Search Results - (Author, Cooperation:Bode)

Bode, Herbert F.; Brinkmann, Günter

Unknown

135 S.

351354412X

Dimensionen der Pädagogik

German

Bode, Fritz

Unknown

90 S.

Handbücher für die praktische naturwissenschaftliche Arbeit

German

Bode, Wilhelm

Unknown

396 S.

Bode, Dietrich; Pientka, Herbert

Unknown

267 S.

3761417764

Materialien-Handbuch Physik Bd. 7

1749-6632

Blackwell Publishing Journal Backfiles 1879-2005

Natural Sciences in General

Electronic Resource

1546-1696

Nature Archives 1869 - 2009

Biology

Process Engineering, Biotechnology, Nutrition Technology

[Auszug] The genus Sorangium synthesizes approximately half of the secondary metabolites isolated from myxobacteria, including the anti-cancer metabolite epothilone. We report the complete genome sequence of the model Sorangium strain S. cellulosum So ce56, which produces several natural products and has ...

Electronic Resource

0012-1606

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Electronic Resource

0012-1606

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Electronic Resource

0012-1606

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Electronic Resource

0012-1606

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Electronic Resource

0009-9120

analysi titrimetric ; chymotrypsin fecal ; diagnosis laboratory ; pancreatic insufficiency ; spectrophotometry

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Medicine

Electronic Resource

0009-9120

analysi titrimetric ; chymotrypsin fecal ; diagnosis laboratory ; pancreatic insufficiency ; spectrophotometry

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Medicine

Electronic Resource

1437-1596

Springer Online Journal Archives 1860-2000

Medicine

Law

Electronic Resource

1432-1335

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

1433-8580

Hepatic coma ; Ammonia ; Amino acids ; Portacaval shunt

Springer Online Journal Archives 1860-2000

Medicine

Summary To elucidate the possible connection between ammonia-induced changes of plasma and cerebrospinal fluid (CSF) amino acid levels and the development of hepatic encephalopathy in dogs, beagle dogs were given an ammonium acetate infusion both before and following portacaval shunt (PCS). During ammonia-induced coma and after recovery in the dogs prior to PCS the plasma and CSF concentrations of most amino acids were decreased. Following PCS the plasma and CSF concentrations of the aromatic amino acids (AAA), phenylalanine and tyrosine, increased and the levels of the branched chain amino acids (BCAA), valine, leucine, and isoleucine, decreased during ammonia-induced coma. The CSF/plasma molar ratio for the AAA exhibited a marked increase after recovery as compared to the value during coma in the Eck-fistula dogs. With respect to the AAA, no correlation was observed between signs of neurologic impairment in the animals and the following parameters: glutamine and methionine levels of CSF, and the plasma molar ratio BCAA/AAA. The data obtained do not support the hypothesis that high concentrations of phenylalanine and tyrosine in the brain may be primarily responsible for altered neurotransmission leading to the development of hepatic encephalopathy.

Electronic Resource

1433-8580

Alkaline phosphatase ; Brush border ; Ethanol ; Intoxikation by ethanol ; Small intestine

Springer Online Journal Archives 1860-2000

Medicine

Summary Single administration of ethanol or alcoholic beverages (5 g ethanol/kg body weight) induces a decrease of the 24 h excretion of fecal intestinal alkaline phosphatase (I-AP) activity of 28% (P〈0.05) in comparison to controls (0.9% saline). Administration of higher amounts of 20% (v/v) ethanol (8 g/kg body weight on 3 consecutive days) yields a decrease of fecal I-AP excretion up to 82% (P〈0.005) in comparison to controls (saturated glucose solution). The interpretation of these results as a toxic effect of ethanol to small intestinal mucosa was supported by measurement of enzymatic activity in the small intestinal mucosa and by morphometric data.

Electronic Resource

1433-8580

Carbohydrate metabolism ; Glucose ; Fructose ; Intestinal mucosa ; Liver

Springer Online Journal Archives 1860-2000

Medicine

Summary The adaptive response of a diet containing 60% fructose on the activity of those enzymes which are involved in the metabolism of fructose was measured in the liver and in the jejunal mucosa of rats over a period of 12 days. Control animals received isocaloric amounts of glucose or starch. Under fructose feeding there was a marked increase in the activity of fructose-1-phosphate aldolase (3-fold), ketohexokinase (2–3-fold), and triokinase (3-fold) in the jejunal mucosa. In the liver, however, a significant increase in enzyme activity could only be seen for triokinase (2–3-fold), whereas the activity of the other enzymes measured were only slightly or not at all altered. The activity of the three enzymes mentioned above were elevated to a maximum within 3 days after feeding the fructose diet. In the following time of observation no major further changes occurred. The results show that fructose feeding in comparison to a glucose or starch containing diet leads to a marked adaptive increase in the activity of those enzymes, which are involved in the breakdown of fructose, only in the jejunal mucosa.

