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Biomedical subjects

A Weber

Publications and source records attributed to A Weber.

At least 505 records · Page 28Linked to original sources
PubMed1983

Haemophilus influenzae b bacteremia and meningitis in infant rabbits after intranasal inoculation.

A suitable model of Haemophilus influenzae meningitis will facilitate better understanding of the pathophysiology, therapy, and prevention of the disease and its sequelae. Bacteremia and meningitis were induced in infant New Zealand white rabbits by intranasal inoculation of H. influenzae type b. Intranasal trypsin prior to challenge significantly increased (p = 0.002) the rate of bacteremia from 64% (7/11) to 100% (45/45). In the trypsin-treated group, H. influenzae b was isolated from the CSF of 89% (25/28) of 17- to 21-day-old rabbits and from 76% (13/17) of 23- to 30-day-old animals, p = 0.3; fatality rates were 88% and 31%, respectively, p = 0.001. Bacteremia developed within 24 hr of inoculation and meningitis within 96 hr. Death occurred 1 to 7 days after the development of meningitis. Histologic evidence of nasopharyngitis and meningitis was found at autopsy. The intranasal route of infection, the age-dependent outcome, the size of the animal, and its low cost and availability make the infant rabbit an appropriate model of H. influenzae b meningitis.

Animals↗
PubMed1983

[Detection of phenylalanine hydroxylase activity in leukocytes and fibroblasts].

Phenylalanine hydroxylase activity measured in leucocytes and fibroblasts by the fluorometric method is nonspecific and can be released by other aromatic hydroxylases. Investigations with the inhibitors p-Cl-phenylalanine, 3-I-tyrosine and 6-F-tryptophan made evident that these results may be caused by the tryptophan hydroxylase and the tyrosine hydroxylase. Phenylalanine hydroxylase activities in leucocytes could also not be measured by radiochemical investigations with [3-14C] phenylalanine (scanner and liquid scintillation technique).

Fibroblasts↗
PubMed1983

Antibody classes and subclasses in circulating immune complexes isolated from mice infected with lactic dehydrogenase virus.

A chronological study of circulating immune complexes (CIC) in lactic dehydrogenase virus (LDV)-infected mice has been performed. The results demonstrate that CIC containing immunoglobulin of the IgM class were isolated between days 3 and 9 post-LDV infection and corresponded to an increase in serum IgM. IgG1-containing CIC were also transient in the serum of LDV-infected mice in that they were isolated only between days 5 and 13. The occurrence of IgG1 CIC did correlate with an increase in total IgG1 in the serum, however, it did correlate with a small (1:10) increase in IgG1 anti-LDV activity. In contrast, CIC containing immunoglobulin of the serum IgG2 subclass were not isolated from LDV-infected serum until 15 days post infection. This chronological appearance of IgG2 CIC did not correlate with the observed increase in total IgG2 concentration in LDV-infected mice on day 7, however, was analogous to the rapid increase in free serum LDV-specific antibody. We propose that the non-specific suppression of the immune response and tumour enhancement during the acute phase of LDV infection could be due to the immunoregulatory properties of IgG1 CIC.

Animals↗
PubMed1982

[Campylobacter jejuni--a "recent" pathogen worthy of study. Present knowledge on its clinical aspects, diagnosis, therapy and epidemiology].

The frequency of human infections caused by Campylobacter (C.) jejuni is thought to be at present as significant as that of the gastroenteric salmonelloses. The clinical symptoms are mostly like enteritis, enterocolitis, acute abdomen or ileitis terminalis. Post-infection reactions are possible not only as arthritis or septicemia but also as meningitis, conjunctivitis, carditis, pneumonia, cholecystitis, peritonitis, urinary tract infection and abortion. Only cultural examinations confirm the diagnosis of an infection with C. jejuni. If chemotherapy is required, erythromycin is the remedy of choice. Animals are an important reservoir for C. jejuni, but the epidemiology of human infections with this microorganism is not well understood.

Adult↗
PubMed1982

[The behavior of the thyrotropin-releasing hormone test in fasting with and without triiodothyronine administration].

It is reported on the performance of the 400 microgram TRH/TSH test in adipose persons in the course of a zero diet and on the effects of an application of 50 micrograms tri-iodothyronine during 7 days on the TRH/TSH test on the same conditions. During total fasting the basic and TRH-stimulating TSH-level shows a slight tendency of decrease, but scarcely significant changes. After application of 50 micrograms tri-iodothyronine an unequivocal suppression of the TSH-concentration in the serum is to be recognized. By these results and with the help of literary data by means of the most sensitive test of the diagnostics of hypothyroidism a general hypofunction of the pancreas could be excluded, as it was supposed in the low T3 syndrome. But tri-iodothyronine deficiency in some tissues is still discussed at present.

