Absence of carriage of glycopeptide-resistant enterococci by at-risk hospitalised patients in Malta.
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Animals↗
Biomedical subjects
M A Borg
Publications and source records attributed to M A Borg.
Bed occupancy and overcrowding as determinant factors in the incidence of MRSA infections within general ward settings.
Methicillin-resistant Staphylococcus aureus (MRSA) incidence and bed occupancy rates at St Luke's Hospital, Malta, were assessed over a 24-month period. A significant positive correlation was established (r=0.463; P<0.05) between new cases of MRSA infections and overall levels of bed occupancy. This would imply that overcrowding may be a relevant factor in MRSA spread within hospitals, even in non-intensive care settings.
Bed Occupancy↗
Hospital laundry workers--an at-risk group for hepatitis A?
Twenty-two laundry personnel at St. Luke's Hospital, Malta, were tested for seropositivity to hepatitis A together with 37 nursing aides working in paediatric and infectious disease wards, matched for age, who were used as controls. IgG antibodies were found in 54.5% of laundry workers and 13.5% of nursing aides [odds ratio (OR) = 7.68; 95% confidence interval (CI) = 1.87-33.83]. Furthermore, laundry personnel consistently handling dirty linen prior to washing showed an OR of 16.50 (CI = 1.19-825.57) as compared with colleagues handling only clean items. These results would suggest that the increased exposure of hospital laundry workers to potentially infected linen can constitute a risk of occupational hepatitis A for this group of employees.
Adult↗
Chronic hypoglycemia and diabetes impair counterregulation induced by localized 2-deoxy-glucose perfusion of the ventromedial hypothalamus in rats.
Previous studies have demonstrated that the ventromedial hypothalamus (VMH) plays a critical role in sensing and responding to systemic hypoglycemia. To evaluate the mechanisms of defective counterregulation caused by iatrogenic hypoglycemia and diabetes per se, we delivered 2-deoxy-glucose (2-DG) via microdialysis into the VMH to produce localized cellular glucopenia in the absence of systemic hypoglycemia. Three groups of awake chronically catheterized rats were studied: 1) nondiabetic (with a mean daily glucose [MDG] of 6.9 mmol/l) BB control rats (n = 5); 2) chronically hypoglycemic nondiabetic (3-4 weeks, with an MDG of 2.7 mmol/l) BB rats (n = 5); and 3) moderately hyperglycemic insulin-treated diabetic (with an MDG of 12.4 mmol/l) BB rats (n = 8). In hypoglycemic rats, both glucagon and catecholamine responses to VMH glucopenia were markedly (77-93%) suppressed. In diabetic rats, VMH 2-DG perfusion was totally ineffective in stimulating glucagon release. The epinephrine response, but not the norepinephrine response, was also diminished by 38% in the diabetic group. We conclude that impaired counterregulation after chronic hypoglycemia may result from alterations of the VMH or its efferent pathways. In diabetes, the capacity of VMH glucopenia to activate the sympathoadrenal system is only modestly diminished; however, the communication between the VMH and the alpha-cell is totally interrupted.
Animals↗
Local ventromedial hypothalamus glucose perfusion blocks counterregulation during systemic hypoglycemia in awake rats.
The ventromedial hypothalamic nucleus (VMH) is necessary for the integrated hormonal response to hypoglycemia. To determine the role of the VMH as a glucose sensor, we performed experiments designed to specifically prevent glucopenia in the VMH, while producing hypoglycemia elsewhere. We used awake chronically catheterized rats, in which local VMH glucose perfusion (100 mM or 15 mM of D-glucose) was combined with a sequential euglycemic-hypoglycemic clamp. In two control groups the VMH was perfused either with (a) an iso-osmotic solution lacking glucose, or with (b) nonmetabolizable L-glucose (100 mM). During systemic hypoglycemia glucagon and catecholamine concentrations promptly increased in the control animals perfused with either 100 mM L-glucose or the iso-osmotic solution lacking glucose. In contrast, glucagon, epinephrine and norepinephrine release was inhibited in the animals in which the VMH was perfused with D-glucose; hormonal secretion was partially suppressed by the VMH perfusion with 15 mM D-glucose and suppressed by approximately 85% when the VMH was perfused with 100 mM D-glucose, as compared with the control groups. We conclude that the VMH must sense hypoglycemia for full activation of catecholamine and glucagon secretion and that it is a key glucose sensor for hypoglycemic counterregulation.
