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Biomedical subjects

B Puschendorf

Publications and source records attributed to B Puschendorf.

At least 145 records · Page 8Linked to original sources
PubMed1984

Increase in histone acetylation and transitions in histone variants during Friend cell differentiation.

Histone acetylation of Murine Erythroleukemia Cells (MELC) has been re-examined. It is demonstrated that sodium butyrate causes hyperacetylation of core histones in inducible as well as non-inducible MELC strains. This indicates that histone hyperacetylation per se is not sufficient to activate genes. However, [3H]acetate incorporation into core histones of the inducible MELC line F4N increases after induction of differentiation with dimethylsulfoxide (DMSO), in contrast to the non-inducible variant F4+. Thus histone acetylation may play a role as an auxiliary mechanism for gene activation (and inactivation). In addition, the appearance of a histone H3 variant during differentiation of MELC is reported.

Acetylation↗
PubMed1984

Depression of histone acetylation by alkylating antitumor agents: significance for antitumor activity and possible biological consequences.

Treatment of Ehrlich ascites tumor cells with the alkylating antitumor agents triaziquonum, N-mustard and cyclophosphamide leads to a reduction in the posttranslational incorporation of 3H-acetate into histones and the extent of histone acetylation in Ehrlich ascites tumor cells. All core histones are affected. The depression of histone acetylation is not the result of a decrease in acetyl-CoA. Evidence is presented for an activation of histone deacetylase by alkylating agents. A reduction of histone deacetylation is observed after exposure to all concentrations of alkylating agents which inhibit cell proliferation. In order to evaluate the biological consequences of a reduction of histone acetylation, the extent of acetylation was modulated by either chemical acetylation or treatment with butyrate. In all cases an increase in histone acetylation leads to an enhancement of the rate of transcription. In accord with previous reports from our laboratory (1), it is concluded that the reduction of histone acetylation affects RNA synthesis. It is emphasized, however, that besides a regulation of transcription, histone acetylation may be involved in other cell functions. Thus, the complete biological consequences of the reduction of histone acetylation remain to be elucidated. In view of the antitumor activity of the alkylating agents it seems noteworthy that hepatoma AS30D cells are characterized by a remarkably higher extent of histone H4-acetylation compared to normal, adult, fetal, or regenerating liver.

Alkylation↗
PubMed1984

Depression of histone acetylation by alkylating antitumor agents in murine cells.

Treatment of Ehrlich ascites tumor cells with the alkylating agent triaziquone [2,3,5-tris(ethyleneimino)benzoquinone-1,4] and nitrogen mustard leads to a reduction of the posttranslational acetylation of histones. Acetylation of all core histones is affected. The reduction of labeling of acetylated sites is accompanied by a dose-dependent decrease in the extent of acetylation as indicated by the level of acetylation of H4. The depression of histone acetylation is expressed at all concentrations of the alkylating agents which cause significant inhibition of tumor cell proliferation. It could be excluded that the observed effects are caused by an impairment of acetyl coenzyme A synthesis.

Acetates↗
PubMed1983

Conservation of the acetylation pattern of histones and the transcriptional activity in Ehrlich ascites tumor cells by sodium butyrate.

Histone deacetylases of Ehrlich ascites tumor cells are active at low temperatures (0-4 degrees C). The so-called hyperacetylated state of histones is the physiological state of histones in intact Ehrlich ascites tumor cells which is conserved by the continuous presence of 10 mM sodium butyrate during the preparation of nuclei and histones. Isolation of histones in the absence of butyrate causes an artificial decrease in histone acetylation. This artificial loss of histone acetylation produces a decrease of the elongation reaction in the RNA synthesis. The initiation of RNA synthesis is not affected.

Acetylation↗
PubMed1983

Myoglobinemia in the early phase of acute myocardial infarction.

Close-meshed determinations of plasma myoglobin, creatine kinase, and its isoenzyme MB were carried out in nine patients admitted to the clinic less than 4 hours after the onset of symptoms in the course of acute myocardial infarction (AMI). Myoglobin clearly appears earlier (mean 2 hours and 30 minutes) in the plasma than creatine kinase (mean 4 hours and 15 minutes) and isoenzyme MB (mean 5 hours and 30 minutes after the onset of symptoms). During the first hours of AMI plasma myoglobin shows multiple peaks in all patients. Because this pattern is observed only with myoglobin but not with creatine kinase, it appears that myoglobin mirrors the early course of the necrosis more distinctly than creatine kinase. Plasma myoglobin was also found elevated after intramuscular injections and a high voltage accident. Myoglobinuria was not detectable after myocardial infarction.

