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Biomedical subjects

A E Davis

Publications and source records attributed to A E Davis.

At least 91 records · Page 5Linked to original sources
PubMed1988

Angioedema induced by a peptide derived from complement component C2.

Synthetic peptides that correspond to the COOH-terminal portion of C2b enhance vascular permeability in human and guinea pig skin. In human studies, 1 nmol of the most active peptide of 25-amino acid residues produced substantial local edema. A pentapeptide and a heptapeptide corresponding to the COOH-terminal sequence of C2b each induced contraction of estrous rat uterus in the micromole range; a peptide of 25 amino acids from this region induced a like contraction of rat uterus at a concentration 20-fold lower than the smaller peptides. The vascular permeability of guinea pig skin was enhanced by doses of these synthetic peptides in a similar fashion as that observed for the concentration of rat uterus. The induction of localized edema by intradermal injection in both the guinea pig and the human proceeds in the presence of antihistaminic drugs, suggesting that there is a histamine-independent component to the observed increase in vascular permeability. Cleavage of C2 with the enzymic subcomponent of C1, C1s, yields only C2a and C2b, and no small peptides, whereas cleavage of C2 with C1s and plasmin yields a set of small peptides. These plasmin-cleaved peptides are derived from the COOH terminus of C2b, and they induce the contraction of estrous rat uterus.

Amino Acid Sequence↗
PubMed1988

Homograft materials in otolaryngology: the risk of transmitting human immunodeficiency virus.

Homograft materials are extensively used in various surgical procedures in otolaryngology, but with the increasing prevalence of human immunodeficiency virus (HIV) in the population this practice must be reviewed. Careful donor selection and antibody testing reduce but do not fully eliminate the risk of an HIV positive donor, and current preservation techniques may not inactivate all viruses. The use of homograft tissues should therefore be reconsidered as autograft or prosthetic material provides a satisfactory alternative in many cases.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Herpes simplex and duodenal ulcer pathology.

An association between Herpes simplex Virus 1 (HSV-1) and duodenal ulcer disease has been suggested. Duodenal ulcers, like HSV-1 lesions, exhibit periodicity in recurrence. Several of the presently available anti-ulcer agents may have an antiviral action. Antibody titres in some studies have shown selective increases to HSV-1 in duodenal ulcer patients. The aim of this study was to determine whether a real association exists between HSV-1 and endoscopically proven duodenal ulcer or duodenal erosive disease. In a prospective study, 27 patients with either duodenal ulcer (16) or duodenal erosions (11) were studied in order to attempt isolation of HSV-1. Acute and convalescent sera were also taken and examined by an enzyme linked-immunoabsorbent assay system for antibody titres to HSV-1. Duodenal biopsies from a further 26 patients with duodenal ulcer or erosive disease were also examined retrospectively for HSV-1 by the immunoperoxidase technique. In no case of either duodenal ulcer or duodenal erosive disease was HSV-1 isolated by any of the above methods, nor was a relationship demonstrated by acute or convalescent HSV-1 antibody titres. Hence, this study does not support an association between HSV-1 and duodenal ulcer or erosive disease.

Duodenal Diseases↗
PubMed1988

Structure of C3f, a small peptide specifically released during inactivation of the third component of complement.

C3f, a peptide presumed to be generated by the combined actions of factors I and H on fluid-phase C3b, has been isolated and sequenced. The peptide is 17 residues long and has a molecular weight of 1,847 daltons. The amino-terminal sequence is, with the exception of a single residue, identical to that deduced for the 46-kilodalton polypeptide seen transiently in the generation of iC3b from C3b, and is in full agreement with the sequence deduced from cDNA analysis. In addition, high-pressure liquid chromatography of the digestion of C3b by factor I has shown that C3f is the sole peptide released during iC3b generation.

Amino Acid Sequence↗
PubMed1988

An ultrastructural study of the mucosal surface of the human inferior concha. I. Normal appearances.

