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Biomedical subjects

W Stenzel

Publications and source records attributed to W Stenzel.

At least 19 recordsLinked to original sources
PubMed1992

Surfactant protein A expression is delayed in fetuses of streptozotocin-treated rats.

The content and distribution of the 26-to 38-kDa surfactant protein (SP-A) and its mRNA were determined in fetuses of control and streptozotocin (STZ)-treated Sprague-Dawley rats using immunohistochemistry, RNA blotting, and in situ hybridization. Female rats were treated with 50 mg/kg STZ before mating, and the fetuses were killed at fetal days 18-21 or on neonatal days 1 and 2 (day of birth = end of day 22). SP-A was barely detectable on fetal day 18 in controls and easily detected by fetal day 21. In the STZ group, SP-A was decreased compared with controls at fetal days 18-21. However, by neonatal days 1-2, there were no significant differences in SP-A levels between groups. SP-A mRNA was detectable at fetal day 18 in controls, but it was decreased in the STZ group at day 18-21 (P less than 0.02) and differences were no longer detected by neonatal days 1-2. SP-A and SP-A mRNA accumulated with advancing gestational age in both groups until neonatal days 1-2. The differences in SP-A and SP-A mRNA levels in the two groups diminished with advancing age but remained significant at fetal day 21. These data suggest that STZ-induced diabetes interferes with normal expression of SP-A in the developing fetal lung.

Animals↗
PubMed1989

Increased binding of epidermal growth factor to placental membranes of intrauterine growth restricted fetal rats.

To examine the relationship between nutrient supply and fetal and placental growth, we examined epidermal growth factor (EGF) binding to membranes prepared from placentas of growth-restricted fetal rats. Intrauterine growth retardation was accomplished by unilateral ligation of the uterine artery; fetal rats on the contralateral uterine horn served as controls. Fetal growth restriction was accompanied by decreased placental wt at 19 and 20 day's gestation and significantly decreased placental glycogen content at 20 and 21 days, 30% and 15%, respectively. Placental DNA content and protein/DNA ratios were similar in the growth-restricted and control groups. Specific binding of 125I-EGF was increased in growth-restricted placentas at 19 and 20 days' gestation by 32% and 16%, respectively. 125I-EGF binding at 20-21 days increased linearly with the extent of placental growth restriction. Competitive binding experiments yielded linear Scatchard plots with an increased receptor density in growth-restricted placenta at 19 and 20 days' gestation, 74% and 60%, respectively. Binding affinities for the EGF receptor were similar in the two groups. The increased binding of EGF to membranes prepared from growth-restricted fetal rats may serve to enhance nutrient uptake under conditions of decreased uterine blood flow.

Animals↗
PubMed1988

Pharmacological properties of the positive inotropic and alpha 1-adrenoceptor blocking agent saterinone.

The pharmacological properties of saterinone [+/-)-1,2-dihydro-5-[4-[2-hydroxy-3-[4-(2-methoxyphenyl)-1-piperazinyl] propoxy]phenyl]-6-methyl-2-oxo-3-pyridine-carbonitrile, BDF 8634) were investigated in isolated organs of the guinea pig and in human platelets. Saterinone was found to be a potent antagonist at vascular alpha 1-adrenoceptors with a pA2-value of 8.46 +/- 0.12. Besides its affinity for alpha 1-adrenoceptors saterinone exerted a positive inotropic effect in the isolated papillary muscle at an EC50-value of 3.2 X 10(-6)mol/l indicating 10-fold greater potency than milrinone. Comparable EC50-values were also found for the inotropic, chronotropic and bronchodilatory actions of the drug, indicating a common mechanism for these effects. The inotropic effects were not mediated by beta-adrenergic or H2-histaminergic receptors, but were shown to involve an elevation of myocardial cyclic adenosine monophosphate (cAMP) content. Saterinone also inhibited crude cAMP phosphodiesterase (PDE) activity in homogenates obtained from guinea pig right ventricles. The IC50-value for PDE-inhibition was 2.3 X 10(-5) mol/l and thus at a higher concentration than the inotropic effect. Saterinone was a potent inhibitor of human platelet aggregation induced by adenosine diphosphate, collagen and arachidonate. Against the latter agonist, saterinone was about 40-fold more effective than acetylsalicylic acid. In conclusion, saterinone exhibited a dual mechanism of action--direct inotropic effects in the myocardium and alpha 1-receptor blockade in the guinea pig vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1988

General pharmacology of the novel centrally acting antihypertensive agent moxonidine.

