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Biomedical subjects

P Collins

Publications and source records attributed to P Collins.

At least 235 records · Page 13Linked to original sources
PubMed1992

The pathogenesis of atheroma and the rationale for its treatment.

Several theories have been proposed to explain the mechanism causing atheroma; these include endothelial cell injury, smooth muscle cell proliferation, lipid deposition and an abnormality of the vasa vasorum. Based on these hypotheses, new therapies aimed at causing regression or preventing the development of atheroma include heparin, calcium antagonists, beta-receptor antagonists, lipid lowering agents and drugs that manipulate platelets.

Animals↗
PubMed1992

Bath-water compared with oral delivery of 8-methoxypsoralen PUVA therapy for chronic plaque psoriasis.

Forty-four patients with chronic plaque psoriasis were randomly allocated to treatment with bath-water-delivered 8-methoxypsoralen (bath 8-MOP) or oral 8-methoxypsoralen (oral 8-MOP) PUVA therapy. There was a significant reduction in extent of the lesions and psoriasis area and severity index (PASI) after 20 treatments with each modality. There was a fourfold reduction in cumulative ultraviolet A (UVA) dose in the bath group. Side-effects of erythema and nausea were less with bath therapy.

Administration, Oral↗
PubMed1992

Psoriasis, psoriatic arthritis and the possible association with Sjögren's syndrome.

Thirty patients with psoriatic arthropathy (PA) were age- and sex-matched with patients with plaque psoriasis alone to investigate a possible link between Sjögren's syndrome (SS) and PA. The results of clinical examination, Schirmer's test, maximal stimulated salivary flow rate, haematological and serological investigations were compared in the two groups. Median maximal stimulated salivary flow rate was significantly reduced in patients with PA suggesting that salivary glands are affected in this condition. One patient with PA had SS.

Adult↗
PubMed1992

The efficacy of methotrexate in psoriasis--a review of 40 cases.

Forty patients with psoriasis treated with methotrexate (MTX) are reviewed. MTX was particularly effective in controlling erythrodermic and generalized pustular psoriasis. The treatment was discontinued in seven patients due to nausea in two and because of abnormal laboratory tests in five. Two patients developed toxic epidermal necrolysis (TEN) and died. Patients under 60 years of age had a liver biopsy before treatment and repeat biopsy after each cumulative MTX dose of 1500 mg. We consider that MTX is the drug of choice for treating difficult psoriasis.

Adult↗
PubMed1992

Hydroxyethyl starch induced acquired von Willebrand's disease.

Hydroxyethyl starch (HES) (Hespan, DuPont) is a widely used synthetic volume expander which in standard doses of up to 1.5l in 24 h has no significant effect on coagulation (Munsch et al. 1988). However, the data sheet states that in large volumes HES may alter the coagulation mechanism. We now report a case of HES induced acquired von Willebrand's disease (vWD) in which severe bleeding occurred.

Adult↗
PubMed1992

Subependymal cells provide a faster response to ependymal injury than astrocytes in the hydrocephalic brain.

Obstructive hydrocephalus was induced in 12-day-old rats by the infusion of kaolin into the cisterna magna. After 7 days, cortical and ependymal lesions were made with thin wire in non-hydrocephalic brains and in hydrocephalic brains. The wounds were allowed to heal for times ranging from 1 day to 10 days post-lesion, after which the animals were perfused and the brains prepared for histology. Paraffin sections of brain containing the ependymal wound were reacted for glial fibrillary acidic protein by the avidin biotin complex technique. Subependymal cells were associated with the ependymal defect from 1 day in both non-hydrocephalic and in hydrocephalic brains. Reactive astrocytes were identified in hydrocephalic wounded brains on day 3. It was not until day 6 that astrocytes and astrocytic processes were seen in association with the subependymal cells at the wound edge, and astrocytic processes were noted along the needle track in the cortex. The results suggest that the extremely rapid response of subependymal cells to ependymal injury is a mechanism distinct from the astrocytes response for repair in the brain.

Animals↗
PubMed1992

Effect of 17 beta-oestradiol on contraction, Ca2+ current and intracellular free Ca2+ in guinea-pig isolated cardiac myocytes.

