Διερεύνηση του άγχους, της κατάθλιψης και της σεξουαλικής λειτουργίας σε γυναίκες με σακχαρώδη διαβήτη τύπου δύο

Ο σακχαρώδης διαβήτης τύπου II αποτελεί μια χρόνια, μεταβολική νόσο. Διάφορες μελέτες καταδεικνύουν ότι οι γυναίκες με σακχαρώδη διαβήτη τύπου II παρουσιάζουν υψηλότερο κίνδυνο εμφάνισης άγχους, κατάθλιψης και σεξουαλικών προβλημάτων σε σύγκριση με τις γυναίκες του γενικού πληθυσμού. Κύριος σκοπός της παρούσας μελέτης ήταν η διερεύνηση του άγχους, της κατάθλιψης και της σεξουαλικής λειτουργίας σε γυναίκες με σακχαρώδη διαβήτη τύπου ΙΙ και η σύγκρισή τους με υγιείς μάρτυρες. Στη μελέτη συμμετείχαν συνολικά 88 προ-εμμηνοπαυσιακές γυναίκες εκ των οποίων 44γυναίκες με σακχαρώδη διαβήτη τύπου ΙΙ και 44 υγιείς μάρτυρες. Οι κλίμακες που χρησιμοποιήθηκαν ήταν ο Δείκτης Γυναικείας Σεξουαλικής Λειτουργίας (ΔΓΣΛ) και η κλίμακα μέτρησης άγχους και κατάθλιψης (HADS). Τα αποτελέσματα της μελέτης έδειξαν ότι γυναίκες με σακχαρώδη διαβήτη τύπου ΙΙ, παρουσίαζαν συγκριτικά με τις υγιείς μάρτυρες στατιστικώς σημαντικά υψηλότερη σεξουαλική δυσλειτουργία καθώς και περισσότερα συμπτώματα σε όλους τους επιμέρους τομείς της γυναικείας σεξουαλικής λειτουργίας: επιθυμία, διέγερση, ύγρανση, οργασμός, ικανοποίηση, πόνος. Επιπροσθέτως, βρέθηκε ότι υψηλότερες τιμές σεξουαλικής δυσλειτουργίας συσχετίζονται με υψηλότερες τιμές κατάθλιψης εντός της ομάδας γυναικών με σακχαρώδη διαβήτη τύπου ΙΙ αλλά όχι εντός της ομάδας ελέγχου. Επιπλέον, ενώ αρχικά στους μονοπαραγοντικούς ελέγχους βρέθηκε ότι οι γυναίκες με σακχαρώδη διαβήτη τύπου II παρουσιάζουν υψηλότερη καταθλιπτική συμπτωματολογία σε σχέση με τις γυναίκες της ομάδας ελέγχου, κατόπιν περεταίρω διερεύνησης με πολλαπλή παλινδρόμηση διαπιστώθηκε ότι η διαφορά αυτή οφείλεται στη συγχυτική επίδραση της σεξουαλικής δυσλειτουργίας, η οποία υπεισέρχεται στην παραπάνω σχέση. Τέλος, οι δυο ομάδες συμμετεχόντων δεν βρέθηκε να διαφέρουν ως προς το άγχος. Η σχέση του σακχαρώδη διαβήτη τύπου ΙΙ με την σεξουαλική δυσλειτουργία στις γυναίκες, η οποία συχνά παραγνωρίζεται, φαίνεται ότι χρήζει περαιτέρω διερεύνησης.Type ΙΙ diabetes mellitus is a chronic, metabolic disease. Several studies have shown that women with type ΙΙ diabetes mellitus have a higher risk of developing anxiety, depression and sexual dysfunction than women in the general population. The main purpose of this study was to investigate the relationship between anxiety, depression and sexual function in woman with type ΙΙ diabetes mellitus, as well as to compare with the control group. Overall, 88 pro-menstrual women, 44 with type two diabetes mellitus and 44 healthy women participated in the study. In this study the scales used were the Female Sexual Function Index (FSFI) and the Anxiety and depression scale (HADS). The results of the study showed that women with type two diabetes have statistically significantly higher sexual dysfunction as well as more symptoms in all the areas of female sexual function compared to the healthy controls: desire, arousal, lubrication, orgasm, satisfaction, pain. In addition, it was found that a higher score in sexual dysfunction correlate with higher score in depression within the group of the women with type two diabetes but not within the control group. In addition, while in the initial one way factor analysis it was found that women with type II diabetes mellitus had a higher depressive symptomatology that the women in the control group, after further investigation with multiple regression, this difference was due to the confounding effect of the sexual dysfunction, which was involved in the above relationship. Finally, the two groups of the participants were not found to differ in the anxiety variable. The relationship between the type II diabetes and the sexual dysfunction in women, which is often overlooked, seems to require further investigation

