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)

Organ transplantation is limited by the number of cadaveric human donor organs that become available. Xenotransplantation - the transplantation of organs and tissues between animal species - would supply an unlimited number of organs and offer many other advantages. The pig has been identified as the most suitable donor animal. Pig organs, when transplanted into humans or nonhuman primates, are, however, rejected hyperacutely within minutes by antibody-mediated complement activation. Human anti-pig antibodies have been identified as being directed against galactose alpha 1-3galactose (alpha Gal) epitopes on pig vascular endothelium. Methods have been successfully developed to prevent hyperacute rejection. These include (i) depletion or inhibition of recipient antibodies or complement and (ii) development of transgenic pigs that express a human complement-regulatory protein (e.g. hDAF). The persistence or return of anti-pig antibody, however, even following the use of hDAF pig organs, eventually leads to what has been variously termed "acute vascular rejection" or "delayed xenograft rejection", which is again believed to be largely antibody-dependent. Nevertheless, experimental pig-to-primate organ xenotransplantation now results in transplant function for days and weeks rather than minutes. Little is yet known of the nature of the acute cellular rejection response that is anticipated to follow, and of any subsequent chronic rejection that may develop. Tolerance to both the alpha Gal epitope and to swine leukocyte antigens (SLA) is being explored using gene therapy techniques and by the induction of hematopoietic cell chimerism. The development of genetically engineered pigs that do not express the alpha Gal epitope is also being pursued. Considerable progress has been made in recent years, but experimental results do not yet warrant the initiation of a clinical trial of organ xenotransplantation. However, trials are already underway of pig cell transplants in patients with diabetes and neurodegenerative conditions, such as Parkinson's disease.
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PMID:Xenotransplantation--state of the art--update 1999. 1020 58

The objective of this paper is to evaluate the health-related quality of life in a community-based population of patients with Parkinson's disease (PD). The PD population consisted of 233 patients and was derived from a wider prevalence study in the county of Rogaland, Norway. The quality of life was measured by the Nottingham Health Profile (NHP) and four general health and well-being questions. The results were compared with quality of life measurements in 100 patients with diabetes mellitus (DM) and 100 healthy elderly people. The control groups had the same age and sex distribution as the patients with PD. This study showed that PD has a substantial impact on the health-related quality of life. Patients with PD had higher distress scores in all measured dimensions of the NHP than the two control groups. The negative impact of PD was highest for physical mobility, emotional reactions, social isolation and energy. Correlation analysis of the quality of life showed that age, duration of levodopa therapy, higher levodopa doses, depression, cognitive impairment and more advanced disease correlated with higher distress scores in patients with PD. The results of this study showed that PD had a broad impact on well-being, more so than DM. The distress related to the severity of the disease, as well as to depressive symptoms and cognitive impairment. An important finding was the underestimated distress related to lack of energy. Copyright 1998 Lippincott Williams & Wilkins
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PMID:Quality of life measurements in patients with Parkinson's disease: A community-based study. 1021 Aug 72

During the period from July 1995 to June 1996 we performed transurethral resection of the prostate (TURP) on 824 patients with benign prostatic hyperplasia (BPH). Among them, 13 were dementia patients between 74 and 96 years old; they presented with urinary hesitancy in 6, retention in 4, frequency in 2 and incontinence in 1 patient. Past history included stroke in 7, hypertension in 6, pulmonary tuberculosis in 4, diabetes in 3, asthma in 2, angina pectoris in 1, Parkinson's disease in 1, pneumonia in 1, and hepatitis in 1. Careful preoperative examination revealed that they were proper candidates for TURP. They underwent TURP under spinal anesthesia. The mean operative time was 34 min, ranging from 20 to 60 min. The adenoma resected weighed 24 g on the average, ranging from 7.5 to 48 g. During surgery, although hypotension was noted in 2 patients, there was no serious morbidity. Their mental condition was well controlled with ketamine and diazepam during and after surgery. Postoperative complications included acute myocardial infarction in 1, multiple gastric ulcer in 1, and decubitus in 1. None died within 3 months after TURP, 3 died there after, and 10 patients were alive at the mean follow-up period of 26 months. Six patients reported good urination, 3 reported some improvement in urination after surgery, although requiring intermittent catheterization and 1 developed mild incontinence. In conclusion, TURP appears to provide some benefit in selected patients with dementia and should not be considered to be a contraindication for such patients.
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PMID:[Transurethral resection of the prostate for patients with dementia]. 1036 42

