Use of an osteocutaneous plantar free flap for salvage of a below-the-knee amputation in a child. A case report.
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Amputation, Surgical↗
Biomedical subjects
B A Taylor
Publications and source records attributed to B A Taylor.
Detection of obesity QTLs on mouse chromosomes 1 and 7 by selective DNA pooling.
The inheritance of obesity has been analyzed in an intercross between the lean 129/Sv mouse strain and the obesity-prone EL/Suz mouse strain. The weights of three major fat pads were determined on 4-month-old mice, and the sum of these weights, divided by body weight, was used as an adiposity index. The strategy of selective DNA pooling was used as a primary screen to identify putative quantitative trait loci (QTLs) affecting adiposity index. DNA pools representing the leanest 15% and fattest 15% of the F2 progeny were compared for differential allelic enrichment using widely dispersed microsatellite variants. To evaluate putative QTLs, individual genotyping and interval mapping were employed to estimate QTL effects and assess statistical significance. One QTL affecting adiposity index, which accounted for 12.3% of phenotypic variance in gender-merged data, was mapped to the central region of Chromosome (Chr) 7. The QTL allele inherited from EL conferred increased adiposity. A second QTL that accounts for 6.3% of phenotypic variance was identified on Chr 1 near D1Mit211. At both QTLs, the data are consistent with dominant inheritance of the allele contributing to obesity. The possible relationships between these QTLs and previously described obesity QTLs, major obesity mutations, and candidate genes are discussed.
Adipose Tissue↗
A genetic linkage map of mouse chromosome 2 extending from thrombospondin to paired box gene 1, including the H3 minor histocompatibility complex.
The classical minor histocompatibility 3 (H3) locus was originally defined by the phenotype of skin graft rejection, which is a complex genetic trait. H3 is now known to be a gene complex comprised of a minimum of two functionally interdependent alloantigen-encoding loci, H3a and H3b. H3a encodes a peptide recognized by cytotoxic T cells, and H3b encodes a peptide that stimulates helper T cells. The H3 complex also contains the beta2-microglobulin gene (B2m), and polymorphisms in B2m contribute to the tissue rejection phenotype. We describe a high-density genetic linkage map of a 16-cM region of mouse Chromosome 2 from thrombospondin (Thbs1) to paired box gene 1 (Pax1). This genetic map includes H3a, H3b, and B2m. Other genes and anonymous loci have also been placed on the map. H3a maps between D2Mit444 and B2m in close vicinity to several known genes. H3b maps 12 cM distal to H3a, and the proprotein convertase subtilisin/kexin type 2 gene (Pcsk2; formerly Nec2) cosegregates with H3b in a high-resolution backcross panel. The H3 complex spans a region that shows conserved synteny to human chromosomes 15q, 2q, and 20p.
Animals↗
Microvascular angiopathy in advanced periodontal disease.
Previous studies have shown a perivascular hyaline thickening affecting restricted regions of the microcirculation in gingivitis and moderate periodontitis and in the pulpal vessels in chronic pulpitis. In the present study of the lesion of advanced periodontitis, immunostaining for type IV collagen and laminin demonstrated widespread deposition of basement membrane material, with manifest involvement of the venous network. Some vessels were associated with an increased deposition of both basement membrane proteins, while others showed preferential deposition of either laminin or type IV collagen. Immunostaining also revealed an extensive trabecular network of type IV collagen throughout the affected gingival tissue that was related to recognizable vessels but was co-extensive with less intense staining for laminin. This network was not associated with viable endothelial cells demonstrable by staining with the endothelial marker Ulex agglutinin (UEA-1). The results indicate extensive vascular pathology in advanced periodontitis that could explain the attenuation of the inflammatory reaction and the restricted ability to develop reparative granulation tissue in this disease.
Adult↗
Comparison of individual surgeon's performance. Risk-adjusted analysis with POSSUM scoring system.
