A simple method for delivery of a subluxed lens.
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Catheterization↗
Biomedical subjects
M Lahav
Publications and source records attributed to M Lahav.
Primary therapy for Cushing's disease with metyrapone.
A 13-year-old boy was diagnosed as suffering from pituitary-dependent Cushing's syndrome. He was treated with 2.0 g of metyrapone daily as the sole treatment for four years. All clinical and biochemical stigmata of Cushing's disease disappeared within a few months. The patient grew 23.0 cm in four years and regained normal health. No significant side effects of metyrapone were noticed. Administering the medication at 2 PM and 8 PM allowed higher cortisol levels in the morning and noon hours than in the evening and night, approximating the normal diurnal variation in cortisol production. We conclude that metyrapone may be considered the sole treatment in patients with Cushing's disease.
Adolescent↗
Inhibition of wall autolysis of staphylococci by sodium polyanethole sulfonate "liquoid".
Liquoid (polyanethole sulfonate) was neither capable of influencing the growth nor the viability of staphylococci. But liquoid induced a suppression of the activity of different autolytic wall systems of normally growing staphylococci, i.e., autolysins which participate in cross wall separation as well as autolysins which are responsible for cell wall turnover. Additionally, the lysostaphin-induced wall disintegration of staphylococci was inhibited by liquoid. However, no indication could be found for a direct inhibition of lytic wall enzymes by liquoid; rather an interaction of liquoid with the target structure for the autolytic wall enzymes, the cell wall itself, was postulated. On the basis of the experimental data with the teichoic acid- mutant S. aureus 52A5 the sites of wall teichoic acid were supposed to be an important target for the binding of liquoid to the staphylococcal cell wall.
Bacteriolysis↗
Drusen measurement from fundus photographs using computer image analysis.
Drusen are yellowish deposits at the level of the retinal pigment epithelium and are frequently associated with age-related maculopathy (ARM). Drusen often change in size and number over time and may be followed by atrophic or exudative macular degeneration. A quantitative method to measure the development of drusen is needed for controlled studies of the natural history, prognosis, and treatment of ARM. An objective method is described using computer image analysis of fundus photographs for the detection and measurement of drusen. This technique enables us to measure both the area of drusen in the macula and the changes in the drusen pattern over time. Evaluation of repeated photographs showed reproducibility of 6.1%, whereas the reproducibility of processing photographic duplicates was 2.3%. Digitization with a high-quality linear array solid state camera did not change reproducibility significantly.
Fundus Oculi↗
Single-dose metyrapone test at 06.00 h: an accurate method for assessment of pituitary-adrenal reserve.
One dose of metyrapone (1.5g) administered at 06.00 h, with subsequent measurement of 11-deoxycortisol and 17-hydroxycorticosteroid (17-OHCS) levels in plasma at 12.00 and 14.00 h, allowed accurate assessment of the pituitary-adrenal reserve. Normal response was defined as achieving a serum 17-OHCS level of more than 10.0 micrograms/100 ml and a 11-deoxycortisol level of more than 6.0 micrograms/100 ml at either 12.00 or 14.00 h. These criteria are based on a group of 18 persons with normal pituitary-adrenal axis, and 86 additional cases responded in this normal range. In this group of 104 subjects, 11-deoxycortisol levels rose to 9.2 +/- 3.5 micrograms/100 ml at noon and 17-OHCS levels to 15.4 +/- 4.7 micrograms/100 ml at 14.00 h. Post-metyrapone 17-OHCS levels were significantly higher than normal cortisol levels at these times (P less than 0.001) and than those observed at 08.00 h on the day of the test, demonstrating stimulation of adrenal corticoid production in addition to blockade of cortisol production by metyrapone. Thirty-one patients found to suffer from secondary adrenal failure showed impaired response. All these patients had limited pituitary-adrenal reserve, either proven by other pituitary-adrenal tests or implicated by severe pituitary disease.
17-Hydroxycorticosteroids↗
Secretory piece and IgA deficiency in a patient with Waldenstrom's macroglobulinemia.
A case of a patient suffering from Waldenstrom's macroglobulinemia who developed diarrhea and mild steatorrhea is described. Laboratory studies revealed low serum IgA, intestinal secretory IgA deficiency, and small intestine bacterial overgrowth as demonstrated by the C14-cholylglycine breath test. These findings suggest that selective IgA deficiency and secretory component deficiency may be contributing factors in the development of diarrhea in Waldenstrom's macroglobulinemia.
Aged↗
[Lymphocyte uroporphyrinogen synthase in the diagnosis of lymphoma and its follow-up].
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Adult↗
Evidence of abnormality of lymphocyte uroporphyrinogen synthase in family members of patients with lymphoproliferative diseases.
Patients with active lymphoproliferative diseases (LPD) were shown to have high activity of lymphocyte uroporphyrinogen synthase (L-UROS), the enzyme which converts porphobilinogen to uroporphyrinogen. The mean L-UROS activity of 64 first-degree relatives of patients with LPD was significantly higher than that of a control group and 45% of these relatives had pathological values of L-UROS. L-UROS activity was also determined in the spouses of 2 patients and was pathologically elevated in both. The pattern of pathological values among family members may indicate the presence of a communicable agent.
