Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Comparative studies of the differences in elderly patients with and without cardiovascular disorders were made in regard to complications occurring during and after operation. The subjects included 38 patients (6 men and 32 women) aged 70 to 99 years (mean: 84 years) at Nagoya City Kouseiin Geriatric Hospital who had orthopedic surgery under general anesthesia, between March 1990 and October 1992. Diseases identified in these subjects were sequelae of cerebrovascular disease (38 subjects), heart disease (22 subjects), hypertension (9 subjects), senile dementia (6 subjects), Parkinson's disease (5 subjects), malignant disease (3 subjects) and diabetes mellitus (2 subjects). They were initially divided into 2 groups according to ultrasonic cardiography: a normal group comprising 20 patients without cardiovascular abnormalities, and a disorder group comprising 18 patients with reduction of left ventricule function, left ventricular hypertrophy and/or valvular disease (more than moderate). All subjects were examined with regard to age, weight, the nutrition index proposed by Onodera, activity of daily living (ADL), cardiac output, left ventricular ejection fraction, serum level of BUN and albumin etc. Moreover, the disorder group subjects were divided into 2 groups according to the presence or absence of heart failure occurring after surgery. In addition to the above-mentioned, we also studied the duration of surgery and anesthesia, and water balance during and after surgery. Results showed that the ADL and nutrition index in the disorder group were lower compared to the normal group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparative studies on complications occurring during and after surgery in elderly patients with and without cardiovascular disorders]. 829 52

Sudden death has been reported in Parkinson's disease (PD), but the cause of death has not been fully clarified. A prolonged QT interval on the electrocardiogram (ECG) of patients without cardiac dysfunction is an independent risk factor for sudden death regardless of etiology. QT prolongation is believed to be related to cardiac autonomic dysfunction. We suspected that QTc intervals, as well as QT intervals, might be related to the clinical characteristics of PD and to the function of the autonomic nervous system in PD and also postulated a relationship between QTc prolongation and sudden death in PD. We investigated the QTc intervals on the ECGs of 48 PD patients (20 males 28 females) aged 64.5 +/- 9.4 years and 44 controls aged 60.0 +/- 8.2 years, and excluded patients with heart disease. QTc intervals were determined by using ECG-8210, ECAPS12 (Nihon-Kohden). The autonomic nervous system was evaluated by measuring CVR-R and performing orthostatic tests. Since the autonomic nervous system is considered to play an important role in the mechanism of diurnal blood pressure variation (DBPV), we assessed DBPV in 19 PD patients by determining blood pressure automatically every 30 minutes for 24 hours with an ambulatory blood pressure monitor (90202, Space Lab). QTc intervals were significantly longer in the PD patients (412 +/- 26 msec) than in the controls (401 +/- 14 msec) (p < 0.02, t-test). QTc prolongation was significantly correlated with severity according to Hoehn and Yahr stage (r = 0.509, p < 0.001), orthostatic hypotension, and decreased CVR-R ratio but not with duration of PD or treatment. The incidence of QTc prolongation was higher in the PD patients with non-dipper type DBPV than in those with the dipper type. Two of the PD patients died suddenly. Their QTc intervals a year before their death were 451 msec and 470 msec, respectively, suggesting that cardiac dysautonomia may have been involved in the cause of their death. These findings suggest that cardiac autonomic dysfunction is related to the severity of PD, and that it may predispose such patients to cardiac disorders including sudden cardiac death.
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PMID:[Prolonged QTc intervals in Parkinson's disease--relation to sudden death and autonomic dysfunction]. 867 3

