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Biomedical subjects

G Koch

Publications and source records attributed to G Koch.

At least 19 recordsLinked to original sources
PubMed1992

Transcription of the chicken anemia virus (CAV) genome and synthesis of its 52-kDa protein.

This paper describes the expression of the chicken anemia virus (CAV) genome, a recently characterized single-stranded circular-DNA virus of a new type [Noteborn et al., J. Virol. 65 (1991) 3131-3139]. The major transcript from the CAV genome is an unspliced mRNA of about 2100 nucleotides (nt). Its transcription start point and poly(A)-addition site are located at nt 354 and 2317 of the CAV sequence, respectively. In vitro translation experiments provide evidence that the major CAV open reading frame encodes a 52-kDa protein by using the fifth AUG as a start codon of the unspliced CAV mRNA.

Blotting, Northern↗
PubMed1992

Posttranslational isoprenylation of rho protein is a prerequisite for its interaction with mastoparan and other amphiphilic agents.

The amphiphilic agents melittin, compound 48/80 and mastoparan inhibit ADP-ribosylation of porcine brain rho protein by Clostridium botulinum exoenzyme C3. However, ADP-ribosylation of recombinant rhoA expressed in E.coli was not inhibited by these agents. Accordingly, steady state GTP hydrolysis by recombinant rhoA was not stimulated by mastoparan, whereas GTP hydrolysis by porcine brain rho was stimulated 2.5-fold in the presence of this wasp venom. After microinjection of recombinant rhoA into Xenopus laevis oocytes the inhibitory effect of mastoparan on C3 ADP-ribosylation was restored. The data suggest that the amphiphilic agents tested are only active at the posttranslationally processed form of rho and that they exert their effects via the C-terminal end.

Adenosine Diphosphate Ribose↗
PubMed1992

Putative invasion-specific proteins in mouse T-cell hybridomas that differ in invasive and metastatic potential.

Fusion of invasive, activated T-lymphocytes with non-invasive BW5147 T-lymphoma cells mainly yields highly invasive (HI), highly metastatic T-cell hybridomas. In addition, several non-invasive (NI), non-metastatic hybrids have been obtained, probably due to loss of involved gene(s) by chromosome segregation. Here we have compared a panel of HI and NI hybrids in a search for proteins specifically expressed by either cell type. MAbs were raised against HI hybrids, but out of more than 1,000 none bound exclusively to HI cells. Furthermore, polyclonal rat, rabbit and chicken antisera did not immunoprecipitate specific proteins from total lysates, and the expression of 18 (T-cell) surface markers did not correlate with invasiveness. These results indicated that the number of differences between HI and NI hybridomas was surprisingly small. This notion was confirmed by 2-dimensional gel electrophoresis. Among 1,000 detectable spots, we found only 2 clear-cut differences between HI and NI T-cell hybridomas, whereas multiple differences were found between individual hybrids. One protein (p130) was expressed at much higher levels by HI than by NI hybrids in this panel, whereas the other (p15) was only seen in NI hybrids. These proteins are primary candidates for a role in invasion.

Animals↗
PubMed1992

ADP-ribosylation of rho proteins is inhibited by melittin, mast cell degranulating peptide and compound 48/80.

The amphiphilic agents melittin, mast cell degranulating peptide and compound 48/80 inhibit the ADP-ribosylation of the small GTP-binding proteins rho by Clostridium botulinum exoenzyme C3. Half-maximal and maximal inhibition (greater than 90%) of ADP-ribosylation occurred at about 8 and 25 micrograms/ml for compound 48/80, at 10 and 45 microM for mast cell degranulating peptide and at 15 and 50 microM for melittin, respectively. In addition, these compounds increase the steady state GTP hydrolysis and the association and dissociation rate of GTP-binding of rho proteins through an increase of GDP/GTP exchange. The data suggest that the amphiphilic agents tested interact with small GTP-binding proteins of the rho protein family.

ADP Ribose Transferases↗
PubMed1992

ADP-ribosylation by Clostridium botulinum C3 exoenzyme increases steady-state GTPase activities of recombinant rhoA and rhoB proteins.

ADP-ribosylation of recombinant rhoA and rhoB proteins by Clostridium botulinum C3 exoenzyme increased steady-state GTP hydrolysis by 50 to 80%. ADP-ribosylation and increase in GTP hydrolysis occurred at similar concentrations of C3, depended on the presence of NAD and were prevented by anti-C3 antibody or heat inactivation of C3. In contrast, GTP hydrolysis by Ile-41 rhoA or Ha-ras, which are no substrates for the transferase, were not affected by C3. ADP-ribosylation facilitated the [3H]GDP release and subsequently, the binding of [3H]GTP to rhoA. The data indicate that the increase in the steady-state GTPase activity by ADP-ribosylation is caused by increasing the rate of GDP release which is suggested to be the rate limiting step of the GTPase cycle of the small GTP-binding proteins.

ADP Ribose Transferases↗
PubMed1992

Clostridium botulinum C3 ADP-ribosyltransferase.

