Bilateral Warthin's tumor.
A case report of bilateral mixed Warthin's tumors with nonuniform uptake demonstrated by Tc-99m pertechnetate imaging is presented. The findings are compared to CT, surgical, and pathology results.
Biomedical subjects
Publications and source records attributed to A Graham.
A case report of bilateral mixed Warthin's tumors with nonuniform uptake demonstrated by Tc-99m pertechnetate imaging is presented. The findings are compared to CT, surgical, and pathology results.
The Hox-2 locus on chromosome 11 represents one of the major clusters of homeo-box-containing genes in the mouse. We have identified two new members (Hox-2.6 and Hox-2.7), which form part of this cluster of seven linked genes, and it appears that the Hox-2 locus is related by duplication and divergence to at least one other mouse homeo box cluster, Hox-1. The Hox-2.6 gene encodes a predicted protein of 250 amino acids, which displays extensive similarity in multiple regions to certain mouse, human, Xenopus, and zebra fish homeo domain proteins. The Drosophila Deformed (Dfd) gene also shares these same regions of similarity, and based on this sequence conservation, we suggest that Hox-2.6 forms part of a vertebrate 'Dfd-like' family. Hox-2.6 is expressed in fetal and adult tissues and is modulated during the differentiation of F9 teratocarcinoma stem cells. In situ hybridization analysis of mouse embryos shows that the Hox-2.6 is expressed in ectodermal derivatives: spinal cord, hindbrain, dorsal root ganglia, and the Xth cranial ganglia. In the central nervous system, expression is observed in the most posterior parts of the spinal cord, with the anterior limit residing in a region of the hindbrain and no expression in the mid- or forebrain. In mesodermal structures, Hox-2.6 is expressed in the kidney, the mesenchyme of the stomach and lung, and the longitudinal muscle layer of the gut. Expression has not been observed in derivatives of embryonic endoderm. The patterns of Hox-2.6 expression in both mesoderm and ectoderm are spatially restricted and may reflect a role for the gene in the response to or establishment of positional cues in the embryo.
The results of recent studies by ourselves and others have demonstrated the feasibility of revascularizing severely ischemic limbs by means of staged arteriovenous reversal at the popliteal level. The results of investigations we did, both clinically and in an animal model, revealed the development of an intense vascular network in the region of the arteriovenous anastomosis as an important component of the revascularization process. To determine the role of ischemia in this process, four groups consisting of three dogs each underwent a popliteal artery to vein anastomosis. In group I, there was no ischemia; group II, distal ischemia only; group III, partial ischemia, and group IV, total ischemia. Angiography at four weeks in all dogs demonstrated that the intense neovascular network seen in previous studies developed only in the limbs of the dogs in group IV. We conclude that the neovascular process seen after creation of arteriovenous reversal develops as a response to severe ischemia. Further studies are needed to better characterize the nature of these vessels, and it is our hope that, in doing so, means of enhancing development of these vessels in order to indirectly revascularize otherwise unsalvagable extremities will be realized.
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Mixed infections of secondary rhesus monkey kidney cells with human rotaviruses carrying rearranged genomes and with bovine rotavirus yielded a high percentage of reassortants. The genotypes of 511 plaque-purified clones raised in either MA104 or BSC-1 cells have been determined and the frequencies of different genotypes have been calculated. It was found that reassortants did not emerge at random; there was non-random association of certain genes; the cell line used to isolate reassortants influenced the result, i.e. host cell factors had a selective effect on a recombinational mixture.
The ionophore monensin inhibited the formation of herpes simplex virus type 2 (HSV-2) particles by about 30% but the yields of infectious particles were reduced to 5% and 1% for cell-associated and extracellular virus, respectively. The presence of monensin did not affect the processing of the two viral glycoproteins gB-2 and gG-2. However, two other glycoproteins, gC-2 and gD-2, were not processed to their fully mature forms in the monensin-treated cells and only the faster moving pgC-2 and pgD-2 were detected. The cell-associated virus particles contained the glycoproteins gB-2, gC-2, gD-2 and gG-2, whereas the extracellular virus particles contained only gG-2 glycoprotein. These results suggest that HSV-2 particles containing all the viral glycoproteins are transported via the Golgi apparatus to the cell surface but that virus particles containing only gG-2 may follow a different pathway for transport and release.
