Biomedical subjects

J L Mueller

Publications and source records attributed to J L Mueller.

14 recordsLinked to original sources

PubMed2006

Imaging cardiac activity by the D-bar method for electrical impedance tomography.

A practical D-bar algorithm for reconstructing conductivity changes from EIT data taken on electrodes in a 2D geometry is described. The algorithm is based on the global uniqueness proof of Nachman (1996 Ann. Math. 143 71-96) for the 2D inverse conductivity problem. Results are shown for reconstructions from data collected on electrodes placed around the circumference of a human chest to reconstruct a 2D cross-section of the torso. The images show changes in conductivity during a cardiac cycle.

Algorithms↗

PubMed2005

Cross-species comparison of Drosophila male accessory gland protein genes.

Drosophila melanogaster males transfer seminal fluid proteins along with sperm during mating. Among these proteins, ACPs (Accessory gland proteins) from the male's accessory gland induce behavioral, physiological, and life span reduction in mated females and mediate sperm storage and utilization. A previous evolutionary EST screen in D. simulans identified partial cDNAs for 57 new candidate ACPs. Here we report the annotation and confirmation of the corresponding Acp genes in D. melanogaster. Of 57 new candidate Acp genes previously reported in D. melanogaster, 34 conform to our more stringent criteria for encoding putative male accessory gland extracellular proteins, thus bringing the total number of ACPs identified to 52 (34 plus 18 previously identified). This comprehensive set of Acp genes allows us to dissect the patterns of evolutionary change in a suite of proteins from a single male-specific reproductive tissue. We used sequence-based analysis to examine codon bias, gene duplications, and levels of divergence (via dN/dS values and ortholog detection) of the 52 D. melanogaster ACPs in D. simulans, D. yakuba, and D. pseudoobscura. We show that 58% of the 52 D. melanogaster Acp genes are detectable in D. pseudoobscura. Sequence comparisons of ACPs shared and not shared between D. melanogaster and D. pseudoobscura show that there are separate classes undergoing distinctly dissimilar evolutionary dynamics.

Animals↗

PubMed2004

Detection and mapping of quantitative trait loci that determine responsiveness of mice to nitrous oxide antinociception.

Exposure to 70% N(2)O evokes a robust antinociceptive effect in C57BL/6 (B6) but not in DBA/2 (D2) inbred mice. This study was conducted to identify quantitative trait loci (QTL) in the mouse genome that might determine responsiveness to N(2)O. Offspring from the F(2) generation bred from B6 and D2 progenitors exhibited a broad range of responsiveness to N(2)O antinociception as determined by the acetic acid-induced abdominal constriction test. QTL analysis was then used to dissect this continuous trait distribution into component loci, and to map them to broad chromosomal regions. To this end, 24 spleens were collected from each of the following four groups: male and female F(2) mice responding to 70% N(2)O in oxygen with 100% response (high-responders); and male and female F(2) mice responding with 0% response (low-responders). Genomic DNA was extracted from the spleens and genotyped with simple sequence length polymorphism MapPairs markers. Findings were combined with findings from the earlier QTL analysis from BXD recombinant inbred mice [Brain Res 725 (1996) 23]. Combined results revealed two significant QTL that influence responsiveness to nitrous oxide on proximal chromosome 2 and distal chromosome 5, and one suggestive QTL on midchromosome 18. The chromosome 2 QTL was evident only in males. A significant interaction was found between a locus on chromosome 6 and another on chromosome 13 with a substantial effect on N(2)O antinociception.

Animals↗

PubMed2001

Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle-Wells syndrome.

Familial cold autoinflammatory syndrome (FCAS, MIM 120100), commonly known as familial cold urticaria (FCU), is an autosomal-dominant systemic inflammatory disease characterized by intermittent episodes of rash, arthralgia, fever and conjunctivitis after generalized exposure to cold. FCAS was previously mapped to a 10-cM region on chromosome 1q44 (refs. 5,6). Muckle-Wells syndrome (MWS; MIM 191900), which also maps to chromosome 1q44, is an autosomal-dominant periodic fever syndrome with a similar phenotype except that symptoms are not precipitated by cold exposure and that sensorineural hearing loss is frequently also present. To identify the genes for FCAS and MWS, we screened exons in the 1q44 region for mutations by direct sequencing of genomic DNA from affected individuals and controls. This resulted in the identification of four distinct mutations in a gene that segregated with the disorder in three families with FCAS and one family with MWS. This gene, called CIAS1, is expressed in peripheral blood leukocytes and encodes a protein with a pyrin domain, a nucleotide-binding site (NBS, NACHT subfamily) domain and a leucine-rich repeat (LRR) motif region, suggesting a role in the regulation of inflammation and apoptosis.

Amino Acid Motifs↗

PubMed2001

Reconstruction of conductivity changes due to ventilation and perfusion from EIT data collected on a rectangular electrode array.

In this paper we demonstrate that conductivity changes caused by ventilation and perfusion in a human subject can be reconstructed from electrical impedance tomography data collected on a rectangular array of electrodes placed on a subject's chest. Currents are applied on the electrodes and the resulting voltages on the electrodes are measured. A 3D reconstruction algorithm is used to reconstruct the conductivity distribution in the region beneath the array. Time traces of the reconstructed conductivity distribution demonstrate the detected changes in conductivity due to ventilation and perfusion.

