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)

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

Fermented papaya preparation is a natural health food that has been commercially sold in Japan for 2 years. It is made by yeast fermentation of Carica Papaya Linn. We examined the antioxidant action of the fermented papaya preparation on free radicals and lipid peroxidation. Free radicals have been related with aging and diseases, such as cancer, diabetes and especially in neurological disorders, for example, Parkinson's disease or Alzheimer's disease. A diet including variable antioxidant foods may therefore help to prevent these illnesses. The free radical scavenging activity of the fermented papaya preparation was examined using an electron spin resonance (ESR) spectrometer. Fermented papaya preparation (50 mg/ml) scavenged 80% of hydroxyl radicals (.OH) as spin adducts of spin trap, 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) (5.27 x 10(15)spins/ml) generated by Fenton reagents. The value of IC50 was 12.5 mg/ml. The oral administration of the fermented papaya preparation for 4 weeks decreased the elevated of lipid peroxide levels in the ipsilateral 30 min after injection of iron solution by iron into the left cortex of rats. The fermented papaya preparation also increased superoxide dismutase activity in the cortex and hippocampus of them. These results suggest that the fermented papaya preparation has antioxidant actions and that it may be prophylactic food against the age related and neurological diseases associated with free radicals.
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PMID:Free radical scavenging activity of fermented papaya preparation and its effect on lipid peroxide level and superoxide dismutase activity in iron-induced epileptic foci of rats. 963 26

Mutations of mitochondrial DNA (mtDNA) are associated with a wide spectrum of disorders encompassing the myopathies, encephalopathies and cardiomyopathies, in addition to organ specific presentations such as diabetes mellitus and deafness. The pathogenesis of mtDNA mutations is not fully understood although it is assumed that their final common pathway involves impaired oxidative phosphorylation. The identification of a specific respiratory chain defect (complex I deficiency) in Parkinson's disease (PD) 10 years ago focused attention on the aetiological and pathogenetic roles that mitochondria may play in neurodegenerative diseases. There is evidence now emerging that mtDNA abnormalities may determine the complex I defect in a proportion of PD patients and it may prove possible to use biochemical analysis of platelet and cybrid complex I function to identify those that lie within this group. Respiratory chain defects of a different pattern have been identified in Huntington's disease (HD) (complex II/III deficiency) and Friedreich's ataxia (FA) complex I-III deficiency). In both these disorders, the mitochondrial abnormality is secondary to the primary nuclear mutation:CAG repeat in the huntingtin gene in HD, and GAA repeat in the frataxin gene in FA. Nevertheless, it appears that the mitochondrion may be the target of the biochemical defects that are the consequence of these mutations. There is a close and reciprocal relationship between respiratory chain dysfunction and free radical generation, and there is evidence for oxidative stress and damage in PD, HD and FA, which together with the mitochondrial defect may result in cell damage. Impaired oxidative phosphorylation and free radical generation may independently adversely affect the maintenance of mitochondrial transmembrane potential (Deltapsim). A fall in Deltapsim is an early event (preceding nuclear fragmentation) in the apoptotic pathway. It is possible therefore that mitochondrial dysfunction in the neurodegenerative disorders may result in a fall in the apoptotic threshold of neurones which, in some, may be sufficient to induce cell death whilst, in others, additional factors may be required. In any event, mitochondria present an important target for future strategies for 'neuroprotection' to prevent or retard neurodegeneration.
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PMID:Mitochondrial dysfunction in neurodegenerative disorders. 971 16

