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Biomedical subjects

D Schreiber

Publications and source records attributed to D Schreiber.

At least 37 records · Page 2Linked to original sources

[Preoperative computer tomography and postoperative classification of brain tumors].

Imaging of different brain tumor types by computed tomography (CT) or contrast-enhanced CT scans is often very similar. Therefore, the exact preoperative CT diagnosis of intracranial neoplasms is difficult. Among 100 cases (88 primary brain tumors, 12 brain metastases), the preoperative classification by CT was correct in 51 and partially correct in 22 cases. A corresponding presumptive CT diagnosis was made in 22 brain neoplasms. 5 cases were misinterpreted. Examples of CT scans and histological pictures are compared and analysed according to the literature.

Brain Neoplasms↗

Structure/activity investigations in eight arylalkyltriazenes comparison of chemical stability, mode of decomposition, and SCE induction in Chinese hamster V79-E cells.

A series of seven 1-aryl-3.3-dialkyltriazenes, including 1-phenyl-3.3-dimethyltriazene (DMPT), 1-phenyl-3.3-di-(trideuteromethyl)-triazene (DMPT-ds), 1-p-methylphenyl-3.3-dimethyltriazene (DMpMPT), 1-p-nitrophenyl-3.3-dimethyltriazene (DMpNPT), 1-phenyl-3.3-diethyltriazene (DEPT), 1-phenyl-3.3-di-n-propyltriazene (DnPrPT) and 1-phenyl-3.3-diisopropyltriazene (DiPrPT) and 1.3-diphenyl-3-methyltriazene (DPMT), was synthesized and characterized by UV/VIS, IR and 1H-NMR spectroscopy. Chemical half-life was determined in phosphate buffer at 37 degrees using UV/VIS spectroscopy. With the exception of DMpNPT, which was stable, the triazenes underwent pH-dependent hydrolytic decomposition (acid catalysis). By means of UV/VIS spectra, TLC and HPLC, phenol, aniline and secondary azocoupling products were identified after complete hydrolytic cleavage of the parent compounds. Pathways of spontaneous hydrolysis are proposed and discussed. Genotoxic activity of the triazenes was assayed by measurement of sister chromatid exchanges (SCE) in V79-E cells without and with rat liver S9 mix as an exogenous metabolizing system. In the direct SCE assay (without S9 mix), all triazenes except DMpNPT exerted a toxic action (cell cycle delay) in a narrow concentration range between no effect and overt cytotoxicity. This non-specific toxicity depended on the pH of the incubation system and was inversely proportional to chemical half-life. The toxicity of these agents is most likely due to the arenediazonium cation which is a relatively stable intermediate. In a sublethal concentration range most triazeness induced significant increases of SCE rates. These are interpreted as an indirect consequence of cytotoxicity. Upon metabolic activation, the compounds were genotoxic in a dose-dependent fashion. Their SCE-inducing capacity depended on the nature of the alkylating species generated, i.e., the alkyldiazonium cation, and on chemical stability. Surprisingly, no deuterium isotope effect was observed in DMPT-d6. The order of genotoxic activity among the aryldialkyltriazenes was DMpNPT much greater than DMPT = DMPT-ds greater than DMpMPT much greater than DEPT greater than DnPrPT greater than or equal to DiPrPT. DPMT was a marginal SCE inducer but very toxic upon metabolic activation. As monooxygenation of DPMT, like spontaneous hydrolysis, should generate a phenyldiazonium cation, the results suggest that arylation of DNA causes a very low SCE induction, if any.

Animals↗

Suppressive macrophages occurring in murine Trypanosoma brucei infection inhibit T-cell responses in vivo and in vitro.

Intraperitoneal injection of Trypanosoma brucei AnTat 1.1 into mice of the C3H.He, BALB/c or C57BL/6 strains resulted in impaired immune responses from day 3 onwards, as measured by the reduction in DNA synthesis in spleen cell populations stimulated with concanavalin A (Con-A) in vitro. Adherent cells from the peritoneum (PC) or from the spleen of infected mice, consisting predominantly of macrophages, caused a 60-80% reduction of the Con-A response in spleen cells from syngeneic recipients 3-4 days after transfer in vivo. Adherent PC from irradiated or athymic mice were equally suppressive. Spleen cells from infected mice reduced the proliferative response of spleen cells from uninfected mice upon co-cultivation in vitro. This dominant suppressive effect was abolished after the selective removal of macrophages from the spleen cell population by treatment with L-leucine methylester. Moreover, the macrophage-depleted spleen cells from infected mice responded normally to Con-A provided they were supplemented with splenic adherent cells from naive mice as a source of accessory cells. Both the cell transfer and co-cultivation experiments suggest that infection with African trypanosomes changes the properties of macrophages to a state which allows them actively to suppress immune responses.

