PubMed Health⌕ Search

Biomedical subjects

M Mantle

Publications and source records attributed to M Mantle.

At least 19 recordsLinked to original sources
PubMed2006

Automated localization of magnetoencephalographic interictal spikes by adaptive spatial filtering.

OBJECTIVE: Automated adaptive spatial filtering techniques can be applied to magnetoencephalographic (MEG) data collected from people with epilepsy. Source waveforms estimated by these methods have higher signal-to-noise ratio (SNR) than spontaneous MEG data, allowing identification and location of interictal spikes. The software tool SAM(g(2)) provides an adaptive spatial filtering algorithm for MEG data that yields source images of excess kurtosis and provides source time-courses in voxels exhibiting high excess kurtosis. The sensitivity and specificity of SAM(g(2)) in epilepsy is unknown. METHODS: Interictal MEG data from 36 patients with intractable epilepsy were analyzed using SAM(g(2)), and results compared with equivalent current dipole (ECD) fit procedures. RESULTS: When SNR of interictal spikes was high (compared to background) with a clear single focus, in most cases there was good agreement between ECD and SAM(g(2)). With multiple foci, there was typically overlap but imperfect concordance between results of ECD and SAM(g(2)). CONCLUSIONS: SAM(g(2)) may in some cases be equivalent to manual ECD fit for localizing interictal spikes with single locus and good SNR. Further studies are required to validate SAM(g(2)) with multiple foci or poor SNR. SIGNIFICANCE: In some cases, SAM(g(2)) might eventually assist or replace manual ECD analysis of MEG data.

Algorithms↗
PubMed2004

Localization of interictal spikes using SAM(g2) and dipole fit.

SAM(g2) is an automated analysis that transforms the MEG data into a functional image of spike-like activity, giving the source waveforms for those locations. Since the source waveforms estimated by SAM have higher signal-to-noise ratio (SNR) than does the raw MEG data, it is possible to automatically mark the location and timing of each spike for comparisons with dipole fit procedures. Both SAM(g2) and equivalent current dipole (ECD) fits were used to analyze MEG interictal spike recordings in 10 patients with cortical dysplasias and medial temporal lobe epilepsy. The ECD fit locations obtained by manual spike classification and latency marking were compared with those found by automated SAM(g2) procedures. When the SNR of interictal activity was high (compared to the background) with a clear single focus, there was excellent agreement between the ECD cluster location and the SAM(g2) maximum. However, when the SNR of spikes was low, manual single ECD location scatter was larger than SAM(g2) reconstructions. When multiple independent interictal spike loci were present, there was some disagreement between SAM(g2) and ECD scatter in the cases of low SNR spikes. When SAM(g2) indicated multiple coupled spike loci, the residual variance for the dipole fit was high and its scatter unacceptably large--even for multiple dipole models. This study demonstrates that SAM(g2) is equivalent to ECD fit for localizing interictal spikes when there is a single locus and good SNR. Further studies are required to validate cases in which there are multiple spike loci or poor SNR.

Action Potentials↗
PubMed2002

An unusual cause of back pain in an achondroplastic man.

A case is described of a 47-year-old man with achondroplasia who presented with lower back pain radiating to his left loin. An intravenous urogram (IVU) showed hydronephrosis on the left side and a dilated left ureter passing down into the left inguinal region. A CT scan confirmed a left inguinal hernia containing the left ureter causing ureteric obstruction. The hernia was repaired using the Lichtenstein technique with the ureter replaced retroperitoneally. A postoperative IVU showed recovery in renal function but with a persistently dilated left ureter that was not obstructed. A review of the literature regarding inguinal herniation involving the ureter is presented.

Achondroplasia↗
PubMed1999

Examination of the metabolic status of rat air pouch inflammatory exudate by high field proton NMR spectroscopy.

High field proton (1H) NMR spectroscopy was employed to investigate the metabolic status of rat air pouch inflammatory exudates obtained subsequent to the induction of inflammation with carrageenan, and the 1H NMR profiles of these fluids were compared and contrasted with those of inflammatory human synovial fluid, rat plasma and human serum. The characteristic biochemical features obtained from 1H NMR analysis of these exudates consisted of (1) substantially elevated levels of lactate (11.40+/-1.46x10-3 mol dm-3 for samples collected at a time point of 24 h post induction) with little or no NMR-detectable glucose, data consistent with a hypoxic environment and consequent anaerobic metabolism in the inflamed air pouch, and (2) high levels of the ketone body 3-d-hydroxybutyrate, providing evidence for an increased utilization of fats for energy by lymphocytes, the predominant leucocytes present in this environment. These phenomena represent a pathological extreme of the abnormal metabolic status of inflammatory human synovial fluids.