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The hydrolysis in vitro of preactivated Intralipid (an artificial triacylglycerol-phospholipid emulsion) by rat adipose tissue lipoprotein lipase is inhibited by rat high-density lipoprotein (HDL). The aim of this work was to investigate whether human lipoprotein lipase was also inhibited, the mechanism of inhibition of the rat enzyme by HDL, and the role of the various individual apolipoproteins. Both human and rat lipoprotein lipase from post-heparin plasma are inhibited by HDL. This inhibition is considerably decreased if the HDL is first made 'apolipoprotein poor' by removal of some transferable apolipoproteins. In contrast, both native and apolipoprotein poor HDL inhibit the hydrolysis of Intralipid by rat hepatic lipase. Apolipoproteins C and E, either free in solution or attached to lipid vesicles, inhibit the hydrolysis of activated Intralipid by rat lipoprotein lipase to a maximum of 85% and 50%, respectively. Apolipoprotein A attached to vesicles gives little inhibition. HDL apolipoprotein and apolipoprotein C compete with the substrate for binding to lipoprotein lipase with apolipoprotein C having a higher affinity for the enzyme than HDL apolipoprotein. The inhibition of lipoprotein lipase by HDL can be explained by the association of the constituent apolipoproteins, in particular apolipoprotein C, with the enzyme so that there is less enzyme available to act on substrate.
Two patients with chronic liver disease developed elevated serum aluminum concentrations and biopsy-proven osteodystrophy. Neither patient had chronic renal failure but both had received aluminum-containing antacids for long periods. We measured biliary and urinary aluminum excretion during antacid loading in patients with normal liver function. Our studies show that biliary excretion is an important route of elimination of orally absorbed aluminum, and we suggest that long-term antacid therapy in patients with severe liver disease be monitored with periodic serum and urinary aluminum determinations to avoid aluminum osteodystrophy.
Pepsinogens (PGA) are the inactive precursors of pepsin, the major acid protease found in the stomach. The PGA gene family exhibits polymorphic variation in human populations that can either be demonstrated by electrophoretic analysis of the proteins or by analysis of the respective genes with cDNA probes. Here, we describe the interrelationships between the most common pepsinogen protein phenotypes and the corresponding pepsinogen haplotypes (A, B, and C) containing different combinations of the PGA3, PGA4, and PGA5 genes. We propose that this unusual genetic variation involving haplotypes that contain three, two, and one genes, respectively, is the result of molecular evolution by gene duplication.
A prospective comparison between digital and visual speculum examination was made in 133 pregnant patients. The coefficient correlation between the two examinations of effacement and dilation of the cervix was 0.74. The present results suggest that cervical evaluation by means of speculum examination in the assessment of pregnant patients with spontaneous rupture of membranes are adequate.
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One of the major bottlenecks in automation and process control of industrial bioprocesses is the lack of suitable sensing devices to accurately measure the concentrations of biomolecules. The measurement of ions (e.g., H(+), NH(4)(+)) and gases (e.g., O(2), CO(2), NH(3)) using standard ion-selective and gas sensing electrodes respectively, is well established. Chemical analysis of biomolecules off-line is generally unreliable, labour intensive and may lead to contamination of the biological systems. Problems of maintaining sterile conditions are especially important when dealing with slow growing mammalian or plant cells in culture. Active research in the development of biosensors for monitoring fermentation processes, food production and pollution control, and for medical and veterinary applications is currently underway. This paper reviews recent approaches toward the development of biosensors which involve a biochemical interaction to measure the concentrations of biomolecules, primarily for the on-line monitoring and control of fermentation processes.
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