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Biomedical subjects

E Kohne

Publications and source records attributed to E Kohne.

At least 73 records · Page 4Linked to original sources
PubMed1979

Hemoglobin A1c (HbA1c) in children with long standing and newly diagnosed diabetes mellitus.

In 35 children with long-standing diabetes mellitus, a significant correlation was found between the hemoglobin A1c (HbA1c)--and the 24-hour urinary glucose excretion. By contrast, 11 newly diagnosed diabetic children had grossly elevated HbA1c-concentrations, but no correlations could be established between the levels of HbA1c and the duration of symptoms, blood glucose, glycosuria, ketonuria and the acid--base status. However, HbA1c and C-peptide were significantly correlated. The elevated HbA1c-concentrations decreased towards normal in all of these 11 children after 2--3 months following adequate therapy. The results suggest that the determination of HbA1c may serve as a valuable metabolic control index in children with long-standing diabetes mellitus, but adds little information in newly diagnosed patients. For the individual diabetic child during the early treatment period, HbA1c may be the index of choice for adequacy of metabolic control.

Acid-Base Equilibrium↗
PubMed1977

Allogeneic bone marrow transplantation in conventional mice: I. Effect of antibiotic therapy on long term survival of allogeneic chimeras.

In the present communication the beneficial effect of long term antimicrobial treatment with poorly absorbable antiboitics on the survival of allogeneic bone marrow chimeras was investigated. The combination of C57Bl mice as bone marrow donors and CBA/CA mice as irradiated recipients (800 rad) was used because of their strong histoincompatibility on the H-2 loci. All allografted recipients received 10 X 10(6) bone marrow cells. The majority of the recipients, which were rendered gnotobiotic by an antimicrobial treatment, achieved stable long term chimerism. In contrast, the conventional chimeras died from secondary disease within 9 weeks after transplantation. As early as 14 days after allogeneic bone marrow grafting the gnotobiotic recipients tolerated the reassociation with a conventional microflora without a change in the rate of mortality. Bone marrow cells (8 X 10(6) i.v.) and spleen cells (2 X 10(6) i.v.) collected from allogeneic chimeras failed to induce graft-versus-host-reaction (GVH) in a second lethally irradiated host. The data indicate, that the high rate of mortality in murine allogeneic bone marrow chimeras results from delayed GVH-reaction and systemic infection. The marrow graft, once established seems to exert tolerance against the allogeneic host. The pathogenesis of the systemic infection has not yet been worked out. It is assumed that it originates from bacteremia, induced by radiation dependent lesions of the epithelial integrity and defected lymphatic tissue in the gut.

Animals↗
PubMed1977

Hemoglobin F Koelliker (alpha2 minus 141 (HC 3) Arg gamma2); a modification of fetal hemoglobin.

An electrophoretically HbA-like hemoglobin component is produced in increasing amounts during storage in hemolysate preparations from macerated tissue (liver, kidney, spleen) of fetuses. Within twenty four hours after hemolysate preparation the "fast moving" fraction increases up to 40 per cent of total hemoglobin, while the concentration of HbA remains constant (5 - 7%) in hemolysates obtained from peripheral blood of the same donor individuals. By structural studies (fingerprint and aminoacid analysis) the HbA-like component was identified as an artefact of HbF, characterized by the absence of the C-terminal arginine of the alpha chains. From experimental data it is concluded, that the break down product results from a digestion of HbF by carboxypeptidase B, the enzyme being released from the macerated tissues. Analogous to a modification of HbA, i.e. Hb Koelliker (alpha2 minus 141 Arg beta2), the structure of the degradation product of HbF is alpha2 minus 141 Arg gamma2 (HbF Koelliker).

Amino Acids↗
PubMed1977

Hb M Milwaukee in a German family.

The second occurrence of Hb M Milwaukee is reported in two members of a German family who had cyanosis since early childhood. Contrary to earlier reports, Hb M Milwaukee exhibits a distinct heat instability. It is suggested, that in this family the variant resulted from a new mutation.

Chromatography, Ion Exchange↗
PubMed1976

[Erythrocyte hypocromia in heterozygous hemoglobin E (beta 26 Glu replaced by Lys)].

A family from south-western Germany with 9 heterozygous carriers of haemoglobin E (beta 26 Glu-Lys) is presented. The abnormal haemoglobin has been identified by different electrophoretic techniques and fingerprint analysis. In contrast to earlier observations, haemoglobin E is even in heterozygous carriers associated with erythrocytic hypochromia with MCH values from 23.6 to 26.2 pg. As an explanation for the hypochromia a decreased haemoglobin synthesis is supposed.

Adult↗
PubMed1976

[Dysfunction of Granulocytes in Children with Frequent Infections].

Eight children with various diseases, who has frequent infections were examined for abnormalities of serum proteins and leucocyte function. Inborn or secondary defects could be recognized by the tests for chemotaxis, the intracellular killing of bacteria as well as yeast and the oxydative metabolism of the granulocytes. The defects were serum- or cell-dependent and they could be detected alone or in combination with other dysfunctions. Three children showed a reduced stimulation of the lymphocytes in addition to the impairment of chemotactic activity or fungicidal cavity.

Adolescent↗
PubMed1975

[HbM Erlangen: alpha2beta263(e7) tyr. New mutation with haemolysis and NADH-methaemoglobin reductase deficiency (author's transl)].

Report on a further hemoglobin M variant, discovered in a boy with congenital cyanosis. Chemical analysis of hemoglobin structure revealed indentity with HbM Saskatoon (= beta63 His leads to Tyr). The abnormal hemoglobin is characterized by normal oxygen transport function. The observed slight constant hemolysis is thought to be due to increased instability of the abnormal hemoglobin molecule. In addition to the hemoglobin anomaly, the activity of NADH-methemoglobin reductase was reduced by approximately 40% of normal. None of the parents presented with an abnormal hemoglobin, indicating that the occurrence of hemoglobin M Erlangen is most likely the result of a new mutation.

Child, Preschool↗
PubMed1975

[Neonatal polycythaemia and haemoglobin types in infants with G-trisomy (author's transl)].

The concentrations of haemoglobin A1, A2, and F were determined quantitatively by column chromatography in 11 newborns with G-trisomy (Down's Syndrome)) and correlated to haematocrit values. In 3 infants the haemoglobin pattern was followed throughout the first six months of life. In connection to the well know polycythaemia, newborns with G-trisomy were found to have significantly higher haemoglobin A1 attaining 35.5 plus or minus 6.6% and A2 equal to 0.79 plus or minus 0.32% as compared to normal infants (HbA1 equal 17.74 plus or minus 4.56%, HbA2 equal to 0.25 plus or minus 0.2%). In G-trisomy the switch-over from synthesis of haemoglobin F to haemoglobin A appears to be initiated earlier than in normal individuals, and it seems even to proceed more rapidly during the first weeks after birth. The amount of adult haemoglobin being synthesized in G-trisomy during the perinatal period may possibly be a response to the increased erythropoiesis, while the influence of chromosomal abnormality seems not to be a specific phenomenon.

Age Factors↗