Air↗
PubMed1997

Sustained gallbladder stasis promotes cholesterol gallstone formation in the ground squirrel.

Although gallbladder stasis exists in most patients with cholesterol gallstones, it is unknown whether stasis is a causative factor of gallstone disease or merely a consequence of it. We studied the impact of sustained gallbladder stasis induced by a cholecystokinin (CCK)-A receptor antagonist (MK-329) on gallstone formation in ground squirrels fed either a trace or a high-cholesterol diet. MK-329 markedly inhibited gallbladder contraction in vitro in response to CCK (at EC100, control: 3.6 +/- 0.5 vs. MK-329: 1.1 +/- 0.3 g; P < .05) and increased gallbladder fasting volume in vivo (control: 462 +/- 66 vs. MK-329: 1,004 +/- 121 microL; P < .05). Whereas the high-cholesterol diet alone (1%-cholesterol diet + placebo) increased the cholesterol saturation index (CSI) in control animals (trace-cholesterol diet + placebo), MK-329 significantly (P < .05) decreased the CSI in both hepatic and gallbladder bile in animals on the trace-(trace-cholesterol diet + MK-329) as well as on the high-cholesterol diets (1%-cholesterol diet + MK-329). The mucin content of the mucus layer on the epithelial surface of the gallbladder wall more than doubled (P < .05) with the high-cholesterol diet; adding MK-329 to the latter group produced a further 82% increase (P < .05). The cholesterol diet + MK-329 group had the highest (100%) incidence of cholesterol crystals that were evident in fresh gallbladder bile, coincident with a shortened nucleation time (2.5 +/- 0.6 days; P < .05 vs. the cholesterol diet + placebo group, 5.8 +/- 1.0 days or the other 2 groups, >21 days). Bile from animals on the trace-cholesterol diet, whether or not receiving MK-329, lacked crystals in bile and exhibited a normal nucleation time (>21 days). Thus, stasis per se may lower the CSI, but its detrimental effect on the gallbladder predominates locally, and so accelerates cholesterol crystal formation in this model.

Animals↗
PubMed1996

Role of 5-HT in cholera toxin-induced mucin secretion in the rat small intestine.

We examined the role of 5-hydroxytryptamine (5-HT) in cholera toxin (CT)-induced mucin secretion in the proximal and distal regions of the rat small intestine. Neither the 5-HT2 receptor antagonist ketanserin nor the cyclooxygenase inhibitor indomethacin was capable of inhibiting choleraic mucin secretion. However, in the presence of the mixed 5-HT3/4 receptor antagonist tropisetron at doses that block both receptor subtypes, the secretory response was reduced to baseline levels in the proximal and distal small intestine. The selective 5-HT3 receptor antagonist ondansetron had no significant effect. These findings suggest that choleraic mucin secretion is mediated primarily through the activation of a 5-HT4-like receptor. Mucin secretion in response to the exogenous application of 5-HT occurs via two pathways: one is mediated by a 5-HT4-like receptor and is capsaicin sensitive but tetrodotoxin (TTX) insensitive, and one lacks the capsaicin-sensitive 5-HT4-mediated response but is TTX sensitive. Both converge on a common pathway that is cholinergic. No significant differences were observed between proximal and distal intestinal segments.

Animals↗
PubMed1994

Binding of Yersinia enterocolitica to purified, native small intestinal mucins from rabbits and humans involves interactions with the mucin carbohydrate moiety.

