Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0030567 (
Parkinson's disease
)
63,064
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Overt copper deficiency is not believed to be a widespread public health concern for most population groups. However, a variety of case studies suggest that under certain circumstances, clinical conditions may predispose individuals to the risk of copper deficiency or copper excess. Acquired copper deficiency has been documented in conditions predisposing to inadequate copper intakes, in
prematurity
, in malabsorption syndromes, and in conditions predisposing to excessive copper losses. In contrast, increases in copper concentrations have been reported in response to stress, inflammation, and infection; in
Parkinson disease
and diabetes mellitus; and in conditions involving an obstruction to bile flow.
...
PMID:Clinical conditions altering copper metabolism in humans. 958 45
Available information on organochlorines and the chronic effects of exposure to them are set out. Organochlorinated compounds are the most persistent pesticides and can be found in all ecosystems. Although they are generally efficient in pest control, they are also a potent environment pollutant and can provoke health problems in man. The evidences of the carcinogenic potential of organochlorines are controversial and insufficient, but they have been related to an increase in the incidence of some kinds of tumors, such as leukemia and solid tumors. Reproductive effects, due to anti-androgenic and estrogenic action, on embryonic virilization, the incidence of abortion and the frequency of
prematurity
, have also been observed. The accumulation of the organochlorines in the adipous tissue is positively correlated to the increase in aging and could be implicated in the development of aging diseases, such as
Parkinson's disease
. The effects of pesticides on human health have not yet been completely elucidated. Genotoxicity is one of the most serious of the possible harmful effects caused by these compounds and calls for special attention in view of the irreversible nature of the process and to the long latency associated with its manifestation.
...
PMID:[Delayed effects of organochlorine pesticides in man]. 987 30
Many pharmacological experiments show that the ionotropic receptor NMDA has both neurotrophic and neuroexcitotoxic effects. The neurotrophic function is manifested in many ways including acceleration of neuronal development, enhancement of neuronal migration, neuroprotection, blockage of apoptosis, prevention of aging and
prematurity
, as well as effects on synaptic plasticity and synaptogenesis. On the other hand, the neuroexcitotoxic function is manifested in its role in neurological and psychiatric diseases such as epilepsy,
Parkinson's disease
and schizophrenia. The present study explores the consequences of complete and partial absence of NMDA-NR1 receptors throughout development. Using DiI tracing in vitro, the development of corpus callosum projection neurons in transgenic mice with deletion of the NMDA-NR1 receptor was observed in visual cortex. Compared to littermate controls, the histogenesis and neuronal development of corpus callosum cells of origin was found to be accelerated in NR1-/- mice. That is, the corpus callosum projection neurons in NR1 knockout mice developed earlier and faster than in littermate heterozygous and wild-type mice. However, the corpus callosum projection neurons in NR1 heterozygous mice developed earlier and faster than in littermate wild-type mice. This suggests that NMDA-NR1 receptors are involved in sequencing and/or temporal regulation of neuronal development, and that there is a gene-dose effect. Studies from other laboratories suggest that the observed phenomenon of
prematurity
or accelerated development is a direct effect of altered expression of genes found in mice with deletion of the NMDA-NR1 receptor.
...
PMID:Corpus callosum and visual cortex of mice with deletion of the NMDA-NR1 receptor: I. Accelerated development of callosal projection neurons. 1293 10