Correlation length and inverse-participation-ratio exponents and multifractal structure for Anderson localization.
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Biomedical subjects
Publications and source records attributed to J Bauer.
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The response of liver macrophages (Kupffer cells) to distinct pathogenic material was investigated by comparing virus- and endotoxin-induced macrophage activation. Endotoxin-induced stimulation and induction with Newcastle disease virus (NDV) or Sendai virus led to the release of the same pattern of prostanoids characterized by a predominant production of prostaglandin E2 (PGE2). With respect to peptide mediators, hepatic macrophages secreted tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 after viral induction and endotoxin treatment, respectively. In response to viruses, however, much more interleukin-6 and TNF-alpha was detected than after endotoxin stimulation. Interferon type I (interferon-alpha/beta), on the other hand, was only detected in the supernatants of macrophages infected with viruses, but not of those exposed to endotoxin. This study also revealed that rat TNF-alpha exists in several soluble species, some of which are glycosylated.
We have generated a series of human macrophage hybridomas by fusing an HGPRT-deficient promonocytic cell line, U937, with macrophages obtained by allowing monocytes to mature into macrophages in teflon bags. The fusions were documented as true hybrids by the acquisition of donor class I molecules, as well as donor derived macrophage surface antigens. The hybridomas represent clonal expansion of individual macrophages, retaining the surface antigen expression and functional capacity of the normal donor cells including cytokine production and stimulation in a mixed lymphocyte reaction. These cell lines differentially express Vmax antigens found on normal macrophages, potentially identifying subpopulations of macrophages. These lines may be useful not only to study normal macrophage function but may be relevant to a variety of disease states where expansion of subpopulations of macrophages identified by Vmax antigens may be important in disease pathogenesis.
A 31-year-old man with Wilson's disease, not treated for the past 4 1/2 years, was admitted to hospital with brain concussion after a fall. While receiving penicillamine, 1 g i.v. four times daily, the neurological signs worsened and akinesia, mutism, tachy- and bradyarrhythmias, as well as transitory respiratory insufficiency developed. Serum copper concentration on the sixth day of treatment was markedly decreased to 28 micrograms/dl, rising to 60 micrograms/dl on the ninth day. 24-hour urinary copper excretion was at first 4500-5000 micrograms. Only after drastic reduction of the penicillamine dosage to 600 mg three times daily was there any improvement and after 11 weeks the patient was again able to walk and was discharged. Marked, mainly hepatic, copper depletion from the high penicillamine dosage was the likely cause of the patient's initial deterioration. To avoid cerebral complications penicillamine should be administered in gradually increasing doses.
Ictal single photon emission computed tomography recordings were performed in 9 patients in the course of 11 seizures. Injections of radionuclide were made an average of 72 seconds after the onset of the seizure as indicated by electroencephalography. All patients also underwent interictal recordings. In 6 patients, the localization of the electroencephalographic focus and the morphological lesions corresponded with the ictal hyperperfusion. This could be seen in single photon emission computed tomography. Seizures triggered by hyperventilation, and seizures of patients with anatomical brain lesions (e.g., cysts, surgical defects, and recent injections of technetium-hexamethylene-propylene-amine-oxime) showed an absent or noncorresponding localization of the ictal recording. The ictal and interictal recording seems suitable as a confirmatory noninvasive method for the localization of the epileptogenic focus, particularly in the preoperative evaluation of epilepsy.
Zieve's syndrome (hyperlipidaemia, anaemia and fatty liver degeneration) may rarely occur with intracranial haemorrhage. Four patients suffering from both diseases are reported. Although it remains unclear whether there is a causal relationship between the two, it seems that hyperlipidaemia may be a major cause of intracranial bleeding. One reason for the small number of reported cases may be that hyperlipidaemic serum levels rapidly decrease after alcohol withdrawal.
Tissue macrophages of the liver (Kupffer cells) release interleukin-6 (IL-6) in vitro. Since Kupffer cells reside in close proximity to hepatocytes, which are major target cells of IL-6, the regulation of IL-6 release by hepatic macrophages has been investigated in this study. Using the hybridoma growth test to detect IL-6, we found that Kupffer cells already maximally release IL-6 at endotoxin concentrations as low as 1.0 ng/ml. The stimulated secretion of IL-6 was increased 4-8-fold by endotoxin when compared to the control macrophages incubated in serum-containing medium alone. The preincubation of macrophages with interferon-gamma enhanced the capacity of Kupffer cells to respond to endotoxin. The secretion of IL-6 could also be induced by interleukin (IL)-1 beta and tumor necrosis factor (TNF-alpha). The most potent inducers, however, were the paramyxoviruses Newcastle Disease Virus and Sendai Virus. The release of IL-6 by macrophages upon stimulation with endotoxin was almost completely inhibited by 1 microM dexamethasone. Whereas 100 nM of prostaglandin E2 (PGE2) inhibited the release of TNF-alpha in rat Kupffer cells, it did not affect the secretion of IL-6.
