Biomedical subjects
Publications and source records attributed to M Simon.
A modification in the introduction of the Kimray-Greenfield filter is described. Rather than advancing the stylet toward the Luer-lok assembly and thereby discharging the filter, the authors propose positioning the carrier containing the closed filter farther into the inferior vena cava, then withdrawing the catheter and carriage while holding the stylet in place. This method reduces the chance for damaging the caval wall.
A case of pulmonary edema following reexpansion of a collapsed lung due to pneumothorax is described and illustrated. The importance of recognizing this relatively uncommon phenomenon is stressed. The development of such edema can be prevented by avoiding application of sudden and excessive negative pleural pressures during the evacuation of a pneumothorax or a pleural effusion. The edema generally occurs in a lung that has been collapsed for more than three days. The importance of the duration of pulmonary collapse in the causation of edema is demonstrated in this patient.
The case history of a patient with tuberous sclerosis with adenoma sebaceum of Pringle, periungual fibromata, epilepsy, retinal phacomata, renal hamartomata and cyst-like lesions of the phalanges is reported. Mosaic trisomy of chromosome 10 was observed in the patient.
Bidirectional fluxes of Na+, K+ and Ca++ were estimated under in vitro conditions through isolated patches of rat peritoneal membranes (parietal and visceral). Morphological (TEM) and functional (changes in fluxes) data are presented to show that mesothelium lining the parietal peritoneum forms a barrier than limits diffusion of ions across this membrane. In addition, it was found that Furosemide and nitroprusside change the permeability of the mesothelium for sodium or potassium, respectively.
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The long distance bactericidal effectiveness of 0.005 ml. 25 percent formalin in 80 percent ethanol applied on a cotton pellet to pulp chambers for one week in unreamed, unirrigated permanent human teeth with initial postive cultures was studied. The results showed 59 percent negative cultures on subsequent examination.
A site-specific inversion event is responsible for phase transition in Salmonella, as indicated by heteroduplex analysis of recombinant molecules carrying the gene coding for H2 flagellin in Salmonella. The inversion region corresponds to approximately 800 base pairs in length, and the inversion process does not appear to be dependent upon the E. coli RecA recombination pathway. Specific deletion derivatives of the cloned fragments no longer produce H2-specific flagella, effectively mapping the H2 gene within about 300 bp of the inversion region. Recombinant products of the hybrid molecules arose spontaneously, and they were used in the mapping of restriction sites within the inversion region. The restriction maps further demonstrate the extent and nature of the inversion.
By indirect immunofluorescence techniques, microtubules and mitochondria were localized in normal rat kidney cells, human WI38 fibroblasts, mouse peritoneal macrophages, and a putative smooth muscle rat cell line, in monolayer culture. The mitochondria were found to be arranged along the cytoplasmic microtubules in each cell type. Disruption of the microtubules with colcemid caused a redistribution of the mitochondria in these cells. There was no correlation between the location of the mitochondria and actin-containing filaments. This evidence suggests that mitochondria are directly or indirectly associated with microtubules in these cells.
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An alloantigen segregating in the double back-cross families, distinct from serologically determinalble transplantation antigens controlled by the major histocompatibility complex (SLA), was detected in pigs by the complement-dependent lymphocytotoxic technique. The system was designated SLB and its product (antigen SLB-A1) was demonstrated in all lymphocytes from the lymph nodes, thymus and peripheral blood, but not in the erythrocytes. Back-cross matings supplied evidence of the dominant heredity of SLB-A1. Detection of further SLB antigens was unsuccessful, so that only two alleles (SLB-A1 and SLB-A-) could be determined in families. Double back-cross families revealed a close linkage between the SLB locus and the L blood group locus. Maximun lod score values were calculated in recombination fraction theta=theta.10.
Previous studies showed that the structural gene for the flagellar hook subunit protein (molecular weight 42,000) was one of a group of flagellar genes located on the Escherichia coli genome near pyrC. Several lines of evidence indicate that the flaK gene is the structural gene for the hook subunit protein. Fla+ strains that were insensitive to chi infection could be isolated as revertants of an FlaK- amber mutant strain but from no other Fla- strain. The hook subunit proteins isolated from such chi-sensitive revertants of the FlaK- strain were shown to be antigenically and electrophoretically different from the hook protein isolated from the wild-type strain. Thus, reversion of a mutation in the flaK gene resulted in alteration of the structure of the hook protein. Furthermore, in programming experiments with hybrid lambda containing flagellar genes, lambdafla with flaK genetic activity programmed the synthesis of a 42,000-molecular weight protein, whereas lambdafla without flaK genetic activity did not.
