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Biomedical subjects

M Staunton

Publications and source records attributed to M Staunton.

13 recordsLinked to original sources
PubMed2005

All radial scars/complex sclerosing lesions seen on breast screening mammograms should be excised.

AIM: To determine the incidence of pre-malignant and malignant conditions in radial scars identified from screening mammograms in women taking part in the UK NHS breast cancer screening programme. METHODS: All women in our screening population from 1988 to 2002 with a radiological diagnosis of radial scar or complex sclerosing lesion confirmed on subsequent histopathology were included in this study. Patients were investigated with fine needle aspiration cytology then localisation biopsy (n=46) or straight to localisation biopsy (n=78). Patients where divided into two groups, one with pure RS/CSL with no associated epithelial features and the second with associated ADH, DCIS or invasive cancer. RESULTS: One hundred and twenty-four lesions were confirmed histologically as radial scar or complex sclerosing lesions. The median age was 58 years. Of the 124 patients, 82 were pure RS/CSL. Forty-two had associated epithelial lesions, 22 patients had ADH and 20 patients had either in situ or invasive carcinoma. Where FNA was performed (n=46), mammograms had shown three lesions suspicious of cancer, which were not proven histologically. Mammograms picked up five malignancies out of the nine RS/CSL with associated cancers. Of these, FNA confirmed malignancy in only two patients. Where FNA was not done (n=78), mammogram had read five pure RS/CSL as cancers. It picked up only four cancers in RS lesions with DCIS/Ca out of 11. CONCLUSION: All screen-detected stellate lesions should be excised due to their association with pre-malignant and malignant conditions.

Breast Neoplasms↗
PubMed2004

Alveolar and plasma concentrations of interleukin-8 and vascular endothelial growth factor following oesophagectomy.

The acute respiratory distress syndrome occurs in approximately 10% of all patients undergoing elective oesophagectomy. Local increases in lung pro-inflammatory cytokines have been previously detected in high-risk patients before the development of the acute respiratory distress syndrome. We hypothesised that similar changes would occur following oesophagectomy. Two groups of patients were studied. In the collapsed lung group (n = 11), interelukin-8 and vascular endothelial growth factor were measured in bronchoalveolar lavage samples obtained from the intra-operative collapsed lung after operation. In the ventilated lung group (n = 10), bronchoalveolar lavage was performed after operation from the ventilated lung and cytokines measured. Cytokines were also measured in peripheral blood samples before and after operation. Bronchoalveolar lavage cytokine levels in both lungs were of an order of magnitude greater than in peripheral blood. Pulmonary pro-inflammatory cytokine release occurs following oesophageal surgery and may indicate subclinical lung injury.

Aged↗
PubMed2000

Neuronal nitric oxide synthase mediates halothane-induced cerebral microvascular dilation.

BACKGROUND: The causes of volatile anesthetic-induced cerebral vasodilation include direct effects on smooth muscle and indirect effects via changes in metabolic rate and release of mediators from vascular endothelium and brain parenchyma. The role of nitric oxide and the relative importance of neuronal and endothelial nitric oxide synthase (nNOS and eNOS, respectively) are unclear. METHODS: Rat brain slices were superfused with oxygenated artificial cerebrospinal fluid. Hippocampal arteriolar diameters were measured using computerized videomicrometry. Vessels were preconstricted with prostaglandin F2alpha (PGF2alpha; halothane group) or pretreated with 7-nitroindazole sodium (7-NINA, specific nNOS inhibitor, 7-NINA + halothane group) or N-nitro-L-arginine methylester (L-NAME; nonselective NOS inhibitor, L-NAME + halothane group) and subsequently given PGF2alpha to achieve the same total preconstriction as in the halothane group. Increasing concentrations of halothane were administered and vasodilation was calculated as a percentage of preconstriction. RESULTS: Halothane caused significant, dose-dependent dilation of hippocampal microvessels (halothane group). Inhibition of nNOS by 7-NINA or nNOS + eNOS by L-NAME similarly attenuated halothane-induced dilation at 0.6, 1.6, and 2.6% halothane. The dilation (mean +/- SEM) at 1.6% halothane was 104 +/- 10%, 65 +/- 6%, and 51 +/- 9% in the halothane, 7-NINA + halothane and L-NAME + halothane groups, respectively. The specificity of 7-NINA was confirmed by showing that acetylcholine-induced dilation was not inhibited by 7-NINA but was converted to constriction by L-NAME. CONCLUSIONS: At clinically relevant concentrations, halothane potently dilates intracerebral arterioles. This dilation is mediated, in part, by neuronally derived nitric oxide. Endothelial NOS does not play a major role in halothane-induced dilation of hippocampal microvessels.