UNLABELLED: Comparison of outcome after colorectal resection among different surgeons is difficult. Crude rates of morbidity and mortality can be misleading because such rates make no allowance for differences in case mix and fitness of patients. AIM: The aim of this study was to compare outcome among five surgeons by means of the simple, well-validated scoring system POSSUM for risk-adjusted analysis. METHODS: A total of 438 patients were studied prospectively. Each patient underwent colorectal resection by one of the five surgeons. Demographic details, operative procedure, and postoperative course were recorded, and physiologic and operative severity scores were determined. Risk of morbidity and mortality was calculated for each patient. RESULTS: Incidence of morbidity varied sharply among the five surgeons, from 13.6 to 30.6 percent, and the 30-day mortality varied from 4.5 to 6.9 percent. However, application of POSSUM to allow risk-adjusted analysis of the data demonstrated that the incidence of morbidity and mortality predicted by POSSUM based on patients physiologic and operative risks factors was very similar to the observed outcome for each surgeon. CONCLUSION: Direct comparison of individual surgeon's performance based on crude rates of morbidity and mortality can be misleading. Risk-adjusted analysis allows more meaningful comparison.
Aged↗
The role of imaging in the diagnosis and management of thoracolumbar burst fractures: current concepts and a review of the literature.
The burst fracture of the spine was first described by Holdsworth in 1963 and redefined by Denis in 1983 as being a fracture of the anterior and middle columns of the spine with or without an associated posterior column fracture. This injury has received much attention in the literature as regards its radiological diagnosis and also its clinical management. The purpose of this article is to review the way that imaging has been used both to diagnose the injury and to guide management. Current concepts of the stability of this fracture are presented and our experience in the use of magnetic resonance imaging in deciding treatment options is discussed.
Humans↗
ALF1, a basic helix-loop-helix transcription factor, maps to mouse chromosome 9.
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Animals↗
Localization of gene encoding the thyroid stimulating hormone receptor (Tshr) on mouse chromosome 12.
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Alleles↗
Ocular retardation mouse caused by Chx10 homeobox null allele: impaired retinal progenitor proliferation and bipolar cell differentiation.
Ocular retardation (or) is a murine eye mutation causing microphthalmia, a thin hypocellular retina and optic nerve aplasia. Here we show that mice carrying the OrJ allele have a premature stop codon in the homeobox of the Chx10 gene, a gene expressed at high levels in uncommitted retinal progenitor cells and mature bipolar cells. No CHX10 protein was detectable in the retinal neuroepithelium of orJ homozygotes. The loss of CHX10 leads both to reduced proliferation of retinal progenitors and to a specific absence of differentiated bipolar cells. Other major retinal cell types were present and correctly positioned in the mutant retina, although rod outer segments were short and retinal lamination was incomplete. These results indicate that Chx10 is an essential component in the network of genes required for the development of the mammalian eye, with profound effects on retinal progenitor proliferation and bipolar cell specification or differentiation. off
Alleles↗
Stimulation of colonic mucin synthesis by corticosteroids and nicotine.
1. We speculated that corticosteroids might cause beneficial stimulation of mucus synthesis, since this is a known action of carbenoxolone, itself a corticosteroid, and has also been proposed as a possible mechanism for the protective effect of smoking on ulcerative colitis. We have therefore compared the effects of corticosteroids including carbenoxolone, and nicotine on mucin synthesis, assessed by incorporation of N-[3H]acetylglucosamine into mucin by colonic epithelial biopsies in culture. 2. In histologically normal biopsies from the left colon, hydrocortisone and prednisolone caused a very marked concentration-dependent increase in mucin synthesis, with maximal effect (580 and 300% of control values respectively) at 6 mumol/l [P < 0.001, n = 35 biopsies (seven patients)] and 1.5 mumol/l [P < 0.001, n = 35 (seven patients)] respectively. The maximal effect of hydrocortisone was significantly greater than that of prednisolone (P < 0.05). Carbenoxolone, 0.17 mmol/l, also increased mucin synthesis in the left colon by 242% [P < 0.05, n = 15 (three patients)]. In contrast, these corticosteroids caused only a small, non-significant increase in mucin synthesis in the histologically normal right colon; fludrocortisone, 2 and 20 mumol/l, and aldosterone, 0.1-10 mumol/l, had no effect. Nicotine significantly increased mucin synthesis (180-220% of control values) between 62.5 nmol/l and 6.25 mumol/l (P < 0.05 at all concentrations) in both the right and left colon. In biopsies from the relatively uninvolved right colon of patients with ulcerative colitis, corticosteroids and nicotine caused relatively smaller increases in mucin synthesis. 3. The marked stimulation of mucin synthesis by corticosteroids suggests that this may account, at least in part, for their therapeutic effect in ulcerative colitis.
