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Biomedical subjects

R Clancy

Publications and source records attributed to R Clancy.

At least 55 records · Page 3Linked to original sources
PubMed1995

Acute on chronic bronchitis: A model of mucosal immunology.

Acute bronchitis has been studied as a model of disturbed mucosal immunoregulation. A new hypothesis relating to the pathogenesis of acute bronchitis has been developed, based on altered host response as the prime mover. Infection-prone subjects had low levels of lysozyme. Effective oral immunization, especially if early, reduced levels of bacterial colonization. Future attention focuses on intra bronchial inflammation and its link to the host-parasite relationship.

Acute Disease↗
PubMed1994

GM-CSF, IL-1 alpha, IL-1 beta, IL-6, IL-8, IL-10, ICAM-1 and VCAM-1 gene expression and cytokine production in human duodenal fibroblasts stimulated with lipopolysaccharide, IL-1 alpha and TNF-alpha.

The role of mucosal fibroblasts in intestinal inflammatory reactions is not known. In this study, we demonstrate that fibroblasts grown from histologically normal human duodenal biopsy tissues expressed mRNA genes for granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-1 alpha, IL-1 beta, IL-6, IL-8, IL-10, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) when stimulated with lipopolysaccharide (LPS) or IL-1 alpha. The increased mRNA expression of GM-CSF, IL-1 alpha, IL-1 beta, IL-6 and IL-8 in response to IL-1 alpha and LPS stimulation was time- and dose-dependent. In contrast, IL-10 was weakly expressed when fibroblasts were stimulated with LPS, IL-1 alpha or tumour necrosis factor-alpha (TNF-alpha), but the expression was enhanced in the presence of cycloheximide combined with optimal concentrations of LPS, IL-1 alpha or TNF-alpha, IL-1 alpha was a more potent stimulator than LPS for GM-CSF, IL-6, IL-8 and IL-10 expression, but not for IL-1 alpha and IL-1 beta. Increased GM-CSF, IL-6 and IL-8 gene expression was associated with the production of cytokine proteins in culture supernatant, but IL-1 alpha and IL-1 beta remained undetectable. Dexamethasone suppressed both gene expression and protein production of GM-CSF, IL-6 and IL-8 when fibroblasts were exposed to IL-1 alpha. TNF-alpha stimulated the release of GM-CSF, IL-6 and IL-8 and, combined with IL-1 alpha, cytokine production was enhanced synergistically. Finally, both LPS and IL-1 alpha up-regulated ICAM-1 and VCAM-1 gene expression. These findings implicate duodenal fibroblasts in the initiation and/or regulation of intestinal inflammation.

Adult↗
PubMed1993

Morphological, phenotypic and functional characteristics of a pure population of CD56+ CD16- CD3- large granular lymphocytes generated from human duodenal mucosa.

Interleukin-2 (IL-2)-dependent large granular lymphocytes (LGL) with a distinctive surface phenotype were generated from histologically normal duodenal biopsy tissues. Immunoperoxidase staining of the mucosa with an anti-CD56 monoclonal antibody revealed LGL localized in the lamina propria rather than in the epithelium. Light and electron microscopy demonstrated azurophilic and electron-dense cytoplasmic granules. Flow cytometry analysis revealed that these cells express CD45, CD56, CD2, CD7, CD11a, CD18, CD69 and the intermediate affinity (p70) IL-2 receptor (IL-2R) but not CD57, CD16, CD3, CD4, CD5, CD8, CD45RA, CD25, or the high affinity p55 IL-2R. The LGL proliferated when cultured in the presence of human rIL-2 but not in the presence of human rIL-4. Functional studies demonstrated that the LGL had strong cytotoxicity against natural killer (NK) target cells, K562, but not NK-resistant targets such as Colo 205, Melanoma and Epstein-Barr virus (EBV)-transformed B-cell lines. The LGL expressed genes for IL-5, IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumour necrosis factor-alpha (TNF-alpha) and the corresponding cytokines were detected in culture supernatant. These results provide evidence for an important role of gut mucosal LGL in the induction and regulation of inflammation and immunity in the gut.

Adult↗
PubMed1992

Cryopreserved allograft veins as alternative coronary artery bypass conduits: early phase results.

