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Biomedical subjects

E Bourke

Publications and source records attributed to E Bourke.

At least 19 recordsLinked to original sources
PubMed2007

Mycosis fungoides--a review of the management of 28 patients and of the recent literature.

BACKGROUND: Mycosis fungoides is an uncommon cutaneous T-cell lymphoma characterized by malignant monoclonal proliferation of T-helper lymphocytes. Its course is variable with a potential for lymphatic and hematogenous involvement. We report the investigations, staging, treatment, follow-up, and outcome of 28 patients. This is the first such study reported from Ireland. METHODS: Twenty-eight patients with mycosis fungoides (14 women, 14 men; average age, 52.5 years) were reviewed over 12 years in the dermatology clinic which assesses an average of 4500 patients per year. All mycosis fungoides patients were referred from their family physicians. The diagnosis was made in all cases from a combination of clinical findings, histology, and immunohistochemistry. TNM staging revealed 11 patients at diagnosis stage IA (T1), 12 at stage IB (T2), four at stage IIB (T3), and one at stage III (T4). RESULTS: The usual male preponderance was not found. Eight patients needed multiple biopsies to establish the diagnosis. Detailed investigations were not useful in the early stages. Patients were followed up over a 12-year period. Thirteen patients died as a result of cutaneous lymphoma. Two patients with stage IA disease progressed rapidly and died, a feature reported in only 10% of patients at this stage. Five patients showed unusual features, including a long history prior to presentation, the development of the rarely reported bullous mycosis fungoides, and aggressive disease beginning at a young age. CONCLUSIONS: Mycosis fungoides is rare; we reviewed 28 patients over 12 years. The prognosis is poor at the later stages; 13 patients died. Two patients who died were unusual in that they rapidly progressed from stage IA disease; however, in the majority of patients with this stage, the prognosis is excellent. Detailed investigations were unhelpful in early stage disease. Close clinical follow-up is essential to identify disease progression.

Adult↗
PubMed2000

Loss of Ikappa B-beta is associated with prolonged NF-kappa B activity in human glial cells.

Nuclear factor-kappaB (NF-kappaB) is an inducible transcription factor central in the regulation of expression of a wide variety of genes and synthesis of several proteins involved in the generation of the immune response and inflammatory processes. In resting cells, NF-kappaB is maintained in an inactive state through cytoplasmic retention by IkappaB inhibitors. Stimulation of cells with a wide variety of inducers results in proteolytic degradation of these IkappaB proteins, leading to activation of NF-kappaB. The present study shows that interleukin-1 (IL-1) causes persistent activation of NF-kappaB in glial cells. Stimulation with IL-1 also causes rapid but transient degradation of IkappaB-alpha and IkappaB-epsilon. However, NF-kappaB remains active even after these IkappaB isoforms have returned to control levels. In contrast, the IkappaB-beta isoform fails to reappear following its initial degradation by IL-1, coincident with sustained activation of NF-kappaB. In addition, in vivo overexpression of the various IkappaB isoforms revealed that IkappaB-beta is the only isoform that has the ability to inhibit IL-1-induced NF-kappaB-driven transcription. The findings also suggest that the inability of IkappaB-alpha and IkappaB-epsilon to modulate NF-kappaB activity is due to their modification in vivo. These findings indicate that IkappaB-beta is the key regulator of the activity of NF-kappaB in human glial cells.

Base Sequence↗
PubMed1999

Antiinflammatory effects of glucocorticoids in brain cells, independent of NF-kappa B.

Glucocorticoids are potent antiinflammatory drugs. They inhibit the expression of proinflammatory cytokines and adhesion molecules. It has recently been proposed that the underlying basis to such inhibition is the induction of the protein I kappa B, which inhibits the transcription factor NF-kappa B. The latter is a key activator of the genes encoding cytokines and adhesion molecules. The present study shows that the synthetic glucocorticoid, dexamethasone, inhibits the induction of the proinflammatory cytokine IL-8 and the adhesion molecules VCAM-1 and ICAM-1 in human 1321N1 astrocytoma and SK.N.SH neuroblastoma cells. However, dexamethasone failed to induce I kappa B or inhibit activation of NF-kappa B by IL-1 in the two cell types. EMSA confirmed the identity of the activated NF-kappa B by demonstrating that an oligonucleotide, containing the wild-type NF-kappa B-binding motif, inhibited formation of the NF-kappa B-DNA complexes whereas a mutated form of the NF-kappa B-binding motif was ineffective. In addition, supershift analysis showed that the protein subunits p50 and p65 were prevalent components in the activated NF-kappa B complexes. The lack of effect of dexamethasone on the capacity of IL-1 to activate NF-kappa B correlated with its inability to induce I kappa B and the ability of IL-1 to cause degradation of I kappa B, even in the presence of dexamethasone. The results presented in this paper strongly suggest that glucocorticoids may exert antiinflammatory effects in cells of neural origin by a mechanism(s) independent of NF-kappa B.

