Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002736 (amyotrophic lateral sclerosis)
19,048 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two employees in a mercuric oxide manufacturing plant developed neurologic changes not previously reported from the exposure to inorganic mercury or elemental mercury vapor. The symptoms, physical findings and laboratory studies resembled those found in amyotrophic lateral sclerosis (ALS) and organic mercury intoxication. Nineteen employees are reported who precipitously developed signs and symptoms which may be regarded to be the early onset of a symptom complex of mercury intoxication that would likely have progressed to the ALS-like syndrome if the progression had not been interrupted by removal of the individuals from exposure to mercury. All symptoms, signs, and laboratory findings returned completely to normal after approximately three months in a mercury free work environment.
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PMID:Inorganic mercury intoxication reminiscent of amyotrophic lateral sclerosis. 72 51

To identify antecedent events contributing to the development of amyotrophic lateral sclerosis, we studied 25 amyotrophic lateral sclerosis patients in whom we tabulated the incidence of factors previously associated with motor neuron disease and compared the incidences with those found in 25 hospitalized patients and 25 normal people. More amyotrophic lateral sclerosis patients reported exposure to lead and mercury, participation in athletics, and consumption of large quantities of milk. Exposure to lead and mercury, athletic participation, and milk ingestion are possible risk factors that may predispose to the development of amyotrophic lateral sclerosis.
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PMID:Antecedent events in amyotrophic lateral sclerosis. 94 26

In a retrospective study of the charts of 39 patients who had motor neuron disease we found that over 50 percent of patients had radiographic abnormalities of bone and over 20 percent had serum calcium concentrations out of the range observed in normal controls. Statistical analysis indicated that, in respect to serum calcium levels, patients who have motor neuron disease are a separate population. These findings, which might reflect a disturbance in bone or calcium metabolism in patients with motor neuron disease, are of interest in view of the known ability of divalent ions other than calcium, such as lead and mercury, to simulate motor neuron disease, and the discovery that patients with proven primary and secondary hyperparathyroidism may have features of amyotrophic lateral sclerosis.
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PMID:Motor neuron disease: retrospective study of associated abnormalities. 127 82

Most frequently encountered causes of intractable pain and intractable medical problems, including headache, post-herpetic neuralgia, tinnitus with hearing difficulty, brachial essential hypertension, cephalic hypertension and hypotension, arrhythmia, stroke, osteo-arthritis, Minamata disease, Alzheimer's disease and neuromuscular problems, such as Amyotrophic Lateral Sclerosis, and cancer are often found to be due to co-existence of 1) viral or bacterial infection, 2) localized microcirculatory disturbances, 3) localized deposits of heavy metals, such as lead or mercury, in affected areas of the body, 4) with or without additional harmful environmental electro-magnetic or electric fields from household electrical devices in close vicinity, which create microcirculatory disturbances and reduced acetylcholine. The main reason why medications known to be effective prove ineffective with intractable medical problems, the authors found, is that even effective medications often cannot reach these affected areas in sufficient therapeutic doses, even though the medications can reach the normal parts of the body and result in side effects when doses are excessive. These conditions are often difficult to treat or may be considered incurable in both Western and Oriental medicine. As solutions to these problems, the authors found some of the following methods can improve circulation and selectively enhance drug uptake: 1) Acupuncture, 2) Low pulse repetition rate electrical stimulation (1-2 pulses/second), 3) (+) Qi Gong energy, 4) Soft lasers using Ga-As diode laser or He-Ne gas laser, 5) Certain electro-magnetic fields or rapidly changing or moving electric or magnetic fields, 6) Heat or moxibustion, 7) Individually selected Calcium Channel Blockers, 8) Individually selected Oriental herb medicines known to reduce or eliminate circulatory disturbances. Each method has advantages and limitations and therefore the individually optimal method has to be selected. Applications of (+) Qi Gong energy stored paper or cloth every 4 hours, along with effective medications, were often found to be effective, as Qigongnized materials can often be used repeatedly, as long as they are not exposed to rapidly changing electric, magnetic or electro-magnetic fields. Application of (+) Qi Gong energy-stored paper or cloth, soft laser or changing electric field for 30-60 seconds on the area above the medulla oblongata, vertebral arteries or endocrine representation area at the tail of pancreas reduced or eliminated microcirculatory disturbances and enhanced drug uptake.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Common factors contributing to intractable pain and medical problems with insufficient drug uptake in areas to be treated, and their pathogenesis and treatment: Part I. Combined use of medication with acupuncture, (+) Qi gong energy-stored material, soft laser or electrical stimulation. 135 50

The distribution of mercury within the brainstem and spinal cord of mice was investigated with the autometallographic technique after intramuscular administration of a single dose of mercuric mercury (HgCl2). Deposits of mercury were localized to motor neurons of the spinal cord and to brainstem motor nuclei; i.e., neurons with their peripheral projections outside the blood-brain barrier. Unilateral ligation of the hypoglossal nerve prior to the injection of HgCl2 prevented the accumulation of mercury deposits in the ipsilateral hypoglossal nucleus. The selective accumulation of mercury in spinal and brainstem motoneurons is most probably due to a leakage of metal-protein complexes from capillaries in muscle into myoneural junctions, followed by uptake into nerve terminals and retrograde axonal transport. The possible link between this process and the development of motor neuron degeneration in ALS is discussed.
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PMID:Inorganic mercury is transported from muscular nerve terminals to spinal and brainstem motoneurons. 138 15