Traditional autologous conduits are sometimes unavailable or unsuitable to permit total revascularization during coronary artery bypass grafting. In these patients the results of using nonautologous alternative conduits has been disappointing. Encouraged by the excellent long-term results seen with cryopreserved allograft valves, a clinical protocol was developed to evaluate the use of a commercially cryopreserved allograft saphenous vein (CPV). Our protocol consisted of using CPV when left internal mammary arteries and autologous saphenous vein grafts were unavailable or unsuitable for complete revascularization. Blood group (ABO) typed CPVs were thawed and implanted as required using standard surgical techniques. From December 1989 through June 1991, 19 of 1,602 patients who underwent coronary revascularization had CPVs implanted (1.2%). There were no operative deaths. An attempt was made to evaluate the patency of all grafts with coronary arteriography or ultrafast computed tomographic scans. Fourteen patients were available for patency evaluation. Patency rate in the 14 patients studied at a mean of 7 +/- 2 months (range, 2 to 16 months) were: internal mammary artery, 93% (14/15); saphenous vein graft, 80% (4/5); and CPV, 41% (7/17). The patency of the CPV was significantly less than the patency rate for the saphenous vein and internal mammary artery (p = 0.004). We conclude that the short-term patency rate of CPVs is inferior to that of autologous vessels. Due to its poor patency, we recommend that CPV should only be used when no other autologous conduit is available.

Aged↗
PubMed1990

Dual mechanisms of inhibition of the immune response by enterocytes isolated from the rat small intestine.

Antigen presentation by enterocytes isolated from the rat small bowel was studied by using T cell proliferation, and immunoregulatory function in an antigen-driven culture system, as indicator systems. Lymph node T cells obtained from rats immunized with ovalbumin (OA) failed to divide when cultured for 4 days in the presence of freshly isolated Ia+ enterocytes and OA. However, cell division was noted when enterocytes were removed after 18 h by Percoll gradient centrifugation, followed by culture of T cells for a further 4 days in the absence of antigen. The failure to divide in the primary culture was due to the secretion by enterocytes of a dialysable non-specific inhibitor. Antigen presentation by enterocytes was specific and was inhibited by monoclonal mouse anti-rat Ia antibody, OX6. An epithelial cell line (REC-2) was established from normal rat small intestine. These cells expressed Ia molecules following incubation with Concanavalin-A stimulated spleen cell supernatant, and were capable of both presenting antigen, and inducing interleukin-2 (IL-2) production, when cultured with primed T cells. Furthermore, Ia+ REC-2 cells functioned as stimulators in a primary mixed lymphocyte reaction (MLR). Both OA-primed T cells activated by enterocytes and antigen, and allogeneic MLR-activated T cells, mediated suppression which was not specific for the initiating antigen. These experiments indicated two mechanisms mediate suppression of cell division in gut mucosa. The contribution of these mechanisms to the control of inflammation at mucosal sites requires investigation.

Animals↗
PubMed1989

Symmetrical thalamic degeneration with calcifications of infancy.

We describe the clinical and radiographic features of three premature infants with symmetric thalamic calcification recognized by computed tomographic scan on days 6, 12, and 49 of life and contrast our findings with those reported in the literature. These lesions follow prepartum or intrapartum hypoxiaischemia and are clinically distinguished by prominent bulbar dysfunction, featuring weak or absent cry, poor feeding, and facial weakness. Neonatal thalamic calcification in premature infants may serve as a radiological marker of an acute, short-lived hypoxic-ischemic event. The presence of brain-stem dysfunction, particularly of lower cranial nerves in association with thalamic calcifications, constitutes a distinctive clinical-radiological entity and usually portends a poor outcome. The presence of these calcifications implies that injury was sustained to diencephalic and brain-stem structures at least 2 to 4 weeks prior to their appearance on computed tomographic scan.

Atrophy↗
PubMed1988

Continuous intracranial pressure monitoring and serial electroencephalographic recordings in severely asphyxiated term neonates.

We report our observations from intensive intracranial pressure (ICP) monitoring and serial clinical neurologic and electroencephalographic examinations in ten asphyxiated full-term neonates, of whom five died and at least two survivors had multiple severe neurologic handicaps. Direct measurements of ICP were obtained by a newly developed infant subarachnoid bolt and/or a transfontanelle pressure transducer. Simultaneous ICPs were recorded and correlated when possible. We noted a dependence of transfontanelle ICP values on application technique and force. In infants with no bleeding diathesis, the subarachnoid bolt was safe and no complications were encountered. Only six infants experienced pathologic elevations of ICP following birth asphyxia, and of these infants only two had sustained, marked increases of ICP. We also noted abundant fluctuations of cerebral perfusion pressure (mean arterial blood pressure minus ICP), but the majority of fluctuations were accounted for by mean arterial pressure changes rather than ICP changes. We found no deterioration of clinical neurologic function as measured by serial mental status examinations and electroencephalogram samples at the time the maximum ICP was measured. We also noted very little change in ICP during most electrographic seizures. In these infants ICP did increase after birth but major ICP elevations were uncommon and did not appear to introduce any acute functional neurologic disturbances. Most changes in cerebral perfusion pressure were attributed to blood pressure rather than ICP changes. It appears unlikely that cerebral edema and elevated ICP play a major role in determining neurologic outcome in some asphyxiated term infants.