Animals↗

[CNS involvement in neurofibromatosis. A postmortem study].

Neurofibromatosis was recorded from 30 in 82,249 postmortem cases (0.036%) at the Medical Academy of Erfurt, Institute of Pathological Anatomy, between June 1, 1945 and December 31, 1986, among them 13 cases of classical peripheral neurofibromatosis generalisata Recklinghausen (NgR) and 17 with CNS involvement. These had been 10 males and 7 females who had died at an age from 8 to 77 years (average age and death being 39 years). CNS lesions were preferentially localised in periventricular sections of the third and fourth ventricles and the cerebral aquaeduct, with diffuse gliosis being recorded from 5 cases. Typical bilateral neurofibromatosis of the acoustic nerve was established from three males aged 19, 26 and 30 years. Spinal neurinoma or neurofibroma, meningioma, an astrocytoma of the cervical spinal cord, and leptomeningeal sarcomatosis were also recorded. Additional skeletal abnormalities were exhibited by four cases. Interest is generally growing in CNS involvement in neurofibromatosis due to the possibility of intravital diagnosis by computed tomography (CT) and magnetic resonance spectroscopy (MRI) and because of possible surgical therapy. Recent studies in molecular genetics, on the other hand, have shown classical NgR to be caused by a lesion to chromosome 17, while bilateral neurofibromatosis of the acoustic nerve was found to be based on a genetic defect to the long arm of chromosome 22.

Adolescent↗

[Microbiological and morphological findings in reactive lymphadenopathy].

An attempt was made by means of microbiological and histomorphological methods for diagnostic elucidation of reactive lymphadenopathies in 52 patients. The serological findings differed from those recorded from clinically intact individuals, in that they included not only increased prevalence of antibodies but also increased antibody titres to cytomegalovirus, influenza virus, and toxoplasma gondii. The dynamic of antibody titres against antigens specific of herpesvirus, influenza virus, and toxoplasma gondii were followed up and enabled positive detection in 11 of 18 patients of active infections with the above pathogens involved. Histologically, the lymph nodes affected were characterised by alterations reminiscent to Piringer lymphadenitis. While, in the course of bacteriological investigations, various bacterial species were isolated from lymph node tissue of 35 patients, direct morphological identification from lymph node sections failed to work. Immature sinus histiocytosis and an increase in phagocytosis activity were among the typical tissue findings.

Adolescent↗

[The pre- and postnatal carcinogenic effect of 3,3-diethyl-1-methyl-1-nitrosourea (DEMNU) in rats following intravenous application].

The pre- and postnatal administration of DEMNU induces a high frequency of tumors when applied via the intravenous route, and the latency periods show a dose dependence (table I). Tumors of the brain, spinal cord and cranial nerves clearly predominate. Furthermore, a large number of neoplasms of kidney, heart and soft tissue was observed (table II). As DEMNU is per se a very stable compound, it is suggested that this agent is metabolized by monooxygenases. 3-Ethyl-1-methyl-1-nitrosourea should be formed as an intermediate product via this pathway, which is relatively stable and might explain the mainly neurotropic carcinogenicity of DEMNU. Species differences in the carcinogenicity of trialkyl-nitrosoureas and the mode of metabolic activation are discussed.

Animals↗

Regulation of hepatic cholesterol ester hydrolase and acyl-coenzyme A:cholesterol acyltransferase in the rat.

