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No abstract available
D'Webi stirbt - Zur gegenwärtigen Krise in der Textilindustrie im Wiesental, am Hoch- und Oberrhein
(1986)
No abstract available
Escherichia coli 536 (06:K15:H31), which was isolated from a case of urinary tract infection, determines high nephropathogenicity in a rat pyelonephritis system as measured by renal bacterial counts 7 days after infection. The loss of S fimbrial adhesin formation (Sfa-) (mannose-resistant hemagglutination [Mrh-] and fimbria production [Fim-]), serum resistance (Sre-), and hemolysin production (Hly-) in the mutaßt 536-21 led to a dramatic reduction of bacterial counts from almost tOS to only 40 cells per g of kidney. The reintroduction of the cloned S fimbrial adhesin determinant (sfa) increases the virulence of the avirulent mutant strain by a factor of 20; almost the same eß'ect was observed after restoration of serum resistance by Integration of an sja+ recombinant cosmid into the chromosome. Additional reintroduction of the my+ phenotype by Iransformation of two hly determinants increased the virulence of the strains. Demolysin production determined increased renal elimination of leukocytes and erythrocytes. Thus all three determinants investigated, S fimbriae, serum resistance, and hemolysin, contribute to the multifactorial phenomenon of E. coli nephropathogenicity.
Scorpions commonly are assumed to hunt on living prey. But under laboratory conditions they also respond very sensitively to dead insects lying on the substrate. In many cases the motionless prey is seized and consumed. It was investigated how this behavior can be elicited. The buthid scorpions Androctonus australis (L.) and Buthus occitanus (Am.) not only find motionless prey again which was stung but managed to escape before dying: They also respond to extracts of the cuticle of prey insects. After touching prey marks' either with the tips of the chelae fingers or the tarsi of the walking legs or the pectine organs specific responses (searching, seizing, feeding) are released at a high rate. Behavioral experiments demonstrate for the first time the chemosensitivity of the pectine organs for which only mechanosensitivity had been proofed formerly. Mechanical as well as contact chemical stimulation of these organs cause scorpions to orient towards the stimulus source which is grasped, retained and consumed or rejected depending on its quality. The probably responsible chemosensitive receptors are already described in the literature. The possible adaptive value and the biological significance of contact chemoreception in prey catching and in other aspects of the life of scorpions is discussed.
A new mouse model for systemic infection with Escherichia coli is presented. Whereas in other models 107_108 bacteria have to be injected into an animal to induce toxic effects resulting in death within 24 hours, now, only 103_104 bacteria of an appropriate strain are required to produce a genuine infection characterized by an increase in the bacterial load over several days. The quantitative determination of bacterial counts per liver allows a more sensitive measurement than recording death rates. Furthermore, few animals are required for a definite result in contrast to the LDso determination of other models. The salient point regarding this new model is that conditioning of animals has to be achieved by incorporating the inoculum into agar which is injected subcutaneously. The resulting infection is completely dependent on the E. colicondistrain used. Whereas a hemolytic, uropathogenic strain is so virulent that an overwhelming infection develops within 48 hours after the injection of 103 bacterial cells, a non-hemolytic variant of this strain is completely avirulent, being unable to multiply in spite of the potentiating agar. The hemolytic E. coli strain ATCC 25922 is intermediate in virulence. The bacterial counts per liver increase steadily until death occurs five to seven days after the injection of 104 bacteria. This bacterial infection can be therapeutically influenced by daily treatment with various drugs. Ciprofloxacin, ceftriaxone and co-trimoxazole are able to cure the infection, whereas amoxicillin given orally is only moderately active against this ATCC strain, which is relatively resistant to amoxicillin.
