 15d-PGJ2, was downregulated in cardiac tissue with I/R injury. Functionally, L-PGDS overexpression mitigates myocardial I/R injury, whereas knockdown exacerbates the damage. Supplementation of 15d-PGJ2 alleviated I/R injury. Mechanistically, 15d-PGJ2 covalently bound to the Ca2+/CaMKII (calmodulin protein kinase II) and induced lipoxidation of its cysteine 495 (CaMKII-δ9) to dampen the formation of CaMKII oligomers and alleviate its overactivation, consequently ameliorating cardiomyocyte death and cardiac injury.CONCLUSIONS:Our study uncovered L-PGDS/15d-PGJ2/CaMKII signaling as a new mechanism underlying I/R-induced cardiomyocyte death. This provides new mechanistic insights and therapeutic targets for myocardial I/R injury and subsequent heart failure. We also showed that lipoxidation is a new post-translational modification type for CaMKII, deepening our understanding of the regulation of its activity.

In Reply We designed the ADAPT-Sepsis trial as a superiority study, addressing a prioritized research funding brief and international evidence gaps. Our sample size estimate, type I error rate, and power were largely driven by a clinical effectiveness outcome (total antibiotic treatment duration to 28 days after randomization) and not safety (28-day all-cause mortality). The resulting sample size estimate allowed us to measure safety with a noninferior 28-day all-cause mortality margin of 5.4%, the narrowest reported to date, as indicated by Dr Bosch and colleagues. We primarily reported trial safety for a reduction in total antibiotic duration for the PCT group compared with standard care using this approach. The 95% CI for the difference in 28-day mortality did not exceed 5.4% and crossed 0. Therefore, we have shown that PCT is not worse than standard care and that there is no difference between PCT and standard care. Furthermore, there were no differences in the survival curves to day 28 (Figure 2B in our article) or day 90 (eFigure 7 in the article’s Supplement 3). Unlike Bosch and colleagues, we do not believe that implementing daily PCT monitoring will result in excess mortality given the totality of our reported trial data and the body of open-label trial evidence. However, given our concealed trial intervention methods, we suggest that future systematic open implementation of our PCT protocol should be informed by evidence (inducing adherence data) to be presented from an in-trial process evaluation.

Millions of people participate in long-distance running, particularly marathons and half-marathons, annually. While the health benefits of regular exercise are well established, long-distance running can cause significant cardiovascular stress, potentially increasing the risk of cardiac arrest in individuals with underlying heart conditions. This concern is particularly notable as the number of middle-aged and elderly runners—a population at higher average cardiovascular risk than younger runners—continues to rise. Understanding the incidence, causes, and outcomes of cardiac arrest in long-distance runners is crucial for informing risk, identifying prevention strategies, and optimizing race-day medical preparedness.

In campo un gruppo di bambini in cura nei reparti oncologici

Objectives
The study aimed to describe the ethical challenges global health programme (GHP) leaders encounter in their day-to-day work and to understand how they address these ethical challenges, as an important first step toward improving the relevance and precision of ethical guidance for GHPs.

Design
We employed a qualitative case study approach using grounded theory data collection and analysis methods.

Setting
GHPs based at a major GHP hub in Decatur, Georgia, USA, providing a wide range of health services to more than 150 countries globally

Participants
Leaders of all 15 GHPs in the programme hub were invited to participate and 9 were available and consented to participate. Two senior leaders of the programme hub also participated in the study.

Results
We identified 10 categories of ethical challenges encountered by GHP leaders: (1) ethical misalignment between funders and implementing partners; (2) budgets functioning as constraints on ethical decision-making; (3) the limited impact of programmes on improving host country capacity; (4) concerns about missed opportunities to benefit host country communities; (5) shortcomings in current ethics guidance (6) issues in data governance, stewardship and management; (7) navigating complex sociocultural contexts; (8) photography in the context of GHPs; (9) trustworthiness and reputational risks and (10) accountability for unintended consequences. The challenges often result in divided or conflicting loyalties for GHP leaders and uncertainty about what to do. We have characterised this form of uncertainty as ‘moral ambiguity,’ which we define as the inability to discern the best ethical way forward when there is tension or conflict among multiple stakeholder interests.

Conclusions
Our findings suggest that moral ambiguity is a common experience for GHP leaders and that current approaches to global health ethics fail to guide and support GHP leaders to recognise and address moral ambiguity and limit the distress it can cause. The experiences of GHP leaders offer important diagnostic insights for improving the way GHPs are imagined, financed, delivered and evaluated.

