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Biomedical subjects

M Ott

Publications and source records attributed to M Ott.

At least 127 records · Page 7Linked to original sources
PubMed1989

Chromosomal mapping of genes encoding mannose-sensitive (type I) and mannose-resistant F8 (P) fimbriae of Escherichia coli O18:K5:H5.

DNA hybridization experiments demonstrated that the gene clusters encoding the F8 fimbriae (fei) as well as the type I fimbriae (pil) exist in a single copy on the chromosome of E. coli O18:K5 strain 2980. In conjugation experiments with appropriate donors, the chromosomal site of these gene clusters was determined. The pil genes were mapped close to the gene clusters thr and leu controlling the biosynthesis of threonine and leucine, respectively. The fei genes were found to be located close to the galactose operon (gal) between the position 17 and 21 of the E. coli chromosomal linkage map.

Bacterial Adhesion↗
PubMed1989

[Duration of pregnancy in higher degree multiple birth].

The relationship of birth-weight and gestational age was analyzed in 39 multiple pregnancies (27 x triplets, 9 x quadruplets, 3 x quintuplets). Prophylactic cerclage has no benefit for the duration of the pregnancy. Premature rupture of the membranes was the major indication to delivery (33.3%) followed by maternal (28.2%) and foetal (28.2%) causes.

Cervix Uteri↗
PubMed1989

[Genetic regulatory mechanisms of bacterial virulence].

Bacterial virulence is due to the action of different virulence factors (e.g. adhesins, toxins, capsules). Virulence factors are encoded by special genes termed as virulence genes or virulence determinants. The degree of virulence of one particular bacterial strain depends on the activity of the corresponding virulence genes. Several mechanisms are involved in the regulation of activity of virulence determinants: plasmids and bacteriophages may be received or lost and chromosomal sequences may be deleted. Such processes are directly responsible for the presence or absence of virulence genes in the bacterial genome. Programmed genetic rearrangements may lead to a switch of promoter sequences and are therefore responsible for a variation of virulence expression. "Jumping" of DNA sequences (transposition) and subsequent recombinational events may also cause antigenic variation of virulence factors. In addition frame shift mutations may influence the expression of virulence genes. Transregulatory factors may also influence the expression of virulence factors of pathogenic bacteria. These systems positively influence the expression of different virulence factors in a coordinative manner. They can be triggered by environmental signals.

Animals↗
PubMed1988

Gene clusters for S fimbrial adhesin (sfa) and F1C fimbriae (foc) of Escherichia coli: comparative aspects of structure and function.

Fimbrial adhesins enable bacteria to attach to eucaryotic cells. The genetic determinants for S fimbrial adhesins (sfa) and for F1C ("pseudotype I") fimbriae (foc) were compared. Sfa and F1C represent functionally distinct adhesins in their receptor specificities. Nevertheless, a high degree of homology between both determinants was found on the basis of DNA-DNA hybridizations. Characteristic differences in the restriction maps of the corresponding gene clusters, however, were visible in regions coding for the fimbrial subunits and for the S-specific adhesin. While a plasmid carrying the genetic determinant for F1C fimbriae was able to complement transposon-induced sfa mutants, a plasmid carrying the genetic determinant for a third adhesin type, termed P fimbriae, was unable to do so. Proximal sfa-specific sequences carrying the S fimbrial structural gene were fused to sequences representing the distal part of the foc gene cluster to form a hybrid cluster, and the foc proximal region coding for the structural protein was ligated to sfa distal sequences to form a second hybrid. Both hybrid clones produced intact fimbriae. Anti-F1C monoclonal antibodies (MAbs) only recognized clones which produced F1C fimbriae, and an anti-S adhesin MAb marked clones which expressed the S adhesin. However, one of four other anti-S fimbriae-specific MAbs reacted with both fimbrial structures, S and F1C, indicating a common epitope on both antigens. The results presented here support the view that sfa and foc determinants code for fimbriae that are similar in several aspects, while the P fimbriae are members of a more distantly related group.

