17,208,553 research outputs found

    Characterization of the haemoglobin-mediated inhibition of the enzymatic activity of bovine serum amine oxidase

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    Haemoglobin has been previously identified as responsible for the decreased enzymatic activity of copper bovine serum amine oxidase (BSAO) in suspensions of human or bovine hemolyzed erythrocytes [Marcocci, L., Pietrangeli, P., Befani, O., Mavelli I., & Mondovi', B. (1991b) Life Chem. Report, 9, 171-177]. This is confirmed by present results on bovine methaemoglobin. Bovine globin and horse skeletal muscle mioglobin showed a similar inhibiting ability, but neither bovine serum albumin nor cytochrome c inhibited BSAO activity under the same experimental conditions. The inhibitory effect of bovine haemoglobin was dependent on pH only at high buffer ionic strength. It was highest in physiological conditions (PBS) where haemoglobin acted as a reversible non competitive inhibitor of BSAO activity, with apparent Ki of 0.5 mM at 37°C. The inhibition was unaffected by partial BSAO deglycosylation (40% of glucidic residues removed) but decreased when haemoglobin lysine groups were derivatised using citraconic anhydride. A possible molecular mechanism underlying the inhibitory effect is discussed

    REVIEW: Giuseppe Marcocci, "L'invenzione di un impero. Politica e cultura nel mondo portoghese (1450-1600)", (Rome: Cacucci, 2011)

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    Review of a book by Giuseppe Marcocci on politics and culture in the Portuguese Empire in the long 15th century

    Familial and Hereditary Forms of Primary Hyperparathyroidism

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    Individuals with a familial predisposition to the development of parathyroid tumors constitute a small minority of all patients with primary hyperparathyroidism (PHPT). These familial syndromes exhibit Mendelian inheritance patterns and the main causative genes in most families have been identified. They include multiple endocrine neoplasia (MEN; types 1, 2A, and 4), hyperparathyroidism-jaw tumor (HPT-JT) syndrome, familial isolated hyperparathyroidism, familial hypocalciuric hypercalcemia (FHH), and neonatal severe PHPT. Each MEN type is associated with the various combinations of specific tumors. MEN1 is characterized by the occurrence of parathyroid, enteropancreatic, and pituitary tumors; MEN2A is characterized by medullary thyroid carcinoma and pheochromocytoma, and MEN4 is characterized by a pathological spectrum similar to that of MEN1 in association with tumors of the adrenal, kidney, and reproductive organs. HPT-JT is characterized by PHPT, ossifying fibromas of maxillary bones, kidney disease, and uterine neoplasias. The prompt diagnosis of these diseases is of great importance for planning appropriate surveillance of the mutant carriers and correct surgical management. The search for mutation is also useful for the identification of the family members who do not carry the mutation and can avoid unnecessary biochemical and instrumental evaluations. Surgery remains the treatment of choice in all familial forms except FHH

    The contribution of light Majorana neutrinos to neutrinoless double beta decay and cosmology

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    Cosmology is making impressive progress and it is producing stringent bounds on the sum of the neutrino masses Sigma, a parameter of great importance for the current laboratory experiments. In this letter, we exploit the potential relevance of the analysis of Palanque-Delabrouille et al. [JCAP 02 (2015) 045] to the neutrinoless double beta decay (0 nu beta beta) search. This analysis indicates small values for the lightest neutrino mass, since the authors find Sigma < 84 meV at 1 sigma C.L., and provides a 1 sigma preference for the normal hierarchy. The allowed values for the Majorana effective mass, probed by 0 nu beta beta, turn out to be < 75 meV at 3 sigma C.L. and lower down to less than 20 meV at 1 sigma C.L.. If this indication is confirmed, the impact on the 0 nu beta beta experiments will be tremendous since the possibility of detecting a signal will be out of the reach of the next generation of experiments

    Italian Society of Endocrinology Consensus Statement: Definition, evaluation and management of patients with mild primary hyperparathyroidism

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    Over the last 50 years, the spectrum of clinical presenta- tion of primary hyperparathyroidism (PHPT) has shifted from a symptomatic disorder, characterized by symptoms of hypercalcemia, nephrolithiasis, and overt bone disease, toward a less symptomatic or asymptomatic disorder . The recognition of the asymptomatic variant of PHPT has markedly increased following the inclusion of serum calcium measurement in the multichannel biochemical screenin

    L-thyroxine therapy induces a fall of thyroid microsomal and thyroglobulin antibodies in idiopathic myxedema and in hypothyroid, but not in euthyroid Hashimoto's thyroiditis.

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    Thyroid microsomal (MAb) and thyroglobulin (TgAb) antibodies were sequentially measured by sensitive and quantitative radioassays in 17 patients with goitrous Hashimoto’s thyroiditis (9 hypothyroid, 8 euthyroid) and in 19 patients with idiopathic myxedema before and at various time intervals up to 24–48 months after the institution of L-thyroxine therapy. Thyroid antibodies were also determined in 5 euthyroid subjects with Hashimoto’s thyroiditis maintained without treatment for a similar period. During L-thyroxine administration a reduction of MAb with respect to the pretreatment level was found in 6 of the 9 (67%) hypothyroid patients with Hashimoto’s thyroiditis and in 16 of the 19 (84%) patients with idiopathic myxedema. The decrease of MAb was highly significant in both groups (p &lt; 0.001 and p &lt; 0.0001, respectively). A fall of TgAb occurred in 2 of the 3 patients (75%) with hypothyroid Hashimoto’s thyroiditis and in 9 of the 10 (90%, p &lt; 0.001) patients with idiopathic myxedema having abnormally elevated pretreatment TgAB levels. No consistent pattern of MAb and TgAb changes was observed in the euthyroid subjects with Hashimoto’s thyroiditis, whether treated or untreated. In the hypothyroid patients with Hashimoto’s thyroiditis a significant association was found between the decrease of MAb and the reduction of goiter size (p &lt; 0.05) occurring during L-thyroxine administration. Moreover, the decrease of MAb and TgAb in idiopathic myxedema was greater (p &lt; 0.05) in the patients with normalized serum TSH (≤ 4 μU/ml) than in those showing only a partial reduction of serum TSH (&gt; 4 μU/ml) under L-thyroxine. It is suggested that the decrease of thyroid antibodies during L-thyroxine therapy could be due to a reduced antigen availability to the immune system, resulting from a decreased stimulation of thyroid tissue by circulating TSH. © 1986, Italian Society of Endocrinology (SIE). All rights reserved
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