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Neste trabalho avaliou-se o efeito das condições de processamento cerâmico na permeabilidade e resistência mecânica de filtros celulares. Esta avaliação compreendeu a fabricação e caracterização de filtros cerâmicos de 8 ppi (poros por polegada linear) no sistema Al2O3-SiC produzidos a partir de suspensões cerâmicas com diferentes ajustes granulométricos. O ajuste granulométrico tem por objetivo otimizar o empacotamento das partículas nos filamentos sólidos e, conseqüentemente, melhorar as propriedades mecânicas do filtro, porém sem comprometer a permeabilidade do mesmo. Neste estudo, a caracterização compreendeu tanto as propriedades reológicas das suspensões selecionadas bem como a caracterização física, fluidodinâmica e mecânica dos filtros obtidos.

We report the case of a boy with chronic septic granulomatosis (CSG) who presented with a marked gastric antrum narrowing which was evaluated by MRI after oral intake of magnetic contrast particles, and after gadolinium i.v. administration. In particular, a mammillated aspect of the gastric wall in the antral region was seen. Follow-up by MRI clearly showed the gradual resolution of hyperemic wall thickness, after medical management. The antral stenosis resolved after 3 months. Magnetic resonance imaging provides detailed evaluation of gastric wall inflammation in course of CSG. [ABSTRACT FROM AUTHOR]

Background: Severely ill patients with coronavirus disease 2019 (COVID-19) show an increased risk of new-onset atrioventricular blocks (AVBs), associated with high rates of short-term mortality. Recent data suggest that the uncontrolled inflammatory activation observed in these patients, specifically interleukin (IL)-6 elevation, may play an important pathogenic role by directly affecting cardiac electrophysiology. The aim of our study was to assess the acute impact of IL-6 changes on electrocardiographic indices of atrioventricular conduction in severe COVID-19., Methods: We investigated (1) the behavior of PR-interval and PR-segment in patients with severe COVID-19 during active phase and recovery, and (2) their association with circulating IL-6 levels over time., Results: During active disease, COVID-19 patients showed a significant increase of PR-interval and PR-segment. Such atrioventricular delay was transient as these parameters rapidly normalized during recovery. PR-indices significantly correlated with circulating IL-6 levels over time. All these changes and correlations persisted also in the absence of laboratory signs of cardiac strain/injury or concomitant treatment with PR-prolonging drugs, repurposed or not., Conclusions: Our study provides evidence that in patients with severe COVID-19 and high-grade systemic inflammation, IL-6 elevation is associated with a significant delay of atrioventricular conduction, independent of concomitant confounding factors. While transient, such alterations may enhance the risk of severe AVB and associated short-term mortality. Our data provide further support to current anti-inflammatory strategies for severe COVID-19, including IL-6 antagonists., Competing Interests: Dr. Pietro Enea Lazzerini received a grant from Roche Italia S.p.A. outside the submitted work, in 2018. The other authors declare no competing interests., (© 2024 The Author(s). Journal of Arrhythmia published by John Wiley & Sons Australia, Ltd on behalf of Japanese Heart Rhythm Society.)

