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Transgender and gender diverse (TGD) individuals face significant healthcare barriers, resulting in inequities and unmet needs. Mobile health (mHealth) applications offer promising solutions by providing accessible, cost-effective, personalized, and gender-affirming care. This systematic review, conducted using PRISMA 2020 guidelines and the PICO framework, screened 5005 records from 4 databases and included 11 articles. The review aimed to identify key features of mHealth apps developed for TGD individuals, focusing on theoretical frameworks, design strategies, and their approaches to addressing healthcare barriers. Key challenges in developing mHealth apps include implementing systemic changes in healthcare settings to combat stigma and discrimination, grounding app development in TGD-specific theoretical frameworks, adequately addressing stressors and protective factors, and overcoming methodological limitations that hinder the evaluation of health outcomes. Overcoming these challenges requires rigorous research methodologies, inclusive designs, reliance on evidence-based TGD frameworks, and stronger collaboration among researchers, healthcare providers, and TGD communities.

Understanding gender identity in transgender and gender-diverse (TGD) individuals is crucial for effective care. The Gender Preoccupation and Stability Questionnaire (GPSQ) measures the preoccupation and stability of gender identity, but no Italian validation is available. This study aimed to translate, culturally adapt and validate the Italian version of the GPSQ in a clinical sample of TGD adults. The GPSQ was translated with a forward-backward method and completed by 151 TGD adults at a gender clinic. Participants also filled out the Symptom Checklist-58 and Body Uneasiness Test. We assessed structural validity (EFA), internal consistency, test-retest reliability, and examined known-groups and predictive validity. The EFA supported a four-factor structure - Gender Identity Instability, Cognitive-Affective Salience, Preoccupation, and Distress/Intervention-Oriented Reflection - with good fit (root mean square error of approximation 0.06; Comparative Fit Index 0.95; Tucker-Lewis Index 0.93; standard root mean square residual 0.04). The GPSQ showed solid internal consistency ( = 0.78; = 0.73) and excellent test-retest reliability ( = 0.98; intraclass correlation coefficient 0.98). Higher scores correlated with psychological distress ( = 0.55, < 0.001) and body image concerns ( = 0.48, < 0.001). Preoccupation was most linked to obsessive-compulsive symptoms, and Cognitive-Affective Salience to body image concerns. Participants not on hormones scored higher ( = 0.010, Cohen's = 0.36). The Italian GPSQ is a reliable and valid tool to assess gender-related preoccupation and identity instability in TGD individuals. Its multidimensional structure makes it useful in both clinical practice and research in the Italian context.

Background: The Gender Variance Scale (GVS) was developed to assess self-perceived masculinity and femininity across diverse gender identities, including binary and non-binary experiences. To date, no validated Italian version was available. Methods: A total of 356 participants (192 transgender and gender-diverse [TGD], 164 cisgender) completed the Italian GVS and the SF-12 Health Survey. Translation and cultural adaptation followed international guidelines. Psychometric evaluation included confirmatory factor analysis (CFA), internal consistency, test–retest reliability (n = 63), convergent validity with health-related quality of life, and group comparisons across gender identity categories. Results: CFA supported the original two-factor model (CFI = 0.916, TLI = 0.905, RMSEA = 0.076, SRMR = 0.053). Internal consistency was high (α = 0.89). The GVS distinguished between gender identity groups: TGD participants scored higher than cisgender peers, and non-binary individuals reported significantly lower scores than both binary groups. Test–retest reliability was strong (r = 0.87–0.99; ICC = 0.992–0.996). Conclusions: The Italian GVS is a valid and reliable measure of gender variance. It provides clinicians, researchers, and educators with a culturally appropriate tool to assess gender expression and support inclusive practices in both community and clinical contexts.

Background: The security measures implemented in response to the COVID-19 emergency have caused complex consequences. The aim of the present study is to examine the repercussions of the pandemic on individuals belonging to gender identity minority groups, who have experienced heightened levels of stress in comparison to the general population. Methods: Online interviews with 12 transgender participants who resided in Italy during the pandemic were conducted and subsequently analyzed following the thematic analysis methodology. Results: The majority of the participants reported an increase in stress levels primarily attributed to the lack of acceptance and support within their familial environments, obstacles encountered in accessing specialized healthcare services, and a lack of support from the broader LGBTQ+ community. Despite these challenges, several participants developed effective coping strategies and a subset of them also benefited from multiple resilience factors, including familial support and assistance from mental health professionals. Conclusions: The outcomes of the present study indicate that the COVID-19 pandemic, while fostering certain protective factors within this population, has also given rise to new and critical mental health concerns. These findings hold significant implications for professionals working with transgender populations, highlighting the necessity of addressing these emerging mental health issues.