Algorithms↗

PubMed1999

A reconstruction algorithm for electrical impedance tomography data collected on rectangular electrode arrays.

A three-dimensional reconstruction algorithm in electrical impedance imaging is presented for determining the conductivity distribution beneath the surface of a medium, given surface voltage data measured on a rectangular array of electrodes. Such an electrode configuration may be desirable for using electrical impedence tomography to detect tumors in the human breast. The algorithm is based on linearizing the conductivity about a constant value. Here, we describe a simple implementation of the algorithm on a four-electrode--by-four-electrode array and the reconstructions obtained from numerical and experimental tank data. The results demonstrate significantly better spatial resolution in the plane of the electrodes than with respect to depth.

Algorithms↗

PubMed1999

Returning to work through job accommodation: a case study.

1. As more people live longer and more active lives the likelihood of experiencing a disability during one's career increases. Although the unemployment rate among people with disabilities is high, workers with disabilities are becoming more common. 2. Effective job accommodation costs only a small fraction of the hundreds of thousands of dollars that would otherwise be paid out in disability benefits and insurance premiums, or wasted in litigation. 3. Job accommodation planning should begin as early as possible in the disability process and include the active involvement of the individual with the disability and appropriate clinicians, as well as the supervisor and coworkers. 4. Successful accommodation is the result of teamwork, The occupational health professional is often the coordinator of a number of internal and external resources in the job accommodation process. Tools are available for sharing information among all those involved in the accommodation process, without compromise of confidential medical or business information.

Accidents, Occupational↗

PubMed1998

Assistive technology and universal design in the workplace.

The terms assistive technology and universal design challenge designers, engineers, and technologists to consider the broadest possible use for the things they create, to make assistive technology as useful to nondisabled persons as to those with disabilities, and to make the products and environments we design as usable as possible for everyone, regardless of age or ability.

Aging↗

PubMed1996

Nitrous oxide antinociception in BXD recombinant inbred mouse strains and identification of quantitative trait loci.

Among inbred mouse strains, DBA/2 mice are unique because of their poor responsiveness to nitrous oxide (N2O) antinociception. As a first step towards identifying candidate genes involved in determining antinociceptive responsiveness to N2O, male mice from the DBA/2 strain, the more responsive C57BL/6 strain, their B6D2F1 offspring, and 22 BXD recombinant inbred (RI) strains derived from DBA/2 and C57BL/6 mice were exposed to N2O and evaluated using the acetic acid abdominal constriction test. When exposed to 70% N2O, C57BL/6, DBA/2 and B6D2F1 mice exhibited antinociceptive responses of 78, 22 and 55%, respectively. The BXD RI strains demonstrated varying degrees of responsiveness to N2O. Cluster analysis revealed one cluster of 16 strains approximating the C57BL/6 progenitor (61.9-100% antinociceptive response to 70% N2O) and another of six strains around the DBA/2 progenitor (9.1-40% antinociceptive response to 70% N2O). The robust strain differences permitted screening the strain means with 1492 marker loci previously mapped in BXD RI strains. Using a QTL analysis specifically tailored to existing mouse RI strains, we found associations at the 0.01 level on seven chromosomes with the most promising marker loci being Il2ra, Hbb, Hmg1rs7 and Gsl5 on chromosomes 2, 7, 16 and 19, respectively (P < 0.002).

Animals↗

PubMed1995

Involvement of nitric oxide in intracerebroventricular beta-endorphin-induced neuronal release of methionine-enkephalin.

Previous work has suggested that the antinociceptive effect of nitrous oxide (N2O) in rats is mediated, at least in part, by beta-endorphin (beta-EP) and that centrally administered beta-EP stimulates release of methionine-enkephalin (ME) in the rat spinal cord. Since inhibition of central nitric oxide (NO) production has been found to suppress N2O antinociception, we examined the possible involvement of NO in the release of spinal cord ME by i.c.v. beta-EP. Urethane-anesthetized, male Sprague-Dawley rats were intrathecally (i.t.) perfused with artificial cerebrospinal fluid (aCSF) and fractions of perfusate were assayed for immunoreactive (i.r.) ME. The beta-EP-induced increase in ME concentration in the i.t. perfusate was significantly suppressed by perfusing the animal with aCSF containing 100 microM L-NG-nitro arginine (L-NOARG), an inhibitor of NO synthase (NOS). The further addition of 50 microM L-arginine (L-ARG), but not D-arginine (D-ARG), to the aCSF reversed the suppression of the ME change by L-NOARG. However, the potency of L-ARG decreased with increasing concentrations of L-ARG. On the other hand, increasing the concentration of L-NOARG in the aCSF to 250 microM failed to produce a greater suppression of the beta-EP-induced increase in ME. These findings suggest that NO may mediate the beta-EP-induced release of ME in the spinal cord and that interference with this mechanism might be an explanation for the antagonism of N2O antinociception in rats by NOS inhibitors.

