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Search Results: 1 - 10 of 192810 matches for " Bryan D Moyer "
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Endoplasmic reticulum degradation impedes olfactory G-protein coupled receptor functional expression
Min Lu, Lena Staszewski, Fernando Echeverri, Hong Xu, Bryan D Moyer
BMC Cell Biology , 2004, DOI: 10.1186/1471-2121-5-34
Abstract: To develop means to increase the functional expression of ORs, we devised an approach to measure activation of the mOREG OR (Unigene # Mm.196680; Olfr73) through coupling to an olfactory cyclic nucleotide-gated cation channel (CNG). This system, which utilizes signal transduction machinery coupled to OR activation in native olfactory sensory neurons, was used to demonstrate that degradation, both by the ubiquitin-proteasome system and autophagy, limits mOREG functional expression. The stimulatory effects of proteasome and autophagy inhibitors on mOREG function required export from the ER and trafficking through the biosynthetic pathway.These findings demonstrate that poor functional expression of mOREG in heterologous cells is improved by blocking proteolysis. Inhibition of ER degradation may improve the function of other ORs and assist future efforts to elucidate the molecular basis of odor discrimination.The sense of smell originates in the olfactory epithelium when olfactory receptors (ORs), members of the seven transmembrane domain G-protein coupled receptor (GPCR) superfamily, bind odorant ligands [1,2]. Despite identification of the first constituents of the ~1000 member OR superfamily over a decade ago, efforts to uncover the molecular basis of odor discrimination have been severely limited by the inability to efficiently express ORs at the plasma membrane in heterologous expression systems [2-6].Recently, we elucidated three specific cellular mechanisms responsible for inefficient OR trafficking to the plasma membrane: ORs are retained within the endoplasmic reticulum (ER) due to inefficient folding and poor coupling to ER export machinery, degraded via the ubiquitin-proteasome system, and sequestered in ER aggregates that are degraded by autophagy [7]. Thus, we have a clearer understanding of the problems associated with OR expression in heterologous cells.To develop rationale means to improve the functional expression of ORs, an approach was devised to qua
Voltage-gated sodium channels in taste bud cells
Na Gao, Min Lu, Fernando Echeverri, Bianca Laita, Dalia Kalabat, Mark E Williams, Peter Hevezi, Albert Zlotnik, Bryan D Moyer
BMC Neuroscience , 2009, DOI: 10.1186/1471-2202-10-20
Abstract: We describe the molecular and histological expression profiles of cation channels involved in electrical signal transmission from apical to basolateral membrane domains. TRPM5 was positioned immediately beneath tight junctions to receive calcium signals originating from sweet, bitter, and umami receptor activation, while PKD2L1 was positioned at the taste pore. Using mouse taste bud and lingual epithelial cells collected by laser capture microdissection, SCN2A, SCN3A, and SCN9A voltage-gated sodium channel transcripts were expressed in taste tissue. SCN2A, SCN3A, and SCN9A were expressed beneath tight junctions in subsets of taste cells. SCN3A and SCN9A were expressed in TRPM5 cells, while SCN2A was expressed in TRPM5 and PKD2L1 cells. HCN4, a gene previously implicated in sour taste, was expressed in PKD2L1 cells and localized to cell processes beneath the taste pore.SCN2A, SCN3A and SCN9A voltage-gated sodium channels are positioned to sense initial depolarizing signals stemming from taste receptor activation and initiate taste cell action potentials. SCN2A, SCN3A and SCN9A gene products likely account for the tetrodotoxin-sensitive sodium currents in taste receptor cells.Taste buds house specialized neuroepithelial cells that sense and transmit information regarding the composition of food [1]. These taste cells express receptors for sweet, bitter, umami (the savory taste of glutamate), sour and salty tastants in apical microvilli facing the saliva [2,3]. Following taste receptor activation, taste cells depolarize and fire action potentials resulting in the release of neurotransmitters to nerve fibers innervating basolateral membranes [4,5]. Segregation of taste receptors at the taste pore from the machinery involved in transmitting signals to nerve fibers is mediated by tight junctions, specialized protein networks that separate apical and basolateral membrane domains [6].Information regarding the composition of food flows from the apical to the basolateral doma
Expression of Genes Encoding Multi-Transmembrane Proteins in Specific Primate Taste Cell Populations
Bryan D. Moyer,Peter Hevezi,Na Gao,Min Lu,Dalia Kalabat,Hortensia Soto,Fernando Echeverri,Bianca Laita,Shaoyang Anthony Yeh,Mark Zoller,Albert Zlotnik
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0007682
Abstract: Using fungiform (FG) and circumvallate (CV) taste buds isolated by laser capture microdissection and analyzed using gene arrays, we previously constructed a comprehensive database of gene expression in primates, which revealed over 2,300 taste bud-associated genes. Bioinformatics analyses identified hundreds of genes predicted to encode multi-transmembrane domain proteins with no previous association with taste function. A first step in elucidating the roles these gene products play in gustation is to identify the specific taste cell types in which they are expressed.
