Disease relevance of MEA1

• These symptoms and findings are characteristic of multiple endocrine adenomatosis (MEA IIb) syndromes [1].
• Three of the Z-E patients exhibited MEA, two having hyperinsulinism and one hyperparathyroidism [2].
• Since PRL-secreting pituitary tumors may occur with variable presentation in MEA-1, periodic measurements of serum PRL levels should be carried out to detect this abnormality [3].
• Three cases are described in which hyperprolactinemia occurred as a feature of multiple endocrine adenomatosis, type 1 (MEA-1); enlargement of the sella turcica varied from gross to absent, and serum prolactin (PRL) levels ranged from 21 to 1,000 ng/ml in these cases [3].
• We evaluated efficacy and toxicity of methotrexate, etoposide and dactinomycin (MEA) as first-line therapy for high risk disease and etoposide and dactinomycin (EA) as second-line therapy for methotrexate-refractory low risk disease in a retrospective analysis of 73 patients (38 MEA, 35 EA) treated since 1986 at a supra-regional centre [4].

Psychiatry related information on MEA1

• Twenty-seven symptoms of 859 treated hypertensive patients were evaluated using a self-administered questionnaire and correlated with the depression (DEP), free-floating anxiety (FFA), phobic anxiety (PHO), obsessionality (OBS) and extraversion (HYS) scores of the Middlesex Hospital Questionnaire [5].
• MEAP was inversely correlated to systemic pain thresholds [6].

High impact information on MEA1

• Like the MEA gene, genes A and B were coordinately transcribed in the testis, which suggests that MEA and genes A and B are members of a gene family [7].
• Sequence properties of the MEA protein include an acidic activation domain, a proline-rich region and two coiled-coil domains indicating protein binding and activation functions [8].
• Purification of MEA, a mast cell growth-enhancing activity, to apparent homogeneity and its partial amino acid sequencing [9].
• MEA was characterized as a glycoprotein with a Mr range between 37,000 and 43,000 [9].
• Inasmuch as MEA was N-terminally blocked during automated Edman-degradation, peptide fragments after digestion with trypsin were used for partial amino acid sequence determination [9].

Chemical compound and disease context of MEA1

• Cysteamine (beta-mercaptoethylamine, MEA) is currently used to treat children with nephropathic cystinosis [10].
• Six healthy subjects, 23 members of three MEA I families, seven patients with malignant pancreatic endocrine tumours and four patients with carcinoid tumours of the gastrointestinal tract were subjected to a standardized test meal, followed by intravenous atropine 60 min after the start of the meal [11].
• Toxicity assays, first evaluated on solid medium MEA, have not shown any toxicity of fluoranthene (1-100 mg.L-1) towards fungi [12].
• OBJECTIVE: To evaluate the efficacy and safety of etoposide/methotrexate/actinomycin D (MEA regimen) as initial chemotherapy and 5-fluorouracil/actinomycin D (FA regimen) as salvage chemotherapy for high-risk gestational trophoblastic tumor (GTT) [13].
• After toxicity identification evaluation (TIE) test of raw wastewater. the inhibition was related to organic nitrogen (TMAH, MEA) and unionized ammonia (free ammonia, NH3) with high pH [14].

Biological context of MEA1

• The genetic conservation and testis-specific expression of the MEA gene support the hypothesis that it plays an important role in mammalian spermatogenesis and/or testis development [7].
• Analysis of vomitus indicated that hydrolysis of the phosphate group of MEAP occurs in the stomach [10].
• HYS was positively associated with the frequency of sexual intercourse in men and negatively with complaints of dyspnoea, tingling in the limbs and a slow walking pace [5].
• In part, this protection seems to have been induced by oxygen consumption in the system due to MEA autoxidation under formation of H2O2 [15].
• However, gpb1-disrupted haploid cells mated and sporulated faster than wild-type cells, both in sporulation (MEA) and in complex medium (YE): when examined 23 h after transfer to sporulation medium, 35% of gpb1-disrupted haploid pairs had undergone conjugation and sporulation, whereas only 3-5% of wild-type haploid pairs had done so [16].

Anatomical context of MEA1

• We have shown that both rat and human liver microsomes metabolize MEA (0.035 nmol/min/mg and 0.069 nmol/min/mg, respectively) and DEA (0.041 nmol/min/mg and 0.040 nmol/min/mg, respectively) [17].
• The percent decrease in leukocyte cystine content obtained with MEA administration (61.9%) was not significantly different from the decrease observed when MEAP was administered (65.3%) [10].
• The syndrome of multiple endocrine neoplasia (MEN or MEA) type 2b is characterized by the association of medullary carcinoma of the thyroid, phaeochromocytoma, ganglioneuromatosis and Marfan-like features [18].
• Conservative treatment of parathyroid gland hyperplasia in the MEA II syndrome is substantiated [19].
• Statistical analysis showed that the Slit sampler and the N6-Andersen sampler in combination with DG18 and MEA gave the best precision and the highest yield in terms of colony forming units per square cubic meter of air (CFU/m3) and number of species isolated [20].

Associations of MEA1 with chemical compounds

• Experiments demonstrated that a thiol-containing reducing agent, mercaptoethylamine (MEA or cysteamine), was the most effective, among other commonly known radical quenchers or singlet oxygen scavengers, in suppressing photobleaching of fluorescein while not reducing the fluorescence quantum yield [21].
• The triplet lifetime of fluorescein was reduced upon adding MEA [21].
• Persistent gestational trophoblastic disease: results of MEA (methotrexate, etoposide and dactinomycin) as first-line chemotherapy in high risk disease and EA (etoposide and dactinomycin) as second-line therapy for low risk disease [4].
• We have determined that both rat and human livers metabolize both CMEPA to MEA (0.308 nmol/min/mg and 0.541 nmol/min/mg, respectively) and CDEPA to DEA (0.350 nmol/min/mg and 0.841 nmol/min/mg, respectively) [17].
• MEA and MEAP appear to be equally effective in their cystine-depleting properties [10].

Analytical, diagnostic and therapeutic context of MEA1

• In conclusion, the MEA and EA chemotherapy regimens for persistent trophoblastic disease are very well tolerated, do not appear to affect future fertility and are associated with excellent, sustained complete response rates [4].
• The cardiac enkephalin, methionine-enkephalin-arginine-phenylalanine (MEAP), alters vagally induced bradycardia when introduced by microdialysis into the sinoatrial (SA) node [22].
• MEA was determined by sodium borohydride reduction followed by high-performance liquid chromatography separation and electrochemical detection [10].
• Cells directly on the top and on the edges of the stimulating microelectrodes in the MEA were preferentially transfected with PI as predicted by the simulations [23].
• Bilateral adrenalectomy is recommended for proved adrenal medullary disease in the MEA II syndrome [19].

References