45,319 research outputs found
Unary FA-presentable semigroups
No full textAutomatic presentations, also called FA-presentations, were introduced to extend nite model theory to innite structures whilst retaining the solubility of interesting decision problems. A particular focus of research has been the classication of those structures of some species that admit automatic presentations. Whilst some successes have been obtained, this appears to be a dicult problem in general. A restricted problem, also of signicant interest, is to ask this question for unary automatic presentations: auto-matic presentations over a one-letter alphabet. This paper studies unary FA-presentable semigroups. We prove the following: Every unary FA-presentable structure admits an injective unary automatic presentation where the language of representatives consists of every word over a one-letter alphabet. Unary FA-presentable semigroups are locally nite, but non-nitely generated unary FA-presentable semigroups may be innite. Every unary FA-presentable semigroup satises some Burnside identity.We describe the Green's relations in unary FA-presentable semigroups. We investigate the relationship between the class of unary FA-presentable semigroups and various semigroup constructions. A classication is given of the unary FA-presentable completely simple semigroups.Peer reviewe
On Property (FA) for wreath products
No full textWe prove that the standard wreath product A \wr B has
Property (FA) if and only if B has Property (FA) and A is a finitely
generated group with finite abelianisation. We also prove an analogous
result for hereditary Property (FA). On the other hand, we
prove that many groups with hereditary Property (FA) are not
quotients of finitely presented groups with the same property
Hypomorphic Mutations in the Central Fanconi Anemia Gene FANCD2 Sustain a Significant Group of FA-D2 Patients with Severe Phenotype. Running title : FA-D2 phenotype and FANCD2 mutations
No full textPremi a l'excel·lència investigadora. Àmbit de les Ciències de la Salut. 2008FANCD2 is an evolutionarily conserved Fanconi anemia (FA) gene that plays a central role in DNA double-strand type damage responses. Using complementation assays and immunoblotting, a consortium of American and European groups assigned 29 FA patients from 23 families and 4 additional unrelated patients to complementation group FA-D2. This amounts to 3 to 6% of FA patients registered in various datasets. Malformations are frequent in FA-D2 patients and hematological manifestations appear earlier and progress more rapidly when compared to patients from all other FA groups combined, as represented by the International Fanconi Anemia Registry, IFAR. FANCD2 is flanked by two pseudogenes. Mutation analysis revealed the expected total of 66 mutated alleles, 34 of which result in aberrant splicing patterns. Many mutations are recurrent and have ethnic associations and shared alleles. There were no biallelic null mutations so that residual FANCD2 protein of both isotypes was observed in all patients' cell lines available. These analyses suggest that unlike in a knock-out mouse model, total absence of FANCD2 is not existing in FA-D2 patients due to constraints on viable combinations of FANCD2 mutations. Although hypomorphic mutations are involved, the result generally is a relatively severe form of FA
Plasma concentrations (g/100 g FA) of selected FA in mice after dietary intervention for 12 weeks<sup>1</sup>.
No full textPlasma concentrations (g/100 g FA) of selected FA in mice after dietary intervention for 12 weeks1.</p
Reduced sensitivity of fa/fa Zucker rats to adrenomedullin
No full textRat adrenomedullin is a peptide vasodepressor that may be of importance in the pathogenesis of hypertensive disease. Because of the known link between obesity and hypertension, we hypothesized that decreased responsiveness to adrenomedullin might be seen in an obese rodent model. In this study, the in vivo vasodilator actions of exogenous adrenomedullin were compared in anesthetized lean (n = 7) and obese (fa/fa) Zucker rats (n = 8). Adrenomedullin dose dependently lowered mean arterial pressure in both phenotypes, but the half-maximal dose (ID50) was 2-fold higher in fa/fa rats (1.7 +/- 0.22 vs. 0.83 +/- 0.06 nmol/kg). Moreover, the duration of effect was markedly reduced in the fa/fa rats, to 1-2 min from about 5 min in the lean animals. There was no evidence for an increased rate of degradation of adrenomedullin in the fa/fa rats. Although the rats used in this study were not hypertensive, adrenomedullin had reduced sensitivity and duration of action. The evidence suggests possible defects at the target receptor or altered metabolism of adrenomedullin in obesity.LR: 20061115; PUBM: Print; JID: 0372712; 0 (Peptides); 0 (Vasodilator Agents); 148498-78-6 (Adrenomedullin); ppublishSource type: Electronic(1
Effect of dietary butter (CON), chia seed (CS) and pumpkin seed (PS) on FA profile (g /100 g FA total methyl ester) in sheep milk.
