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Biomedical subjects

K Morris

Publications and source records attributed to K Morris.

At least 127 records · Page 7Linked to original sources
PubMed1998

Short normal children and environmental disadvantage: a longitudinal study of growth and cognitive development from 4 to 11 years.

The aim of this investigation was to follow up a sample of exceptionally short but medically healthy children, and a normal comparison group, previously studied at 4 years of age. They lived in an inner-city area which was, on objective criteria, seriously disadvantaged in socioeconomic terms. When first seen at 4 years, cases were significantly impaired in cognitive abilities relative to comparisons, although firstborns were much less severely affected. Of the original 46 cases, 45 were assessed again at 11 years. Most continued to live in the same geographical area. Case children remained exceptionally short, even when parental stature was taken into account, although a degree of catch-up had occurred. One third had special educational needs, and a similar proportion had been referred for speech therapy. Verbal and nonverbal cognitive skills of both case and comparison children had, on the whole, changed little and group differences persisted. In conclusion, short normal children from socioeconomically disadvantaged backgrounds are at high risk of educational failure at elementary school.

Analysis of Variance↗
PubMed1997

Influence of filtration on platelet transfusion reactions. Northern Ireland Haematology Audit Group [corrected].

In a retrospective analysis two methods for preventing platelet transfusion reactions are compared. The first group of patients received platelets filtered in the hospital blood bank and were subsequently given filtered and washed platelets if they developed reactions. The second group received platelets filtered at the bedside. In the group receiving platelets filtered in the hospital blood bank there was a very low rate of reaction (2/101 = 2%) and no patients receiving filtered and washed platelets (0/91) developed a reaction. In the group receiving platelets filtered at the bedside there was a reaction rate of 19/95 (20%). Further, two of these reactions were categorised as very severe, the patients showing hypotensive collapse. We conclude that filtering platelets in the hospital blood bank is significantly more effective than bedside filtration in preventing platelet transfusion reactions.

Adult↗
PubMed1997

Upregulation of aquaporin-2 water channel expression in chronic heart failure rat.

Aquaporin-2 (AQP2) mediates vasopressin-regulated collecting duct water permeability. Chronic heart failure (CHF) is characterized by abnormal renal water retention. We hypothetized that upregulation of aquaporin-2 water channel could account for the water retention in CHF. Male rats underwent either a left coronary artery ligation, a model of CHF, or were sham operated. 31-33 d after surgery, mean arterial pressure (MAP) and cardiac output were measured in conscious animals, and the animals were killed 24 h later. Cardiac output (CO) and plasma osmolality were significantly decreased and plasma vasopressin increased in the CHF as compared to the sham-operated rats. Both mRNA and protein AQP2 were significantly increased in the kidneys of the CHF rats. The effect of oral administration of a nonpeptide V2 vasopressin receptor antagonist, OPC 31260, was therefore investigated. OPC 31260 induced a significant increase in diuresis, decrease in urinary osmolality, and rise in plasma osmolality in the OPC 31260-treated CHF rats as compared to untreated CHF rats. The mRNA and protein AQP2 were significantly diminished in both cortex and inner medulla of the treated CHF rats. In conclusion, an early upregulation of AQP2 is present in CHF rats and this upregulation is inhibited by the administration of a V2 receptor antagonist. The results indicate a major role for vasopressin in the upregulation of AQP2 water channels and water retention in experimental CHF in the rat.

Animals↗
PubMed1997

Completed hepatitis C lookback in Northern Ireland.

Hepatitis C virus screening of blood donors was introduced in September 1991 using a second-generation enzyme-linked immunoassay (ELISA) and subsequent confirmatory testing with immunoblot (RIBA) and polymerase chain reaction (PCR). In April 1995 a lookback exercise was announced by the Department of Health, the purpose of which was to trace, counsel, investigate and, if necessary, treat individuals who may have been infected with HCV through blood and blood products prior to screening. A total of 231,321 donations have been screened, of which 553 were found to be reactive. Subsequent confirmatory tests identified 24 HCV-positive donors; 13 were repeat donors who had given a total of 164 units. Ninety-three units were traced and 117 components were identified as having been issued to hospitals. Twenty-five recipients requiring follow-up were identified, of which three were assessed by their GPs as not requiring counselling. Of 22 recipients of potentially infectious units 12 showed no evidence of exposure to HCV. We discuss these results in detail.

