Galactic Effects on Habitability

The galactic environment has been suspected to influence planetary habitability in many ways. Very metal-poor regions of the Galaxy, or those largely devoid of atoms more massive than H and He, are thought to be unable to form habitable planets. Moreover, if such planets do form, the young system is subjected to close stellar passages while it resides in its stellar birth cluster. Various potential hazards remain after clusters disperse. For instance, central galactic regions may present risks to habitability via nearby supernovae, gamma ray bursts (GRBs), and frequent comet showers. In addition, planets residing within very wide binary star systems are affected by the Galaxy, as local gravitational perturbations from the Galaxy can increase the binary's eccentricity until it destabilizes the planets it hosts. Here we review the most recent work on the main galactic influences over planetary habitability. Although there must be some metallicity limit below which rocky planets cannot form, recent exoplanet surveys show that they form around stars with a very large range of metallicities. Once formed, the probability of star clusters destabilizing planetary systems only becomes high for rare, extremely long-lived clusters. Regarding threats to habitability from supernovae, GRBs, and comet showers, many recent studies suggest that their hazards are more limited than originally thought. Finally, denser regions of the Galaxy enhance the threat that very wide binary companions pose to planetary habitability, but the probability that a very wide binary star disrupts habitability will always be substantially below 100% for any environment. While some Milky Way regions must be more hospitable to habitable planets than others, it is difficult to state that habitable planets are confined to any well-defined region of the Galaxy or that any other particular region of the Galaxy is uninhabitable.Comment: Invited review chapter, accepted for publication in the "Handbook of Exoplanets"; 19 pages; 2 figure

Sex-specific impact of patterns of imageable tumor growth on survival of primary glioblastoma patients

BACKGROUND: Sex is recognized as a significant determinant of outcome among glioblastoma patients, but the relative prognostic importance of glioblastoma features has not been thoroughly explored for sex differences. METHODS: Combining multi-modal MR images, biomathematical models, and patient clinical information, this investigation assesses which pretreatment variables have a sex-specific impact on the survival of glioblastoma patients (299 males and 195 females). RESULTS: Among males, tumor (T1Gd) radius was a predictor of overall survival (HR = 1.027, p = 0.044). Among females, higher tumor cell net invasion rate was a significant detriment to overall survival (HR = 1.011, p \u3c 0.001). Female extreme survivors had significantly smaller tumors (T1Gd) (p = 0.010 t-test), but tumor size was not correlated with female overall survival (p = 0.955 CPH). Both male and female extreme survivors had significantly lower tumor cell net proliferation rates than other patients (M p = 0.004, F p = 0.001, t-test). CONCLUSION: Despite similar distributions of the MR imaging parameters between males and females, there was a sex-specific difference in how these parameters related to outcomes

Regulation of the hepatitis C virus RNA replicase by endogenous lipid peroxidation

Oxidative tissue injury often accompanies viral infection, yet there is little understanding of how it influences virus replication. We show that multiple hepatitis C virus (HCV) genotypes are exquisitely sensitive to oxidative membrane damage, a property distinguishing them from other pathogenic RNA viruses. Lipid peroxidation, regulated in part through sphingosine kinase-2, severely restricts HCV replication in Huh-7 cells and primary human hepatoblasts. Endogenous oxidative membrane damage lowers the 50% effective concentration of direct-acting antivirals in vitro, suggesting critical regulation of the conformation of the NS3-4A protease and the NS5B polymerase, membrane-bound HCV replicase components. Resistance to lipid peroxidation maps genetically to transmembrane and membrane-proximal residues within these proteins and is essential for robust replication in cell culture, as exemplified by the atypical JFH1 strain of HCV. Thus, the typical, wild-type HCV replicase is uniquely regulated by lipid peroxidation, providing a mechanism for attenuating replication in stressed tissue and possibly facilitating long-term viral persistence.Daisuke Yamane, David R McGivern, Eliane Wauthier, MinKyung Yi, Victoria J Madden, Christoph Welsch, Iris Antes, Yahong Wen, Pauline E Chugh, Charles E McGee, Douglas G Widman, Ichiro Misumi, Sibali Bandyopadhyay, Seungtaek Kim, Tetsuro Shimakami, Tsunekazu Oikawa, Jason K Whitmire, Mark T Heise, Dirk P Dittmer, C Cheng Kao, Stuart M Pitson, Alfred H Merrill Jr, Lola M Reid, Stanley M Lemo