Analysis of Variance↗
PubMed1999

Dexmedetomidine modulates cardiovascular responses to stimulation of central nervous system pressor sites.

UNLABELLED: Halothane attenuates the alterations in arterial pressure (BP) and heart rate (HR) produced by central nervous svstem (CNS) stimulation. We examined the effects of the alpha2-adrenergic agonist dexmedetomidine, with and without halothane, on cardiovascular regulation during CNS pressor site stimulation in chronically instrumented cats. Stimuli trains via bipolar stimulating electrodes in the hypothalamus and reticular formation elicited pressor responses. Dexmedetomidine-induced (15 microg/kg PO) bradycardia was greater in the presence of halothane. CNS stimulation increased BP and HR, which were dose-dependently attenuated by halothane (hypothalamic stimulation 71 +/- 9 mm Hg at control, 25 +/- 5 and 15 +/- 3 mm Hg at 1.0% and 1.5% halothane, respectively). Although dexmedetomidine alone did not alter pressor responses, halothane plus dexmedetomidine attenuated pressor responses in a potentially synergistic fashion (hypothalamic stimulation 67 +/- 8 mm Hg at control, 2 +/- 1 and 1 +/- 0.4 mm Hg at 1.0% and 1.5% halothane, respectively). These results suggest differences in the disruptive effects of CNS-mediated cardiovascular responses by halothane and dexmedetomidine, and that dexmedetomidine has an anesthetic-sparing effect on these CNS-mediated cardiovascular control mechanisms, potentiating the depressant effect of halothane. IMPLICATIONS: A new potential anesthetic adjunct, dexmedetomidine, does not attenuate brain-mediated increases in blood pressure, but the combination of dexmedetomidine and the anesthetic halothane acts to modulate central cardiovascular responses.

Adrenergic alpha-Agonists↗
PubMed1999

Pretreatment with dexmedetomidine: altered indices of anesthetic depth for halothane in the neuraxis of cats.

UNLABELLED: The sedative and anesthetic-sparing ability of the alpha2-adrenergic agonist dexmedetomidine is well documented. In this study, we identified the effects of halothane, with and without dexmedetomidine, on hemodynamic and electroencephalographic (EEG) variables and quantified the concentration of halothane resulting in various anesthetic depth indices mediated through the central nervous system (CNS) in chronically instrumented cats. Halothane was given alone or after dexmedetomidine (15 microg/kg p.o.). In both groups, four indices of anesthetic depth--minimum alveolar anesthetic concentration (MAC; no movement to noxious stimuli), MAC(BAR) (no autonomic response to noxious stimuli), MAC(BS) (EEG burst suppression), and MAC(ISOELECTRIC) (EEG isoelectricity)--were determined. Halothane decreased arterial blood pressure, heart rate, and higher frequency components of the EEG before the onset of burst suppression and isoelectricity. Dexmedetomidine pretreatment augmented the actions of halothane on arterial pressure, heart rate, and the EEG. Dexmedetomidine reduced the halothane concentrations resulting in MAC (from 1.22% +/- 0.06% to 0.89% +/- 0.08%) and MAC(BAR) (from 1.81% +/- 0.05% to 1.1% +/- 0.10%), but not those resulting in MAC(BS) (3.01% +/- 0.17% vs 3.14% +/- 0.10%) or MAC(ISOELECTRIC) (4.39% +/- 0.26% vs 4.65% +/- 0.12%). These results suggest that dexmedetomidine does not alter various CNS-mediated indices of anesthetic action to equivalent degrees and that there are dissimilar degrees of an anesthetic-sparing action at different levels of the neuraxis. IMPLICATIONS: The anesthetic adjuvant dexmedetomidine seems to differentially alter central nervous system-mediated indices of anesthetic action. Lower brainstem or spinal determinants of anesthetic depth (movement and hemodynamic responses) are more attenuated than those of higher brain functions, such as the electroencephalogram.

