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Biomedical subjects

C A Morris

Publications and source records attributed to C A Morris.

At least 19 recordsLinked to original sources
PubMed1995

Genetic factors affecting antibody responses to four species of nematode parasite in Romney ewe lambs.

Serum levels of antibodies (Ab) and immunoglobulin G1 (IgG1) to the larval (L3) stage of the internal parasites Cooperia curticei and Trichostrongylus colubriformis and levels of Ab to the L3 stages of Haemonchus contortus and Ostertagia circumcincta were determined in 1432 Romney ewe lambs which were born on one farm in 1990 and 1991 and were the progeny of 63 rams. The objectives were to estimate heritabilities of, and genetic correlations among, the serum concentrations in newly weaned lambs under commercial conditions and to estimate genetic correlations of Ab and IgG1 with production traits. Lambs were exposed to a natural parasite challenge on pasture, following an anthelmintic drench at weaning. Blood and faecal samples from 4- to 6-month-old lambs were then taken when the mean faecal nematode egg count of a monitor group reached 800-1500 eggs g-1. Heritabilities for the serum levels of the four Abs ranged from 0.25 +/- 0.05 to 0.37 +/- 0.06. Heritabilities for the level of IgG1 developed against C. curticei was 0.19 +/- 0.04 and against T. colubriformis, 0.18 +/- 0.05. Genetic correlations between Abs for the 4 species were high, averaging 0.84, and between the two IgG1s it was 0.82. The genetic correlations between Ab or IgG1 levels and weight or gain traits were negative (for the 6 significant values out of 18), with yearling fleece weight positive (for the 2 significant values out of 6), whilst those with loge faecal egg count were all negative (average -0.15).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Complement inhibition by human vitronectin involves non-heparin binding domains.

Vitronectin (complement S-protein), a multifunctional glycoprotein, inhibits complement-mediated cytolysis at two identified stages of terminal complement complex (TCC) formation: blocking of C5b-7 membrane binding, and prevention of C9 polymerization. However, the functional domain(s) of vitronectin involved in these reactions remains incompletely defined. In order to identify the complement inhibition site, a 12-kD heparin binding fragment and two other internal fragments (53 kD and 43 kD) of vitronectin were isolated after cyanogen bromide (CNBr) treatment of the native molecule. Potent inhibition of guinea pig erythrocyte (GPE) reactive lysis was demonstrated with native vitronectin, total CNBr digest and the 53-kD and 43-kD fragments, but only very poorly by the heparin binding 12-kD peptide. Similarly, the 43-kD fragment blocked the binding of C5b-7 to immobilized vitronectin, whereas the 12-kD fragment had no effect. These data localize the C5b-7 binding site to a 43-kD internal region. Further characterization of the fragments was carried out in an assay which detected C9 polymerization in the presence of C5b-8. Polymerized material was separated by PAGE, detected by autoradiography and quantified after excision from the gels. Results showed that polymerization did not occur in the presence of the 53-kD and 43-kD fragments. However, the 12-kD heparin binding fragment had no effect. It is proposed that prevention of C5b-8-induced C9 polymerization resides at a site in an internal region of the vitronectin molecule.

Amino Acid Sequence↗
PubMed1995

Ostrich slaughter and fabrication: 1. Slaughter yields of carcasses and effects of electrical stimulation on post-mortem pH.

A commercial ostrich slaughter protocol was developed. Ostriches (n = 7 males and n = 7 females) averaged 95.54 kg live weight and yielded 55.91-kg carcasses. By-product yields were measured. The most significant by-products by weight were full viscera (8.29 kg), hide (6.71 kg), full gizzard and crop (5.80 kg), and abdominal fat (4.11 kg). Sex had no effect on slaughter yields. Post-mortem temperature declines were measured on five separate muscles and showed that chilling for 24 h was sufficient to adequately chill the deep muscle temperature to under 4 C. The effect of electrical stimulation on post-mortem pH decline also was investigated and had no effect.

Animals↗
PubMed1995

Strong correlation of elastin deletions, detected by FISH, with Williams syndrome: evaluation of 235 patients.