Moxonidine (4-chloro-N-(4, 5-dihydro-1H-imidazol-2-yl)-6-methoxy-2-methyl-5-pyrimidinamine, BDF 5895) reduces blood pressure and heart rate in rats with genetic hypertension (SHR/Okamoto) and in rats with renovascular hypertension (Goldblatt 1 k/1 c). The hypotensive action was also confirmed in renal-hypertensive dogs. The hypotensive action is preceded by a reduction in plasma noradrenaline concentration, thus reflecting a reduction in sympathetic activity. In anesthetized cats, administration of moxonidine into the vertebral artery induces a greater hypotensive effect than i.v. injection of same doses, indicating the central nervous system as the site of hypotensive action. Similar to clonidine, the hypotensive action of moxonidine is abolished by pretreatment of the animals with a selective alpha 2-antagonist. Direct application of moxonidine into the cisterna magna of anesthetized rabbits revealed a 10-fold greater hypotensive potency than clonidine, in contrast to i.v. application where moxonidine was 10-fold less potent than clonidine. At least 10-fold higher doses of moxonidine were needed to cause side effects (sedation, inhibition of gastric secretion), when compared with clonidine. Interruption of presynaptic noradrenergic pathways completely abolished the hypotensive action of moxonidine. Thus moxonidine is endowed with a specific central site of action, presumably by stimulating central presynaptic alpha 2-adrenoceptors. This specific central hypotensive action enables a greater dissociation between the antihypertensive effect on the one hand, and the side effects on the other.

Administration, Oral↗
PubMed1978

[The influence of non-metabolizable alpha- and beta-glycosides on the regulation of sorbose fermentation of salmonellae (author's transl)].

Fermentation of sorbose by late positive Salmonella wildtype cultures and by mutant strains splitting this sugar promptly is restrained by the beta-glucoside salicine and likewise by 1-o-methyl-alpha-D-glucopyranoside (MGP), but is not influenced by lactose or sucrose. In growing cultures salicine works more powerful on sorbose utilization than MGP while in dense suspensions of non-multiplying bacteria the relations are reversed. Among the majority of wildtype strains this suppressive effect is diminished or abolished by dimethylsulfoxide (DMSO), but there are strains in which the glucoside effect is enhanced by DMSO. The sorbose fermentation lag in the presence of salicine or MGP is detectable, too, in dense suspensions of promptly splitting Salmonella mutant strains in media poorly supplied with nitrogen and must therefore be attributed to a non-mutative event. From prior work (Stenzel, 1977c) we got some evidence that this event might depend on an inhibition of enzyme induction. Targets and mode of action of the alpha- and beta-glucoside largely seem to be identical, though possibly there might exist minor differences.

Benzyl Alcohols↗
PubMed1977

[Suppression of sorbose fermentation of Salmonellae by salicine (author's transl)].

Fermentation of sorbose by Salmonellae splitting this sugar with delay is restrained to a varying degree in presence of salicine, depending on the concentration of this glycoside. There is no support that salicine might become metabolized in this process. A similar salicine effect on the delayed fermentation of dulcitol has not been seen.

Fermentation↗
PubMed1977

[On the genetics of the delayed attack of substrates by strains of the Salmonella group (author's transl)].

The delayed attack of sugar alcohols by Salmonellae essentially goes back on a mutative event but doesnot represent a phenotypical or genotypical uniform phenomenon. The - frequently occuring - regularly split of sugars is caused by a simple looking fixed rate mutative event, and is characterized by an only moderate variation of the latent period preceding acid formation. In contrast, irregularly delayed splitting strains attack the substrate varying and, when occasion arises, with an extremely uncertain latency. Fermentation capacity of some strains attacking dulcitol irregularly can be induced by irradiation with ultraviolet light, and can be reduced to a certain degree by treatment with acridine orange, but cannot be transferred to other strains by conjugation. We presume that at least the uv inducible type of irregularly delayed splitting is governed by an episomal genetical element which is active only in the autonomous state but is repressed when being integrated within the chromosome.

Culture Media↗
PubMed1977

[Effects of dimethylsulfoxide and salicine on the delayed adaption on sorbose and dulcitol of Salmonellae (author's transl)].

Among the majority of Salmonella strains splitting sorbose or dulcitol with delay dimethylsulfoxide shortens the latent period preceding acid formation and abolishes the deceleration of sorbose adaption caused by salicine. In other strains, especially S. paratyphi B cultures, DMSO doesn't touch sorbose adaption directly but amplifies the restraing effect of salicine. From the whole of our findings it can be concluded that in the first group of strains sorbose adaption starts with segregation of adaptive sorbose permease positive mutants, followed by the - salicin-sensitive - induction of this permease, the appearance of mutants aditionally metabolizing sorbose constitutively, and, finally, the substrate-promoted particular growth of adapted cells. The latter category of strains, however, apparently possesses a wild type (constitutive or adaptive?) sorbose permease but splits off mutants with adaptive metabolizing enzymes the induction of which is salicine-sensitive. The amplification of the salicine effect by DMSO found in these strains might be refered to an enhancement of salicine uptake caused by DMSO.

