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"Putnam, James"
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Art and artifact : the museum as medium
\"The increasing trend towards collaborations between practising artists and museum curators has in some cases involved the rehanging of existing collections or redesigning of gallery spaces. In this way the probing instinct of the creative mind counterbalances the sense of permanence and order associated with the museum in a constructive dialogue involving elements of the past, present and future.\"--BOOK JACKET.
Book
Sequences Sufficient for Programming Imprinted Germline DNA Methylation Defined
Epigenetic marks are fundamental to normal development, but little is known about signals that dictate their placement. Insights have been provided by studies of imprinted loci in mammals, where monoallelic expression is epigenetically controlled. Imprinted expression is regulated by DNA methylation programmed during gametogenesis in a sex-specific manner and maintained after fertilization. At Rasgrf1 in mouse, paternal-specific DNA methylation on a differential methylation domain (DMD) requires downstream tandem repeats. The DMD and repeats constitute a binary switch regulating paternal-specific expression. Here, we define sequences sufficient for imprinted methylation using two transgenic mouse lines: One carries the entire Rasgrf1 cluster (RC); the second carries only the DMD and repeats (DR) from Rasgrf1. The RC transgene recapitulated all aspects of imprinting seen at the endogenous locus. DR underwent proper DNA methylation establishment in sperm and erasure in oocytes, indicating the DMD and repeats are sufficient to program imprinted DNA methylation in germlines. Both transgenes produce a DMD-spanning pit-RNA, previously shown to be necessary for imprinted DNA methylation at the endogenous locus. We show that when pit-RNA expression is controlled by the repeats, it regulates DNA methylation in cis only and not in trans. Interestingly, pedigree history dictated whether established DR methylation patterns were maintained after fertilization. When DR was paternally transmitted followed by maternal transmission, the unmethylated state that was properly established in the female germlines could not be maintained. This provides a model for transgenerational epigenetic inheritance in mice.
Journal Article
Mummy
Documents the history and significance of mummies, both natural and man-made, and describes the principles and ceremonies associated with them.
BOOK
Ghrelin Prevents Disruption of the Blood–Brain Barrier after Traumatic Brain Injury
Significant effort has been focused on reducing neuronal damage from post-traumatic brain injury (TBI) inflammation and blood–brain barrier (BBB)-mediated edema. The orexigenic hormone ghrelin decreases inflammation in sepsis models, and has recently been shown to be neuroprotective following subarachnoid hemorrhage. We hypothesized that ghrelin modulates cerebral vascular permeability and mediates BBB breakdown following TBI. Using a weight-drop model, TBI was created in three groups of mice: sham, TBI, and TBI/ghrelin. The BBB was investigated by examining its permeability to FITC-dextran and through quantification of perivascualar aquaporin-4 (AQP-4). Finally, we immunoblotted for serum S100B as a marker of brain injury. Compared to sham, TBI caused significant histologic neuronal degeneration, increases in vascular permeability, perivascular expression of AQP-4, and serum levels of S100B. Treatment with ghrelin mitigated these effects; after TBI, ghrelin-treated mice had vascular permeability and perivascular AQP-4 and S100B levels that were similar to sham. Our data suggest that ghrelin prevents BBB disruption after TBI. This is evident by a decrease in vascular permeability that is linked to a decrease in AQP-4. This decrease in vascular permeability may diminish post-TBI brain tissue damage was evident by decreased S100B.
Journal Article
Vagal nerve stimulation protects cardiac injury by attenuating mitochondrial dysfunction in a murine burn injury model
Mitochondria play a central role in the integration and execution of a wide variety of apoptotic signals. In the present study, we examined the deleterious effects of burn injury on heart tissue. We explored the effects of vagal nerve stimulation (VNS) on cardiac injury in a murine burn injury model, with a focus on the protective effect of VNS on mitochondrial dysfunction in heart tissue. Mice were subjected to a 30% total body surface area, full‐thickness steam burn followed by right cervical VNS for 10 min. and compared to burn alone. A separate group of mice were treated with the M3‐muscarinic acetylcholine receptor (M3‐AchR) antagonist 4‐DAMP or phosphatidylinositol 3 Kinase (PI3K) inhibitor LY294002 prior to burn and VNS. Heart tissue samples were collected at 6 and 24 hrs after injury to measure changes in apoptotic signalling pathways. Burn injury caused significant cardiac pathological changes, cardiomyocyte apoptosis, mitochondrial swelling and decrease in myocardial ATP content at 6 and 24 hrs after injury. These changes were significantly attenuated by VNS. VNS inhibited release of pro‐apoptotic protein cytochrome C and apoptosis‐inducing factor from mitochondria to cytosol by increasing the expression of Bcl‐2, and the phosphorylation level of Bad (pBad136) and Akt (pAkt308). These protective changes were blocked by 4‐DAMP or LY294002. We demonstrated that VNS protected against burn injury–induced cardiac injury by attenuating mitochondria dysfunction, likely through the M3‐AchR and the PI3K/Akt signalling pathways.
Journal Article
US Community Bank Failure: An Empirical Investigation
There are clear differences in institutional risk profiles between community and noncommunity banks. We hypothesize that these dissimilarities impact community bank failure risk through bank-specific covariates relating to asset quality and earnings in a way that is disparate from the salient findings in the literature on non-community banks. Consistent with our differential impact hypothesis we find that community banks which reduce their proportion of consumer lending or compensation, as a percentage of total assets, have increased failure risk. These findings appear to be unique to the community banking industry.
Journal Article
