Search PubMed⌕ Search

Biomedical subjects

C M Taylor

Publications and source records attributed to C M Taylor.

At least 73 records · Page 4Linked to original sources
PubMed1995

Soluble circulating cell adhesion molecules in haemolytic uraemic syndrome.

Plasma concentrations of soluble vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-selectin) and intercellular adhesion molecule-1 (sICAM-1) were measured by enzyme-linked immunosorbent assay in four groups of children. Group 1 consisted of 20 patients with acute diarrhoea-associated haemolytic uraemic syndrome (D+HUS), the aetiology of HUS being verocytotoxin-producing Escherichia coli infection in each case. Controls consisted of 11 patients who had previously had D+HUS (group 2), 12 with chronic renal failure (group 3) and 8 healthy controls (group 4). When compared with healthy controls, the acute D+HUS group had higher sVCAM-1 (median 1,875 ng/ml, range 1,200-6,450 ng/ml vs. 1,200 ng/ml, range 975-2,125 ng/ml), von Willebrand factor antigen, (1.9 U/ml, range 0.85-5.1 U/ml vs. 0.55 U/ml, range 0.3-1.57 U/ml), white cell count (WBC, 14.5 x 10(9)/l, range 7.8-43.1 10(9)/l vs. 8.9 10(9)/l, range 5.7-10.8 10(9)/l) and neutrophil count (PMN, 10.1 x 10(9)/l, range 4.3-26.5 10(9)/l vs. 4.3 10(9)/l, range 3.7-6.6 10(9)/l), all P < 0.005, and sICAM-1 was reduced (230 ng/ml, range 130-340 ng/ml vs. 400 ng/ml, range 260-690 ng/ml), P < 0.05. Within the acute D+HUS group there was a significant correlation between sICAM-1 and PMN (r = 0.56, P < 0.01). There was no correlation between any adhesion molecule and plasma creatinine or von Willebrand factor. Comparing the acute HUS group with children with chronic renal failure, WBC (P < 0.001), PMN (P < 0.01) and sVCAM-1 (P < 0.01) were significantly elevated, but there was no difference between the von Willebrand factor (P = 0.08) or the sICAM-1 (P > 0.1). sVCAM-1 is elevated and sICAM-1 decreased in acute D+HUS. This pattern of altered adhesion molecule concentration is unlike that in adults with vasculitis and suggests that different endothelial regulatory factors are at play.

Acute Disease↗
PubMed1995

Characteristic phenotype in congenital nephrotic syndrome.

We present three children with congenital nephrotic syndrome and previously undescribed facial features. These include: (1) small mouth (intercommissural distance < 3rd percentile); (2) tented upper lip; (3) small nose (interalar distance -2 SD below mean); (4) fullness of cheeks giving a 'jowly' appearance; (5) overhanging outer thirds of upper eyelids. These features may reflect prolonged tissue oedema and protein malnutrition in utero and early life. CONCLUSION Characteristic facial features in congenital nephrotic syndrome may reflect intra-uterine malnutrition.

Facial Expression↗
PubMed1995

Boundaries.

Explore the source record for details and available documents.

Ethics, Nursing↗
PubMed1995

Linkage of posterior polymorphous corneal dystrophy to 20q11.

Posterior polymorphous dystrophy (PPMD) is an autosomal dominant disorder of the cornea that is clinically recognized by the presence of vesicles on the endothelial surface of the cornea. The corneal endothelium is normally a single layer of cells that lose their mitotic potential after development is complete. In PPMD, the endothelium is often multi-layered and has several other characteristics of an epithelium including the presence of desmosomes, tonofilaments, and microvilli. These abnormal cells retain their ability to divide and extend onto the trabecular meshwork to cause glaucoma in up to 40% of cases. A large family with 21 members affected with PPMD was genotyped with short tandem repeat polymorphisms distributed across the autosomal genome. Linkage was established with markers on the long arm of chromosome 20. The highest observed LOD score was 5.54 (theta = 0) with marker D20S45. Analysis of recombination events in four affected individuals revealed that the disease gene lies within a 30cM interval between markers D20S98 and D20S108.

Chromosome Mapping↗
PubMed1995

Linkage of autosomal dominant iris hypoplasia to the region of the Rieger syndrome locus (4q25).

Iris hypoplasia is an autosomal dominant disorder which is frequently associated with glaucoma. This glaucoma is usually resistant to medical therapy and can lead to blindness. A large family of Scandinavian descent with a five generation history of iris hypoplasia was studied. Fifteen individuals were found to have iris hypoplasia, nine of whom had associated glaucoma. In an attempt to identify the chromosomal location of the disease-causing gene, this family was genotyped with short tandem repeat polymorphisms (STRPs) known to map to loci previously associated with glaucoma. The juvenile glaucoma locus at 1q25 and a congenital glaucoma locus on 6p were both statistically excluded. However, significant linkage was demonstrated at the Rieger syndrome locus at 4q25. The highest observed LOD score was 3.70 (theta = 0) and was obtained with marker D4S1616. Three recombination events were observed in affected individuals that together demonstrate that the disease-causing gene lies between markers ACT3E03 and D4S1611, an interval of approximately 7 cM. These results suggest that autosomal dominant iris hypoplasia and Rieger syndrome are allelic.