Global burden of 288 causes of death and life expectancy decomposition in 204 countries and territories and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021

BACKGROUND Regular, detailed reporting on population health by underlying cause of death is fundamental for public health decision making. Cause-specific estimates of mortality and the subsequent effects on life expectancy worldwide are valuable metrics to gauge progress in reducing mortality rates. These estimates are particularly important following large-scale mortality spikes, such as the COVID-19 pandemic. When systematically analysed, mortality rates and life expectancy allow comparisons of the consequences of causes of death globally and over time, providing a nuanced understanding of the effect of these causes on global populations. METHODS The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 cause-of-death analysis estimated mortality and years of life lost (YLLs) from 288 causes of death by age-sex-location-year in 204 countries and territories and 811 subnational locations for each year from 1990 until 2021. The analysis used 56 604 data sources, including data from vital registration and verbal autopsy as well as surveys, censuses, surveillance systems, and cancer registries, among others. As with previous GBD rounds, cause-specific death rates for most causes were estimated using the Cause of Death Ensemble model-a modelling tool developed for GBD to assess the out-of-sample predictive validity of different statistical models and covariate permutations and combine those results to produce cause-specific mortality estimates-with alternative strategies adapted to model causes with insufficient data, substantial changes in reporting over the study period, or unusual epidemiology. YLLs were computed as the product of the number of deaths for each cause-age-sex-location-year and the standard life expectancy at each age. As part of the modelling process, uncertainty intervals (UIs) were generated using the 2·5th and 97·5th percentiles from a 1000-draw distribution for each metric. We decomposed life expectancy by cause of death, location, and year to show cause-specific effects on life expectancy from 1990 to 2021. We also used the coefficient of variation and the fraction of population affected by 90% of deaths to highlight concentrations of mortality. Findings are reported in counts and age-standardised rates. Methodological improvements for cause-of-death estimates in GBD 2021 include the expansion of under-5-years age group to include four new age groups, enhanced methods to account for stochastic variation of sparse data, and the inclusion of COVID-19 and other pandemic-related mortality-which includes excess mortality associated with the pandemic, excluding COVID-19, lower respiratory infections, measles, malaria, and pertussis. For this analysis, 199 new country-years of vital registration cause-of-death data, 5 country-years of surveillance data, 21 country-years of verbal autopsy data, and 94 country-years of other data types were added to those used in previous GBD rounds. FINDINGS The leading causes of age-standardised deaths globally were the same in 2019 as they were in 1990; in descending order, these were, ischaemic heart disease, stroke, chronic obstructive pulmonary disease, and lower respiratory infections. In 2021, however, COVID-19 replaced stroke as the second-leading age-standardised cause of death, with 94·0 deaths (95% UI 89·2-100·0) per 100 000 population. The COVID-19 pandemic shifted the rankings of the leading five causes, lowering stroke to the third-leading and chronic obstructive pulmonary disease to the fourth-leading position. In 2021, the highest age-standardised death rates from COVID-19 occurred in sub-Saharan Africa (271·0 deaths [250·1-290·7] per 100 000 population) and Latin America and the Caribbean (195·4 deaths [182·1-211·4] per 100 000 population). The lowest age-standardised death rates from COVID-19 were in the high-income super-region (48·1 deaths [47·4-48·8] per 100 000 population) and southeast Asia, east Asia, and Oceania (23·2 deaths [16·3-37·2] per 100 000 population). Globally, life expectancy steadily improved between 1990 and 2019 for 18 of the 22 investigated causes. Decomposition of global and regional life expectancy showed the positive effect that reductions in deaths from enteric infections, lower respiratory infections, stroke, and neonatal deaths, among others have contributed to improved survival over the study period. However, a net reduction of 1·6 years occurred in global life expectancy between 2019 and 2021, primarily due to increased death rates from COVID-19 and other pandemic-related mortality. Life expectancy was highly variable between super-regions over the study period, with southeast Asia, east Asia, and Oceania gaining 8·3 years (6·7-9·9) overall, while having the smallest reduction in life expectancy due to COVID-19 (0·4 years). The largest reduction in life expectancy due to COVID-19 occurred in Latin America and the Caribbean (3·6 years). Additionally, 53 of the 288 causes of death were highly concentrated in locations with less than 50% of the global population as of 2021, and these causes of death became progressively more concentrated since 1990, when only 44 causes showed this pattern. The concentration phenomenon is discussed heuristically with respect to enteric and lower respiratory infections, malaria, HIV/AIDS, neonatal disorders, tuberculosis, and measles. INTERPRETATION Long-standing gains in life expectancy and reductions in many of the leading causes of death have been disrupted by the COVID-19 pandemic, the adverse effects of which were spread unevenly among populations. Despite the pandemic, there has been continued progress in combatting several notable causes of death, leading to improved global life expectancy over the study period. Each of the seven GBD super-regions showed an overall improvement from 1990 and 2021, obscuring the negative effect in the years of the pandemic. Additionally, our findings regarding regional variation in causes of death driving increases in life expectancy hold clear policy utility. Analyses of shifting mortality trends reveal that several causes, once widespread globally, are now increasingly concentrated geographically. These changes in mortality concentration, alongside further investigation of changing risks, interventions, and relevant policy, present an important opportunity to deepen our understanding of mortality-reduction strategies. Examining patterns in mortality concentration might reveal areas where successful public health interventions have been implemented. Translating these successes to locations where certain causes of death remain entrenched can inform policies that work to improve life expectancy for people everywhere. FUNDING Bill & Melinda Gates Foundation