Background/Objectives : Arterial stiffness (AS) is an independent predictor of cardiovascular events and is associated with a poor prognosis. While AS may represent a novel therapeutic target, recent evidence shows that it is sexually dimorphic. The aim of this study was to evaluate relative sex differences in arterial stiffness and their possible impact on the outcome of acute ischemic stroke. Methods : We retrospectively evaluated a cohort of adult patients with the following inclusion criteria: acute ischemic stroke, which occurred within 24 h from the onset of symptoms, confirmed through neuroimaging examinations, additional evaluations including extracranial and transcranial arterial ultrasound examinations, transthoracic echocardiography, a 12-lead resting ECG, and continuous 24 h in-hospital blood pressure monitoring. Based on the 24 h blood pressure monitoring, the following parameters were evaluated: systolic blood pressure, diastolic blood pressure, mean blood pressure, pulse pressure, and arterial stiffness index (ASI). The modified Rankin scale (mRS) was assessed at 90 days to evaluate the 3-month clinical outcome, defining an unfavorable outcome as an mRS score ≥ 3. To assess the factors associated with unfavorable outcomes, a stepwise logistic regression model was performed on the total sample size, and the analyses were replicated after stratifying by sex. Results : A total of 334 patients (176 males, 158 females) were included in the analysis. There was a significant sex-dependent impact of ASI on the 90-day unfavorable Rankin score (mRS score ≥ 3) as only men had a reduced likelihood of favorable outcomes with increasing arterial stiffness (OR:1.54, 95% CI: 1.06-2.23; P-interaction = 0.023). Conclusions : The influence of ASI on the 3-month functional outcome after acute ischemic stroke is at least in part sex-related, suggesting that, in males, higher ASI values are associated with a worse outcome.

Background: Advanced atrioventricular block (AVB), that is, higher than second-degree Mobitz-1, is an abnormal finding in athletes. Despite intensive investigation, in several cases the pathogenesis remains unknown, but frequently pacemaker implantation is still indicated. Increasing evidence points to circulating anti-Ro/Sjögren syndrome-related antigen A (SSA) antibodies cross-reacting with L-type calcium channel and inhibiting the related current as an epidemiologically relevant and potentially reversible cause of isolated AVB in adults. The aim of the study was to determine the prevalence of anti-Ro/SSA-associated advanced AVBs in a large sample of young athletes., Methods and Results: A total of 2536 consecutive athletes aged <40 years without a history of cardiac diseases/interventions were enrolled in a cross-sectional study. Resting and exercise electrocardiography was performed, and those presenting any AVB were further evaluated by 24-hour Holter ECG. Athletes with second-degree AVBs and their mothers underwent anti-Ro/SSA testing. Moreover, purified immunoglobulin G from subjects with anti-Ro/SSA-positive and anti-Ro/SSA-negative advanced AVB were tested on L-type calcium current and L-type-calcium channel expression using tSA201 cells. The global prevalence of advanced AVB in the overall sample was ≈0.1%, but the risk considerably increased (2%) when intensely trained postpubertal male subjects were selectively considered. While none of the athletes with advanced AVB showed heart abnormalities, in 100% of cases anti-Ro/SSA antibodies were detected. Ex vivo experiments showed that immunoglobulin G from anti-Ro/SSA-positive but not -negative subjects with advanced AVB acutely inhibit L-type calcium current and chronically downregulate L-type-calcium channel expression., Conclusions: Our study provides evidence that advanced AVB occurs in young athletes, in most cases associated with anti-Ro/SSA antibodies blocking L-type calcium channels. These findings may open new avenues for immunomodulating therapies to reduce the risk of life-threatening events in athletes, avoiding or delaying pacemaker implantation.

Background: Although accumulating data indicate that IL-6 (interleukin-6) can promote heart rate-corrected QT interval (QTc) prolongation via direct and indirect effects on cardiac electrophysiology, current evidence comes from basic investigations and small clinical studies only. Therefore, IL-6 is still largely ignored in the clinical management of long-QT syndrome and related arrhythmias. The aim of this study was to estimate the risk of QTc prolongation associated with elevated IL-6 levels in a large population of unselected subjects., Methods and Results: An observational study using the Veterans Affairs Informatics and Computing Infrastructure was performed. Participants were US veterans who had an ECG and were tested for IL-6. Descriptive statistics and univariate and multivariate regression analyses were performed to study the relationship between IL-6 and QTc prolongation risk. Study population comprised 1085 individuals, 306 showing normal (<5 pg/mL), 376 moderately high (5-25 pg/mL), and 403 high (>25 pg/mL) IL-6 levels. Subjects with elevated IL-6 showed a concentration-dependent increase in the prevalence of QTc prolongation, and those presenting with QTc prolongation exhibited higher circulating IL-6 levels. Stepwise multivariate regression analyses demonstrated that increased IL-6 level was significantly associated with a risk of QTc prolongation up to 2 times the odds of the reference category of QTc (e.g. QTc >470 ms men/480 ms women ms: odds ratio, 2.28 [95% CI, 1.12-4.50] for IL-6 >25 pg/mL) regardless of the underlying cause. Specifically, the mean QTc increase observed in the presence of elevated IL-6 was quantitatively comparable (IL-6 >25 pg/mL:+6.7 ms) to that of major recognized QT-prolonging risk factors, such as hypokalemia and history of myocardial infarction., Conclusions: Our data provide evidence that a high circulating IL-6 level is a robust risk factor for QTc prolongation in a large cohort of US veterans, supporting a potentially important arrhythmogenic role for this cytokine in the general population.