Genome-Wide Analysis of Gene Expression in Primate Taste Buds Reveals Links to Diverse Processes
Peter Hevezi, Bryan D. Moyer, Min Lu, Na Gao, Evan White, Fernando Echeverri, Dalia Kalabat, Hortensia Soto, Bianca Laita, Cherry Li, Shaoyang Anthony Yeh, Mark Zoller, Albert Zlotnik
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0006395
Abstract: Efforts to unravel the mechanisms underlying taste sensation (gustation) have largely focused on rodents. Here we present the first comprehensive characterization of gene expression in primate taste buds. Our findings reveal unique new insights into the biology of taste buds. We generated a taste bud gene expression database using laser capture microdissection (LCM) procured fungiform (FG) and circumvallate (CV) taste buds from primates. We also used LCM to collect the top and bottom portions of CV taste buds. Affymetrix genome wide arrays were used to analyze gene expression in all samples. Known taste receptors are preferentially expressed in the top portion of taste buds. Genes associated with the cell cycle and stem cells are preferentially expressed in the bottom portion of taste buds, suggesting that precursor cells are located there. Several chemokines including CXCL14 and CXCL8 are among the highest expressed genes in taste buds, indicating that immune system related processes are active in taste buds. Several genes expressed specifically in endocrine glands including growth hormone releasing hormone and its receptor are also strongly expressed in taste buds, suggesting a link between metabolism and taste. Cell type-specific expression of transcription factors and signaling molecules involved in cell fate, including KIT, reveals the taste bud as an active site of cell regeneration, differentiation, and development. IKBKAP, a gene mutated in familial dysautonomia, a disease that results in loss of taste buds, is expressed in taste cells that communicate with afferent nerve fibers via synaptic transmission. This database highlights the power of LCM coupled with transcriptional profiling to dissect the molecular composition of normal tissues, represents the most comprehensive molecular analysis of primate taste buds to date, and provides a foundation for further studies in diverse aspects of taste biology.
The Effect of Retrofit Technologies on Formaldehyde Emissions from a Large Bore Natural Gas Engine  [PDF]
Daniel B. Olsen, Bryan D. Willson
Energy and Power Engineering (EPE) , 2011, DOI: 10.4236/epe.2011.34071
Abstract: Formaldehyde is an air toxic that is typically emitted from natural gas-fired internal combustion engines as a product of incomplete combustion. The United States Environmental Protection Agency (EPA) regulates air toxic emissions, including formaldehyde, from stationary reciprocating internal combustion engines. National air toxic standards are required under the 1990 Clean Air Act Amendments. This work investigates the effect that hardware modifications, or retrofit technologies, have on formaldehyde emissions from a large bore natural gas engine. The test engine is a Cooper-Bessemer GMV-4TF two stroke cycle engine with a 14” (35.6 cm) bore and a 14” (35.6 cm) stroke. The impact of modifications to the fuel injection and ignition systems are investigated. Data analysis and discussion is performed with reference to possible formaldehyde formation mechanisms and in-cylinder phenomena. The results show that high pressure fuel injection (HPFI) and precombustion chamber (PCC) ignition significantly reduce formaldehyde emissions
In memoriam P.E. de Josselin de Jong (8 July 1922-1 January 1999)
L.E. Visser,D.S. Moyer
Bijdragen tot de Taal-, Land- en Volkenkunde , 1999,
Abstract:
On Pebbling Graphs by their Blocks
D. Curtis,T. Hines,G. Hurlbert,T. Moyer
Mathematics , 2008,
Abstract: Graph pebbling is a game played on a connected graph G. A player purchases pebbles at a dollar a piece, and hands them to an adversary who distributes them among the vertices of G (called a configuration) and chooses a target vertex r. The player may make a pebbling move by taking two pebbles off of one vertex and moving one pebble to a neighboring vertex. The player wins the game if he can move k pebbles to r. The value of the game (G,k), called the k-pebbling number of G, is the minimum cost to the player to guarantee a win. That is, it is the smallest positive integer m of pebbles so that, from every configuration of size m, one can move k pebbles to any target. In this paper, we use the block structure of graphs to investigate pebbling numbers, and we present the exact pebbling number of the graphs whose blocks are complete. We also provide an upper bound for the k-pebbling number of diameter-two graphs, which can be the basis for further investigation into the pebbling numbers of graphs with blocks that have diameter at most two.
