Is depression a real risk factor for acute myocardial infarction mortality? A retrospective cohort study

Background: Depression has been associated with a higher risk of cardiovascular events and a higher mortality in patients with one or more comorbidities. This study investigated whether continuative use of antidepressants (ADs), considered as a proxy of a state of depression, prior to acute myocardial infarction (AMI) is associated with a higher mortality afterwards. The outcome to assess was mortality by AD use. Methods: A retrospective cohort study was conducted in the Veneto Region on hospital discharge records with a primary diagnosis of AMI in 2002-2015. Subsequent deaths were ascertained from mortality records. Drug purchases were used to identify AD users. A descriptive analysis was conducted on patients' demographics and clinical data. Survival after discharge was assessed with a Kaplan-Meier survival analysis and Cox's multiple regression model. Results: Among 3985 hospital discharge records considered, 349 (8.8%) patients were classified as AD users'. The mean AMI-related hospitalization rate was 164.8/100,000 population/year, and declined significantly from 204.9 in 2002 to 130.0 in 2015, but only for AD users (-40.4%). The mean overall follow-up was 4.64.1years. Overall, 523 patients (13.1%) died within 30days of their AMI. The remainder survived a mean 5.3 +/- 4.0years. After adjusting for potential confounders, use of antidepressants was independently associated with mortality (adj OR=1.75, 95% CI: 1.40-2.19). Conclusions: Our findings show that AD users hospitalized for AMI have a worse prognosis in terms of mortality. The use of routinely-available records can prove an efficient way to monitor trends in the state of health of specific subpopulations, enabling the early identification of AMI survivors with a history of antidepressant use

Our products are safe (don’t tell anyone!). Why don’t supermarkets advertise their private food safety standards?

Large retail chains have spent considerable resources to promote production protocols andtraceability across the supply chain, aiming at increasing food safety. Yet, the majority of consumers areunaware of these private food safety standards (PFSS) and retailers are not informing them. This behaviordenotes a pooling paradox: supermarkets spend a large amount of money for food safety and yet they forgetto inform consumers. The result is a pooling equilibrium where consumers cannot discriminate among highquality and low quality products and supermarkets give up the potential price premium. This paper providesan economic explanation for the paradox using a contract-theory model. We found that PFSSimplementation may be rational even if consumers have no willingness to pay for safety, because thestandard can be used as a tool to solve asymmetric information along the supply chain. Using the PFSS,supermarkets can achieve a separating equilibrium where opportunistic suppliers have no incentive to acceptthe contract.Even if consumers exhibit a limited (but strictly positive) willingness to pay for safety, advertisingmay be profit-reducing. If the expected price margin is high enough, supermarkets have incentive to supplyboth certified and uncertified products. In this case, we show that, if consumers perceive undifferentiatedproducts as “reasonably safe”, supermarkets may maximize profits by pooling the goods and selling them asundifferentiated. This result is not driven by advertising costs, as we derive it assuming free advertising.[...

Accumulation of Dry Matter, Protein and Total Available Carbohydrate in Berseem under Different Cutting Regimes

The effect of different cutting regimes on physiology and morphology of aerial parts and roots in 6 bcrseem (Trifolium alexadrium L.) genotypes was evaluated. Observations were carried out on individual plants at 4 stages of development: fourth and eighth internode elongation, early flowering and physiological seed maturity. The results showed that the genotypes were characterised by highest values of dry matter in the aerial and root parts at the early flowering stage. Variability among genotypes was observed

The Role of LRRK2 in Parkinson's Disease

This thesis focuses on the role of the leucine rich repeat kinase 2 (LRRK2) gene in Parkinson’s disease (PD). PD is the second most frequent human neurodegenerative disorder after Alzheimer’s disease. The etiology of PD remains unknown in most cases, but several genetically-determined forms have been recently identified, which are greatly promoting our understanding of the disease mechanisms. Mutations in the LRRK2 gene were initially identified through positional cloning within the PARK8 locus in families with autosomal dominant inheritance of PD. Subsequent studies, included some of those described in this thesis, have delineated LRRK2 mutations as the most frequent, known cause of familial and sporadic PD

Autophagy in motor neuron disease: Key pathogenetic mechanisms and therapeutic targets

Autophagy is a lysosome-dependant intracellular degradation process that eliminates long-lived proteins as well as damaged organelles from the cytoplasm. An increasing body of evidence suggests that dysregulation of this system plays a pivotal role in the etiology and/or progression of neurodegenerative diseases including motor neuron disorders. Herein, we review the latest findings that highlight the involvement of autophagy in the pathogenesis of amyotrophic lateral sclerosis (ALS) and the potential role of this pathway as a target of therapeutic purposes. Autophagy promotes the removal of toxic, cytoplasmic aggregate-prone pathogenetic proteins, enhances cell survival, and modulates inflammation. The existence of several drugs targeting this pathway can facilitate the translation of basic research to clinical trials for ALS and other motor neuron diseases

Uncompleted Emergency Department Care (UEDC): A 5-year population-based study in the Veneto Region, Italy

Introduction: Uncompleted visits to emergency departments (UEDC) are a patient safety concern. The purpose of this study was to investigate risk factors for UEDC, describing not only the sociodemographic characteristics of patients who left against medical advice (AMA) and those who left without being seen (LWBS), but also the characteristics of their access to the emergency department (ED) and of the hospital structure. Methods: This was a cross sectional study on anonymized administrative data in a population-based ED database. Results: A total of 9,147,415 patients attended EDs in the Veneto Region from 2011 to 2015. The UEDC rate was 28.7\u2030, with a slightly higher rate of AMA than of LWBS (15.3\u2030 vs 13.4\u2030). Age, sex, citizenship, and residence were sociodemographic factors associated with UEDC, and so were certain characteristics of access, such as mode of admission, type of referral, emergency level, waiting time before being seen, and type of medical issue (trauma or other). Some characteristics of the hospital structure, such as the type of hospital and the volume of patients managed, could also be associated with UEDC. Conclusion: Cases of UEDC, which may involve patients who leave AMA and those who LWBS, differ considerably from other cases managed at the ED. The present findings are important for the purpose of planning and staffing health services. Decision-makers should identify and target the factors associated with UEDC to minimize walkouts from public hospital EDs

