Biomedical subjects

Paul T Kelly

Publications and source records attributed to Paul T Kelly.

4 recordsLinked to original sources

PubMed2006

Normobaric hypoxia inhalation test vs. response to airline flight in healthy passengers.

INTRODUCTION: There is little data available to determine the normal response to normobaric hypoxia inhalation testing (NHIT) and air travel. Quantifying a healthy response may assist in the evaluation of passengers considered at risk for air travel. The aims of this study were: (1) to quantify the degree of desaturation in healthy subjects during a NHIT and air travel; and (2) assess the validity of the NHIT when compared with actual in-flight responses. METHODS: There were 15 healthy adults (age 23-57; 10 women) who volunteered for this study. Preflight tests included lung function, arterial blood gas, pulse oximetry (SpO2), and NHIT (inspired oxygen 15%). SpO2 and cabin pressure were measured continuously on each subject during a commercial air flight (mean cabin altitude 2178 m; range 1719-2426 m). In-flight oxygenation was compared with the preflight NHIT. RESULTS: Lung function testing results were normal. There was significant desaturation (SpO2) during the NHIT (pre: 98 +/- 2%; post: 92 +/- 2%) and at cruising altitude (pre: 97 +/- 1%; cruise: 92 +/- 2%). There was no difference between the final NHIT SpO2 and the mean in-flight SpO2. There was a significant difference between the lowest in-flight SpO2 (88 +/- 2%) vs. the lowest NHIT SpO2, (90 +/- 2%). DISCUSSION: Oxygen saturation decreases significantly during air travel in normal individuals. In this group of healthy passengers the NHIT approximates some, but not all, aspects of in-flight oxygenation. These results can be used to describe a normal response to the NHIT and air-travel.

Adult↗

PubMed2005

Postsynaptic IP3 receptor-mediated Ca2+ release modulates synaptic transmission in hippocampal neurons.

Ca(2+)-dependent mechanisms are important in regulating synaptic transmission. The results herein indicate that whole-cell perfusion of inositol 1,4,5-trisphosphate receptor (IP(3)R) agonists greatly enhanced excitatory postsynaptic current (EPSC) amplitudes in postsynaptic hippocampal CA1 neurons. IP(3)R agonist-mediated increases in synaptic transmission changed during development and paralleled age-dependent increases in hippocampal type-1 IP(3)Rs. IP(3)R agonist-mediated increases in EPSC amplitudes were inhibited by postsynaptic perfusion of inhibitors of Ca(2+)/calmodulin, PKC and Ca(2+)/calmodulin-dependent protein kinase II. Postsynaptic perfusion of inhibitors of smooth endoplasmic reticulum (SER) Ca(2+)-ATPases, which deplete intracellular Ca(2+) stores, also enhanced EPSC amplitudes. Postsynaptic perfusion of the IP(3)R agonist adenophostin (AdA) during subthreshold stimulation appeared to convert silent to active synapses; synaptic transmission at these active synapses was completely blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Postsynaptic IP(3)R-mediated Ca(2+) release also produced a significant increase in spontaneous EPSC frequency. These results indicate that Ca(2+) release from intracellular stores play a key role in regulating the function of postsynaptic AMPARs.

2-Amino-5-phosphonovalerate↗

PubMed2005

Activation of postsynaptic Ca(2+) stores modulates glutamate receptor cycling in hippocampal neurons.

We show that activation of postsynaptic inositol 1,4,5-tris-phosphate receptors (IP(3)Rs) with the IP(3)R agonist adenophostin A (AdA) produces large increases in AMPA receptor (AMPAR) excitatory postsynaptic current (EPSC) amplitudes at hippocampal CA1 synapses. Co-perfusion of the Ca(2+) chelator bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid strongly inhibited AdA-enhanced increases in EPSC amplitudes. We examined the role of AMPAR insertion/anchoring in basal synaptic transmission. Perfusion of an inhibitor of synaptotagmin-soluble n-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor SNARE-mediated exocytosis depressed basal EPSC amplitudes, whereas a peptide that inhibits GluR2/3 interactions with postsynaptic density-95 (PDZ) domain proteins glutamate receptor interacting protein (GRIP)/protein interacting with C-kinase-1 (PICK1) enhanced basal synaptic transmission. These results suggest that constitutive trafficking and anchoring of AMPARs help maintain basal synaptic transmission. The regulation of postsynaptic AMPAR trafficking involves synaptotagmin-SNARE-mediated vesicle exocytosis and interactions between AMPARs and the PDZ domains in GRIP/PICK1. We show that inhibitors of synaptotagmin-SNARE-mediated exocytosis, or interactions between AMPARs and GRIP/PICK1, attenuated AdA-enhanced increases in EPSC amplitudes. These results suggest that IP(3)R-mediated Ca(2+) release can enhance AMPAR EPSC amplitudes through mechanisms that involve AMPAR-PDZ interactions and/or synaptotagmin-SNARE-mediated receptor trafficking.

Adenosine↗

PubMed2004

Tracker: continuous HMMER and BLAST searching.

SUMMARY: Tracker is a web-based email alert system for monitoring protein database searches using HMMER and Blast-P, nucleotide searches using Blast-N and literature searches of the PubMed database. Users submit searches via a web-based interface. Searches are saved and run against updated databases to alert users about new information. If there are new results from the saved searches, users will be notified by email and will then be able to access results and link to additional information on the NCBI website. Tracker supports Boolean AND/OR operations on HMMER and BLASTP result sets to allow users to broaden or narrow protein searches. AVAILABILITY: The server is located at http://jay.bioinformatics.ku.edu/tracker/index.html. A distribution package including detailed installation procedure is freely available from http://jay.bioinformatics.ku.edu/download/tracker/.

Database Management Systems↗