Of the more than 30 genes required for flagellar function, 6 are located between pyrC and ptsG on the Escherichia coli genetic man. This cluster of genes is called flagellar region I. Four-point transductional crosses were used to establish the position and order of the region I flagellar genes with respect to the outside markers ptsG and pyrC. Bacteriophage lambda-E. coli hybrids that contained most of the genes necessary for flagellar formation were constructed. The properties of specific hybrids that carried the region I fla genes were examined by genetic complementation and by measuring the capacity of the hybrids to direct the synthesis of specific polypeptides. The results of these tests with lambda hybrids and with a series of deletion mutations derived from the lambda hybrids demonstrated the existence of at least six flagellar-specific cistrons. These directed the synthesis of polypeptides with the following apparent molecular weights: flaV, 11,000; flaK, 42,000; flaL, 30,000 and 27,000; flaM, 38,000; flS, 60,000; and flaT, 35,000. Plasmid ColE1-E. coli hybrids with region I flagellar genes were also used to program the synthesis of polypeptides in minicell-producing strains. The polypeptides synthesized in these experiments were identical to polypeptides of the hook-basal body structure and helped to confirm the assignment of genes to specific polypeptides. The synthesis of all of these polypeptides was regulated by the same mechanism that regulates the synthesis of other flagellar-related structural components.
Serum ferritin concentrations were found to be raised, often considerably, in 58 of 76 black patients with primary liver cancer (PLC). No correlation could be demonstrated between the serum ferritin concentration and several other measurements, including the following: hepatic iron stores measured chemically, the size of the tumour, serum transaminase values, and the presence or absence of cirrhosis in the non-tumorous liver. There was, however, a negative correlation between serum ferritin and alpha-foetoprotein concentrations. Ferritin was purified from PLC tissue obtained from three patients at necropsy and the distribution of isoferritins was determined by isoelectric focusing. Acidic isoferritins similar to those previously found in PLC tissue were obtained. Their acidic nature was confirmed chromatographically using DEAE cellulose. Because the serum ferritin in patients with PLC probably consists of a mixture of normal and acidic isoferritins, it is likely that the serum assay used in the present study underestimated the actual concentrations present. With the development of an assay which utlises a specific antibody against acidic PLC isoferritins, serum ferritin may prove to be a second marker for PLC.
Serum levels of vitamin A, its specific carrier protein retinol-binding protein (RBP), and zinc were determined in 34 cases of idiopathic hemochromatosis, 33 cases of alcoholic cirrhosis, 10 cases of non-alcoholic cirrhosis, and in 35 normal controls. In both alcoholic and non-alcoholic cirrhosis, vitamin A and RBP levels were very significantly reduced, whereas a significantly low zinc was observed only in the alcoholic cirrhosis group. In idiopathic hemochromatosis, vitamin A values were significantly lower compared to normals, whereas serum RBP levels were normal and serum zinc was very close to that of the controls. A significant correlation was found between vitamin A and RBP levels in the entire group of 112 patients. These results, (1) in alcoholic and non-alcoholic cirrhosis, confirm a dramatic vitamin A deficiency and the major role played by decreased RBP, but tend to deemphasize the possible role of zinc deficiency; (2) in idiopathic hemochromatosis, affirm a significant serum vitamin A deficiency supposedly by a different mechanism from that of alcoholic cirrhosis since in idiopathic hemochromatosis plasma RBP levels are normal. The role of this vitamin A disorder should be considered in the interpretation of clinical signs of idiopathic hemochromatosis such as ichthyosis and visual disorders.
Vitamin C status was studied, by means of leucocyte ascorbic acid concentrations, in 67 cases of idiopathic hemochromatosis subdivided into 44 untreated and 25 treated cases (2 patients belonging to both subgroups) and compared to 31 normal subjects and 37 alcoholic cirrhosis patients. The control groups exhibited the following mean levels (+/- SEM): 34.4 +/- 1.9 microgram/10(8) WBC in normals and 22.0 +/- 1.8 microgram/10(8) WBC in alcoholic cirrhosis. In idiopathic hemochromatosis the mean levels were: for the untreated group 19.5 +/- 1.7 microgram/10(8) WBC and for the treated group 34.3 +/- 2.3 microgram/10(8) WBC. These results (1) affirm an important vitamin C deficiency in the untreated disease; (2) suggest that iron overload is the main causal factor in view of the striking difference--to date unreported--between untreated and treated cases of idiopathic hemochromatosis. Besides its possible theoretical interests, this vitamin C deficiency is responsible in idiopathic hemochromatosis for a significant underestimation of the desferrioxamine-induced urinary iron excretion.
Two cases of fatal heat stroke, concerning a 20 year-old soldier and a 44 year-old psychiatric patient, treated with neuroleptics, are reported. The clinical picture, starting suddenly with coma and hyperthermia, was quite identical for both. Secondarily, while hyperthermia decreases and the conscience improved partially, an hemorrhagic syndrome similar to a consumption coagulopathy, acute renal insufficiency and acute hepatic failure appear. Death occurred after aggravated neurological disorders and respiratory distress. The anatomical lesions spread on all the viscera include tubular nephritis, and hepatic centro-lobular necrosis and an interstitial and alveolar oedema with hemorrhages and hyaline membranes in the lungs.