Adaptation, Physiological↗
PubMed1976

[Sorbose in Salmonella diagnosis (author's transl)].

From 1525 Salmonella strains checked for fermentation of sorbose the majority failed to attack this sugar or split it with distinct delay. None of these cultures showed production of acid from sorbose prior to the third day of incubation. In contrast, sorbose was attacked within 24 hours by 74 out of 100 Ballerup-Bethesda strains. As an easy and reliable basis test combination for performing a minimal biochemical Salmonella diagnosis a series consisting of Kligler's medium and media containing urea, lysine, lactose, sucrose, sorbose, and salicin is suggested.

Salmonella↗
PubMed1975

[Serotype 185 and E. coli O115 - two distinct bioseropathotypes (author's transl)].

E. coli O115 strain 27w and TRABULSI's serotype 185 have been subjected by us to comparing examinations of the serological behaviour of their cell wall and their protoplasmatic antigens, of their biochemical and cultural behaviour and their pathogenicity for the mucous membranes of guinea-pigs. As a result of this inquiry it was found, that E. coli O115 27w and the dysentery-provoking serotype 185 are biological distinct bacteria which only share a minor cross relationship of their O-antigens, and which should not be classified together.

Animals↗
PubMed1975

[Occurrence of the cathode-bound group antigen of the dysentery bacilli in Escherichieae types of intermediate character (author's transl)].

Protoplasmatic antigens of 28 strains of 27 Escherichieae types not accepted as Shigellae have been examined for the occurrence of a cathode-bound group antigen (KGA). From the tested cultures of non-dysentery-provoking types E. coli O28 E1073(z) TAYLOR, E. coli O32, E. coli O115 (27w), Alkalescens-Dispar O1, A.-D. O1 var. Koji, A.-D. O2, A.-D. O3, A.-D. O4, A.-D. O5, A.-D. O6, A.-D. O7, and the intermediate serotypes H62 and 6275-52 no one possessed KGA, and likewise one of the two examined E. coli O136 cultures proved to be KGA-negative. In contrast, KGA was found in the dysentery types 147, 792, 185, Sh. guanabara, E. coli O124, E. coli O136 (one strain), E. coli O143, E. coli O144, and E. coli O152, in the Shigella-like serotypes 2044-54 and 1831, in the E. coli serotypes O112a,b:K68 and RUCHMAN, which have been suspected to provoke dysentery but are showing the biochemical behavior of typical E. coli, finally in Alkalescens-Dispar O8, which is known to be apathogenic for mucous membranes. After, all, KGA seems to be a constituent of all dysentery bacilli, but might be absent in individual cultures. On the other hand, KGA exceptionally seems to be found also in Escherichieae types not enteropathogenic for men.

Antigens, Bacterial↗
PubMed1975

[Pathogenicity factors of gramnegative enteropathogenic bacteria and pathogenesis of intestinal diseases (author's transl)].

Enterotoxins as produced by the majority of enteropathogenic bacteria play a central role in the pathogenesis of cholera and E. coli enteritis but are obviously of little significance as to the development of Salmonella enteritis and dysentery. Pathology of Salmonella enteritis and dysentery results from multiplication of bacteria within the bowel wall and from the damage of tissue caused thereby. The lipopolysaccharides (endotoxins) of invasive enteropathogenic bacteria do not possess the character of a primary pathogenicity factor but operate as a protective agent versus bactericidal mechanisms of the macroorganism and probably also as an agent toxic for the tissue.

Animals↗
PubMed1975

[The cathode bound group antigen of dysentery-provoking escherichieae (author's transl)].

Antigens from disrupted cells of dysentery-provoking and of non-enteropathogenic Escherichieae were submitted to immunoelectrophoresis on cellulose acetate stripes at pH 8.0. Among 6 immune sera produced for this purpose by immunizing rabbits against desintegrated dysentery bacteria, only one contained a precipitine reacting with an antigen similar to the "generic antigen" of BELAYA. This - at pH 8.0 - cathode-bound group antigen (KGA) could not only be found in virulent but also in 5 attenuated cultures and in 5 from 6 avirulent strains of several dysentery types. Only the - apathogenic - type culture 1111/55 of dysentery-provoking E. coli O 136 showed no KGA-reaction. Some sources of methodical errors responsible for false outcomes of immunopherogrammes have been discussed.

Antigens, Bacterial↗