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)

A case history of a patient who developed mammary cancer (T1N1bMo) after 5 1/2 years of continuous treatment with Levodopa for Parkinson's disease is presented. The prolactin inhibition by the Levodopa was verified, and the clinical and mammographic growth, the doubling time, and the labeling index of the tumor were determined. The results were not significantly different than those obtained from patients with breast cancer not under treatment with Levodopa. The rapid growth and evolution of this tumor suggests that prolactin does not have an inducer or promoter effect in mammary cancer.
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PMID:Breast cancer in a patient under levodopa treatment. 67 56

Parkinson's disease, a neurologic disorder characterized by a dopamine deficit within the striatum, may be improved by transplantation of polymer encapsulated neurosecretory cells. Surrounding cells with a selectively permeable barrier offers several advantages, including preventing immune rejection and tumor formation while allowing functional efficacy. Bovine adrenal medullary chromaffin cells, or PC12 cells, a rat-derived pheochromocytoma cell line, were encapsulated within polyelectrolyte-based microcapsules or thermoplastic-based macrocapsules. Histologic and biochemical analyses revealed that both types of cells survived and that neurotransmitter release from capsules was sustained for several months in vitro, irrespective of the encapsulation method employed. Both of the encapsulation systems protected the enclosed cells from an immunologic challenge in vitro, and prevented immune rejection when cell containing capsules were implanted in an immunologically incompatible host. Chromaffin or PC12 cell containing capsules implanted into the dopamine (DA) depleted striatum of rats reduced the lesion associated functional deficit. These results suggest that encapsulated neurosecretory cell implants may be useful in treating various central nervous system (CNS) deficits, particularly in cases involving a specific neurochemical lesion.
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PMID:Polymer encapsulated neurotransmitter secreting cells. Potential treatment for Parkinson's disease. 134 91

Available evidence suggests that blood vessels indigenous to solid CNS and peripheral tissues grafted to the brain are sustained and maintain the morphological and permeability characteristics they manifest in normal life. Furthermore, these vessels of graft origin anastomose (albeit not rapidly) with vessels of the surrounding host tissue predominantly at the host-graft interface and less so, or not at all, within the graft itself. For these reasons, blood-brain and brain-blood barriers, evident in the late fetal and neonatal CNS, can be expected to exist within CNS grafts placed intracerebrally or extracerebrally, providing the graft remains viable. Peripheral neural and non-neural tissues not possessing cellular barriers to circulating macromolecules do not acquire such barriers subsequent to their transplantation within the CNS. The absence of a blood-brain barrier in the adrenal gland grafted intracerebrally may be relevant for the treatment of Parkinson's disease with blood-borne therapeutics. Compared to solid tissue grafts, cell suspension grafts have the potential of becoming vascularized rapidly. That cell suspensions of neurons and of glia are supplied with BBB vessels of host origin and that the permeability characteristics of host BBB vessels are altered by a tumor cell suspension reaffirm the belief that the type of transplanted cell/tissue indeed determines the permeability characteristics of the blood vessels supplying it. The suspected immunologic privilege of the CNS is not absolute. Eventual host rejection of allografts placed within the third ventricle may be a dual consequence of the absence of a BBB at the level of the host median eminence and involvement of the minor histocompatibility complex.
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PMID:Angiogenesis and the blood-brain barrier in solid and dissociated cell grafts within the CNS. 170 57

A chart review from 151 dysphonic patients over the age of 60 was done to define aging related voice disorders. Overwhelmingly, patients suffered from dysphonia due to disease processes associated with aging rather than to physiologic aging alone. These include: 1. central neurological disorders affecting laryngeal function (e.g., stroke, Parkinson's disease, essential tremor, Alzheimer's disease); 2. benign vocal fold lesions (e.g., Reinke's edema, benign and dysplastic epithelial lesions); 3. inflammatory disorders (e.g., laryngitis sicca, medication effect); 4. laryngeal neoplasia; and 5. laryngeal paralysis. Typical laryngeal findings of vocal fold bowing and breathiness consistent with presbylarynges were present in only six patients. Presbylarynges is not a common disorder and should be a diagnosis of exclusion made only after careful medical and speech evaluation.
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PMID:Dysphonia in the aging: physiology versus disease. 173 85

