Suzaku Observation of HCG 62: Temperature, Abundance, and Extended Hard X-ray Emission Profiles

We present results of 120 ks observation of a compact group of galaxies HCG~62 ($z=0.0145$) with Suzaku XIS and HXD-PIN\@. The XIS spectra for four annular regions were fitted with two temperature {\it vapec} model with variable abundance, combined with the foreground Galactic component. The Galactic component was constrained to have a common surface brightness among the four annuli, and two temperature {\it apec} model was preferred to single temperature model. We confirmed the multi-temperature nature of the intra-group medium reported with Chandra and XMM-Newton, with a doughnut-like high temperature ring at radii 3.3--6.5$'$ in a hardness image. We found Mg, Si, S, and Fe abundances to be fairly robust. We examined the possible ``high-abundance arc'' at $\sim 2'$ southwest from the center, however Suzaku data did not confirm it. We suspect that it is a misidentification of an excess hot component in this region as the Fe line. Careful background study showed no positive detection of the extended hard X-rays previously reported with ASCA, in 5--12 keV with XIS and 12--40 keV with HXD-PIN, although our upper limit did not exclude the ASCA result. There is an indication that the X-ray intensity in $r<3.3'$ region is $70\pm 19$% higher than the nominal CXB level (5--12 keV), and Chandra and Suzaku data suggest that most of this excess could be due to concentration of hard X-ray sources with an average photon index of $\Gamma=1.38\pm 0.06$. Cumulative mass of O, Fe and Mg in the group gas and the metal mass-to-light ratio were derived and compared with those in other groups. Possible role of AGN or galaxy mergers in this group is also discussed.Comment: 29 pages with 9 figures, accepted for publication in PASJ Vol 60, second Suzaku special issu

Purinergic Signaling Induces Cyclooxygenase-1-Dependent Prostanoid Synthesis in Microglia: Roles in the Outcome of Excitotoxic Brain Injury

Cyclooxygenases (COX) are prostanoid synthesizing enzymes constitutively expressed in the brain that contribute to excitotoxic neuronal cell death. While the neurotoxic role of COX-2 is well established and has been linked to prostaglandin E2 synthesis, the role of COX-1 is not clearly understood. In a model of N-Methyl-D-aspartic acid (NMDA) induced excitotoxicity in the mouse cerebral cortex we found a distinctive temporal profile of COX-1 and COX-2 activation where COX-1, located in microglia, is responsible for the early phase of prostaglandin E2 synthesis (10 minutes after NMDA), while both COX-1 and COX-2 contribute to the second phase (3–24 hours after NMDA). Microglial COX-1 is strongly activated by ATP but not excitatory neurotransmitters or the Toll-like receptor 4 ligand bacterial lipopolysaccharide. ATP induced microglial COX-1 dependent prostaglandin E2 synthesis is dependent on P2X7 receptors, extracellular Ca2+ and cytoplasmic phospholipase A2. NMDA receptor activation induces ATP release from cultured neurons leading to microglial P2X7 receptor activation and COX-1 dependent prostaglandin E2 synthesis in mixed microglial-neuronal cultures. Pharmacological inhibition of COX-1 has no effect on the cortical lesion produced by NMDA, but counteracts the neuroprotection exerted by inhibition of COX-2 or observed in mice lacking the prostaglandin E2 receptor type 1. Similarly, the neuroprotection exerted by the prostaglandin E2 receptor type 2 agonist butaprost is not observed after COX-1 inhibition. P2X7 receptors contribute to NMDA induced prostaglandin E2 production in vivo and blockage of P2X7 receptors reverses the neuroprotection offered by COX-2 inhibition. These findings suggest that purinergic signaling in microglia triggered by neuronal ATP modulates excitotoxic cortical lesion by regulating COX-1 dependent prostanoid production and unveil a previously unrecognized protective role of microglial COX-1 in excitotoxic brain injury

高血圧患者におけるアンジオテンシン II-レニンフィードバック機構に対するL/N型カルシウムチャネル拮抗薬の影響

Objectives. Cilnidipine, an L-/N-type calcium channel blocker (CCB), has unique organ-protective properties due to suppression of hyperactivity in the sympathetic nervous system and renin-angiotensin system (RAS). In this study, we hypothesized that cilnidipine might exert a renoprotective effect by suppressing the RAS. Methods. A total of 25 hypertensive patients receiving a RAS inhibitor were randomly assigned to a cilnidipine (n = 12) or amlodipine (n = 13) group. The effects of cilnidipine on proteinuria and angiotensin II–renin feedback were assessed. Results. After 6 months of treatment, both systolic and diastolic blood pressures were significantly reduced to a similar extent in both groups. The urine albumin-to-creatinine ratio was significantly lower in the cilnidipine group (p < 0.05) than in the amlodipine group. Amlodipine increased plasma angiotensin I and angiotensin II levels (p < 0.05), whereas cilnidipine did not. Interestingly, the cilnidipine group had a higher ratio of angiotensin-(1–7) (Ang-(1–7)) to angiotensin II in plasma than the amlodipine group (p < 0.05). Conclusions. The L-/N-type CCB cilnidipine, but not amlodipine, decreased urinary albumin excretion in hypertensive patients. Cilnidipine also increased the ratio of Ang-(1–7) to angiotensin II in plasma, which might be one factor underlying its beneficial effects

The 150th anniversary of Nagasaki University School of Medicine: recovery from the atomic disaster and evolution of the department of neurosurgery.

NAGASAKI IS LOCATED on the western edge of Japan, closer to the Asian continent. Because of this geographical proximity, Nagasaki became a gateway for the introduction of continental culture and civilization to Japan. After the port of Nagasaki was opened for trade with the Portuguese in 1571, Nagasaki had a central role in cultural exchange with the West and China until the latter half of the 19th century. As a result of the political situation, students came to Nagasaki from all over Japan to obtain information on Western science, especially in medicine, turning Nagasaki into a hub for modern academic studies. The first medical facility in Japan educating doctors in the Western style was founded in Nagasaki in 1857. Despite the tragedy of World War II, the medical school arose again. More than 10 000 physicians have completed their studies at the medical school since its founding. The Department of Neurosurgery at Nagasaki University had its origins within the Second Department of Surgery and became an independent department in 1973. The post of professor was assumed by Kazuo Mori and succeeded in 1991 by Shobu Shibata and in 2003 by Izumi Nagata, who holds the post at the time of this writing. Neurosurgery is dynamic and constantly changing at Nagasaki University with work in progress on technological, diagnostic, and surgical innovations that permit the treatment of highly complex cases. In 2007, the 150th anniversary of the founding of Nagasaki University School of Medicine was celebrated with a number of commemorative events