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Biomedical subjects

R Bergmann

Publications and source records attributed to R Bergmann.

At least 55 records · Page 3Linked to original sources
PubMed1992

Simultaneous study of the biodistribution of radio-yttrium complexed with EDTMP and citrate ligands in tumour-bearing rats.

The influence of the ligands ethylenediaminetetramethylene phosphonic acid (EDTMP) and citrate (CIT) on the biodistribution of radio-yttrium in rats bearing a DS-carcinosarcoma was compared. 88Y-EDTMP and 87Y-CIT were i.v. injected into the same animals. Faster blood clearance and higher renal excretion were observed for the EDTMP-ligand. Of high practical interest is the reduced liver uptake of radio-yttrium (by one order of magnitude) with the EDTMP complex. Since bone and tumour accumulation is only weakly influenced, high tumour-to-liver ratios (up to 14) were observed. We propose to use EDTMP or similar complex ligands for liver blocking when radionuclides like 90Y, 169Yb, 225Ac or other group 3 elements are to be applied in endoradionuclide therapy technique.

Animals↗
PubMed1991

Experimental and clinical main forms of hypoxic-ischaemic brain damage and their monitoring.

A short review of main pathogenetic forms of hypoxic-ischaemic brain damage and its consequences for causally orientated therapy and monitoring is given. Different pathogenetic components act in several combinations. In these processes disturbances of the cardio-vascular system, of the haemorheology mainly at the level of microvessels, and disturbances of the blood brain barrier are involved. Furthermore, there are relevant disturbances of the neuronal metabolism such as accumulation of cytosolic Ca++ or disturbances caused by the effect of radicals, lipid peroxidation and changes of protein synthesis. Nowadays, chances of a cause-related therapy are increased by improved evaluation of main pathogenetic components especially regarding secondary brain damage. To evaluate these components in detail, animal models must be more clinically related, especially regarding long-term studies. The increasing knowledge about critical thresholds of reversible and irreversible brain changes also favours effective cerebral function monitoring. The main conclusions from previous experimental as well as clinically related studies indicate the necessity of very early therapeutical interventions.

Brain↗
PubMed1991

Interaction between systemic circulation and brain injuries in newborns.

In several studies different pathogenetic mechanisms of metabolic and/or cardiovascular origin were shown depending on the type of hypoxic or hypoxic/hypercapnic stress and conditions of animals (normal developed or intrauterine growth retarded newborn piglets). Thus, in normal-weight piglets the prevention of compensatory hyperventilation owing to severe hypoxia (artificially ventilated animals) leads to critical, i.e. lethal acidosis. In intrauterine growth retarded piglets, a severe hypoxia cannot be vitally compensated because of the restricted circulatory centralization. Moreover, a limited cerebrovascular dilatation during moderate hypoxia/hypercapnia produces a critical state of the metabolic supply in those animals.

Adaptation, Physiological↗
PubMed1991

Investigations of cerebral glucose utilization into the newborn brain: a [18F]-FDG positron emission tomography study using a high resolution multiwire proportional chamber detector device.

An experimental approach is presented, where for the first time positron emission tomography (PET, the most important method for in vivo measuring the key functions of brain physiology and metabolism) was applied together with other techniques for quantitative-topological estimation of key parameters such as rCMRGlu in normal and disturbed brain function states in the newborn period.

Animals↗
PubMed1990

Synthesis and antihypertensive activity of 4-(1,2-dihydro-2-oxo-1-pyridyl)-2H-1-benzopyrans and related compounds, new potassium channel activators.

The synthesis and antihypertensive activity of 4-(1,2-dihydro-2-oxo-1-pyridyl)-2H-1-benzopyran-3-ols are described. The unsubstituted pyridone adduct lead compound 7e is highly active, with substituents on the pyridone ring leading to a decrease in activity. Strongly electron-withdrawing substituents at the C-6 position are required for optimal activity. When the 2-pyridone ring is replaced by other heterocycles such as 4-pyridone, pyrimidone, pyridazinone, pyrazinone, and 1,4-butanesultam, the activity is maintained. The removal of the 3-hydroxy function (----17a) does not significantly reduce the activity. The elimination of water from the chromanols leads to the formation of the chromenes, which are among the most potent antihypertensives known. The influence of diverse substituents, in particular heterocyclic C-6 substituents, was investigated in the 4-(2-oxo-1-pyrrolidinyl)chroman-3-ol series. Chromanols esterified at the 3-hydroxy group with short-chain acids, maintain their activity. The epoxidation of the chromene double bond also produces active compounds. The rearrangement of the epoxides 22 produces the 3-keto compounds 23 and the enol derivatives 25. The reduction of the ketone 23a produces cis-chromanol 7ab along with its trans isomer 7e. All compounds were tested for oral antihypertensive activity in spontaneously hypertensive rats with a dose of 1 mg/kg; for selected compounds ED30 values as well as the duration of the antihypertensive effect were determined. 4-(1,2-Dihydro-2-oxo-1-pyridyl)-2,2-dimethyl-2H-1-benzopyran-6- carbonitrile (18a) is under development as a coronary vasodilator and a drug for treating angina pectoris.

