Personality traits and disorders among adult adhd patients: Do they vary between males and females?

INTRODUCTION: Patients with Attention Deficit/Hyperactivity Disorder (ADHD) have shown an increased risk of developing a DSM Cluster B (i.e., Borderline, OR=13.16; Antisocial, OR=3.03; Narcissistic, OR=8.69) and DSM Avoidant Personality Disorder (PD; OR=9.77; Miller et al., 2008). Although different comorbidities affect males and females with ADHD (Kooij et al., 2013), gender differences in personality traits and disorders have not yet been investigated. OBJECTIVES: To describe gender differences in personality traits and disorders among a sample of adult outpatients with ADHD. METHODS: A consecutive sample of DSM-5 ADHD outpatients was recruited at the Adult ADHD Center of the “San Luigi” University Hospital (Orbassano (TO), Italy) between Jan 2017 and Jan 2018. Patients’ personality was assessed by Millon Clinical Multiaxial Inventory (MCMI-III; Zennaro et al, 2008). RESULTS: The study sample consisted of 82 males and 31 females. Sixty percent of men vs. 77% of women had a personality disorder ( CONCLUSIONS: Women with ADHD showed a higher frequency of personality disorders and higher rate of Masochistic PD than men. Moreover, the two most important clusters detected in women included severe personality components (i.e., Borderline and Paranoid) when compared with men. Further studies on larger samples should be conducted to confirm more severe personality profiles in women than in men. DISCLOSURE: No significant relationships

New perspectives in cancer biology from a study of canonical and non-canonical functions of base excision repair proteins with a focus on early steps

Alterations of DNA repair enzymes and consequential triggering of aberrant DNA damage response (DDR) pathways are thought to play a pivotal role in genomic instabilities associated with cancer development, and are further thought to be important predictive biomarkers for therapy using the synthetic lethality paradigm. However, novel unpredicted perspectives are emerging from the identification of several non-canonical roles of DNA repair enzymes, particularly in gene expression regulation, by different molecular mechanisms, such as (i) non-coding RNA regulation of tumour suppressors, (ii) epigenetic and transcriptional regulation of genes involved in genotoxic responses and (iii) paracrine effects of secreted DNA repair enzymes triggering the cell senescence phenotype. The base excision repair (BER) pathway, canonically involved in the repair of non-distorting DNA lesions generated by oxidative stress, ionising radiation, alkylation damage and spontaneous or enzymatic deamination of nucleotide bases, represents a paradigm for the multifaceted roles of complex DDR in human cells. This review will focus on what is known about the canonical and non-canonical functions of BER enzymes related to cancer development, highlighting novel opportunities to understand the biology of cancer and representing future perspectives for designing new anticancer strategies. We will specifically focus on APE1 as an example of a pleiotropic and multifunctional BER protein

Enzymatically active apurinic/apyrimidinic endodeoxyribonuclease 1 is released by mammalian cells through exosomes

The apurinic/apyrimidinic endodeoxyribonuclease 1 (APE1), the main AP-endonuclease of the DNA base excision repair pathway, is a key molecule of interest to researchers due to its unsuspected roles in different nonrepair activities, such as: I) adaptive cell response to genotoxic stress, ii) regulation of gene expression, and iii) processing of microRNAs, which make it an excellent drug target for cancer treatment. We and others recently demonstrated that APE1 can be secreted in the extracellular environment and that serum APE1 may represent a novel prognostic biomarker in hepatocellular and non-smallcell lung cancers. However, the mechanism by which APE1 is released extracellularly was not described before. Here, using three different approaches for exosomes isolation: Commercial kit, nickel-based isolation, and ultracentrifugation methods and various mammalian cell lines, we elucidated the mechanisms responsible for APE1 secretion. We demonstrated that APE1 p37 and p33 forms are actively secreted through extracellular vesicles (EVs), including exosomes from different mammalian cell lines. We then observed that APE1 p33 form is generated by proteasomal-mediated degradation and is enzymatically active in EVs. Finally, we revealed that the p33 form of APE1 accumulates in EVs upon genotoxic treatment by cisplatin and doxorubicin, compounds commonly found in chemotherapy pharmacological treatments. Taken together, these findings provide for the first time evidence that a functional Base Excision Repair protein is delivered through exosomes in response to genotoxic stresses, shedding new light into the complex noncanonical biological functions of APE1 and opening new intriguing perspectives on its role in cancer biology

TCO Optimization in Si Heterojunction Solar Cells on p-type Wafers with n-SiOx Emitter☆

Abstract Silicon heterojunction solar cells have largely demonstrated their suitability to reach high efficiencies. We have here focused on p-type c-Si wafers as absorber, considering that they share more than 90% of the solar cell market. To overcome some of the issues encountered in the conventional (n)a-Si:H/(p)c-Si configuration, we have implemented a mixed phase n-type silicon oxide (n-SiOx) emitter in order to gain from the wider bandgap and lower activation energy of this material with respect to (n)a-Si:H. The workfunction of the transparent conductive oxide layer (WTCO) plays also a key role, as it may induce an unfavourable band bending at the interface with the emitter. We have here focused on AZO, a promising alternative to ITO. Different layers with varying WTCO were prepared, by changing relevant deposition parameters, and were tested into solar cells. The experimental results have been explained with the aid of numerical simulations. Finally, for the n-SiOx/(p)c-Si heterojunction with optimized WTCO a potential conversion efficiency well over 23% has been estimated

By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy

Basal-like breast cancer is an aggressive tumor subtype with a poor response to conventional therapies. Tumor formation and relapse are sustained by a cell subset of Breast Cancer Stem Cells (BrCSCs). Here we show that miR-100 inhibits maintenance and expansion of BrCSCs in basal-like cancer through Polo-like kinase1 (Plk1) down-regulation. Moreover, miR-100 favors BrCSC differentiation, converting a basal like phenotype into luminal. It induces the expression of a functional estrogen receptor (ER) and renders basal-like BrCSCs responsive to hormonal therapy. The key role played by miR-100 in breast cancer free-survival is confirmed by the analysis of a cohort of patients' tumors, which shows that low expression of miR-100 is a negative prognostic factor and is associated with gene signatures of high grade undifferentiated tumors. Our findings indicate a new possible therapeutic strategy, which could make aggressive breast cancers responsive to standard treatments