1. The effect of 17 beta-oestradiol on cardiac cell contraction, inward Ca2+ current and intracellular free Ca2+ ([free Ca2+]i) was investigated in guinea-pig single, isolated ventricular myocytes. The changes of cell length were measured by use of a photodiode array, the voltage-clamp experiments were performed with a switch clamp system and [free Ca2+]i was measured with the Ca2+ indicator, Fura-2. 2. 17 beta-Oestradiol (10, 30 microM) caused a decrease in cell shortening at both 22 and 35 degrees C. This negative inotropic effect was accompanied by a decrease in action potential duration mainly brought about by a shortening of the plateau region of the action potential. 17 beta-Oestradiol (10, 30 microM) induced a similar decrease in cell shortening in voltage-clamped and current-clamped cells. 3. In Fura-2 loaded cells, 17 beta-oestradiol (10 and 30 microM) decreased systolic Fura-2 fluorescence to 72 +/- 7% and 47 +/- 4% (n = 6, P less than 0.001) of control respectively. 17 beta-Oestradiol (10 microM) had no significant effect on diastolic Fura-2 fluorescence, but at higher concentration (30 microM) induced a slight decrease in resting Fura-2 fluorescence. The effect of 17 beta-oestradiol was reversible after 1-2 min of washout of the steroid. 4. 17 beta-Oestradiol (10 and 30 microM) decreased the peak inward Ca2+ current (ICa), which was sensitive to [Ca2+]o, dihydropyridines and isoprenaline, to 59 +/- 3% and 39 +/- 5% (n = 7 approximately 9, P less than 0.01) respectively, without producing any significant change in the shape of the current-voltage relationship.5. The recovery time of ICa from inactivation was delayed by 17beta-oestradiol (10microM). The inhibitory effect of 17beta-oestradiol on ICa was less at a holding potential of -80 mV than at -40 mV.6. We conclude that 17beta-oestradiol has a negative inotropic effect on guinea-pig single ventricular myocytes by inhibiting ICa and so reducing systolic [Ca2+]i. 17beta-Oestradiol may therefore have a Ca2+ channel blocking property in guinea-pig isolated ventricular myocytes.

Action Potentials↗
PubMed1992

An association between hypocholesterolaemia and colorectal carcinoma in an Irish population.

A group of 114 Irish patients with primary adenocarcinoma of the large bowel had significantly lower serum cholesterol concentrations than an age and sex matched group drawn from the general population. The hypocholesterolaemiac trait was manifest in male and female patients. Rigorous control procedures established that it was neither an artefact of nutritional compromise nor of preoperative bowel preparatory protocols. The data suggested that the appreciable hypocholesterolaemia observed was not influenced by the pathological stage or degree of differentiation of the tumour.

Adenocarcinoma↗
PubMed1992

Acute effect of 17 beta-estradiol on rabbit coronary artery contractile responses to endothelin-1.

We assessed the acute effect of 17 beta-estradiol on coronary artery constrictor responses to endothelin-1. 17 beta-Estradiol significantly shifted endothelin-1, calcium, or BAY K 8644 concentration-dependent contraction curves to the right in endothelium-denuded coronary arteries isolated from nonpregnant female rabbits. The -log 50% effective dose (ED50) of calcium in high KCl medium (100 mM) was 3.8 +/- 0.11 in control and 3.2 +/- 0.1 and 2.8 +/- 0.12 after incubation with 17 beta-estradiol (1 and 10 microM, respectively). The -log ED50 of BAY K 8644 (KCl 15 mM) was 7.8 +/- 0.1 in control and 7.4 +/- 0.08 and 7.2 +/- 0.05 in the presence of 17 beta-estradiol (1 and 10 microM, respectively). The -log ED50 of endothelin-1 was 9.2 +/- 0.08 in control and 8.8 +/- 0.1, 8.4 +/- 0.07, and 8.1 +/- 0.12 after incubation with 17 beta-estradiol (3, 10, and 30 microM, respectively). Similar results were obtained from coronary arteries of male rabbits. These increases of -log ED50 values were significant (P less than 0.05 or 0.01). 17 beta-Estradiol and verapamil induced dose-dependent relaxation in both endothelium-intact or -denuded coronary arteries submaximally precontracted by endothelin-1. NG-monomethyl-L-arginine had no effect on relaxation induced by 17 beta-estradiol, whereas it eliminated relaxation induced by acetylcholine in rings with an intact endothelium. These data suggest that 17 beta-estradiol attenuates the rabbit coronary artery contraction induced by endothelin-1 via an endothelium-independent mechanism, possibly by affecting calcium influx.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Hypercholesterolaemia: simvastatin and pravastatin alter cholesterol metabolism by different mechanisms.

