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Biomedical subjects

B Heuberger

Publications and source records attributed to B Heuberger.

6 recordsLinked to original sources
PubMed1996

Lack of bioavailability of dichlorobenzidine form diarylide azo pigments: molecular dosimetry for hemoglobin and DNA adducts.

The hypothetical release of 3,3'-dichlorobenzidine (DCB) from two insoluble azo pigments and from a soluble azo dye was investigated in female Wistar rats for a 4 week treatment with 0.2% (w/w) Colour Index Pigment 13 (PY13) or 0.2% (w/w) Colour Index Pigment Yellow 17 (PY17) in the diet or 0.06% (w/v) Colour Index Direct Red 46 (DR46) in the drinking water. Steady-state DCB-hemoglobin adduct levels were determined by GC/MS with negative chemical ionization as well as DCB-DNA adduct levels in the liver by (32)P-postlabelling and compared with the respective adduct levels obtained in animals after treatment for 4 weeks with 0.00024, 0.0012 or 0.006% (w/v) DCB in the drinking water. A dose-proportional increase in adduct levels from 8.1 ng/g hemoglobin and 2.6 ng/g DNA (relative adduct level, RAL, 3.3x10(-9)) to 160 ng/g hemoglobin and 45.4 ng/g DNA (RAL 56.1x10(-9)) was observed in the DCB-treated rats. In rats treated with DR46 total adduct levels of 17.7 ng/g hemoglobin and 5.2 ng/g DNA (RAL 6.4x10(-9))were determined. No hemoglobin of DNA adducts were found in rats treated with PY17 in the diet, at a limit of detection of 0.1 ng/g hemoglobin and 0.08 ng/g DNA (RAL 0.1x10(-9)). In animals treated with PY13 in the diet no adducts or only minimal amounts slightly above the limit of detection could be identified. Taking into consideration that PY13 was contaminated with 0.02% of the respective soluble monoazo compound, it is concluded that the small amounts of DCB detected have been released from the contaminating soluble monoazo compound and not from insoluble PY13. The results of the present study demonstrate the lack of bioavailability of DCB from the diarylide azo pigments PY17 and PY13.

3,3'-Dichlorobenzidine↗
PubMed1986

[Cholecystitis in accident surgery].

Out of a large number of cholecystectomies four cases are reported. In some cases, the gallbladder was involved in the traumatic lesion itself but there are also cases, in which the cholecystitis developed independently of the primary lesion. Beside abdominal trauma which leads to a disruption of the organ wall we also see an inflammatory disease of the gallbladder after perforation during liver blind punction. In another case a patient with gall stone history developed acute cholecystitis after operative treatment of a collum femuris fracture. The fourth case shows acute cholecystitis which also arose after operative treatment of bone fracture in an acalculous bile vesicle. Acute cholecystitis after severe trauma not inflicting the organ itself is a severe, life threatening complication. One step to acute acalculous cholecystitis is the sludge formation in the gallbladder which can be recognized by ultrasonography. The pathogenetic mechanisms which lead to sludge phenomenon and later to acute cholecystitis are multifactorial. Some theories which try to explain this phenomenon are discussed. In each case the development of cholecystitis after trauma is a dangerous complication which urgently demands nonconservative treatment.

Adult↗
PubMed1982

Immunosuppressive effect of cyclosporin A in two lymphocyte transfer models in rats: comparison of in vivo and in vitro treatment.

The immunosuppressive effect of CS-A was first studied in the assay for local GvHR. 3 X 10(6) viable spleen cells from LEW rats were injected into one foot pad of LEW X BN hybrids and both PLN were weighed 7 days later. Treatment of the recipients with 3 doses of 50 mg/kg/day of CS-A suppressed this local GvHR. The effect was more pronounced when treatment started at the time of cell transfer rather than a few days before peak response. In vitro incubation of the cellular inoculum with CS-A also prevented local GvHR. Histology of the PLN confirmed the quantitative results expressed by the PLN index. CS-A was further investigated in the EAE model in LEW rats. It protected rats sensitised with spinal cord emulsified in complete Freund's adjuvant for as long as they were treated with CS-A. Treatment delayed until after the appearance of EAE also markedly improved their condition. Oral treatment of recipients with 50 mg/kg/day CS-A prevented the development of adoptive EAE following the transfer of lymphoid cells conditioned in vitro. The presence of 0.1-1.0 microgram CS-A in the medium of the sensitised lymphoid cells also inhibited the adoptive transfer of EAE. Finally, if the cells for the adoptive transfer were derived from CS-A-treated sensitised donors, they failed to induce EAE. Histological examination supported the symptomatic findings.

Animals↗
PubMed1982

Induction of androgen receptor formation by epithelium-mesenchyme interaction in embryonic mouse mammary gland.

The role of tissue interaction in the development of hormone responsiveness was studied in the embryonic mammary gland of the mouse, which becomes sensitive to testosterone on day 14. Previously, the mesenchyme had been identified as the sole target tissue for the hormone, although it was also demonstrated that its response to testosterone required the presence of mammary epithelium. Using autoradiography, we now show that [3H]testosterone or [3H]5 alpha-dihydrotestosterone is bound only by those mesenchymal cells closest to the epithelial mammary bud. When mammary epithelia were experimentally associated with mesenchyme of the mammary region and cultured together for 3 days in vitro, they also became surrounded by several layers of [3H]testosterone-binding mesenchymal cells. Correspondingly, this tissue association was accompanied by a substantial increase of androgen-binding sites in the explants. No hormone-building mesenchymal cells were seen in combinations with epidermis or pancreas epithelium; only salivary epithelium showed a weak positive effect. From these results we conclude that mammary epithelium induces the formation of androgen receptors in adjacent mesenchyme and thereby controls the development of androgen responsiveness in this tissue.

Animals↗
PubMed1982

Cyclosporin receptors on human lymphocytes.

Utilizing (3H) cyclosporin C (3H CS-C), a dihydroderivative of cyclosporin A (CS-A), an assay for cyclosporin receptors on human peripheral blood lymphocytes was developed. The specific binding of (3H) CS-C was saturable, time-dependent, and reversible. A Kd of 1.2 x 10(-7) M and a maximum binding capacity (Bmax) of 7 pmol/10(6) cells was calculated from equilibrium binding studies. A Scatchard analysis confirmed a single population of high affinity binding sites and about 7 x 10(5) sites/cell. Kinetic analysis of specific binding at 37 degrees C yielded a pseudo-first order rate association constant of 1.1 x 10(6) M-1 min-1 and a zero order dissociation rate constant of 0.19 min-1. The Kd 1.7 x 10(-7) M calculated from kinetic studies agreed well with the value of 1.2 x 10(-7) M determined in equilibrium binding studies. Regarding the specificity of binding, (3H) CS-C binding to lymphocytes was inhibited with CS-A and CS-C; however, no inhibition with the biologically inert keto-CS-A was observed. Mitogens and various growth factors did not compete for the binding site when added simultaneously with the radiolabel. However, pretreatment with T cell mitogens such as PHA, Con A, or the OKT3 antibody reduced (3H) CS-C binding significantly. These results suggest that the binding site for CS-A is closely associated with the mitogenic receptor on lymphocytes.

Antibodies, Monoclonal↗