The content of chlorinated hydrocarbons (CHC) was determined by means of capillary column gas chromatography in samples of fat tissue from 183 healthy children, 46 children with malignant tumors and 33 children with benign tumors or congenital malformations. The highest concentrations were found for total polychlorobiphenyls (PCB) (mean = 1.614 ppm), followed by the DDT group (mean = 0.556 ppm, HCB (mean = 0.097 ppm), the HCH isomers (mean = 0.083 ppm), dieldrin (mean = 0.020 ppm) and total heptachlor (mean = 0.010 ppm). Neonates displayed high concentrations in the adipose tissue before the first uptake of food. In the first six months of life, the concentrations of total PCB, the individual PCB components as well as DDT and HCB decreased significantly. In the second year of life, they rose again to the initial values and then remained relatively constant during the rest of childhood. The regional differences with regard to total CHC residues were slight, so that the CHC exposure cannot be reduced by a change of domicile within West Germany (FRG). Children with congenital malformations or benign or malignant tumors do not display raised concentrations of CHC.

Adipose Tissue↗

PubMedDate not supplied

Toxic reactions of oxidized LDL on cells of acute myeloid leukemia.

In AML patients LDL concentration of the serum is reduced due to the high LDL receptor activity of the AML cells. This phenomenon enables the use of LDL particles as vehicles for drug targeting. Toxic lipid peroxides and aldehydes were introduced into LDL particles by the simple but effective oxidation with 10 microM CuSO4. Up to 250 nmol peroxides and 6 nmol malondialdehyde were formed per mg LDL protein within 30 h of oxidation. This oxidized LDL is effectively taken up by AML cells of the FAB type M3 and M5 indicating the presence of scavenger receptors on these cells. Within 96 h 61-84% of the AML cells are killed by the oxidized LDL. Our results open a possibility to achieve specificity for targeting lipophilic antineoplastic drugs towards AML cells using oxidized LDL as vehicles. The use of oxidized LDL as drug carrier is recommended for purging of AML bone marrow because hematopoietic stem cells that don't possess scavenger receptors are protected from toxic action.

Copper Sulfate↗

PubMedDate not supplied

[Polysaccharide specific humoral immunodeficiency in ectodermal dysplasia. Case report of a boy with two affected brothers].

We report a now three year old male patient with ectodermal dysplasia and a polysaccharide specific humoral immunodeficiency. Immunological investigations showed compromised production of IgA, IgM, and IgG2. Isohaemagglutinins still were not detectable at the age of three years. Repeated vaccination with polyvalent pneumococcal polysaccharide vaccine did not result in production of specific antibodies. Two brothers showed clinical signs of ectodermal dysplasia. The elder brother died from pneumococcal sepsis at the age of 3 years. The younger brother suffers from chronic inflammatory gastrointestinal disease with ulcerations in all parts of the gastrointestinal system. Thus, a possible association between polysaccharide specific humoral immunodeficiency and ectodermal dysplasia may be considered.

Anti-Bacterial Agents↗

PubMedDate not supplied

[Resectability of malignant soft tissue tumors. Retrospective analysis of patients in the CWS 86 study].

A retrospective analysis of patients in the CWS-86 study with regard to the primary resectability of malignant soft tissue tumours was carried out. The aim was to find out how the topographical region, tumour size, histology and experience of the surgeon determined whether the tumour was primarily resectable. The survival rate, local relapse and metastatic rate were the end points of assessment. Although the number of patients in the groups was small, there was some suggestion that the topographical site of the primary tumour was a prognostic factor. The results showed that with regard to the resectability of the primary tumour and prognosis, it is possible to separate high and low risk regions. This initial classification could influence the therapeutic strategy.

Adolescent↗

PubMedDate not supplied

Apoptosis of cultured neuroblastoma cells is induced by ceramide and not by ligation of the Fas/Apo-1/CD95 receptor.

The expression of the Fas/APO-1/CD95 receptor on the neuroblastoma cell lines IMR-32, Kelly, SK-N-SH, LS and SiMa was investigated. The induction of apoptosis was attempted by incubation with Fas antibody IgM and IgG, Fas ligand and with ceramide. All neuroblastoma cell lines proved to be positive for Fas/APO-1/CD95 receptor expression by FACS. However, propidium iodide staining in FACS showed that neither incubation with the Fas antibody nor with the Fas ligand resulted in convincing apoptosis of the neuroblastoma cells. On the other hand, incubation with ceramide rapidly led to all signs of apoptosis morphologically and in the FACS. Therefore, other pathways than Fas/Apo-1/CD95 ligation must be of significance for the apoptosis of these neuroblastoma cell lines.

Apoptosis↗

PubMedDate not supplied

Inhibition of the membrane localization of p21 ras proteins by lovastatin in tumor cells possessing a mutated N-ras gene.

Mutated ras genes are found in a variety of human tumors. For biological activity the gene product p21 ras needs to be bound to the cell membrane by a farnesyl residue. Treatment of tumor cells with lovastatin reduces the availability of farnesyl pyrophosphate for the modification of the ras proteins. The membrane localization of p21 ras has been reduced by 30-36% after the tumor cells have grown in the presence of 10 microM lovastatin for 7 days. The extent of the inhibition depends on the growth kinetics of the cell lines.

Acute Disease↗

PubMedDate not supplied

Inhibition of farnesyl-protein-transferase in neuroblastoma cells by alpha-hydroxyfarnesylphosphonate.

Oncogenic Ras is responsible for malignant transformation in a variety of tumors. Farnesylation of Ras by farnesyl-protein-transferase (FPTase) is necessary for membrane localization of Ras-proteins, a prerequisite for its biological activity. Although mutations in ras genes are rare in neuroblastoma inactivation of Ras by inhibition of the FPTase is of interest in neuroblastoma. In this tumor, amplification of N-myc is frequently observed and expression of N-myc is induced via Ras signaling. Farnesyl-protein-transferase of neuroblastoma cells is inhibited by alpha-hydroxyfarnesylphosphonate. In homogenates of the cell line SK-N-AS an ID50 = 6.5 microM is estimated, in SK-N-SH the ID50 is 3.4 microM. The consequences of the inhibition of FPTase on the membrane localization was examined by immunoblots. Western blots of membrane proteins analysed with H-ras and N-ras specific antibodies revealed that H-ras protein is more sensitive to the inhibition of FPTase than N-ras protein. After culturing neuroblastoma cells for 24 hrs in the presence of 20 microM alpha-hydroxyfarnesylphosphonate H-ras protein completely dissappeared from the membrane fraction whereas N-ras protein was only affected by 50%. K-ras was not detectable on Western blots of three neuroblastoma cell lines. The experiments showed that FPTase inhibitors are effective in neuroblastoma cells but for complete inactivation of N-ras stronger conditions are required than for H-ras.

Alkyl and Aryl Transferases↗

PubMedDate not supplied

[Arrhythmias in mitral valve prolapse].

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Adolescent↗