The patient with Parkinson's disease often needs concomitant treatment for disorders that accompany the disease, such as depression, insomnia or constipation, or for frequent concomitant alterations such as dizziness, high blood pressure or heart disease. The many drugs that can worsen motor symptoms in Parkinson's disease must be avoided, especially if use will be prolonged. Not all drugs that induce or aggravate parkinsonism have the same potency. We describe 3 groups: 1) drugs that invariably induce or aggravate parkinsonism if taken long enough or at high enough doses; 2) drugs that only provoke parkinsonism in some individuals, and 3) drugs that interfere with the action of levodopa. Knowledge of these drugs is essential for all doctors who treat patients with Parkinson's disease.
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PMID:[Drug treatment of frequent disorders in patients with Parkinson's disease]. 869 42

Methionine metabolism and transmethylation are central to the metabolism and differentiation of all known cells. In enkaryotic organisms, methionine metabolism and transmethylation are of paramount importance in modification and regulation of proteins, lipids, and nucleic acids. The differential methylation of genes regulates their expression in the myriad of cells in eukaryotic organisms. Disruption and abnormalities in methionine metabolism and transmethylation seems to be associated with the major diseases of mankind, including cancer, heart disease, aging, obesity, and Parkinson's disease. In this review, we describe how aberrant and abnormal methionine metabolism and transmethylation are related to these major diseases. Most importantly, we review and hypothesize how the developing therapeutic recombination methioninase (rMETase) can be utilized to cure or prevent all of these diseases.
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PMID:Methioninase: a therapeutic for diseases related to altered methionine metabolism and transmethylation: cancer, heart disease, obesity, aging, and Parkinson's disease. 923 67

Physical disorders and pharmacotherapy for all 134 people with mental retardation ages 65 years and over living in Leicestershire, United Kingdom, were examined. Results were compared with a randomly selected group of 73 younger adults with mental retardation. Group comparisons revealed higher rates of urinary incontinence, immobility, hearing impairments, arthritis, hypertension, and cerebrovascular disease among the older group. The younger group had higher rates of dermatological disorders; congenital heart disease; ear, nose, and throat (ENT) disorders; and neurological disorders (excluding Parkinson disease). The older group took more drugs for physical illness. The effect of ageing on physical morbidity outweighs the effect of people with more severe mental retardation dying younger: Older people with mental retardation have significant physical health needs.
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PMID:Clinical study of the effects of age on the physical health of adults with mental retardation. 960 67

In the past 40 years, transplantation has moved from an experimental form of therapy used almost exclusively for renal failure to an accepted treatment for end-stage kidney disease, heart disease, liver disease, lung disease, and diabetes mellitus. Tissue transplantation for conditions from thermal injury to Parkinson disease is being investigated. The primary barrier in transplantation medicine is the immunologic reaction of the recipient to donor organs and tissues. Currently available drugs permit excellent short-term graft survival but have not led to reliable long-term survival. Recent advances in the understanding of this immune response have suggested new approaches to induction of immunologic tolerance and reduction of late graft losses. Because of the excellent short-term success of current agents, integration of these new approaches into clinical trials is challenging and raises important questions about the design of such trials.
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PMID:What's new in transplant immunology: problems and prospects. 963 35

To evaluate whether lazabemide has proarrhythmic or hypotensive potency in Parkinson's disease (PD), we conducted an 8-week, double-blind, placcbo-controlled, parallel group study with use of 24-hour ambulatory electrocardiographic (ECG) monitoring. Fifty-one patients with PD who did not have clinically apparent heart disease were randomized in a double-blind fashion to receive either lazabemide (n = 25) or placebo (n = 26) treatments. Lazabemide therapy did not induce clinically significant arrhythmias. A paroxysmal atrioventricular (AV) block, which progressed from first-degree AV block, was found in one patient in the lazabemide group. This was determined not to be a new AV block. However, the causality of lazabemide in prolongation of the pause was not ruled out completely. In addition, the asymptomatic fall in systolic blood pressure seen 3 minutes after standing up was observed to be more pronounced in the lazabemide group than in the placebo group. The mean decrease of systolic blood pressure was 10 mmHg greater in the lazabemide group than in the placebo group. In conclusion, lazabemide did not induce any clinically significant arrhythmias in patients without clinically apparent heart disease. However, it may increase the asymptomatic, orthostatic drop in systolic blood pressure.
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PMID:Safety study of lazabemide (Ro19-6327), a new MAO-B inhibitor, on cardiac arrhythmias and blood pressure of patients with Parkinson's disease. 1062 94