Plasmid-bearing (but not plasmid-cured) Yersinia enterocolitica is known to bind to purified small intestinal mucins from rabbits and humans. This study examined which region(s) of the mucin molecule is important for bacterial adherence. Pronase digestion of mucin and removal of nonglycosylated or poorly glycosylated peptide regions had no effect on bacterial binding, suggesting that plasmid-bearing Y. enterocolitica interacts with mucin carbohydrate. Periodate oxidation also did not alter bacterial adherence, indicating that vicinal hydroxyl groups in the mucin sugars are not important for binding. Boiling of mucin, depolymerization by reduction of disulfide bonds, or removal of noncovalently associated lipid actually enhanced bacterial adherence, suggesting that plasmid-bearing Y. enterocolitica can interact with additional domains in the mucin molecule revealed by these treatments. These domains were destroyed by pronase digestion. In delipidated mucin (but not in reduced or boiled mucin), binding to these domains appeared to be hydrophobic since it could be prevented by treatment of bacteria with tetramethyl urea. Oligosaccharides obtained from both human and rabbit small intestinal mucins were capable of inhibiting attachment of plasmid-bearing (but not plasmid-cured) Y. enterocolitica to mucin. After removal of terminal and backbone sugar residues by treatment of mucin with trifluoromethanesulfonic acid, binding of plasmid-bearing bacteria increased significantly when N-acetylgalactosamine, either alone or with galactose attached, was revealed, indicating that core regions of the sugar side chains are involved in bacterial binding. Adherence of plasmid-cured organisms was unaffected by trifluoromethanesulfonic acid treatment of mucin. We concluded that virulent Y. enterocolitica interacts with the carbohydrate moiety of native small intestinal mucin through a plasmid-mediated process. When mucin becomes denatured, binding of the organism can increase through hydrophobic and nonhydrophobic interactions with (most likely) the mucin protein.

Animals↗
PubMed1993

Characterization of quail intestinal mucin as a ligand for endogenous quail lectin.

The S-type lectins have been shown to be components of mucosal scrapings, and in avian systems these lectins have been localized immunohistochemically to the mucosal surface and goblet cells of the intestine. The interaction of lectin specifically with purified mucin has not, however, been established. Quail intestinal mucin was purified by two subsequent isopycnic density-gradient centrifugations in CsCl and chromatography on Sepharose Cl-2B. Purified mucin, obtained from the void volume of the Sepharose column, was characterized by SDS/PAGE, amino acid and carbohydrate analyses, sensitivity to thiol reduction, and cross-reactivity with antibody preparations to rat and human intestinal mucins on Western blots. Antibody raised against purified quail mucin partially cross-reacts with purified rat, rabbit and human intestinal mucins, and specifically labels the mucosal surface and goblet cells of quail intestine by the immunoperoxidase technique. Protein eluted by lactose from an affinity matrix composed of quail intestinal mucin possessed the same molecular mass on SDS/PAGE as intestinal lectin and reacted on Western blots with a lectin-specific antibody. The data clearly demonstrate the co-localization of lectin and mucin in the quail intestine and also the ability of the lectin to specifically interact with the purified mucin, raising the question of the role of endogenous lectins in secretions.

Amino Acids↗
PubMed1993

Growth in and breakdown of purified rabbit small intestinal mucin by Yersinia enterocolitica.

The mucus lining of the gastrointestinal tract serves as a protective barrier over the epithelial surface that must be crossed by invading bacteria seeking entry into the mucosa. The gel-forming component of mucus is mucin, a large polymeric glycoprotein. The present study examined the growth of Yersinia enterocolitica (with and without its virulence plasmid) in purified rabbit small intestinal mucin and the ability of bacteria to degrade mucin. Both virulent and nonvirulent organisms showed enhanced growth in mucin-supplemented media compared with unsupplemented media, but only at 37 degrees C and not at 25 degrees C. The effects of mucin were not specific because medium supplemented with bovine serum albumin also enhanced bacterial growth at 37 degrees C. Purified mucin was broken down into lower-molecular-weight components (assessed by monitoring its elution profile on a Sepharose CL-2B column) by plasmid-bearing Y. enterocolitica but not by plasmid-cured organisms. Culturing virulent Y. enterocolitica at 25 degrees C completely suppressed its capacity to degrade mucin, suggesting that this activity depends on plasmid expression. These results were confirmed in similar studies with purified rabbit colonic mucin. Mucin-degrading activity could be demonstrated in spent culture media from virulent Y. enterocolitica incubated at 37 degrees C but not in bacterial membrane preparations. Changes in the elution profiles of small intestinal and colonic mucins exposed to plasmid-bearing Y. enterocolitica at 37 degrees C were consistent with proteolytic depolymerization. The ability to grow well in mucin may help Y. enterocolitica to colonize the intestine, while the production of a mucin-degrading enzyme(s) by plasmid-bearing organisms may assist pathogenic strains to solubilize and penetrate the mucus gel layer.

Animals↗
PubMed1993

Adhesion of Yersinia enterocolitica to purified rabbit and human intestinal mucin.