Acetylglucosamine↗
MRI of 'idiopathic' juvenile scoliosis. A prospective study.
In a prospective trial we performed MRI of the spine and hind brain in 31 patients with scoliosis of onset between the ages of four and 12 years. In eight patients (26%) there was a significant neuroanatomical abnormality; there were six cases of Chiari-1 malformation associated with a syrinx, one isolated Chiari-1 malformation and one astrocytoma of the cervical spine. Four of these patients had left-sided curves. There were no clinical features which could reliably identify those patients with abnormalities on MRI. In particular, the unilateral absence of abdominal reflexes was found to be non-specific (1 of 8 of patients with neuroanatomical abnormalities (12.5%) v 2 of 23 with normal scans (8.7%). In view of the established risks of surgical correction of scoliosis in the presence of undecompressed syringomyelia and the possible improvement that may follow decompression of the foramen magnum, we feel that MRI of all patients with scoliosis of juvenile onset should be obligatory.
Child↗
Encyclopedia of the mouse genome V. Mouse chromosome 10.
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Animals↗
Positional cloning of the nude locus: genetic, physical, and transcription maps of the region and mutations in the mouse and rat.
Mutations in the nude locus in mice and rats produce the pleiotropic phenotype of hairlessness and athymia, resulting in severely compromised immune system. To identify the causative gene, we utilized modern tools and techniques of positional cloning. Specifically, spanning the region in which the nude locus resides, we constructed a genetic map of polymorphic markers, a physical map of yeast artificial chromosomes and bacteriophage P1 clones, and a transcription map of genes obtained by direct cDNA selection and exon trapping. We identified seven novel transcripts with similarity to genes from Drosophila, Caenorhabditis elegans, rat, or human and three previously identified mouse genes. Based on our transcription mapping results, we present a novel approach to estimate the number of genes in a region and estimate that the nude locus resides in a region approximately threefold enriched for genes. We confirm a recently published report that the nude phenotype is caused by mutations in a gene encoding a novel winged helix or fork head domain transcription factor, whn (Nehls et al., Nature 372: 103-107, 1994). We report as well the mutations in the rat rnu allele and the complete coding sequence of the rat whn mRNA.
Amino Acid Sequence↗
Octreotide inhibits the growth and development of three types of experimental liver metastases.
A study was performed to assess the effects of octreotide on the growth and development of liver metastases in rats. Tumour was induced by intraportal injection of three tumorigenic cell lines (the fibrosarcoma HSN and colonic adenocarcinomas K12/Tr and WB2054M) in syngeneic rats. Octreotide treatment (2 micrograms subcutaneously for 3 or 4 weeks) was started 18 h and 1 week after tumour induction; a delay in treatment of 1 week allowed micrometastases to develop. Treatment with octreotide significantly (P < 0.001) reduced the median hepatic replacement of liver by tumour compared with that of control rats given saline (controls: HSN 76.4 per cent, K12/Tr 17.5 per cent, WB2054M 43.9 per cent; octreotide treatment delayed 18 h: HSN 2.7 per cent, K12/Tr 0.6 per cent, WB2054M 1.3 per cent; octreotide treatment delayed 1 week: HSN 9.3 per cent, K12/Tr 2.5 per cent, WB2054M 2.3 per cent). These results clearly indicate that octreotide significantly inhibits the growth and development of experimental liver metastases. Further studies are required both to delineate the mechanism of action and to investigate these effects in a clinical setting.
Animals↗
Typing recombinant inbred mouse strains for microsatellite markers on chromosomes 10, 16, 18, 19, and X.