Adhesins, Escherichia coli↗
PubMed1987

Comparison of the genetic determinant coding for the S-fimbrial adhesin (sfa) of Escherichia coli to other chromosomally encoded fimbrial determinants.

DNA probes specific for different regions of the S-fimbrial adhesin (sfa) determinant were constructed and hybridized with DNA sequences coding for P (F8 and F13), mannose-sensitive hemagglutinating type 1 (F1A), and F1C fimbriae. While the sfa and F1C DNA determinants exhibited homology along their entire lengths, the P-fimbrial and type 1-fimbrial determinants exhibited homology to regions of the sfa cluster responsible for the control of transcription and, to a minor extent, to regions coding for proteins involved in biogenesis and/or adhesion of the fimbriae and for the N-terminal part of the fimbrillin subunit.

Adhesins, Escherichia coli↗
PubMed1986

Analysis of the genetic determinants coding for the S-fimbrial adhesin (sfa) in different Escherichia coli strains causing meningitis or urinary tract infections.

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 Escherichia 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 O83:K1 isolates, were serologically related. The Sfa-specific antibodies did not cross-react with P fimbriae, but did cross-react with F1C fimbriae. Furthermore the sfa+ recombinant DNAs and some cloned sfa-flanking regions were used as probes in Southern experiments. Chromosomal DNAs isolated from O18:K1 and O83:K1 meningitis strains with and without S fimbriae and from uropathogenic O6: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 O7:K1 isolate. With the exception of small alterations in the sfa-coding region the genetic determinants for S fimbriae were identical in uropathogenic O6:K+ and meningitis O18:K1 and O83:K1 strains. The sfa determinant was also detected on the chromosome of K1 isolates with an Sfa-negative phenotype, and specific cross-hybridization signals were visible after blotting against F1C-specific DNA. In addition homology among the different strains was observed in the sfa-flanking regions.

Adhesins, Escherichia coli↗
PubMed1979

[Creatine kinase and creatine isoenzyme activities in newborn. Development of the organ-typical isoenzyme pattern during the fetal period (author's transl)].

The activity of the creatine kinase isoenzyme was measured in the serum of 133 healthy newborn. In contrast to the conditions in the adult, a normal range of 0-45 U/1 was found. No creatine kinase BMB activities were established. The increased creatine kinase-MB activities in newborn could be explained by means of an examination of the creatine kinase isoenzyme pattern in the skeleton muscle of foetuses and newborn. Depending upon the gestation age, creatine kinase-MB activity levels were found amounting to as much as a multiple of ten of the adult levels. Due to the deviation of the creatine kinase isoenzyme distribution in the organ tissue of newborn, identified in this study for the first time, creatine kinase-MB activity seems to be unsuitable as an indicator of myocardial damage during the neonatal period.

Creatine Kinase↗
PubMed1975

Metabolic transformation of colchicine, III. Inhibition of phosphatases by the metabolite O10-demethylcolchicine (colchiceine) and their reactivation by divalent cations.

Colchicine and some of its metabolites and derivatives were investigated regarding their inhibitory action against alkaline phosphatases from E. coli and calf intestine, and against acid phosphatase from potato. Colchicine itself was essentially ineffective, also its metabolites O2-demethyl- and O3-demethylcolchicine. The metabolite O10-demethylcolchicine (= colchiceine) was found to be a powerful, non-competitive inhibitor for all three phosphatases with Ki in the range of 0.45-6.0mM. Amongst the derivatives of colchicine, colchiceyltaurine proved to be a non-competitive inhibitor of acid phosphatase (Ki=3.0mM); desacetylcolchiceine behaved like colchiceine. The inhbitory actions of colchiceine and desacetylcholchiceine could be completely reversed by the addition of Mg2, Ca2, or Zn2, respectively. This interaction with divalent cations demonstrates a novel type of action of the metabolite colchiceine when compared with its mother alkaloid and is possibly of major biological significance.

Acid Phosphatase↗
PubMedDate not supplied

Overexpression of Mad transcription factor inhibits proliferation of cultured human hepatocellular carcinoma cells along with tumor formation in immunodeficient animals.

