University of Messina

Prolonged monitoring with implantable cardiac monitors (ICMs) effectively detects subclinical atrial fibrillation (SCAF) in patients with cryptogenic stroke (CS). Understanding SCAF progression to higher burdens can affect decisions regarding oral anticoagulant (OAC) and antiarrhythmic therapies. This analysis aimed to quantify initial SCAF burden, its progression, and predictors of progression in CS patients. This multicenter project collected demographics, stroke characteristics, and SCAF daily burden in CS patients implanted with ICM. SCAF progression was defined as an increase in daily burden from initial detection, categorized as: 5 min to 1 h, 1-6 h, 6-24 h, 24 h for < 7 days, and 24 h for ≥ 7 days. Of 593 patients (70.0 ± 11.3 years, 42% female, median CHA2DS2-VASc score 4.7 ± 1.4) monitored over a median of 24.6 months, 32.7% had SCAF detected. While initial SCAF daily burden was < 1 h in 38.7% of SCAF patients, 53.3% progressed to a higher SCAF daily burden, with 30.6% reaching the 24 h burden by 36 months. Higher CHA2DS2-VASc scores and stroke severity were associated with SCAF progression. OAC therapy was initiated in 91.2% patients with a maximum SCAF daily burden < 1 h, while in 98.0% of those with a maximum daily burden ≥ 1 h (p = 0.042). Over half of CS patients with SCAF progressed to a higher burden, and about one-third reached a 24 h SCAF daily burden. These findings highlight the importance of continuous monitoring in CS patients for early SCAF detection and personalized therapy, considering SCAF burden progression and the patient's risk profile.

Peroxisome proliferator-activated receptor gamma (PPAR-γ) is a key regulator of adipose tissue expansion, coordinating adipocyte physiological differentiation and maturation. In this study we evaluated the PPAR-γ effects of perfluorooctanoic acid (PFOA), a perfluorinated alkylated environmental obesogen, associated with an increased risk of diabetes, during adipogenic differentiation of 3T3-L1 murine cells. In particular, using in vitro monoculture (differentiating preadipocytes exposed to PFOA) or co-culture systems (differentiating preadipocytes in contact with PFOA-induced dysfunctional mature adipocytes) we examined adipocytes morphology and biological functions such as adipogenesis, insulin sensitivity and lipolytic response to adrenergic compounds. Exposure to PFOA (0.1-10μM) promoted adipocyte hypertrophy inducing the formation of larger lipid vacuoles. These effects were also evident in the co-culture system, where paracrine factors released by PFOA-induced hypertrophic adipocytes influenced preadipocytes differentiation. Furthermore, both in the mono-culture and in the co-culture systems, PFOA exposure induced a metabolically unhealthy adipocyte phenotype affecting insulin sensitivity. Finally, findings obtained in mono-culture system evidence that these effects induced by PFOA may be related to its capability to affect lipid metabolism and pro/anti-inflammatory adipokine expression. This study, therefore, draws attention on PFOA as an obesogenic factor promoting adipocyte metabolic dysregulation and dysfunctional paracrine signaling.

The present study investigates the bed-load dynamics of non-buoyant microplastic particles subjected to wave forcing, with emphasis on the phase-resolved relationship between particle motion and near-bed hydrodynamics. Specifically, five groups of PLA particles, differing in shape and density, were tested in a wave flume under five regular wave conditions representative of intermediate-depth coastal environments. Based on high quality video analysis, particle mobilisation occurred when the modified Shields parameter for plastics exceeded the incipient-motion threshold derived from previous work. The experiments highlighted a residual onshore drift that depends on the particle characteristics and increases with wave steepness, resulting from asymmetries in the near-bed velocity field. For the first time, a link has been established between the phase-resolved particle velocity, normalised by the near-bed flow velocity, and the ratio of the modified Shields number for plastics to the incipient motion threshold, revealing a clear non-linear dependence between particle mobility and the applied force. • Phase-resolved experiments investigate non-buoyant microplastics under waves. • Blob-analysis tracking quantifies oscillatory motion and onshore drift. • Particle velocity follows a power-law relation with excess shear stress. • Results reveal a unified scale for sediment and plastic transport.

Cardiovascular diseases remain the leading cause of morbidity and mortality worldwide. Low-density lipoprotein cholesterol (LDL-C) plays a central role in atherogenesis and cardiovascular events. In real-world primary care, many patients at high and very-high cardiovascular risk (HCVR) do not achieve recommended LDL-C targets. This study evaluated whether an audit and feedback (A&F) intervention could improve lipid management in HCVR patients managed in general practice. We conducted a retrospective-prospective observational study involving general practitioners (GPs). GPs were classified as active, participating in A&F training and feedback sessions, or controls, contributing data only. Patient-level data were extracted from electronic medical records across three 18-month observation periods (T0, T1, and T2). Active GPs received tailored performance reports and educational sessions after T0 and T1. Main outcomes included completeness of clinical data recording, LDL-C target attainment (<70mg/dL), lipid-lowering treatment patterns, and treatment adherence. Compared with baseline, active GPs showed significant improvements in the recording of LDL-C (+18.3%), HbA1c (+5.7%), body mass index (+17.1%), smoking status (+4.4%), and alcohol consumption (+14.4%). LDL-C target attainment increased from 6.1% at T0 to 14.5% at T2, exceeding the proportion observed in controls at T2 (8.7%). The use of lipid-lowering therapy among active GPs increased from 48.9% at T0 to 61.3% at T2, while high-intensity therapy increased from 9.1% to 17.6%. Treatment adherence improved over time, with a higher proportion of patients adherent to high-intensity therapy and a reduction in non-adherent low-intensity therapy. An audit and feedback intervention supported by a multidisciplinary team improved data completeness and lipid management in high-risk patients in the primary care setting.

