Three pyrone glucosidic derivatives from Conyza albida

Three new pyrone glucosidic derivatives, together with the known pyromeconic acid glucoside, three acytelenes and two eudesmanes, were obtained from the aerial parts of Conyza albida. The structures were elucidated by high field NMR spectroscopy.     

A mechanism for shock following stomach rupture in the newborn

BACKGROUND: Stomach rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. METHODS: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating stomach rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. RESULTS: Endotoxin feeding alone caused endotoxemia (0.49 +/- 0.12 ng/mL; P < 0.05) in 10-day-old rats, while plasma endotoxin concentration in controls was less than 0.04 ng/mL. However, the endotoxemia did not cause disruption of glucose regulation or death. Injection of HCl alone did not increase plasma endotoxin concentrations and did not alter glucose regulation. However, HCl injection into endotoxin-fed rats induced endotoxemia (211.1 +/- 70.5 ng/mL; P < 0.05), hypoglycemia, lactacidemia and mortality (45%; P < 0.05). CONCLUSION: Early development of shock following stomach rupture may be in part due to endotoxin translocation and endotoxemia.     

The CD24/P-selectin binding pathway initiates lung arrest of human A125 adenocarcinoma cells

Carbohydrates on tumor cells have been shown to play an important role in tumor metastasis. We demonstrated before that CD24, a Mr 35,000-60,000 mucine-type glycosylphosphatidylinositol-linked cell surface molecule, can function as ligand for P-selectin and that the sialylLex carbohydrate is essential for CD24-mediated rolling of tumor cells on P-selectin. To investigate the role of both antigens more closely, we transfected human A125 adenocarcinoma cells with CD24 and/or fucosyltransferase VII (Fuc TVII) cDNAs. Stable transfectants expressed CD24 and/or sialylLex. Biochemical analysis confirmed that in A125-CD24/FucTVII double transfectants, CD24 was modified with sialylLex. Only double transfectants showed rolling on P-selectin in vivo. When injected into mice, double transfectants arrested in the lungs, and this step was P-selectin dependent because it was strongly enhanced in lipopolysaccharide (LPS) pretreated wild-type mice but not in P-selectin knockout mice. CD24 modified by sialylLex was required on the tumor cells because the LPS-induced lung arrest was abolished by removal of CD24 from the cell surface by phosphatidylinositol-specific phospholipase C. A125-FucTVII single transfectants expressing sialylLex but not CD24 did not show P-selectin-mediated lung arrest. The sialylLex epitope is abundantly expressed on human carcinomas, and significant correlations between sialylLex expression and clinical prognosis exist. Our data suggest an important role for sialylLex-modified CD24 in the lung colonization of human tumors.     

Bilateral pheochromocytoma and islet cell adenoma of the pancreas

An 18-year-old woman with bilateral pheochromocytomas and an asymptomatic islet cell adenoma of the pancreas represents the 11th patient to be described with this combination of endocrine tumors. No other components of any multiple endocrine adenomatosis (MEA) syndromes were present. Because of this "overlap syndrome," in which tumors that have traditionally been considered to be components of separate and mutually exclusive MEA syndromes have occurred concomitantly in the same patient, a question is raised regarding the validity of a rigid classification of these various MEA syndromes. The possibility of a pancreatic tumor should be kept in mind in any patient with a pheochromocytoma, especially if it is bilateral of multicentric in origin.     

Changes of neuronal activity in areas CA1 and CA3 during anoxia and normoxic or hyperoxic reoxygenation in juvenile rat organotypic hippocampal slice cultures

In neonates, asphyxia is usually followed by hyperoxic treatment. In order to study whether hyperoxic reoxygenation might cause additional impairment of neuronal function, we subjected organotypic hippocampal slice cultures of juvenile rats (7 DIV, P6-8) to 30 min anoxia followed by 60 min hyperoxic or normoxic reoxygenation (95% or 19% O2, respectively). Spontaneous and evoked field potentials as well as [Ca2+]o were recorded in the pyramidal layer of area CA1 or area CA3. In area CA1, 30 min of anoxia led to decline of evoked field potential amplitudes by on average 67% and to profound changes in field potential characteristics and Ca2+ homeostasis which were not related to outcome after reoxygenation. Hyperoxic reoxygenation resulted first in a fast recovery of the field potential amplitude to 82% of the control value and then, in 75% of slice cultures, in a large negative field potential shift accompanied by a prolonged decrease of [Ca2+]o and loss of excitability outlasting the experiment. Recovery of field potential amplitude under normoxic conditions stayed poor, with a first increase to 51% and a second decrease to 22%. In contrast, field potential amplitude in area CA3 recovered to 80% of the initial amplitude, irrespective of the reoxygenation mode. The selective loss of function during hyperoxic reoxygenation in area CA1 might be a first sign of neuronal injury that we observed 1 h after end of hyperoxic reoxygenation in a previous study. Whether the poor outcome after normoxic reoxygenation would favour long-term recovery remains to be determined.