Animals↗
PubMed1990

4-Heterocyclyloxy-2H-1-benzopyran potassium channel activators.

The reaction of 2,4-dihydroxypyridine (2) with 3,4-epoxy-3,4-dihydro-2,2-dimethyl-2H-1-benzopyran-6-carbonitrile (1) yielded the 4-[(1,2-dihydro-2-oxo-4-pyridyl)oxy] compound 3a, accompanied by small amounts of the isomeric 4-(1,2-dihydro-4-hydroxy-2-oxo-1-pyridyl) compound 4. This could also be prepared by hydrogenation of the benzyloxy derivative 5. Reaction of 3,6-pyridazinediol (10) with 1 (R = CN) gave the 4-[(1,6-dihydro-6-oxo-3-pyridazinyl)oxy] compound 11a, which in turn rearranged on heating with NaH in DMSO into the 4-(1,6-dihydro-3-hydroxy-6-oxo-1-pyridazinyl) compound 12. A series of 6-substituted analogues (R = CO2Me, CSNH2, NO2, Br) of 3a and 11a were synthesized. N-Alkylation led to compounds 14a-c (R = Me, Et, CHMe2). The 4-heterocyclyloxychromenes 9 and 16a were obtained by alkaline hydrolysis of their 3-camphorsulfonates. The racemic pyridazinyloxy compounds 11a and 14a could be resolved via their diastereomeric camphorsulfonates or camphanates. The differences between the 4-heterocyclyloxychromanols and the isomeric N-substituted compounds 4 and 12 were elucidated in the course of extensive NMR investigations. While in DMSO the former appeared to be conformationally flexible molecules the latter were rigid. All compounds were tested for oral antihypertensive activity in spontaneously hypertensive rats, using doses of 1 mg/kg. High and long lasting activities were found for the pyridyloxy compounds 3a and 3d, the pyridazinyloxy compound 11a, and its N-alkylation products, as well as for the 3S,4R-enantiomers 20a and 22a. (-)-(3S,4R)-3,4-Dihydro-4-[(1,6-dihydro-1-methyl-6-oxo-3- pyridazinyl)oxy]-3-hydroxy-2,2-dimethyl-2H-1-benzopyran-6-carbonitrile (22a) was selected for further development.

Animals↗
PubMed1989

Thiolutin inhibits utilization of glucose and other carbon sources in cells of Escherichia coli.

Thiolutin was found to inhibit the utilization of glucose and other growth substrates in Escherichia coli. The inhibition was detected by a sharp drop of the respiration rate after addition of the antibiotic. The actual function affected was allocated to the cytoplasmic membrane of the bacterial cells by the following evidence: --spheroplasts were affected like intact cells, --individual reactions of either the electron transport chain or the glycolytic pathway were not inhibited, --glucose consumption in the culture stopped and the cells accumulated guanosine tetraphosphate as under starvation conditions, --activation of the cell's apo-glucose dehydrogenase restored respiration via bypassing the glucose phosphotransferase system. It was concluded that the transport of certain substrates across the membrane was inhibited.

Anti-Bacterial Agents↗
PubMed1989

Lipid profile of body builders with and without self-administration of anabolic steroids.

Twenty-four top-level body builders [13 anabolic steroid users (A); 11 non-users (N)] and 11 performance-matched controls (C) were examined to determine the effect on lipids, lipoproteins and apolipoproteins of many years of body building with and without simultaneous intake of anabolic steroids and testosterone. After an overnight fast, triglycerides (TG), total cholesterol (TOTC), high density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC), the HDLC subfractions HDL2C and HDL3C, as well as apolipoprotein A-I (Apo A-I), apolipoprotein A-II (Apo A-II) and apolipoprotein B (Apo B) were determined. Both A and N, compared to C, showed significantly lower HDLC and higher LDLC concentrations, with the differences between A and C clearly pronounced. In a subgroup of 6 body builders taking anabolic steroids at the time of the study, HDLC, HDL2C, HDL3C, Apo A-I and Apo A-II were all significantly lower and LDLC was significantly higher than in a second subgroup of 7 body builders who had discontinued their intake of anabolic steroids at least 4 weeks prior to the study. In some single cases HDLC was barely detectable (2-7 mg.dl-1). The TG and TOTC remained unchanged. The present findings suggest that many years of body building among top-level athletes have no beneficial effect on lipoproteins and apolipoproteins. Simultaneous use of anabolic steroids results in part in extreme alterations in lipoproteins and apolipoproteins, representing an atherogenic profile. After discontinuing the use of anabolic steroids, the changes in lipid metabolism appear to be reversible.

