Prosthetic valve endocarditis due to Listeria.
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Biomedical subjects
Publications and source records attributed to M Ravid.
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Sodium dodecyl sulphate polyacrylamide gel electrophoresis and reversed-phase high-performance liquid chromatography (HPLC) were used consecutively for the isolation of amyloid protein A (protein AA) from amyloid fibrils. Highly purified protein AA was obtained and determined by electrophoretic and amino acid analyses. The heterogeneity of protein AA was shown by HPLC. The isoforms of protein AA had different hydrophobicities, although they were equal in size and similar in amino acid composition. Compared with the conventional amyloid separation procedure (gel permeation chromatography), this technique is rapid, requires only small amounts of amyloid fibrils and may provide new information on amyloid proteins.
The occurrence of late congestive heart failure (CHF) as the first clinical manifestation of doxorubicin-induced cardiac toxicity is unusual in children and very rare in adults. However, subclinical cardiac dysfunction is commonly detected in children years after treatment with doxorubicin containing regimens. We report a 58 year old woman who developed stage IV CHF 7 years after completion of doxorubicin treatment for carcinoma of the ovary. Occult cardiac dysfunction was first demonstrated by radionuclide angiography 6 years prior to the occurrence of the clinical manifestations. This unique course of the disease and the management of the CHF are discussed.
Colchicine has been used in diverse clinical settings such as gout, familial Mediterranean fever, liver cirrhosis, Behcet's disease and pericarditis. It also has an antimitotic potential hitherto unexplored due to its narrow therapeutic toxic ratio. The aim of the present study was to compare the effectiveness and the toxicity of colchicine and three analogues: thiocolchicine, 2,3 dimethyl-colchicine and 3-dimethylthiocolchicine in the blockage of amyloid synthesis in a murine model. 3-demethylthiocolchicine was equipotent to colchicine in the blockage of casein induced amyloidogenesis. However, it was markedly less toxic (LD50 11.3 mg kg-1 vs. 1.6 mg kg-1). Thiocolchicine was toxic (LD50 1.0 mg kg-1) and 2,3 didemethyl-colchicine was far less effective. The effect of 3-dimethylthiocolchicine on polymorphonuclear leukocytes was then compared to colchicine. The effect of this analogue on inhibition of chemotaxis was equivalent to that of colchicine whereas the latter was superior to the analogue in the suppression of phagocytosis (by a ratio of 2:1) and in the inhibition of bactericidal activity (by a ratio of 10:1). Since in therapeutic concentrations the only detectable effect of colchicine on PMNs is inhibition of chemotaxis, our data may point to 3-demethylthiocolchicine as an optional, perhaps superior alternative to colchicine for some of its therapeutic indications.
A new liver biopsy instrument taking the form of a suction biopsy syringe with two pistons and a Menghini needle, is described. A vacuum is first created, and the whole procedure is effected by a continuous uninterrupted movement into the liver and instantaneous withdrawal. The syringe is held in one hand. The procedure is very simple and requires minimal training. A total of 118 biopsies have been performed. The specimens were suitable for histopathological examination. Pain was minimal and there were no complications.
BACKGROUND: The deleterious effect of hypertension on the course of diabetic retinopathy and the protective influence of antihypertensive therapy are well known. There is, however, little information about the long-term effect of different levels of blood pressure within the normal range on the evolution of renal function in type II diabetes. METHODS: One hundred ninety-five young normotensive patients with recent-onset type II diabetes, normal renal function, and no proteinuria were followed up for 14 years. Plasma glucose, creatinine, and urinary protein levels and blood pressure were determined periodically. RESULTS: Thirty patients developed hypertension; among them, 18 developed proteinuria (0.3 g/L). Among 144 patients who remained normotensive, 30 developed proteinuria. The mean decline in renal function (decline in reciprocal creatinine [100/creatinine level], expressed as a percentage of the initial value) was 26% for normotensive patients, 43% for normotensive patients with nephropathy, 39% for hypertensive patients, and 52% for hypertensive patients with nephropathy. The degree of metabolic control was not associated with the presence of proteinuria or with the severity of renal impairment. There was a significant association between the mean blood pressure over the whole observation period and the degree of impairment in renal function. This association was significant also in the patients who remained normotensive with and without proteinuria. CONCLUSIONS: Minor elevation of blood pressure as well as values in the upper normal range may be associated with acceleration of renal damage in type II diabetes.
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An 83-year-old patient developed agranulocytosis following six months of enalapril 10 mg/d. The patient also had received verapamil for three years. Upon discontinuation of both drugs the white blood cell count was rapidly restored. Cases of agranulocytosis due to angiotensin-converting enzyme inhibitors, mainly captopril, have been previously described. We could, however, find no single case associated with verapamil. This, and the very long exposure of the patient to verapamil, support the assumption that this life-threatening complication might have been caused by enalapril.