Adult↗
PubMed1983

Inhibition of tumor growth by an alkylation of the plasma membrane.

The effect of nitrogen mustard (2-chloro-N-2-chloroethyl-N-methylethanamine), Trenimon (2,3,5-trisethyleneiminobenzoquinone-1,4), chlorambucil (4-[p-(bis[2-chloroethyl]amino)-phenyl]butyric acid) and phosphamide mustard (N,N-bis(2-chloroethyl)-diamidophosphoric acid) on Na+/K+-ATPase, membrane fluidity and cell multiplication was studied. With the exception of chlorambucil which does not affect Na+/K+-ATPase all concentrations of the other alkylating agents which inhibit cell multiplication of Ehrlich ascites tumor cells depress the activity of the Na+/K+-ATPase. All alkylating agents--including chlorambucil--caused an increase in the apparent degree of fluorescence polarization after labelling of the plasma membrane with 1,6-diphenyl-1,3,5-hexatriene (DPH). This effect is interpreted as a decrease in membrane fluidity caused by the alkylating drugs. The decrease in membrane fluidity is due to a direct interaction of the alkylating agent with the plasma membrane and is expressed at all concentrations of the drug which inhibit cell proliferation. No effect on membrane fluidity is observed after treatment of cells resistant to nitrogen mustard. The biological consequence of a decrease in membrane fluidity was investigated by growing Friend erythroleukemia cells in the presence of 10 mM cholesterol hemisuccinate. This procedure raises the microviscosity of the plasma membrane and depresses cell proliferation.

Alkylating Agents↗
PubMed1982

Cell-cycle-dependent effects of sodium-n-butyrate in Physarum polycephalum.

Sodium-n-butyrate affects the length of the mitotic cycle of Physarum polycephalum. Application during S- or early G2-period results in a delay of the subsequent mitosis, whereas application later in the cycle has no delaying effect. Interestingly, the second mitotic cycle after application is considerably shortened when butyrate has been administered during S- or early G2-period of the preceding cycle. In comparison, other homologous short-chain fatty acids were tested; the retarding effect on mitosis increases with the number of carbon atoms, although only butyrate can shorten the second mitotic cycle. It is shown that butyrate causes an immediate depression of synthesis of DNA, RNA and protein. After a certain time-interval the plasmodium overcomes the butyrate block. DNA synthesis is fully recovered and the inhibition of RNA and protein synthesis is even overcompensated until the next mitosis, as reflected by elevated levels of RNA and protein.

Butyrates↗
PubMed1981

[Possible malignant hyperthermia as reaction to an overdose of myotonolytic, antidepressive and sedative drugs (author's transl)].

A 51-year-old male patient with no history of musculo-skeletal or myopathic abnormalities, but suffering from manic-depressive psychosis, attempted suicide with an overdose of dolpersin hydrochloride (Mydocalm), dipenzepine hydrochloride (Noveril), meprobamate (Mepronox) and nitrazepam (Mogadon). He developed high fever, muscle rigidity, tachycardia, arrhythmias, hypotension and mottled cyanosis, symptoms well-known in persons with malignant hyperthermia, an autosomally inherited disease of skeletal muscle. There is also discussed the manifestation and the symptoms of an acute rhabdomyolysis. The diagnosis was confirmed by chemical pathological laboratory findings, including respiratory and metabolic acidosis, myoglobinaemia accompanied by myoglobin diuresis, and elevated creatine phosphokinase (CPK values up to 2790 U/l). Electron microscopic examination of muscle tissue revealed signs of myolysis and mitochondrial reactions with pleoconic hyperplasia. No inhalation anaesthetics or skeletal muscle relaxants, such as succinyl choline, were used in this case. Therefore, malignant hyperthermia might have been induced by a combination of drugs which were not known to induce this abnormal muscular reaction. However, the muscle relaxant effect of dolpersin hydrochloride may have acted as a possible inducer of the attack.

Bipolar Disorder↗
PubMed1981

Interaction of the alkylating antitumor agent 2,3,5-tris(ethyleneimino)benzoquinone with the plasma membrane of Ehrlich ascites tumor cells.