The term neurodegenerative denotes a process rather than a state. In contrast, most research on such disorders, whether clinical or experimental, represents only a slice of time. Their progressive nature is mostly confined to speculation instead of being codified in research protocols. Research on cancer, also a degenerative disease, is much more often framed in terms of process. Part of the difference is accounted for by the impact of quantitative modeling, which enjoys a long history in both basic and clinical cancer research and which originated in attempts to describe and understand tumor development. Analogous questions are posed by neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. Among the issues that modeling could help to clarify are the properties and sources of the age-specific incidence rate, which resembles that for cancer, and the pharmacokinetics governing the toxic products of neurotransmitter metabolism. Neurodegenerative disorders maintain a research advantage because functional measures, mostly inaccessible to cancer investigators, serve as the ultimate index of progression. Their exploitation, however, in longitudinal studies remains inadequate.
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PMID:Cancer and the dynamics of neurodegenerative processes. 174 29

We have recorded movement-related cortical potentials (MRCPs) preceding voluntary finger extension in patients with Parkinson's disease and in patients with brain tumors that may involve the motor system. Three components of potential shifts preceding the voluntary movement were identified in all subjects. There were no differences between the healthy subjects and those with Parkinson's disease, or between pre- and postoperative recordings from the same parkinsonian patients in terms of onset latencies and gradients of these potential shifts. There was no evidence of MRCPs from the depth electroencephalogram recorded from the thalamic ventrolateral (VL) nucleus. After removal of the cerebellar dentate nucleus along with a tumor, MRCPs were still identified. After removal of tumors from the supplementary motor cortex and frontal association cortex, a part of the MRCPs preceding the voluntary movement was absent. The generation of MRCPs was considered not to be greatly affected by the cerebellar system because: (1) no MRCPs were detected from the thalamic VL nucleus, which is the relay nucleus of the dentato-rubro-thalamic pathway, believed to be related to voluntary movement; (2) destruction of the VL nucleus did not cause any changes in the MRCPs recorded at other sites, and (3) the MRCPs did not disappear when the dentate nucleus, an output system, was excised.
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PMID:Analysis of premovement components of movement-related cortical potentials in patients with Parkinson's disease or brain tumors. 208 Mar 36

Using radioimmunoassay methods the authors assayed the concentration of biochemical neoplasm markers (BMN) in 106 patients with neurological diseases (M-56, F-50) in the serum, and in 20 cases in the cerebrospinal fluid. In certain cases these markers were present, and sometimes their concentration was raised: ferritin in multiple sclerosis from 200 to 1365 ng/ml, in ischaemic stroke up to 327.9 ng/ml, in Parkinson's disease up to 423 ng/ml in the serum. In some cases of other diseases the levels of carcinoembryonic antigen (CEA), acid prostatic phosphatase (PAP) and alpha-fetoprotein (AFP) were raised, similarly as that of human chorionic gonadotropin (HCG). Further studies are being conducted on BMN, including also other markers (CA 125, CA 199), with monoclonal antibodies, beta-endorphins and prostaglandins in neurological diseases, including multiple sclerosis. It is suggested (Nowak) that BMN may have an indirect role in the aetiology and pathogenesis of certain diseases of the nervous system and that they may have connections with prostaglandins.
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PMID:[Biochemical neoplasm markers in selected neurological diseases]. 243 40

