Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0276640 (TEM)
 20,729 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ampicillin-resistant Haemophilus influenzae does occur now in the FRG. In one isolate a plasmid with resistance genes (R-factor) could be demonstrated as cause of the ampicillin resistance. This R-factor influences production of a beta-lactamase of the TEM type which destroys ampicillin. The infectious nature of the ampicillin resistance was proven by the fact that it was transferable to other bacterial species through cocultivation. Parallel to ampicillin resistance tetracycline resistant Haemophilus influenzae has occurred in the FRG. Here the resistance was equally bound to plasmids. These R-factors are infectious as well. Molecular analysis of the 3 isolated resistance factors in Haemophilus influenzae showed that they carry the same resistance genes which are known from R-factors of Enterobacteriaceae. In the therapy of purulent infections due to Haemophilus influenzae such as childhood meningitis one can no longer rely on general ampicillin sensitivity of the offender. Apart from ampicillin and tetracycline resistant Haemophilus influenzae chloramphenicol resistance has been observed in a few cases.
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PMID:[Infectious resistance to antibiotics in Haemophilus influenzae (author's transl)]. 30 40

The emergence of resistance to ampicillin and other antibiotics in Haemophilus influenzae has been a relatively recent event. In contrast, drug resistance has been rampant in the Enterobacteriaceae for many years. Ampicillin-resistance in H. influenzae is almost invariably attributable to possession of the TEM (Type III a)beta-lactamase. As is common in other bacteria the gene specifying this enzyme is plasmid-borne in Haemophilus. Some ampicillin-resistant strains of H. influenzae can transfer the TEM beta-lactamase gene to other strains of Haemophilus, to Escherichia coli and to Pseudomonas aeruginosa. The features of such transfer are unusual and lead for example, to the induction of adenine requirement in recipient strains of P. aeruginosa. Crypticity measurements of beta-lactamase activity show that in comparison to P. aeruginosa or E. coli, the outer membrane of H. influenzae affords only a weak penetration barrier to beta-lactam antibiotics. This may have consequences for the stability and distribution of beta-lactamase production in Haemophilus spp. which are discussed. A comparison of the molecular properties of R-plasmids determining a variety of resistances and carried by strains of H. influenzae isolated in diverse geographical locations has revealed unexpected homologies. A series of such plasmids of similar molecular weights (about 30 X 10(6)) differ substantially only in the transposable resistance genes that they carry. A model based on these findings is presented to explain the acquisition of ampicillin- and other resistances by Haemophilus.
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PMID:beta-lactamases and R-plasmids of Haemophilus influenzae. 30 59

In two cases of trichocellular leukaemia, specimens of blood, bone marrow and the spleen were evaluated not only by means of SEM and TEM but also with a view to their phagocytic and immunological properties. While immunological investigation rather suggested a B lymphocytic aetiology of the process, phagocytosis of Ferrocide (not, however, of latex) seemed to justify, in one case, also histoendothelial aetiology.
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PMID:[Trichocellular leukemia--ultrastructural study of tumor cells and various functional parameters]. 30 67

We have predicted the secondary structures of four beta-lactamases (Bacillus cereus, Bacillus licheniformis, Staphylococcus aureus, and Escherichia coli R-TEM) by the statistical method of Chou & Fasman as well as by the information theory method of Garnier et al. The secondary structures of all four beta-lactamases are of the alpha/beta type (Levitt & Chothia's nomenclature), with helices at N- and C-termini. There are about eight short regions each of alpha-helical (30--50%) and beta-strand (10--20%) structure separated by about 20 reverse turns. The conformation of the Gram-positive and Gram-negative beta-lactamases are generally similar although a few differences are predicted between the S.aureus and E.coli structures. Surprisingly, the two bacilli structures differ significantly in three short regions. In all four enzymes the region near the catalytically-implicated tyrosine has similar secondary structure. The secondary structure of hen egg white lysozyme, a penicillin-binding enzyme, as well as T4 phage lysozyme, has similarities to the N-terminal half of the penicillin-destroying beta-lactamases.
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PMID:Predicted secondary structures of four penicillin beta-lactamases and a comparison with two lysozymes. 31 76

The corneal endothelium of three species (man, dog, and guinea pig) was examined for glycosaminoglycans by using TEM, REM, and EDAX (energy-dispersive analysis of X-rays). Since no clear results can be determined by using ruthenium red (RR) alone, a testicular hyaluronidase was used to digest the glycocalyx. After incubation with hyaluronidase, the dark RR borderline of the outer leaflet of the cell membrane became more fluffy when examined by using TEM and REM. When EDAX was applied, the Ru peak became smaller compared with the S peak. These impressive results had not been found when the material was fixed in glutaraldehyde for 24 h before incubation. Considering the individual results, it can be concluded that RR, even wouthout OsO4, marks the acid groups of glycosaminoglycans that might be in the cell membrane, as well as other acid groups. There was no difference in the results among the three species used in this experiment. Some pictures showed that RR/OsO4 penetrates through the intercellular space into the Descemet's membrane.
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PMID:[Proof of glycosaminoglycans in the corneal endothelium]. 31 22

The authors draw the attention on the existence of an "Immotile-cilia Syndrome" in patients with chronic respiratory infections of unknown origin. The study of the ultra structure of the ciliae (TEM, SEM) in a case of Kartagener Syndrome supports the existence of an "Immotile-cilia Syndrome".
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PMID:[Ultrastructure of the nasal mucosa cilia in the Kartagener syndrome]. 31 80