Chromosomes, Human, Pair 4↗
PubMed1994

Peptide synthesis catalyzed by an antibody containing a binding site for variable amino acids.

Monoclonal antibodies, induced with a phosphonate diester hapten, catalyzed the coupling of p-nitrophenyl esters of N-acetyl valine, leucine, and phenylalanine with tryptophan amide to form the corresponding dipeptides. All possible stereoisomeric combinations of the ester and amide substrates were coupled at comparable rates. The antibodies did not catalyze the hydrolysis of the dipeptide product nor hydrolysis or racemization of the activated esters. The yields of the dipeptides ranged from 44 to 94 percent. The antibodies were capable of multiple turnovers at rates that exceeded the rate of spontaneous ester hydrolysis. This achievement suggests routes toward creating a small number of antibody catalysts for polypeptide syntheses.

Antibodies, Catalytic↗
PubMed1994

Assessment of retinol-binding protein excretion in normal children.

Retinol-binding protein (RBP) is a low molecular weight protein freely filtered at the glomerulus. The fractional tubular reabsorption of RBP is 99.97% and increased excretion is therefore a sensitive marker of tubular dysfunction. We obtained early-morning urine specimens from 151 well children, from newborn to 16 years of age. RBP was measured using an enzyme-linked immunosorbent assay, albumin by a radioimmunoassay and creatinine by a modified Jaffé reaction. Protein excretion was assessed by calculating the protein:creatinine ratio for early-morning urine samples. We found a fall in both RBP and albumin excretion with increasing age, particularly in the 1st year of life, with a much wider variation in values from the infants studied. The mean excretion of RBP for children aged 0-6 months [51.4 (0.6-4,719) micrograms/mmol] was significantly higher (P < 0.001) than the mean for children aged 6 months to 16-years [15.0 (3.8-60) micrograms/mmol]. It has been shown that measurement of tubular proteinuria using the RBP: creatinine ratio is useful in the assessment of children with renal disease and we propose a value two standard deviations above the geometric mean for the age of the patient as an upper limit of normal.

Adolescent↗
PubMed1994

Dental needs of pre-retirement and retired people in an inner-city area.

Perceived and normative dental needs were assessed for people of pre-retirement (55-64 years) and retirement age (65-74 years) in Camberwell, London, using a postal questionnaire and dental examination. Of the pre-retirement group, 77% were dentate compared with 65% in the older cohort. The younger age-group were more likely to believe teeth were more important and to perceive a need for dental care. People who attended for the examination were more likely to perceive a need for (64% and 15% respectively) and want treatment (39% and 17%) than non-examinees. Also, they were more likely to be unhappy with their appearance (43% and 20%) and to be in pain (42% and 21%). Treatment need was similar for both groups with regard to restorative and extraction needs. However, the retirement group were more likely to have deep periodontal pockets (33% and 8%) and a greater normative need for denture care.

Aged↗
PubMed1994

Three autosomal dominant corneal dystrophies map to chromosome 5q.

The two most common autosomal dominant dystrophies of the corneal stroma are lattice corneal dystrophy type I and granular dystrophy. A third autosomal dominant stromal dystrophy (Avellino) has also been recognized. Chromosome linkage analysis of four families with Avellino dystrophy mapped the disease-causing gene to chromosome 5q. Subsequent linkage analysis of two families with typical lattice dystrophy and two with typical granular dystrophy also revealed significant linkage with the same markers. Thus, each of three clinically and histopathologically distinct phenotypes is independently linked to 5q. The maximum combined lod score using all 114 affected patients was 28.6 with marker D5S393. None of the 14 known human amyloid-associated genes map to chromosome 5.

Alleles↗
PubMed1994

Children exposed to disaster: I. Epidemiology of post-traumatic symptoms and symptom profiles.

OBJECTIVE: To determine the range and severity of post-traumatic stress disorder (PTSD) symptoms exhibited by children after exposure to a natural disaster. METHOD: Three months after Hurricane Hugo struck Berkeley County, South Carolina, 5,687 school-aged children were surveyed about their experiences and reactions related to the storm. Self-reports of PTSD symptoms were obtained by use of a PTSD Reaction Index. RESULTS: Significant variation in the prevalence of PTSD symptoms was found across race, gender, and age groups. Self-reported symptoms were used to derive a post-traumatic stress syndrome classification according to DSM-III-R guidelines for the diagnosis of PTSD. More than 5% of the sample reported sufficient symptoms to be classified as exhibiting this post-traumatic stress syndrome. Females and younger children were more likely to receive this classification. At the symptom level, females reported more symptoms associated with emotional processing and emotional reaction to the trauma. Males were more likely to report symptoms related to cognitive and behavioral factors. Younger children were more likely to report symptoms overall. CONCLUSIONS: Children exposed to a high magnitude natural disaster report sufficient symptoms to establish a DSM-III-R derived classification of a PTSD syndrome. Differences between gender, age, and race groups appear to be related to differential risk of exposure, reporting biases, as well as a differential risk for developing post-traumatic symptoms.

