Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatobiliary imaging with the various technetium-labeled IDA compounds is more than 90% sensitive and specific for the diagnosis of acute cholecystitis. Causes of false-positive studies include chronic cholecystitis, cystic-duct obstruction by tumor, prolonged fasting, the nonfasting state, pancreatitis, alcoholism, parenteral hyperalimentation, and severe intercurrent illness. A case of congenital absence of the gallbladder is submitted as another cause of a false-positive scan.
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PMID:Congenital absence of the gallbladder: another cause of false-positive hepatobiliary image. 672 25

We studied the clinical features, pathology, and molecular genetics of a family (Mo) with an autosomal dominant disinhibition, frontal lobe dementia, parkinsonism, and amyotrophy. We examined seven affected members and gathered clinical information on another six. The mean onset was at age 45 years. Personality and behavioral changes (disinhibition, withdrawal, alcoholism, hyperphagia) were the first symptoms in twelve. There was early memory loss, anomia, and poor construction with preservation until late of orientation, speech, and calculations. All affected members examined had rigidity, bradykinesia, and postural instability. Mean duration to death was 13 years. We studied the neuropathology of six individuals, five of whom had been examined in life. There was atrophy and spongiform change in the frontotemporal cortex, and neuronal loss and gliosis in the substantia nigra and amygdala. Two individuals, including one with fasciculations and muscle wasting, had anterior horn cell loss. There were no Lewy bodies, neurofibrillary tangles, or amyloid plaques. We call this disorder the "disinhibition-dementia-parkinsonism-amyotrophy complex" (DDPAC), based on the clinical syndrome found in this family and linkage to chromosome 17.
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PMID:Clinical characteristics of a family with chromosome 17-linked disinhibition-dementia-parkinsonism-amyotrophy complex. 793 62

Wernicke's encephalopathy (WE) is a thiamine deficiency disorder and is characterized clinically by the triad of ocular abnormalities, ataxia and disturbances of consciousness. We report on 3 patients with WE, of whom 2 had insufficient thiamine substitution. In the first patient symptoms disappeared during thiamine substitution. In the second patient acute WE was the terminating event in the sequence of parenteral nutrition, lactic acidosis and cardio-pulmonary decompensation. Possibly due to hereditary deficits WE developed in the third patient despite sufficient thiamine substitution. Attention to thiamine deficiency should be paid in all patients with history of alcoholism, malnutrition, malabsorption, tumors, inflammation, other severe diseases and in parenteral hyperalimentation. In order to prevent WE thiamine should be substituted with at least 100 mg/day i.v. or i.m.
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PMID:Wernicke's encephalopathy--causes to consider. 804 22

Two hundred one non-treatment seeking women with alcoholism, anxiety disorders, alcoholism and anxiety disorders, or neither alcoholism nor anxiety disorders were interviewed to assess core psychopathology associated with eating disorders using the Eating Disorders Examination and DSM-IIIR psychiatric diagnoses using the Schedule of Affective Disorders and Schizophrenia-Lifetime version. Alcoholic women had significantly higher mean scores on each of the Eating Disorders Examination subscales of Restraint, Overeating, Eating Concern, Shape Concern, and Weight Concern compared with nonalcoholic women. Women with anxiety disorders had significantly elevated scores on subscales of Overeating, Eating Concern, and Weight Concern compared with women without anxiety disorders. Women with both alcoholism and anxiety disorders had higher rates of bulimia nervosa and/or eating disorder NOS compared with women with either disorder alone. Implications of these findings are discussed in the context of the co-morbid association between alcoholism, eating disorders, and anxiety disorders.
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PMID:Eating pathology among women with alcoholism and/or anxiety disorders. 890 68