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Initial results of magnetic source localization by means of multichannel recording using a 10 or a 31 channel system are reported. Simultaneous magnetoencephalographic (MEG) and electroencephalographic (EEG) (scalp, sphenoidal and foramen oval) recording, as well as magnetic resonance imaging (MRI) with a fixed head position, permits the projection of brain structures and the source localized from MEG into a three-dimensional coordinate system. From 8 patients investigated it can be clearly seen that the method is of diagnostic relevance for patients with temporal lobe epilepsy. Results are demonstrated for 3 patients with interesting findings concerning the anatomical correlation with source localization. The findings indicate that MRI-correlated magnetic source localization by means of multichannel recordings provides important advantages in epilepsy research. (1) Increased precision permits noninvasive localization. Deeper sources in the temporal lobe are localized from MEG combined with scalp or minor invasive EEG. (2) Investigation time is considerably shortened. (3) Single events can be localized for supplementary presurgical information concerning the three-dimensional anatomical localization of focal epileptic activity in the brain.
In a model of colon cancer in rats the bacterial extract OM-89 was found to have antitumor properties. We have shown that OM-89 induced the complete regression of numerous peritoneal tumor nodules measuring 1-5 mm in 46% of rats, and inhibited the growth of microscopic tumors in 42% of rats. OM-89 was effective when injected ip at the dose of 50 mg/kg, twice a week for 2 weeks. It was ineffective at the same dose when given orally every day for 14 or 21 days. The traces of endotoxins (0.0005%) were probably not involved in the antitumor effect of OM-89. No side-effects were observed.
Comparative analyses of cereal samples pretreated with or without beta-glucosidase indicate the presence of zearalenone-glycoside. To examine the stability of zearalenone-glycoside during digestion, mixed feed was artificially contaminated with synthesized zearalenone-4-beta-D-glucopyranoside (395 micrograms/kg) and fed to a pig over a period of 14 days. The metabolites detected in feces and urine samples were zearalenone and alpha-zearalenol. These results demonstrate that zearalenone-4-beta-D-glucopyranoside is decomposed during digestion and the aglucone, zearalenone, is released. Since zearalenone-glycoside is not detected during routine analysis, but hydrolysed during digestion, it seems likely that such "masked mycotoxins" are involved in cases of mycotoxicoses.
The biosynthesis and secretion of M-type and Z-type alpha 1-antitrypsin was studied in human monocytes. In monocytes of PiMM individuals alpha 1-antitrypsin represented 0.08% of the newly synthesized proteins and 0.44% of the secreted proteins. Two molecular forms of alpha 1-antitrypsin could be identified: a 51-kDa intracellular form, susceptible to endoglucosaminidase H, thus representing the high-mannose type precursor form and a 56-kDa form resistant to endoglucosaminidase H which was secreted into the medium. Inhibition of de novo glycosylation by tunicamycin impaired the secretion of M-type alpha 1-antitrypsin by about 75% whereas inhibition of oligosaccharide processing by the mannosidase II inhibitor swainsonine did not alter the secretion of M-type alpha 1-antitrypsin. alpha 1-Antitrypsin secreted by human monocytes was functionally active as measured by complex formation with porcine pancreatic elastase. Even unglycosylated alpha 1-antitrypsin secreted by human monocytes treated with tunicamycin formed a complex with elastase. In monocytes of PiZZ individuals the secretion of alpha 1-antitrypsin was decreased. 72% of newly synthesized M-type alpha 1-antitrypsin, but only 35% of newly synthesized Z-type alpha 1-antitrypsin were secreted during a labeling period of 3 h with [35S]methionine. The 51-kDa form of Z-type alpha 1-antitrypsin accumulated intracellularly, whereas the 56-kDa form was secreted. Inhibition of oligosaccharide processing by swainsonine did not alter the decreased secretion of Z-type alpha 1-antitrypsin, whereas inhibition of de novo glycosylation by tunicamycin blocked the secretion of Z-type alpha 1-antitrypsin completely.