Electronic Resource

1433-8580

Fructose absorption ; Glucose absorption ; Ileum ; Jejunum ; Small intestine

Springer Online Journal Archives 1860-2000

Medicine

Summary The influence of feeding isocaloric diets containing either 65% of fructose (F 65) or 65% of glucose (G 65) were studied on the uptake of both sugars in segments of rat proximal jejunum and distal ileum. The hexose absorption was compared to that obtained in animals receiving isocaloric amounts of a diet containing 30% of glucose (G 30). Feeding fructose (F 65) for 3 days resulted in a 2.5-fold increase of fructose uptake in the jejunum and a 40% increase in the ileum as compared to group G30. When fructose (F65) was administered instead of G 65 the uptake of fructose was enhanced by 75% in the jejunum and 35% in the ileum. Stimulation of glucose absorption in segments of the proximal and distal small intestine by diets F 65 and G 65 was nearly identical as compared to the values of group G 30. The stimulation of the uptake of fructose induced by fructose feeding parallels an adaptive increase in the activity of enzymes involved in fructose metabolism in the mucosa of the small intestine.

Electronic Resource

1432-1440

Springer Online Journal Archives 1860-2000

Medicine

Summary 1. In order to elucidate the mechanism involved in the triglyceride accumulation in the liver induced by ethanol, studies have been carried out on the effects of ethanol on the level of metabolites and coenzymes of the energy producing metabolism and the triglyceride content in the liver of rats fed a standard diet or low protein diet. The latter treatment markedly inhibits the oxidation of ethanol. 2. In rats fed the standard diet ethanol produced a pronounced increase in the reduction state of the cytoplasmic NAD-system measured by the ratio lactate/pyruvate andα-glycerophosphate/dihydroxyacetonephosphate. In the initial phase following ethanol administration the increase in the reduction of the mitochondrial NAD-system, calculated on the quotientβ-hydroxybutyrate/acetoacetate, was less marked than the cytoplasmic NAD-system. However in contrary to the latter with increasing duration of the influence of ethanol the reduction state of the mitochondrial NAD-system showed further elevation. 3. In rats fed the standard diet, ethanol produced a fourfold accumulation of triglycerides within 12 hours. During ethanol oxidation the levels ofβ-hydroxybutyrate and acetoacetate increased steadily. 4.|As a result of the distinctly inhibited rate of ethanol oxidation no increase in the reduction of the cytoplasmic NAD-system in the liver was observed in animals fed the protein deficient diet following ethanol treatment. Conversely the accumulation of triglycerides in the liver was even more pronounced than in the controls kept on the standard regimen. The concentration of the fatty acid metabolitesβ-hydroxybutyrate and acetoacetate and the redoxquotient of this substrate couple in the liver and in the blood also increased more markedly in the protein deficient group. 5. In man the effects of a single oral load of ethanol on the redoxquotients lactate/pyruvate andβ-hydroxybutyrate/acetoacetate in the blood are analogous to the alterations observed in animal experiments. 6. From these results it is concluded that following acute ethanol administration the fatty acids leading to increased triglyceride content of the liver are predominantly of extrahepatic origin. The accumulation of fat is probably independent of metabolic changes in the liver caused by the alcohol oxidation itself.

Zusammenfassung 1. In der vorliegenden Arbeit wurde untersucht, ob für die Fetteinlagerung in die Leber durch Alkoholzufuhr vorwiegend eine Neusynthese von Fettsäuren als Folge von Stoffwechseländerungen in der Leber durch die Alkoholoxydation selbst verantwortlich ist oder eine Mobilisierung von Fettsäuren aus dem peripheren Fettgewebe. Zu diesem Zweck wurde der Einfluß von Äthanol auf den Gehalt an Metaboliten und Coenzymen des energieliefernden Stoffwechsels sowie von Triglyceriden in der Leber von Ratten bestimmt, bei denen die Alkoholoxydation normal oder durch Fütterung einer proteinarmen Kost stark eingeschränkt war. 2. Alkohol führt bei normal ernährten Ratten in kurzer Zeit zu einer deutlichen Zunahme der Reduktion des cytoplasmatischen NAD-Systems der Leber, gemessen an den Quotienten Lactat/Pyruvat undα-Glycerophosphat/Dihydroxyacetonphosphat. Der Reduktionsgrad des mitochondrialen NAD-Systems nimmt, gemessen an dem Quotientenβ-Hydroxybutyrat/Acetoacetat nach Alkoholzufuhr initial weniger ausgeprägt zu. Er steigt jedoch, im Gegensatz zu dem des cytoplasmatischen NAD-Systems, mit der Dauer der Alkoholeinwirkung weiter an. Der Quotient NADH/NAD, der sich aus dem Gehalt der Leber an NADH und NAD berechnet, nimmt unter Alkohol ebenfalls zu. 3. Der Triglyceridgehalt der Leber steigt unter Äthanoleinwirkung bei normal ernährten Ratten innerhalb von 12 Std auf das 4fache des Ausgangswertes an. Der Spiegel der Ketokörperβ-Hydroxybutyrat und Acetoacetat nimmt in der Leber und im Blut in Gegenwart von Alkohol kontinuierlich zu. 4. Bei proteinarm ernährten Tieren bleibt infolge der stark verminderten Oxydationskapazität für Alkohol die Zunahme der Reduktion des cytoplasmatischen NAD-Systems nach Alkoholzufuhr aus, gemessen an den Quotienten Lactat/Pyruvat undα-Glycerophosphat/Dihydroxyacetonphosphat. Die Triglycerideinlagerung in die Leber ist dagegen noch ausgeprägter als bei den normal ernährten Kontrollen. Auch die Konzentration der Fettsäuremetabolitenβ-Hydroxybutyrat und Acetoacetat und der Redox-Quotient dieses Substratpaares nehmen in der Leber und im Blut stärker zu als bei den Normaltieren. 5. Beim Menschen verhalten sich die Redox-Quotienten Lactat/Pyruvat undβ-Hydroxybutyrat/Acetoacetat im Blut nach einmaliger oraler Alkoholgabe analog den bei den Tierversuchen beobachteten Veränderungen. 6. Aus den Ergebnissen wird geschlossen, daß die Fettsäuren für die vermehrte Triglycerideinlagerung in die Leber nach akuter Alkoholgabe vorweigend extrahepatischen Ursprungs sind. Die Fetteinlagerung ist weitgehend unabhängig von Stoffwechseländerungen in der Leber durch die Alkoholoxydation selbst.