A\(_1\) adenosine receptors from rat brain membranes were solubilized with the zwitterionic detergent 3-[3-( cholamidopropyl)dimethylammonio]-1-propanesulfonate. The solubilized receptors retained all the characteristics of membrane-bound A\(_1\) adenosine receptors. A high and a low agonist affinity state for the radiolabelled agonist (R)-\(N^6\)-[\(^3\)H]phenylisopropyladenosine([\(^3\)H]PJA) with K\(_D\) values of 0.3 and 12 nM, respectively, were detected. High-affinity agonist binding was regulated by guanine nucleotides. In addition agonist binding was still modulated by divalent cations. The solubilized A\(_1\) adenosine receptors could be labelled not only with the agonist [\(^3\)H]PIA but also with the antagonist I ,3-diethyi-8-[\(^3\)H]phenylxanthine. Guanine nucleotides did not affect antagonist binding as reported for membrane-bound receptors. These results suggest that the solubilized receptors are still coupled to the guanine nucleotide binding protein N; and that all regulatory functions are retained on solubilization. Key Words: A1 adenosine receptors - Solubilization- Rat brain membranes. Klotz K.-N. et al. Characterization of the solubilized A1 adenosine receptor from rat brain membranes. J. Neurochem. 46, 1528-1534 (1986).
Insulin receptors were solubilized from rat liver microsomes by the nonionic detergent Triton X-100. After gel filtration of the extract on Sepharose CL-6B, two insulin-binding species (peak I and peak li) were obtained. The structure and binding properties of both peaks were characterized. Gel filtration yielded Stokes radii of 9.2 nm (peak I) and 8.0 nm (peak Il). Both peaks were glycoproteins. At 4°C peak 1 showed optimal insulin binding at pH 8.0 and high ionic strength. In contrast, peak li bad its binding optimum at pH 7.0 and low ionic strength, where peak I bindingwas minimal. For peak I the change in insulin binding under different conditions of pH and ionic strength was due to a change in receptor affinity only. For peak 11 an additional change in receptor number was found. Both peaks yielded non-linear Scatchard plots under most of the buffer conditions examined. At their binding optima at 4 oc the high affinity dissociation constants were 0.50 nM (peak I) and 0.55 nM (peak II). Sodium dodecyl sulfatejpolyacrylamide gel electrophoresis of peak I revealed five receptor bands with Mr 400000, 365000, 320000, 290000, and 245000 under non-reducing conditions. For peak II two major receptor bands with M\(_r\) 210000 and 115000 were found. The peak II receptor bands were also obtained aftermild reduction of peak I. After complete reduction both peaks showed one major receptor band with M\(_r\) 130000. The reductive generation of the peak II receptor together with molecular mass estimations suggest that the peak I receptor is the disulfide-linked dimer of the peak II receptor. Thus, Triton extracts from rat liver microsomes contain two receptor species, which are related, but differ considerably in their size and insulin-binding properties.
E. coli stcains isolated from patients with urinary tcact infecrions (UTn very often possess mannose"sensitive (MS) and mannose-resistant (MR) adherence facmrs (fimbriae). According to their receptor specificity the mannose-resistant adhesins can be divided inm several types, P, S, M and X. We have cloned rhe determinants of rhree groups of UTI E. coli adhesins, MS, p and S, and prepared specific aorisera against the fimbriae antigens. 189 hernagglutination (HA+) -positive stcains, 96 fecal isolates and 93 strains isoJated from UTI . have been tesred with rhese specific antisera and further characterized by receptor specific : HA, HA parteras and further of rhe "common 0 serogroups" 01, 02, 04, 06, 07, 08, 018, ' 025, 075, most prevalenr in UTI, and hemolysin production. · 68 (73 %) of the UTI srrains a.nd 50 (52%) of the fecal isolates showed P-receptor specificiry; 16 (17%) of the uropathogenic bacteria and 33 (34%) of the fecal strains exhibited S, M or X-fimbriae antigens. 24% of rhe P-hemagglutinating (P+) strains reacted wirb P (F8)-specific antiserum. In contrast, more than three quaner of the s+-srrains were agglutinated by S-specific antiserum. HA-pattern VJ and 018 amigen were found to be associared with P-fimbriae strains, wbereas HA-pattern V and VII and the 0 anrigens 02 (M-type), 06 and 018 (5-type) occurred most frequently in p- -strains. A high percentage of P-fimbriated strains showed mannose-sensitive hemagglurination and hemolysin production.