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In order to evaluate the possible cardiosparing effect of a prolonged infusion of doxorubicin as compared with the standard mode of administration 62 consecutive patients with metastatic carcinoma of the breast or carcinoma of the ovary Stage III or IV were prospectively randomized to receive doxorubicin either as a rapid infusion over 15 to 20 minutes at 8 AM or as a continuous infusion over 6 hours, 8 AM to 2 PM. The remaining protocol was identical for the two groups. The cardiotoxic effect of doxorubicin was evaluated by history and physical examination and by the decline in resting ventricular ejection fraction (LVEF) as determined by gated pool radionuclide angiography with technetium 99m (99mTc) and by the decline in the height of the QRS complexes in the standard leads of the echocardiogram (ECG). Initially there were 31 patients in each group. The cumulative dose of doxorubicin, was 410 mg/m2 +/- 42 SD in the standard infusion group and 428 mg/m2 +/- 48 SD in the 6-hour infusion group. The mean decline in LVEF after a cumulative doxorubicin dose of 300 mg/m2 was 17% in the first group and only 4.1% in the second. After 400 mg/m2 the mean fall in LVEF was 21% in the first group and 6% in the second. The mean decline in QRS voltage after 300 mg/m2 was 29% and 1.5%, respectively. Four patients, all in the standard infusion group, developed congestive heart failure. These data suggest that slow infusion of doxorubicin is associated with reduced cardiotoxicity.
Standardization of the measurement of amyloid degrading activity (ADA) by diffusion of serum in amyloid-impregnated agar plates may either indicate or exclude with reasonable certainty the presence of systemic AA amyloidosis. In certain cases, it may obviate the need for a diagnostic biopsy. The sera of 38 patients with systemic amyloidosis were tested and compared with sera of 38 controls matched for age, serum creatinine and albumin blood levels, and with sera of 48 additional controls with the same basic diseases as the amyloidotic patients but without amyloidosis. The difference between ADA of amyloidotic and control patients was significant, with no overlap in the range of activity between the two groups. A positive correlation was found between ADA and serum albumin concentration in the nonamyloidotic matched controls but not in patients with amyloidosis. Our data do not support the view that the decline in ADA of sera of amyloidotic patients is due to hypoalbuminemia.
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A case of advanced ovarian carcinoma in pregnancy is described. The entity is usually difficult to diagnose; when it does occur, the objective should be to optimize both fetal and maternal outcome.
It has been suggested that reserpine blocks expression of delayed hypersensitivity (DH) reactions by depleting tissue mast cells of serotonin, thereby preventing a T cell-dependent release of mast cell serotonin necessary to localize and to amplify the DH response. However, reserpine blocks expression of DH in mast cell-deficient mice. Recently, we showed that the ability of reserpine to interfere with the expression of contact sensitivity was independent of an effect on mast cells, but reflected an effort of the drug on effector T cell function. In the present study we evaluated the mechanisms by which reserpine abrogates the expression of T cell functions. By using human peripheral blood mononuclear cells or enriched T cell populations we found that the drug inhibited, in a dose-dependent fashion, the proliferation of T cells after mitogen stimulation. Reserpine also interfered with the mitogen-induced IL-2 production by these cells, but the IL-2 receptor expression, as measured by immunofluorescence, was unaffected. Despite this, in the continuous presence of reserpine, exogenous IL-2 did not bypass reserpine inhibition of PHA-induced proliferation. By using the fluorescent indicator quin-2 we have demonstrated that preincubation with reserpine prevented the increase of cytosolic free calcium, which accompanies PHA-induced proliferative responses of human T lymphocytes. These results identify the sites of action of reserpine in human T lymphocytes and are sufficient to explain its ability to block cell-mediated immune responses in vitro and in vivo.
The samples of normal and uremic sera were ultrafiltered, separated on SEP-PAK C18 cartridges and subjected to sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The serum material extracted from the slab gel was purified from SDS and further fractionated by reverse-phase high performance liquid chromatography (HPLC). The obtained fractions were examined by amino acid analysis and mass spectrometry. An increased number of moderately polar fractions containing bound amino acids was found in sera of uremic patients on hemodialysis. Two most prominent uremic fractions corresponded to N-benzoylglycine (hippuric acid) (fraction I, k' = 9,4) and phenylacetylglutamine (fraction II, k' = 9,7). Increased amounts of bound glutamine, glycine, serine, leucine, asparagine, alanine, valine, phenylalanine were found in other moderately polar uremic fractions. These fractions (k' range from 12.1 to 13.2) contained no free amino acids, nor any other known small uremic serum compounds; they were considered as peptide 'middle molecules' (MM) of a molecular mass smaller than 1700.
A hygroma of the left kidney was found at surgery in a thirty-five-year-old woman, who presented with anemia, hypertension, and a left abdominal mass. There was a very high sedimentation rate and fine needle aspiration yielded bizarre cells which raised the possibility of malignancy. Compression of the kidney by the cystic structure probably interfered with renal blood flow and was responsible for the elevated blood pressure which receded to normal after removal of the cyst and the left kidney.
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