On September 14 through 16, 1988, a meeting on the use of human fetal tissue in transplantation was held at the National Institutes of Health, Bethesda Maryland, USA. The meeting sponsored by NIH for the Human Fetal Tissue Transplantation Research Panel, a consultant group to the Advisory Committee to the Director. The consultant group was convened to deal with the scientific, judicial and moral questions associated with research involving transplantation of human fetal tissue obtained after induced abortions. The first day of the meeting was devoted to presentations addressing scientific issues. Included among the speakers was Dr. Lars Olson, Professor of Neurobiology, Karolinska Institute, Stockholm, who described the use of transplanted human fetal tissue in the treatment of patients with Parkinson's disease and Dr. Eugene Redmond, Professor of Psychiatry, Yale University School of Medicine, who showed results of work with transplantation of tissue to correct induced Parkinson-like disease in monkeys. Other speakers addressed the present, past or potential use of fetal tissue in the treatment of diabetes, immune disorders, and other diseases, as well as the use of fetal cells in the production of biologicals. At the conclusion of the meeting the panel did not recommend that research be halted on fetal tissue within the context discussed, although the recommendation of the committee is not binding, and an additional assembly of the panel will probably occur before the final recommendation to an NIH advisory committee is made in November. Other meetings on this subject include a meeting on the use of fetal tissue sponsored by the American Association of Tissue Banks, March 6-7, 1989, in Washington D. C. (Crystal City) and a meeting June 10, 1989, the day before the annual meeting of the Tissue Culture Association, USA, in Orlando, Florida, on fetal cells and ownership of cultured cells and products derived from clinical specimens. Following are statements to the Human Fetal Tissue Transplantation Research Panel presented September 14, 1988, by Dr. David Barnes, Associate Professor of Biochemistry and Biophysics in the Environmental Health Sciences Center at Oregon State University, USA, who was asked to address for the panel recent advances in cell culture related to fetal tissue, and Dr. Robert E. Stevenson, Director of the American Type Culture Collection, President of the Tissue Culture Association, USA, and Chairman of the Committee on Cells and Tumors of the American Association of Tissue Banks.
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PMID:Meeting report: human fetal tissue transplantation research panel. 291 16

In a Nigerian town with a stable population of 20,000, a door-to-door survey was conducted, using a questionnaire involving a complete census and a simple neurological evaluation which had previously showed a 95% sensitivity and an 80% specificity for detecting neurological disease. Positive responders were evaluated and categorised, using agreed criteria for diagnoses. Nearly 100% cooperation was obtained. Life prevalence ratio for at least one episode of headache was 51/1000. Crude point prevalence ratio for migrainous headache was 5.3/100, and peak age-specific ratio was in the first decade. Prevalence ratio for epilepsy was 533/100,000 and peak age-specific prevalence ratio occurred in the 5-14 years age groups. The prevalence ratio for peripheral nerve disorders was 268/100,000, and age-specific prevalence ratio for tropical neuropathy increased with age. Prevalence ratio for stroke was rather low at 58/100,000, but was probably due to the people's attitude to the disabled elderly and high mortality of stroke which showed annual mortality rate of 70/100,000 which increased with age to 1519/100,000 per year in the eighth decade. Crude prevalence ratios (cases per 100,000) for others are 112 for neurological complications (including sciatica) of spondylosis, 15 each for poliomyelitis, motor neurone disease, development speech disorders, 10 each for syncope, hereditary neuropathies. Parkinson's disease, benign essential tremor, primary cerebellar degeneration, cerebral palsy, mental retardation, organic psychosis (probable intracranial tumor) and 5 each for muscular dystrophy, pyomyositis, spina bifida occulta, alcohol dependence and cerebral malaria. The implications of the findings are important for development of community neurological services in the developing countries.
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PMID:Neurological disorders in Nigerian Africans: a community-based study. 303 73

We report 5 cases of bilateral abductor paralysis of the vocal cords (Gerhardt syndrome) with attacks of nocturnal asphyxia in patients with Parkinson disease, Shy-Drager syndrome, amyotrophic lateral sclerosis and tumor of the posterior cranial fossa.
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PMID:Bilateral abductor paralysis of the vocal cords in the course of neurological diseases: report of 5 cases. 335 25


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