Anti-Inflammatory Agents↗
PubMed1996

Interlaboratory study of the analysis of ampicillin by liquid chromatography.

A liquid chromatographic method for the analysis of ampicillin was examined in a collaborative study involving seven laboratories. The method included an isocratic part, which is used in the assay. The isocratic part is similar to the assay method for ampicillin of the US Pharmacopeia XXIII Revision. When the isocratic part is combined with gradient elution, the method is suitable for purity control. Six samples of ampicillin (anhydrous, trihydrate and sodium salt) with varying purity were analysed. The main component and related substances were determined. An analysis of variance proved the absence of consistent laboratory bias. The laboratory-sample interaction was significant. Estimates of the repeatability and reproducibility of the method, expressed as standard deviations of the result of the determination of ampicillin, were calculated to be about 0.9 and 1.1 respectively.

Ampicillin↗
PubMed1993

Assessment of hypocalcemia and hypercalcemia.

Methodologic aspects including causes of factitious hypocalcemia and hypercalcemia are summarized. The differential diagnosis of hypocalcemia is reviewed under three main headings: hypoalbuminemia, hypocalcemia with decreased parathyroid hormone (PTH) action or activity, and hypocalcemia with normal PTH action and activity. The differential diagnosis of hypercalcemia is subdivided into three broad categories: hyperproteinemia, PTH-mediated hypercalcemia, and non-PTH-mediated hypercalcemia. The causes of hypocalcemia and hypercalcemia are outlined with a focus on pathophysiology and clinicochemical sequelae. A laboratory perspective is emphasized in outlining management strategies.

Calcium↗
PubMed1993

Assessment of hyperphosphatemia and hypophosphatemia.

Methodologic aspects including causes of factitious hyperphosphatemia and hypophosphatemia are summarized. The differential diagnosis of hyperphosphatemia is reviewed under its three broad causes: decreased glomerular filtration rate, increased exogenous or endogenous phosphate load, and increased renal tubular phosphate reabsorption. The differential diagnosis of hypophosphatemia is reviewed under its three broad causes: inadequate gastrointestinal input, excess phosphate losses, and transcellular shifts. The consequences of hyperphosphatemia and hypophosphatemia are outlined with a focus on pathophysiologic and clinicochemical sequelae. A laboratory perspective is emphasized in outlining management strategies.

Diagnosis, Differential↗
PubMed1992

The kidney in sickle cell anemia.

New insights into the physical chemistry and molecular epidemiology of sickle cell anemia have improved our understanding of the pathophysiology of the associated nephropathy, the predictors of this complication, and genetic and other factors that may modify it. In this article, we analyze the current clinicopathologic knowledge with reference to the predilection to nephropathy and the protection from hypertension, as well as the altered renal physiology of the sickle cell state that underlies both these phenomena. In the early stages of sickle cell anemia, the kidney is characterized by impaired function of the renal medulla, as evidenced by reduced capacity to concentrate, acidify, and excrete potassium into the urine. Meanwhile, the cortex functions supranormally, as evidenced by increased renal plasma flow and glomerular filtration rate, proximal tubular function, and urinary diluting capacity. In addition to the complications of hematuria and papillary necrosis, renal insufficiency supervenes in a subgroup of patients. The morphology of the glomerulopathy generally differs between children and adults; in the latter group there is a particularly poor prognosis and markedly shortened life expectancy. Renal replacement therapy has nonetheless been successful. Although hypertension may be found at this stage, it is extremely rare before the onset of significant renal impairment. The possible mechanism of this protection is discussed, with a focus on the compelling need for further investigation in light of the newly gained basic understanding of this hematorenal syndrome.

Adult↗
PubMed1991

Effects of maleic acid on renal phosphorus transport: role of dietary phosphorus.

