Search

We investigate critical masses of and circular geodesics around doubly-degenerate stars (DDSs) which are composed of cold nuclear matter as well as cold Fermionic dark matter (DM). We here consider asymmetric dark Fermion with self-interaction as a DM candidate. These stars have core-envelope structures and are categorized into baryon-enveloped and DM-enveloped, according to the composition of their envelope. It is seen that the baryon-enveloped and DM-enveloped classes have their own critical masses determined mainly by the dominant component in their envelope. For a typical parameter sets, we see that a balanced mixture of two species may lead to smaller masses than if the either of the species is dominant. We also show that for a highly DM-enveloped case circular orbits in the vacuum region terminates at the innermost stable circular orbit (ISCO) in vacuum, but circular orbits of smaller radius are possible in the DM-envelope forming a gap between the ISCO and the inner orbits., Comment: 8 pages, 12 figures

To clarify mechanisms involved in the development of autoimmune hepatitis (AIH), we recently developed a mouse model of spontaneous AIH by inducing a concurrent loss of Foxp3(+) regulatory T cells and programmed cell death 1 (PD-1)-mediated signaling. Fatal AIH in these mice was characterized by severe T-cell infiltration and huge production of antinuclear antibodies (Abs). This study aims to identify induction sites, responsible T-cell subsets, and key molecules for induction of AIH.

Heparanase is an enzyme that cleaves heparan sulfate proteoglycans, an important component of the extracellular matrix to generate heparan sulfate fragments, leading to the remodeling of the extracellular matrix and the basement membrane particularly during cancer metastasis. A growing body of evidence suggests that heparanase serves multiple functions in normal tissues including the central nervous system. In this study, we showed that heparanase is expressed in reactive astrocytes in the peri-infarct lesion of a rat brain whose middle cerebral artery was transiently occluded for 90 min. RT-PCR and Western blot analyses revealed that heparanase expression was markedly upregulated during the subacute phase of ischemia (from 3 to 7 days post-reperfusion (dpr)). As revealed by immunohistochemical study, heparanase was localized in astrocytes located in the peri-infarct region. Heparanase+ astrocytes expressed nestin that is known as a marker of reactive astrocytes. Infiltrated neutrophils were weakly heparanase+. After 7 dpr, the expression level of heparanase+ astrocytes considerably decreased. Therefore, the maximum expression of heparanase by astrocytes may correlate with the time of migration of reactive astrocytes toward the ischemic core, which may result in astrogliosis. These findings suggest a novel role of heparanase in the pathophysiology of brain ischemia.