C3 and C3-like ADP-ribosyltransferases modify the low-molecular-mass GTP-binding proteins Rho and Rac. ADP-ribosylation occurs in asparagine-41, which is located in the putative effector region of these highly conserved regulatory proteins. First studies indicate that the Rho proteins are somehow involved in the regulation of cytoskeletal proteins, e.g., microfilament proteins. Although the precise mechanism of the interaction of the C3 substrate with cytoskeletal elements is unclear, it appears that the ADP-ribosylation by C3 renders the GTP-binding protein biologically inactive. Thus C3 and/or C3-like ADP-ribosyltransferases may be useful instruments with which to study the physiological functions of its eukaryotic substrates. Moreover, those studies may help to elucidate whether these exoenzymes are of pathophysiological and pathogenetic relevance in diseases caused by clostridia producing these agents.

ADP Ribose Transferases↗
PubMed1992

Cure profiles of visible-light-cured Class II composite restorations in vivo and in vitro.

The degrees of conversion of posterior composite material in Class II restorations performed in vivo and in vitro were studied by means of the Raman spectroscopy method. Class II restorations in 13 contralateral pairs of premolars were analyzed. The average difference of the ratio I 1610 cm-1/I 1640 cm-1 between the in vivo- and in vitro-performed restorations was 0.42. This indicates a higher grade of conversion in the in vivo situation.

Bicuspid↗
PubMed1992

Effect of vitamin A deficiency and Newcastle disease virus infection on IgA and IgM secretion in chickens.

The effect of vitamin A deficiency or the lentogenic La Sota strain of Newcastle disease virus (NDV) infection, or both, on immunoglobulin (IgA and IgM) levels in bile and plasma were investigated. In addition, tissue distribution of IgA-, IgG- and IgM-containing cells was studied to establish the source of these Ig. Chickens (1-d-old) with limited vitamin A reserves were fed ad lib. on diets containing either marginal or adequate levels of vitamin A. At 4 weeks of age, half the chickens in each group were infected with NDV. The number of IgA- and IgM-containing cells was not significantly affected by vitamin A deficiency, demonstrating that neither class-switching nor homing of Ig-containing cells is influenced by vitamin A deficiency. Although bile IgM levels were not significantly different in vitamin A-deficient chickens compared with normal chickens, IgA levels were significantly lower. This decrease was even more pronounced in deficient NDV-infected chickens, despite the higher number of IgA-containing cells found in these birds. These results, together with the slightly increased levels of IgA in plasma of vitamin A-deficient chickens, suggest that the hepatobiliary transport of IgA is impaired by vitamin A deficiency and possibly also by NDV infection, although disturbed secretion by IgA-containing cells cannot be excluded.

Animals↗
PubMed1992

The relationship between plasma beta-endorphin, opioid receptor activity, and silent myocardial ischemia.

OBJECTIVE: To investigate the role of the opioid system in the pathophysiology of silent ischemia through opiate antagonism with naloxone, and to determine the reproducibility of resting and postexercise beta-endorphin levels in predominantly asymptomatic patients with coronary artery disease. DESIGN: Randomized, double-blind, placebo-controlled crossover trial. SETTING: A University hospital referral center. PATIENTS: Ten patients with prior evidence of silent exercise-induced ischemia were studied. INTERVENTION: An infusion of saline placebo or naloxone at two dose regimens of 0.015 mg/kg or 0.15 mg/kg before supine exercise testing during three separate occasions for each patient. OUTCOME MEASURES: Plasma beta-endorphin was measured at rest, immediately after exercise, and 5 min poststress. Timing and severity of angina and exercise hemodynamics were also determined. RESULTS: Seven of 10 patients reported no angina, whereas the other three experienced angina with placebo and after administration of naloxone at both doses. The severity and duration of angina was consistently noted to decrease in these patients after naloxone administration, especially after low-dose naloxone relative to placebo. There were no apparent correlations between beta-endorphin levels and the characteristics of angina in these three patients, nor between beta-endorphin and hemodynamic responses in all patients in the study. CONCLUSIONS: (a) naloxone failed to precipitate angina in this population of patients with silent ischemia; (b) naloxone appears to exert an analgesic effect at low doses; and (c) a variability of 5 pM at rest and 13 pM after exercise might be expected in predominantly asymptomatic patients due to random variation, which is comparable with results found in normal subjects.

Aged↗
PubMed1992

Location of antigenic sites defined by neutralizing monoclonal antibodies on the S1 avian infectious bronchitis virus glycopolypeptide.

Neutralizing monoclonal antibodies directed against five antigenic sites on the spike (S) S1 glycopolypeptide of avian infectious bronchitis virus (IBV) were used to select neutralization-resistant variants of the virus. By comparing the nucleotide sequence of such variants with the sequence of the IBV parent strain, we located five antigenic sites on the amino acid sequence of the S1 glycopolypeptide. The variants had mutations within three regions corresponding to amino acid residues 24 to 61, 132 to 149 and 291 to 398 of the S1 glycopolypeptide. The location of three overlapping antigenic sites on the IBV spike protein was similar to the location of antigenic sites on the spike protein of other coronaviruses.

Antibodies, Monoclonal↗
PubMed1992

Interrelationships between left ventricular volume and output during exercise in healthy subjects.