The effects of maleic acid on renal phosphate (Pi) transport were examined by clearance and brush-border membrane vesicle (BBMV) transport studies. In normal rats, maleic acid 50 mg.kg body wt-1.h-1 increased the phosphaturia (P less than 0.001). Intraperitoneal administration of a similar dose of maleic acid decreased the BBMV uptake of Pi but not glucose. In rats fed a low-phosphate diet (0.03%), the maleic acid-induced phosphaturia was blunted, but the inhibitory effect on the BBMV transport of Pi persisted. In chronic parathyroidectomized rats fed a low-phosphate diet, where the filtered load of Pi was higher than in the previous groups, the phosphaturia was abolished, but the inhibition of the BBMV transport of Pi was sustained. Both the in vitro incubation of BBMVV and in vivo administration of maleic acid were associated with a competitive inhibition of Pi transport. These studies indicate that the maleic acid-induced phosphaturia is expressed at the apical membrane entry step of Pi, and the enhanced distal tubular reabsorption accounts for the lack of phosphaturia in dietary Pi deprivation.

Animals↗
PubMed1990

Naproxen-induced nephropathy in systemic lupus erythematosus.

A 34-year-old female with an 8-month history of systemic lupus erythematosus and intermittent naproxen use presented with acute oliguric renal failure, hypoalbuminemia, 4+ proteinuria, and an active urinary sediment. The clinical picture suggested a rapidly progressive lupus glomerulonephritis. Renal biopsy, however, demonstrated chronic, active interstitial nephritis without evidence of immune deposits by immunofluorescence or electron microscopy. Nonsclerotic glomeruli revealed diffuse foot process fusion without cellular proliferation. These findings were consistent with nonsteroidal anti-inflammatory drug induced nephropathy. Discontinuation of naproxen and institution of corticosteroid therapy was followed by improvement in renal function and remission of nephrotic syndrome. This case represents the first report of nonsteroidal antiinflammatory drug nephropathy associated with systemic lupus erythematosus.

Acute Kidney Injury↗
PubMed1989

The effect of local anaesthetics on epinephrine absorption following rectal mucosal infiltration.

This study was undertaken to investigate the effects of lidocaine and bupivacaine on epinephrine absorption following rectal mucosal infiltration, to assess the cardiovascular and metabolic effects of the absorbed epinephrine and to compare the systemic absorption of the local anaesthetics employed. Three groups of five greyhounds received 1.5 micrograms.kg-1 of epinephrine 1:200,000 in lidocaine 0.5 per cent, bupivacaine 0.5 per cent or 0.9 per cent saline. Plasma epinephrine, lidocaine, bupivacaine, lactate, glucose and potassium concentrations were measured at 1, 2, 5, 10, 15 and 30 minutes following infiltration. Plasma epinephrine concentrations were significantly higher in the lidocaine group at one and two minutes following infiltration. Plasma bupivacaine concentrations were significantly higher than plasma lidocaine concentrations throughout the study period. There were no significant differences in metabolic or biochemical indices within or between the three groups. A local vasodilatory action of lidocaine may enhance epinephrine absorption. Differences in hepatic uptake and rate of metabolism may explain the increased plasma bupivacaine measured. Lidocaine may be the local anaesthetic of choice for ano-rectal procedures, especially when large volumes of local anaesthetic are being infiltrated.

Absorption↗
PubMed1989

Hypocomplementemic proliferative glomerulonephritis with C3 nephritic-factor-like activity in multiple myeloma.

Advanced renal failure, nephrotic-range proteinuria due to proliferative glomerulonephritis and multiple myeloma with circulating IgG2 lambda and free lambda light-chain paraproteins occurred in a 31-year-old male. Commonly established causes of renal failure in multiple myeloma were excluded. Immunofluorescence revealed heavy granular glomerular deposition of C3. Serum C3 was decreased, and C3c was increased. C3 nephritic-factor (C3 NeF)-like activity was demonstrated in the serum. Plasmapheresis and chemotherapy resulted in a decrease in paraprotein concentration up to 90%, a decrease in C3 NeF-like activity to negligible, normal serum complement levels and a marked improvement in both renal function and proteinuria. With reference to the literature, the possibility of a syndrome of paraproteinemia, C3 NeF-like activity and glomerulonephritis is forwarded.

Adult↗
PubMed1989

Effects of malonate administration on renal ammoniagenesis in intact dogs.

