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Biomedical subjects

G McBride

Publications and source records attributed to G McBride.

At least 19 recordsLinked to original sources
PubMed2002

Sudden infant death syndrome in Indigenous and non-Indigenous infants in north Queensland, 1990-1998.

OBJECTIVE: To compare the epidemiology of sudden infant death syndrome (SIDS) in Indigenous and non-Indigenous infants in north Queensland, and to assess the quality of data recorded for SIDS deaths. METHODS: Records were obtained for SIDS cases from all coronial courts in north Queensland from 1990 to 1998. Demographic characteristics, ethnicity, age at death, sleeping and feeding patterns, smoking incidences and autopsy findings were compared. Incidences, medians and univariate associations were generated where appropriate. RESULTS: There were 83 248 live births for the 9-year period; 71 389 non-Indigenous and 11 859 Indigenous births. There were 69 SIDS deaths (0.83 per 1000 live births). Overall, recording of demographic and death scene data was poor. Thirty-eight autopsies (55%) were performed by specialist pathologists. There were 22 (32%) non-Indigenous and 22 (32%) Indigenous SIDS deaths (25 ethnicity unknown), giving an estimated relative risk of 2.82 (95% CI 2, 4). Median age at death was 13.1 weeks (range 1-83 weeks) with 14% of deaths occurring in the neonatal period for both groups. Sleeping position was not recorded in 42% of cases and co-sleeping was not recorded in 27% of cases. Bed sharing was more common amongst Indigenous infants. Fifty-two per cent of SIDS cases occurred in the wet season and 48% in the dry season. CONCLUSIONS: Data recorded for SIDS deaths in north Queensland are poor, preventing specific conclusions concerning SIDS risk factors. However, SIDS rates may be up to three-fold higher in the Indigenous population. A uniform system of post-mortem and death scene data reporting is needed urgently.

Autopsy↗
PubMed2000

Intubating LMA guided awake fibreoptic intubation in severe maxillo-facial injury.

PURPOSE: To describe control of the airway in a patient with severe maxillo-facial injury using intubating laryngeal mask guided awake fibreoptic intubation. CLINICAL FEATURES: A 110 kg man presented with a severe facial injury due to a horse kick. Local examination showed a large transverse gaping laceration just beneath the nose, exposing the lower nasal cavities through to the posterior nasopharynx. It was planned to perform a surgical tracheostomy before surgical fixation of the maxilla and nasal bones. Considering the patient's weight, short neck and difficulty in lying flat, surgical tracheostomy under general anesthesia was considered the best option. Under topical anesthesia, an intubating laryngeal mask was introduced followed by a fibreoptic bronchscope. The endotracheal tube was threaded over the bronchoscope and airway control achieved. CONCLUSIONS: The use of an intubating laryngeal mask avoids the need for manipulation of the head and neck and acts as a 'shield' for the fibreoptic bronchoscope from surrounding blood in patients with maxillo-facial injury. The use of the fibreoptic bronchoscope ensures intubation under vision.

Adult↗
PubMed1997

Myringotomy and ventilation tube insertion: a ten-year follow-up.

Eighty children who had myringotomy performed for otitis media with effusion in 1984 were reviewed in 1994. This had involved surgery on 158 ears. Three aspects of ear condition were studied: hearing loss, tympanic membrane perforation, and tympanosclerosis. Hearing losses were present in 13 ears (8.2 per cent), involving 10 children (12.5 per cent), although losses were under 20 dB in seven of these ears (five patients). Of the six ears with losses more than 20 dB (3.8 per cent), in five patients bilateral losses of 30 dB were due to a recurrence of effusions, a large dry posterior perforation was the cause of a 30 dB loss, an infected anterior perforation had caused a 30 dB loss, an ear which had a cholesteatoma, and had a mastoidectomy and ossiculoplasty in 1987, had a 30-40 dB loss, and one ear which had a Type 1 tympanoplasty in 1994 had a 50 dB loss. Therefore in only three ears (1.9 per cent) could hearing loss be associated directly with myringotomy and ventilation tube insertion. Perforations had persisted unilaterally in seven patients, three having had tympanoplasties. Of the remaining perforated tympanic membranes, two were free of symptoms, one had only a slight hearing loss, and one had a more significant loss with recurrent infection. Tympanosclerosis was only found in those ears which had ventilation tubes inserted (and not those which had myringotomy only), occurring in 48 ears (31 per cent, of 39 per cent of those which had a ventilation tube inserted). There was no link between tympanosclerosis and hearing loss. The site of tympanosclerosis was not restricted to the site of myringotomy, and in many cases was present only in other areas of the tympanic membrane. There was a tendency for more extensive tympanosclerosis to occur in those ears which had more ventilation tube insertions. The risk of perforation in particular lends support to a policy of 'watchful waiting'.