A study is presented of normal human nasal mucosa. Tissue was taken from a defined site on the inferior concha to minimise individual variation and was studied using scanning and transmission electron microscopy. Three cell types were found at the epithelial surface; ciliated and non-ciliated columnar cells and goblet cells. The distribution of cell types varied greatly between specimens, perhaps owing to environmental factors. All cells bore microvilli which showed minor structural differences between the cell types. Two important features were common to all microvilli. Cytoplasmic filaments were seen running parallel to the long axis of the structure; these may be involved in microvillar motility. Also found was a prominent surface glycocalyx. This may help maintain the volume and viscosity of periciliary fluid; it may also prevent adhesion and tangling of microvilli and cilia. A notable feature of the cilia seen on transmission electron microscopy was the presence of occasional ciliary crowns; these claw-like projections from the cilial tips may be involved in the propulsion of mucus. The goblet cells showed apocrine secretory droplets which were extruded intact into the nasal lumen. This may help to preserve the integrity of the mucous and periciliary fluid layers. We conclude that the mechanism of mucus secretion and transport in the nose may involve several surface structures including ciliary crowns and microvilli. Their function is not yet clear and further study is indicated.

Adult↗
PubMed1987

Role of maintenance sucralfate in prevention of duodenal ulcer recurrence.

Fifty-nine patients who had duodenal ulcers that were healed following sucralfate administration in a dose of 1 g four times a day were randomly entered into a double-blind, placebo-controlled, 12-month maintenance study to determine whether sucralfate 1 g twice daily prevents recurrence of duodenal ulceration. Patients were assessed endoscopically at four, eight, and 12 months after healing or earlier if clinical relapse occurred. Of the original 59 patients, 53 showed healing with six weeks of therapy, and the remaining six patients required 10 weeks of treatment. Nine patients were subsequently lost to follow-up because of non-compliance, leaving 50 patients for the analysis, 24 who received sucralfate and 26 who received placebo. There were 10 ulcer recurrences in the sucralfate group and the ulcers in 14 (58 percent) patients remaining healed at the end of 12 months. In contrast, there were 21 recurrences in the placebo group with the ulcers in five patients (19 percent) remaining healed at 12 months. Patients who received placebo experienced recurrence more quickly than those who received sucralfate and there was no difference between the two groups in terms of symptomatic and asymptomatic recurrence. There was no alteration in serum aluminium and phosphate levels throughout the study. Smoking seemed to have no adverse effect on recurrence once initial healing had been achieved. Sucralfate is, therefore, an effective and safe maintenance treatment for duodenal ulcer disease.

Aluminum↗
PubMed1987

Metabolism of C4 and linkage analysis in a kindred with hereditary incomplete C4 deficiency.

We studied a kindred in which C4 deficiency had been discovered. Unlike families with total absence of C4, in this kindred C4 deficiency was found to be incomplete, autosomal dominant, not caused by null alleles, and not associated with a high incidence of systemic lupus erythematosus. The deficient state was caused by hyposynthesis of C4, not by hypercatabolism. The locus for incomplete C4 deficiency was not closely linked to the major histocompatibility complex. The abnormal autosomal dominant allele is, apparently, rare, and how it causes decreased synthesis of C4 is unknown.

Adult↗
PubMed1987

The effect of protein deficiency on systemic release of rat mucosal mast cell protease II during Nippostrongylus brasiliensis infection and following systemic anaphylaxis.