Adolescent↗
PubMed1994

Children exposed to disaster: II. Risk factors for the development of post-traumatic symptomatology.

OBJECTIVE: To examine the influence of subject and exposure variables on the development of post-traumatic stress disorder (PTSD) symptoms and syndrome in children exposed to disaster. METHOD: Three months after Hurricane Hugo, 5,687 school-aged children were surveyed about their experiences and reactions to the hurricane. Self-reports of PTSD symptoms were obtained by use of a PTSD Reaction Index. RESULTS: The presence of PTSD symptoms was strongly related to children's reported severity of the hurricane, degree of home damage sustained, and continued displacement; however, children's level of trait anxiety and their reported emotional reactivity during the hurricane were more strongly related to the presence of PTSD symptoms than were the exposure factors. Different sets of risk factors appeared to differentially influence the development of the three DSM-III-R PTSD symptom clusters. Little evidence for a differential effect of the risk factors between females and males and younger and older children was found. CONCLUSIONS: Level of trait anxiety appears to be the single strongest risk for the development of severe post-traumatic reactions. The higher rate of post-traumatic symptoms in females and younger children in combination with the absence of differential reaction to the risk factors suggests that females and younger children are more likely to develop posttraumatic reactions following a disaster.

Adaptation, Psychological↗
PubMed1994

Anti-idiotypic activity against anti-myeloperoxidase antibodies in pooled human immunoglobulin.

We investigated the ability of six different pooled human immunoglobulin (PHIG) preparations to inhibit the binding of anti-myeloperoxidase (MPO) antibodies to MPO. All six PHIG preparations inhibited the binding of anti-MPO antibodies from six sera to MPO in a concentration-dependent manner in the concentration range 0.016-10 mg/ml. There was considerable variation in the ability of each PHIG preparation to inhibit the binding of anti-MPO antibody in a given serum. Further differences were seen in the ability of a given PHIG to inhibit anti-MPO binding in different sera. F(ab')2 fragments from two PHIG preparations also inhibited in a concentration-dependent manner anti-MPO binding to MPO in all six sera in the concentration range 0.002-2.65 mg/ml, with a maximum inhibition of 42%. Little inhibition was seen with F(ab')2 of normal human IgG from individual donors (1.8-12.2% at the maximum concentration of 2 mg/ml). F(ab')2 fragments from three anti-MPO containing sera and two affinity-purified anti-MPO antibodies were eluted by affinity chromatography from Sepharose-bound PHIG F(ab')2 and showed anti-MPO antibody activity. We have shown that PHIG and F(ab')2 fragments of PHIG inhibit anti-MPO binding to MPO, and further that F(ab')2 fragments of PHIG bind to F(ab')2 fragments of anti-MPO antibodies. These observations indicate binding between the variable regions of PHIG and the antigen binding site of anti-MPO antibodies, and are consistent with an anti-idiotypic reaction. The variability seen in the inhibitory effect of the different PHIG preparations in anti-MPO-positive sera implies differences in their anti-idiotype content, while the variability of the inhibitory effect of a particular PHIG preparation between different sera suggests heterogeneity in the idiotypic repertoire of anti-MPO antibodies. Such variations in the inhibitory effect of different PHIG preparations on antibody binding may be an important determinant of their therapeutic effect.

Animals↗
PubMed1994

Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression and function on cultured human glomerular epithelial cells.

Glomerular epithelial cells are involved in extracapillary inflammation (crescents) but the mechanisms of this extracapillary accumulation of macrophages, epithelial cells and occasional lymphocytes are unknown. Human glomerular parietal epithelial cells express ICAM-1 and VCAM-1 on immunohistological stains of renal biopsies. We studied the expression of these cell adhesion molecules on cultured human glomerular epithelial cells (HGEC), their regulation by pro-inflammatory cytokines, and their role in mediating the adhesion of concanavalin A (Con A)-activated peripheral blood mononuclear cells. Human glomerular epithelial cells in culture constitutively express ICAM-1 and VCAM-1. The expression of ICAM-1 was not significantly altered by tumour necrosis factor-alpha (TNF-alpha) (P = 0.32), IL-1 beta (P = 0.24), interferon-gamma (IFN-gamma) (P = 0.66) or IL-4 (P = 0.85). VCAM-1 expression was increased by all four cytokines, but only significantly so by IL-4 (P = 0.0001). Con A-stimulated, monocyte-depleted peripheral blood lymphocytes bound to human glomerular epithelial cells, median 28.9% (range 14.5-37.9%). This adherence was significantly inhibited by anti-ICAM-1 (P = 0.03) and anti-LFA-1 (P = 0.02), but not by anti-VCAM-1 (P = 0.13) or by antibody to von Willebrand factor (P = NS). The interaction between ICAM-1 on HGEC and LFA-1 on mononuclear cells may be important in the pathogenesis of extracapillary inflammation in glomerulonephritis.

Cell Adhesion↗