Adult↗
Addison's disease due to metastases to the adrenal glands.
A 43 year old patient with Addison's disease secondary to extensive metastases to both adrenal glands is presented. Thirty two previously reported cases are reviewed; in only 13 cases was the diagnosis of Addison's disease confirmed biochemically. Reasons for the apparent rarity of Addison's disease in spite of the frequency of adrenal metastases are discussed. The need to consider the possibility of Addison's disease complicating known malignant disease arising in other tissues is stressed.
Addison Disease↗
Eosinophilic pleural effusion: a review of 36 cases.
36 cases of eosinophilic pleural effusion (EPE) are reviewed. The etiologies were: traumatic 25%, congestive heart failure (CHF) 14%, infectious 8.5%, idiopathic 8.5% and miscellaneous 11%. 33% (12 patients) had a tumoral etiology, yet in only 1 patient could all additional etiologies for EPE be ruled out. Hence, the conclusion is that EPE is rarely caused by a tumoral etiology, and that other etiologies should be considered. The comparison of pleural fluid and peripheral blood findings disclosed no significant difference among the various subgroups.
Adult↗
Reduced toxicity of liposome-associated amphotericin B injected intravitreally in rabbits.
The ocular toxicity of liposome-intercalated amphotericin B and commercial amphotericin B were compared after intravitreal injection in healthy pigmented rabbits. Ophthalmoscopic observations over 5 weeks following a single intravitreal injection showed vitreal band formation and focal retinal damage after doses of commercial amphotericin B as low as 5 micrograms. Such lesions were not seen in animals given liposomal amphotericin B in doses up to 20 micrograms. Histopathologic examination showed areas of retinal atrophy or necrosis in five of 16 rabbits given commercial amphotericin B in doses of 5-20 micrograms but in none of 16 rabbits given the same doses of liposomal amphotericin B (P = 0.02). Small white vitreal bodies were seen clinically in virtually all animals given liposomal amphotericin B or "empty" (drug-free) liposomes but in only a few animals given commercial amphotericin B; these deposits may represent residual lipid. Concentrations of amphotericin B ranged from 0.4 to 1.0 micrograms per ml of vitreous humor 5 weeks after injection of 5-20 micrograms of either formulation. These studies indicate that liposome association markedly reduces the ocular toxicity of amphotericin B.
Amphotericin B↗
Legionnaires' disease: new etiologic agents.
Two patients with pneumonitis due to legionellosis are described. The etiologic diagnosis was based on high titers of immunoglobulin (Ig)M class antibodies (1/2048 and 1/512) detected by indirect immunofluorescence. The etiologic agents were presumed to be Legionella bozemanii in one case and either L. bozemanii or L. longbeachae in the other. Both patients made an uneventful recovery. Infections with these organisms have not been described in Israel previously.
Aged↗
Persistence of staphylococcal cell-wall components in inflammatory sites may be due to the modulation by sulphated polyelectrolytes of autolytic wall enzymes: a working hypothesis.
The interaction of leucocytes with Staphylococcus aureus results in killing of the bacterial cells, but large portions of the bacterial cell walls persist apparently phagocytic cells for long periods. The mechanisms of biodegradation of staphylococci by leucocyte factors have shown that degradation of cell walls in vitro may be the result of the activation, by leucocyte kationic proteins, of the bacterial autolytic wall enzymes that are responsible for degrading the cell walls from within. This process is markedly inhibited by sulphated polysaccharides like dextran sulphate, by heparin, or by polyanetholesulfonate (liquoid). These anionic polyelectrolytes have also been shown to inhibit the lysis of staphylococci treated with bacteriolytic concentrations of penicillin G. Staphylococci injected intraarticularly into the knee joint of rats underwent massive plasmolysis, but structures compatible with cell walls (peptidoglycan) persisted within macrophages in the inflammatory sites, for long periods. It is postulated that the inability of leucocytes to degrade staphylococcal cell-wall components may be the result of the interference, by anionic polyelectrolytes likely to accumulate in the inflammatory sites, with the activation of the autolytic systems. Alternatively, anionic polyelectrolytes may coat the bacterial cells and interfere with the binding of the autolytic enzymes with their corresponding substrates.
Animals↗
Poly-L-arginine and an N-formylated chemotactic peptide act synergistically with lectins and calcium ionophore to induce intense chemiluminescence and superoxide production in human blood leukocytes. Modulation by metabolic inhibitors, sugars, and polyelectrolytes.
