Lovastatin is used for the treatment of hypercholesterolemia. It functions by inhibiting the enzyme, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (EC 1.1.1.34), that is required for the conversion of 3-hydroxy-3-methylglutaryl-coenzyme A to mevalonic acid. Since biosynthesis of both cholesterol and coenzyme Q (CoQ) requires mevalonic acid as a precursor, it was considered that lovastatin therapy would also result in a lowering of cellular CoQ levels. This study was conducted to determine whether lovastatin treatment does decrease CoQ levels and whether such decreases can be prevented by CoQ supplementation. Forty-five adult male Holtzman rats were randomly assigned to one of three treatment groups. Controls were fed ground laboratory rat chow ad libitum. The other two groups were fed ground laboratory rat chow containing 400 mg of lovastatin per kg of diet ad libitum. One of the lovastatin-fed groups received CoQ10 (15 mg per kg of body weight) daily via stomach intubation. After 4 weeks, samples of heart, liver, and blood were analyzed for CoQ concentrations. Results indicated that CoQ concentrations in all tissues analyzed were decreased in lovastatin-treated rats. Lovastatin-treated animals that were supplemented with CoQ10 had blood, heart, and liver CoQ10 CoQ10 (the subscript indicates the number of isoprene units in the side chain) is an important participant in electron transport in the respiratory chain in mammalian mitochondria (2-9). Evidence has been accumulating over the last two decades that this coenzyme may be important in a variety of clinical conditions. Essential hypertension, periodontal disease, lichen planus, doxorubicin-induced cardiotoxicity, cardiac output in heart patients, renal ischemia survival, and hepatic damage by antineoplastic drugs (mitomycin C and 5-fluorouracil dry syrup) have been reported to improve or be mitigated by CoQ10 treatment (10-24). It is likely and very important that some, if not most, of the side effects associated with the use of lovastatin in treatment of hypercholesterolemia are due to a decrease in CoQ10 levels.Known side effects of lovastatin include marked, persistent increases in serum transaminases, myalgia, myositis, increased creatine kinase levels, renal failure, and, in mice, tumors of liver, lung, and stomach (2). Therefore, it is plausible that many of the side effects associated with the use of lovastatin in treatment of hypercholesterolemia are due to a decrease in CoQ10 levels.This study in the rat model was undertaken to determine whether lovastatin treatment does indeed decrease CoQ levels and whether such decreases can be prevented by CoQ supplementation. METHODSForty-five adult male Holtzman rats were randomly assigned to one of three treatment groups (15 rats per group). Group I (controls) were fed ground laboratory rat chow (Purina) ad libitum. Groups II (lovastatin treatment group) and III (lovastatin plus CoQ treatment group) were fed ground laboratory rat chow containing 400 mg of lovastatin per kg of diet ad libitum. The lov...

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Preventing negative health outcomes following marital transitions can promote personal recovery and well-being. We used the Health and Retirement Study (HRS) (2012, 2014) to test whether social relationship quality moderated the association between marital transition and change in depressive symptomology among U.S. adults aged 50 and older (n = 3,705). Marital status transitions between 2012 and 2014 included remained married/partnered, divorced/separated, and widowed. Depressive symptomology was measured using the Center for Epidemiological Studies Depression Scale 8 Short Form (CES-D 8). Social support, social contact, and social strain were indicators of social relationship quality. Change in depressive symptomology was modeled using autoregressive multiple regression. Social relationship quality appeared to influence depressive symptomatology for those experiencing divorce/separation. Compared to individuals who remained married/partnered, depressive symptomatology in those experiencing separation/divorce decreased among those reporting low social support, increased among those reporting high social support, and increased among those who reported low social strain. Limitations and clinical implications are discussed.

Recent research shows that unsuccessful tender offers may affect target share returns for two years past the offer's announcement. This note examines target returns in the interim between the announcement and one year after the offer's withdrawal. Analyzing a recent sample of targets that did not get another bid in the year following a failed tender offer, this study reaches two conclusions. First, all of an offer's premium disappears by the time failure becomes public. Second, excess returns are zero in the post‐failure year. An explanation that is based on the causes of the tender offers' failures is presented.

Despite the burgeoning literature linking social integration and cognitive function, studies that focus on the potential cognitive benefits associated with friendships are limited. Using eight waves of nationally representative data from the Health and Retirement Study (1998-2012), we investigated whether two distinct forms of social interaction with friends—(1) getting together for a chat/social visit and (2) providing informal helping to friends—were associated with cognitive function (assessed with a modified version of the Telephone Interview for Cognition Status) among individuals aged 50 and older (person N = 29,951) over a 14-year observation period. Multilevel models revealed robust evidence for within-person linkages between both forms of social interaction with friends and better cognitive function. The study findings are discussed in the context of declining social interaction with one’s friends reported over the past several decades in the United States, which are partly driven by increasing leisure trends characterized by in-home entertainment.