Effects of Gas on Formation and Evolution of Stellar Bars and Nuclear Rings in Disk Galaxies

We run self-consistent simulations of Milky Way-sized, isolated disk galaxies to study formation and evolution of a stellar bar as well as a nuclear ring in the presence of gas. We consider two sets of models with cold or warm disks that differ in the radial velocity dispersions, and vary the gas fraction $f_{\rm gas}$ by fixing the total disk mass. A bar forms earlier and more strongly in the cold disks with larger $f_{\rm gas}$, while gas progressively delays the bar formation in the warm disks . The bar formation enhances a central mass concentration which in turn makes the bar decay temporarily, after which it regrows in size and strength, eventually becoming stronger in models with smaller $f_{\rm gas}$. Although all bars rotate fast in the beginning, they rapidly turn to slow rotators. In our models, only the gas-free, warm disk undergoes rapid buckling instability, while other disks thicken more gradually via vertical heating. The gas driven inward by the bar potential readily forms a star-forming nuclear ring. The ring is very small when it first forms and grows in size over time. The ring star formation rate is episodic and bursty due to feedback, and well correlated with the mass inflow rate to the ring. Some expanding shells produced by star formation feedback are sheared out in the bar regions and collide with dust lanes to appear as filamentary interbar spurs. The bars and nuclear rings formed in our simulations have properties similar to those in the Milky Way

Effects of Gas on Formation and Evolution of Stellar Bars and Nuclear Rings in Disk Galaxies

We run self-consistent simulations of Milky Way-sized, isolated disk galaxies to study the formation and evolution of a stellar bar as well as a nuclear ring in the presence of gas. We consider two sets of models with cold or warm disks that differ in the radial velocity dispersions, and vary the gas fraction f_(gas) by fixing the total disk mass. A bar forms earlier and more strongly in the cold disks with larger f_(gas), while gas progressively delays the bar formation in the warm disks. The bar formation enhances a central mass concentration, which in turn causes the bar to decay temporarily, after which it regrows in size and strength, eventually becoming stronger in models with smaller f_(gas). Although all bars rotate fast in the beginning, they rapidly turn to slow rotators. In our models, only the gas-free, warm disk undergoes rapid buckling instability, while other disks thicken more gradually via vertical heating. The gas driven inward by the bar potential readily forms a star-forming nuclear ring. The ring is very small when it first forms and grows in size over time. The ring star formation rate is episodic and bursty due to feedback, and is well correlated with the mass inflow rate to the ring. Some expanding shells produced by star formation feedback are sheared out in the bar regions and collide with dust lanes to appear as filamentary interbar spurs. The bars and nuclear rings formed in our simulations have properties similar to those in the Milky Way

Beclin 1 functions as a negative modulator of MLKL oligomerisation by integrating into the necrosome complex

Necroptosis is a form of regulated cell death caused by formation of the necrosome complex. However, the factors modulating this process and the systemic pathophysiological effects of necroptosis are yet to be understood. Here, we identified that Beclin 1 functions as an anti-necroptosis factor by being recruited into the necrosome complex upon treatment with TNF alpha, Smac mimetic, and pan-caspase inhibitor and by repressing MLKL oligomerisation, thus preventing the disruption of the plasma membrane. Cells ablated or knocked-out for Beclin 1 become sensitised to necroptosis in an autophagy-independent manner without affecting the necrosome formation itself. Interestingly, the recruitment of Beclin 1 into the necrosome complex is dependent on the activation and phosphorylation of MLKL. Biochemically, the coiled-coil domain (CCD) of Beclin 1 binds to the CCD of MLKL, which restrains the oligomerisation of phosphorylated MLKL. Finally, Beclin 1 depletion was found to promote necroptosis in leukaemia cells and enhance regression of xenografted-tumour upon treatment with Smac mimetics and caspase inhibitors. These results suggest that Beclin 1 functions as a negative regulator in the execution of necroptosis by suppressing MLKL oligomerisation

Retroperitoneal Giant Liposarcoma

Retroperitoneal liposarcoma is an infrequent, locally aggressive malignancy. We report two cases of huge retroperitoneal liposarcomas. The presence of a palpable abdominal mass was a common symptom of the two patients. Preoperative imaging study showed huge retroperitoneal tumors. Both patients underwent complete surgical resections, and a negative microscopic margin was achieved in both cases. The histopathologic diagnosis was a well-differentiated retroperitoneal liposarcoma. Neither of the two patients developed a recurring tumor during the 1.5 years of follow-up

A two-photon fluorescent probe for lysosomal zinc ions

The selective detection of zinc ions in lysosomes over that in cytosol is achieved with a fluorescent probe, which enabled the fluorescence imaging of endogenous zinc ions in lysosomes of NIH 3T3 cells as well as mouse hippocampal tissues by two-photon microscopy under excitation at 900 nm.open

Could a Growth Spurt Cause Linear Focal Elastosis Like Striae Distensae?

Linear focal elastosis (LFE) is characterized by several asymptomatic, yellow, palpable, irregularly indurated, striae-like lines extending horizontally across the middle and lower back. A focal increase in elastic fibers is a hallmark of the disease as seen from biopsy specimens. The pathogenesis of LFE is unclear, as is the association between LFE and striae distensae (SD). However, the prevailing opinion is that LFE represents an excessive regenerative process of elastic fibers and is analogous to keloidal repair of SD. Although the timing of onset of LFE and SD was not synchronous in our patient, the triggering factor was the same, which was the growth spurt. This case is supporting the putative association between LFE and SD