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Biomedical subjects

R Wilson

Publications and source records attributed to R Wilson.

At least 253 records · Page 14Linked to original sources
PubMed1997

Lung pathology in high-altitude pulmonary edema.

Autopsy findings in 10 cases of high-altitude pulmonary edema have been collected from published articles and personal observations. All cases were males with a mean age of 37 years (22-62). The altitude of occurrence was from 8400 to 17 500 feet. The mean combined lung weight in nine cases was 1682 g (1200-3000 g). Cerebral edema was present in five of eight cases. The most frequency pulmonary findings in addition to diffuse edema consisted of leukocyte infiltrates, alveolar hemorrhages, thrombi in small pulmonary arteries, and alveolar hyaline membranes. Pulmonary infarction was present in only one case. Right ventricular dilatation was commonly present. The left ventricle was normal. No significant coronary disease was present.

Adult↗
PubMed1997

Attitudes toward obstetrics training. Residents surveyed at McGill University and University of Montreal.

OBJECTIVE: To determine family medicine residents' attitudes toward family practice training in obstetrics and neonatology before and after implementation of a modified obstetrics curriculum at McGill University (MG). DESIGN: Two-group pretest and posttest. Fifty-seven respondents, 31 at MG, 26 at University of Montreal (UM), were case matched as first-year and second-year residents. SETTING: Departments of Family Medicine at MG and UM. PARTICIPANTS: Family medicine residents at MG and UM. INTERVENTION: A modified obstetrics curriculum was introduced at MG (study group); no modifications were introduced at UM (control group). First- and second-year residents' attitudes toward the adequacy of training were assessed through responses to a questionnaire administered in July 1992 and July 1994. MAIN OUTCOME MEASURES: Changes in response scores before and after implementation of the modified curriculum. RESULTS: Repeated multivariate analysis of variance (MANOVA) showed respondents believed family practice obstetrics training was adequate in general, but that family practitioners were inadequately trained in emergency obstetric skills. Scores for items assessing neonatology skills increased significantly in the MG group after the intervention. CONCLUSIONS: Residents' overall confidence in their obstetrics training did not appear to improve, but this might be due to a time lag between curriculum modification and attitudinal change. McGill residents' confidence in neonatology skills improved significantly after curriculum modification.

Adult↗
PubMed1997

Nocturnal ophthalmic arterial hemodynamics in primary open-angle glaucoma.

PURPOSE: Recent studies have found nocturnal reductions in systemic arterial blood pressure associated with progressive visual field loss in glaucoma. Although ocular ischemia has been hypothesized to link these two phenomena, it remains unknown if perfusion of the eye is reduced during the night in patients with glaucoma. PATIENTS AND METHODS: Nine patients with primary open-angle glaucoma (POAG) and stable visual fields who were free from systemic hypertension, as well as nine age- and gender-matched controls, were studied at 9:00 P.M., and then during sleep at 12:00, 3:00, and 6:00 A.M. Systemic blood pressure, intraocular pressure (IOP), and color Doppler imaging (CDI) of the ophthalmic artery were measured at each time. RESULTS: Arterial blood pressure and ophthalmic artery peak systolic and end-diastolic velocities were similar and were unchanged over time, in both groups. In contrast, the ophthalmic arterial resistance index decreased as the night progressed (p < 0.05), identically in controls and patients. In patients with glaucoma, CDI indices were independent of changes in arterial pressure, IOP, or calculated ocular perfusion pressure. CONCLUSION: Patients with POAG characterized by stable visual fields who were free from systemic hypertension exhibited normal ophthalmic arterial hemodynamics at night; there was no evidence of ocular ischemia or vasoconstriction.

Blood Pressure↗
PubMed1997

The effect of rolipram, a type IV phosphodiesterase inhibitor, on Pseudomonas aeruginosa infection of respiratory mucosa.

