Kinematics of Circumgalactic Gas: Feeding Galaxies and Feedback

We present observations of 50 pairs of redshift z ~ 0.2 star-forming galaxies and background quasars. These sightlines probe the circumgalactic medium (CGM) out to half the virial radius, and we describe the circumgalactic gas kinematics relative to the reference frame defined by the galactic disks. We detect halo gas in MgII absorption, measure the equivalent-width-weighted Doppler shifts relative to each galaxy, and find that the CGM has a component of angular momentum that is aligned with the galactic disk. No net counter-rotation of the CGM is detected within 45 degrees of the major axis at any impact parameter. The velocity offset of the circumgalactic gas correlates with the projected rotation speed in the disk plane out to disk radii of roughly 70 kpc. We confirm previous claims that the MgII absorption becomes stronger near the galactic minor axis and show that the equivalent width correlates with the velocity range of the absorption. We cannot directly measure the location of any absorber along the sightline, but we explore the hypothesis that individual velocity components can be associated with gas orbiting in the disk plane or flowing radially outward in a conical outflow. We conclude that centrifugal forces partially support the low-ionization gas and galactic outflows kinematically disturb the CGM producing excess absorption. Our results firmly rule out schema for the inner CGM that lack rotation and suggest that angular momentum as well as galactic winds should be included in any viable model for the low-redshift CGM.Comment: Accepted for publication in the Astrophysical Journa

Hyper-entanglement between pulse modes and frequency bins

Hyper-entanglement between two or more photonic degrees of freedom (DOF) can enhance and enable new quantum protocols by allowing each DOF to perform the task it is optimally suited for. Here we demonstrate the generation of photon pairs hyper-entangled between pulse modes and frequency bins. The pulse modes are generated via parametric downconversion in a domain-engineered crystal and subsequently entangled to two frequency bins via a spectral mapping technique. The resulting hyper-entangled state is characterized and verified via measurement of its joint spectral intensity and non-classical two-photon interference patterns from which we infer its spectral phase. The protocol combines the robustness to loss, intrinsic high dimensionality and compatibility with standard fiber-optic networks of the energy-time DOF with the ability of hyper-entanglement to increase the capacity and efficiency of the quantum channel, already exploited in recent experimental applications in both quantum information and quantum computation

Cardiac myocyte-specific knock-out of calcium-independent phospholipase A2γ (iPLA2γ) decreases oxidized fatty acids during ischemia/reperfusion and reduces infarct size

Calcium-independent phospholipase A(2)γ (iPLA(2)γ) is a mitochondrial enzyme that produces lipid second messengers that facilitate opening of the mitochondrial permeability transition pore (mPTP) and contribute to the production of oxidized fatty acids in myocardium. To specifically identify the roles of iPLA(2)γ in cardiac myocytes, we generated cardiac myocyte-specific iPLA(2)γ knock-out (CMiPLA(2)γKO) mice by removing the exon encoding the active site serine (Ser-477). Hearts of CMiPLA(2)γKO mice exhibited normal hemodynamic function, glycerophospholipid molecular species composition, and normal rates of mitochondrial respiration and ATP production. In contrast, CMiPLA(2)γKO mice demonstrated attenuated Ca(2+)-induced mPTP opening that could be rapidly restored by the addition of palmitate and substantially reduced production of oxidized polyunsaturated fatty acids (PUFAs). Furthermore, myocardial ischemia/reperfusion (I/R) in CMiPLA(2)γKO mice (30 min of ischemia followed by 30 min of reperfusion in vivo) dramatically decreased oxidized fatty acid production in the ischemic border zones. Moreover, CMiPLA(2)γKO mice subjected to 30 min of ischemia followed by 24 h of reperfusion in vivo developed substantially less cardiac necrosis in the area-at-risk in comparison with their WT littermates. Furthermore, we found that membrane depolarization in murine heart mitochondria was sensitized to Ca(2+) by the presence of oxidized PUFAs. Because mitochondrial membrane depolarization and calcium are known to activate iPLA(2)γ, these results are consistent with salvage of myocardium after I/R by iPLA(2)γ loss of function through decreasing mPTP opening, diminishing production of proinflammatory oxidized fatty acids, and attenuating the deleterious effects of abrupt increases in calcium ion on membrane potential during reperfusion

A chemical genetic approach reveals distinct EphB signaling mechanisms during brain development.

EphB receptor tyrosine kinases control multiple steps in nervous system development. However, it remains unclear whether EphBs regulate these different developmental processes directly or indirectly. In addition, given that EphBs signal through multiple mechanisms, it has been challenging to define which signaling functions of EphBs regulate particular developmental events. To address these issues, we engineered triple knock-in mice in which the kinase activity of three neuronally expressed EphBs can be rapidly, reversibly and specifically blocked. We found that the tyrosine kinase activity of EphBs was required for axon guidance in vivo. In contrast, EphB-mediated synaptogenesis occurred normally when the kinase activity of EphBs was inhibited, suggesting that EphBs mediate synapse development by an EphB tyrosine kinase-independent mechanism. Taken together, our data indicate that EphBs control axon guidance and synaptogenesis by distinct mechanisms and provide a new mouse model for dissecting EphB function in development and disease

Update of the keratin gene family: evolution, tissue-specific expression patterns, and relevance to clinical disorders.

Intermediate filament (IntFil) genes arose during early metazoan evolution, to provide mechanical support for plasma membranes contacting/interacting with other cells and the extracellular matrix. Keratin genes comprise the largest subset of IntFil genes. Whereas the first keratin gene appeared in sponge, and three genes in arthropods, more rapid increases in keratin genes occurred in lungfish and amphibian genomes, concomitant with land animal-sea animal divergence (~ 440 to 410 million years ago). Human, mouse and zebrafish genomes contain 18, 17 and 24 non-keratin IntFil genes, respectively. Human has 27 of 28 type I "acidic" keratin genes clustered at chromosome (Chr) 17q21.2, and all 26 type II "basic" keratin genes clustered at Chr 12q13.13. Mouse has 27 of 28 type I keratin genes clustered on Chr 11, and all 26 type II clustered on Chr 15. Zebrafish has 18 type I keratin genes scattered on five chromosomes, and 3 type II keratin genes on two chromosomes. Types I and II keratin clusters-reflecting evolutionary blooms of keratin genes along one chromosomal segment-are found in all land animal genomes examined, but not fishes; such rapid gene expansions likely reflect sudden requirements for many novel paralogous proteins having divergent functions to enhance species survival following sea-to-land transition. Using data from the Genotype-Tissue Expression (GTEx) project, tissue-specific keratin expression throughout the human body was reconstructed. Clustering of gene expression patterns revealed similarities in tissue-specific expression patterns for previously described "keratin pairs" (i.e., KRT1/KRT10, KRT8/KRT18, KRT5/KRT14, KRT6/KRT16 and KRT6/KRT17 proteins). The ClinVar database currently lists 26 human disease-causing variants within the various domains of keratin proteins