Blood Banks↗
PubMed1997

Gastroprotection in neurosurgery: the practice in Great Britain.

The indications for gastroprotection concurrent with corticosteroid use or as prophylaxis for stress ulceration in the neurosurgical intensive care unit remain unclear. The purpose of this study was to determine to what extent gastroprotection is practised in neurosurgical units in the British Isles. Data were obtained by questionnaire circulated at the end of 1988 and 1994. Of 92 surgeons who replied in 1988, 49 routinely used a gastroprotective agent with corticosteroids and 47 in patients at risk of stress ulceration. This compares with 63 out of 89 surgeons using a gastroprotective agent with steroid administration and 60 using prophylaxis for stress ulceration in 1994. The gastroprotective agent of choice in 1988 was an H2 antagonist (76) followed by antacids (36). In 1994, it was again an H2 antagonist (69), but sucralfate (15) was now the second most common agent used. The number of reported peptic ulcer complications among those surgeons who did not routinely use gastroprotective agents was no higher than those who did. Our findings indicate an increase in the administration of gastroprotective agents within neurosurgery. However, the use of H2 antagonists in the intensive care unit and the use of gastroprotective agents with corticosteroids may not be warranted.

Adrenal Cortex Hormones↗
PubMed1997

Hippocampal atrophy is not a major determinant of regional hypometabolism in temporal lobe epilepsy.

PURPOSE: The pathophysiologic basis for the [18F]fluorodeoxyglucose positron-emission tomography (FDG-PET) temporal lobe hypometabolism in patients with hippocampal sclerosis (HS) is uncertain. We tested the hypothesis that hippocampal atrophy, which is strongly correlated with hippocampal cell loss, is largely responsible for the regional hypometabolism in HS. METHODS: Regions of interest (ROIs) on FDG-PET scanning were determined in the medial, lateral, and posterior temporal lobe, thalamus, and basal ganglia. A right/left asymmetry index for each ROI was calculated. These results were correlated with hippocampal magnetic resonance imaging (MRI) volume ratios. RESULTS: There was no correlation between the magnitudes of the FDG-PET asymmetry index and the MRI volume ratio for the mesial or lateral temporal regions (r = -0.09, r = -0.04). When the right/left asymmetry index was compared with the right/left hippocampal volume ratio, correlations for the mesial temporal ROI (r = 0.79, p < 0.0001) and lateral temporal ROI (r = 0.57, p < 0.0005) were found. These, however, simply indicated that both tests accurately reflect the side of the epileptogenic region. The concordance of the side of relative hypometabolism of the FDG-PET with the side of the hippocampal atrophy was higher for the mesial temporal region (100%) than for the lateral (77.5%). CONCLUSIONS: The lack of correlation between the magnitudes of the ratios argues against hippocampal atrophy and cell loss having a central role in the FDG-PET temporal hypometabolism.

Adult↗
PubMed1997

Dietary modulation of phase 1 and phase 2 activities with benzo(a)pyrene and related compounds in the intestine but not the liver of the channel catfish, Ictalurus punctatus.

These studies demonstrated that intestinal mucosa of the channel catfish contained activities comparable with liver for several phase 2 xenobiotic-metabolizing enzymes, and showed that CYP1A-dependent monooxygenase activities were inducible in intestine but not liver by dietary exposure to low concentrations of the Ah agonist, beta-naphthoflavone (BNF). The diets administered were laboratory-prepared, semisynthetic pellets of known composition, commercial chow, or chow supplemented with BNF at 10 or 100 mg BNF/kg chow. Very low intestinal benzo(a)pyrene hydroxylase [aryl hydrocarbon hydroxylase (AHH)] and ethoxyresorufin O-deethylase (EROD) activities were found in catfish fed the semisynthetic diet. Intestinal EROD and AHH activities were elevated by the commercial chow diet and further induced by supplementation with 10, but not 100, mg BNF/kg diet. In vitro studies showed that catfish EROD and AHH activities were sensitive to inhibition by BNF, with mean IC50 values of 0.078 and 2.2 microM, respectively. Thus, residues of BNF retained in intestinal mucosa may have masked monooxygenase induction in catfish fed the 100 mg BNF/kg diet. Microsomal UDP-glucuronosyltransferase and cytosolic PAPS-sulfotransferase activities with 3-hydroxybenzo(a)pyrene as substrate were largely unaffected by the diets studied, and intestinal activities were similar to hepatic activities. Glutathione S-transferase activity was slightly induced in intestinal, but not hepatic cytosol of catfish treated with BNF at the 10 mg/kg diet level relative to chow controls. Epoxide hydrolase activity with styrene oxide as substrate was not affected by diet in intestinal microsomes.

