Birthrates and delay times of Type Ia supernovae

Type Ia supernovae (SNe Ia) play an important role in diverse areas of astrophysics, from the chemical evolution of galaxies to observational cosmology. However, the nature of the progenitors of SNe Ia is still unclear. In this paper, according to a detailed binary population synthesis study, we obtained SN Ia birthrates and delay times from different progenitor models, and compared them with observations. We find that the Galactic SN Ia birthrate from the double-degenerate (DD) model is close to those inferred from observations, while the birthrate from the single-degenerate (SD) model accounts for only about 1/2-2/3 of the observations. If a single starburst is assumed, the distribution of the delay times of SNe Ia from the SD model is a weak bimodality, where the WD + He channel contributes to the SNe Ia with delay times shorter than 100Myr, and the WD + MS and WD + RG channels to those with age longer than 1Gyr.Comment: 11 pages, 2 figures, accepted by Science in China Series G (Dec.30, 2009

Identification of a novel TSC2 c.3610G > A, p.G1204R mutation contribute to aberrant splicing in a patient with classical tuberous sclerosis complex: a case report

Background: Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterized by hamartomas in any organ systems. Mutations in the TSC1 or TSC2 gene lead to the dysfunction of hamartin or tuberin proteins, which cause tuberous sclerosis complex. Case presentation: We describe the clinical characteristics of patients from a Chinese family with tuberous sclerosis complex and analyze the functional consequences of their causal genetic mutations. A novel heterozygous mutation (c.3610G > A) at the last nucleotide of exon 29 in TSC2 was identified. On the protein level, this variant was presumed to be a missense mutation (p.Gly1204Arg). However, the splicing assay revealed that this mutation also leads to the whole TSC2 exon 29 skipping, besides the wild-type transcript. The mutated transcript results in an in-frame deletion of 71 amino acids (p.Gly1133_Thr1203del) and its ratio with the normal splice product is of about 44:56. Conclusions: The novel c.3610G > A TSC2 mutation was identified in association with tuberous sclerosis complex. And it was proven to code both for a missense-carrying transcript (56%), and for an isoform lacking exon 29 (44%)