The prevalence, consequences, and resistance to treatment of obesity make it one of the most difficult psychological and medical problems in society today. The incidence of obesity is greater in Mexican Americans than in Caucasians. The purpose of this study was to apply the Transtheoretical Model of Behavior Change on a sample of Mexican American women in weight-loss study. Questionnaires assessing the stages and processes of change were shortened, translated, and administered to subjects. Cluster analyses were conducted to determine the stage of change profiles, with five distinct profiles emerging. These profiles are consistent with those reported in previous research on smoking, psychotherapy, alcoholism, and overeating. Relationships among stages, processes, and profiles of change were examined and found to be consistent with previous research. This study supports the use of the Transtheoretical Model with Mexican American women who were enrolled in a behaviorally oriented weight-loss program. Results of the study are limited owing to a small sample size; however, it does provide a foundation to incorporate Hispanic populations in future studies pertaining to stages and processes of behavior change.
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PMID:Application of the transtheoretical model of behavior change for obesity in Mexican American women. 976 1

The relationship between desirable and undesirable aspects of masculinity and femininity and drinking and eating was investigated. A sample of 144 university women in Australia completed questionnaires that assessed masculinity and femininity, reported drinking, alcohol dependence, eating restraint, frequency of dieting, and overeating. Evidence of a common underlying dimension linking aspects of problem drinking and overeating to undesirable masculine characteristics was found. The results are consistent with the view that women engage in excessive consummatory behaviors such as binging to deal with their gender-role conflict.
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PMID:Relation of drinking and eating to masculinity and femininity. 987 67

Ethanol toxicity on liver is a function of duration of alcoholism, amount of daily intake of alcohol and patient's nutrition. The threshold of alcohol toxicity on the liver is about 40 g of ethanol daily in men and 20-30 g in women, however liver cirrhosis develops in no more than 8-20% of patients exceeding this values. Ethanol is oxidized in the liver to acetaldehyde--a compound considerably more toxic than ethanol itself. Despite small amount of alcohol dehydrogenase (ADH) found in gastric mucosa, the metabolism of ethanol in this site may have an important hepatoprotective effect. The oxidation of ethanol is associated with a change of hepatocyte redox homeostasis, which leads to a number of metabolic disorders such as lactic acidosis, hyperlipidaemia and hyperuricaemia. Chronic ethanol consumption does not influence ADH activity, but has a profound stimulatory effect on microsomal enzymes, in particular cytochrome CYP2E1. This fact is responsible for development in alcoholic liver associated with rise of oxygen consumption, excessive production of free radicals and increased metabolism of ethanol, vitamin A and testosterone. Ethanol and acetaldehyde have a deleterious effect, both the direct and indirect, on hepatocytes e.g., generating radical oxygen species and damaging intestinal mucosal barrier. Cellular oxidative stress that is caused by both an excess of free radicals and the antioxidatives' deficiency (glutathion, vitamin E, phosphatidylcholine), may be the principal factor responsible for progression of alcoholic liver disease. Among other factors accelerating alcohol-related liver lesion there are certain drugs, high fat diet, infection with HCV and genetic factors (female sex, enzymatic polymorphic forms of ADH and ALDH, hemochromatosis). Great importance in pathogenesis of necrotic and inflammatory hepatic events is being attributed to portal endotoxaemia and cytokines induced within the liver, in particular TNF-alpha and interleukin 8. These cytokines play a key role in development of alcoholic hepatitis, which clinical severity ranges from subclinical to fatal forms. Apart from abstinence, the treatment of alcohol liver disease is based on hyperalimentation, since alcoholism is generally associated with protein malnutrition. In severe forms of alcohol hepatitis corticosteroids are recommended.
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PMID:[Alcoholic liver disease]. 1290 Dec 71

In non-addicted patients, several states such as alcoholism, previous valvular heart disease or prosthetic valve replacement, immunodeficiency states, prolonged intravenous hyperalimentation, permanent pacemakers, and some congenital heart diseases can provide the predisposing factors for tricuspid valve endocarditis. It is an extremely rare occurrence in patients with normal native cardiac valves. In this report, we present a case of a 67-year-old woman with tricuspid native valve endocarditis related to Candida parapsilosis which is a very rare cause of infective endocarditis and carries a high mortality risk. An operation was indicated for the patient due to persistent enlarging vegetation on tricuspid valve, severe tricuspid regurgitation, septic pulmonary emboli and finally uncompensated respiratory and heart failure. She underwent tricuspid valve replacement with bioprothesis three years ago and now she is in a satisfactory condition without any medical treatment.
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PMID:Candida parapsilosis tricuspid native valve endocarditis: 3-year follow-up after surgical treatment. 1829 75