The identification of a majority of the polypeptides in mitochondria would be invaluable because they play crucial and diverse roles in many cellular processes and diseases. The endogenous production of reactive oxygen species (ROS) is a major limiter of life as illustrated by studies in which the transgenic overexpression in invertebrates of catalytic antioxidant enzymes results in increased lifespans. Mitochondria have received considerable attention as a principal source---and target---of ROS. Mitochondrial oxidative stress has been implicated in heart disease including myocardial preconditioning, ischemia/reperfusion, and other pathologies. In addition, oxidative stress in the mitochondria is associated with the pathogenesis of Alzheimer's disease, Parkinson's disease, prion diseases, and amyotrophic lateral sclerosis (ALS) as well as aging itself. The rapidly emerging field of proteomics can provide powerful strategies for the characterization of mitochondrial proteins. Current approaches to mitochondrial proteomics include the creation of detailed catalogues of the protein components in a single sample or the identification of differentially expressed proteins in diseased or physiologically altered samples versus a reference control. It is clear that for any proteomics approach prefractionation of complex protein mixtures is essential to facilitate the identification of low-abundance proteins because the dynamic range of protein abundance within cells has been estimated to be as high as 10(7). The opportunities for identification of proteins directly involved in diseases associated with or caused by mitochondrial dysfunction are compelling. Future efforts will focus on linking genomic array information to actual protein levels in mitochondria.
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PMID:Applied proteomics: mitochondrial proteins and effect on function. 1188 66

Manganese superoxide dismutase (MnSOD) is the enzyme that converts toxic O(2)(-) to H(2)O(2) in mitochondria. Previous reports showed that a deficiency of MnSOD in mice was neonatal lethal. Therefore, a model mouse was not available for the analysis of the pathological role of O(2)(-) injuries in adult tissues. To explore an adult-type model mouse, we designed tissue-specific MnSOD conditional knockout mice using a Cre-loxp system. First, we crossbred MnSOD flox mice with transgenic mice expressing Cre recombinase under the control of the chicken actin promoter (CAG). We confirmed that CAG MnSOD knockout mice were completely deficient in MnSOD and died as neonates, validating the use of the Cre-loxp system. Next, we generated liver-specific MnSOD-deficient mice by crossbreeding with Alb-Cre transgenic mice. MnSOD activity and protein were both significantly downregulated in the liver of liver-specific MnSOD knockout mice. However, no obvious morphological abnormality was observed in the liver when biochemical alterations such as lipid peroxidation were not detectable, suggesting a redundant or less important physiological role for MnSOD in the liver than previously thought. In the present study, we successfully generated tissue-specific MnSOD conditional knockout mice that would provide a useful tool for the analysis of various age-associated diseases such as diabetes mellitus, Parkinson's disease, stroke, and heart disease, when crossbred with tissue-specific transgenic Cre mice.
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PMID:Model mice for tissue-specific deletion of the manganese superoxide dismutase (MnSOD) gene. 1217 43

A major factor in the context of evaluating depression in the elderly is the role of medical problems. With aging there is a rapid increase in the prevalence of a number of medical disorders, including cancer, heart disease, Parkinson's disease, Alzheimer's disease, stroke, and arthritis. In this article, we hope to bring clarity to the definition of comorbidity and then discuss a number of medical disorders as they relate to depression. We evaluate medical comorbidity as a risk factor for depression as well as the converse, that is, depression as a risk factor for medical illness. Most of the disorders that we focus on occur in the elderly, with the exception of HIV infection. This review focuses exclusively on unipolar disorder. The review summarizes the current state of the art and also makes recommendations for future directions.
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PMID:Comorbidity of depression with other medical diseases in the elderly. 1236 69


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