Characterization of a monoclonal antibody against the fimbrial F8 antigen of Escherichia coli
(1986)
A monoclonal lgG 1 antibody against F8 fimbriae was obtained with the hybridoma technique using spieen cells from C3H/f rnice immunised with a fimbrial preparation of Escherichia coli 2980 (018ac: K5: H-: FIC, F8) and Sp 2/0 Ag8 myeloma cells. The hybrid cells were cloned twice by lirniting dilution and grown in tissue culture. The monoclonal antibody was purified from culture supernatants on Protein A Sepharose. lt reacted with F8 fimbriae in colony blot, enzyme-linked immunosorbent assay (ELISA) and immunoblot after electrotransfer from sodium dodecyl sulphate-polyacrylarnide gel electrophoresis (SOS-PAGE) of fimbrial preparations. The antibody bound to and agglutinated F8-fimbriated bacteria.
Cardioventilator responses were studied in anaesthetized rats after injections of TRH into either the lateral (i.c.v. lat) or the fourth (i.c.v. IV) cerebral ventricles. TRH induced a morerapid hypertensive effect i.c.v. IV than i.c.v. lat. Blocking of the cerebral aqueduct abolished the hypertensive and tachypnoeic effects of TRH i.c.v. lat but not those of TRH i.c.v. IV. It is concluded that TRH increased blood pressure and ventilation rate via brain stem structures close to the fourtli ventricle.
Purified S fimbriae and an Escherichia coli strain carrying the recombinant plasmid pANN801-4 that encodes S fimbriae were tested for adhesion to frozen sections of human kidney. The fimbrlae and the bacteria bound to the same tissue domains, and in both cases the binding was specifically inhibited by the receptor analog of S fimbria, sialyl(a2-3)1actose. S fimbriae bound specifically to the epithelial elements in the kidneys; to the epithelial cells of proximal and distal tubules as weil as of the collecting ducts and to the visceral and parietal glomerular epithelium. In addition, they bound to the vascular endothelium of glomerull and of the renal Interstitium. No blnding to connective tissue elements was observed. The results suggest that the biological functlon of S fimbriae is to mediate the adheslon of E. coli to human epithelial and vascular endothellal ceUs.
No abstract available
Arthur Adamov
(1986)
No abstract available
Recently we have described the molecular cloning of the genetic determinant coding for the S-fimbrial adhesin (Sfa), a sialic acid-recognizing pilus frequently found among extraintestinal Eschenchili coli isolates. Fimbriae from the resulting Sfa + E. coli K-12 clone were isolated, and an Sfa-specific antiserum was prepared. Western blots indicate that S fimbriae isolated from different uropathogenic and meningitis-associated E. coli strains, including 083:Kl isolates, were serologically related. The Sfa-specific antibodies did not cross-react with P fimbriae, but did cross-react with FlC fimbriae. Furthermore the sja+ recombinant DNAs and some cloned s/a-flanking regions were used as probes in Southem experiments. Chromosomal DNAs isolated from 018:Kl and 083:Kl meningitis strains with and without S fimbriae and from uropathogenic 06:K + strains were hybridized against these sfa-specific probes. Only one copy of the sfa determinant was identified on the chromosome of these strains. No sfa-specific sequences were observed on the chromosome of E. coli K-12 strains and an 07:Kl isolate. With the exception of small alterations in the sfa-coding region the genetic determinants for S fimbriae were identical in uropathogenic 06:K + and meningitis 018:Kl and 083:Kl strains. The sfa determinant was also detected on the chromosome of Kl isolates with an Sfa-negative phenotype, and specific cross-hybridization signals were visible after blotting against FlC-specific DNA. In addition homology among the different strains was observed in the sfa-flanking regions.