To better characterize the relationship between left ventricular volume response and improved ventricular ejection and output during supine exercise in normal subjects, 36 healthy asymptomatic volunteers (age 39 +/- 17 yr) were studied with radionuclide ventriculography during recumbent bicycle ergometry. Relative changes in left ventricular end-diastolic and end-systolic volume were measured at rest and during exercise by a modification of the radionuclide counts-based method that accounted for variability in stress blood pool counts. A biphasic response was noted in left ventricular end-diastolic volume with an initial increase in early exercise (8.5 +/- 11% at 200 kpm/min and 11 +/- 12% at 300 kpm/min) followed by a progressive and significant decline at peak exercise (-3.3 +/- 18% at 547 +/- 140 kpm/min; P < 0.05). There was substantial variation in end-diastolic volume response at peak exercise in the group as a whole, which could be more closely related to changes in end-systolic volume (r = 0.84, P < 0.0001) than in heart rate (r = -0.57, P < 0.01) or age (r = 0.36, P < 0.05) of the study subjects. Despite the decline in ventricular filling, systolic function appeared to improve dramatically at peak exercise (change in left ventricular ejection fraction 15.5 +/- 6.4, P < 0.0001). Although not directly related to increasing systolic ejection, end-diastolic volume was directly related to the percent change in stroke volume at peak exercise among the study subjects (r = 0.88, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Susceptibility of thymocytes for infection by chicken anemia virus is related to pre- and posthatching development.

To investigate the age-dependent mechanism of susceptibility for chicken anemia virus (CAV) infection, we inoculated embryos and chickens of ages between day 9 of embryonic development and day 28 after hatching with CAV. Chicken embryos inoculated at days 9 and 11 of development showed no CAV-infected cells in the thymus, nor in other lymphoid organs. Many CAV-infected cells were detected in the thymic cortex of all chicken embryos inoculated at days 13 and 16 of development and of all chickens inoculated 1, 3, and 7 days after hatching. All embryos and chickens that contained CAV-infected cells in the thymus also contained CAV-infected cells in the bone marrow, but not in the bursa of Fabricius or the spleen. In chickens inoculated at days 14 and 21, only few CAV-infected cells were detected in the thymus, whereas these cells were not detected in thymi of 28-day-old inoculated chickens. Depletion of the thymic cortex was only detected in chickens inoculated from day 16 of embryonic development till day 21 after hatching. Only hematocrit values of the chickens inoculated 1 and 3 days after hatching were below normal. The rationale for the simultaneous susceptibility of cells of the T-cell lineage and cells of the erythrocyte lineage is discussed. As far as the thymus is concerned, the absence of clinical and microscopical signs of CAV infection in older chickens and the inability of CAV to infect embryos at days 9 and 11 of embryonic development may be caused by a lack of susceptible thymocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Alpharetrovirus↗
PubMed1992

L-696,474, a novel cytochalasin as an inhibitor of HIV-1 protease. III. Biological activity.

L-696,474, an inhibitor of the HIV-1 protease, was discovered in extracts of the fungal culture Hypoxylon fragiforme (MF5511; ATCC 20995). L-696,474 is a novel cytochalasin with a molecular weight of 477 and an empirical formula of C30H39NO4. L-696,474 inhibited HIV-1 protease activity with an IC50 of 3 microM and the mode of inhibition was competitive with respect to substrate (apparent Ki = 1 microM). Furthermore, L-696,474 was not a slow-binding inhibitor. The inhibition due to L-696,474 was also independent of the HIV-1 protease concentration. L-696,474 was inactive against pepsin, another aspartyl protease; stromelysin, a zinc-metalloproteinase; papain, a cysteine-specific protease or human leucocyte elastase, a serine-specific protease. Two other novel cytochalasins (L-697,318 and L-696,475) isolated from the same culture were inactive against the HIV-1 protease. Commercially available cytochalasins B, C, D, E, F, H and J were inactive while cytochalasin A was as active as L-696,474 against the HIV-1 protease.

Cytochalasins↗
PubMed1992

Oral health in preschool children living in Sweden. Part II--A longitudinal study. Findings at three years of age.

Scientific epidemiological studies of dental health in children three years of age are relatively few in Sweden. The aim of this study was to describe the oral health of three-year-old children living in Sweden, with special reference to immigration and failure to attend health examinations. All of 671 children requested to take part in an earlier investigation (Wendt et al. 1991) were invited for a new dental examination at three years of age. A total of 632 children were examined. At the age of three years 71.7 per cent of the children were caries free. Of the children with caries, 33.5 per cent were immigrants and of the total number of immigrants, 50.5 per cent had caries compared to 21.9 per cent of the non-immigrant children. Among those children, who failed to attend the earlier investigations at one or two years of age, 61.5 per cent had caries at the age of three. Compared to studies on dental health in three-year-old children from the 70's and 80's (Hugoson et al. 1986), this study shows that dental health in three-year-old children has not improved significantly during the last decade. Furthermore, this study supports the suggestion that special preventive dental programmes should be developed for immigrant children and that extra attention should be paid to children who fail to attend health examinations and their families.

Child, Preschool↗