Occult Hemothorax after Transcatheter Aortic Valve Implantation (TAVI)  [PDF]
Kenneth D. Eichenbaum,Bryan Noorda,Walter Bethune,Dennis E. Feierman
Open Journal of Anesthesiology (OJAnes) , 2013, DOI: 10.4236/ojanes.2013.35059
Abstract: We present a case of occult hemothorax, a rare but dangerous complication resulting from cannulation of the internal jugular vein. To date we are not aware of any case reports of bleeding sequelae resulting from direct parenchymal lung injury. The insidious nature of this complication, in which the clinical presentation occurred several hours after central venous cannulation, provides an important reminder for clinicians to follow up central line placement with imaging studies. In this case, the latent period prior to the appearance of clinical manifestations of hemorrhage along with the patient’s subsequent acute decompensation raises questions as to the nature of the underlying injury and mechanisms of both detection and prevention. The patient underwent two right video-assisted thoracoscopic surgical explorations, the first revealed ongoing venous bleeding from within the parenchyma of the right upper lobe which was controlled by a wedge resection. She was ultimately discharged home and, as of the time of this writing, appears to have recovered completely, suffering no long-term sequelae as a result of this complication.
Occult Hemothorax after Transcatheter Aortic Valve Implantation (TAVI)  [PDF]
Kenneth D. Eichenbaum, Bryan Noorda, Walter Bethune, Dennis E. Feierman
Open Journal of Anesthesiology (OJAnes) , 2013, DOI: 10.4236/ojanes.2013.35059
Abstract:

We present a case of occult hemothorax, a rare but dangerous complication resulting from cannulation of the internal jugular vein. To date we are not aware of any case reports of bleeding sequelae resulting from direct parenchymal lung injury. The insidious nature of this complication, in which the clinical presentation occurred several hours after central venous cannulation, provides an important reminder for clinicians to follow up central line placement with imaging studies. In this case, the latent period prior to the appearance of clinical manifestations of hemorrhage along with the patient’s subsequent acute decompensation raises questions as to the nature of the underlying injury and mechanisms of both detection and prevention. The patient underwent two right video-assisted thoracoscopic surgical explorations, the first revealed ongoing venous bleeding from within the parenchyma of the right upper lobe which was controlled by a wedge resection. She was ultimately discharged home and, as of the time of this writing, appears to have recovered completely, suffering no long-term sequelae as a result of this complication.

Impaired Wheel Running Exercise in CLC-1 Chloride Channel-Deficient Myotonic Mice
Michelle Moyer
Frontiers in Physiology , 2011, DOI: 10.3389/fphys.2011.00047
Abstract: Background: Genetic deficiency of the muscle CLC-1 chloride channel leads to myotonia, which is manifested most prominently by slowing of muscle relaxation. Humans experience this as muscle stiffness upon initiation of contraction, although this can be overcome with repeated efforts (the “warm-up” phenomenon). The extent to which CLC-1 deficiency impairs exercise activity is controversial. We hypothesized that skeletal muscle CLC-1 chloride channel deficiency leads to severe reductions in spontaneous exercise. Methodology/Principal Findings: To examine this quantitatively, myotonic CLC-1 deficient mice were provided access to running wheels, and their spontaneous running activity was quantified subsequently. Differences between myotonic and normal mice in running were not present soon after introduction to the running wheels, but were fully established during week 2. During the eighth week, myotonic mice were running significantly less than normal mice (322 ± 177 vs 5058 ± 1253 m/day, P = 0.025). Furthermore, there were considerable reductions in consecutive running times (18.8 ± 1.5 vs 59.0 ± 3.7 min, P < 0.001) and in the distance per consecutive running period (58 ± 38 vs 601 ± 174 m, P = 0.048) in myotonic compared with normal animals. Conclusion/Significance: These findings indicate that CLC-1 chloride deficient myotonia in mice markedly impairs spontaneous exercise activity, with reductions in both total distance and consecutive running times.
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