Background: In ∼50% of severe atrioventricular blocks (AVBs) occurring in adults <50 years, the underlying etiology remains unknown. Preliminary evidence from case reports suggests that autoimmunity, specifically the presence of circulating anti-Ro/SSA antibodies in the patient (acquired form), in the patient's mother (late-progressive congenital form), or in both (mixed form), could be involved in a fraction of idiopathic AVBs in adults by possibly targeting the L-type calcium channel (Ca v 1.2) and inhibiting the related current (I CaL )., Objectives: The purpose of this study was to evaluate whether anti-Ro/SSA antibodies are causally implicated in the development of isolated AVBs in adults., Methods: Thirty-four consecutive patients with isolated AVB of unknown origin and 17 available mothers were prospectively enrolled in a cross-sectional study. Anti-Ro/SSA antibodies were assessed by fluoroenzyme-immunoassay, immuno-Western blotting, and line-blot immunoassay. Purified immunoglobulin-G (IgG) from anti-Ro/SSA-positive and anti-Ro/SSA-negative subjects were tested on I CaL and Ca v 1.2 expression using tSA201 and HEK293 cells, respectively. Moreover, in 13 AVB patients, the impact of a short course of steroid therapy on AV conduction was evaluated., Results: Anti-Ro/SSA antibodies, particularly anti-Ro/SSA-52kD, were found in 53% of AVB-patients and/or in their mothers, most commonly an acquired or mixed form (two-thirds of cases) without history of autoimmune diseases. Purified IgG from anti-Ro/SSA-positive but not anti-Ro/SSA-negative AVB patients acutely inhibited I CaL and chronically down-regulated Ca v 1.2 expression. Moreover, anti-Ro/SSA-positive sera showed high reactivity with peptides corresponding to the Ca v 1.2 channel pore-forming region. Finally, steroid therapy rapidly improved AV conduction in AVB-patients with circulating anti-Ro/SSA antibodies but not in those without., Conclusions: Our study points to anti-Ro/SSA antibodies as a novel, epidemiologically relevant and potentially reversible cause of isolated AVB in adults, via an autoimmune-mediated functional interference with the L-type calcium channels. These findings have significant impact on antiarrhythmic therapies by avoiding or delaying pacemaker implantation., Competing Interests: Funding Support and Author Disclosures This work was supported by Ministero dell’Istruzione, dell’Università e della Ricerca (MIUR), Progetti di Rilevante Interesse Nazionale (PRIN), and Bando 2017, protocollo 2017XZMBYX (to Dr Lazzerini and Dr Capecchi); a Merit Review grant I01 BX002137 from Biomedical Laboratory Research & Development Service of Veterans Affairs Office of Research and Development (to Dr Boutjdir); National Heart, Lung, and Blood Institute grant 1R01HL164415-01 (to Dr Boutjdir); and U.S. Department of Defense award number W81XWH-21-1-0424 (to Dr Boutjdir). Dr Lazzerini has received a grant from Roche Italia S.p.A. outside the submitted work. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2023 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: Heart rate-corrected QT interval (QTc) prolongation is prevalent in patients with severe coronavirus disease 2019 (COVID-19) and is associated with poor outcomes. Recent evidence suggests that the exaggerated host immune-inflammatory response characterizing the disease, specifically interleukin-6 (IL-6) increase, may have an important role, possibly via direct effects on cardiac electrophysiology. The aim of this study was to dissect the short-term discrete impact of IL-6 elevation on QTc in patients with severe COVID-19 infection and explore the underlying mechanisms., Methods: We investigated the following mechanisms: (1) the QTc duration in patients with COVID-19 during the active phase and recovery, and its association with C-reactive protein (CRP) and IL-6 levels; (2) the acute impact of IL-6 administration on QTc in an in vivo guinea pig model; and (3) the electrophysiological effects of IL-6 on ventricular myocytes in vitro ., Results: In patients with active severe COVID-19 and elevated IL-6 levels, regardless of acute myocardial injury/strain and concomitant QT-prolonging risk factors, QTc was significantly prolonged and rapidly normalized in correlation with IL-6 decrease. The direct administration of IL-6 in an in vivo guinea pig model acutely prolongs QTc duration. Moreover, ventricular myocytes incubated in vitro with IL-6 show evident prolongation in the action potential, along with significant inhibition in the rapid delayed rectifier potassium current (I Kr )., Conclusion: For the first time, we demonstrated that in severe COVID-19, systemic inflammatory activation can per se promote QTc prolongation via IL-6 elevation, leading to ventricular electric remodeling. Despite being transitory, such modifications may significantly contribute to arrhythmic events and associated poor outcomes in COVID-19. These findings provide a further rationale for current anti-inflammatory treatments for COVID-19, including IL-6-targeted therapies., Competing Interests: PL received a grant from Roche Italia S.p.A. outside the submitted work in 2018. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Lazzerini, Accioli, Acampa, Zhang, Verrengia, Cartocci, Bacarelli, Xin, Salvini, Chen, Salvadori, D’errico, Bisogno, Cevenini, Marzotti, Capecchi, Laghi-Pasini, Chen, Capecchi and Boutjdir.)