We have investigated the effect of rolipram, a type IV phosphodiesterase inhibitor, on Pseudomonas aeruginosa infection of the respiratory mucosa of an organ culture model and on the reduction in intracellular cAMP levels seen in human nasal epithelial cells incubated with P. aeruginosa culture filtrate. We have compared rolipram with salmeterol, a long-acting beta-2 agonist, and have also studied the effect of the two agents together. Infected organ cultures had significantly (P < or = .05) increased epithelial damage. Rolipram significantly (P < or = .05) reduced P. aeruginosa-induced epithelial damage and reduced the total number of bacteria adhering to the respiratory mucosa (P < or = .04) in a concentration-dependent manner, although neither rolipram nor salmeterol affected P. aeruginosa growth in broth cultures. Rolipram reduced P. aeruginosa-induced mucosal damage more than salmeterol (P < or = .03). The effect of the two agents was neither additive nor synergistic. Rolipram, salmeterol and both agents together significantly (P < or = .01) increased intracellular cAMP levels in epithelial cells treated with P. aeruginosa culture filtrate. Rolipram alone increased cAMP more than salmeterol or both agents together (P < or = .01), probably because of an interaction between the two agents. These results suggest that agents that elevate intracellular cAMP protect the epithelium during bacterial infection. Rolipram is more effective than salmeterol in preventing P. aeruginosa-induced epithelial damage.

Bacterial Adhesion↗
PubMed1996

Peripheral kappa 1-opioid receptor-mediated analgesia in mice.

When injected directly into the tail, U50,488H is a potent analgesic in the tailflick assay (ED50 3.1 micrograms). The analgesic activity is lost if the radiant heat is focused 1 cm away from the site of injection. The kappa 1-opioid receptor antagonist nor-binaltorphimine given systemically reverses the local analgesic response of U50,488H, but the antagonist is 100-fold more potent when injected directly into the tail. Intrathecal antisense treatment with a probe targeting the mRNA encoding the kappa 1-opioid receptor blocks the local analgesic actions of U50,488H in the tail, suggesting that U50,488H is acting on dorsal ganglia neurons.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1996

Type-III procollagen assembly in semi-intact cells: chain association, nucleation and triple-helix folding do not require formation of inter-chain disulphide bonds but triple-helix nucleation does require hydroxylation.

Procollagen assembly is initiated within the endoplasmic reticulum by three alpha-chains associating via their C-propeptides (C-terminal propeptides). To study the requirements for the association of procollagen monomers at synthesis we have reconstituted the initial stages in the folding, assembly and modification of procollagen using semi-permeabilized cells. By translating a type-III procollagen "mini-gene' which lacks part of the triple-helical domain, we demonstrate that these cells efficiently carry out the assembly of hydroxylated, triple-helical, procollagen trimers and allow the identification of specific disulphide-bonded intermediates in the folding pathway. Mutant chains, which lack the ability to form inter-chain disulphide bonds within the C-propeptide, were still able to assemble within this system. Furthermore, characterization of the trimeric molecules formed suggested that inter-chain disulphide bonds had formed within the C-telopeptide (C-terminal telopeptide). However, when hydroxylation of prolyl and lysyl residues was inhibited no inter-chain disulphide bonds were formed in the C-telopeptide, indicating that hydroxylation is required for the initial nucleation of the triple-helical domain. Mutant chains which lacked the ability to form inter-chain disulphide bonds within the C-propeptide or the C-telopeptide could still assemble to form trimeric triple-helical molecules linked by inter-chain disulphide bonds within the N-propeptide (N-terminal propeptide). These results indicate that inter-chain disulphide bond formation within the C-propeptide or the C-telopeptide is not required for chain association and triple-helix formation.

Amino Acid Sequence↗
PubMed1996

Monocyte chemoattractant protein-1: receptor interactions and calcium signaling mechanisms.

Monocyte chemoattractant protein-1 (MCP-1) is a member of the Cys-Cys chemokine family. Two related MCP-1 receptors have been identified (CC-CKR2A and CC-CKR2B), although the precise kinetics of ligand binding and calcium signaling of these receptors has yet to be investigated. To examine this more closely, the human MCP-1 receptors were cloned and expressed in Chinese hamster ovary (CHO) cells. Membranes prepared from cells expressing CC-CKR2B bind MCP-1 selectively and with high affinity (Kd = 120 pM). MCP-1 stimulation of recombinant CHO cells expressing CC-CKR2B induces a rapid increase in intracellular Ca2+ through both receptor-operated Ca2+ channels and mobilization of Ca2+ from intracellular stores, and leads to a rapid temperature-dependent internalization of the ligand/receptor complexes. In contrast, recombinant CHO cells expressing CC-CKR2A, and membranes prepared from these cells, fail to bind detectable levels of MCP-1. However, MCP-1 stimulation of cells expressing CC-CKR2A induces a small but significant increase in intracellular Ca2+. Repeated stimulation of these cells with MCP-1 leads to a potentiation of the response to a level comparable to that seen in cells expressing CC-CKR2B. These observations suggest that the levels of cell surface CC-CKR2A are controlled by novel mechanisms.

