Anxiety and depression in keratotic oral lichen planus: a multicentric study from the SIPMO

Objectives: Oral lichen planus with exclusive keratotic reticular, papular, and/or plaque-like lesions (K-OLP) is a clinical pattern of OLP that may be associated with a complex symptomatology and psychological alteration. The aim of the study was to evaluate the prevalence of anxiety (A) and depression (D) in patients with K-OLP, analyzing the potential predictors which can affect mental health status. Methods: Three hundred K-OLP patients versus 300 healthy controls (HC) were recruited in 15 Italian universities. The Numeric Rating Scale (NRS), Total Pain Rating Index (T-PRI), and Hamilton Rating Scales for Depression and for Anxiety (HAM-D and HAM-A) were administered. Results: The K-OLP patients showed statistically higher scores in the NRS, T-PRI, HAM-D, and HAM-A compared with the HC (p-value < 0.001**). A and D were found in 158 (52.7%) and 148 (49.3%) K-OLP patients. Strong linear correlations were identified between HAM-A, HAM-D, NRS, T-PRI, and employment status and between HAM-D, HAM-A, NRS, T-PRI, employment status, and female gender. Multivariate logistic regression revealed that HAM-D and HAM-A showed the greatest increase in the R2 value for A and D in the K-OLP patients, respectively (DR2 = 55.5% p-value < 0.001**; DR2 = 56.5% p-value < 0.001**). Conclusions: The prevalence of A and D is higher in the K-OLP patients compared with the HC, also found in K-OLP subjects without pain, suggesting that the processing of pain may be in a certain way independent of the processing of mood. Clinical relevance: Mood disorders and pain assessment should be carefully performed in relation to K-OLP to obtain a complete analysis of the patients

How future surgery will benefit from SARS-COV-2-related measures: a SPIGC survey conveying the perspective of Italian surgeons

COVID-19 negatively affected surgical activity, but the potential benefits resulting from adopted measures remain unclear. The aim of this study was to evaluate the change in surgical activity and potential benefit from COVID-19 measures in perspective of Italian surgeons on behalf of SPIGC. A nationwide online survey on surgical practice before, during, and after COVID-19 pandemic was conducted in March-April 2022 (NCT:05323851). Effects of COVID-19 hospital-related measures on surgical patients' management and personal professional development across surgical specialties were explored. Data on demographics, pre-operative/peri-operative/post-operative management, and professional development were collected. Outcomes were matched with the corresponding volume. Four hundred and seventy-three respondents were included in final analysis across 14 surgical specialties. Since SARS-CoV-2 pandemic, application of telematic consultations (4.1% vs. 21.6%; p &lt; 0.0001) and diagnostic evaluations (16.4% vs. 42.2%; p &lt; 0.0001) increased. Elective surgical activities significantly reduced and surgeons opted more frequently for conservative management with a possible indication for elective (26.3% vs. 35.7%; p &lt; 0.0001) or urgent (20.4% vs. 38.5%; p &lt; 0.0001) surgery. All new COVID-related measures are perceived to be maintained in the future. Surgeons' personal education online increased from 12.6% (pre-COVID) to 86.6% (post-COVID; p &lt; 0.0001). Online educational activities are considered a beneficial effect from COVID pandemic (56.4%). COVID-19 had a great impact on surgical specialties, with significant reduction of operation volume. However, some forced changes turned out to be benefits. Isolation measures pushed the use of telemedicine and telemetric devices for outpatient practice and favored communication for educational purposes and surgeon-patient/family communication. From the Italian surgeons' perspective, COVID-related measures will continue to influence future surgical clinical practice

Biochemical pathways analysis of intracellular and extracellular signaling in failing human ventricular myocytes: differential signal transducers and activators of transcription (STAT) proteins modulation.