Background Systemic inflammation and male hypogonadism are 2 increasingly recognized "nonconventional" risk factors for long-QT syndrome and torsades de pointes (TdP). Specifically, inflammatory cytokines prolong, while testosterone shortens the heart rate-corrected QT interval (QTc) via direct electrophysiological effects on cardiomyocytes. Moreover, several studies demonstrated important interplays between inflammation and reduced gonad function in men. We hypothesized that, during inflammatory activation in men, testosterone levels decrease and that this enhances TdP risk by contributing to the overall prolonging effect of inflammation on QTc. Methods and Results We investigated (1) the levels of sex hormones and their relationship with inflammatory markers and QTc in male patients with different types of inflammatory diseases, during active phase and recovery; and (2) the association between inflammatory markers and sex hormones in a cohort of male patients who developed extreme QTc prolongation and TdP, consecutively collected over 10 years. In men with active inflammatory diseases, testosterone levels were significantly reduced, but promptly normalized in association with the decrease in C-reactive protein and interleukin-6 levels. Reduction of testosterone levels, which also inversely correlated with 17-β estradiol over time, significantly contributed to inflammation-induced QTc prolongation. In men with TdP, both active systemic inflammation and hypogonadism were frequently present, with significant correlations between C-reactive protein, testosterone, and 17-β estradiol levels; in these patients, increased C-reactive protein and reduced testosterone were associated with a worse short-term outcome of the arrhythmia. Conclusions During systemic inflammatory activation, interleukin-6 elevation is associated with reduced testosterone levels in males, possibly deriving from an enhanced androgen-to-estrogen conversion. While transient, inflammatory hypotestosteronemia is significantly associated with an increased long-QT syndrome/TdP risk in men.