Williams syndrome (WS) is generally characterized by mental deficiency, gregarious personality, dysmorphic facies, supravalvular aortic stenosis, and idiopathic infantile hypercalcemia. Patients with WS show allelic loss of elastin (ELN), exhibiting a submicroscopic deletion, at 7q11.23, detectable by FISH. Hemizygosity is likely the cause of vascular abnormalities in WS patients. A series of 235 patients was studied, and molecular cytogenetic deletions were seen in 96% of patients with classic WS. Patients included 195 solicited through the Williams Syndrome Association (WSA), plus 40 clinical cytogenetics cases referred by primary-care physicians. Photographs and medical records of most WSA subjects were reviewed, and patients were identified as "classic" (n = 114) or "uncertain" (n = 39). An additional 42 WSA patients were evaluated without clinical information. FISH was performed with biotinylated ELN cosmids on metaphase cells from immortalized lymphoblastoid lines from WSA patients and after high-resolution banding analysis on clinical referral patients. An alpha-satellite probe for chromosome 7 was included in hybridizations, as an internal control. Ninety-six percent of the patients with classic WS showed a deletion in one ELN allele; four of these did not show a deletion. Of the uncertain WS patients, only 3 of 39 showed a deletion. Of the 42 who were not classified phenotypically, because of lack of clinical information, 25 patients (60%) showed a deletion. Thirty-eight percent (15/40) of clinical cytogenetics cases showed an ELN deletion and no cytogenetic deletion by banded analysis. These results support the usefulness of FISH for the detection of elastin deletions as an initial diagnostic assay for WS.

Abnormalities, Multiple↗
PubMed1994

Relative topography of biologically active domains of human vitronectin. Evidence from monoclonal antibody epitope and denaturation studies.

A panel of monoclonal antibodies to human vitronectin was used to define some epitopes for the multifunctions of this protein. Separate antibodies were identified which strongly inhibited cell spreading activity and which prevented binding to collagen. A third group interfered with the ability of vitronectin to inhibit complement-mediated guinea pig erythrocyte reactive lysis. None of the antibodies from these three groups prevented heparin binding, providing evidence that this reaction occurs at a fourth location; a different monoclonal antibody partially inhibited the binding of heparin. The relative accessibility of each biologically active epitope was assessed by the differential binding of the monoclonals to native and denatured vitronectin. Reactivity of the antibody which inhibited heparin binding greatly increased upon denaturation of vitronectin, implying that this region is normally inaccessible in the native form of the molecule. By contrast, epitopes for cell spreading, collagen binding, and inhibition of terminal complement complex lysis were destroyed by denaturation. On the basis of denaturation data and epitope mapping by competitive exclusion of monoclonal antibodies, a Venn diagram was constructed to represent overlap of monoclonal antibody epitopes in the tertiary structure. Linear epitopes for the antibodies were identified using cyanogen bromide and plasmin-derived peptides from vitronectin. The antibody which strongly inhibited cell binding reacted with a region containing the RGD site, whereas linear epitopes for collagen binding and complement inhibition appeared to reside in a 43-kDa peptide representing the internal region of the amino acid sequence, excluding the heparin-binding site. The latter two epitopes were differentiated from each other by reactivity of the antibody which inhibited collagen binding toward a smaller 20-kDa plasmin-derived peptide.

Animals↗
PubMed1994

Inadequate response to intradermal hepatitis A vaccine.

To assess the efficacy of the intradermal route of administration of hepatitis A vaccine we conducted a study in hospital laboratory workers. Forty-three volunteers were given three different combinations of intradermal and intramuscular hepatitis A vaccine and compared with 18 controls given intramuscular vaccine only. The geometric mean titres (GMT) after one, two and three intradermal doses of 0.1 ml each were 4.5, 28 and 143 IU l-1 respectively. The GMT after one intramuscular dose in the controls was 163 IU l-1. The results indicate that the response to intradermal hepatitis A vaccine is poor and its use cannot be recommended.

Administration, Cutaneous↗
PubMed1994

A gene for Crouzon craniofacial dysostosis maps to the long arm of chromosome 10.