Child↗
PubMed1993

Exon skipping causes alteration of the COOH-terminus and deletion of the phospholipase C gamma 1 interaction site in the FGF receptor 2 kinase in normal prostate epithelial cells.

Polymerase chain reaction analysis revealed an mRNA in rat prostate that results from alternate splicing of exon 16 in the heparin-binding fibroblast growth factor receptor kinase type 2 gene (FGFR2). The absence of exon 16 and the shift in reading frame at the exon 15-17 junction predicts an expression product (FGFR2-2) with a unique COOH-terminus that does not exhibit the major autophosphorylation site (tyrosine 789) required for interaction of phospholipase C gamma 1 with the full-length FGFR2-1 isoform. Nuclease protection analysis revealed that the FGFR-2 splice variant is expressed in quantities equal to or greater than the FGFR2-1 isoform in normal prostate tissue. When combined with the same FGFR2 extracellular domain, co-expression of the two COOH-terminal variants may mediate effect of the same FGF ligand on different signal transduction pathways.

Alternative Splicing↗
PubMed1993

Exon switching and activation of stromal and embryonic fibroblast growth factor (FGF)-FGF receptor genes in prostate epithelial cells accompany stromal independence and malignancy.

Stroma and the heparin-binding fibroblast growth factor (FGF) family influence normal epithelial cell growth and differentiation in embryonic and adult tissues. The role of stromal cells and the expression of isoforms of the FGF ligand and receptor family were examined during malignant progression of epithelial cells from a differentiated, slowly growing, nonmalignant model rat prostate tumor. In syngeneic hosts, a mixture of stromal and epithelial cells resulted in nonmalignant tumors which were differentiated and slowly growing. In the absence of the stromal cells, epithelial cells progressed to malignant tumors which were independent of the stroma and undifferentiated. The independence of the malignant epithelial cells from stromal cells was accompanied by a switch from exclusive expression of exon IIIb to exclusive expression of exon IIIc in the FGF receptor 2 (FGF-R2) gene. The FGF-R2(IIIb) isoform displays high affinity for stromal cell-derived FGF-7, whereas the FGF-R2(IIIc) isoform does not recognize FGF-7 but has high affinity for the FGF-2 member of the FGF ligand family. The switch from expression of exclusively exon IIIb to exclusively exon IIIc in the resident FGF-R2 gene was followed by activation of the FGF-2 ligand gene, the normally stromal cell FGF-R1 gene, and embryonic FGF-3 and FGF-5 ligand genes in malignant epithelial cells. Multiple autocrine and potentially intracrine ligand-receptor loops resulting from these alterations within the FGF-FGF-R family may underlie the autonomy of malignant tumor cells.

Animals↗
PubMed1992

Substitution of putative half-cystine residues in heparin-binding fibroblast growth factor receptors. Loss of binding activity in both two and three loop isoforms.

Alternate use of an exon coding for an 89-residue NH2 terminal immunoglobulin-like disulfide loop results in isoforms of the heparin-binding fibroblast growth factor receptor (FGF-R) with three (FGF-R alpha) and two (FGF-R beta) Ig-like loops in the extracellular domain. Both FGF-R alpha and FGF-R beta isoforms exhibit qualitatively similar ligand-binding activities. In this report, we show by site-directed mutagenesis and analysis of ligand-binding activity in transfected cells that substitution of a cysteine that potentially forms an intra-loop disulfide in either juxtamembrane Loop II or III disrupted maturation and formation of the ligand-binding site in both FGF-R alpha and FGF-R beta isoforms. Neither three loop FGF-R alpha constructions coding for intact Loops I and II adjacent to defective Loop III nor intact Loops I and III separated by defective Loop II exhibited ligand-binding activity. In addition, a two-loop molecule of tandem Loops I and III was inactive. The results suggest that single Loops I, II, or III of FGF-R are insufficient to form a ligand-binding site. Loop I does not form an independent ligand-binding site with either Loop II or III, but interacts with a common ligand-binding site formed by Loops II and III (Xu, J., Nakahara, M., Crabb, J. W., Shi, E., Matuo, Y., Fraser, M., Kan, M., Hou, J., and McKeehan, W. L. (1992) J. Biol. Chem. 267, 17792-17803, 1992).

Amino Acid Sequence↗