Introduction
Deep brain stimulation (DBS) is a proven effective treatment for Parkinson’s disease (PD). However, titrating DBS stimulation parameters is a labourious process and requires frequent hospital visits. Additionally, its current application uses continuous high-frequency stimulation at a constant intensity, which may reduce efficacy and cause side effects. The objective of the AI-DBS study is to identify patient-specific patterns of neuronal activity that are associated with the severity of motor symptoms of PD. This information is essential for the development of advanced responsive stimulation algorithms, which may improve the efficacy of DBS.

Methods and analysis
This longitudinal prospective observational cohort study will enrol 100 patients with PD who are bilaterally implanted with a sensing-enabled DBS system (Percept PC, Medtronic) in the subthalamic nucleus as part of standard clinical care. Local neuronal activity, specifically local field potential (LFP) signals, will be recorded during the first 6 months after DBS implantation. Correlations will be tested between spectral features of LFP data and symptom severity, which will be assessed using (1) inertial sensor data from a wearable smartwatch, (2) clinical rating scales and (3) patient diaries and analysed using conventional descriptive statistics and artificial intelligence algorithms. The primary objective is to identify patient-specific profiles of neuronal activity that are associated with the presence and severity of motor symptoms, forming a ‘neuronal fingerprint’.

Ethics and dissemination
Ethical approval was granted by the local ethics committee of the Amsterdam UMC (registration number 2022.0368). Study findings will be disseminated through scientific journals and presented at national and international conferences.

Objectives
Identifying the underlying cause of acute coma is crucial for improving outcomes in this time-sensitive medical emergency. This study aimed to explore the clinical characteristics, incidence, causes and outcomes of acute coma.

Design
A nationwide population-based retrospective cohort study.

Participants
Among 99 217 322 emergency department (ED) visits between 2000 and 2017, 419 480 acute coma events were identified. After excluding visits with only acute coma diagnosis codes lacking detailed information, individuals without socio-demographic data or those with prior nursing home residence or disability, a total of 205 747 first-ever acute coma cases constituted the final research cohort.

Primary and secondary outcome measures
The primary outcomes included the acute coma event rate, incidence rates stratified by age and underlying causes categorised into 23 clinical groups by the Agency for Healthcare Research and Quality Clinical Classification Software (CCS). Secondary outcomes assessed were reversible coma, hospitalisation rates, 30-day mortality, 1-year medical utilisation and long-term functional outcomes. Cox regression models identified factors influencing long-term mortality.

Results
The overall event rate for acute coma was 4.23 per 1000 ED visits, and the incidence rate was 0.93 per 1000 person-years. The median age of cases was 58.27 years (SD 23.04), with a male predominance (58.90%). Infection and central nervous system (CNS)-related causes were most prevalent. Of these cases, 45.49% experienced reversible coma, 41.66% required hospitalisation and the 30-day mortality group accounted for 12.85%. CNS and drug-related causes contributed to increased 30-day mortality, while psychiatric, alcohol, women’s health and perinatal care, and seizure are causes linked to reversible coma. Patients frequently required intensive care (26.54%), life-sustaining treatments (41.09%) or experienced disability (6.57%) within one year. Generalised estimating equations revealed significantly lower odds of reversible coma for CNS (adjusted OR (aOR), 0.68; 95% CI: 0.62 to 0.74; p

Cormann, ‘lavorare per proteggere bambini nel mondo digitale’

Cormann, ‘lavorare per proteggere bambini nel mondo digitale’

Cormann, ‘lavorare per proteggere bambini nel mondo digitale’

Objectives
To investigate the outcomes of patients with ST-elevation myocardial infarction (STEMI) who were treated with coronary artery bypass grafting (CABG) surgery.

Design
Retrospective nationwide cohort study.

Setting
Patients with STEMI in Finland who were treated with CABG between January 2004 and December 2018.

Participants
1069 patients (mean age: 66.4, 21.4% women).

Primary outcome measure
All-cause mortality (median follow-up 6.4 years) and usage of evidence-based secondary preventive medication early after CABG.

Results
In-hospital mortality among the total cohort was 10.0%, with a significant decrease (p90% of patients and ACE inhibitors/angiotensin II receptor blockers by 70% of patients after discharge from the hospital. The proportion of high-dose statin users increased from 33.1% in 2004–2008 to 63.1% in 2014–2018. ADP inhibitors were used by 29.0% of patients, but the proportion increased during the study.

Conclusions
Contemporary in-hospital and long-term outcomes of CABG-treated patients with STEMI are acceptable. In-hospital mortality has decreased, and the usage of secondary prevention medications after CABG procedures has increased in recent years.