Animals↗
PubMed1996

Inhibition of cyclic 3'-5'-guanosine monophosphate-specific phosphodiesterase selectively vasodilates the pulmonary circulation in chronically hypoxic rats.

While it is known that nitric oxide (NO) is an important modulator of tone in the hypertensive pulmonary circulation, the roles of cyclic 3'-5'-guanosine monophosphate (cGMP) and cGMP-phosphodiesterase (PDE) are uncertain. We found that isolated lung perfusate levels of cGMP were over ninefold elevated in hypertensive vs. normotensive control rats. 98-100% of lung cGMP hydrolytic activity was cGMP-specific PDE5, with no significant decrease in PDE activity in hypertensive lungs, suggesting that the elevation in cGMP was due to accelerated production rather than reduced degradation. In pulmonary hypertensive rat lungs, in vitro, cGMP-PDE inhibition by E4021[1-(6-chloro-4-(3,4-methylbenzyl) amino-quinazolin-2-yl)piperdine-4-carboxylate], increased perfusate cGMP threefold, reduced hypoxic vasoconstriction by 58 +/- 2%, and reduced baseline pulmonary artery pressure by 37 +/- 5%. In conscious, pulmonary hypertensive rats, intravenous administration of E4021 reduced hypoxic vasoconstriction by 68 +/- 8%, pulmonary artery pressure by 12.6 +/- 3.7% and total pulmonary resistance by 13.1 +/- 6.4%, with no significant effect on cardiac output, systemic pressure, and resistance. Comparison of E4021 to inhaled nitric oxide demonstrated that cGMP-PDE inhibition was as selective and as effective as inhaled NO.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1996

Comparison of vascular nitric oxide production and systemic hemodynamics in cirrhosis versus prehepatic portal hypertension in rats.

Nitric oxide (NO) is postulated to play a role in the pathogenesis of arterial vasodilation in chronic portal hypertension. This present study investigates the relationship between systemic hemodynamics and the vascular production of NO, as estimated by measuring cyclic guanosine monophosphate (cGMP) in aortic tissue in two models of chronic portal hypertension in the rat: the partial portal vein ligation (PVL) model and CCl4-induced cirrhosis. NOS was also examined by Western blotting in aortic and mesenteric vessels. Sham-operated rats and rats given phenobarbital were used as controls. PVL rats and rats with cirrhosis and ascites showed a typical pattern of a hyperdynamic circulatory state, when compared with their respective controls: mean arterial pressure; PVL: 113 +/- 2 versus 124 +/- 2, P < .01 and cirrhotics: 103 +/- 5 versus 130 +/- 4 mm Hg, P < .01. Cardiac index; PVL: 32 +/- 2 versus 26 +/- 1, P < .01 and cirrhotics: 51 +/- 3 versus 30 +/- 1 mL . min-1 . 100 gm-1, P < .0001. Systemic vascular resistance; PVL: 3.7 +/- 0.1 versus 4.9 +/- 0.2, P < .01 and cirrhotics: 2.1 +/- 0.2 versus 4.4 +/- 0.2 mm Hg . min-1 100 g-1, P < .0001. Aortic cGMP was markedly increased in cirrhotic rats with ascites (728 +/- 83 fmol/ mg protein) as compared with phenobarbital-treated controls (244 +/- 31 fmol/mg, P < .001). This increase was abolished by chronic administration of N(omega)-nitro-L-arginine methyl ester. By contrast, PVL rats had an aortic cGMP concentration similar to sham-operated controls (282 +/- 16 fmol/mg vs. 274 +/- 33 fmol/mg, P = not significant) and significantly lower than that found in cirrhotic rats with ascites. Expression of cirrhotic aortic endothelial nitric oxide synthase (eNOS) was increased but PVL aortic eNOS did not differ from that of controls, whereas the mesenteric eNOS was increased in both PVL and cirrhotic rats as compared with the controls. These results suggest that vascular NO production is higher in cirrhotic rats than in PVL rats. This increased production may contribute to the more marked abnormalities in systemic hemodynamics seen in experimental cirrhosis as compared with PVL.

Animals↗