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Introduction: Drug-drug interactions (DDIs) can reduce therapeutic efficacy and increase the duration and cost of hospitalization so that patients are sometimes exposed to significant complications and even death. Patients in the intensive care unit (ICU) are at higher risk of DDIs for a variety of reasons, including impaired absorption, decreased metabolism, and renal failure. The main objective of this study was to evaluate frequency, clinical ranking and risk factors of potential DDIs in the ICUs of 3 teaching hospitals in Ardabil. Methods : In this descriptive-analytical cross-sectional study, drug prescriptions 355 patients admitted to the ICUs were studied. Patient information including age, sex, diagnosis, number of prescribers, number of drugs, length of stay, and status of patients' discharge (recovery or death) were recorded and checked using the online software up to date and the book Drug Interaction Facts. Finally, the data were statistically analyzed using the SPSS software. Results : The number of patients studied was 355. The mean age of the patients were 51.88 ± 23.22 years, and on average, 8.45 drugs had been prescribed for each patient. The total number of DDIs was 1597 among which class X was 1.4%, class D was 26.2%, and class C was 67.7%. Four hundred ninety-seven unique pairs of DDIs were identified. Age, number of prescribed drugs and length of stay in ICU were associated with prevalence of DDIs. Age and number of drugs were also identified as the risk factors of patients' discharge caused by death. Conclusion : DDIs can complicate health state of patients in ICUs and may increase the length of hospital stay. Setting up computerized systems to alert drug interactions in hospital wards and pharmacotherapeutic intervention by clinical pharmacist can minimize DDIs. [ABSTRACT FROM AUTHOR]

Following the introduction and application of pesticides in human life, they have always been along with health concerns both in acute poisoning and chronic toxicities. Neurotoxicity of pesticides in chronic exposures has been known as one of the most important human health problems, as most of these chemicals act through interacting with some elements of nervous system. Pesticide-induced neurotoxicity can be defined in different categories of neurological disorders including neurodegenerative (Alzheimer, Parkinson, amyotrophic lateral sclerosis, multiple sclerosis), neurodevelopmental (attention deficit hyperactivity disorder, autism spectrum disorders, developmental delay, and intellectual disability), neurobehavioral and neuropsychiatric (depression/suicide attempt, anxiety/insomnia, and cognitive impairment) disorders some of which are among the most debilitating human health problems. In this review, neurotoxicity of pesticides in the mentioned categories and sub-categories of neurological diseases have been systematically presented in relation to different route of exposures including general, occupational, environmental, prenatal, postnatal, and paternal. [ABSTRACT FROM AUTHOR]

Objective(s): Diabetes is a metabolic disease with an increasing prevalence for which finding new and efficient therapeutic approaches has always been a challenge. Preserving integrity and functionality of pancreatic β-cells as the only source of insulin in the body is such a case. To achieve this goal different cellular targets have been proposed among which pancreatic estrogen receptors have gotten much attention. In this work, we evaluated the integrity and function of islets of Langerhans under the influence of factors known to intervene with estrogen receptors. Cadmium, a toxic heavy metal, has been recently shown to interact with estrogen receptors but its toxicity in the pancreatic islets regarding this mechanism remains unclear. Materials and Methods: Isolated islets of Langerhans from the pancreas of rats were grouped and treated with cadmium chloride and also cadmium chloride plus β-estradiol. After 24 hr incubation, parameters of cellular viability, oxidative stress, apoptosis, and insulin secretion were measured. Results: The results indicated that cadmium reduced viability of the islets along with an increase in the formation of reactive oxygen species and apoptosis markers, and β-estradiol, in turn, was able to alleviate these disturbances to some extent, implicating the protective role of β-estradiol against pancreatic toxicity of cadmium. Conclusion: It can be concluded that modification of estrogen receptors in the endocrine pancreas and especially β-cells may be a promising target to find a new therapeutic strategy for diabetes and even uncovering mechanisms of environmental toxicants that have been known as risk factors of diabetes. [ABSTRACT FROM AUTHOR]