The role of endothelin-1 in patients with congenital heart disease with left to right shunt.and secondary pulmonary hypertension

Endothelin-1 (ET-1) is a 21–amino acid polypeptide produced by vascular endothelial cells that has vasoconstrictor properties and induces vascular smooth muscle cell proliferation. Both vasoconstriction and myofibroblast proliferation are considered to be responsible for the genesis of pulmonary hypertension (PH). Congenital heart disease (CHD) with left to right shunt type lesion is often associated with pulmonary hypertension. Endothelin-1 concentrations are increased in patients with congenital heart disease (CHD) with left to right shunt. It is unclear whether pressure or flow is the key regulator of endothelin-1 in these patients.In our study, we enrolled 31 patients with congenital heart disease, with isolated left to right shunt type lesion (atrial septal defect, ventricular septal defect and patent ductus arteriosus) and pulmonary vascular resistance less than 3 U.m. Prior to angiography was performed, a blood sample of 3 ml was obtained from the main PA and PV. Hemodynamic variables were measured during cardiac catheterization. 11 children with normal cardiac anatomy and no left to right shunt formed our control group. Plasma ET-1 levels were determined by radioimmunoassay (RIA) Endothelin 1-21 Specific [125 I] Assay System, Amersham Biosciences, UK.. Differences in patients’ profile, hemodynamics and ET-1 levels between PH and non-PH group were tested with the Mann-Whitney test and linear regression analysis. There were neither significant differences in age, nor in gender distribution among the two groups of patients (with PH and non-PH) and the normal subjects. Plasma ET-1 levels among the subgroups of patients with ASD, VSD, and PDA did not differ significantly. Also plasma ET-1 concentrations in the PH group were not significantly higher than those in the non-PH group. The Mann-Whitney U test displayed that there is no correlation between Qp/Qs and plasma ET-1 concentration of pulmonary artery (p=0.647) or pulmonary vein (p=0.133). Significant positive correlation was found between plasma ET-1 concentration at PV and mean pulmonary artery pressure (p=0.009), not only for the entire group of patients but also for two subgroups, with or without pulmonary hypertension. The multiple forward stepwise regression analysis, applied as an equivalent method, produced similar results to Mann-Whitney U test method, Conclusions: Children with the CHD of Atrial Septal Defect, Ventricular Septal Defect and Patent Ductus Arteriosus associated with left-to-right shunt, display increased plasma ET-1 levels in comparison with healthy children. Children belonging to the same group of CHD with left-to shunt and PH, develop higher ET-1 plasma concentrations compared to children without PH. Pulmonary blood pressure constitutes the main factor of plasma ET-1 levels increase in children with the above CHD and left-to-right shunt. The present study displayed that ET-1 plasma levels cannot serve as a diagnostic or prognostic indicator of disease severity, in children with the above three congenital heart diseases.