Biomedical subjects

A F Muhleman

Publications and source records attributed to A F Muhleman.

5 recordsLinked to original sources

PubMed1986

The ferret: a new model of oral ethanol injury involving the liver, bone marrow, and peripheral blood lymphocytes.

We have developed a model of oral ethanol ingestion in the ferret by providing a complete liquid diet in which 21% of the total caloric intake is given as ethanol. After 3 weeks of ethanol treatment, migration inhibitory factor activity from ferret lymphocytes was significantly decreased when compared to animals fed a dextrose-substituted, identical liquid diet. Lymphocyte blastogenesis in response to the mitogen, phytohemagglutinin, was also decreased after 6 weeks of ethanol ingestion. Histopathologically, hepatic cell degeneration, fat deposition, and "Mallory body-like" material were present after 11 weeks of therapy. Bone marrow aspirate cells from the iliac crest of ethanol-fed animals showed vacuolization in both erythroid and myeloid elements after 6 weeks of ethanol ingestion. Mean ferret weights were not significantly different between the ethanol and dextrose control groups; serum ethanol and acetaldehyde concentrations were somewhat higher over the study period compared to those seen in human alcoholics. Therefore, we have designed a small animal model of the toxic effects of alcohol in which multiple organ systems exhibited evidence of ethanol-related disease.

Alcoholism↗

PubMed1985

Factor VIII inhibitors: in vivo decrease of inhibitory activity during calcium infusion.

The effect of parenteral calcium on altering the activity of factor VIII inhibitors has been studied in three patients, two nonhemophiliacs and one hemophiliac. The patients were studied during both intravenous calcium infusion, factor VIII replacement, and combinations thereof. When compared to factor VIII replacement alone, a greater diminution of inhibitory activity was noted whenever calcium was infused prior to and during factor VIII replacement. This was demonstrated by both conventional coagulation assays and an agarose gel method. These observations could have therapeutic implications and may aid in further understanding the relationship of calcium to factor VIII and its inhibitor.

Blood Coagulation↗

PubMed1979

A factor V inhibitor: in vitro interference by calcium.

A patient with a factor V inhibitor resistant to all standard methods of therapy was recently reported. Because of this resistance, further investigation of the inhibitor was carried out employing the inhibitory plasma, serum, and isofocused fraction. It has subsequently been shown in vitro by use of the prothrombin time, partial thromboplastin time, and Russell's viper venom time that the activity of the inhibitor is diminished by the addition of calcium chloride or calcium gluconate to the inhibitory plasma, serum, or isofocused fraction before the addition of normal pooled plasma. This inhibitor, an IgG4 (lambda) immunoglobulin appears to have a high calcium binding affinity and is markedly potentiated in acid pH. These findings suggest that there may be a role in vivo for calcium infusion as part of the clinical management of such an inhibitor and that the metabolic acidosis associated with hemorrhagic shock may potentiate this type of inhibitor.

Calcium↗

PubMed1979

A monoclonal IgG4 (lambda) with factor V inhibitory activity.

A monoclonal IgG4 (lambda) with inhibitory activity to human coagulation factor V was isolated from the serum of a patient with a fatal hemorrhagic diathesis by using a combination of DE-52 ion exchange chromatography and isoelectric focusing techniques. Using the criteria for defining a monoclonal immunoglobulin of restricted mobility on protein electrophoresis, immunoelectrophoresis, and isoelectric focusing, as well as neutralization with class, subclass, and light chain type antisera, we are the first to demonstrate a factor V inhibitor as a monoclonal IgG4 (lambda) detectable in serum or plasma.

Chromatography, Ion Exchange↗

PubMed1978

Hemorrhagic death associated with a high titer factor V inhibitor.

An acquired bleeding diathesis was first noted in a 51-year-old patient 11 days following an exploratory laparotomy. Laboratory studies indicated the cause of bleeding to be the development of a circulating anticoagulant which inhibited factor V activity. The inhibitor, an immunoglobulin of the IgG class, was separated by use of Sephadex G-200 filtration, disc electrophoresis, and isoelectric focusing. Despite vigorous immunosuppressive, antifibrinolytic, and replacement therapy, including the use of a "prothrombin complex" and plasmaphoresis, the bleeding diathesis could not be reversed and the patient died of hemorrhage. Although inhibitors to factor V are not usually associated with major life-threatening hemorrhage, this case demonstrates that the development of such an inhibitor can be an ominous finding. The use of an aminoglycoside antibiotic in this and other patients so reported may be one of the contributing causes to the development of such an inhibitor.

Antibodies↗