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Biomedical subjects

G Hurst

Publications and source records attributed to G Hurst.

At least 19 recordsLinked to original sources
PubMed2005

Voice recognition for radiology reporting: is it good enough?

AIM: To compare the efficiency and accuracy of radiology reports generated by voice recognition (VR) against the traditional tape dictation-transcription (DT) method. MATERIALS AND METHODS: Two hundred and twenty previously reported computed radiography (CR) and cross-sectional imaging (CSI) examinations were separately entered into the Radiology Information System (RIS) using both VR and DT. The times taken and errors found in the reports were compared using univariate analyses based upon the sign-test, and a general linear model constructed to examine the mean differences between the two methods. RESULTS: There were significant reductions (p<0.001) in the mean difference in the reporting times using VR compared with DT for the two reporting methods assessed (CR, +67.4; CSI, +122.1s). There was a significant increase in the mean difference in the actual radiologist times using VR compared with DT in the CSI reports; -14.3s, p=0.037 (more experienced user); -13.7s, p=0.014 (less experienced user). There were significantly more total and major errors when using VR compared with DT for CR reports (-0.25 and -0.26, respectively), and in total errors for CSI (-0.75, p<0.001), but no difference in major errors (-0.16, p=0.168). Although there were significantly more errors with VR in the less experienced group of users (mean difference in total errors -0.90, and major errors -0.40, p<0.001), there was no significant difference in the more experienced (p=0.419 and p=0.814, respectively). CONCLUSIONS: VR is a viable reporting method for experienced users, with a quicker overall report production time (despite an increase in the radiologists' time) and a tendency to more errors for inexperienced users.

England↗
PubMed2001

Risk factors associated with the presence of Sarcocystis neurona sporocysts in opossums (Didelphis virginiana).

Sarcocystis neurona is the most important cause of equine protozoal myeloencephalitis (EPM) in horse in the Americas. The only known definitive host for this parasite in the United States is the opossum (Didelphis virginiana); however, despite the importance of the disease, the epidemiology of the parasite in the definitive host is poorly understood. To begin addressing these data gaps, potential risk factors were evaluated for their association with the presence of sporocysts of S. neurona in opossums live-trapped in March 1999 and November 1999 to May 2000. Sporocysts of S. neurona were found in 19 of the 72 animals examined. Potential risk factors evaluated were locality, trap date, age, gender, the presence of young in the pouch of females, and body condition score. Variables that were associated with the presence of S. neurona sporocysts were used in logistic regression analysis. Of the factors examined, season and body condition score were associated with increased odds of an animal harboring sporocysts.

Age Factors↗
PubMed2001

Prevalence of Sarcocystis neurona sporocysts in opossums (Didelphis virginiana) from rural Mississippi.

Sarcocystis species sporocysts were found in intestinal scrapings from 24 of 72 opossums (Didelphis virginiana) from rural Mississippi. The number of sporocysts in each opossum varied from a few ( < 100000) to 187 million. Sporocysts from 24 opossums were bioassayed for Sarcocystis neurona infections by feeding to gamma-interferon knockout (KO) mice. S. neurona was detected in the brains of KO mice fed sporocysts from 19 opossums by immunohistochemical staining with anti-S. neurona specific polyclonal rabbit serum, and by in vitro culture from the brains of KO mice fed sporocysts. The isolates of S. neurona from opossums were designated SN16-OP to SN34-OP. Merozoites from 17 of 19 isolates tested at the 25/396 locus were identical to previously described S. neurona isolates from horses. The high prevalence of S. neurona sparocysts in D. virginiana suggests that this opossum constitutes an ample reservoir of infection in the southern United States.

Animals↗
PubMed1999

Purification and characterization of a complex from placental syncytiotrophoblast microvillous membranes which inhibits the proliferation of human umbilical vein endothelial cells.