Cholesterol exists within the hepatocyte as free cholesterol and cholesteryl ester. The proportion of intrahepatic cholesterol in the free or ester forms is governed in part by the rate of cholesteryl ester formation by acyl-coenzyme A:cholesterol acyltransferase (ACAT) and cholesteryl ester hydrolysis by neutral cholesterol ester (CE) hydrolase. In other cell types both ACAT and CE hydrolase activities are regulated in response to changes in the need for cellular free cholesterol. In rats, we performed a variety of experimental manipulations in order to vary the need for hepatic free cholesterol and to examine what effect, if any, this had on the enzymes that govern cholesteryl ester metabolism. Administration of a 20-mg bolus of lipoprotein cholesterol or a diet supplemented with 2% cholesterol resulted in an increase in microsomal cholesteryl ester content with little change in microsomal free cholesterol. This was accomplished by an increase in cholesteryl esterification as measured by ACAT but no change in CE hydrolase activity. An increased need for hepatic free cholesterol was experimentally induced by intravenous bile salt infusion or cholestyramine (3%) added to the diet. ACAT activity was decreased with both experimental manipulations compared to controls, while CE hydrolase activity did not change. Microsomal cholesteryl ester content decreased significantly with little change in microsomal free cholesterol content. Addition of exogenous liposomal cholesterol to liver microsomes from cholestyramine-fed and control rats resulted in a 784 +/- 38% increase in ACAT activity. Nevertheless, the decrease in ACAT activity with cholestyramine feeding was maintained. These studies allowed us to conclude that changes in hepatic free cholesterol needs are met in part by regulation of the rate of cholesterol esterification by ACAT without a change in the rate of cholesteryl ester hydrolysis by CE hydrolase.

Animals↗

[Intracranial ependymoma with extraneural metastases].

A report is given on a 14-year-old boy with an ependymoma of the brain which was 3 times operated upon. At autopsy, a widespread leptomeningeal and intraventricular dissemination was found. Extraneural metastases developed in the soft tissues of the neck as well as in the pleura and lung on the left side. Immunohistochemically, the cells of the brain tumor and extraneural metastases of the neck showed a positive GFAP-reaction. According to Tables 17 to 19 of Jänisch and co-workers (1976; 1988) and Table 1 of this paper, 48 intracranial, intraspinal and ectopic (subcutaneous sacrococcygeal) ependymomas with extraneural metastases were collected from the literature.

Adolescent↗

[A simple method for the isolation of GFAP and its use for the study of brain tumors].

A simple method is described in this paper for the production of a polyclonal antiserum against GFAP. The antiserum was tested on 212 primary brain tumours which had been selected from biopsy and autopsy material of the Institute of Pathological Anatomy at the Medical Academy of Erfurt, GDR. 52 of 81 astrocytomas (64%) and 26 of 47 glioblastomas (55%) gave GFAP-positive results. GFAP-negative responses were primarily recorded from tumours with severe anaplasia. GFAP was found in all 22 ependymomas tested. Epithelioid ependymomas, however, exhibited lower immunological reactions than tanycytic variants. Isomorphic oligodendrogliomas, meningiomas, medulloblastomas, and brain metastases of carcinomas were GFAP-negative. The possibility is discussed in some detail of falsely negative results on account of too little biopsy material or insufficient fixation of tumour tissue.

Animals↗

Fibrin glue on the Cohn I fraction basis in repairing cerebral and dura defects--an experimental study on rats.

The rat skulls were operated upon using a trephine osteoplastically, and a defined cerebral and dura defect was induced. The repair of the cerebral defect was performed with Cohn I glue, or in combination with collageneous fleece. The dura defect was repaired by suture and/or glueing of a split skin or pedicle galeal-periostal flap. Thanks to using Cohn I glue, at all times sufficient venous hemostasis could be achieved, and in combination with collagen fleece the repair was at an optimum. The histological check-up demonstrated that neurotoxic side-effects were absent and there were no conglutinations with the dura. Suturing of the dura was highly time-consuming and impossible when the dura had been removed near the bone. The use of Cohn I adhesive permitted ready and defect repair commonly applicable. At high tension the combined suture-glueing technique proved to be superior.

Animals↗

[Hamartoma of the liver in childhood].

Liver hamartoma is one of the very rare findings in childhood. It is a dysontogenetic malformation that grows clinically manifest with tumour-like appearance in the first or second year of age. Cystic and solid formations are described in this report. Findings are usually clearly delimited from clinically intact liver parenchyma. In surgical extirpation, that delimitation should be stringently observed to avoid unnecessary blood loss. The prognosis generally is good and should not be jeopardised by delay of surgical therapy. Reported are two cases of liver hamartoma, with both patients being laparotomised at the age of one and a half years.

Hamartoma↗