Electronic Resource

1432-1440

Alkoholstoffwechsel ; Alkoholismus ; Fruktose ; Mikrosomen ; Phenobarbital ; Alcohol metabolism ; Alcoholism ; Fructose ; Microsomes

Springer Online Journal Archives 1860-2000

Medicine

Summary The effect of phenobarbital (PB) pretreatment and of chronic alcoholism on blood ethanol elimination rate (BEER) was investigated in man. In order to gain additional information concerning the mechanism of possible changes BEER was determined before and during intravenous infusion of fructose, a compound known to increase the NADH-oxidizing capacity of the liver and thereby stimulating alcohol oxidation rate. Following PB-treatment (300 mg/day for 5–6 days,n=8) a marked increase in unstimulated (U-) BEER was obtained. But the fructose stimulated (FS-) BEER was not significantly changed by PB-treatment. In chronic alcoholics (n=15) U-BEER values above the upper limit (x+2 S D) obtained in healthy controls, were observed only when the time of sobriety was less than one week (n=6). Values of FS-BEER in chronic alcoholics with increased basal alcohol oxidation rates were in the same range as those of healthy controls. In 5 out of the 6 alcoholics in whom the values were elevated on admission, BEER decreased significantly after withdrawal of alcohol for 2–4 weeks. Since FS-BEER was nearly identical in all conditions tested, the distinct changes in U-BEER are probably independent of changes in the activity of enzymes involved in alcohol oxidation. It is assumed that alcohol metabolism in man is mainly controlled by the rate of NADH reoxidation in the liver.

Zusammenfassung Es wurde der Einfluß einer Vorbehandlung mit Phenobarbital (PB) und eines chronischen Alkoholabusus auf die Geschwindigkeit der Blutalkoholelimination (BAE) beim Menschen untersucht. Es wurde die BAE vor und während einer intravenösen Fruktoseinfusion gemessen. Fruktosezufuhr erhöht die Kapazität der Leber zur NADH-Oxidation und kann hierdurch die Alkoholoxidation stimulieren. Durch PB-Vorbehandlung (300 mg/Tag für 5–6 Tage,n=8) nahm die unstimulierte (U-) BAE im Mittel um 50% zu. Die durch Fruktose stimulierte (FS-) BAE wurde durch PB-Vorbehandlung jedoch nicht signifikant beeinflußt. Bei chronischen Alkoholikern (n=15) wurden U-BAE-Werte, die über dem Bereich der bei gesunden Kontrollen gefundenen Abbauraten lagen, nur dann beobachtet, wenn die Dauer des Alkoholentzugs weniger als eine Woche betrug (n=6). Bei den chronischen Alkoholikern mit erhöhter U-BAE lagen die Werte der FS-BAE im gleichen Bereich wie bei den gesunden Kontrollen. Bei 5 der 6 Alkoholiker mit erhöhten Werten der U-BAE konnte letztere 2–4 Wochen nach Beginn des Alkoholentzugs erneut bestimmt werden. Die Werte waren in allen Fällen im Vergleich zu den Ausgangsbefunden deutlich vermindert. Die FS-BAE blieb somit durch Phenobarbital-Behandlung und chronischen Alkoholkonsum nahezu unbeeinflußt. Gleiches gilt, wie in einer vorangehenden Mitteilung gezeigt wurde, für längeres Fasten. Hieraus wird geschlossen, daß die deutlichen Änderungen der U-BAE vermutlich unabhängig von Aktivitätsänderungen der am Alkoholabbau beteiligten Enzyme sind.

Electronic Resource