Various cationic polyelectrolytes (poly-alpha-amino acids and histones), lectins, the chemotactic peptide, f-methionyl-leucyl-phenylalanine (fMLP), the calcium ionophore A23187, and phorbol myristate acetate (PMA) were investigated regarding their capacity to induce luminol-dependent chemiluminescence (LDCL) and superoxide production by human blood leukocytes. Although when tested individually, poly-L-arginine (PARG), phytohemagglutinin (PHA), concanavalin A (Con A), or fMLP induced only a low to moderate LDCL response, very intense synergistic CL reactions were obtained by mixtures of PARG + PHA, PARG + Con A, PARG + PHA + fMLP, Ca2 + ionophore + PARG + PHA + fMLP, and PARG + PMA. The sequence of addition of the various agents to WBC in the presence of luminol absolutely determined the intensity of the LDCL signals obtained, the highest reactions being achieved when the WBC were preincubated for 2-3 min with A23187 followed by the sequential addition of fMLP, PARG, and PHA. These "multiple hits" induced CL reactions which were many times higher than those obtained by each factor alone. On the other hand, neither poly-L-lysine, poly-L-ornithine, poly-L-histidine, nor poly-L-asparagine, when employed at equimolar concentrations, cooperated efficiently with PHA and fMLP to trigger synergistic LDCL responses in leukocytes. Concomitantly with the induction of LDCL, certain ligand mixtures also triggered the production of superoxide. The LDCL which was induced by the "cocktail" of agents was markedly inhibited by sodium azide (93% inhibition), but to a lesser extent by catalase (10% inhibition) or by superoxide dismutase (20%-60% inhibition). On the other hand, scavengers of singlet oxygen and OH (sodium benzoate, histidine) did not affect the synergistic LDCL responses induced by these multiple ligands. Cytochalasin B also markedly inhibited the LDCL responses induced either by soluble stimuli or by streptococci preopsonized either with histone or with polyanethole sulfonate. The LDCL responses which were induced by mixtures of PARG and concanavalin A were also strongly inhibited by mannose, alpha-methyl mannoside, and poly-L-glutamic acid. The data suggest that the LDCL responses induced by the soluble ligands involved a myeloperoxidase-catalyzed reaction. The possible employment of "cocktails" of ligands to enhance the bactericidal effects of PMNs, macrophages, and natural killer cells on microbial cells and mammalian targets is discussed.
Antimetabolites↗
The modulation of placental lactogen secretion by calcium: studies with cultured human term trophoblast.
Previous reports have documented the negative regulatory effect of calcium ion on the secretion of human placental lactogen by the placenta. Human term trophoblasts were dispersed from term placenta and maintained in monolayer cell culture. Incubation of the cultured trophoblast with EGTA produced a dose-dependent stimulation of placental lactogen secretion. The calcium ionophore A23187 inhibited hormone secretion. This inhibitory effect was eliminated by the addition of the calcium-calmodulin complex inhibitor trifluoperazine. It is concluded that calcium exerts a negative regulatory effect on the secretion of placental lactogen by a mechanism which requires the action of the calcium-calmodulin complex.
Calcimycin↗
Correlation between HbA1c, purified insulins, diabetic control, and insulin antibodies in diabetic children.
Insulin antibodies were determined in sera from 38 children diagnosed as having juvenile diabetes for a duration of 0.7-15.2 years (median = 4.9 years). 8 children were treated with purified porcine insulins from the beginning of their disease, 16 children with bovine insulin NPH alone, and 14 children with non-purified, of whom 9 were later transferred to purified insulins. Serum insulin antibodies were measured by non-specific and specific methods using beef (B) and pork (P) antigens as described by Welborne and Sebriakova, respectively. 12/38 children had insulin binding levels similar to those of normal children, irrespective of the type of insulin used. The concentration of antibodies using radiolabelled B or P insulins as antigens were strongly correlated, by both the non-specific (p less than 0.01) and the specific (p less than 0.01) methods. Children with better score for diabetic control had significantly lower levels of insulin antibodies against B (p less than 0.05) and P (p less than 0.05) than those with poor diabetic control. There was also a significant positive correlation between mean HbA1c concentration and both B and P mean insulin antibody concentration (p less than 0.01). Finally, patients treated with purified porcine insulin had significantly lower levels of antibodies than patients with non-purified bovine insulin (p less than 0.05).
Adolescent↗
HLA antigens A, B, C and DR in hay-fever families of similar environmental conditions.
Investigation of 98 members (healthy and affected) belonging to 17 hay-fever families, for clinical picture, total and specific IgE and HLA A, B, C and DR is presented. There was no significant correlation between hay-fever, total or specific IgE and a certain HLA antigen or haplotype. There was, however, an association between hay-fever and same haplotype within 4 of the 17 families.
Adult↗
Survey of immunoglobulin E levels in atopic families in Israel.
Two hundred and ten members belonging to two consecutive generations of 41 atopic families (healthy and affected by clinical atopic manifestations) were investigated for basal immunoglobulin E (IgE) levels and clinical picture. The results show overall increased IgE levels, above standard values in the whole population studied, and a significant correlation between clinical atopy and high IgE levels in the children of the group. Within these families recessive inheritance of abnormally high IgE levels suggests that their high IgE levels are due to a genetically transmitted defect in IgE suppression.
Adolescent↗