Aerospace medicine and biology: A continuing bibliography with indexes (supplement 352)

This bibliography lists 147 reports, articles and other documents introduced into the NASA Scientific and Technical Information System during July 1991. Subject coverage includes: aerospace medicine and psychology, life support systems and controlled environments, safety equipment, exobiology and extraterrestrial life, and flight crew behavior and performance

Keeping up with environmental change:The importance of sociality

In the current era of rapid climate change, populations are facing environments in which food availability can quickly decline or become highly unpredictable. These conditions may require a high degree of flexibility of individuals and populations to adequately respond to such changes. We propose that the evolution of such high flexibility may be facilitated in social animals that form groups and cooperate in important tasks that critically affect survival and reproduction and ultimately affect adaptive capacity. We argue that sociality is likely to be a key, yet largely overlooked factor that shapes rather than limits the potential for phenotypic plasticity. Cooperatively breeding species are most suitable for studying the influence of both the physical and the social environmental conditions on shaping the phenotypic plasticity of individuals. Cooperative breeders display variation in group size and structure, and in the extent of cooperation and competition between their members. In addition, immigrants may impose costs and/or benefits on other group members, as well as on the whole group. In cooperative breeders, we elucidate why and how group formation and interactions between group members can provide adaptive benefits to some or all individuals in the group. Observed adjustments in social behaviour may be strategic and ultimately enhance individual fitness benefits, and thus improve group and population persistence. Future studies should examine how ecology and sociality together shape the adjustment of animals to rapid and extreme environmental change. In addition to identifying how changes in physical and social factors impact individual behaviour, group formation and sociality, it is crucial to assess associated costs and benefits by exploring the life histories of all group members. Understanding this requires population models, as they integrate all the critical life-history phases, and different types of sociality. We are confident that future research into the ecology and social dynamics will reveal new avenues for the adaptive ability of cooperative breeders and other social species

Biological embedding of maternal postpartum depressive symptoms: The potential role of cortisol and telomere length.

Although maternal postpartum depressive symptoms (PDS) are associated with child behavior problems, the underlying biological mechanisms are poorly understood. Thus, the current study focused on 193 healthy mother-child dyads and investigated child cortisol and telomere length as potential mediating factors. At 3 and 6 months postpartum, mothers reported on PDS. At age 6, children provided saliva and buccal swab samples. At age 10, mothers and children reported on child behavior problems. Structural equation modelling revealed (a) no association between PDS and child behavior problems and thus no possibility of mediation, but that (b) lower cortisol forecast more child-reported internalizing problems, and (c) shorter telomere length predicted more child-reported internalizing and externalizing problems. These findings raise mediational questions about the determinants of these biomarkers

A systematic approach to cancer: evolution beyond selection.

Cancer is typically scrutinized as a pathological process characterized by chromosomal aberrations and clonal expansion subject to stochastic Darwinian selection within adaptive cellular ecosystems. Cognition based evolution is suggested as an alternative approach to cancer development and progression in which neoplastic cells of differing karyotypes and cellular lineages are assessed as self-referential agencies with purposive participation within tissue microenvironments. As distinct self-aware entities, neoplastic cells occupy unique participant/observer status within tissue ecologies. In consequence, neoplastic proliferation by clonal lineages is enhanced by the advantaged utilization of ecological resources through flexible re-connection with progenitor evolutionary stages

Role of the Transcription Factor CREB in the NMDA Receptor Antagonist-Induced Attention Deficits

