Are molecular filters really necessary?
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Biomedical subjects
Publications and source records attributed to G Koch.
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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.
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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.
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.
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)
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)
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.
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.
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Amalgam (ANA 2000), composite resin (Occlusin), and glass ionomer cement (ChemFil) were compared in conventional Class II restorations in second primary molars. Twenty-five restorations of each material were placed by two dentists in 50 patients. The restorations were evaluated during a three year period using the USPHS criteria. Great differences could be found between the materials. The failure rate (USPHS ratings Charlie) was after three years 8 per cent for the amalgam, 16 per cent for the composite resin and 60 per cent for the glass ionomer cement restorations.
Anticardiolipin-antibodies are antibodies to phospholipids which were first detected in patients with arterial thrombosis and lupus erythematosus. In this prospective study, IgG- and IgM-anticardiolipin-antibodies were determined in patients with cerebral and/or peripheral artery disease but without autoimmune disorders. 123 randomly selected patients (88 males, 35 females; mean: 65 +/- 10, range: 41-85 years) were included and divided into four groups: 18 patients with isolated cerebrovascular disease (group A), 35 patients with peripheral artery disease only (group B), 35 patients suffering from cerebral and peripheral artery disease (group C) and 35 patients as controls (group D). In family history, cholesterol, blood sugar and prothrombin time the four patient groups did not differ significantly, whereas patients of group B and C were more often smokers than those in groups A and D. However, IgG-anticardiolipin-antibody-levels were significantly elevated in patients with cerebral and peripheral artery disease compared to controls (p less than 0.01). The highest values were seen in group C where patients suffered from cerebral and peripheral artery disease (n.s.). On the other hand, IgM-anticardiolipin-antibody-levels did not show any differences in the four groups. Furthermore, there was no correlation between vascular risk factors and/or laboratory findings with IgG- and IgM-antibody-levels. Thus, elevated IgG-anticardiolipin-antibodies appear to be independent markers for severe cerebral and peripheral artery disease and should be determined in patients at increased risk.
Mastoparan, which has been shown to active G proteins, inhibits the ADP-ribosylation of 20 kDa human platelet membrane proteins catalyzed by Clostridium botulinum exoenzyme C3 half-maximally and maximally (90%) at 20 and 100 microM concentrations, respectively. Inhibition of ADP-ribosylation was enhanced by GTP-gamma S. Mastoparan increased GTP hydrolysis by porcine brain rho protein and stimulated GTP binding in a concentration dependent manner. The data suggest that mastoparan not only interacts with heterotrimeric G proteins but also with low molecular mass GTP-binding proteins of the rho/rac family.
The avian immune system is reviewed. The avian immune system differs from that of mammals, mainly in the presence or absence of lymphoid organ and in the histology of these organs, in the antibody response, in the generation of diversity of antibodies, and in the transfer of maternal immunity. The chicken immune system is mainly discussed, since most of the research on the avian immune system has been performed using this bird.
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18 patients who had fulfilled the NINCDS-ADRDA criteria for "possible AD" took part in a clinical study to evaluate the effect of the cholinesterase inhibitor Galanthamine, 30 mg/day. Neuropsychological und social parameters were rated. This open clinical pilot-study showed no statistic significant change in neuropsychological test-results. However after 1 year treatment 6 patients are still taking the drug. According to their care-persons there was a positive changes in competence of everyday-routine and/or in the emotional situation.
Visual symptoms are often among the first complaints of patients suffering from Alzheimer's disease and several studies showed a delay in flash visual evoked potentials. Hinton et al. (1986) described optic nerve degenerations in patients with Alzheimer's disease and Sadun published a dropout of retinal ganglion cells that range from 30% to 60%. The reduction of neurotransmitters, especially of acetylcholine, found in the brain might also occur in the retina. Therefore we examined the retinal functions of patients suffering from Alzheimer's disease. In eight patients the pattern-electroretinograms and the scotopic and photopic luminance-electroretinograms were recorded and compared to an age-matched control group. We could not find any abnormalities in the pattern- and the luminance electroretinograms of patients with Alzheimer's disease. Although cholinergic cells have been found in the retina, our results did not reveal an involvement of retinal functions in Morbus Alzheimer.