Adolescent↗
PubMed1982

[Enteral yersiniosis--a serious disease? Current knowledge of clinical aspects, diagnosis and therapy].

Enteral yersiniosis is caused either by Y. enterocolitica 0-group I (syn. serotype 0:3) and 0-group V (syn. serotype 0:9) or Y. pseudotuberculosis type I-VI. The clinical symptoms are mostly like enteritis, enterocolitis, acute abdomen, mesenteric lymphadenitis, or ileitis terminalis. Post-infection reactions are possible like septicemia, arthritis and erythema nodosum. Only cultural and serological examinations confirm the diagnosis of enteral yersiniosis. In the judgement of serological results it is necessary to consider the cross-reactions of Y. enterocolitica 0-group V to Brucella abortus, Brucella melitensis and Brucella suis and also to the antigenic community of Y. pseudotuberculosis type II respectively IV to Salmonella group B respectively D. With exception of septicemia, it is not necessary to treat enteral yersiniosis with antibiotics.

Abdomen, Acute↗
PubMed1982

Potentiated state of the tropomyosin actin filament and nucleotide-containing myosin subfragment 1.

The main purpose of this study was to determine whether potentiation of acto-S-1 ATPase activity (activity higher than that obtained with tropomyosin-free actin) could be caused by nucleotide-containing acto-S-1 complexes. In addition, we wanted to know whether these complexes also have a positive cooperative effect on their own apparent binding constant under conditions where nucleotide-free acto-S-1 complexes cause potentiation of ATPase activity. Using calcium-saturated troponin-tropomyosin actin filaments, we observed potentiation of ATPase activity in the presence of 5.0 mM magnesium 5'-adenylyl imidodiphosphate (MgAMPPNP) and calculated that the ability of acto-S-1-AMPPNP complexes to cause potentiation must have been very similar to that of nucleotide-free acto-S-1 complexes. In extension of earlier studies, potentiated acto-S-1 ATPase activity was characterized by an increase in Vmax and, as observed before, a lowering of the apparent Km for subfragment 1 (S-1). Under conditions similar to those that produce the potentiation of acto-S-1 ATPase activity, the apparent actin binding constant of nucleotide-free S-1 was increased about 3-5 fold while the apparent binding constant of AMPPNP to actin-bound S-1 was reduced to (2.5-10) x 10(2) M-1 compared to that of about (1-5) x 10(3) M-1 for S-1 bound to tropomyosin-free actin. Under the same conditions, the apparent binding constant of S-1-AMPPNP to actin was not increased. We suggest that a potentiated state of the tropomyosin actin filament is produced by the cooperative action of acto-S-1 or acto-S-1-AMPPNP complexes. The potentiated state is characterized by an increase in the Vmax of the acto-S-1 ATPase activity, increased binding constants for S-1 and S-1-ADP, and increased binding of tropomyosin to actin.

Actins↗
PubMed1982

Development and expression of cytoplasmic antigens in Purkinje cells recognized by monoclonal antibodies. Studies in neurologically mutant mice.

Five monoclonal antibodies reacting with intracellular constituents of Purkinje cells were investigated by means of indirect immunofluorescence on fresh-frozen sections of the cerebellum and retina from developing and adult normal and mutant mice. Antibodies PC1, PC2 and PC3, which recognize Purkinje cells, but no other cerebellar neuron type, label these cells from day 4 onward. PC4 antigen is expressed in addition to Purkinje cells also in granule cells and neurons of deep cerebellar nuclei and appears in Purkinje cells at day 4. M1 antigen (Lagenaur et al. 1980) is first detectable in Purkinje cell bodies by day 5; it is also detectable in deep cerebellar neurons. In the adult retina, only PC4 antigen is detectably expressed and is localized in the inner segments of photoreceptor cells. The neurological mutants weaver, reeler, jimpy and wobbler show detectable levels of these antigens in Purkinje cells. However, the mutants staggerer and Purkinje cell degeneration are abnormal in expression PC1, PC2, PC3, and M1 antigens. Staggerer never starts to express the antigens during development, whereas Purkinje cell degeneration first expresses the antigens, but then loses antigen expression after day 23. PC4 antigen is detectable in the remaining Purkinje cells in staggerer and Purkinje cell degeneration mice at all ages tested in this study. Deep cerebellar neurons are positive for both antigens, PC4 and M1, in all mutants and at all ages studied. In retinas of staggerer and Purkinje cell degeneration mutants. PC4 antigen is normally detectable in the inner segments of photoreceptor cells, even when these have started to degenerate in the case of Purkinje cell degeneration.

Animals↗