Animals↗

PubMed1993

Strain-dependent differences in responsiveness of mice to nitrous oxide (N2O) antinociception.

N2O antinociception was assessed in eight inbred and two outbred mouse strains. Results indicated the following order of responsiveness among the 10 strains: A/J (most sensitive), C57BL/6ByJ, C57BL/6J, BALB/cByJ, C3H/HeJ, Swiss-Webster, CXBK/ByJ, ICR, CBA/J and DBA/2J (least sensitive). These results demonstrate significant strain-dependent differences in antinociceptive responsiveness to N2O. The weak antinociceptive response to N2O in the DBA/2J strain, which is sensitive to morphine and U-50, 488H, indicates some underlying neurobiological difference in the DBA/2J mouse that imparts resistance to N2O. The responsiveness of CXBK/ByJ mice to N2O indicates that mu-opioid receptors may not play an important role in N2O antinociception in mice.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1993

Dose-dependent antagonism and potentiation of nitrous oxide antinociception by naloxone in mice.

Administration of the anesthetic gas nitrous oxide (N2O) evoked a concentration-dependent antinociceptive effect in mice as assessed by the abdominal constriction test. Depending on the dose and route of pretreatment with the opioid receptor blocker naloxone, the N2O drug effect was either antagonized or potentiated. After s.c. pretreatment with milligram per kilogram doses of naloxone, dose-related antagonism occurred; picogram per kilogram doses potentiated N2O-induced antinociception. The i.c.v. pretreatment with microgram quantities of naloxone also antagonized N2O antinociception in a dose-related fashion; i.c.v. pretreatment with femtogram doses was without effect. On the other hand, intrathecal (i.t.) pretreatment with femtogram quantities of naloxone potentiated N2O antinociception; i.t. pretreatment with microgram quantities continued to antagonize the antinociceptive effect. The same pattern of interaction was observed in mice challenged with the kappa opioid analgesic drug trans (+- 3,4-dichlow-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl] benzeneacetamide methane sulfonate (U-50, 488H) after s.c., i.c.v. or i.t. pretreatments with high and low doses of naloxone. These results 1) demonstrate further similarities in the opioid receptor mediation of N2O and U-50, 488H antinociceptive effects and also 2) support the concept of high-affinity spinal opioid receptors, whose blockade by s.c.- or i.t.- but not i.c.v.-administered low-dose naloxone can potentiate the antinociceptive effects of both N2O and U-50,488H. These findings suggest that the antinociceptive effect of N2O might be modulated by a descending opioid system that inhibits analgesia.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1992

Contrasting influences of 5-hydroxytryptamine receptors in nitrous oxide antinociception in mice.

5-Hydroxytryptamine (5-HT) mechanisms may play a role in opioid-mediated antinociception. Since opioid mechanisms have been implicated in nitrous oxide antinociception, this study was conducted to determine the possible role of 5-HT receptors in nitrous oxide antinociception. Male Swiss Webster mice were pretreated with one of two 5-HT receptor blockers and then tested in the acetic acid abdominal constriction test for their antinociceptive response to nitrous oxide, the kappa-opioid agonist U-50,488H, or the mu-opioid agonist sufentanil. Results indicate that the 5-HT3 receptor blocker ICS-205,930 antagonized both nitrous oxide and U-50,488H effects but not that of sufentanil. Mianserin, a 5-HT1c/5-HT2 receptor blocker, effects but not that of sufentanil. Mianserin, a 5-HT1c/5-HT2 receptor blocker, potentiated effects of both nitrous oxide and U-50,488H but not that of sufentanil. These findings show similarities in nitrous oxide and U-50,488H antinociception and further support our hypothesis that nitrous oxide works through central kappa-opioid mechanisms in mice. The results also suggest different roles for 5-HT receptor subtypes in mediating or modulating the antinociceptive effect of nitrous oxide.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMedDate not supplied

Antagonism of nitrous oxide antinociception in mice by intrathecally administered antisera to endogenous opioid peptides.

Previously it was demonstrated that nitrous oxide antinociception in the mouse abdominal constriction test is mediated by kappa-opioid receptors. Since nitrous oxide is thought to cause the neuronal release of endogenous opioid peptide to stimulate opioid receptors, this study was designed to identify the opioid peptides involved, especially in the spinal cord, by determining whether nitrous oxide antinociception can be differentially inhibited by intrathecally (i. t.) administered antisera to different opioid peptides. Male NIH Swiss mice were pretreated i.t. with rabbit antisera to opioid peptides then exposed 24 h later to one of three different concentrations of nitrous oxide in oxygen. Dose-response curves constructed from the data indicated that the antinociceptive effect of nitrous oxide was significantly antagonized by antisera to various dynorphins (DYNs) and methionine-enkephalin (ME), but not by antiserum to beta-endorphin (beta-EP). The AD(50) values for nitrous oxide antinociception were significantly elevated by antisera to DYNs and ME but not beta-EP. These findings of this study support the hypothesis that nitrous oxide antinociception in the mouse abdominal constriction test involves the neuronal release of DYN and ME in the spinal cord.

Analgesics, Non-Narcotic↗