The signs of pre-eclampsia are thought to arise from maternal endothelial dysfunction caused by circulating factors of placental origin. Syncytiotrophoblast microvillous membranes (STBM) cause endothelial disruption and inhibit proliferation in vitro. Significantly increased amounts of STBM can be detected in blood from pre-eclamptic women and could contribute to endothelial dysfunction in vivo. This study purified a complex from STBM which inhibits the proliferation of cultured human endothelial cells. Integral membrane proteins were solubilized with sucrose monolaurate. Anion exchange chromatography yielded two peaks of anti-proliferative activity. Only the second peak was specific to STBM and was subjected to further separation by Sephacryl S-200 gel filtration chromatography (GFC). A single peak of specific activity eluted close to the void volume, at a position unaltered by added denaturing agents, guanidium chloride or urea. On Sephacryl S-300 GFC, two peaks were obtained of 410 and 820 kDa, with similar anti-proliferative activity and protein components (by SDS-polyacrylamide gel electrophoresis). The major protein bands were as integrins alpha5 and alpha v, dipeptidyl peptidase IV, alpha-actinin, transferrin, transferrin receptor, placental alkaline phosphatase and monoamine oxidase A.

Actinin↗
PubMed1999

Supernatants from co-cultured endothelial cells and syncytiotrophoblast microvillous membranes activate peripheral blood leukocytes in vitro.

There is evidence for both endothelial cell and peripheral blood leukocyte (PBL) activation in pre-eclampsia. Syncytiotrophoblast microvillous membranes (STBM) are shed in greater quantities from the placenta in pre-eclampsia, disrupt cultured endothelial cells in vitro and may be the immediate cause of the maternal syndrome. The aim of this study was to determine if endothelial cells co-cultured with STBM release factors that can activate PBL in vitro. Flow cytometry was used to measure changes in intracellular free ionized calcium ([Ca2+]i), pH (pHi) and reactive oxygen species (iROS) as indices of leukocyte activation. PBL from male non-pregnant donors was exposed to supernatants from human umbilical vein endothelial cells (HUVEC) cultured with STBM. The time course of changes in [Ca2+]i, pHi and iROS was determined and compared with appropriate control measurements. The test supernatants caused significant activation of granulocytes and monocytes in terms of increases in [Ca2+]i and falls in pHi and release of iROS. Lymphocytes responded only with respect to increases in iROS. The results define a possible mechanism for the activation of PBL in pre-eclampsia, as being secondary to endothelial cell activation caused by circulating STBM shed in excess amounts from the placenta.

Calcium↗
PubMed1997

Preclinical characterization of MDL 27,192 as a potential broad spectrum anticonvulsant agent with neuroprotective properties.

The compound 5-(4-chlorophenyl)-2,4-dihydro-4-ethyl-3H-1,2,4-triazol-3-one (MDL 27,192) was evaluated in a variety of rodent models to assess its anticonvulsant profile and its potential neuroprotective activity. MDL 27,192 demonstrated anticonvulsant activity in a wide range of epilepsy models that are genetically-based (audiogenic seizures in the seizure susceptible DBA/2J or Frings mouse; spike wave seizures in genetic absence epilepsy rats of Strasbourg (GAERS), electrically-based (MES seizures in mice and rats, corneally-kindled seizures in rats) and chemically-based (bicuculline, PTZ, picrotoxin, 3-mercaptopropionic acid, quinolinic acid and strychnine). When compared to valproate, orally administered MDL 27,192 was 17-48-fold more potent as an anticonvulsant and showed a safety index one to three-fold greater. Following a timed intravenous administration of PTZ to mice, MDL 27,192, but not phenytoin or carbamazepine, consistently increased the latencies to first twitch and clonus. MDL 27,192 was active in a genetic model of absence epilepsy, the GAERS rat model. These data indicate that MDL 27,192 likely exerts its anticonvulsant action by affecting seizure spread and by raising seizure threshold. MDL 27,192 did not display any signs of tolerance following subchronic (15 day) administration. In tests of neuroprotective potential, MDL 27,192 reduced infarct volume in a permanent middle cerebral artery occlusion model of focal cerebral ischemia in rats and reduced the loss of hippocampal dentate hilar neurons in an animal model of unilateral head injury. In summary, MDL 27,192 possesses a broad-spectrum anticonvulsant profile. The potential for reduced tolerance and neuroprotective activity are additional positive features of MDL 27,192's preclinical profile.

Animals↗
PubMed1997

Continuous small-dose tranexamic acid reduces fibrinolysis but not transfusion requirements during orthotopic liver transplantation.