BACKGROUND: Dominant negative regulation of critical cell cycle molecules could perturb survival of cancer cells and help develop novel therapies. METHODS: To perturb the activity of c-Myc, which regulates G0/G1 transitions, we overexpressed Mad1 protein with an adenoviral vector, AdMad. Studies were conducted with established cell lines, including HepG2, HuH-7 and PLC/PRF/5 liver cancer cells, RAT-1A embryonic fibroblasts and U373MG astrocytoma cells. RESULTS: After AdMad-treatment, transduced cells exhibited decreased proliferation rates in culture conditions. RAT-1A embryonic fibroblasts and U373MG astrocytoma cells showed accumulations in G0/G1, whereas HepG2 and HuH-7 cells accumulated in G0/G1, and additionally in G2/M, albeit to a lesser extent. An in vitro assay using hepatocyte growth factor to stimulate proliferation in HuH-7 cells showed blunting of growth factor responsiveness, along with inhibition of cell cycle progression in AdMad-treated cells. No cytotoxicity was observed in AdMad-treated cells in culture, although cells lost clonogenic capacity in soft agar. In vivo assays using HepG2 cell tumors in immunodeficient mice showed that overexpression of AdMad prevented tumorigenesis. CONCLUSIONS: These studies indicate roles of Mad in G2/M, as well as the potential of manipulating cell cycle controls for treating liver cancer.

Adenoviridae↗
PubMedDate not supplied

Picture archiving and communications systems (PACS).

Although there has been a recent increase in interest in picture archiving and communications systems (PACS) topics, little has been published to assist the non-technical person in understanding the complexities of the technologies required for a PACS implementation. This issue of Current Problems in Radiology defines each PACS component and explains why each is important in a system design. PACS installations at the University of Florida are used as examples to tie the concepts together. The infrastructure required for PACS consists of the information system interfaces, networks, and databases. Information system interfaces guarantee consistent patient data across all platforms and reduce labor requirements by eliminating duplicate data entry. Data networks move information from the originating location to users around the hospital, clinic, campus, city, or world. In the PACS environment, the data consist of patient and study information as well as images and information about these images. Databases organize the data from multiple sources into a coherent package that can be queried for many different purposes, such as retrieving images, reviewing patient and study information, studying practice statistics, and performing outcomes analysis. PACS components consist of acquisition nodes, archives, and output devices. Acquisition nodes may include "digital modalities" such as CT, MRI, nuclear medicine, and computed radiography (CR), along with devices to convert from analog to digital, such as digitizers and frame grabbers. Options for archives are discussed along with configuration schemes. Output devices include both hard copy (film and paper prints) and soft copy (workstations for display and diagnosis). Finally, a description of the PACS installations at the University of Florida is presented, with comments on some of the difficulties and complexities encountered. A discussion of the cost and benefits of PACS is included, along with a forecast of the future of PACS.

Computer Systems↗
PubMedDate not supplied

Acetylation of the HIV-1 Tat protein by p300 is important for its transcriptional activity.

The human immunodeficiency virus 1 (HIV-1) Tat protein activates transcriptional elongation by recruiting the positive transcription elongation factor (pTEFb) complex to the TAR RNA element, which is located at the 5' extremity of all viral transcripts [1-3]. Tat also associates in vitro and in vivo with the transcriptional coactivator p300/CBP [4-6]. This association has been proposed to recruit the histone acetyltransferase (HAT) activity of p300 to the integrated HIV-1 promoter. We have observed that the purified p300 HAT domain acetylates recombinant Tat proteins in vitro and that Tat is acetylated in vivo. The major targets of acetylation by p300 are lysine residues (Lys50 and Lys51) in the arginine-rich motif (ARM) used by Tat to bind RNA and for nuclear import. Mutation of these residues in full-length recombinant Tat blocked its acetylation in vitro. Furthermore, mutation of these lysine residues to arginine markedly decreased the synergistic activation of he HIV promoter by Tat and p300 or by Tat and cyclin T1. These results demonstrate that acetylation of Tat by p300/CBP is important for its transcriptional activation of the HIV promoter.

Acetylation↗