Adult↗
PubMed1989

[Preventing iron deficiency in breast-fed infants by suitable supplementary food. A prospective, controlled study].

Iron deficiency may develop in prolonged breast feeding. Introduction of beikost (supplementary nutrition) is recommended in Germany for infants after 4 months of age. In a prospective study 73 exclusively breastfed infants at the age of 16 weeks were assigned to one of two feeding groups: 35 infants received a meat vegetable dinner fortified with iron-2-sulfate (3 mg iron per 100 kcal) as their first supplementary food. At 20 weeks of age a milk based rice cereal (MBRC) without iron fortification was added as a second beikost meal. The other group comprised 38 infants who first received a MBRC fortified with iron-3-pyrophosphate (3 mg iron per 100 kcal). At 20 weeks of age a non iron fortified vegetable potato dinner was introduced. After 6 months of age the iron fortified meat vegetable dinner was offered to all infants once a day. 26 infants who did not receive this dinner but otherwise were consulted and treated identically served as controls at 12 months of age. At 6 months of age values of hemoglobin, MCV, serum iron, ferritin, and transferrin saturation were higher in the meat dinner group compared to the cereal first group. At 12 months of age this was also true for the meat dinner group compared to the controls. However, the differences were minor and statistically not significant. Whereas most of the indicators of iron nutritional status were within the lower normal range, and total iron intake was below the levels recommended by German and American authorities, recommending two iron fortified beikost meals between age 7 and 12 months appears to be justified.

Anemia, Hypochromic↗
PubMed1988

[Breast feeding as "alternative" nutrition? An orientation aid in the field spanning ideology and current status].

Recommending breast feeding supports a trend "back to nature". However, there are believers in the unbiased goodness of nature, who claim effects of mothers milk, e.g. protection from the evils of civilization, that are not confirmed by current scientific knowledge. As nature is not uniquely good (it feeds the donkey and the lion), and as biology is not perfect, breast feeding does not guarantee an uneventful infancy and childhood. There is even a pathology of breast feeding that the pediatrician should be familiar with.- The proven benefits, claimed effects, and some risks of breast feeding are reviewed on the basis of research results, and conclusions are drawn to make breast feeding as uneventful an experience as possible. Potential fields of research are being identified.

Breast Feeding↗
PubMed1987

[Kinetics of membrane-bound aldehyde dehydrogenase from Acinetobacter calcoaceticus].

In recent investigations we were able to demonstrate that the NADP-dependent aldehyde dehydrogenase of Acinetobacter calcoaceticus is an inducible enzyme localized in intracytoplasmic membranes limiting alkane inclusions. Long-chain aliphatic hydrocarbons and alkanols are inducers of the enzyme. It was purified by us and now kinetically characterized using the enzyme-micelle form, which contains bacterial phospholipids and a detergent (sodium cholate), too. The pH optimum of aldehyde dehydrogenase was determined to be at pH 10. The enzyme showed substrate inhibition (by aldehyde excess). The Ks and Km values of the leading substrate NADP+ were found to be 8.6 X 10(-5) and 10.3 X 10(-5)M independent of the chain-length of the aldehydes. The Km values of the aldehydes decreased depending on increasing chain-length (butanal: 1.6 X 10(-3), decanal: 1.5 X 10(-6)M). The Ki values (for inhibition by aldehyde excess) showed a similar behaviour (butanal: 7.5 X 10(-3), decanal: 3.5 X 10(-5)M) as well as the optimal aldehyde concentrations inducing the "maximal" reaction velocity (butanal: 5mM, decanal: 6 microM). The number of inhibiting aldehyde molecules per enzyme-substrate complex was determined to be n = 1. NADPH showed product inhibition kinetics (Ki(NADPH) = 2.2 X 10(-4)M), fatty acids did not. We were unable to measure a reverse reaction. The following ions and organic compounds were non-competitive inhibitors of the enzyme: Sn2+, Fe2+, Cu2+, BO3(3-), CN-, EDTA, o-phenanthroline, p-chloromercuri-benzoate, mercaptoethanol, phenylmethylsulfonyl fluoride, and diisopropylfluorophosphate; iodoacetate did not influence enzyme activity. Chloral hydrate was a competitive inhibitor of the aldehydes. Ethyl butyrate activates the enzyme, dependent on the chain-length of the aldehyde substrates.

Acinetobacter↗