Adrenergic alpha-Agonists↗
PubMed1998

The effects of graded hypoxia on intraparenchymal arterioles in rat brain slices.

Hypoxia-induced changes in intracerebral arterioles, the major determinants of local cerebral oxygen delivery, are not well understood. Hippocampal arteriolar diameters were measured in rat brain slices using computerized videomicroscopy. In group 1 (control), artificial cerebrospinal fluid oxygen tension (PO2) was maintained at 500 mmHg. In groups 2 and 3, PO2 was gradually reduced to anoxia (95% N2/5% CO2). In group 3, prostaglandin F2a alpha was given to approximate physiological myogenic tone. PCO2 and pH were controlled. Graded hypoxia progressively dilated vessels (PO2 300 mmHg = 2.4 +/- 1.2%, 4.2 +/- 1.6%; PO2 90 mmHg = 15.4 +/- 3.0%, 14.5 +/- 1.8%; groups 2 and 3, respectively). The presence of preconstriction did not influence the extent of hypoxia-induced dilation. This vasorelaxation may be important in maintaining cerebral oxygen delivery during microvascular hypoxia.

Animals↗
PubMed1994

Auditory sensory gating, hippocampal volume, and catecholamine metabolism in schizophrenics and their siblings.

Schizophrenia may result from the concerted action of several pathophysiological factors. This pilot study compared the distribution of measurements of three such putative factors in 11 schizophrenics and their siblings: a neurophysiological deficit in auditory sensory gating, diminished hippocampal volume, and increased catecholamine metabolism. Abnormal auditory sensory gating was found in all schizophrenics in the 11 families studied and in 8 of their 20 siblings. Compared with the schizophrenics, the clinically unaffected siblings with abnormal auditory gating had larger hippocampal volume. There was no similar difference for the siblings with normal gating. The siblings with abnormal auditory gating also had lower homovanillic acid levels than the other siblings. The data suggest that a familial neuronal deficit, identified by diminished sensory gating, may be a necessary, but not sufficient factor in the pathogenesis of schizophrenia. Individuals with this deficit are generally clinically unaffected, except for schizophrenics, who also have other abnormalities, such as diminished hippocampal volume and increased catecholamine metabolism.

Acoustic Stimulation↗
PubMed1990

Sensory gating deficits in psychiatric inpatients: relation to catecholamine metabolites in different diagnostic groups.

Acutely ill psychiatric inpatients were examined for a deficit in sensory gating, measured as failure to suppress the P50 wave of the auditory-evoked response to the second of paired stimuli. Previously, we had found that in mania, this sensory gating deficit is correlated with increased plasma-free levels of the noradrenergic metabolite 3-methoxy, 4-hydroxyphenylglycol (pMHPG), whereas in schizophrenia, there is no correlation with catecholamine metabolism. To assess the generalizability of these findings, we examined inpatients with a broader range of diagnoses, including those with multiple DSM III-R Axis I, II, and III diagnoses. The patients were grouped into three diagnostic spectra for analysis: schizophrenic, manic, and depressive. In the schizophrenic patients, there was no relationship between pMHPG or other catecholamine metabolites and the sensory gating deficit. In manic patients, however, a positive correlation between pMHPG level and the sensory gating deficit was again observed. This relationship did not extend to the depressive patients, who uniquely showed sensory gating deficits that correlated negatively with the severity of their illness. The data suggest that sensory gating deficits are common to these three diagnostic spectra, but the deficits in each group have different relationships to catecholamine metabolism and symptom severity that may reflect differences in the underlying neuronal pathophysiology of these illnesses.

Adult↗