Despite the reticence of certain prominent scientists, there will be no moratorium on clinical xenotransplantation in the USA and a limited number of well-controlled trials will be enabled. There has already been some advances in cell and tissue xenografts with encapsulated porcine pancreas cells and porcine foetal neurones in patients with diabetes and Parkinson's disease. However, because of some porcine viruses are able to develop in human tissues, current and planned trials have been interrupted until routine viral detection tests are available. Several attempts have been made in the past, with animal organs (kidney, heart, liver) from various non-human primate species and conventional immunotherapy without success. Another major question now, is the choice of the animal donor species. Phylogenetically dose to man, non-human primates would be a right and logical choice. But, because of their procurement problems, it is likely that most future trials will be conducted with porcine organs from more performant transgenic animals, more powerful immunosuppressors and new therapeutic strategies based on the natural tolerance mechanisms.
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PMID:[Xenografts: clinical trials and perspectives]. 976 76

Sleep disorders are common and well documented in patients with Parkinson's disease (PD). However, most data on sleep in patients with PD are derived from selected patient populations. This community-based survey evaluated the prevalence of and risk factors for sleep disturbances in an unselected group of 245 patients with PD and two control groups of similar age and sex distribution: 100 patients with another chronic disease (diabetes mellitus) and 100 healthy elderly persons. Nearly two thirds of the patients with PD reported sleep disorders, significantly more than among patients with diabetes (46%) and healthy control subjects (33%). About a third of the patients with PD rated their overall nighttime problem as moderate to severe. The most common sleep disorders reported by the patients with PD were frequent awakening (sleep fragmentation) and early awakening. Sleep initiation showed no significant difference compared with the control groups. Pain and cramps were not more prevalent among the patients with PD, but they were more likely to report sleep disturbed by myoclonic jerks. Use of sedatives was common in all three groups but significantly higher in the PD group than in the healthy elderly. Symptoms of depression and duration of levodopa treatment showed a significant correlation with sleep disorders in the PD group. This community-based study confirms that sleep disorders are common and distressing in patients with PD. The strong correlation between depression and sleep disorders in patients with PD underlines the importance of identifying and treating both conditions in these patients.
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PMID:A community-based study of sleep disorders in patients with Parkinson's disease. 982 12

Prevalence of chronic constipation is around 3% in youth, 8% in middle age, and 20% in the elderly, respectively. There are three etiologic groups: 1. Diet poor in fibre. Most constipated persons, however, do not eat less fibre than controls. 2. Organic diseases accompanied by constipation such as autonomous neuropathies (e.g. in diabetes), endocrine disorders, and neurologic diseases (e.g. Parkinsons disease). 3. Functional outlet obstruction. This may be due to disturbed sphincter function, internal rectal prolapse, or rectocele. The basic treatment of all forms of constipation consists in a diet rich in fibre. In selected cases of functional outlet obstruction, surgery may be successful. Otherwise, treatment with laxatives is justified.
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PMID:[Diagnosis and therapy of constipation]. 988 Oct 37

The use of animal cells, tissues, or organs for humans is being investigated as an alternative to allotransplantation and as therapy for a broad range of disease states including diabetes, Parkinson's disease, and neurologic pain control. The risk of transmitting novel infections with these tissues, xenozoonoses, has led to much debate. It is well recognized that infections are a hazard with the use of all biologic agents. In addition, infections from human donors remain a major cause of morbidity and mortality after allotransplantation. Accordingly the potential for animal microbial agents to be pathogenic in the human recipient after xenotransplantation and be transmissible to others must be critically examined. Along with laboratory-based research, clinical trials must be conducted in a manner to evaluate the transmission of potential animal infections. Pretransplant evaluation should include discussions with the candidate and, if possible, with close contacts. Information must be provided as to the potential risks of infection and transmission to others. Behavioral modifications which can decrease spread of infections should be emphasized. Serial samples should be obtained from the patients at defined intervals and if recipients become ill. In addition, archiving samples for future evaluation is critical. Prospective evaluation will enhance the ability to define and understand the spectrum of xenogeneic infections.
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PMID:Xenozoonoses and the xenotransplant recipient. 992 10