Crouzon craniofacial dysostosis (CFD) is an autosomal dominant craniofacial disorder characterized by premature craniosynostosis, shallow orbits and hypoplastic maxilla. To map the gene responsible, we have used a mapping strategy of testing for linkage to known developmental genes. Analysis of a large kindred established linkage between CFD and three loci (D10S190, D10S209 and D10S216) that span a 13 cM region on chromosome 10q. A maximum pairwise lod score of 4.42 (theta = 0) at D10S190 was obtained and the addition of a second kindred produced a combined pairwise lod score of 5.32 (theta = 0) at the same locus. The developmental gene, PAX2, located within this region, is an attractive candidate gene.

Chromosome Mapping↗
PubMed1994

Supravalvular aortic stenosis associated with a deletion disrupting the elastin gene.

Supravalvular aortic stenosis (SVAS) is an inherited vascular disease that can cause heart failure and death. SVAS can be inherited as an autosomal dominant trait or as part of a developmental disorder, Williams syndrome (WS). In recent studies we presented evidence suggesting that a translocation disrupting the elastin gene caused SVAS in one family while deletions involving the entire elastin locus caused WS. In this study, pulsed-field, PCR, and Southern analyses showed that a 100-kb deletion of the 3' end of the elastin gene cosegregated with the disease in another SVAS family. DNA sequence analysis localized the breakpoint between elastin exons 27 and 28, the same region disrupted by the SVAS-associated translocation. These data indicate that mutations in the elastin gene cause SVAS and suggest that elastin exons 28-36 may encode critical domains for vascular development.

Aortic Stenosis, Subvalvular↗
PubMed1994

Crossbreeding of Ayrshire, brown Swiss, and Sahiwal cattle for annual and lifetime milk yield in the lowland tropics of Kenya.

Records from 1577 cows born from 1973 to 1983 on a ranch in lowland Kenya were analyzed for age at first calving, lactation length, lactational milk yield, calving interval, annual milk yield, and, for cows born from 1973 to 1979, number of calvings, productive lifetime in the herd, and lifetime milk yield. Partial lifetime yield (< or = 4 lactations) was studied for all cows. Rotational crosses of Ayrshire and Sahiwal, the crosses between them (interbreds), and the crosses sired by Brown Swiss from the rotational crosses were compared. The Ayrshire-sired rotational crosses yielded 4.8% more milk during a 19-d longer lactation and with a calving interval that was 14 d longer than those sired by Sahiwal. Milk yield for completed lactations of interbred cows was 4.5% less, and milk yield of Brown Swiss crosses was 9.5% more, than the average of the rotational crosses. Lifetime milk yields were 48% greater for the rotational crosses sired by Ayrshire than for those sired by Sahiwal. Interbreds yielded 34% less than the average of the rotational crosses. Over partial lifetimes, the rotational crosses sired by Ayrshire yielded 45% more milk than those sired by Sahiwal; the interbreds and the crosses sired by Brown Swiss yielded 34% less and 62% more milk, respectively, than the mean of the rotational crosses.

Animals↗
PubMed1993

Williams syndrome: autosomal dominant inheritance.

Williams syndrome (WS) usually occurs sporadically. Few familial cases of Williams syndrome have been described, and those reports have often lacked photographic documentation. We describe 3 families, including a 3-year-old boy and his 34-year-old father, a 2-year-old girl and her 30-year-old mother, and a 3-year-old girl and her 31-year-old mother. None of these patients has supravalvular aortic stenosis or chromosome abnormalities. In all 3 families, the parent with Williams syndrome was diagnosed after the identification of the syndrome in the affected child.

Abnormalities, Multiple↗
PubMed1993

Supravalvular aortic stenosis cosegregates with a familial 6; 7 translocation which disrupts the elastin gene.

Supravalvular aortic stenosis (SVAS) is an autosomal dominant disorder characterized by abnormalities of development of the great vessels. SVAS is also commonly part of Williams syndrome. Linkage to the elastin gene on chromosome 7q11 has recently been reported in two kindreds with SVAS. Previous reports of patients with 7q11 deletions have noted great vessel abnormalities in some. We report on a family in which SVAS is cosegregating with a balanced reciprocal translocation, t(6:7) (p21.1;q11.23), providing further evidence that SVAS is the result of a mutation of elastin at 7q11.23 region. The propositus of the translocation family has some minor anomalies which occur in Williams syndrome, suggesting that elastin abnormalities may cause some of the abnormalities found in Williams syndrome.

