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    Cancers Falsehoods and also Harmful Facts about Fb along with other Social networking: A Brief Document.

    of AChA infarcts. The objective of the study was to determine the prevalence of anxiety symptoms and describe the association with illness severity, quality of life (QOL) and current medications among patients with BPAD who are currently in remission. A descriptive cross-sectional study conducted among outpatient clinic patients at the University Professorial Unit of University of Ruhuna, Sri Lanka. The study population consisted of patients diagnosed with BPAD and who are currently in remission. Anxiety symptoms among BPAD patients were assessed using the DASS-21 anxiety subscale and QOL was assessed using WHOQoL-BREF. Medications and severity of illness related information were gathered from both the patent and from their medical records. The study population consisted of 145 patients. The prevalence of anxiety among patients with BPAD who are currently in remission was 48.3 % (95 %CI 40.0-56.6). Multiple logistic regression revealed that being anxious was independently associated with currently not being married (aOR 2.92) and currently not being employed (aOR 2.1). Presence of anxiety significantly reduced the QOL in all the domains. Having anxiety was significantly associated with having one or more relapses within the past three years (aOR 4.1), one or more hospital admissions within the past three years (aOR 6.1), needing more psychoactive medications to maintain a euthymic state (aOR 7.7), and one or more suicidal attempts in the past (aOR 6.5). Anxiety was highly prevalent among patients with BPAD. Those with anxiety experienced significantly lower QOL and were found to be having significantly high adverse outcomes from the disease. mTOR inhibitor V.OBJECTIVE We address two questions relevant to infants’ exposure to potentially toxic arsenolipids, namely, are the arsenolipids naturally present in fish transported intact to a mother’s milk, and what is the efficiency of this transport. METHODS We investigated the transport of arsenolipids and other arsenic species present in fish to mother’s milk by analyzing the milk of a single nursing mother at 15 sampling times over a 3-day period after she had consumed a meal of salmon. Total arsenic values were obtained by elemental mass spectrometry, and arsenic species were measured by HPLC coupled to both elemental and molecular mass spectrometry. RESULTS Total arsenic increased from background levels (0.1 μg As kg-1) to a peak value of 1.72 μg As kg-1 eight hours after the fish meal. The pattern for arsenolipids was similar to that of total arsenic, increasing from undetectable background levels ( less then 0.01 μg As kg-1) to a peak after eight hours of 0.45 μg As kg-1. Most of the remaining total arsenic in the milk was accounted for by arsenobetaine. The major arsenolipids in the salmon were arsenic hydrocarbons (AsHCs; 55 % of total arsenolipids), and these compounds were also the dominant arsenolipids in the milk where they contributed over 90 % of the total arsenolipids. CONCLUSIONS Our study has shown that ca 2-3 % of arsenic hydrocarbons, natural constituents of fish, can be directly transferred unchanged to the milk of a nursing mother. In view of the potential neurotoxicity of AsHCs, the effects of these compounds on the brain developmental stage of infants need to be investigated. mTOR inhibitor Fluoride compounds are known as hazardous environmental pollutants that can enter the body with drinking water. Chronic exposure to fluoride leads to development of oxidative stress and can lead to activation of nuclear factor κB (NF-κB). The aim of this work is to clarify the role of NF-kB activation in production of reactive nitrogen and oxygen species, activity of antioxidant enzymes and intensity of lipid peroxidation (LPO) in gastric mucosa of rats during chronic fluoride intoxication. MATERIALS AND METHODS We carried out the study on 18 mature male rats of the Wistar line. The animals were divided into 3 groups control animals (6), group of chronic fluoride intoxication (6), and animals (6), which received the NF-κB inhibitor, namely ammonium pyrrolidine dithiocarbamate (PDTC) in a dose of 76 mg / kg (iNF-κB group) during modeling of chronic fluoride intoxication. To assess the development of oxidative stress we studied superoxide production (O2-), activity of superoxide dismutase (SOD), catalase (CAT) and concentration of free malondialdehyde (MDA). We also assessed NO production and concentration of its metabolites (peroxynitrite, nitrosilated thiol groups, nitrites). RESULTS Chronic fluoride intoxication leads to NO hyperproduction with subsequent increase in concentration of its later metabolites (peroxynitrite, nitrosilated thiol groups, nitrites). Production of O2- increases, SOD activity decreases, CAT activity increases and MDA concentration also increases. Inhibition of NF-kB activation by PDTC normalizes the parameters studied. CONCLUSIONS Activation of NF-κB during chronic fluoride intoxication leads to the development of hyperproduction of NO and development of oxidative-nitrosative stress. Patients with acute olfactory disorders typically present to the otolaryngologist with both acute hyposmia and less often with anosmia. With the onset of COVID-19 we have noticed an increase in the number of patients who have presented with new onset of complete smell loss to the senior author’s practice in Tehran, Iran. This anosmia and the frequency with which patients present is highly unusual. Coronaviruses have been known to cause common cold symptoms. COVID-19 infections have been described as causing more severe respiratory infections and the symptoms reported by authors from Wuhan, China have not specifically included anosmia. We describe patients who have presented during a two-week period of the COVID-19 pandemic with complete loss of sense of smell. Most had either no symptoms or mild respiratory symptoms. Many had a normal otolaryngologic exam. A relationship between COVID-19 and anosmia should be considered during the pandemic. We hypothesize that the mechanism of injury is similar to that of other coronavirus infections that cause central and peripheral neurologic deficits.