A unique challenge posed by advancing scientific knowledge about the biology of human behavior is how to integrate that understanding with the desire to hold ourselves--and one another--morally accountable. As human beings, we are something more than just passive agents whose behavior is the sum product of biologic determinism. Because of the existence of the mind, we are also active agents with the capacity to influence, at least to some extent, our own destinies. Behavior may be determined, but it is not predetermined. We are one of its determinants. Misconduct by a person of sound mind should not be attributed improperly to brain pathology. On the other hand, suffering, legitimate mental disorder, and associated impairments should not be trivialized. Historically, persons who once were labeled "lazy" are often more appropriately understood by modern standards as clinically depressed. Frequently they are more in need of pharmacologic treatments that alter brain chemistry than "a kick in the behind." Gluttony, one of the original cardinal sins, is often more properly understood as morbid obesity, a condition that deserves appropriate medical care. Persons who have alcoholism, once judged morally as "bums in the gutter," are more frequently referred to treatment facilities, such as The Betty Ford Clinic. One should not approach the issue of human sexual behavior without at least some appreciation of moral values and scientific research. Although clearly some persons choose to act in a sexually selfish and self-indulgent fashion with wanton disregard, others seem to be more genuinely burdened and struggle to integrate their sexual desires into an otherwise healthy and fully responsible lifestyle. When a person, whether male or female, seems to be so driven that it becomes difficult to master erotic desires and he or she experiences difficulty serving his or her own best longterm interests, the concept of sexual compulsivity seems to be relevant. Ultimately, a better understanding of any associated neuropathologies may help to facilitate future treatments and public acceptance. The possibility exists, at least in some instances, that a sexually compulsive individual is less an example of a bad person deserving of punishment than a "broken mind" in need of repair. In time, increased knowledge about the precise workings of the brain in reciprocally initiating and sustaining the sexual interests of the mind may facilitate a much clearer appreciation of the issues at hand.
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PMID:Basic science and neurobiological research: potential relevance to sexual compulsivity. 1899 3

The experimental question is whether hypothalamic opioids, known to stimulate consummatory behavior, control a link to the nucleus accumbens (NAc). It was hypothesized that opioids injected in the hypothalamic paraventricular nucleus (PVN) alter the balance of dopamine (DA) and acetylcholine (ACh) in the NAc in a manner that fosters appetite for food or ethanol. Rats were implanted with two guide shafts, one in the NAc to measure extracellular DA and ACh by microdialysis and the other in the PVN for microinjection of opioid mu- and delta-agonists, an antagonist, or saline vehicle. The compounds tested were morphine, the mu-receptor agonist [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-Enkephalin (DAMGO), the delta-receptor agonist D-Ala-Gly-Phe-Met-NH2 (DALA), and the opioid antagonist naloxone methiodide (m-naloxone). Morphine in the PVN increased the release of accumbens DA (+41%) and decreased ACh (-35%). Consistent with this, the opioid antagonist m-naloxone decreased DA (-24%) and increased ACh (+19%). In terms of receptor involvement, DAMGO dose-dependently increased DA to up to 209% of baseline. Simultaneously, ACh levels were markedly decreased to 55% of baseline. The agonist DALA produced a smaller but significant, 34% increase in DA, without affecting ACh. In contrast, control injections of saline had no significant effect. These results demonstrate that mu- and delta-opioids in the PVN contribute to the control of accumbens DA and ACh release and suggest that this circuit from the PVN to the NAc may be one of the mechanisms underlying opiate-induced ingestive behavior as well as naltrexone therapy for overeating and alcoholism.
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PMID:Opioids in the hypothalamus control dopamine and acetylcholine levels in the nucleus accumbens. 1994 54


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