Background Recent data suggest that systemic inflammation can negatively affect atrioventricular conduction, regardless of acute cardiac injury. Indeed, gap-junctions containing connexin43 coupling cardiomyocytes and inflammation-related cells (macrophages) are increasingly recognized as important factors regulating the conduction in the atrioventricular node. The aim of this study was to evaluate the acute impact of systemic inflammatory activation on atrioventricular conduction, and elucidate underlying mechanisms. Methods and Results We analyzed: (1) the PR-interval in patients with inflammatory diseases of different origins during active phase and recovery, and its association with inflammatory markers; (2) the existing correlation between connexin43 expression in the cardiac tissue and peripheral blood mononuclear cells (PBMC), and the changes occurring in patients with inflammatory diseases over time; (3) the acute effects of interleukin(IL)-6 on atrioventricular conduction in an in vivo animal model, and on connexin43 expression in vitro. In patients with elevated C-reactive protein levels, atrioventricular conduction indices are increased, but promptly normalized in association with inflammatory markers reduction, particularly IL-6. In these subjects, connexin43 expression in PBMC, which is correlative of that measured in the cardiac tissue, inversely associated with IL-6 changes. Moreover, direct IL-6 administration increased atrioventricular conduction indices in vivo in a guinea pig model, and IL-6 incubation in both cardiomyocytes and macrophages in culture, significantly reduced connexin43 proteins expression. Conclusions The data evidence that systemic inflammation can acutely worsen atrioventricular conduction, and that IL-6-induced down-regulation of cardiac connexin43 is a mechanistic pathway putatively involved in the process. Though reversible, these alterations could significantly increase the risk of severe atrioventricular blocks during active inflammatory processes.

Purpose: Carpal tunnel syndrome (CTS) is a neuropathy caused by compression of the median nerve in the carpal tunnel. Our purpose was to evaluate the role of high-resolution ultrasonography (US), performed with a 10-13 MHz probe, in the detection of morphovolumetric changes of the median nerve to confirm the clinical diagnosis., Materials and Methods: Fifty healthy volunteers were examined first by US; subsequently we studied 294 wrists in 186 symptomatic patients, calculating the cross-sectional area of the median nerve at three levels: before the median nerve enters the carpal tunnel, at the carpal tunnel inlet and at the outlet. US was considered diagnostic for CTS when the median nerve area increased at the inlet or flattening was present along the carpal tunnel., Results: Ultrasonography showed pathologic findings in 267 wrists: in 261 cases morphovolumetric changes of the median nerve were found; in six cases anatomic variant of the median nerve was detected. Surgery was performed in 277 cases and all patients became symptom-free. The sensitivity of US was 96.3 % ., Conclusions: Our study confirms that quantitative ultrasonographic assessment is a useful support in confirming the clinical diagnosis of CTS.

Purpose: Carpal Tunnel Syndrome (CTS) is a neuropathy caused by compression of the median nerve at the level of the wrist, which is caused by different pathologic conditions. In some cases it has been associated with anatomic variations of the median nerve, mainly with the early duplication of the nerve inside the carpal tunnel (III Group of Lanz). The treatment of CTS is mainly surgical consisting in decompression by transection of the transverse carpal ligament, which is better performed by endoscopic release. The aim of our study was to evaluate the possibility to detect this anatomic variant by integrated imaging and assess the value of this information for planning treatment., Material and Methods: We report 6 cases of bifid median nerve examined by Ultrasonography (US) using mechanic sectorial and linear array transducers operating at 10 to 13 MHz, and by MR imaging using 0.2 T equipment., Results: In all cases US transverse scans showed two adjacent oval formations with a structure similar to that of the median nerve. CONCLUSIONS. MR imaging confirmed the sonographic findings in all cases. All patients underwent open surgical treatment by decompression of the median nerve; in all cases an early duplicated median nerve was confirmed.