Haemoglobin interference in the determination of bilirubin was compared in 7 different methods using the Jendrassik-Grofprocedure, the Jendrassik-Grof-Nosslin rhodification, and the more recent procedures using nitrophenyldiazonium, 2,5-dichlorophenyIdiazonium, 2,4-dichloraniline, and a direct reading method. To a variable degree, haemoglobin decreased the apparent absorption of the reaction product in all procedures. The extent of this decrease depended on the reagent used, the wavelength, incubation time, bilirubin concentratiori and the type of blank used. In an attempt to elucidate the mechanism of interference, haemoglobin was found to destroy the bilirubin diazo-compound whereas haemiglobin was ineffective. Likewise, storage of haemolytic samples for several days led to a disappearance of haemoglobin. H 2 O 2 , which had no effect in the absence of haemoglobin, potentiated the action of haemoglobin on diazobilirubin coupling.From our observations it can be concluded that haemoglobin disturbs the diazo-bilirubin reaction by a dual mechanism. H2Ü2, formed from oxyhaemoglobin by autoxidation, destroys the diazo bilirubin colour. In accordance with this explanation, potassium iodide stabilized the diazo compound against the peroxidative effect of oxyhaemoglobin; stabilization was not effective with Superoxide dismutase, mannitol or ascorbate. Studien zur Störung der Bilirubinbestimmung durch HämoglobinZusammenfassung: Die Störung der Bilirubinbestimmung durch Hämoglobin wurde durch Vergleich 7 verschiedener Verfahren untersucht. Diese umfassen die Jendrassik-Grof-Methode, die Modifikation nach Jendrassik-Grof-Nosslin sowie die neueren Verfahren mit Nitrophenyldiazonium, 2,5-Dichlorophenyldiazonium, 2,4-Dichloroanilin, sowie eine direkt-photometrische Methode. Hämoglobin verminderte die Absorption des Reaktionsprodukts bei allen Verfahren, jedoch in verschiedenem Maße. Das Ausmaß der Störung hängt nicht nur vom Reagenz ab, sondern auch von der verwendeten Wellenlänge, der Inkubationszeit, der Bilirubinkonzentration und der Art der Leerwertbildung. Beim Versuch, den Mechanismus der Störung zu erhellen, fanden wir, daß Hämoglobin den Diazobilirubinkomplex zerstörte. Hämiglobin hatte dagegen keinen Einfluß. Ebenso blieb die Störung aus, wenn man hämolytische Proben über Tage lagerte. H 2 O 2 , das in Abwesenheit von Hämoglobin keinen Effekt auf die Diazoreaktion hatte, potenzierte die Wirkung des Hämoglobins auf die Diazobilirubinkopplungsreaktion. Aus den Ergebnissen kann geschlossen werden, daß Hämoglobin auf zweifache Weise die Diazobilirubinreaktion stört: Aus Oxyhämoglobin gebildetes H 2 O 2 und die peroxidative Wirkung zerstören offensichtlich den Diazobilirubinkomplex. Im Einklang mit dieser Vorstellung zeigte Kaliumiodid, nicht aber Superoxiddismutase, Mannit oder Ascorbat eine stabilisierende Wirkung auf den Diazokomplex gegen die peroxidative Wirkung des Oxyhämoglobins.

This technique allows for the first time to measure the mucociliary clearance at various locations inside the nose of a patient in a short and easy to perform procedure, which up to now necessitated extensive or experimental set-ups. Besides the establishment of a register of mucociliary clearance at various anatomical localisations inside the nose (olfactory epithelium, conchae, surrounding of the ostiae etc.), we intend to verify if this technique can be used as a new diagnostic tool to obtain a deeper insight into some pathologic alterations or uncharacteristic symptoms ("post-nasal-drip") or drug-effects in the nose and in the tracheo-bronchial system.

This report presents the state of current knowledge regarding the importance of basement membrane (BM) for the growth of benign and malignant tumours with special emphasis on tumours of the head and neck. The BM forms a barrier that has to be destroyed by infiltrative tumour cells. Recent immunohistochemical analyses have revealed both quantitative and qualitative changes in the BM composition following malignant transformation of the epithelial cells, thereby allowing malignant ingrowth into the stroma. This BM pattern, however, may also allow an early diagnosis of tumour invasion. Additionally, carcinomas of the larynx demonstrate a correlation between the amount of preserved BM deposition and the grade of tumour differentiation. This fact may also be important in tumour prognosis.

Sudden failure of an occasional patient afflicted with Addison-Biermer's disease (Addisonian pernicious anemia) to respond to adequate amounts of purified liver extracts in the absence of factors known to interfere with a therapeutic response has been observed by us during the past few years in the Minneapolis General Hospital. The occurrence of a refractory state for no apparent reasons has also been noted by others (1 to 4). Because little is known about the chemical nature of the liver factor (anti-pernicious anemia factor) or the physiologic dose, including the development of a progressive anemic state under adequate amounts of purified liver extracts, we felt justified in publishing an observation which we believe may indicate one of the mechanisms responsible for a sudden refractory behavior of certain patients. We could demonstrate in a male afflicted with Addisonian pernicious anemia that fatty liver and fatty metamorphosis of the bone marrow organ were apparently factors in the development of a progressive anemic state.Without further administration of liver extract, the progressive anemic state was brought into remission by means of the administration of a 5 per cent solution of choline chloride (Merck), 20 ml. intravenously for 16 successive days. The doses were given at a rate of 1 ml. per minute.The first dose caused flushing and some nausea after 10 ml. were administered. No significant drop in blood pressure was observed. The successive doses were well tolerated. CASE HISTORYThe patient, a male, who -for several years responded in a characteristic manner to the administration of liver extracts intramuscularly and maintained a normal peripheral blood status on 3 ml. monthly of fairly crude liver extracts containing about % to 2 U.S.P. units per ml., developed a progressive anemic state when purified liver extracts were substituted containing about 10 and 15 U.S.P. units

Zusammenfassung:Neben der seit langem bekannten erhöhten nicht-enzymalischen Glucosylierung von Hämog/obinen sind bei Diabetikern auch andere Blut-und Gewebeproteine höher glucosyliert als bei Normalpersonen. Diese chemische Modifikation der freien Aminogruppen von Proteinen kann zur Änderung ihrer Struktur bzw. ihrer Funktion führen, wie an einigen Beispielen gezeigt wird. Die mögliche Holle der nicht-enzymatischen Glucosylierung bei der Entwicklung diabetischer Spätkomplikationen wird diskutiert.Schlüsselwörter: Diabetes -nichtenzymatische Glucosylierung -postribosomale Modifikation -Stoffwechseleinstellungdiabetische SpätschädenSummary:Not only hemoglobin but also other blood proteins and tissue proteins are nonenzymatically glucosylated in diabetic patients to a higher extent. This chemical modification of free amino groups may alter the structure or function of proteins. The possible role of nonenzymatic glucosylation for the development of diabetic late complications is discussed.