Mitochondria contain the respiratory chain enzyme complexes that carry out oxidative phosphorylation and produce the main part of cellular energy in the form of ATP. Mitochondrial DNA (mtDNA) encodes essential subunits of the respiratory chain and is thus critical for maintaining cellular energy production. The first pathogenic mtDNA mutations were reported in 1988, and today more than 50 disease-causing mtDNA mutations have been identified. In addition, mtDNA mutations have been implicated in ageing and in common disorders such as diabetes mellitus, heart failure and Parkinson's disease. This review will summarize recent advances in the rapidly expanding field of mitochondrial medicine.
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PMID:Mitochondrial medicine--recent advances. 1044 21

The objective of this study was to investigate the frequency of excessive daytime sleepiness (EDS) and the beneficial effect of sleep on motor performance in an unselected community-based sample of patients with Parkinson's disease (PD). Furthermore, we wanted to identify possible risk factors to these phenomena. Detailed information on somnolence and sleep during daytime, as well as sleep benefit (SB) on awakening, was collected through a questionnaire among 245 patients with PD. Daytime somnolence was graded in groups of no somnolence, mild daytime sleepiness, and EDS. In addition, the occurrence of somnolence in the patients with PD was compared with the occurrence among control groups of patients with diabetes mellitus and of healthy elderly subjects. The correlations between EDS and SB and various motor- and non-motor symptoms of PD were evaluated. Among the patients with PD, 15.5% experienced EDS, significantly more than in the patients with diabetes mellitus (4%) and the healthy control subjects (1%). The frequency of mild daytime sleepiness was similar (10%) in patients with PD and control subjects. The patients with EDS had significantly higher staging of PD, were more disabled, and showed a higher frequency of cognitive decline compared with the patients without somnolence. They also had been using levodopa for a longer time and had more hallucinations. The occurrence of nocturnal sleeping problems and the use of sleeping pills was similar in the two groups, as was the mean age at examination, duration of PD, and presence of fluctuations and dyskinesias. SB was found in 42.2% of the patients with PD. These patients had been using levodopa for significantly longer and had significantly more fluctuations and dyskinesias compared with the patients without SB. Our results suggest that mild daytime sleepiness may be a result of normal aging, whereas more severe EDS can be explained by the neuropathologic changes of PD. The data from this community-based study confirms the previously reported high frequencies of SB.
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PMID:Excessive daytime sleepiness and sleep benefit in Parkinson's disease: a community-based study. 1058 65

In November 1998 biologists announced that they had discovered a way to isolate and preserve human stem cells. Since stem cells are capable of developing into any kind of human tissue or organ, this was a great scientific coup. Researchers envision using the cells to replace damaged organs and to restore tissue destroyed by, for example, Parkinson's disease, diabetes, or even Alzheimer's. But, since stem cells are taken from aborted embryonic and fetal tissue or "leftover" in vitro embryos, their use raises large ethical issues. The National Institutes of Health (NIH) recently decided to fund research employing, not stem cells, but "cell lines" derived from them. The NIH has essentially made an ethical determination, finding sufficient "distance" between cell lines and abortion. Can Catholic universities sponsoring biological research agree with this finding? Probably not. In Catholic teaching, the concept of "complicity" would likely preclude such research. However, Catholic teaching would probably allow research done with stem cells obtained from postpartum placental tissue and from adult bone marrow and tissue. These cells, which lack the pluripotency of embryonic and fetal stem cells, are nevertheless scientifically promising and do not involve the destruction of human life.
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PMID:Stem cell research: licit or complicit? Is a medical breakthrough based on embryonic and fetal tissue compatible with Catholic teaching? 1062 80