Le malattie cardiovascolari costituiscono la principale causa di morte nei paesi occidentali, in particolare lo scompenso cardiaco è la sottoclasse con la più rapida crescita nell’ultimo decennio. La fisiopatologia dell’ipertrofia miocardica e l’evoluzione dell’insufficienza cardiaca rappresentano l’epifenomeno di complesse e molteplici vie biochimiche responsabili della trasduzione del segnale intra ed extra-cellulare. Diversi studi clinici hanno rivelato su modelli animali il coinvolgimento d’importanti mediatori proteici che giocano un ruolo chiave nella fisiopatologia cardiaca, e in particolare, di una via intracellulare di trasduzione del segnale, la via JAK(Janus-activated kinase) /STAT (signal transducer and activator of transcription), indotta da diversi mediatori, tra cui l’Angiotensina (Ang) II, fattore determinante nel rimodellamento cardiaco. Come sperimentalmente dimostrato, la fosforilazione di ERK1/2 (extracellular signal-regulated kinase) indotta da Angi II è ridotta nei cardiomiociti umani isolati da cuori scompensati (FM), indipendentemente dalla causa specifica che ha condotto all’insufficienza cardiaca, diversamente la fosforilazione di JAK2 risulta aumentata, contrariamente a quanto accade nelle cellule miocardiche provenienti da cuori “sani” (NFM). Nonostante l’attivazione di JAK2 indotta da Ang II risulta potenziata nei cardiomiociti FM, rimangono ancora inesplorati i fenomeni che sottendono la modulazione degli STAT, in particolare tra l’effetto cardioprotettivo di STAT3 e l’effetto pro-infiammatorio di STAT2 e STAT5. Pertanto abbiamo studiato l’attivazione differenziale degli STAT conseguente alla fosforilazione di JAK2 nei cardiomiociti isolati, ottenuti da cuori umani scompensati (n=16), e da cuori umani sani (n=6) o ratti adulti (data la scarsa disponibilità di cuori umani sani utilizzabili per prelievo). Nei NFM la fosforilazione di JAK2 è seguita dall’attivazione di STAT3 (205%±43% a 30 min) senza alcuna risposta di STAT2 o STAT5. Diversamente nei FM è stato osservato un incremento di STAT2 (229%±36%) e STAT5 (224%±44%) senza alcuna risposta di STAT3. L’attivazione degli STAT è modulata negativamente dall’antagonismo selettivo dei recettori AT1, ma non degli AT2. I risultati di questo lavoro sperimentale dimostrano un opposto pattern di attivazione degli STAT studiati tra i cardiomiociti FM e NFM. In altri termini, l’alterazione della risposta degli STAT indotta da JAK2 nei cardiomiociti “scompensati”, e il ruolo relativo di alti livelli di glucosio, come precedentemente dimostrato, potrebbero essere rilevanti nella progressione dell’ipertrofia miocardica nei diabetici e nell’evoluzione della insufficienza cardiaca di qualunque eziologia.Cardiovascular disease remains the number one cause of mortality in the Western world, with heart failure representing the fastest growing subclass over the past decade. Although signal-transduction pathways are inherently complex and abundant, studies in animal models have revealed important mediators of cardiac hypertrophy from proteins; in particular, recent reports have shown that the JAK-STAT intracellular signal transduction pathway plays a central role in cardiac pathophysiology. Angiotensin II (Ang II)-induced extracellular signal-regulated kinase (ERK)1/2 phosphorylation is reduced in human ventricular failing cardiomyocytes (FM), whereas Janus-activated kinase (JAK)2 phosphorylation is enhanced as compared to non-failing myocardial cells (NFM). Although Ang II-induced JAK2 phosphorylation was reported to be enhanced in failing human cardiomyocytes, the downstream balance between cardio-protective signal transducer and activator of transcription (STAT) 3 and the pro-inflammatory (STAT2 and STAT5) response remains unexplored. Therefore STATs phosphorylation following JAK2 activation were investigated in isolated cardiomyocytes obtained from failing human hearts (n=16), and from non-failing (NF) hearts from humans (putative donors, n=6) or adult rats. In NF myocytes JAK2 activation was followed by STAT3 phosphorylation (205%±43% at 30 min) with no STAT2 or STAT5 response. Conversely in failing myocytes STAT2 (229%±36%) and STAT5 (224%±44%) phosphorylation responses were observed with no STAT3 response. STAT activation was blunted by AT1 but not AT2 antagonism. According to the present findings, an opposite pattern of STAT response characterises FM as compared to NFM. The altered JAK2 induced STATs response in human failing cardiomyocytes, as well as the relative role of glucose, may be of relevance for myocardial hypertrophy in diabetics and the further progression of heart failure due to the selective activity of the STATs involved

Infectious aortitis or acute aortic syndrome-that is the question

Differential diagnosis between rare, acute aortitis, and common, dissection, forms of acute aortic syndrome

Long-Term Follow-Up Study of Temporary Tricuspid Valve Detachment as Approach to VSD Repair without Consequent Tricuspid Dysfunction

Temporary tricuspid valve detachment improves the operative view of certain congenital ventricular septal defects (VSDs), but its long-term effects on tricuspid valve function are still debated. From 2002 through 2012, we performed a prospective study of 68 children (mean age, 1.28 \ub1 1.01 yr) who underwent transatrial closure of VSDs following temporary tricuspid valve detachment. Sixty patients had conoventricular and 8 had mid-muscular VSDs. All were in sinus rhythm. Seventeen patients had systemic pulmonary artery pressures. Preoperative echocardiograms showed trivial-to-mild tricuspid regurgitation in 62 patients and tricuspid dysplasia with severe regurgitation in 6 patients. Patients were clinically and echocardiographically monitored at 30 postoperative days, 3 months, 6 months, every 6 months thereafter for the first 2 years, and then once a year. No in-hospital or late death was observed at the median follow-up evaluation of 5.9 years. Mean intensive care unit and hospital stays were 1.6 \ub1 1.1 and 7.3 \ub1 2.7 days, respectively. Residual small VSDs occurred in 3 patients, and temporary atrioventricular block in one. After VSD repair, 62 patients (91%) had trivial or mild tricuspid regurgitation, and 6 moderate. Five of these last had severe tricuspid regurgitation preoperatively and had undergone additional tricuspid valve repair during the procedure. The grade of residual tricuspid regurgitation remained stable postoperatively, and no tricuspid stenosis was documented. All patients were in New York Heart Association class I at follow-up. Temporary tricuspid valve detachment is a simple and useful method for a complete visualization of certain VSDs without incurring substantial tricuspid dysfunction