Background: Genetic causes of growth failure should be suspected in patients born small for gestational age (SGA) who fail to show postnatal catch-up growth, present with severe short stature (SS), and exhibit a poor or absent response to growth hormone (rhGH) therapy. Mutations in the insulin-like growth factor 1 receptor (IGF1R) gene are associated with impaired growth, intrauterine growth restriction (IUGR), low birth weight and/or length, and postnatal SS. Case Description: A 9-year-old boy, born SGA for birth length, was evaluated for severe SS. Common causes of SS were excluded. At 9 years and 7 months of age, his height was 112.6 cm (-3.99 SDS), weight 18 kg (-3.79 SDS), and BMI 14.2 kg/m2 (-1.8 SDS); pubertal development was Tanner stage 1. The target height was 158 cm (-2.62 SDS). Bone age was delayed by approximately one year compared with chronological age. Serum IGF-1 levels were within the upper-normal range for age. GH therapy (0.035 mg/kg/day) was initiated due to the lack of catch-up growth in an SGA subject. After three years of treatment, the height gain was only 0.5 SDS. IGF-1 levels showed a transient treatment-related increase, followed by persistent normalization during ongoing therapy. Next-generation sequencing (NGS) analysis identified novel heterozygous paternal nonsense variant in the IGF1R gene: c.3498C>G (p.Tyr1166Ter). At 12 years of age, impaired fasting glucose and reduced glucose tolerance were detected; consequently, it was decided to discontinue rhGH therapy, also in light of the IGF1R mutation and the lack of height recovery. Conclusions: This case underlines the critical role of genetic testing in the evaluation of patients born SGA. The coexistence of SGA status and an IGF1R gene mutation may provide a clear explanation for both the poor response to rhGH therapy and the increased risk of alterations in glucose metabolism. An extensive narrative review of the literature on growth outcomes and glucose metabolism abnormalities during GH treatment in SGA patients carrying IGF1R variants was also performed.

Vein grafting may provide a valuable option in microvascular free flap reconstruction for head and neck cancer when direct anastomosis is not feasible. This study assesses indications and outcomes, reappraises prevailing assumptions, and delineates clinical contexts in which the technique could enhance reconstructive reliability and success. This retrospective study evaluates the use of vein grafts in microvascular free flap reconstruction for head and neck malignancies. Among 51 consecutive patients treated at S. Marco Hospital, University of Catania (2021-2024), 11 underwent vein grafting. In 4 cases, grafting was adopted as a secondary measure following anastomotic failure or excessive vessel distance that precluded direct anastomosis; in 7, it was planned from the outset due to anticipated vessel misalignment or insufficient pedicle length. The external jugular vein served as the graft conduit in all cases. Among 11 patients, 5 underwent radial forearm flap, 2 fibular flap, 2 anterolateral thigh (ALT), and 2 latissimus dorsi flap. Four patients underwent radiotherapy, whereas 2 are still awaiting evaluation. Only 1 case resulted in flap necrosis, requiring surgical revision. Complications were minimal, with 1 case of wound dehiscence. No cases of venous thrombosis, arterial insufficiency, or total flap loss occurred beyond the single necrosis case. The overall flap survival rate was 91%. Vein grafting is a safe, effective adjunct for head and neck free flap reconstruction, particularly when pedicle-recipient mismatch or thrombosis precludes direct anastomosis, and can improve outcomes in complex cases.

A dispetto della distanza dai fronti di guerra egiziano e siriano, i paesi maghrebini presero posizione nella guerra arabo-israeliana dell’ottobre 1973 schierando forze militari (Marocco, Algeria, Tunisia), esercitando pressioni economiche e diplomatiche, mobilitando l’opinione pubblica. Il contributo esamina, a partire dal punto di vista del Maghreb, la congiuntura del 1973 quale banco di prova del panarabismo rivisitando la periodizzazione ad quem del nazionalismo arabo. La spinta solidale e unitaria registratasi nel Maghreb nel corso della guerra e le pregresse iniziative di unificazione maghrebina sono messe a raffronto, da una parte, con le agende politiche statuali informate a pragmatismo e ragion di stato e, dall’altra con l’ideologia del terzomondismo che sussumeva la causa arabo-palestinese nel proprio registro discorsivo. Le fonti primarie e secondarie consultate – frammenti di archivi, stampa e letteratura coeva, discorsi alle Nazioni Unite, memorialistica – consentono di seguire da vicino il dispiegarsi della fase discendente del nazionalismo arabo mostrando la sfasatura tra la forza del sentimento e la validità del progetto politico.