Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied 13 patients with lipoamide dehydrogenase (LAD) deficiency, originating from seven Ashkenazi Jewish families. Their disease was characterized by recurrent attacks of vomiting, abdominal pain, and encephalopathy accompanied by elevated liver transaminases, prolonged prothrombin time, and occasionally associated with lactic and ketoacidemia or with myoglobinuria. Two patients who presented neonatally suffered from residual neurological damage with attention deficit hyperactive disorder, mild ataxia, motor incoordination, muscle hypotonia, and weakness. Nine patients who presented in early childhood or later suffered from exertional fatigue between decompensation episodes but were otherwise asymptomatic. Two patients died because of intractable metabolic acidosis and multi-organ failure. In all patients LAD activity was reduced to 8 to 21% of the control in muscle or lymphocytes. In four patients LAD protein in muscle was reduced to 20 to 60% of the control. Direct sequencing of the cDNA of the LAD gene showed that 12 of the 14 mutated alleles carried the G229C mutation and two carried an insertion mutation 105insA (Y35X). The patients who presented neonatally and had more severe sequelae were compound heterozygotes for the two mutations; patients who presented in early childhood or later were homozygous for the G229C mutation. Using an allele-specific oligonucleotide hybridization technique, nine heterozygotes for the G229C mutation were identified among 845 anonymous individuals of Ashkenazi Jewish origin disclosing a carrier rate of 1:94. Because of the significant morbidity associated with the disease, screening for the G229C mutation among Ashkenazi Jewish couples should be considered.
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PMID:Molecular basis of lipoamide dehydrogenase deficiency in Ashkenazi Jews. 993 85

The effect of RCMF-magnetic therapy apparatus on signal substances was studied. The radioimmunoassay (RIA) suggested that the magnetic field increased beta-endorphin markedly in plasma. ELISA indicated that the magnetic field inhibited vomiting reaction induced by chemotherapy drug, with reversible decrease of serotonin (5-HT) level in brains, small intestine tissue and serum. Furthermore, the bioeffect of magnetic fields on 5-HT level presented a typical window effect and post-effect, and the inhibitory effect of magnetic field on the emesis was parallel to the decrease level of 5-HT. This result implied that the decrease of 5-HT might be the basis of rotating constant magnetic field (RCMF) inhibiting drug-induced emesis. The nitric acid reductase-spectrophotometry and nicotinamide adenine dinucleotide-diaphorase/arginine-vasopressin (AVP) cytochemistry technique showed that the magnetic field induced nitric oxide (NO) increase in hypothalamus and the high NO(A) level lasted for 3 hours. The results suggested that NO(A) increases after the treatment of the magnetic field in hypothalamus, which may result from strong expression of NO-ergic neuron in paraventricular hypothalamic nucleus (PVN), periventricular hypothalamic nucleus (PEN) and supraoptic nucleus (SON). The coexistence of NO and AVP may play an important role in the regulation of endocrine and neuroendocrine by the magnetic field. And our data also confirmed that the magnetic field increased the content of NO so strongly that high NO level lasted for 3 hours, also made neuropeptide Y (NPY) cell in medulla stained heavily.
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PMID:Molecular mechanism of effect of rotating constant magnetic field on organisms. 1872 1