Predictors of Outcome in Patients with Pulmonary Hypertension Undergoing Mitral and Tricuspid Valve Surgery

Background and Objectives: Pulmonary hypertension (PH) secondary to left-sided valvular heart disease is associated with poor cardiac surgical outcome compared with patients without PH. Our objective was to investigate the prognostic factors of surgical outcome in patients with PH undergoing mitral valve (MV) and tricuspid valve (TV) surgery, in order to risk stratify their management. Materials and Methods: This is a retrospective observational study on patients with PH who underwent MV and TV surgery from 2011 to 2019. The primary outcome was all-cause mortality. The secondary outcomes were post-op respiratory and renal complications, length of intensive care unit stay and length of hospital stay. Results: Seventy-six patients were included in this study. The all-cause mortality was 13% (n = 10), with mean survival of 92.6 months. Among the patients, 9.2% (n = 7) had post-op renal failure requiring renal replacement therapy and 6.6% (n = 5) had post-op respiratory failure requiring intubation. Univariate analysis demonstrated that pre-operative left ventricular ejection fraction (LVEF), peak systolic tissue velocity at the tricuspid annulus (S’) and etiology of MV disease were associated with respiratory and renal failure. Tricuspid annular plane systolic excursion (TAPSE) was associated with respiratory failure only. S’, type of operation, LVEF, urgency of surgery, and etiology of MV disease were found to be predictive of mortality. After excluding redo mitral surgery, all statistically significant findings remain unchanged, with the addition of right ventricular (RV) size being associated with respiratory failure. In the subgroup analysis of routine cases (n = 56), patients with primary mitral regurgitation who underwent mitral valve repair had better survival outcome. Conclusions: Urgency of surgery, etiology of MV disease, type of operation (replacement or repair), S’ and pre-op LVEF are prognostic indicators in this small cohort of patients with PH undergoing MV and TV surgery. A larger prospective study is warranted to validate our findings

Effects of angiotensin II type 1 receptor antagonist and temperature on prolonged cardioplegic arrest in neonatal rat myocytes.

Cardioplegic arrest is a model of ischemia/reperfusion injury and results in the death of irreplaceable cardiac myocytes by a programmed cell death or apoptosis. Signal transducers and activators of transcription (STAT) signaling pathways play an important role in the modulation of apoptosis after ischemia and reperfusion. Angiotensin II type 1 (AT1) receptor antagonist added to cardioplegia could represent an additional modality for enhancing myocardial protection during cardioplegic arrest. To test that hypothesis, we studied the effect of AT1 receptor antagonism and cardioplegia temperature perfusion on STATs modulation during cardioplegic arrest in neonatal rat hearts. Isolated, nonworking hearts (n = 4 per group) from neonatal rats were perfused aerobically in the Langendorff mode according to the following scheme: Dulbecco's Modified Eagle's Medium solution (Group 1); cold (4°C) modified St. Thomas' Hospital no. 2 (MSTH2) cardioplegic solution (Group 2); cold (4°C) MSTH2 cardioplegic solution plus AT1 antagonist (Valsartan) (Group 3); and warm (34°C) MSTH2 cardioplegic solution (Group 4). Thus, myocytes were isolated by enzymatic digestion, and STAT1, STAT2, STAT3, and STAT5 were investigated in Western blot studies. Times to arrest after cardioplegia were 6-10 s for all groups with the exception of Group 1 (spontaneous arrest after 12-16 s). Total cardioplegia delivery volume was about 300 mL in 15 min. Perfusion with cold MSTH2 supplemented with AT1 receptor antagonist (Group 3) induced a significant reduction in STAT1, STAT2, and STAT5 tyrosine phosphorylation versus other groups (P < 0.05). The decreased activation of STAT1, STAT2, and STAT5 observed in Group 3 was accompanied by reduction of interleukin-1β (P < 0.05). On the other hand, STAT3 activation was significantly reduced in Groups 1 and 4 (P < 0.05). Only perfusion with AT1 receptor antagonist supplemented with cold MSTH2 significantly decreases the inflammatory response of the neonatal rat cardiomyocytes without affecting antiapoptotic influence provided by activation of STAT3. Therefore, AT1 receptor antagonist could play a pivotal role in cytoprotective effect and cardiac recovery in neonates and infants