Animals↗
Resistance to neuroglycopenia: an adaptive response during intensive insulin treatment of diabetes.
Counterregulation and awareness of hypoglycemia begins at lower plasma glucose levels in insulin-dependent diabetes mellitus (IDDM) subjects given intensive insulin treatment. To determine whether these changes are associated with an alteration in the susceptibility of the brain to mild hypoglycemia, we compared central nervous system responses to hypoglycemia in 8 intensively treated (hemoglobin A1, 8.3 +/- 0.2%; normal, <8%) and 11 conventionally treated IDDM patients (hemoglobin A1, 14.6 +/- 1.3%) with those in 10 healthy subjects. Plasma glucose was lowered from approximately 4.6 mmol/L in 0.5-0.6 steps using the clamp technique. Glucose levels triggering hormonal responses and perception of hypoglycemic symptoms were significantly lower in intensively treated patients compared to their poorly controlled counterparts (P < 0.05), and hormonal responses were suppressed compared to those in healthy controls. Similarly directed changes occurred in the level of circulating glucose required to alter cortical evoked potentials during hypoglycemia. A greater reduction in plasma glucose was required to alter P300 event-related potentials in the intensively treated patients (2.2 mmol/L) compared to those in the conventionally treated and nondiabetic groups (approximately 3.5 and approximately 3.0 mmol/L, respectively). We conclude that intensively treated IDDM patients are resistant to changes in cortical evoked potentials induced by mild hypoglycemia. This may explain why intensively treated IDDM counterregulate and experience hypoglycemic symptoms at a lower glucose level than conventionally treated patients.
Adaptation, Physiological↗
Local ventromedial hypothalamus glucopenia triggers counterregulatory hormone release.
To test the hypothesis that nuclei of the ventromedial hypothalamus (VMH) play a key role in the detection of counterregulatory responses to hypoglycemia, we delivered the glucopenic agent 2-deoxyglucose via bilaterally placed microdialysis probes into the VMH of conscious, chronically catheterized rats. The goal was to produce cellular glucopenia localized to the VMH. The volume of brain tissue exposed to 2-deoxyglucose was determined by adding [3H]2-deoxyglucose to the dialysate; its distribution in cerebral tissue was almost exclusively limited to the VMH. Rats with microdialysis probes placed into the frontal lobes served as a control group. Local perfusion of 2-deoxyglucose (but not glucose) into the VMH caused a prompt twofold increase in plasma glucose in association with a striking elevation of plasma glucagon (3.5-fold), epinephrine (30-fold), and norepinephrine (3.5-fold). No effect was seen when 2-deoxyglucose was delivered into the frontal lobes. We conclude that glucopenia localized to the VMH triggers the release of counterregulatory hormones that defend against hypoglycemia. Thus, the neurons that sense glucopenia may be situated in the VMH.
Animals↗
Ventromedial hypothalamic lesions in rats suppress counterregulatory responses to hypoglycemia.
The central nervous system has been implicated in the activation of counterregulatory hormone release during hypoglycemia. However, the precise loci involved are not established. To determine the role of the ventromedial hypoglycemia, we performed hypoglycemic clamp studies in conscious Sprague-Dawley rats with bilateral VMH lesions produced by local ibotenic acid injection 2 wk earlier. Rats with lesions in the lateral hypothalamic area, frontal lobe, sham operated (stereotaxic needle placement into hypothalamus without injection), and naive animals served as control groups. The clamp study had two phases. For the first hour plasma glucose was fixed by a variable glucose infusion at euglycemia (approximately 5.9 mM). Thereafter, for an additional 90 min, glucose was either allowed to fall to (a) mild hypoglycemia (approximately 3.0 mM) or (b) more severe hypoglycemia (approximately 2.5 mM). Glucagon and catecholamine responses of lateral hypothalamic area-, frontal lobe-lesioned, sham operated, and naive animals were virtually identical at each hypoglycemic plateau. In contrast, glucagon, epinephrine, and norepinephrine responses in the VMH-lesioned rats were markedly inhibited; hormones were diminished by 50-60% during mild and by 75-80% during severe hypoglycemia as compared with the other groups. We conclude that the VMH plays a crucial role in triggering the release of glucagon and catecholamines during hypoglycemia.
Animals↗