Serum rat mucosal mast cell protease II (RMCPII) was measured in protein-deficient rats to assess mucosal mast cell (MMC) activation during primary infection with the nematode, Nippostrongylus brasiliensis, and during systemic anaphylaxis produced by Nippostrongylus antigen in immune animals. In the first study, serum RMCPII increased 4-fold by day 15 after infection. By day 20, serum RMCPII continued to rise in protein-deficient animals, but decreased in nutritionally normal animals. This was associated with impaired worm rejection in protein-deficient rats. During systemic anaphylaxis, serum RMCPII was elevated in three groups of protein-deficient rats on 6%, 8% and 10% low protein diets and in nutritionally normal rats. All protein-deficient rats exhibited 3 to 7-fold less mucosal permeability of the small intestine to Evan's blue dye injected intravenously compared to nutritionally normal animals following anaphylactic stimulation. These results demonstrated that MMC are activated during infection in protein deficiency, and suggest that reduced MMC function does not explain delay in worm expulsion. Impaired mucosal anaphylaxis in protein deficiency could not be attributed to a failure of MMC response.

Anaphylaxis↗
PubMed1987

Prevention of duodenal ulcer occurrence. Double-blind comparison of ranitidine and cimetidine.

We compared ranitidine and cimetidine in maintenance therapy to prevent duodenal ulcer recurrence over a period of 24 months. Endoscopic examination at the end of 12 months showed that the ulcers of 26 of 31 patients (84%) on ranitidine in a dose of 150 mg remained healed and of 10 of 13 (77%) patients on cimetidine in a dose of 400 mg at night remained healed. Thirty-four patients continued in an open evaluation of ranitidine in a dose of 150 mg at night for a further 12-month period, and during this time there were four further recurrences. Life table estimates of duodenal ulcer recurrence during the 2-year period showed no significant difference between the two forms of treatment.

Adult↗
PubMed1987

Molecular basis for the deficiency of complement 1 inhibitor in type I hereditary angioneurotic edema.

Hereditary angioneurotic edema (HANE) results from deficiency of complement 1 inhibitor (C1 INH). In type I HANE, C1 INH is present in serum at levels 5-30% of normals. Using cultured monocytes and biosynthetic labeling of proteins, C1 INH was detected in supernatants of cells from HANE patients at levels 20% of those detected in normals. The intracellular reduction of C1 INH in patients' monocytes approached 50%. The study of C1 INH messenger RNA (mRNA) by Northern blot analysis indicated that in HANE patients' monocytes a message of normal size is present at about half the concentration of that from normal cells. One of the patients analyzed showed the presence of a genetically inherited abnormal mRNA (1.9 kb) in addition to the normal mRNA (2.1 kb). Southern blot analysis of DNA from peripheral blood leukocytes did not show any difference in quantity or in sizes of endonuclease restriction fragments between patients and normals. The defect(s), therefore, in type I HANE is pretranslational, but is not due to a deletion or to a major chromosomal rearrangement.

Angioedema↗
PubMed1987

Restriction fragment length polymorphism of the C1 inhibitor gene in hereditary angioneurotic edema.

Hereditary angioneurotic edema (HANE) results from the deficiency of the inhibitor of the first component of human complement (C1-INH). It is inherited as an autosomal dominant trait. Heterogeneity of this defect has been shown at the protein and mRNA level. Southern blot analysis of genomic DNA was performed after digestion with six different restriction endonucleases in 24 families affected with type 1 HANE (low antigenic and functional C1-INH levels) and five with type 2 (low functional C1-INH levels and normal or elevated levels of dysmorphic C1-INH). Blots were hybridized with a C1-INH cDNA probe of 1,227 bp. With one enzyme (Pst I), two different patterns of restriction fragment length polymorphism (RFLP) were detected. One was present in one kindred with type 1 HANE and the other appeared the same in one type 1 and in one type 2 family, thus indicating that each RFLP resulted from a different mutation. Analysis of a total of 34 members of these three families suggested that the polymorphisms are tightly linked to the mutation responsible for the disease. Using a 170-bp probe we showed that the three different mutations leading to these polymorphisms are located in the same region of the C1-INH gene. These data suggest that different mutations in the same region of the C1-INH gene are responsible for C1-INH deficiency in these families. Most of these mutations are probably point mutations or other "minor" defects and do not appear to be due to major deletions or rearrangements.