B-lymphocyte derived mouse myeloma cells P3X63Ag8U.1 were used to study the change of the negative surface charge density which occurs during a final maturation step of mouse and human B-cells. These cells showed a uniform EM distribution curve as long as they lived within a clone. However, when they grew in suspension at low density, a part of them increased their electrophoretic mobility (EM). Cells with enhanced EM were isolated by free flow electrophoresis. They showed lower proliferation and clone forming activity but higher alkaline phosphatase activity than cells with unchanged low EM. The study suggests that the increase of the EM and of the alkaline phosphatase activity are parallel events associated with B cell progression from the proliferative to the Ig secretion stage.
In a number of neurological diseases, e.g. Guillain-Barré syndrome, patients are at high risk for a bradyarrhythmia or asystolia. Sometimes a cardiac pacemaker is needed for prophylaxis or for emergency therapy. The usual temporary insertion of a transvenous stimulating electrode has many disadvantages and a high incidence of complications. We report on our initial experience with the non-invasive technique of transcutaneous stimulation via superficial electrodes. The advantages of this method are discussed.
OM-89, a proteinaceous extract from Escherichia coli with very low endotoxin content, was tested for its capacity to stimulate in vitro cells involved in the immune response. OM-89 induced a marked proliferation of mouse spleen cells; E. coli lipopolysaccharide (LPS) at the same concentration as present in OM-89 was totally ineffective. Passage through nylon wool strongly decreased the OM-89-induced effect, suggesting that the responding lymphocytes were of the B lineage. Exposure of bone marrow-derived macrophages to OM-89 promoted glucose oxidation through the hexose monophosphate shunt pathway and the capacity to generate superoxide upon phorbol myristate acetate (PMA) stimulation. These effects were not blocked by polymyxin B, whereas this compound completely prevented induction of similar metabolic activation by E. coli lipopolysaccharide. In addition, OM-89 treatment induced marked PMA-dependent superoxide and hydrogen peroxide release by macrophages from the LPS low responder mouse strain C3H/HeJ. Incubation with recombinant murine interferon-gamma and OM-89, but not with either compound alone, led to functional activation, as shown by the killing of tumor target cells, and by the destruction of the intracellular parasite Leishmania enrietti by macrophages of both LPS-responsive and unresponsive mouse strains. These experiments indicate that OM-89 can stimulate metabolic and functional activities of lymphocytes and macrophages that are important for host defense.
Adsorption of the mycotoxin ochratoxin A by activated charcoal, various bentonites (acid, alkaline, neutral), and hydrated sodium calcium aluminosilicate was tested in vitro as well as in feeding experiments with pigs. In vitro tests showed that the 1% addition of activated charcoal leads to complete adsorption of ochratoxin A from aqueous solutions. This effect was not influenced by pH-values ranging from 3-8. In contrast, adsorption by bentonite and hydrated sodium calcium aluminosilicate occurred primarily in the acid range (pH 3-4). Dietary addition of hydrated sodium calcium aluminosilicate (1%) and acid bentonite (1%, 10%) to ochratoxin A-contaminated feed (1.0 mg/kg) had no effect on the blood or tissue levels of the toxin in pigs. The addition of 1% activated charcoal caused a slight decrease of ochratoxin A in the blood, whereas a tenfold dosage resulted in a 50% to 80% reduction of ochratoxin A levels in both blood and tissue. Reduction of ochratoxin A absorption via the dietary administration of activated charcoal (5%) was confirmed in a 16 week feeding experiment. However, this experiment also showed the serum level of vitamin E to be lower than in the controls receiving adsorbent-free feed.
The incidence of chronic radiation enteritis appears to have risen in recent years due to the increasing utilization of radiotherapy for abdominal and pelvic malignancies. The etiology, pathogenesis, and management of radiation enteritis are discussed. Two case reports exemplify the progressive nature of the disease. Case 1 demonstrates the classical picture of multiple exacerbations and remissions of partial small bowel obstruction and the eventual need for surgical management ten years after radiation therapy. Case 2 presents the more severe sequelae of an acute perforation with a 14-yr latency period. Predisposing factors in the progression of radiation injury include excessive radiation, underlying cardiovascular disease, fixation of the bowel, and an asthenic habitus. In both cases, radiation injury was localized to a discrete segment of bowel; therefore, resection with a primary end-to-end anastomosis was performed. In addition, diseased bowel was eliminated and, therefore, would not cause further complications such as intractable bleeding or fistula formation. The review focuses on current knowledge which may be applied to the treatment and prevention of radiation enteritis.
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