PurposeThis study aimed at evaluating the efficacy and safety of high-dose (> 0.2 L/kg of treated plasma per day) coupled plasma filtration-adsorption (CPFA) in treating patients with septic shock.MethodsMulticentre, randomised, adaptive trial, performed in 12 Italian intensive care units (ICUs). Patients aged 14 or more, admitted to the ICU with septic shock, or had developed it during the stay were eligible. The final outcome was mortality at discharge from the last hospital at which the patient received care.ResultsBetween May 2015, and October 2017, 115 patients were randomised. The first interim analysis revealed a number of early deaths, prompting an unplanned analysis. Last hospital mortality was non-significantly higher in the CPFA (55.6%) than in the control group (46.2%, p = 0.35). The 90-day survival curves diverged in favour of the controls early after randomisation and remained separated afterwards (p = 0.100). An unplanned analysis showed higher mortality in CPFA compared to controls among patients without severe renal failure (p = 0.025); a dose–response relationship was observed between treated plasma volume and mortality (p = 0.010).ConclusionThe COMPACT-2 trial was stopped due to the possible harmful effect of CPFA in patients with septic shock. The harmful effect, if present, was particularly marked in the early phase of septic shock. Patients not requiring renal replacement therapy seemed most exposed to the possible harm, with evidence of a dose–response effect. Until the mechanisms behind these results are fully understood, the use of CPFA for the treatment of patients with septic shock is not recommended.

Introduction Chronic obstructive pulmonary disease (COPD) is a frequent cause of morbidity and mortality. Dysregulated and enhanced immune-inflammatory responses have been described in COPD. Recent data showed impaired immune responses and, in particular, of interferon (IFNs) signaling pathway in these patients. Aim To evaluate in peripheral lung of COPD patients, the expression of some of the less investigated key components of the innate immune responses leading to IFN productions including: IFN-receptors (IFNAR1/IFNAR2), IRF-3 and MDA-5. Correlations with clinical traits and with the inflammatory cell profile have been assessed. Methods Lung specimens were collected from 58 subjects undergoing thoracic surgery: 22 COPD patients, 21 smokers with normal lung function (SC) and 15 non-smoker controls (nSC). The expression of IFNAR1, IFNAR2, IRF-3 and MDA-5, of eosinophils and activated NK cells (NKp46+) were quantified in the peripheral lung by immunohistochemistry. Results A significant increase of IRF-3 + alveolar macrophages were observed in COPD and SC compared with nSC subjects. However, in COPD patients, the lower the levels of IRF-3 + alveolar macrophages the lower the FEV1 and the higher the exacerbation rate. The presence of chronic bronchitis (CB) was also associated with low levels of IRF-3 + alveolar macrophages. NKp46 + cells, but not eosinophils, were increased in COPD patients compared to nSC patients ( p  < 0.0001). Conclusions Smoking is associated with higher levels of innate immune response as showed by higher levels of IRF-3 + alveolar macrophages and NKp46 + cells. In COPD, exacerbation rates, severe airflow obstruction and CB were associated with lower levels of IRF-3 expression, suggesting that innate immune responses characterize specific clinical traits of the disease.

Air pollution is a risk factor for respiratory infections and asthma exacerbations. We previously reported impaired Type-I and Type-III interferons (IFN-β/λ) from airway epithelial cells of preschool children with asthma and/or atopy. In this study we analyzed the association between rhinovirus-induced IFN-β/λ epithelial expression and acute exposure to the principal outdoor air pollutants in the same cohort. We studied 34 children (17asthmatics/17non-asthmatics) undergoing fiberoptic bronchoscopy for clinical indications. Bronchial epithelial cells were harvested by brushing, cultured and experimentally infected with Rhinovirus Type 16 (RV16). RV16-induced IFN-β and λ expression was measured by quantitative real time PCR, as was RV16vRNA. The association between IFNs and the mean exposure to PM10, SO2 and NO in the day preceding bronchoscopy was evaluated using a Generalized Linear Model (GLM) with Gamma distribution. Acute exposure to PM10 and NO was negatively associated to RV16-induced IFNβ mRNA. For each increase of 1ug/m of NO we found a significative decrease of 2.3x10 IFN-β mRNA copies and for each increase of 1ug/m of PM10 a significative decrease of 1x10 IFN-β mRNA copies. No significant associations were detected between IFN-λ mRNA and NO nor PM10. Increasing levels of NO (but not PM10) were found to be associated to increased RV16 replication. Short-term exposure to high levels of NO and PM10 is associated to a reduced IFN-β expression by the airway epithelium, which may lead to increased viral replication. These findings suggest a potential mechanism underlying the link between air pollution, viral infections and asthma exacerbations.