In the dog kidney in vivo, malonate augmented ammoniagenesis from both amide and nonamide nitrogen sources, similar to previous in vitro investigations using incubating canine renal tubules. This was highly significant in alkalotic dogs, where it was accompanied by decreased renal tissue concentrations of glutamate. Changes in renal ammonia metabolism were less evident in acidotic dogs where a markedly decreased glomerular filtration rate was noted following malonate administration. Under conditions of complete ureteric obstruction which effectively abolished glomerular filtration, malonate significantly augmented ammoniagenesis above baseline in acidotic dogs. These in vivo results with malonate have similarities to those seen in dogs subjected to an acid challenge alone and suggest that the adaptation in renal ammoniagenesis under both circumstances occurs via enhanced deamination of glutamate pools.

Acidosis↗
PubMed1989

Effect of hypocalcemia on renal phosphorus handling in the rat: interaction with dietary phosphorus and PTH.

The effect of Na-EGTA induced hypocalcemia was investigated in chronically parathyroidectomized (PTX) rats. In dietary inorganic phosphorus (Pi) replete animals, reduction in the plasma calcium to 1.37 +/- 0.03 mM at constant filtered loads of Pi had no effect on tubular reabsorption of phosphorus (85 +/- 3 vs. 83 +/- 2 micrograms/ml, NS). In dietary Pi-deprived rats, where an elevation of plasma calcium is a known accompaniment, similar reduction in plasma calcium concentration also failed to alter (89 +/- 2 vs. 90 +/- 2 micrograms/ml, NS) phosphorus reabsorption. Resistance to parathyroid hormone (PTH) in dietary Pi deprivation was confirmed. Super imposition of PTH on EGTA induced hypocalcemia during dietary Pi deprivation, however, resulted in a significant reduction in tubular Pi reabsorption (81 +/- 2 vs. 67 +/- 3 micrograms/ml, p less than 0.05) with full restoration of its phosphaturic action. These changes were unaccompanied by differences in urinary adenosine 3',5'-cyclic phosphate (cAMP). In conclusion, hypocalcemia per se does not alter the renal handling of phosphorus at constant plasma Pi concentrations. The elevation in the plasma calcium associated with dietary Pi deprivation does not contribute importantly to the hypophosphaturia of dietary Pi deprivation. Hypocalcemia, however, abolishes the resistance to PTH observed in Pi deprivation.

Animals↗
PubMed1989

Effects of physiologic hyperinsulinemia on renal phosphate handling in the rat: a role for calcium.

In a recent study in acutely parathyroidectomized, fasted rats, infused with parathyroid hormone (PTH), superimposition of euglycemic hyperinsulinemia within the physiologic range completely reversed the decline in tubular reabsorption of Pi (TRPi) induced by PTH. As an extension of these observations on insulin as a counterregulator of Pi homeostatis, the present results demonstrated that similar insulin administration prevented a decrease in TRPi when PTH infusion was superimposed. This was, moreover, observed in the fed state and at doses of insulin which did not stimulate renal cortical Na-K-ATPase activity. Subsequent studies addressed the role of insulin in a PTH-independent phosphaturic state, namely that induced by Pi loading. Under such conditions and while the resultant hypocalcemia of hyperphosphatemia was circumvented by the addition of calcium to the infusate, insulin substantially increased the renal tubular reabsorptive capacity for Pi, thereby demonstrating an antiphosphaturic action of insulin independent of PTH. Furthermore, when increased filtered loads of Pi and PTH administration were combined during insulin infusion, TRPi was greater than when PTH was administered alone during similar insulin infusion. When calcium infusion did not accompany Pi loading with a resultant fall in serum calcium, euglycemic hyperinsulinemia did not affect TRPi, indicating abolition of the antiphosphaturic action of insulin by hypocalcemia.

Animals↗
PubMed1988

Minimal change glomerulonephropathy and interstitial infiltration with mycosis fungoides.

The nephrotic syndrome developed in a patient with mycosis fungoides shortly after systemic involvement by his tumor occurred. Renal biopsy examination revealed atypical lymphocytic interstitial infiltration and changes consistent with minimal change glomerulonephropathy. The patient's proteinuria decreased following steroid therapy. This is the first report of an association between minimal change glomerulonephropathy and a proven T-cell malignant lymphoma. The implications are discussed with reference to the literature.

Humans↗