No full textEffect of dietary butter (CON), chia seed (CS) and pumpkin seed (PS) on FA profile (g /100 g FA total methyl ester) in sheep milk.</p
Fatty acid composition (g/100 g FA) of crocodile oil and palm oil.
No full textFatty acid composition (g/100 g FA) of crocodile oil and palm oil.</p
The effect of pertussis toxin on insulin secretion from obese (fa/fa) Zucker rats
No full textThe obese (fa/fa) Zucker rat is a genetic model of childhood-onset obesity in humans. Pathological changes seen in this rat include, among others, a pronounced hyperinsulinemia in the presence of normoglycemia. The etiology of elevated blood levels of insulin is unknown. These studies investigated the role of the inhibitory guanine nucleotide binding protein G\sb{\rm i} of adenylate cyclase in the endocrine pancreas. The hypothesis was that function of G\sb{\rm i} in obese rats was compromised, resulting in loss of inhibitory pathways. This loss of inhibition could contribute to hypersecretion of insulin.To test this hypothesis, two separate sets of experiments were performed. Initially isolated pancreatic islets of lean and obese Zucker rats were used. The second experiment employed an isolated perfused pancreas preparation. The function of inhibitory hormones of insulin secretion reported to act via G\sb{\rm i}, including epinephrine, somatostatin and galanin, were tested. Pertussis toxin was used to inactivate G\sb{\rm i} both 'in vivo' and in isolated islets. (Abstract shortened by UMI.).Source: Masters Abstracts International, Volume: 30-03, page: 0652
Identification of biochemical defects in pancreatic islets of fa/fa rats: a developmental study
No full textAdult obese (fa/fa) Zucker rats hypersecrete insulin in response to glucose and other secretagogues. Functional changes in islet alpha 2-adrenoceptors (8) and glycolytic regulation (9) have been reported. In this study, the development of these biochemical lesions in islets isolated from suckling (3 week old) and weanling (5 week old) lean and fa/fa rats was investigated and compared to results in adult animals. Glucose (15 mM)-induced insulin secretion was inhibited by mannoheptulose (MH) in lean (n = 8) but not fa/fa (n = 10) adult rats, indicating loss of sensitivity of glucokinase to competitive inhibition. Sensitivity to MH was somewhat reduced in the islets of 3- and 5-week-old fa/fa (n = 7 and 12) compared to lean (n = 15 and 9) rats, requiring 30-100 fold higher concentrations to achieve significant inhibition. At 3 weeks of age fa/fa rats did not differ from lean controls in either islet insulin content or body weight, but both parameters were increased in fa/fa rats by 5 weeks. The presence of altered alpha 2-adrenoceptor function in fa/fa rats could not be confirmed in this study. Unlike the previous report, prazosin did not antagonize alpha 2-agonist mediated inhibition of insulin secretion. The presence of defective regulation of the glycolytic pathway by mannoheptulose in suckling and weanling rats may contribute to development of hyperinsulinemia in fa/fa rats.LR: 20061115; PUBM: Print; JID: 9305691; 0 (Receptors, Adrenergic, alpha); 11061-68-0 (Insulin); 50-99-7 (Glucose); 654-29-5 (Mannoheptulose); EC 2.7.1.2 (Glucokinase); ppublishSource type: Electronic(1
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