Asphyxia Neonatorum↗
PubMed1988

Genetic disorders and major extracardiac anomalies associated with the hypoplastic left heart syndrome.

All pediatric autopsies of patients with hypoplastic left heart syndrome seen during an 11-year interval were reviewed to determine the frequency of underlying chromosomal and single-gene defects and idiopathic major extracardiac anomalies associated with this common, lethal congenital heart abnormality. Of 83 patients identified, nine had underlying chromosomal abnormalities, four had single-gene defects, ten had one or more major extracardiac anomalies without an identifiable chromosomal or mendelian disorder, and two were infants of insulin-dependent diabetic mothers. Overall, 23 patients (28%) had a genetic disorder and/or major extracardiac anomaly. The substantial prevalence of genetic causes of and major extracardiac anomalies associated with hypoplastic left heart syndrome underscores the need for a detailed genetic evaluation for all patients with hypoplastic left heart syndrome.

Abnormalities, Multiple↗
PubMed1986

Cerebral metabolic effects of neonatal seizures measured with in vivo 31P NMR spectroscopy.

In vivo phosphorus 31 nuclear magnetic resonance (31P NMR) spectroscopy was used to evaluate changes in cerebral high-energy phosphate compounds in 8 infants with seizures. During the study 4 babies had seizures that caused a 50% decrease in the phosphocreatine to inorganic phosphate (PCr/Pi) ratio. Focal seizures caused lateralized decreases in the PCr/Pi ratio; generalized seizures caused bilateral decreases. Postictal spectra had increased PCr/Pi ratios, presumably due to postictal inhibition. Interictal 31P NMR spectra were normal. One patient's seizures were successfully treated with intravenously administered phenobarbital during NMR data acquisition, causing an immediate increase in the PCr/Pi ratio from 0.7 to 1.2. These studies indicate that cerebral PCr concentration decreases by approximately 33% and that oxidative metabolism increases by approximately 45% during neonatal seizures. Five babies had PCr/Pi ratios of less than 0.8 during seizures and subsequently developed long-term neurological sequelae, which suggests that neonatal seizures may cause or exacerbate cerebral injury by increasing cerebral metabolic demands above energy supply.

Adenosine Triphosphate↗
PubMed1986

Clinical predictors of computed tomography in epileptic children.

The purpose of this study was to determine which clinical characteristics correlated with abnormal computed tomographic (CT) scans in epileptic children. Thirty variables were examined. Of these, four variables (presence of inherited or congenital disease, focal motor findings, developmental delay, and early onset of seizures) correlated with CT scan outcome. Partial seizures per se were not highly associated with abnormal CT scans. A crude decision rule based on these results correctly classified the CT scan result in 94% of the patients who were clinically predicted not to have a parenchymal abnormality.

Brain↗
PubMed1986

The epidemiology of malaria in a population surrounding Madang, Papua New Guinea.

Malaria is prevalent throughout coastal and lowland Papua New Guinea. Recent changes, including a shift from predominance of Plasmodium vivax to Plasmodium falciparum, appearance of chloroquine-resistant P. falciparum and decreased effectiveness of vector control programs have been observed. Epidemiological features of malaria were studied through four six-month surveys of a population of 16,500 in Madang Province from 1981-1983. Baseline data on parasitology, splenic enlargement, serology, hemoglobin levels, prevalence of 4-aminoquinolines, utilization of mosquito nets and incidence of fever were collected for use in future evaluation of malaria control measures including possible field trials of an antimalarial vaccine. Prevalence of parasitemia (all species, all ages) varied from 35.0% to 42.7% over the four surveys each of which covered a random sample of 25% of the population. The ratio of parasite species was: P. falciparum 70:P. vivax 25:P. malariae 5 in the dry seasons, shifting slightly in favor of P. falciparum during the wet seasons. Intense year-round transmission was indicated by decreasing parasite prevalence and splenic enlargement with age, low density asymptomatic parasitemias and high prevalence of antimalarial antibodies (i.e., greater than 80% of the population over five years of age was ELISA-positive). Levels of endemicity varied geographically, presence of 4-aminoquinolines in urine samples was relatively common (12.7% positive) and chloroquine resistance was widespread (81.6% in vitro, 46.6% in vivo).

Adolescent↗