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Biomedical subjects

A Koller

Publications and source records attributed to A Koller.

174 records · Page 10Linked to original sources
PubMed1975

[Congenital pernicious anemia (author's transl)].

Pernicious anemia is a rare disease of the pediatric age-group. Two kinds of pernicious anemia are known for this period, the "congenital" and the "iuvenile" form. Both are characterized by a megaloblastic anemia and a deficiency of the intrinsic-factor. The congenital form unusually begins before the second year of age and does not have changes of the mucous membranes of the stomach. The iuvenile form also called "adolescent or auto-immune pernicious anemia" has its beginning in the later childhood and shows like the adult form atrophy of the mucous membrane of the stomach, anacidity and antibodies against the intrinsic factor and parietalcells. A patient with congenital pernicious anemia is presented; the symptoms, diagnosis, differentialdiagnosis and therapy of this disease is reviewed.

Age Factors↗
PubMed1975

Evidence supporting a proposed mechanism explaining the inverse relationship between guanidinoacetate and guanidinosuccinate in human urine.

A proposed mechanism [Clin. Chem. 19, 668 (1973)] for the inverse relationship between guanidinoacetate (I) and guanidinosuccinate (II) in human urine is explored. The mechanism proposes that canavaninosuccinate (III) may be reduced to form homoserine and II or, alternatively, that the III may be acted upon by a lyase to form canavanine and fumarate. The canavanine would then proceed to transamidinate to glycine to form I. This study demonstrates for the first time that lyase activity for converting III to canavanine and fumarate exists in human liver and kidney extracts. Transamidination from canavanine to glycine to form I is also readily accomplished with human tissue. Reductive cleavage of III to II and homoserine has been demonstrated before [Clin. Chem. 15, 397 (1969)]. The optimum pH for the lyase reaction is 6.5, for the reductive cleavage it is 8.7. In following the course of the lyase reaction, we developed a technique whereby the fumarate formed was hydrated with fumarase (EC 4.2.1.2) and then dehydrogenated with malate dehydrogenase (EC 1.1.1.37). The changes in absorbance of NADH formed in the reaction were then measured and used to determine the amount of fumarate formed, as a measure of lyase activity. Canavanino-succinate lyase activity follows pseudo-first-order reaction kinetics. The Michaelis constant of this lyase was 6.16 X 10-4 mol/liter, for argininosuccinate lyase 9.74 X 10-4 mol/liter. These data suggest that the binding affinity for III to the enzyme is greater than that for argininosuccinate. Glycine added to the reaction acts as an activator, probably because it removes the canavanine from the reaction mixture. On the other hand, arginine acts as an inhibitor of III-lyase. Other substances tested, such as canavanine, fumarate, and argininosuccinate had no effect on the reaction kinetics.

Acetates↗
PubMed1975

Hepatic synthesis of canavaninosuccinate from ureidohomoserine and aspartate, and its conversion to guanidinosuccinate.

This study continues the exploration of the mechanism for the formation of guanidinoacetate and guanidinosuccinate in the human [Clin. Chem. 21, 235 (1975)]. In this report we describe the formation of canavaninosuccinate from ureidohomoserine and aspartate by a human or bovine liver extract that had high argininosuccinate synthetase (EC 6.3.4.5) activity, and the subsequent formation of guanidinosuccinate by reductive cleavage. In the presence of ATP the optimum pH for the synthetic reaction is 8.4. This reaction can be carried out in either a tris(hydroxymethyl)aminomethane or borate buffer. Subsequent addition of dithiothreitol in the presence of Fe2+ resulted in the cleavage of some of the synthesized canavaninosuccinate to form guanidinosuccinate and homoserine. Synthesis of canavaninosuccinate was strongly inhibited by added argininosuccinate, less so by canavaninosuccinate, arginine, canavanine, glycine, or 2,3-dimercaptopropanol. The Km values for the substrates of the synthetic reaction are 3.6 X 10(-4) mol/liter for aspartate, 1.6 X 10(-3) mol/liter for ureidohomoserine, and 2.92 X 10(-5) mol/liter for ATP. These values are higher than those obtained when the synthesis of argininosuccinate was studied, except for ATP, which yielded a lower value. All of the reactions in the proposed mechanism have now been demonstrated except for the synthesis of canaline from aspartate.

