Community Interventions to Promote Mental Health and Social Equity.

(Reprinted with permission from (2020) 21: 35).

Exploring well-being: medical students and staff.

Background: Mental illness in young people is a major public health challenge, with a higher prevalence amongst medical students. This study explores the perspectives of both students and staff in relation to the provision of well-being support within one medical school in the United Kingdom.

Methods: A total of 17 second-year medical students and five members of academic and well-being staff at Liverpool Medical School participated in one-to-one semi-structured interviews.

Adverse effect of catechol-O-methyltransferase (COMT) Val158Met met/met genotype in methamphetamine-related executive dysfunction.

Introduction: The Val allele of the Val158Met single-nucleotide polymorphism of the catechol-o-methyltransferase gene (COMT) confers greater catabolism of dopamine (DA) in the prefrontal cortex (PFC) than the Met allele. Met/Met homozygotes typically outperform Val-carriers on tests of executive function (EF), perhaps resulting from increased DA bioavailability. Methamphetamine (METH) causes large releases of DA, which is associated with neurotoxicity and executive dysfunction in chronic METH users.

Community Interventions to Promote Mental Health and Social Equity.

Purpose Of Review: We review recent community interventions to promote mental health and social equity. We define community interventions as those that involve multi-sector partnerships, emphasize community members as integral to the intervention, and/or deliver services in community settings. We examine literature in seven topic areas: collaborative care, early psychosis, school-based interventions, homelessness, criminal justice, global mental health, and mental health promotion/prevention.

Peripheral ammonia and blood brain barrier structure and function after methamphetamine.

An effect of the widely abuse psychostimulant, methamphetamine (Meth), is blood-brain-barrier (BBB) disruption; however, the mechanism by which Meth causes BBB disruption remains unclear. Recently it has been shown that Meth produces liver damage and consequent increases in plasma ammonia. Ammonia can mediate oxidative stress and inflammation, both of which are known to cause BBB disruption.

Multimodality treatment of intrahepatic cholangiocarcinoma: A review.

Intrahepatic cholangiocarcinoma (iCCA) is the second most common primary hepatic cancer in the United States. Currently, curative treatment involves aggressive surgery. Chemotherapy and radiation treatments have been used for unresectable tumors with some success.

Epidemiology of severe sepsis: 2008-2012.

Introduction: Severe sepsis continues to be a significant burden on society.

Methods: Using the International Classification of Diseases, Ninth Revision, Clinical Modification codes, we analyzed the Healthcare Cost and Utilization Project National Inpatient Sample in order to estimate epidemiologic trends of severe sepsis from the years 2008 to 2012. The 2010 US Census, which included 308,745,538 individuals, was used to calculate incidence per 100,000 persons.

Suprahepatic Gallbladder.

Introduction: Suprahepatic gallbladders have been reported in the literature dating back to 1965. However, their etiology and consequences remain unclear.

Methods: A case of a patient being treated for biliary dyskinesia with an incidental finding of suprahepatic gallbladder is presented along with a literature review on the causes, effects, and management of a suprahepatic gallbladder.

Ammonia mediates methamphetamine-induced increases in glutamate and excitotoxicity.

Ammonia has been identified to have a significant role in the long-term damage to dopamine and serotonin terminals produced by methamphetamine (METH), but how ammonia contributes to this damage is unknown. Experiments were conducted to identify whether increases in brain ammonia affect METH-induced increases in glutamate and subsequent excitotoxicity. Increases in striatal glutamate were measured using in vivo microdialysis.

Methamphetamine causes acute hyperthermia-dependent liver damage.

Methamphetamine-induced neurotoxicity has been correlated with damage to the liver but this damage has not been extensively characterized. Moreover, the mechanism by which the drug contributes to liver damage is unknown. This study characterizes the hepatocellular toxicity of methamphetamine and examines if hyperthermia contributes to this liver damage.

Neurotoxicity of methamphetamine and 3,4-methylenedioxymethamphetamine.

Amphetamines are a class of psychostimulant drugs that are widely abused for their stimulant, euphoric, empathogenic and hallucinogenic properties. Many of these effects result from acute increases in dopamine and serotonin neurotransmission. Subsequent to these acute effects, methamphetamine and 3,4 methylenedioxymethamphetamine (MDMA) produce persistent damage to dopamine and serotonin nerve terminals.

Peripheral ammonia as a mediator of methamphetamine neurotoxicity.

Ammonia is metabolized by the liver and has established neurological effects. The current study examined the possibility that ammonia contributes to the neurotoxic effects of methamphetamine (METH). The results show that a binge dosing regimen of METH to the rat increased plasma and brain ammonia concentrations that were paralleled by evidence of hepatotoxicity.