Angioedema↗
PubMed1986

Purification and chemical composition of gpL115, the human lymphocyte surface sialoglycoprotein that is defective in Wiskott-Aldrich syndrome.

gpL115, the surface sialoglycoprotein that is defective in lymphocytes of Wiskott-Aldrich syndrome patients has been purified from large scale cultures of the lymphoblastoid line CEM. The purification entails cell lysis and solubilization of gpL115 with the detergent Nonidet P-40, sequential affinity chromatography on lentil lectin-Sepharose, wheat germ lectin-Sepharose, and, after treatment with sialidase, on peanut lectin-Sepharose. Sepharose CL-6B gel filtration removes residual protein contaminants and transfers asialo-gpL115 from Nonidet P-40-containing to sodium dodecyl sulfate-containing buffer. The yield, 1300 micrograms of homogeneous protein/10(11) cells, represents greater than 60% recovery. The amino acid composition of gpL115 has several atypical features including low lysine content, high proline content, and very high content of hydroxyamino acids (12.5 residues of serine and 12.5 residues of threonine/100 amino acids). Total carbohydrate content of gpL115 is very high, i.e. 52% for the asialo-molecule. The major carbohydrate residues of asialo-gpL115 are galactose and N-acetylgalactosamine in approximately equimolar amounts (25 and 22 residues/100 amino acids, respectively) plus severalfold lower amounts of N-acetylglucosamine, fucose, and mannose.

Amino Acids↗
PubMed1986

Ultrastructure and composition of bovine conglutinin.

Conglutinin binds in a Ca2+-dependent manner to the carbohydrate portion of zymosan and cell-bound iC3b (complement subcomponent C3b cleaved by Factor I in the presence of factor H) similarly to lectin-like proteins that participate in the clearance of plasma glycoproteins. This carbohydrate-binding protein has been found to include both collagenous and non-collagenous domains. Electron micrographs of bovine conglutinin are presented in which conglutinin appears as a tetramer of four 'lollipop' structures emanating from a central hub. The stem region, linking each head to the central hub, is quite stiff, whereas the hub-stem junction is a flexible hinge. From electron micrographs of a pepsin digest of conglutinin, the linkage region is identified as the collagenous portion of the macromolecule. Conglutinin is a multimer of a single polypeptide chain. From sedimentation equilibria of unreduced as compared with reduced and alkylated conglutinin, there are determined to be three disulphide-linked chains. These data, combined with information on the subunit polypeptide of conglutinin, suggest a model for conglutinin in which four disulphide-linked trimers are associated via the N-termini to form the intact macromolecule as viewed in the electron microscope. The ultrastructure of conglutinin appears ideally suited to its lectin-like function.

Animals↗
PubMed1986

Blood loss during Nippostrongylus brasiliensis infection in the rat.

Faecal blood loss was measured during Nippostrongylus brasiliensis infection in the DA rat using 51Cr-labelled red blood cells (r.b.c.s). In an initial study, faecal blood loss was measured on day 7 of primary infection with 3000 larvae administered subcutaneously (s.c.), and found to be 0.03 ml/24 h in uninfected animals and 0.14 ml/24 h in infected animals. In a further experiment, blood loss was measured on the day before infection and for 13 days after primary s.c. infection with 5000 larvae. Faecal blood loss was 0.05 ml/24 h or less until day 3, began to rise from day 5, reached a peak of 0.51 ml/24 h on day 8, and fell until day 13. This was closely associated with the rise and fall of the pooled faecal egg count. Direct worm count confirmed a high worm burden on day 7 and expulsion by day 14. The effect of the worm burden on the haemoglobin concentration (Hb) was measured in a further experiment and showed a fall in Hb with a mean worm burden of 726 compared to that of 47 or 284 worms. The study concluded that there is minimal background blood loss in uninfected rats but that infection with N. brasiliensis is a cause of intestinal blood loss and this is associated with a fall in Hb concentration that is dependent on the worm burden.

Analysis of Variance↗