The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin, reduced low-density-lipoprotein (LDL) cholesterol in hypercholesterolaemic patients by 40% (P less than 0.001). The reduction in LDL cholesterol was accompanied by a significant decrease in the esterified/free cholesterol ratio of the patients' LDL from 2.51 +/- 0.13 to 2.06 +/- 0.14 (P less than 0.01). This change led to a significant increase (P less than 0.05) in the capacity of the LDL to suppress [14C]acetate incorporation into cholesterol in mononuclear leucocytes. Furthermore, [14C]acetate incorporation into the patients mononuclear leucocytes was significantly lower (P less than 0.02) following drug treatment (117 +/- 22 vs. 162 +/- 29 nmol/mg cell protein). Comparison of simvastatin with another HMG-CoA reductase inhibitor pravastatin, showed similar reduction in LDL cholesterol. Pravastatin treatment however, did not result in a reduction in the LDL esterified/free cholesterol ratio or in the changes in cellular cholesterol synthesis and its regulation by LDL which accompanied simvastatin treatment. The activity of the enzyme acyl-coenzyme A: cholesterol acyltransferase (ACAT) in patients' mononuclear cells remained unchanged after treatment with either drug. Results of the study show that while the drugs are equally effective in lowering LDL cholesterol, simvastatin has additional compositional effects on LDL which increase its capacity to regulate mononuclear leucocyte cholesterologenesis.

Adult↗
PubMed1991

Migration patterns of donor astrocytes after reciprocal striatum-cerebellum transplantation into newborn hosts.

Fragments of striatum or cerebellum from E 25 rabbit embryo were implanted into either the striatum or the mesencephalon of newborn mice. Implanted rabbit astrocytes were selectively identified by monoclonal antibodies to the GFAP which are unable to combine with mouse GFAP. Previous investigations had shown that xenogenic astrocytes have the capacity to migrate in host CNS. The purpose of this study was to compare the patterns of migration of transplant-derived astroglial cells according to the topographic origin of the transplant and location of the grafting site. We found that the migration pattern of the grafted cells from any of both selected sites of implantation was independent from the topographic origin of the transplant. The routes as well as the distances of migration were similar after homo- or heterotopic transplantation. We conclude that astroglial cells or their precursors do not express information which would direct them to move specifically toward a defined region in the host brain according to the region of origin in the donor.

Animals↗
PubMed1991

Host response during successful engraftment of fetal xenogenic astrocytes: predominance of microglia and macrophages.

Grafting of fetal rabbit brain fragments into the brains of newborn mice results in the successful establishment and migration of xenogenic astrocytes in the majority of recipients. This can be demonstrated by the use of Tp-GFAP1 monoclonal antibody which binds with rabbit, but not with murine glial fibrillary acidic protein. In the first phase, donor astrocytes are found in more than 80% of recipients 3 and 4 weeks after grafting. In the second phase, there is a decline and disappearance of donor astrocytes by the tenth week. We have recently demonstrated that the decline and disappearance of donor astrocytes was co-incident with infiltration of T cells into the brain, compatible with T-cell-mediated graft rejection. In the present studies, we wished to characterize the types of host cells responding during the period of graft success, in the first 4 weeks after transplantation. It was found that responses by microglia, macrophages, and astrocytes occurred promptly and were sustained throughout this period. Host responses occurred at the graft site and at sites of migration. Examination of sham transplanted control mice revealed responses by the same types of cells. No expression of donor Ia antigen was observed, and the expression of Ia antigen by the host was variable and of low magnitude. T cells were rarely present in transplanted brains during this period. Taken together with previous findings, the present studies demonstrate a clear difference in the host response in the brain at the time when xenogenic astrocytes migrate and survive compared to the period when they disappear.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Drugs acting at D-1 and D-2 dopamine receptors induce identical purposeless chewing in rats which can be differentiated by cholinergic manipulation.