The effect of the alkylating agent 2,3,5-tris(ethyleneimino)benzoquinone (Trenimon) on the uptake of 2-aminoisobutyric acid, 1-aminocyclopentane-1-carboxylic acid (cycloleucine), 3-O-methyl-D-glucose, and 86Rb was studied. All transport studies were performed at nonsaturating conditions where the specific transport system was rate limiting for the uptake. The activities of all systems are reduced after treatment with the alkylating agent. The impairment of the plasma membrane is expressed 30 sec after exposure to the drug, as measured by the 86Rb uptake, and lasts for at least 12 hr according to the reduced 3-O-methyl-D-glucose uptake. Inhibition of protein synthesis by cycloheximide for 2 hr does not affect the uptake of 86Rb. The short interval which is necessary before an inhibition of 86Rb uptake can be registered and the resistance of the 86Rb transport system to an inhibition of protein synthesis are considered as indicative for a direct alkylation of a membrane constituent. Treatment with the alkylating agent increases the cyclic adenosine 3':5'-monophosphate of the cells. This effect is not due to an effect on adenylate cyclase or the membrane-bound cyclic adenosine 3':5'-monophosphate phosphodiesterase. In view of the known correlations between plasma membrane functions and the regulation of cell division, it is proposed that the growth inhibition by Trenimon of Ehrlich ascites tumor cells may be caused by its interaction with the plasma membrane.

Alkylating Agents↗
PubMed1981

Urinary excretion of cyclic guanosine 3'.5'-monophosphate in children with malignant tumours.

The present study shows an increased urinary cyclic guanosine 3'.5'-monophosphate (cyclic GMP) excretion rate in children of all age groups bearing malignant tumours or lymphomas. The incidence of increased cyclic GMP excretion was highly significant (79%). Follow-up studies of up to three years have revealed that during periods of remission of malignant disease the urinary cyclic GMP excretion drops to near normal values, whereas recurrences are accompanied by a new increase of cyclic GMP excretion.

Age Factors↗
PubMed1980

[Diagnosis of hypercalciuria in calcium nephrolithiasis (author's transl)].

An increased calcium excretion in 24-hour urine was found in 32 of 42 out-patients with recurrent calcium nephrolithiasis (calcium excretion > 300 mg in males, > 250 mg in females). Subsequent hospitalization of the 32 patients revealed the following diagnosis after a calcium tolerance test: absorptive hypercalciuria in 18, renal hypercalciuria in 4, primary hyperparathyroidism in 2 and dietary hypercalciuria in 7. Normocalciuria in 10 out-patients was confirmed in 6; in one instance there was, however, primary hyperparathyroidism, in 3 there was absorptive hypercalciuria. In one patient it was not possible to classify the hypercalciuria. Total as well as nephrogenic cAMP showed wide scatter and was unsuitable, therefore, in differential diagnosis. In 2 of 3 cases of hyperparathyroidism the serum level of parathormone was distinctly elevated.

Calcium↗
PubMed1979

[Estimation of myocardial damage after open-heart surgery by CK isoencymes (author's transl)].

After 12 cases of open-heart surgery serum activities of CK and CKMB have been registrated. To make a more exact statement about myocardial damage the portion of CKMB out of the CK-activity has been evaluated by the way of a mathematic programm. The results verify the statement that after aortic valve replacement the CKMB portion is higher than the average, and that after intraoperative complications the highest CKMB portions have been reached. No myocardial infarction occurred.

Aortic Valve↗
PubMed1978

[Differential diagnosis between skeletal muscle lesions and myocardial damage in multiple injury by determination of myocardial-specific creatine phosphokinase (CK-MB) (author's transl)].

The serum level of the myocardial-specific isoenzyme of creatine phosphokinase, CK-MB was determined in 50 patients with severe multiple injuries or following extensive surgery. It is concluded that whenever the proportion of CK-MB exceeds 10% of the total creatine phosphokinase activity myocardial damage has occurred, especially since equivalent ECG changes were registered in this group of patients.

Contusions↗
PubMed1978

[Postoperative fructose infusion in a case of presumed hereditary fructose intolerance (author's transl)].

Hereditary fructose intolerance (HFI) was diagnosed in a 61 year-old male patient on account of liver dysfunction followed by prolonged shock immediately after the administration of a fructose and lactose infusion postoperatively. The diagnosis of HFI was based on an increased value of fructose, hypoglycaemia, lactic acidosis and diminution of the phosphate level in combination with the typical family history. The patient's children showed a normal reaction to fructose administration. The therapy included glucose, insulin and heparin administration, balance of acidosis and partial exchange of blood, which resulted in improvement in the glucose level, coagulation factors and acidosis, but could not prevent further liver damage and uraemia with a fatal outcome.

Acidosis↗
PubMed1978

[The value of CKMB in multiple trauma and high voltage injuries].

The paper deals with a new aspect in patients with polytrauma using a method to distinguish between myocardial or skeletal muscle damage. The isoenzyme CKMB of kreatine kinase is found to be characteristic for myocardial damage when increasing to more than 10% of the whole enzyme activity. It should be mentioned that this elevation is also seen in other disorders. Therefore the correlation to ECG changes is important in considering the diagnosis.

Adolescent↗