A total of 57 different microsatellite variants have been typed in one or more of five different sets of recombinant inbred (RI) mouse strains. The present report concentrates on markers for Chromosomes (Chrs) 10, 16, 18, 19 and X. These markers extend the regions swept in these RI strains, provide reference markers for integrating RI and conventional maps, and provide additional estimates of genetic distances. Multilocus maps, based on maximum likelihood analysis of present and previously published RI SDPs on five chromosomes, are presented. Unexpectedly, three microsatellite markers, previously assigned to Chr 10, detected polymorphic fragments mapping to other chromosomes.
Animals↗
Acute pouchitis and deficiencies of fuel.
PURPOSE: Acute pouchitis is a troublesome complication after restorative proctocolectomy. Deficiency of fuel, especially short chain fatty acids (SCFA), produced by anaerobic bacterial fermentation of saccharides, is implicated in ulcerative and diversion colitis. Our hypothesis was that SCFA deficiency occurs in acute pouchitis, and correction of the deficiency is associated with resolution of pouchitis. METHODS: Thirty-two patients were studied, 10 with histologically confirmed acute pouchitis and 22 with healthy pouches. Stool concentrations of SCFA (acetic, propionic, butyric, and valeric acids) were determined by gas-liquid chromatography. Quantitative bacteriologic studies of stool were carried out, and four-quadrant pouch biopsies were assessed by a pathologist who was unaware of the clinical state. Patients with pouchitis were treated for six weeks with metronidazole and given dietary advice to increase their intake of fermentable saccharides. RESULTS: Stool concentrations of SCFA were significantly less in pouchitis patients compared with patients with healthy pouches (340 mumol/g (range, 124-492) vs. 93 (range, 44-136) P < 0.01). No differences in anaerobic or aerobic counts were seen. Resolution of pouchitis was associated with a significant increase in SCFA, but anaerobic counts fell. CONCLUSION: Deficiency of SCFA is implicated in acute pouchitis.
Acetates↗
In vitro and in vivo enhancement of ddI activity against Rauscher murine leukemia virus by ribavirin.
Ribavirin has been reported to enhance the activity of ddI against HIV. We explored this enhancement of antiviral activity in Rauscher murine leukemia virus (RMuLV) models in vitro and in vivo. The significant finding in these studies was that combinations of the drugs exhibited virus titer reductions that were greater than would be expected if the drug interactions were simply additive. These effects were designated synergistic by the method of Prichard and Shipman (Prichard, M.N. and Shipman, C., Jr. (1990). A three-dimensional model to analyze drug-drug interaction, Antiviral Res. 14, 181-206). In addition to the antiviral synergy, we also observed some synergistic toxicity in the animal model.
Animals↗
Effect of octreotide infusion on hepatic and tumour blood flow in two experimental models of liver metastases.
OBJECTIVE: To investigate the effects of octreotide infusion on hepatic and tumour blood flow in rats with experimentally induced liver tumours. DESIGN: Blood flow was determined in tumour-bearing rats using a dual reference microsphere technique before and after intravenous infusion of octreotide. METHODS: Tumours were induced in syngeneic rats by intraportal injection of K12-Tr and WB2054-M adenocarcinoma cells. Hepatic arterial and portal venous inflow, tumour blood flow and systemic arterial pressure were determined before and after octreotide infusion (0.05 microgram/min). RESULTS: In rats with K12-Tr tumours there was no change in tumour blood flow, hepatic arterial flow or portal venous inflow after octreotide infusion. In contrast, in rats with WB2054-M tumours, octreotide infusion resulted in a significant reduction in the blood flow to the hepatic tumour (from 0.37 to 0.135 ml/min/g) but had no effect on hepatic artery or portal venous inflow. CONCLUSION: The reduction in blood flow to tumours derived from WB2054-M cells could, at least in part, explain the inhibitory effect of octreotide on the growth and development of these tumours. However, octreotide had no effect on blood flow to tumours derived from K12-Tr cells, suggesting that the analogue must inhibit tumour growth by other mechanisms.
Adenocarcinoma↗