Purposeless chewing in rats was dose dependently increased by acute administration of the dopamine D-1 receptor agonist SKF 38393 (5-20 mg/kg), the D-2 receptor antagonist sulpiride (10-100 mg/kg) and the D-2 receptor agonist quinpirole (0.05-0.25 mg/kg). Only high doses of the D-1 receptor antagonist SCH 23390 (1 and 5 mg/kg) induced purposeless chewing. SCH 23390 (0.05 mg/kg) blocked SKF 38393 (20 mg/kg)-induced purposeless chewing, but had no effect on the purposeless chewing induced by sulpiride (100 mg/kg) or quinpirole (0.1 mg/kg). A dose of SKF 38393 (5 mg/kg) which did not itself induce chewing, potentiated the increase in purposeless chewing observed after administration of sulpiride (100 mg/kg). Administration of SKF 38393 (20 mg/kg) and quinpirole (0.1 mg/kg) did not induce purposeless chewing but stereotyped licking was observed. Administration of sulpiride (100 mg/kg) with quinpirole (0.1 mg/kg) produced an incidence of purposeless chewing not different from that observed when either compound was administered alone. Acute administration of the cholinergic agonist pilocarpine (0.5-4.0 mg/kg) or the cholinesterase inhibitor physostigmine (0.05-0.2 mg/kg) increased the frequency of purposeless chewing in rats. Co-administration of pilocarpine (0.5 mg/kg) with sulpiride (100 mg/kg) increased the frequency of purposeless chewing above that seen when either compound was administered alone. Co-administration of pilocarpine (0.5 mg/kg) with SKF 38393 (20 mg/kg) increased the frequency of purposeless chewing in an additive manner. Co-administration of physostigmine (0.1 mg/kg) with sulpiride (100 mg/kg) but not SKF 38393 (20 mg/kg), increased the frequency of purposeless chewing above that observed when either compound was administered alone. Quinpirole (0.1 mg/kg)-induced purposeless chewing was not affected by co-administration with either pilocarpine (0.5 mg/kg) or physostigmine (0.1 mg/kg). The anticholinergic agent scopolamine (0.1 mg/kg) blocked the purposeless chewing induced by either SKF 38393 (20 mg/kg) or sulpiride (100 mg/kg), but had no effect on the purposeless chewing induced by quinpirole (0.1 mg/kg). Contrary to previous reports, acute manipulation of D-1 or D-2 receptor function can both enhance purposeless chewing behaviour in rats.(ABSTRACT TRUNCATED AT 400 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1991

Oral vaccination of calves against experimental salmonellosis using a double aro mutant of Salmonella typhimurium.

An attenuated derivative of the fully calf virulent Salmonella typhimurium strain ST4/74 was constructed by introducing stable mutations into genes aroA and aroD rendering the strain dependent for growth on aromatic compounds. The strain (BRD562) was used to vaccinate orally ten Friesian calves 7 days after birth with approximately 10(10) live organisms. The only effects of vaccination in the calves was a transient faecal excretion of the organism, mild transient diarrhoea and mild pyrexia in one animal. Two of these animals were tested for the presence of BRD562 at necropsy 56 days after birth but none were shown to be infected. Eight of the vaccinated calves were subjected to an oral challenge infection with ST4/74 28 days after vaccination and seven out of the eight animals survived. The only effect of challenge in the surviving calves was mild pyrexia and transient excretion of ST4/74 in their faeces; only one of the seven animals was found to be infected at necropsy 28 days after challenge. The eighth challenged calf scoured severely and was killed in extremis 7 days after challenge. Four unvaccinated control calves infected orally with ST4/74 28 days after birth all scoured severely and were euthanased for humane reasons 5-7 days later. This study suggests that vaccination with an attenuated strain of S. typhimurium harbouring mutations in two aro genes is a safe and effective way of protecting young calves against experimental S. typhimurium infection.

Administration, Oral↗