Strains of Escherichia coli and Salmonella typhimurium carrying R plasmids, which were obtained from ampicillin-resistant clinical isolates of E. coli and Klebsiella spp. and specified either the type IIIa (TEM-type) or type Va (oxacillin-hydrolyzing) beta-lactamase, are resistant not only to ampicillin but also to carbenicillin and sulbenicillin. The latter two derivatives, however, are poorly hydrolyzed in vitro by the beta-lactamases. Although values of K(m) of the enzymes are lower for sulbenicillin and carbenicillin than for ampicillin, the ratios of V(max) to K(m) for sulbenicillin and carbenicillin are not high enough to explain the high resistance in E. coli bearing the R plasmid. Two mutants of the plasmids conferring a temperature-sensitive ampicillin resistance were induced by nitrosoguanidine treatment. It was confirmed that E. coli CSH2, harboring the mutant plasmid, produces a temperature-sensitive beta-lactamase and is resistant only at low temperatures (below 33 degrees C), but not at 42 degrees C, to ampicillin, sulbenicillin, and carbenicillin simultaneously. It is thus concluded that beta-lactamase itself is responsible for the mechanism of resistance not only to ampicillin but also to sulbenicillin and carbenicillin, even though the enzyme as determined in cell-free extracts hydrolyzes the latter two drugs poorly. An unknown barrier for sulbenicillin and carbenicillin directed by beta-lactamase in E. coli strains carrying R (bla) plasmids is postulated.
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PMID:Beta-lactamase-directed barrier for penicillins of Escherichia coli carrying R plasmids. 32 24

The effect of a large tracheal tube cuff on the rabbit tracheal mucosa was investigated by phase contrast microscopy and scanning (SEM) and transmission (TEM) electron microscopy. The tube was left in the trachea for 15 min. The cuff was either uninflated or inflated to a cuff-to-tracheal wall pressure (C-T pressure) of up to 100 mmHg. The uninflated cuff caused superficial damage to the epithelial lamina over regions where a cartilage was situated. When the cuff was inflated, it resulted in an increase of the mucosal damage, the extent of which was directly related to the pressure in the cuff. This took the form of both widening of the injured areas and penetration of the damage to deeper regions. At a C-T pressure of 100 mmHg the damage involved almost the entire mucosa and only small unaffected mucosal regions remained. At this stage it appeared as if the basement membrane had also begun to disintegrate. It is well known that a small cuff easily causes deep ulceration in the mucosa overlying the cartilages. From this investigation it was concluded that a large cuff causes the same type of ulceration if 1) the cuff wall is not sufficiently thin and pliable, and 2) if the cuff is overinflated enough to dilate the trachea to a diameter exceeding the cuff-diameter. At that moment there will be circumferential tension in the cuff and the sealing physics of the large cuff will become the sealing physics of a small (high pressure) cuff. A large cuff, properly handled, is more benign to the trachea than a small cuff. In order to avoid overinflation of the large cuff, the intracuff pressure (= C-T pressure) should always be measured by means of a four-way stopcock and an aneroid manometer. In the case of extended periods of mechanical ventilation with a high airway pressure, the resulting tracheal diameter at the cuff site should be checked radiographically.
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PMID:The trachea and cuff-induced tracheal injury. An experimental study on causative factors and prevention. 33 78

After treatment of postmeiotic stages of spermatogenesis of the mouse with TEM, dose and stage of spermatogenesis-dependent disturbances of the early embryonic development can be observed both in vivo and after in vitro culture of the embryos. The observations in both systems can be correlated. The embryo-culture system thereby enables analysis of the expression of mutagen-induced damage more accurately than the in vivo dominant lethal test. With the doses used (0.2 and 0.4 mg/kg) TEM-treatment of the fathers did not affect the rate of fertilized and cleaving eggs during the first three weeks post-treatment but severely disturbed the further development of the embryos at all stages up to implantation, exhibiting a maximum effect on morulae.
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PMID:Expression of TEM-induced damage to postmeiotic stages of spermatogenesis of the mouse during early embryogenesis. I. Investigations with in vitro embryo culture. 34 36

RDEC-1 is a piliated strain of Escherichia coli that was isolated from and produces diarrhea in rabbits without invading the mucosa or synthesizing one of the classical enterotoxins. Previous histological and fluorescent-antibody studies of RDEC-1 diarrhea revealed an acute inflammatory response and large numbers of RDEC-1 associated with (adhering to) the mucosal surface of the ileum, cecum, and colon. The purpose of the present investigation was to further elucidate the histopathology by scanning (SEM) and transmission (TEM) electron microscopy. SEM revealed aggregates of bacteria on the surface of the gut; their distribution was patchy in the ileum and diffuse in the cecum and colon. Bacteria were in contact with each other and appeared to be closely associated with the epithelial surface. TEM showed that the brush border region of the epithelial cells was found to be in varying stages of degeneration, and the bacteria could not be seen adhering to the mucosal cells unless the brush border was absent. Bacteria were in close contact only with epithelial cells that had lost their brush border. The space between the bacteria and the epithelial cells was 11 nm, and it appeared to be filled, in most cases, with densely stained material. This E. coli rarely penetrated epithelial cells, but when it did; it was found in the supranuclear region and never reached the lamina propria. From previous and present studies, it seems probable that RDEC-1 produces diarrhea in rabbits by a mechanism that may be cytotoxic and differs from the classic mechanisms by which E. coli produces diarrhea.
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PMID:Scanning and transmission electron microscopic study of Escherichia coli O15 (RDEC-1) enteric infection in rabbits. 34 19


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