Virtually all cells in humans depend on mitochondrial oxidative phosphorylation to generate energy, accounting for the remarkable diversity of clinical disorders associated with mitochondrial DNA mutations. However, certain tissues are particularly susceptible to mitochondrial dysfunction, resulting in recognizable clinical syndromes. Mitochondrial DNA mutations have been linked to seizures, strokes, optic atrophy, neuropathy, myopathy, cardiomyopathy, sensorineural hearing loss, diabetes mellitus, and other clinical features. Mitochondrial DNA mutations also may play an important role in aging, as well as in common age-related neurodegenerative disorders such as Parkinson's disease. Therefore, it is becoming increasingly important for clinicians to recognize the clinical syndromes suggestive of a mitochondrial disorder, and to understand the unique features of mitochondrial genetics that complicate diagnosis and genetic counseling.
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PMID:Mitochondrial disorders: clinical and genetic features. 1007 67

Xenotransplantation is considered increasingly as a solution to the current shortage of human organs for allotransplantation. In addition, it is being investigated as a treatment for a number of other diseases such as Parkinson's disease, diabetes mellitus, and acquired immunodeficiency disease. The potential risk of novel zoonotic infections is a concern associated with these procedures. Accordingly, the role of animal microbial agents must be critically examined. This review examines the concerns and proposed mechanisms for xenogeneic infections and details what is known and what still needs to be learned as the field of xenotransplantation progresses. Emphasis is placed on microbial agents of baboons and swine because they are currently the most common species considered as donor sources for xenotransplantation.
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PMID:Xenotransplant-associated infections. 1009 20

In 1988, a moratorium on the use of federal funds for fetal tissue transplantation research (FTTR) halted the promise of a cure for millions of Americans suffering from Parkinson's disease, diabetes, and other debilitating conditions. Since the moratorium began, private and international experimentation continues with mixed success. In the foreground, however, the debate rages over federal funding for fetal tissue transplantation from induced abortions into humans. In the House of Representatives and the Senate, the debate culminated with the passage of the National Institutes of Health (NIH) Revitalization Amendments. In addition to authorizing NIH programs, the $5.4 billion bill included measures designed to overturn the moratorium on federal funding for the transplantation research. Brimming with controversy, the bill was forwarded to the White House where it met President Bush's promised veto. The veto was sustained when the House failed to rally the two-thirds majority vote necessary to override a veto, leaving the moratorium intact and the controversy alive. Modified measures were introduced in both Houses of Congress, but a Senate filibuster in the last hours of the session foreclosed a second veto and placed the bill on the 1993 calendar. The field of fetal tissue research, currently a fraction of human health research but with the potential for a six billion dollar industry, is the focus of inevitable controversy. FTTR, as a sub-field, presents a volatile combination of the politics of abortion, the international research race, and the cries of millions of Americans suffering from Parkinson's disease and other crippling debilitations. Thus, using fetal tissue as a potential cure commands the interest and the passion of many. FTTR from induced abortions distinguishes itself from federally approved fetal tissue research because it connects a potentially beneficial health pursuit with a critically divisive moral issue of our day--abortion. By its very nature, FTTR cannot automatically enjoy the approval given to other research pursuits, primarily because at its very core lies an unresolved ethical issue. This issue is found in the connection between the procedures of aborting the fetus, harvesting the tissue, and transplanting it into a needy recipient. Unlike transplantation from ectopic pregnancies or spontaneous abortions, which are permitted by the ban, FTTR directly links decisions and procedures immersed in the moral controversy over induced abortion. This Comment outlines the debate over the transplantation research affected by the moratorium on the use of federal funds for FTTR. Whether fetal tissue from induced abortions should be procured for transplantation into humans, and if so, how its use can be regulated is a significant contemporary challenge for public policy makers. Part I of this Comment delineates the formation of public policy on the issue. Part II explains the content of the NIH Amendments as a new direction for public policy. Part III discusses the potential benefits and risks of federal funding of FTTR. Finally, part IV addresses whether the executive ban or the legislative measure is a sound, farsighted public policy.
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PMID:Bioethical catch-22: the moratorium on federal funding of fetal tissue transplantation research and the NIH revitalization amendments. 1012 47


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