Η ΕΤ-1 αποτελεί τον ισχυρότερο ενδογενή αγγειοσυσταλτικό παράγοντα και ενοχοποιείται για τη δημιουργία της πνευμονικής αρτηριακής υπέρτασης. Οι ασθενείς με συγγενείς καρδιοπάθειες και αριστεροδεξιά διαφυγή εμφανίζουν κατά την εξέλιξη της νόσου αυξημένο κίνδυνο ανάπτυξης πνευμονικής υπέρτασης. Αυξημένα επίπεδα ΕΤ-1 έχουν βρεθεί σε παιδιά με δευτεροπαθή πνευμονική υπέρταση που οφείλεται σε συγγενή καρδιοπάθεια. Σκοπός της παρούσας μελέτης είναι ο προσδιορισμός των παραγόντων που σχετίζονται με αυξημένα επίπεδα ενδοθηλίνης-1 σε παιδιά με συγγενή καρδιοπάθεια που χαρακτηρίζεται από μία μόνο ανατομική ανωμαλία (μεσοκολπική επικοινωνία ή μεσοκοιλιακή επικοινωνία ή ανοικτό αρτηριακό πόρο) και από αριστεροδεξιά διαφυγή και η διερεύνηση της δυνατότητας αξιοποίησης των επιπέδων αυτών ως δεικτών διαγνωστικών ή προγνωστικών της σοβαρότητας της νόσου. Τον πληθυσμό της μελέτης αποτέλεσαν 31 παιδιά με συγγενή καρδιοπάθεια, καθώς και 11 υγιή παιδιά. Όλοι οι ασθενείς είχαν χαμηλές πνευμονικές αντιστάσεις (Rp<3 U.mΤα δείγματα αίματος των υγιών παιδιών ελήφθησαν από περιφερική αρτηρία και φλέβα ενώ των ασθενών από την κύρια πνευμονική αρτηρία και τις πνευμονικές φλέβες κατά τη διάρκεια του καρδιακού καθετηριασμού. Τα επίπεδα της ενδοθηλίνης-1 στο πλάσμα εκτιμήθηκαν με ραδιοανοσολογική μέθοδο RIA (Endothelin 1-21 specific [125 I] Assay System, Amersham Biosciences UK) .Δύο μέθοδοι χρησιμοποιήθηκαν για τη στατιστική ανάλυση, ο έλεγχος U Mann-Whitney και η βηματική πολλαπλή παλινδρόμηση. Τα επίπεδα της ΕΤ-1 στο πλάσμα δεν συναρτώνται με την ηλικία των ασθενών και το είδος της καρδιακής ανωμαλίας. Ο μέσος όρος των επιπέδων της ΕΤ-1 των ασθενών είναι υψηλότερος από τον αντίστοιχο των υγιών. Ο έλεγχος Mann-Whitney U test έδειξε ότι δεν υπάρχει συσχέτιση του λόγου Qp/Qs με τα επίπεδα της ΕΤ-1 στην πνευμονική αρτηρία (p=0,647) και τα επίπεδα της ΕΤ-1 στις πνευμονικές φλέβες (p=0.133), καθώς και ότι η συσχέτιση της μέσης πίεσης της πνευμονικής αρτηρίας και των επιπέδων της ΕΤ-1 των πνευμονικών φλεβών είναι σημαντική (p=0.009). Η βηματική παλινδρόμηση κατέληξε σε όμοια αποτελέσματα με εκείνα της μεθόδου Mann-Whitney U test, δηλαδή ότι η πνευμονική πίεση αποτελεί τον καθοριστικό παράγοντα για την αύξηση των επιπέδων της ΕΤ-1 στις πνευμονικές φλέβες τόσο στο σύνολο των ασθενών όσο και στις δύο υποομάδες ασθενών με και χωρίς πνευμονική υπέρταση. Συμπεράσματα: Παιδιά με μεσοκολπική επικοινωνία, ή μεσοκοιλιακή επικοινωνία ή ανοικτό αρτηριακό πόρο στα οποία η διαφυγή είναι αριστεροδεξιά εμφανίζουν αυξημένα επίπεδα ενδοθηλίνης-1 στο πλάσμα σε σχέση με υγιή παιδιά. Παιδιά με τις ίδιες συγγενείς καρδιοπάθειες, αριστεροδεξιά διαφυγή και επιπλέον πνευμονική υπέρταση εμφανίζουν υψηλότερα επίπεδα ΕΤ-1 από παιδιά χωρίς πνευμονική υπέρταση. Η πίεση της πνευμονικής αρτηρίας αποτελεί τον κύριο παράγοντα αύξησης των επιπέδων της ΕΤ-1 στο πλάσμα του αίματος σε παιδιά με τις παραπάνω συγγενείς καρδιοπάθειες και αριστεροδεξιά διαφυγή. Από την παρούσα μελέτη δεν προέκυψε ότι τα επίπεδα της ΕΤ-1 στο πλάσμα του αίματος παιδιών με τις τρεις αυτές συγγενείς καρδιοπάθειες μπορούν να αποτελέσουν διαγνωστικό ή προγνωστικό δείκτη της σοβαρότητας της νόσου

