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H Pearson

Publications and source records attributed to H Pearson.

At least 19 recordsLinked to original sources

Determination of the sedimentation constants for total suspended solids and the algal component in a full-scale primary facultative pond operating at high wind velocities under tropical conditions.

This study evaluated the amount, distribution and sedimentation constant of solids in a full-scale primary facultative pond operating mostly under high wind conditions and the contribution made by the algal biomass. Solids deposition rates were measured using sedimentation traps placed in the inlet and outlet zones of the pond. Most sludge accumulation occurred, not surprisingly, in the inlet zone A1 with a sludge volume of 9072.m3 accumulating over an operating time of approximately 3 years. However, sludge deposition within this zone was uneven and affected by wind action. Mean proportionality constant (K) values for solids sedimentation were 3.02 and 5.70 for depths of 50 cm and 100 cm respectively for A1. In contrast in zone A3, (the outlet zone), reduced K values of 1.38 and 3.22 were obtained for depths of 50 cm and 100 cm respectively. The algal sedimentation constant varied from 0.8 d(-1) in zone A1 to 0.02 d(-1) in A3. These data suggest that in this large facultative pond the wind, blowing predominantly from the direction of the outlets towards the pond inlets, had a greater influence on solids deposition than the bulk hydraulic flow and also kept the pond completely mixed for most of the time.

Biomass↗

Two become one.

Explore the source record for details and available documents.

Animals↗

Acute hyperhomocysteinaemia affects pulse pressure but not microvascular vasodilator function.

AIMS: Raised homocysteine (hcy) levels are associated with premature coronary artery disease, but the underlying vascular mechanism and the extent to which hcy affects small vessel vasodilator responses (especially non-nitric oxide mediated pathways) are unclear. METHODS: This double-blind, placebo-controlled crossover study in 14 healthy male subjects evaluated the effects of single-dose oral methionine 15 g (to induce acute hyperhomocysteinaemia) on cutaneous microvascular vasodilator responses to incremental-dose iontophoretic administration of acetylcholine (Ach) and sodium nitroprusside (SNP) using laser Doppler fluximetry (LDF), and the effects on von Willibrand factor (vWF) levels and systemic haemodynamics. RESULTS: Methionine administration produced a three fold rise in plasma hcy levels at 8 h, which was accompanied by a significant increase in pulse pressure (53 vs 49 mmHg, P < 0.05) but no change in heart rate. Acute hyperhomocysteinaemia had no significant effect on incremental microvascular vasodilator dose-response curves to Ach and SNP, or circulating levels of vWF. CONCLUSIONS: The present study shows that acute hyperhomocysteinaemia increases pulse pressure (a marker of large vessel stiffness) but has no effect on endothelial-dependent (non-NO-mediated) microvascular vasodilation.

Acetylcholine↗

Antenatal screening for HPA-1a by flow cytometry.

Pregnant women who attended antenatal clinics at King George V Hospital, the Birth Centre or were referred by obstetricians from February 19 July, 1996 were screened for the platelet antigen HPA-1a by flow cytometry. Forty out of 2,300 (1.7%) were found to be negative for this antigen. Of the 28 women followed throughout their pregnancy, none developed antibody to HPA-1a. Platelet counts performed on samples from 17 babies born to 17 of these mothers were all normal. This study proves the simplicity and rapidity of flow cytometry for platelet antigen screening. The results were comparable with the Solid Phase Red Cell Adherence (SPRCA) method and with PCR. The lack of a plentiful supply of specific antibody and the rarity of fetomaternal alloimmune thrombocytopenia (FMAIT) argue against the introduction of routine screening for maternal HPA-1a status at the present time.

Adolescent↗

A review of pathological diagnoses made from 87 canine splenic biopsies.

The pathological findings in 87 cases of canine splenic abnormality recognised clinically by abdominal palpation or radiography, or at exploratory laparotomy, are presented. The most common diagnosis was of splenic neoplasia (n = 38) and the most frequently recognised canine splenic neoplasm was haemangiosarcoma (17 of 38 cases). Benign splenic enlargement secondary to nodular hyperplasia (n = 6), haematoma (n = 16) or non-specific changes including congestion, haemorrhage, extramedullary haemopoiesis and haemosiderin deposition (n = 14) was also recognised. A diagnosis of non-specific pathology was more frequently recorded when portions of spleen, as opposed to the entire organ, were submitted for assessment. Splenic infarction, with (n = 3) or without (n = 7) torsion, abscessation (n = 2) and focal mast cell proliferation (n = 1) accounted for the remainder of the cases. Clinical follow-up was available for 35 cases and revealed good long-term survival in cases of splenic haematoma or haemangioma, with relatively poor survival with a diagnosis of splenic haemangiosarcoma or anaplastic sarcoma. A range of splenic disorders was recognised in dogs of the labrador breed (16 of 87 cases) and three of 17 cases of haemangiosarcoma occurred in German shepherd dogs. The possible predisposition of dogs of these breeds to splenic disorders is discussed.

Abscess↗

Effect of body position on oesophageal and gastric pressures in the anaesthetised dog.

