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Biomedical subjects

B Gilpin

Publications and source records attributed to B Gilpin.

8 recordsLinked to original sources

Elucidation of potential transmission routes of Campylobacter in New Zealand.

Campylobacter is the most commonly reported notifiable disease in New Zealand. The cost of Campylobacter infections in the country during 1994 was estimated as dollar 61.7M although the true cost was probably higher. Investigation of the main environmental reservoirs and routes of transmission to humans is necessary to formulate the most appropriate intervention strategies. This project investigated the reservoirs of Campylobacter in a defined geographical area within New Zealand and compared strains isolated from humans and environmental sources within this area as a prelude to investigating the likely transmission routes to humans. Campylobacter jejuni was commonly found in faeces from dairy cows, beef cattle, sheep and ducks, chicken carcasses, sheep offal and surface waters and C. coli was commonly found in sheep faeces. Preliminary analysis of Penner types was suggestive of transmission to humans from dairy and beef cattle and possibly from sheep.

Animals↗

The use of chemical and molecular microbial indicators for faecal source identification.

Identifying the source of faecal pollution is important to enable appropriate management of faecal pollution of water. We are developing and evaluating a combination of these microbial and chemical indicators better able to identify the source of faecal pollution. These assays make use of a combination of direct PCR, culturing, and colony hybridisation to identify source specific species of Bifidobacterium, Rhodococcus and Bacteroides. In conjunction with assays for (a) fluorescent whitening agents and (b) faecal sterols and stanols, these indicators were able to identify human derived faecal pollution in river water containing inputs from septic tanks, municipal oxidation ponds, farmed animals and feral animals. Differentiating amongst the animal sources was more difficult and will require development of molecular assays for organisms specific to each animal group.

Agriculture↗

Tetranectin in slow intra- and extrafusal chicken muscle fibers.

Tetranectin is a C-type lectin that occurs in the mammalian musculoskeletal system. In the present report we describe the first studies on an avian tetranectin. A full-length chicken tetranectin cDNA was isolated. Comparison of the deduced amino acid sequence of chicken tetranectin with mouse and human tetranectin showed an identity of 67 and 68%, respectively. Northern blot analysis demonstrated broad expression of chicken tetranectin mRNA, which was first detected on embryonic day 4. Tetranectin protein was detected in chicken serum and egg yolk. Since muscle is one of few tissues in which tetranectin protein is retained, we examined the distribution of tetranectin in various muscle types in chicken. Myofibers strongly positive for tetranectin were observed in several muscles including m. tibialis ant. and m. sartorius (from embryonic day 10 to adult). Using antibodies to fast and slow myosin heavy chains (MHC) and double immunostaining techniques, we found that tetranectin was restricted to slow (type I) muscle fibers. Similarly only slow intrafusal fibers accumulated tetranectin. The pattern of immunostaining in chickens differs markedly from that seen in mouse muscles, indicating that tetranectin performs a role in muscle that is not associated with a hitherto recognized muscle type or function.

Adaptation, Physiological↗

The cysteine-rich domain of human ADAM 12 supports cell adhesion through syndecans and triggers signaling events that lead to beta1 integrin-dependent cell spreading.

The ADAMs (a disintegrin and metalloprotease) family of proteins is involved in a variety of cellular interactions, including cell adhesion and ecto- domain shedding. Here we show that ADAM 12 binds to cell surface syndecans. Three forms of recombinant ADAM 12 were used in these experiments: the cys-teine-rich domain made in Escherichia coli (rADAM 12-cys), the disintegrin-like and cysteine-rich domain made in insect cells (rADAM 12-DC), and full-length human ADAM 12-S tagged with green fluorescent protein made in mammalian cells (rADAM 12-GFP). Mesenchymal cells specifically and in a dose-dependent manner attach to ADAM 12 via members of the syndecan family. After binding to syndecans, mesenchymal cells spread and form focal adhesions and actin stress fibers. Integrin beta1 was responsible for cell spreading because function-blocking monoclonal antibodies completely inhibited cell spreading, and chondroblasts lacking beta1 integrin attached but did not spread. These data suggest that mesenchymal cells use syndecans as the initial receptor for the ADAM 12 cysteine-rich domain-mediated cell adhesion, and then the beta1 integrin to induce cell spreading. Interestingly, carcinoma cells attached but did not spread on ADAM 12. However, spreading could be efficiently induced by the addition of either 1 mM Mn(2+) or the beta1 integrin-activating monoclonal antibody 12G10, suggesting that in these carcinoma cells, the ADAM 12-syndecan complex fails to modulate the function of beta1 integrin.

ADAM Proteins↗

Chronic abruption-oligohydramnios sequence.

OBJECTIVE: To determine outcome in patients with chronic abruption. STUDY DESIGN: A retrospective review was performed of all patients delivering at a tertiary medical center during a 54-month period. All patients with a diagnosis of placental abruption with oligohydramnios or ruptured membranes were included. Chronic abruption-oligohydramnios sequence (CAOS) was defined by the following criteria: (1) clinically significant vaginal bleeding in the absence of placenta previa or other identifiable source of bleeding, (2) amniotic fluid volume initially documented as normal, and (3) oligohydramnios (amniotic fluid index < or = 5) eventually developing without concurrent evidence of ruptured membranes. RESULTS: Twenty-four patients with CAOS were identified. Fourteen had first evidence of abruption at < 20 weeks' gestational age. A clot was identified between the chorion and uterus in 18/24. The mean gestational age at the first bleeding episode was 19.4 +/- 5.5 (SD) weeks, with the mean gestational age at delivery 28.1 +/- 4.5 weeks. Preterm premature membrane rupture occurred in 15/24. In these 15 there was a mean of 11.5 +/- days between the diagnosis of oligohydramnios and of ruptured membranes. Patients whose first blood occurred at < 20 weeks' gestation delivered at a gestational age of 26.1 +/- 3.9 weeks versus 33.0 +/- 5.3 weeks for the control group. CONCLUSION: CAOS can occur in pregnancies complicated by abruptio placentae. If it develops, the mean gestational age at delivery is 28 weeks.

Abruptio Placentae↗