Molecular Profiling of Malignant Pleural Effusions with Next Generation Sequencing (NGS): Evidence that Supports Its Role in Cancer Management

Malignant pleural effusions (MPEs) often develop in advanced cancer patients and confer significant morbidity and mortality. In this review, we evaluated whether molecular profiling of MPEs with next generation sequencing (NGS) could have a role in cancer management, focusing on lung cancer. We reviewed and compared the diagnostic performance of pleural fluid liquid biopsy with other types of samples. When applied in MPEs, NGS may have comparable performance with corresponding tissue biopsies, yield higher DNA amount, and detect more genetic aberrations than blood-derived liquid biopsies. NGS in MPEs may also be preferable to plasma liquid biopsy in advanced cancer patients with a MPE and a paucicellular or difficult to obtain tissue/fine-needle aspiration biopsy. Of interest, post-centrifuge supernatant NGS may exhibit superior results compared to cell pellet, cell block or other materials. NGS in MPEs can also guide clinicians in tailoring established therapies and identifying therapy resistance. Evidence is still premature regarding the role of NGS in MPEs from patients with cancers other than lung. We concluded that MPE processing could provide useful prognostic and theranostic information, besides its diagnostic role

Plasma Urotensin II levels in children and adolescents with chronic kidney disease: a single-centre study

Abstract Background Increased plasma Urotensin II (UII) levels have been found in adults with renal diseases. Studies in children are scarce. The objective of the study is to estimate plasma UII levels in subjects with chronic kidney disease (CKD) stages 3 to 5 and renal transplant recipients (RTR). In addition, the correlation of UII with anthropometric features and biochemical parameters was assessed. Methods Fifty-four subjects, aged 3 to 20 years old, 23 with CKD, 13 with end-stage kidney disease (ESKD) undergoing hemodialysis (HD) and 18 RTR were enrolled. A detailed clinical evaluation was performed. Biochemical parameters of renal and liver function were measured. Plasma UII levels were measured in all patients and in 117 healthy controls, using a high sensitive enzyme immunoassay (EIA) kit. All data were analyzed using STATA™ (Version 10.1). Results Median UII and mean log-transformed UII levels were significantly higher in CKD and RTR patients compared to healthy subjects (p < 0.001). HD patients had higher but not statistically significant UII and log-UII levels than controls. UII levels increased significantly at the end of the HD session and were higher than controls and in line to those of other patients. The geometric scores of UII in HD (before dialysis), CKD and RTR patients increased respectively by 42, 136 and 164% in comparison with controls. Metabolic acidosis was associated with statistical significant change in log-UII levels (p = 0.001). Patients with metabolic acidosis had an increase in UII concentration by 76% compared to those without acidosis. Conclusions Children and adolescents with CKD, particularly those who are not on HD and RTR, have significantly higher levels of UII than healthy subjects. UII levels increase significantly at the end of the HD session. The presence of metabolic acidosis affects significantly plasma UII levels

Explainable AI-based identification of contributing factors to the mood state change of children and adolescents with pre-existing psychiatric disorders in the context of COVID-19 related lockdowns in Greece

The COVID-19 pandemic and accompanying restrictions have significantly impacted lives globally. There is an increasing interest in examining the influence of this unprecedented situation on our mental well-being, with less attention towards the impact of elongation of COVID-19 related measures on youth with a pre-existing psychiatric/developmental disorder. The majority of studies are focusing on individuals, such as students, adults, youths, among others, with little attention to be given to the elongation of COVID-19 related measures and their impact to a special group of individuals, such as children and adolescents with diagnosed developmental and psychiatric disorders. In addition, most of these studies adopt statistical methodologies to identify pair-wise relationships among factors, an approach that limits the ability to understand and interpret the impact of various factors. In response, this study aims to adopt an explainable machine learning approach to identify factors that explain the deterioration or amelioration of mood state in youth clinical sample. The purpose of this study is to identify and interpret the impact of the most contributing features of mood states change to the prediction output, via an explainable machine learning pipeline. Among all the machine learning classifiers, Random Forest model achieved the highest accuracy, with 76% Best AUC-ROC Score and 13 features. Explainability analysis showed that stress or positive changes derived from the imposing restrictions and COVID-19 pandemic are the top two factors that could affect mood state

Correction: Ntakolia et al. An Explainable Machine Learning Approach for COVID-19’s Impact on Mood States of Children and Adolescents during the First Lockdown in Greece. <i>Healthcare</i> 2022, <i>10</i>, 149

Argyris Stringaris was initially included as an author in the original publication [...