Animals↗
PubMed1996

The effect of mutations in genes required for lipopolysaccharide synthesis on Haemophilus influenzae type b colonization of human nasopharyngeal tissue.

Haemophilus influenzae type b (Hib) is an upper respiratory tract commensal that can cause invasive disease, particularly in young children. Lipopolysaccharide (LPS) has been implicated as a major virulence determinant of Hib, and changes in LPS structure may influence bacterial interactions with the respiratory mucosa. We have examined the effect of variations in LPS on the interaction of Hib with human nasal turbinate tissue maintained in an organ culture model with an air-interface, by using isogenic derivatives of strains RM153 (Eagan) and RM7004 expressing truncated LPS due to mutations in genes contained within the chromosomal loci lic1 and lic2 (lic1lic2) or in the galE and galK genes (galEK). Tissue was infected with an inoculating dose of 2.3-3.3 x 10(6) colony forming units (cfu) in 2 microliters of PBS and maintained for 24 h. By scanning electron microscopy the percentage of the organ culture surface exhibiting epithelial damage increased from 5.3 +/- 1.4 in controls to 12.5 +/- 6.4-26.3 +/- 9.1 following infection, with no significant difference between parent strains and their derivatives. There was significant bacterial tropism for mucus, and to a lesser extent damaged cells, which was not influenced by the LPS phenotype. All strains caused separation of epithelial cells, adhered to non-luminal cell surfaces, and invaded the epithelium intercellularly. We conclude that Hib associated with mucus and damaged epithelium, and infrequently with normal epithelium, but changes in the LPS phenotype did not affect the interaction between Hib and the mucosal surface of human nasal turbinate tissue.

Bacterial Adhesion↗
PubMed1996

The effect of bacterial toxins on levels of intracellular adenosine nucleotides and human ciliary beat frequency.

Toxins that slow ciliary beat are virulence determinants of bacteria that infect or invade ciliated epithelial surfaces. We have previously shown that the effect of the Pseudomonas aeruginosa toxin pyocyanin on ciliary beat is associated with a fall in intracellular cAMP and ATP. We have now investigated whether reduction in intracellular adenosine nucleotides might be a common mechanism of action of other bacterial toxins which slow ciliary beat. Two other P. aeruginosa toxins, 1-hydroxyphenazine (1-HP) and rhamnolipid, and two Haemophilus influenzae fractions produced by gel filtration of broth cultures were tested. The effect on human nasal epithelium ciliary beat frequency (CBF), and intracellular cAMP and ATP were measured, and the effect of two pharmacological agents, dibutyryl cAMP and salmeterol, on these changes was assessed. 1-HP, rhamnolipid and the two H. influenzae fractions slowed CBF before there was significant release of lactate dehydrogenase from the cells. The toxins also caused a fall in intracellular cAMP and ATP. Dibutyryl cAMP and salmeterol at the concentrations used do not increase baseline CBF, but diminished the fall in CBF and intracellular adenosine nucleotides. The cAMP and ATP levels in these studies were combined with those previously obtained with pyocyanin. there was a good correlation between cAMP and ATP levels and CBF. Bacterial toxins which slow CBF may act by causing a fall in intracellular adenosine nucleotides, and agents which stimulate cAMP may prevent toxin-induced slowing of ciliary beat.

Adenine Nucleotides↗
PubMed1996

Carcinogenic risks of inorganic arsenic in perspective.

Induction of cancer by inorganic arsenic occurs inconsistently between species and between routes of exposure, and it exhibits different dose-response relationships between different target organs. Inhaled or ingested arsenic causes cancer in humans but not in other species. Inhaled arsenic primarily induces lung cancer, whereas ingested arsenic induces cancer at multiple sites, including the skin and various other organs. Cancer potency appears to vary by route of exposure (ingestion or inhalation) and by organ site, and increases markedly at higher exposures in some instances. To understand what might explain these inconsistencies, we reviewed several hypotheses about the mechanism of cancer induction by arsenic. Arsenic disposition does not provide satisfactory explanations. Induction of cell proliferation by arsenic is a mechanism of carcinogenesis that is biologically plausible and compatible with differential effects for species or differential dose rates for organ sites. The presence of other carcinogens, or risk modifiers, at levels that correlate with arsenic in drinking water supplies, may be a factor in all three inconsistencies: interspecies specificity, organ sensitivity to route of administration, and organ sensitivity to dose rate.

Aged↗