The mechanism of the uranyl ion photoinitiated polymerization of acrylamide has been studied in aqueous solutions and in acetone. Steady‐state and dynamic luminescence quenching studies show that initiation proceeds through a thermally activated bimolecular interaction between *UO22+ and monomer involving electron or charge transfer. Results from various studies show that the mechanism previously suggested for this process, involving energy transfer, is incorrect. ESR studies suggest that initiation involves formation of a uranium(V)‐radical pair. Polymerization then proceeds through a radical mechanism in both solvents. With the exception of the chloride, the yields do not depend upon the counter‐ion. Polymer is frequently produced with adsorbed uranyl ions, which can be separated by dialysis. In agreement with previous studies, photopolymerization proceeds without significant overall reduction in the uranyl concentration. It is shown that this is probably due to any intermediate uranium(V) being reoxidized by monomer, with concurrent thermal initiation of polymerization.
Introduction Alcohol consumption has devastating psychosocial and health consequences, with effects on cognitive functions. Recent studies have highlighted that patients with diagnosis of alcohol dependence syndrome have cognitive deficits in executive function, visuospatial ability, attention, procedural memory, verbal fluency and processing speed. Objectives The aim of this study is to characterize the sociodemographic and clinical patterns of the study sample and the cognitive deterioration severity and type. Methods A retrospective observational study was conducted with patients who had alcohol use disorder diagnosis at Dual Pathology Outpatient and Inpatient Unity, Psychiatry Department, at Coimbra Hospital and University Center, Portugal. Patients were admitted from 1/1/2016 and 30/09/2021, and submitted at neuropsychological structured evaluation. From the initial sample, major neurocognitive disorder, intellectual development disorder, cerebrovascular accident, traumatic brain injury and neurosurgery were excluded. Results The results show significant cognitive impairment in executive function, memory, verbal fluency and visuospatial ability. Conclusions Our results support the hypothesis of widespread impairment resulting from alcohol consumption. Cognitive impairment can limit the psychotherapeutic intervention, the adherence to pharmacological therapy and abstinence maintenance. The sheer presence of alcohol use disorder should encourage a neuropsychological evaluation. Further studies are needed in this area to prevent and outline an early intervention. Disclosure No significant relationships.
IntroductionDrug use and misuse continue to create public health challenges in the world, leading to overdose deaths, infections, and other chronic health conditions. Illegal addictive drugs can lead to functional or structural impairment of the central nervous system (CNS). Because clinical findings alone are often nonspecific, and some patients are unlikely to admit substance abuse, the neuroimaging may play an important role in establishing the diagnosis and initiating treatment.ObjectivesWe aim to provide an overview of the structural imaging findings on computed tomography (CT), magnetic resonance (MR) imaging related to chronic and acute abuse of commonly addictive substances, including cannabis, alcohol, cocaine, and opioids.MethodsNon systematic review of the literature on the subject and description of three clinical cases.ResultsPathomecanisms of drugs misuse include excitotoxicity, which may lead to an acute or subacute leukoencephalopathy, and vascular complications, including vasoconstriction, vasculitis, or hypertension, which may lead to intracranial hemorrhage or ischemia. Alcohol abuse may lead to Wernicke-Korsakoff syndrome, revealing in MR bilateral symmetrical hyperintense signals on T2-weighted; Marchiafava-Bignami disease (MBD) is a very rare condition which may present hypodense lesions in the corpus callosum; and alcoholic cerebellar degeneration is a common type of acquired cerebellar ataxia and may present cerebellar volume loss localized to the anterior superior vermis. One of our clinical cases is a female, 39 years, and present cocaine induced multifocal leukoencephalopathy, associated with inflammatory/immune mediated mechanism. Other clinical case (female, 24 years) demonstrate spongiform leukoencephalotpathy from “chasing” heroin, with a characteristic presentation.ConclusionsThe main pathomechanisms related to the abuse of drugs are ischemia, hemorrhage, and leukoencephalopathy related to excitotoxicity of the drug or its derivatives. Clinical findings are nonspecific, highlighting the need to recognize these complications at both CT and MR imaging. Therefore, diagnostic imaging modalities can play a pivotal role in the recognition and timely management of drug-related complications in the CNS.Disclosure of InterestNone Declared
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