Adult↗
PubMed1993

A human vascular disorder, supravalvular aortic stenosis, maps to chromosome 7.

The pathogenesis of vascular disease is unclear, but genetic factors play an important role. In this study we performed linkage analyses in two families with supravalvular aortic stenosis, an inherited vascular disorder that causes narrowing of major arteries and may lead to cardiac overload and failure. DNA markers on the long arm of chromosome 7 (D7S371, D7S395, D7S448, and ELN) were linked to supravalvular aortic stenosis in both families with a combined logarithm of likelihood for linkage (lod score) of 5.9 at the ELN locus. These findings indicate that a gene for supravalvular aortic stenosis is located in the same chromosomal subunit as elastin, which becomes a candidate for the disease gene.

Aortic Valve Stenosis↗
PubMed1993

The elastin gene is disrupted by a translocation associated with supravalvular aortic stenosis.

To identify genes involved in vascular disease, we investigated patients with supravalvular aortic stenosis (SVAS), an inherited vascular disorder that causes hemodynamically significant narrowing of large elastic arteries. Pulsed-field gel and Southern analyses showed that a translocation near the elastin gene cosegregated with SVAS in one family. DNA sequence analyses demonstrated that the translocation disrupted the elastin gene and localized the breakpoint to exon 28. Taken together with our previous study linking SVAS to the elastin gene in two additional families and existing knowledge of vascular biology, these data suggest that mutations in the elastin gene can cause SVAS.

Amino Acid Sequence↗
PubMed1993

Hemizygosity at the elastin locus in a developmental disorder, Williams syndrome.

Williams syndrome (WS) is a developmental disorder affecting connective tissue and the central nervous system. A common feature of WS, supravalvular aortic stenosis, is also a distinct autosomal dominant disorder caused by mutations in the elastin gene. In this study, we identified hemizygosity at the elastin locus using genetic analyses in four familial and five sporadic cases of WS. Fluorescent in situ hybridization and quantitative Southern analyses confirmed these findings, demonstrating inherited and de novo deletions of the elastin gene. These data indicate that deletions involving one elastin allele cause WS and implicate elastin hemizygosity in the pathogenesis of the disease.

Adult↗
PubMed1993

Assessment of DNA fingerprinting for determining genetic diversity in sheep populations.

Genomic DNA, prepared from 12 animals from four sheep flocks, was digested with either HaeIII or HinfI and probed with three DNA fingerprinting probes. Mean DNA fingerprint band sharing and band frequency calculated for each flock were used to estimate genetic diversity. Each of the DNA fingerprinting systems showed the same trend in diversity within the sampled flocks, and greater diversity between the flocks than within the flocks. DNA fingerprinting therefore provides a useful measure of genetic diversity in sheep.

Analysis of Variance↗
PubMed1993

Vitronectin-mediated inhibition of complement: evidence for different binding sites for C5b-7 and C9.

In the activated complement system, vitronectin (complement S-protein) occupies the metastable membrane binding site of the nascent precursor complex C5b-7, so that the newly formed SC5b-7 is unable to insert into cell membranes. Some evidence also indicates that vitronectin limits on-going membrane-associated pore formation by inhibiting C9 polymerization. It has been assumed that these two stages of terminal complement complex (TCC) inhibition take place through charge interactions between the heparin-binding region of vitronectin and homologous cysteine-rich sequences of the late complement proteins C6, C7, C8 and C9. We examined SC5b-7 formation and inhibition of C9 binding in the TCC using separate haemolytic assays. The mode of action of vitronectin in these assays was compared with two 15mer peptides which span residues 348-379 of the heparin-binding region, and a heparin-affinity polypeptide, protamine sulphate. The results showed that vitronectin acts predominantly through SC5b-7 production with a lesser effect on the inhibition of C9 lytic pore formation. In contrast, protamine sulphate did not prevent C5b-7 membrane attachment, but was a potent inhibitor of C9-mediated lysis. The peptides did not inhibit C5b-7 membrane insertion and only one affected C9 binding. These data suggest that the two stages of TCC inhibition involve separate binding sites on the vitronectin molecule. The site for association with nascent C5b-7 is unknown, whereas inhibition of C9 binding and pore formation takes place through the heparin-binding region.

Amino Acid Sequence↗