The pathogenic relation of chronic mercurialism and amyotrophic lateral sclerosis (ALS) was evaluated clinically on 83 ex-mercury workers who were poisoned or exposed to mercury vapor about 18 years ago at one of the biggest mercury mines in Hokkaido, as well as on the causes of 65 expired workers in the cohort. The 83 ex-mercury workers were subdivided into two groups according to severity of mercury poisoning: 31 ex-workers who had been hospitalized for treatment of mercury poisoning and the remaining 52 ex-workers severely exposed to mercury vapor but not hospitalized. Neurologic examinations and measurements of mercury contents in the blood, urine, and hair samples in the 83 cases, failed to disclose any pathogenicity of mercury to ALS. Among these 148 including the 65 deceased cases, no ALS cases were found. Further clinical and epidemiological studies should be required on mercury poisoning as one of the risk factors in the development of ALS, especially in relation to selenium.
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PMID:[A clinical evaluation of the inorganic mercurialism--its pathogenic relation to amyotrophic lateral sclerosis]. 176 67

The mercury and selenium content in the hair of 13 ALS cases was studied by neutron activation analysis. The total mercury content of the hair was 3.70 +/- 2.73 ppm (mean +/- standard deviation) in the ALS patients as a whole, 4.46 +/- 3.16 ppm in the ALS patients from the middle of Kii Peninsula, and 2.49 +/- 1.38 ppm in the ALS patients from other region. As the comparison, mercury content was 2.43 +/- 0.79 ppm in the patients with Parkinsonism, and 2.10 +/- 1.13 ppm in the patients with multiple sclerosis (MS). The selenium content of the hair was 0.36 +/- 0.35 ppm for all ALS patients as a whole, 0.45 +/- 0.25 ppm in the ALS patients from the middle of the Kii Peninsula, and 0.21 +/- 0.47 ppm in the ALS from other region. There were no cases with higher values than mean values of control group, except one case from other regions. It is well known that the selenium decreases the toxicity of mercury in the human body. From these data mercury with low content of selenium might be one of the environmental factors which are thought to be involved in producing of ALS.
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PMID:[Amyotrophic lateral sclerosis and mercury--preliminary report]. 208 36

The causes of human amyotrophic lateral sclerosis (ALS) and the spinal muscular atrophies (SMA) are, almost without exception, unknown. This ignorance has stimulated the search for animal models to obtain insight into the etiology, pathogenesis and biochemical mechanisms underlying the human disorders. None of the 38 animal models, described in this review, provides an exact animal copy of a specific human motor neuron disease. Most of the models reproduce certain structural or physiological aspects of their human counterparts. The various experimental models can be classified according to the pathogenetic mechanism involved and according to the structural changes observed. Models based on experimentally induced disease, include heavy metals and trace elements (lead intoxication in guinea pigs, rabbits, rats, cats and primates; mercury intoxication in rats; aluminium intoxication in rabbits; swayback in goat kids; calcium and magnesium deficient rabbits and primates and calcium deficient cynomolgus monkeys), toxins (IDPN, vincristine, vinblastine, podophyllotoxin, colchicine, maytansine, maytanprine, L-BMAA, lectins, adriamycin), nutritional factors (ascorbic acid deficient guinea pigs), virus infection (spongiform polioencephalomyelitis, attenuated poliovirus, lactate dehydrogenase-elevating virus), and immunological factors (immunization with motor neurons). Hereditary models comprise hereditary canine spinal muscular atrophy, hereditary neurogenic amyotrophy in the pointer dog, Stockard paralysis, Swedish Lapland dog paralysis, "wobbler" mouse, "shaker" calf, and hereditary spinal muscular atrophy in zebra foals, crossbred rabbits,
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PMID:Animal models of amyotrophic lateral sclerosis and the spinal muscular atrophies. 267 Dec 67

In middle of Kii peninsula, one of the biggest mercury mine in Japan had been present until about 10 years ago. The mercury contents in water and fish are reported to be higher in this district. So we investigated the mercury in hair of patients and normal controls. In this study the subjects are 23 cases of ALS including 15 cases in Nara and Mie and 8 cases in other prefectures except in Kii peninsula, 14 cases with ataxia, 11 cases with other degenerative diseases like Parkinson's disease and Alzheimer's disease, 25 cases of cerebrovascular disease as compared to 26 normal controls. The hair are taken from 3 areas on head of patients and normal controls. They are washed in 2% sodium lauryl sulfate and stirred in distilled water several times, and they are soaked in acetone and dried in filter paper. They are inserted in fire and vaporized mercury are measured (Zeeman Effect Mercury Analyzer) in ppm. The hair mercury concentration is 2.81 ppm in ALS in total, 3.62 ppm in ALS in Nara and Mie and 1.39 ppm in outside of Kii Peninsula, 2.34 ppm in ataxia, 1.83 ppm in other degenerative diseases, 1.66 ppm in cerebrovascular disease and 1.44 ppm in normal controls. Statistically it is significant (p less than 0.05) between that in ALS in Nara and Mie and that in normal controls. 6 cases (40%) with ALS in Nara and Mie have the value above the mean +2 standard deviation of controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mercury in hair of patients with ALS]. 280 5

A retrospective case-control study of occupational heavy metal exposure was conducted using 66 amyotrophic lateral sclerosis (ALS) patients and 66 age- and sex-matched controls. Cases were ascertained primarily through a neurology support and research clinic. The self-administered questionnaire probed potential exposure to nine heavy metals: aluminum, lead, lead alkyl, magnesium, manganese, mercury, mercury alkyl, nickel and selenium. Using McNemar's test and a Mantel Haenszel extended analysis, no association was found between heavy metal exposure and the pathogenesis of ALS in this patient population. Demographic factors, fracture history, immunizations, travel and other variables were similar in ALS patients and controls.
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PMID:Amyotrophic lateral sclerosis and occupational heavy metal exposure: a case-control study. 374 67


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