The effect of body position on lower oesophageal sphincter pressure (LOSP), gastric pressure and barrier pressure (BrP) was investigated in 40 dogs anaesthetised for neutering procedures. The dogs were placed in lateral recumbency followed by dorsal recumbency (group 1) or vice versa (group 2). LOSP decreased significantly in the animals which were positioned initially in lateral recumbency, when they were then placed in dorsal recumbency, while those initially positioned in dorsal recumbency showed no significant change in their LOSP or BrP when their position was altered to lateral recumbency. When the data from both groups were pooled, LOSP and BrP were significantly lower when the dogs were in dorsal compared to lateral recumbency (P < 0.05).

Anesthesia↗

Pertussis toxin treatment increases glutamate release and dihydropyridine binding sites in cultured rat cerebellar granule neurons.

This study was designed to examine the ability of pertussis toxin to block various responses due to (-)-baclofen in cultured cerebellar granule neurons of the rat. Treatment with pertussis toxin for 3 h markedly reduced the ability of (-)-baclofen to stimulate GTPase in membranes, and its ability to inhibit forskolin-stimulated adenylyl cyclase in intact cells, whereas the ability of (-)-baclofen to inhibit glutamate release was not affected at 3 h, but was abolished after 16 and 48 h treatment with pertussis toxin. The amount of ADP-ribosylation of Gi/Go due to pertussis toxin in intact cells correlated well with the former two effects, but not with the prevention of the ability of baclofen to inhibit glutamate release. Pertussis toxin treatment for up to 48 h did not significantly affect the levels of Gs, Gi and Go in membranes from granule neurons determined by immunoblotting. Pertussis toxin treatment for 16 or 48 h but not 3 h increased the total amount of stimulated release of glutamate by about 40% under normal conditions, and by 84% under depolarizing conditions. In parallel experiments it was observed that pertussis toxin treatment for 16 h increased the number of dihydropyridine binding sites by about 90% on intact granule neurons. Whole-cell calcium channel currents, recorded under several conditions in the cells, were not increased in amplitude by pertussis toxin treatment for up to 48 h, although the ability of baclofen to inhibit calcium channel currents was blocked by pertussis toxin. These results indicate that the pertussis toxin-induced increase in glutamate release may be due to an increase in dihydropyridine binding sites, possibly localized to the presynaptic terminals.

Adenosine Diphosphate Ribose↗

Acidified chloroquine treatment for the removal of class I HLA antigens.

With the aim of reducing the damage to platelets while effectively removing class I HLA antigens from their surfaces, we developed a new method using acidified chloroquine diphosphate. Platelets were treated with a 0.2 M solution of chloroquine diphosphate (pH 4.0). More than 90% of the platelets remained viable after treatment. While a marked reduction in reactions of acidified chloroquine-treated platelets with multispecific HLA antisera was noted in comparison with phosphate-buffered-saline-(PBS)-treated platelets, reactions with platelet-specific antibodies were preserved. This was demonstrated by immunofluorescence tests and solid-phase and monoclonal antibody immobilization of platelet antigen assays. Aggregation responses, though reduced in comparison with PBS-treated platelets, were still preserved after acidified chloroquine treatment. Ultrastructural analysis did not show any significant difference from PBS-treated platelets. We conclude that treatment of platelets with acidified chloroquine diphosphate is a simple and effective method for removing class I HLA antigens from their surfaces with minimal damage to their structure and function.

Blood Platelets↗

N-methyl-D-aspartate responses in rat cerebellar granule cells are modified by chronic depolarisation in culture.

Following culture in high (25 mM) K+ conditions cerebellar granule cells only respond with a rise in cytosolic free calcium concentration ([Ca2+]i after removal of external Mg2+. When granule cells are grown in low (5 mM) K+ N-methyl-D-aspartate (NMDA) exerts a neurotrophic effect. We show that at the critical time for this effect NMDA will elicit a rise in [Ca2+]i in 5 mM K+ cultures even in the presence of Mg2+ and that growth in 25 mM K+ induces the rapid appearance of a Mg2+ block of NMDA receptors in granule cells. This suggests firstly, that a rise in [Ca2+]i could be involved in the neurotrophic effect of NMDA and secondly, that the characteristics of the NMDA responses in granule cells are modified as a result of growth under depolarising conditions.

Animals↗

Relationship Between Intracellular Free Calcium Concentration and NMDA-induced Cerebellar Granule Cell Survival In Vitro.

The survival of cerebellar granule cells in culture is stimulated by activation of the N-methyl-d-aspartate (NMDA) class of glutamate receptors. Activation of these receptors at the key period for cell survival in vitro (3 days; 3DIV) resulted in a sustained elevation of intracellular free calcium concentration [Ca2+]i over the same concentration range of NMDA that led to granule cell survival. Agents that release Ca2+ from intracellular stores led to only small, transient elevations of [Ca2+]i and were unable to stimulate granule cell survival. Addition of the Ca2+ ionophore ionomycin to granule cell cultures at 3DIV resulted in increased granule cell number at 7DIV. The ability of ionomycin to stimulate granule cell survival was related to the [Ca2+]i elicited, indicating that a rise in [Ca2+]i is sufficient to activate the processes leading to granule cell survival and that the extent of the elevation in [Ca2+]i is crucially important in determining granule cell fate.

Journal Article↗