Interactions between Yersinia enterocolitica and purified intestinal mucins from rabbit and humans were investigated. Plasmid-bearing virulent organisms (but not plasmid-free nonvirulent bacteria) bound well to both mucins, suggesting that adherence was controlled by the virulence plasmid. Examination of binding to 14 different preparations of purified human intestinal mucin (8 preparations obtained from normal subjects and 6 samples from patients with cystic fibrosis) revealed no differences between normal and cystic fibrotic mucins in ability to serve as a binding substrate for virulent Y. enterocolitica. Analyses of binding curves suggested the presence of a single type of noninteracting receptor for Y. enterocolitica in both rabbit and human mucins with similar (but not necessarily identical) structures. Virulent bacteria bound to polystyrene through hydrophobic interactions that could be disrupted by treating the organisms with tetramethyl urea. In contrast, binding of plasmid-bearing Y. enterocolitica to intestinal mucin was not susceptible to tetramethyl urea and therefore does not appear to involve hydrophobic interactions. Prior incubation of organisms with mucin significantly inhibited binding to polystyrene, suggesting that mucin can mask hydrophobic adhesins on the bacterial surface. Hapten inhibition studies revealed that the monosaccharides galactose and N-acetylgalactosamine and the disaccharide lactose could markedly reduce (but not abolish) bacterial adherence to mucin but other monosaccharides and the RGD peptide had no effect on mucin binding. We conclude that virulent Y. enterocolitica is capable of interacting with the carbohydrate moiety of intestinal mucin. These interactions appear to be plasmid mediated and not hydrophobic.

Animals↗
PubMed1993

Neural mediation of cholera toxin-induced mucin secretion in the rat small intestine.

We examined the role of enteric nerves in cholera toxin (CT)-induced mucin secretion in proximal and distal regions of rat small intestine. Stimulation of intestinal loops with 120 micrograms (1.5 mumol) CT using an in vitro open-loop model resulted in an approximately four-fold increase in luminal mucin content over unstimulated controls in both regions of the gut. Prior treatment of loops with tetrodotoxin had no effect on the amount of mucin released in response to CT. However, permanent destruction of primary sensory afferent nerves by neonatal treatment of rats with capsaicin reduced the mucin response to CT to baseline levels in both regions. In normal animals, atropine resulted in approximately 40% inhibition of mucin secretion in both the proximal and distal small intestine. The atropine-sensitive secretory response appears to be a component of the capsaicin-sensitive response. These results suggest that choleraic mucin secretion is mediated primarily by a capsaicin-sensitive neurogenic pathway involving local activation of sensory nerves, which may then elicit mucin secretion through interaction with cholinergic nerves.

Animals↗
PubMed1992

Mucin and protein release in the rabbit jejunum: effects of bethanechol and vagal nerve stimulation.

The role of the vagus nerve and cholinergic mechanisms in the control of rabbit jejunal mucin and protein release was investigated in vivo. In anesthetized animals, a 10-cm segment of the jejunum was cannulated and perfused with saline. Perfusate was collected and analyzed for mucin (by immunoassay) and protein. Bilateral cervical vagotomy had no effect on basal mucin or protein output, suggesting that the vagus nerve does not exert a tonic control on jejunal macromolecule secretion. Electrical stimulation of the vagi did not alter mucin release, even in the presence of muscarinic cholinergic (scopolamine) or adrenergic (propranolol and phentolamine) blockade. In contrast, protein output increased significantly after vagal stimulation, an effect inhibited by scopolamine. In both vagotomized and vagally intact rabbits, the cholinergic agonist bethanechol (200 micrograms/kg intraperitoneally) induced a scopolamine-sensitive increase in both mucin and protein output. Predominantly serum proteins were released into intestinal perfusates after vagal or cholinergic stimulation. It is concluded that the extrinsic vagus nerve does not regulate rabbit jejunal mucin secretion in vivo and that cholinergic control of intestinal goblet cells is implemented entirely by the intrinsic enteric nervous system. In addition, cholinergic or vagal stimulation increases intestinal vascular and epithelial permeability, resulting in the passage of serum proteins into the lumen, possibly by opening tight junctions and paracellular pathways.

Animals↗
PubMed1991

Effects of hydrogen peroxide, mild trypsin digestion and partial reduction on rat intestinal mucin and its disulphide-bound 118 kDa glycoprotein.