This article reviews evidence for the occurrence of atypical parkinsonism in Afro-Caribbean and Indian ethnic minority subjects living in western countries, particularly the UK. Current information on the frequency, pattern, and prevalence of Parkinson's disease and parkinsonism in these communities is unclear and controversial. While several workers have suggested that there is a low prevalence of Parkinson's disease in populations of African origin, other workers have suggested a higher prevalence of Parkinson's disease in African Americans. Furthermore, little information is available in relation to the pattern of parkinsonism in these subjects. A recent phenomenologic study of parkinsonism in the French West Indies by Caparros-Lefebvre and colleagues has indicated a significantly increased frequency of atypical parkinsonism in local non-white subjects. Since 1995, we have been studying the pattern and frequency of parkinsonism in Afro-Caribbean and Indian (originating from the Indian subcontinent) patients living in the UK, with London serving as the coordinating center. Our results indicate that there is a three- to fourfold increase in the frequency of occurrence of sporadic atypical parkinsonism characterized by levodopa hyporesponsiveness, bradykinesia-dominant disease, and early cognitive dysfunction in these patients even after exclusion of patients with clinically probable multiple system atrophy, progressive supranuclear palsy, and Lewy body dementia. These findings are similar to observations made in the French West Indies. Ongoing studies in India suggest that atypical parkinsonism also affects local patients, and the pattern of parkinsonism tends to differ from Afro-Caribbean subjects in the UK. Studies are currently underway to unravel the mechanism of increased frequency of atypical parkinsonism in these ethnic groups and include genetic studies addressing polymorphisms of enzymes metabolizing levodopa, dietary neurotoxin screen and functional imaging studies of the striatum using positron emission tomography. Furthermore, the contribution of diabetes mellitus and hypertension, commonly seen in these ethnic groups, is also being examined.
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PMID:Atypical parkinsonism in Afro-Caribbean and Indian origin immigrants to the UK. 1063 37

The plasma soluble melanins (PSM) form spontaneously in vitro and in vivo and their formation involves oxidative polymerization and copolymerization of dopa, catecholamines, homogentisic acid, 3-hydroxyanthranilic acid, p-aminophenol, p-phenylenediamine, and other end(ex)ogenous ortho and para polyhydroxy-, (poly)hydroxy(poly)amino- and polyamino-phenyl compounds. The build up of PSM is visible within 2-3 h after the start of incubation at 37 degrees C with 1 mg/ml of plasma. PSM also form similarly in blood and these processes cause hemolysis. The mean quantity of PSM in normal human plasma is 1.61+/-0.1 (S.D.) mg/ml (n = 20) and in normal human urine is 1.1+/-1.2 g/24 h collection (n = 8). They contribute to the yellow color of plasma and urine. Antioxidants delay the formation of PSM. The deposited melanins also form from these precursors. Reactive oxygen side products (ROSP) are generated during and after melanogenesis. Melanins in vivo are generally associated with proteins or with proteins and lipids. The PSM-protein-lipid complexes are called plasma soluble lipofuscins (PSL), because they have histochemical and fluorescence properties similar to those of solid lipofuscins. The soluble and deposited melanins (SDM) and their intermediates have similar toxic chemical reactivities. The oxidizing quinoid (they can produce partially and completely substituted conjugates) and the semiquinoid free radical intermediates are also moieties in most human melanin structures. Soluble melanins formed from dopa, or dopamine, or norepinephrine in weak alkaline solution have been shown to be toxic to human CD4+ lymphoblastic cells (MT-2) at higher than 10 microg/ml concentrations. Alkaptonuria with high levels of homogentisic acid in the plasma is a potentially fatal disease, exhibiting the toxic effects of the homogentisic acid melanin (soluble and deposited), its intermediates and the ROSP. Patients with alkaptonuria develop arthritis and often suffer from other diseases too, including cardiovascular disease (frequent cause of death) and kidney disease. Pheochromocytoma, with high levels of catecholamines in the plasma is another potentially fatal disease. The catecholamine PSM of pheochromocytoma have very light yellow or practically no colors, due to the concentrations and chemical structures. Pheochromocytomas can cause hypertension, cardiovascular disease (frequent cause of death), kidney disease, stroke, cancer, amyloid formation and can mimic many other diseases, including acute pancreatitis, carcinoid, neuroblastoma, psychiatric illness, hypercalcemia, retinal vascular lesions, and diabetes mellitus. Pheochromocytoma is potentially fatal even in patients without hypertension. Following trauma and surgery, heavily pigmented eyes are apt to experience greater inflammation than lightly pigmented eyes. In Parkinson's disease those neurons are lost first in the substantia nigra and locus ceruleus which contain the greatest amounts of neuromelanins. The antihypertensive alphamethyldopa causes Parkinson's syndrome. It forms PSM in a short time in vitro. The side effects of L-dopa (immobility episodes alternate with normal or involuntary movements; psychotic abnormalities) suggest that the SDM, their intermediates and the ROSP present naturally in vivo are involved in the cause of Parkinson's disease and Alzheimer's disease. There is a large overlap between these two diseases. (ABSTRACT TRUNCATED)
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PMID:The probable involvement of soluble and deposited melanins, their intermediates and the reactive oxygen side-products in human diseases and aging. 1124 35