Tranexamic acid (TA) is a synthetic drug that inhibits fibrinolysis. It has been administered to decrease the use of blood products during cardiac surgery and orthotopic liver transplantation when infused in larger doses. A small-dose infusion of aprotinin causes a reduction in fibrinolysis and blood product requirement during orthotopic liver transplantation without apparent risk of intravascular thrombosis. This prospective study was designed to investigate whether a small-dose infusion of TA would be equally effective in reducing fibrinolysis and blood product transfusions during orthotopic liver transplantation. A double-blind, controlled study was undertaken to compare the efficacy of a small-dose TA infusion with that of a placebo. Thirty-two consecutive patients were randomized either to the TA group (n = 16), which received an intravenous infusion of 2 mg x kg(-1) x h(-1), or to the control group (n = 16), which received an identical volume of normal saline. Coagulation values were measured, a field rating was made by the surgeon, and a thromboelastogram was produced at four predetermined intervals throughout the case-before TA infusion was started, after portal vein ligation, 10 min after reperfusion, and at the end of surgery. Intraoperative transfusion requirements were recorded during the procedure and for the first 24 h postoperatively. A record was kept of any intraoperative epsilon-aminocaproic acid administered for uncontrolled fibrinolysis. The thromboelastogram clot lysis index was significant for lysis in the control group during both the anhepatic and the neohepatic phases (P < 0.01 and P < 0.05, respectively) when compared with the TA group. Fibrin degradation products were significantly increased (>20 microg/mL) in the control group at reperfusion (P < 0.03) and at the end of surgery (P < 0.01). D-dimers were also significantly increased (>1 mg/L) in the control group at the end of surgery (P < 0.04). Nine of the 16 control patients versus 3 of the 16 TA patients required epsilon-aminocaproic acid rescue for fibrinolysis. There were no other significant differences between groups. Transfusion requirements during surgery and for the first 24 h postoperatively did not differ significantly between the two groups. We conclude that the use of small-dose TA reduces fibrinolysis but not transfusion requirements during orthotopic liver transplantation.

Aminocaproic Acid↗
PubMed1995

Neural adaptation of imaginary visual motion.

Observers made time-to-contact judgements about an imagined moving object that passed through an area of the visual field previously adapted to a single direction of real motion. The direction of imagined motion varied relative to the direction of adapting motion. When imagined motion was in the same direction as that experienced during adaptation, imagined speed was slowed; when imagined motion was in the opposite direction, its speed was increased; when adaptation and imagined motions were orthogonal, imagined speed was unaffected. The particular influence that prior adaptation has on imagined speed suggests that imagined motion and real vision may engage common neural mechanisms without being functionally equivalent. Negative aftereffects observed in imagined motion imply that the imagination represents movement as an inference from position changes of static images.

Eye Movements↗
PubMed1995

Monitoring interval cancers in breast screening programmes: the east Anglian experience. Quality Assurance Management Group of the East Anglian Breast Screening Programme.

Interval cancer rates are a major determinant of the success of a screening programme. In the Swedish two county study, on which the United Kingdom programme is based, a 39% reduction in mortality was observed in screened women aged 50-64. Using data from the Swedish study, the relationship between interval cancer incidence and the likely future effect on breast cancer mortality was quantified. In East Anglia, as elsewhere in the United Kingdom, interval cancers rates are nearly double those obtained in Sweden: interval cancer rates in the first, second, and third years respectively, after a negative screen were 24%, 59%, and 79% of the expected underlying incidence in the absence of screening. The corresponding figures from the two county study were 17%, 30%, and 56%. From these it was estimated that the mortality reduction in East Anglia will be 21%, which is lower than the 35% observed in invited women in this age group in the Swedish two county study and the 25% specified in the Health of the Nation target. In a rereading exercise, using screening mammograms from women who were screen normal, who had screen detected cancers, or who subsequently developed interval cancers, four out of five radiologists recommended recall for around 70% of the original mammograms (classed as screen normal at time of screening) from 33 interval cancers. This suggests that sensitivity is a contributory factor to the higher interval cancer rates in East Anglia.

Aged↗
PubMed1994

Prolongation of the intravascular retention of hemoglobin modified with a long-chain fatty acid derivative.

To develop hemoglobin (Hb) derivatives with an increased circulatory half-life, Hb was chemically modified with long chain fatty acid analogs. One compound, sodium 1-hexadecyl 6-(2-iodoacetamido)hexyl phosphate, specifically modified the Cys-93 beta residues of human hemoglobin (HbA) as determined by sulfhydryl titration analysis. The resulting modified Hb derivative, FAHbA, was isolated and was shown to have a two-fold longer circulatory half-life than native HbA in a rat low-dose acute transfusion model.