Microscopic Polyangiitis With Selective Involvement of Central and Peripheral Nervous System : A Case Report

Background: Microscopic polyangiitis (MPA) is a necrotizing vasculitis that affects predominantly small-sized vessels in many organ systems. The disease generally causes glomerulonephritis, pulmonary damage, arthritis, and neuropathy. An exclusive involvement of both central nervous system (CNS) and peripheral nervous system (PNS) is extremely rare. Case Presentation: A 62-year-old woman was admitted to our hospital with a 3 months history of right foot drop, recently complicated by intense myalgia, arthralgia, and allodynia to tactile, vibratory, and pressure stimuli. Since blood tests revealed elevated inflammatory indexes, we suspected either infectious or immune-mediated disorders. Chest radiograph, blood culture series, and echocardiogram revealed normal findings, while urinalysis showed a bacterial infection that was successfully treated. The neurophysiological findings were compatible with multiple mononeuritis, and a brain MRI evidenced ischemic lesions of both basal ganglia and thalamus. A wide-spectrum autoantibody assay revealed the presence of high-titer perinuclear anti-neutrophil cytoplasmic antibodies specific for myeloperoxidase (MPO-ANCA). According to these findings, the diagnosis of MPA was made, and the patient was successfully treated with intravenous (IV) methylprednisolone, followed by two doses of rituximab. Conclusions: An assessment of both CNS and PNS should be included in the diagnostic evaluation of MPA. The involvement of the PNS may raise the risk of a relapsing course and treatment failure, therefore it should be considered in the choice of induction and maintenance therapy

HOPS-associated neurological disorders (HOPSANDs): linking endolysosomal dysfunction to the pathogenesis of dystonia

The homotypic fusion and protein sorting (HOPS) complex is the structural bridge necessary for the fusion of late endosomes and autophagosomes with lysosomes. Recent publications linked mutations in genes encoding HOPS complex proteins with the aetiopathogenesis of inherited dystonias (i.e. VPS16, VPS41, and VPS11). Functional and microstructural studies conducted on patient-derived fibroblasts carrying mutations of HOPS complex subunits displayed clear abnormalities of the lysosomal and autophagic compartments. We propose to name this group of diseases HOPS-associated neurological disorders (HOPSANDs), which are mainly characterized by dystonic presentations. The delineation of HOPSANDs further confirms the connection of lysosomal and autophagic dysfunction with the pathogenesis of dystonia, prompting researchers to find innovative therapies targeting this pathway

Peri-ictal and inter-ictal headache in children and adolescents with idiopathic epilepsy: a multicenter cross-sectional study.

PURPOSE: Headache in epileptic population ranges from 8% to 15%. The aim of this paper was to study the clinical and temporal characteristics of primary headache comorbidity in idiopathic epileptic children. METHODS: From June 2006 to June 2009, a cross-sectional multi-center study involving five Italian Child Neurology University Centers (two in Rome, one in Chieti, one in Naples, and one in L'Aquila) was conducted. Among 1,264 consecutively newly diagnosed, idiopathic, partial, or generalized, epileptic children, according to ILAE diagnostic criteria (aged between 5 and 15 years of age), we selected 142 children (11.2%) (130 of whom completed the study) who showed an associated peri-ictal and/or inter-ictal headache diagnosed according to the International Headache Society Criteria. Rare cases of "ictal epileptic headache", in which headache represents the sole ictal epileptic manifestation, were excluded from this study. RESULTS AND CONCLUSIONS: Post-ictal headaches were most frequent (62%). Pre-ictal headaches were less common (30%). Inter-ictal headaches were described in 57.6%. Clear migrainous features were present in 93% of pre-ictal and 81.4% of post-ictal headaches. Inter-ictal headaches meet criteria for migraines in 87%. The association between partial epilepsy and migraine without aura is most common and reported in 82% of our patients with peri-ictal headache and in 76.5% of patients with post-ictal headache

In vitro models of multiple system atrophy from primary cells to induced pluripotent stem cells

Multiple system atrophy (MSA) is a rare neurodegenerative disease with a fatal outcome. Nowadays, only symptomatic treatment is available for MSA patients. The hallmarks of the disease are glial cytoplasmic inclusions (GCIs), proteinaceous aggregates mainly composed of alpha-synuclein, which accumulate in oligodendrocytes. However, despite the extensive research efforts, little is known about the pathogenesis of MSA. Early myelin dysfunction and alpha-synuclein deposition are thought to play a major role, but the origin of the aggregates and the causes of misfolding are obscure. One of the reasons for this is the lack of a reliable model of the disease. Recently, the development of induced pluripotent stem cell (iPSC) technology opened up the possibility of elucidating disease mechanisms in neurodegenerative diseases including MSA. Patient specific iPSC can be differentiated in glia and neurons, the cells involved in MSA, providing a useful human disease model. Here, we firstly review the progress made in MSA modelling with primary cell cultures. Subsequently, we focus on the first iPSC-based model of MSA, which showed that alpha-synuclein is expressed in oligodendrocyte progenitors, whereas its production decreases in mature oligodendrocytes. We then highlight the opportunities offered by iPSC in studying disease mechanisms and providing innovative models for testing therapeutic strategies, and we discuss the challenges connected with this technique