This thesis is the result of a multidisciplinary approach which combines behavioral, biochemical and neurochemical assays to identify and delineate the molecular mechanisms involved in the control of attention. Blockade of prefrontocortical glutamate NMDAR is associated with attentional performance deficits as assessed in a task capable of measuring selective attention and response control such as the five choice serial reaction time (5-CSRT) task. I investigated whether phosphorylation of proteins linked to the PKA/CREB pathway in the prefrontal cortex (PFC) and in subcortical regions may be affected by NMDAR blockade. Pharmacological experiments using western blot and immunohistochemical techniques clearly demonstrated that increased CREB phosphorylation (p-CREB) in the PFC but not in subcortical regions may be associated to deficits in attention performance caused by the blockade of prefrontocortical NMDAR with the selective antagonist CPP. Attempts has been made to identify the intracellular pathways responsible for CPP-induced p-CREB changes by examining different protein kinases upstream to CREB such as protein kinase A (PKA), extracellular regulated protein kinases 1/2 (ERK1/2) and calcium/calmodulin kinase II (CaMKII). However, the precise role of these kinases in NMDAR antagonist induced changes in p-CREB is unclear and deserves further studies. The hypothesis that attention deficits induced by NMDAR blockade in the PFC might reflect excessive glutamate (GLU) release in the PFC was investigated by assessing the effects of intracortical CPP on attention, GLU release and p-CREB under basal conditions and in rats pre-treated with the mGlu2/3 receptor agonist LY379268. The results provide evidence that enhanced GLU release in the PFC and CREB phosphorylation are associated to attention deficit. As there are evidences that drug responses may be modulated by the behavioural state of animals, I evaluated the effect of blockade of NMDAR in the PFC on p-CREB in rats performing the 5-CSRT task. Intriguingly, I found that in these rats CPP-induced p-CREB in the PFC was decreased as opposed to the increase found in behaviourally naive rats at the same time point, suggesting that the direction of CPP-induced p-CREB changes critically depends on the behavioural state of animals. Moreover CPP-induced cognitive impairments were prevented by the intracortical administration of Sp-cAMP suggesting that the activation of the PKA/CREB cascade in the PFC is required for the correct performance of the task. In conclusion the present thesis support the role of CREB and provide new information on the mechanisms involved in the control of attention and executive functions associated with some neuropsychiatric disorders

Cell based therapy following cortical injury in Rhesus monkeys reduces secondary injury and enhances neurorestorative processes

While physical rehabilitation facilitates some recovery, it is uncommon for patients to recover completely from stroke. Cell based therapies derived from stem cells have produced promising results in enhancing recovery in pre-clinical studies, but the mechanism is not yet completely understood. We previously evaluated human umbilical tissue-derived cells (hUTC) in our non-human primate model of cortical injury, limited to the hand area of primary motor cortex. hUTC treatment, injected intravenously 24 hours after injury, resulted in significantly greater recovery of fine motor function compared to treatment with vehicle. Based on these striking findings, in the current study, we investigated the hypothesis that hUTC treatment leads to functional recovery through reducing cytotoxic responses and enhancing neurorestorative processes following cortical injury. Brain sections were assessed using histological techniques to quantify perilesional oxidative damage, hemosiderin accumulation, microglial activation, Betz cell number, synaptic density, and astrocytic complexity. Brain sections outside of the primary area of injury were also assessed for microglial activation in white matter pathways, cell activation through c-Fos in premotor cortices, and neurogenesis in neurogenic niches. Finally, blood samples from throughout the recovery period and CSF samples from 16 weeks after injury were analyzed for BDNF levels. In the perilesional area, hUTC treatment was associated with lower oxidative damage and hemosiderin accumulation, but not with a difference in microglial activation. hUTC also resulted in a trend toward higher astrocyte complexity and synaptic density in the lesion area, but no difference in ipsilesional Betz cell number. Further, hUTC treatment led to more microglia in white matter pathways, higher c-Fos activation in ventral premotor cortex, and a trend toward higher neurogenesis in the hippocampus. Finally, BDNF levels were higher in blood with hUTC treatment one week after injury, but there was no change beyond one week in blood serum or in CSF, when compared with vehicle. Taken together, these results suggest that hUTC treatment modulates immune responses, limits perilesional damage and cell death, enables neuroplasticity and reorganization, and enhances acute neurotrophic factor secretion. While many cell therapies are currently undergoing clinical trials, this study advances our understanding of the mechanism of cell based therapies

Distribution and connectivity of messenger molecules in the control of energy metabolism : focus on neuropeptides and calcium binding proteins