Animals↗
PubMedDate not supplied

Meconium analysis for cocaine: a validation study and comparison with paired urine analysis.

We established the validity of a drug-screening method to detect the presence of cocaine or benzoylecgonine or both in meconium and then undertook an analysis of results from urine and meconium specimens obtained concurrently from neonates within 3 days of birth. Meconium specimens from 82 consecutive newborns were analyzed using fluorescence polarization immunoassay (FPIA), Kinetic Interaction of Microparticles in Solution (KIMS), and gas chromatography-mass spectrometry (GC-MS). Each meconium specimen was analyzed by all three methods. Fifty-four paired urine and meconium specimens were obtained over a 13-month period from a neonatal intensive care unit. Urine drug testing was performed by immunoassay (enzyme multiplied immunoassay [EMIT] technique), whereas meconium specimens utilized FPIA with GC-MS confirmation on all but one specimen (due to insufficient quantity). Ten true positives were found by GC-MS, 10 positives were found by FPIA, and 70 positives were found by KIMS. Of the 54 paired samples, 39 samples tested negative for cocaine in both urine and meconium; four specimens were positive by both routes; 10 specimens were negative in urine but positive in the meconium; and one specimen tested positive in urine but negative in the meconium. Thus, 9.3% of the urine specimens tested positive, and 25.9% of meconium samples tested positive (p = .011; McNemar's Test). We conclude that screening meconium specimens by FPIA followed by GC-MS confirmation of screened positives yields highly accurate determinations of the presence of cocaine or benzoylecgonine or both in meconium and that testing of meconium for cocaine and its metabolites is more sensitive than testing of urine.

Cocaine↗
PubMedDate not supplied

17beta-estradiol restores endothelial nitric oxide release to shear stress in arterioles of male hypertensive rats.

BACKGROUND: Endothelial nitric oxide (NO)-mediated responses are impaired in arterioles of male spontaneously hypertensive rats (SHR), but they are still present in female SHR. We hypothesized that in vitro incubation of arterioles of male SHR with estrogen will restore NO-mediated responses by upregulation of endothelial NO synthase. METHODS AND RESULTS: Responses to increases in perfusate flow (from 0 to 25 microL/min) and to the calcium ionophore A23187 (5 x 10(-8) to 10(-6) mol/L), norepinephrine (NE; 10(-7) to 3 x 10(-7) mol/L), sodium nitroprusside (SNP; 10(-8) to 10(-6) mol/L), and adenosine (ADO; 10(-6) to 5 x 10(-5) mol/L) were studied in cannulated and pressurized gracilis muscle arterioles ( approximately 75 microm in diameter) isolated from 12-week-old male SHR before and after incubation with 10(-9) mol/L 17beta-estradiol (17beta-E(2)) for 16 to 18 hours. After incubation with 17beta-E(2), basal diameter of arterioles was significantly increased (by approximately 10%), and flow-induced dilation was significantly enhanced (79.8+/-2.9 versus 103.7+/-3.7 microm at 25 microL/min), resulting in a lowered shear stress (62.0+/-9.1 versus 32.5+/-4.2 dyne/cm(2)). Also, vasoconstrictions to A23187 were reversed to dilations (-18.7+/-2.2 versus 18.8+/-1.7 microm), and constrictions to NE were significantly attenuated (-30.7+/-3.0 versus -21.2+/-2.8 microm). These alterations were eliminated by ICI 182,780 (10(-7) mol/L), an estrogen receptor antagonist; 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole (10(-5) mol/L), a transcription inhibitor; or N(omega)-nitro-L-arginine methyl ester (10(-4) mol/L), an inhibitor of NO synthase, whereas they were not affected by aminoguanidine (5 x 10(-5) mol/L), a specific inhibitor of inducible NO synthase. Arteriolar responses were not altered by incubation with 17alpha-estradiol. CONCLUSIONS: Estrogen, via a receptor-mediated pathway, upregulates endothelial NO synthase gene expression, leading to increased NO production, and restores the regulation of wall shear stress in arterioles of male SHR.

Adenosine↗