Restless legs syndrome (RLS) is a perplexing, debilitating, and fairly common condition that can be challenging to manage. Hallmark symptoms include an increase in the severity of sensations during rest and an irresistible urge to move the affected limbs. RLS often occurs concomitantly with periodic limb movement disorder. There are no known causes of RLS, but likely triggers include heredity, iron and vitamin deficiencies, caffeine, and alcohol. Chronic conditions such as diabetes, peripheral neuropathy, and Parkinson's disease can worsen and prolong RLS symptoms. Symptom management begins by establishing proper nutrition intake and improved sleep hygiene. If these fail, conservative pharmacologic treatment is appropriate, with regimens chosen from dopaminergic agents, benzodiazepines, opioids, and anticonvulsants.
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PMID:Restless legs syndrome. How to provide symptom relief with drug and nondrug therapies. 1077 1

Though mitochondria have been a major source of energy production in eukaryotae since 15-20 billion years previously, existence of disorders due to primary abnormalities of their DNA has not been known until very recent years. In 1962, Luft et al reported the first case of such myopathy, and another case reported in 1967 by Shy et al was also the first case of generalized disorder with mitochondrial abnormalities. Since then, many case reports have followed including MELAS and other encephalomyopathies. Finally, in 1989, deletion of mitochondria DNA was found by Folt et al. Today, these disorders were able to be classified as follows: 1) LHON and A1555G type deafness as strictly limited non-syndromic type, 2) encephalomyopathies and their incomplete forms due to common and other deletions of mitochondria DNA, 3) encephalomyopathies and their incomplete forms including MIDD, diabetes mellituis, cardiomyopathy, deafness due to point mutations of mitochondria DNA related MELAS and others, 4) Neurodegenerative types including Parkinson's disease, Alzheimer's disease, cerebellar degeneration, and amyotrophic lateral sclerosis, or neurologic disorders mimic to such diseases, 5) Mitochondrial involvement not due to primary abnormalities of mitochondria DNA. Possible mechanisms were discussed, but sufficient knowledge is lacking so far to clarify pathophysiology of these disorders and the role of deleterious DNA in aging. Possible effective therapeutic strategies were also discussed, but further development of research works on these disorders in the 21st century are needed to answer these questions.
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PMID:[Current and future aspects of mitochondrial diseases]. 1079 Oct 75


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