Feeding is an essential and complex behavior which aims to provide the energy required for maintaining physiological homeostasis. The drive to feed is a powerful stimulus arising from metabolic demands, and reinforced by evolutionary pressure. The current epidemic in obesity, and associated disorders such as diabetes, makes it clinically vital to understand the mechanisms behind the control of energy metabolism. Feeding is a process governed by the central nervous system (CNS); particularly through the interplay between different hypothalamic nuclei. At the heart of the feeding neuro-circuitry lies the arcuate nucleus (ARC) which acts as a metabolic sensor, taking stock of the supply and demands of energy in the body, and coordinating food intake and energy expenditure. The work in this thesis aimed to explore the neuro-anatomical substrate of metabolic control, and the mediators involved. The ARC contains two distinct sets of functionally antagonistic neurons. One group of neurons express the orexigenic peptides, neuropeptide Y (NPY) and agouti gene related peptide (AGRP); while the other set expresses the anorexigenic peptides, proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript. In paper V, we describe the histochemistry of NPY/AGRP and POMC neurons with regard to their anatomical interrelationship at the cell body and terminal level. A common experimental problem is that the ARC NPY cell bodies are difficult to distinguish and visualize in electrophysiological experiments and for immunohistochemistry. Therefore, in paper III, a novel transgenic mouse which expresses bright Renilla green fluorescent protein in NPY neurons was generated. Using this model, a comprehensive map of NPY-expressing cells in the CNS was generated and the effects of the satiety-inducing gut-brain bombesin peptides on ARC neurons were explored. Bombesin was found to exert powerful depolarizing actions on NPY and POMC neurons alike. Calcium binding proteins (CaBPs) have been used extensively to delineate neuronal populations, but the ARC has not yet been subjected to such analysis. In Paper IV we show that three major CaBPs (calbindin D-28k, calretinin, and parvalbumin) are all expressed in the ARC, but displayed little co-localization with previously described cell groups. One exception was POMC neurons, of which distinct subpopulations stained for calbindin D-28k and calretinin, respectively. Another CaBP, nucleobindin 2 (NUCB2; also known as nesfatin), has recently been proposed as a central anorexigenic mediator. In Paper I, the CNS distribution of this protein was shown to include nuclei that participate in all three output channels of metabolic control, i.e. behavioral, endocrine and autonomic modulation. Our data also suggest that NUCB2 may not act as a cleaved and secreted messenger as proposed, but rather may play an intracellular role. The wide distribution of NUCB2 in the neuroendocrine system prompted us to explore this protein in the pancreas (Paper II). We show that NUCB2 is exclusively expressed in insulin-producing β cells, and that islet NUCB2 is dramatically decreased in the diabetic Goto-Kakizaki rat, an effect that is normalized by fasting. These data indicate that NUCB2 may play a role in metabolic control also outside of the CNS

Creating Knowledge, volume 4, 2011

The College of Liberal Arts and Sciences, through the deliberations and efforts of its task force on “Students Creating Knowledge”, chaired by Professor Ralph Erber, associate dean for research in the College of Liberal Arts and Sciences, committed itself to a number of new strategic initiatives that would enhance and enrich the academic quality of the student experience within the college. Chief among these initiatives was one that would encourage students to become actively engaged in creating scholarship and research and give them a venue for the publication of their essays. The first volume of “Creating Knowledge: The LA&S Student Research Journal” was published in 2008. I am now extremely pleased to be able to introduce the fourth volume of Creating Knowledge. This year’s publication, like the ones that preceded it, gives considerable testimony to the creativity, hard work and sophistication of our undergraduate scholars. It is through the continuing, annual publication of this undergraduate student journal that we aim to encourage students across the college and the university to understand that leadership within their disciplines requires them to not only be familiar with the knowledge base of the discipline, but to have the experience of being actively engaged in understanding how creative work and/or scientific discoveries are created through research, scholarship and the dissemination and sharing of knowledge. I want to congratulate, first and foremost, the many student scholars whose work is featured in this fourth volume of the journal. I also want to thank the students and faculty who served to make this publication possible—those who served on the editorial board that shaped this journal and who reviewed the many submissions of student work. In accomplishing this task all of you have participated in what is the heart of scholarship—the contributions to enabling and sustaining an intellectual community—one which we hope will lead you to make similar contributions beyond the college and DePaul University. To one and all, my most sincere congratulations and gratitude. Chuck Suchar Deanhttps://via.library.depaul.edu/ckgallery/1003/thumbnail.jp