Animals↗
PubMed1988

Serial residual volumes in men with prostatic hypertrophy.

Thirty men with prostatic hypertrophy were scanned on 3 occasions on the day before TURP. Five commonly used formulae to estimate residual urine were used. All of these methods are subject to large degrees of error; 66% of these patients had residual volumes that varied significantly on the same day. We suggest that it is of no clinical value to perform a single residual urine measurement in patients with prostatic hypertrophy.

Aged↗
PubMed1986

Effects on the rabbit carotid body of stimulation by almitrine, natural high altitude, and experimental normobaric hypoxia.

Rabbits were given intraperitoneal injections of almitrine in ascending doses for 5 weeks. They were compared with a control group and with a group of rabbits which had been exposed from birth to the natural hypobaric hypoxia found at Cerro de Pasco (433 m) in the Peruvian Andes. A further group of animals was placed in an experimental normobaric chamber for either 3 or 6 months to subject them to the same degree of hypoxia as that occurring in Cerro. The carotid bodies of the rabbits in all these groups were processed for light and electron microscopy, and examined both qualitatively and quantitatively. The carotid bodies in the group given almitrine showed no changes in their size or in the population of their glomic cells when compared with controls. In contrast, the carotid bodies of Peruvian rabbits were greatly enlarged with a disproportionate increase in the population of the light variant of chief cell. Rabbits from the hypoxic chamber also had enlarged carotid bodies but those killed after 3 months showed an increase in the dark variant of chief cell, whereas after 6 months this cell was reduced in number. There was also intense cytoplasmic vacuolation. Election microscopy confirmed these changes and revealed that dark cells had larger, more pleomorphic granules than the light variant. Vacuolation of the granules in light cells was most pronounced in Peruvian rabbits, but was uncommon in animals exposed to hypoxia for 3 months. We suggest that the dark cell responds to the early stages of hypoxia but later matures into the light variant of chief cell.

Almitrine↗
PubMed1986

The carotid bodies in coarctation of the aorta.

The carotid bodies were found to be enlarged at the necropsy of a 61-year-old man with congenital coarctation of the aorta. The enlargement was found to be due to hyperplasia of the sustentacular (type II) cells and considered to be a response to systemic hypertension. The proliferation of these cells had compressed the small remaining cores of chief (type I) cells which contain catecholamines and peptides. This case is illustrative of the fact that the carotid bodies may enlarge in some forms of congenital heart disease. The histological changes in the glomic tissue in any one type of congenital cardiac anomaly appear to be related to the nature of the underlying physiological disturbance. Thus the raised intravascular pressure in the upper part of the body in coarctation of the aorta appears to lead to hyperplasia of sustentacular cells.

Adult↗
PubMed1986

The carotid bodies in a case of ventricular septal defect.

A woman of 62 years with Turner's syndrome died in congestive cardiac failure secondary to a large ventricular septal defect with biventricular hypertrophy. During her last few months the lifelong left-to-right shunt underwent reversal exposing her carotid bodies to hypoxaemia. The carotid bodies were not enlarged, thus demonstrating that hyperplasia of glomic tissue is not brought about by increased myocardial mass per se. They were, however, abnormally cellular with more dark cells ( a variant of chief cells), many of which were abnormally large and showed ultrastructural features of metabolic activity. These changes may represent the earliest histological response of the carotid body to hypoxaemia and later, the dark cells may mature into the more familiar and common light variant. It seems likely that this dark cell activity precedes, probably by a long period, the sustentacular cell hyperplasia and proliferation of nerve axons which we have reported elsewhere as the chronic reaction of the carotid bodies to hypoxaemia.

Cardiomegaly↗
PubMed1985

Histological changes associated with ageing of the human carotid body.

A qualitative and quantitative histological study was made of the carotid bodies obtained at necropsy from 47 subjects ranging in age from 14 to 100 years. With increasing age there is a loss of more than a third of the amount of glomic tissue with a diminution in the size of the lobules. In young people the basic histological pattern of clusters, composed of cores of chief cells with surrounding rims of sustentacular cells, has commonly superimposed on it prominence of the dark variant of chief cells. In middle-aged subjects there is proliferation of sustentacular cells which appear to merge imperceptibly into fibrosis of the lobules and becomes associated with diffuse or focal infiltrates of lymphocytes.

Adolescent↗