Asthma is the most common chronic respiratory disorder worldwide and accounts for a huge health and economic burden. Its incidence is rapidly increasing but, in parallel, novel personalized approaches have emerged. Indeed, the improved knowledge of cells and molecules mediating asthma pathogenesis has led to the development of targeted therapies that significantly increased our ability to treat asthma patients, especially in severe stages of disease. In such complex scenarios, extracellular vesicles (EVs i.e., anucleated particles transporting nucleic acids, cytokines, and lipids) have gained the spotlight, being considered key sensors and mediators of the mechanisms controlling cell-to-cell interplay. We will herein first revise the existing evidence, mainly by mechanistic studies in vitro and in animal models, that EV content and release is strongly influenced by the specific triggers of asthma. Current studies indicate that EVs are released by potentially all cell subtypes in the asthmatic airways, particularly by bronchial epithelial cells (with different cargoes in the apical and basolateral side) and inflammatory cells. Such studies largely suggest a pro-inflammatory and pro-remodelling role of EVs, whereas a minority of reports indicate protective effects, particularly by mesenchymal cells. The co-existence of several confounding factors—including technical pitfalls and host and environmental confounders—is still a major challenge in human studies. Technical standardization in isolating EVs from different body fluids and careful selection of patients will provide the basis for obtaining reliable results and extend their application as effective biomarkers in asthma.

Head and neck squamous cell carcinoma remains challenging to treat with no improvement in survival rates over the past 50 years. Thus, there is an urgent need to discover more reliable therapeutic targets and biomarkers for HNSCC. Matriptase, a type-II transmembrane serine protease, induces malignant transformation in epithelial stem cells through proteolytic activation of pro-HGF and PAR-2, triggering PI3K-AKT-mTOR and NFKB signaling. The serine protease inhibitor lympho-epithelial Kazal-type-related inhibitor (LEKTI) inhibits the matriptase-driven proteolytic pathway, directly blocking kallikreins in epithelial differentiation. Hence, we hypothesized LEKTI could inhibit matriptase-dependent squamous cell carcinogenesis, thus implicating kallikreins in this process. Double-transgenic mice with simultaneous expression of matriptase and LEKTI under the keratin-5 promoter showed a prominent rescue of K5-Matriptase+/0 premalignant phenotype. Notably, in DMBA-induced SCC, heterotopic co-expression of LEKTI and matriptase delayed matriptase-driven tumor incidence and progression. Co-expression of LEKTI reverted altered Kallikrein-5 expression observed in the skin of K5-Matriptase+/0 mice, indicating that matriptase-dependent proteolytic pathway inhibition by LEKTI occurs through kallikreins. Moreover, we showed that Kallikrein-5 is necessary for PAR-2-mediated IL-8 release, YAP1-TAZ/TEAD activation, and matriptase-mediated oral squamous cell carcinoma migration. Collectively, our data identify a third signaling pathway for matriptase-dependent carcinogenesis in vivo. These findings are critical for the identification of more reliable biomarkers and effective therapeutic targets in Head and Neck cancer.

Chronic obstructive pulmonary disease (COPD) is a frequent cause of morbidity and mortality. Dysregulated and enhanced immune-inflammatory responses have been described in COPD. Recent data showed impaired immune responses and, in particular, of interferon (IFNs) signaling pathway in these patients. To evaluate in peripheral lung of COPD patients, the expression of some of the less investigated key components of the innate immune responses leading to IFN productions including: IFN-receptors (IFNAR1/IFNAR2), IRF-3 and MDA-5. Correlations with clinical traits and with the inflammatory cell profile have been assessed. Lung specimens were collected from 58 subjects undergoing thoracic surgery: 22 COPD patients, 21 smokers with normal lung function (SC) and 15 non-smoker controls (nSC). The expression of IFNAR1, IFNAR2, IRF-3 and MDA-5, of eosinophils and activated NK cells (NKp46+) were quantified in the peripheral lung by immunohistochemistry. A significant increase of IRF-3 + alveolar macrophages were observed in COPD and SC compared with nSC subjects. However, in COPD patients, the lower the levels of IRF-3 + alveolar macrophages the lower the FEV1 and the higher the exacerbation rate. The presence of chronic bronchitis (CB) was also associated with low levels of IRF-3 + alveolar macrophages. NKp46 + cells, but not eosinophils, were increased in COPD patients compared to nSC patients (p < 0.0001). Smoking is associated with higher levels of innate immune response as showed by higher levels of IRF-3 + alveolar macrophages and NKp46 + cells. In COPD, exacerbation rates, severe airflow obstruction and CB were associated with lower levels of IRF-3 expression, suggesting that innate immune responses characterize specific clinical traits of the disease.