Brain damage after hypoxia-ischemia (HI) occurs in an age-dependent manner. Neuroprotective strategies assumed to be effective in the adult might have deleterious effects in the immature brain. In order to create effective therapies, the complex pathophysiology of HI in developing brain requires exploring new mechanisms. Critical determinants of neuronal survival after HI are the extent of vascular dysfunction, inflammation, and oxidative stress, followed later by tissue repair. The key enzyme of these processes in human body is arginase (ARG) that acts via bioavailability of nitric oxide, and synthesis of polyamines and proline. ARG is expressed throughout the brain in different cells, however, little is known about the effect of ARG in pathophysiological states of brain, especially hypoxia-ischemia. Here, we summarize the role of ARG during neurodevelopment, as well as in various brain pathologies.
The present study examined whether exercise duration was associated with elevated and/or sustained elevations of postexercise adenosine 3',5'-cyclic monophosphate (cAMP) by measuring cAMP levels in skeletal muscle for up to 4 h after acute exercise bouts of durations that are known to either produce (60 min) or not produce (10 min) mitochondrial proliferation after chronic training. Treadmill-acclimatized, but untrained, rats were run at 22 m/min for 0 (control), 10, or 60 min and were killed at various postexercise (0, 0.5, 1, 2, and 4 h) time points. Fast-twitch white and red (quadriceps) and slow-twitch (soleus) muscles were quickly excised, frozen in liquid nitrogen, and assayed for cAMP with a commercial kit. Unexpectedly, cAMP contents in all three muscles were similar to control (nonexercise) at most (21 of 30) time points after a single 10- or 60-min run. Values at 9 of 30 time points were significantly different from control (P < 0.05); i.e., 3 time points were significantly higher than control and 6 were significantly less than control. These data suggest that the cAMP concentration of untrained skeletal muscle after a single bout of endurance-type exercise is not, by itself, associated with exercise duration.
It is widely acknowledged that university research and information exchange between academic and industrial science play vital roles in technological innovation, yet little is known about the process of university-industry linkage and its economic results. In 1982, the National Science Foundation's Division of Industrial Science and Technological Innovation (NSF/ISTI) began sponsorship of a major research project exploring the process of information exchange between academia and the business world, as well as the relationship of such linkage to the complex process of technological innovation. From 1982 to 1985, the Productivity Improvement Research Section of NSF/ISTI provided approximately $400,000 to support a feasibility study and a two-phase research project focusing on university-industry linkages in the State of Michigan (Grant #ISI-8313945).
The cellular responses to hypoxia or hypoxia‐ischemia (HI) are governed largely by the hypoxia‐inducible factor (HIF) family of transcription factors. Our previous studies show that HIF‐1α induction is an important factor that mediates protective effects in the brain after neonatal HI. In the present study, we investigated the contribution of another closely related HIF α isoform, HIF‐2α, specifically the neuronal HIF‐2α, to brain HI injury. Homozygous transgenic mice with a floxed exon 2 of HIF‐2α were bred with CaMKIIα‐Cre mice to generate a mouse line with selective deletion of HIF‐2α in forebrain neurons. These mice, along with their wildtype littermates, were subjected to HI at postnatal day 9. Brain injury at different ages was evaluated by the levels of cleaved caspase‐3 and spectrin breakdown products at 24 hr; and histologically at 6 days or 3 months after HI. Multiple behavioral tests were performed at 3 months, prior to sacrifice. Loss of neuronal HIF‐2α exacerbated brain injury during the acute (24 hr) and subacute phases (6 days), with a trend toward more severe volume loss in the adult brain. The long‐term brain function for coordinated movement and recognition memory, however, were not impacted in the neuronal HIF‐2α deficient mice. Our data suggest that, similar to HIF‐1α, neuronal HIF‐2α promotes cell survival in the immature mouse brain. The two HIF alpha isoforms may act through partially overlapping or distinct transcriptional targets to mediate their intrinsic protective responses against neonatal HI brain injury.
different worlds, and insists that the theme of Romans is far bigger than the fate of the individual or even the relationship between Israel and the Gentiles. It is nothing less than the redemption of the cosmos from the power of sin and death. This novel approach to the question of the role of women in the New Testament bypasses the usual texts and concentrates on passages whose significance has hitherto been ignored. Most of the chapters in this book have been published previously, as independent essays, which means that there is inevitably some repetition, but this is not excessive. By attempting to see the images in context, Gaventa has made a real contribution to Pauline theology.
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