The role of the disulphide-bound 118 kDa glycoprotein of rat intestinal mucin is unknown, although it has been proposed to serve as a 'link' component for the mucin monomers. The present studies investigated release or destruction of the 118 kDa glycoprotein (monitored by gel electrophoresis and Western-blot analysis) during progressive breakdown of the mucin polymer (assessed by Sepharose 2B chromatography). H2O2 gradually destroyed the 118 kDa glycoprotein and dissociated the mucin polymer into components of similar size to the monomers. After 3 h, mucin samples contained almost no 118 kDa glycoprotein or its breakdown products, but 50% of the mucin was still eluted in the void volume of a Sepharose 2B column. Although mild trypsinolysis had little effect on the Sepharose 2B elution profile of the mucin, the 118 kDa glycoprotein was completely cleaved into 54-56 kDa and 60-66 kDa fragments which remained disulphide-bound to the high-molecular-mass mucin. Increasing levels of thiol reduction resulted in progressive loss of disulphide bonds, release of the 118 kDa glycoprotein and depolymerization of the mucin. Although approx. 40% of the mucin in partially reduced samples was recovered in the Sepharose 2B void volume, this material contained no 118 kDa glycoprotein and apparently consisted of disulphide-bound mucin monomers. Thus the 118 kDa glycoprotein may be destroyed by H2O2, extensively cleaved by trypsin or released by reduction without completely dissociating the mucin into monomers. Therefore the 118 kDa glycoprotein may not function as a 'link' component for all of the mucin monomers in the native polymer.

Animals↗
PubMed1991

Intestinal mucin secretion in streptozotocin-diabetic rats: lack of response to cholinergic stimulation and cholera toxin.

In diabetic rats, intestinal mucin secretion is unusually high compared with that in normal rats. These studies demonstrate that mucin synthesis is also increased in the diabetic intestine. alpha- and beta-adrenergic agonists or antagonists did not affect mucin output in either normal or diabetic animals, suggesting that altered release in diabetes was not due to goblet cells responding abnormally to adrenergic agents. The cholinergic agonist bethanechol caused a dose-dependent and atropine-sensitive increase in mucin secretion from the normal intestine but had no effect on mucin release from diabetic tissue. Atropine alone did not reduce mucin secretion from the diabetic intestine to levels found in normal tissue. Cholera toxin caused an approximately fivefold increase in mucin output from normal rats but had no effect on mucin secretion from diabetic animals. Thus, goblet cell responses to cholinergic stimulation and cholera toxin in the diabetic intestine are markedly impaired. However, loss of cholinergic control does not appear to be responsible for altered baseline mucin secretion in diabetes.

Animals↗
PubMed1991

Effects of Yersinia enterocolitica infection on rabbit intestinal and colonic goblet cells and mucin: morphometrics, histochemistry, and biochemistry.

The effects of Yersinia enterocolitica on intestinal goblet cells were investigated in New Zealand white rabbits. Animals infected with Y enterocolitica were compared with weight matched and pair fed controls. Goblet cell hyperplasia developed in the distal small intestine of infected rabbits on day 1, in the mid small intestine on day 3, and in the upper small intestine on day 6. In all regions hyperplasia persisted throughout the 14 day study. The degree of hyperplasia was greater in the distal small intestine than the upper and mid regions. Goblet cells in the proximal colon of infected animals seemed to respond as those in the distal small intestine. Thus goblet cell hyperplasia developed more rapidly and to a greater extent in the ileocaecal region where mucosal injury was most severe. These changes resulted directly from Y enterocolitica infection since goblet cell numbers did not increase in pair fed controls. Histochemically, goblet cell mucins from infected rabbits were unchanged at either six or 14 days. Biochemical analysis, however, established that purified mucins from animals on day 6 after infection were less sialylated (in the small intestine) and more sulphated (in the small intestine and proximal colon). In addition, mucins from the distal small intestine and the proximal colon seemed to contain fewer but longer oligosaccharide chains.

Amino Acids↗
PubMed1991

The ocular effects of hyoscine-n-butylbromide ("Buscopan") in radiological practice.

"Buscopan" (hyoscine-n-butylbromide, HBB) is a smooth muscle relaxant regularly used in radiological and endoscopic procedures. One unwanted effect is temporary impairment of visual accommodation. Near and distance vision were assessed in 100 patients undergoing barium meal and barium enema studies. Visual testing was performed prior to the examination and repeated immediately before leaving the radiology department. Completed data was obtained in 90 patients. Of these, 37 were given a conventional 20 mg intravenous dose of HBB, 37 were given glucagon and 16 received no drug. No patient showed any impairment of distance vision. Minor abnormalities of near vision were observed in five patients. All had been given HBB. They were aged 50 years or less and had been retested 12-21 min after administration of the drug. It is suggested that the degree of visual impairment observed is not sufficient to impair driving ability. Routine questioning concerning history of glaucoma is unlikely to be of value; more appropriate would be a warning to seek urgent medical advice if eye pain or visual loss is experienced.

Barium Sulfate↗