Biomedical subjects
Publications and source records attributed to R B Davis.
Fixed payment schemes have transformed departments that were once revenue centers into cost centers, and created the need to carefully manage resources and streamline procedures to improve operational efficiency. One key department in the hospital where these changes are having an impact is Pharmacy.
A case of reticular erythematous mucinosis associated with chronic idiopathic thrombocytopenic purpura and circulating immune complexes is described. We compare reticular erythematous mucinosis with the similar plaquelike cutaneous mucinosis. We discuss the apparent photosensitivity of reticular erythematous mucinosis and its possible relationship with altered states of immune function such as diabetes, thyroid disease, and neoplasia. The somewhat varied but characteristic histopathologic findings and staining are reviewed, including the characteristic perivascular and occasional perifollicular lymphocytic infiltrate and Alcian blue-positive dermal mucin. Treatment with antimalarial drugs still appears to be the most uniformly successful therapeutic approach to the management of this chronic dermatosis. Further research efforts should be directed at understanding its link with altered states of immune function.
Based on work with adolescents at a mental health center and an alcohol education program, some of the difficulties children of alcoholics experience in separating from their homes are considered. These difficulties are described in terms of organizing fantasies in which adolescents use relationships outside of their homes to work through unresolved feelings about their families.
We have evaluated the possible role of platelet functional abnormalities as a contributory cause of thrombosis during pregnancy and to the increased fetal mortality and morbidity among women who smoke. Fifty-three pregnant women were enrolled and evaluated on two separate prenatal visits held between the 20th and 36th week of pregnancy and, when possible, post partum. Smoking status was evaluated by personal statement and alveolar carbon monoxide levels. Women in the smoking group deliberately avoided cigarettes for at least 20 minutes before sampling. Plasma levels of beta-thromboglobulin, thromboxane B2, and 6-Keto PGF1 alpha were evaluated. A significant increase in 6-Keto PGF1 alpha was noted among smoking women as pregnancy advanced. 6-Keto PGF1 alpha levels decreased among non-smoking women while beta-thromboglobulin increased significantly between the 20th and 33rd week of pregnancy in non-smokers. Platelet aggregation, both in platelet rich plasma and in whole blood (by impedance aggregometry), was evaluated by five different parameters and four different aggregating agents. Significant differences between the non-smoking and smoking pregnant women were noted for selected age cohorts and aggregating agents. An increase in platelet reactivity among smokers was observed in whole blood by impedance aggregometry with adenosine diphosphate and in two age cohorts using platelet rich plasma. In two groups in which aggregation was significantly accelerated among non-smokers, epinephrine was used as the aggregating agent.
P16 is a small polypeptide originally found in GH3 rat pituitary tumor cells whose expression is tightly linked to the expression of rat GH (rGH) at a genetic level. It is estimated to be 3-5 kilodaltons smaller than rGH and exhibits the same complex response to T3, dexamethasone, and insulin in GH3 cells as does rGH. P16 was also found in high but variable abundance in anterior but not posterior pituitary. To approach the question of whether it arises from a unique gene or derives instead from the rGH gene by a posttranscriptional mechanism, we have measured its structural relatedness to rGH by peptide mapping techniques. From partial peptide maps of rGH and P16 by V8 protease, it appeared that the two proteins were related by loss of a common, small peptide. Both proteins also contained many tryptic peptides in common. Cleavage by N-chlorosuccinimide at tryptophan residues showed that rGH and P16 both contained the same N-terminal peptide but differed in their C-termini. Hence, P16 differs from rGH by loss of an amino acid segment somewhere in the C-terminus. Charge calibration of two-dimensional gels indicated that P16 was more acidic than rGH by at least five negative charges. These observations taken together imply that rGH gives rise to P16 by a highly specific cleavage in the C-terminus mostly likely between residues 152 and 156. This region also harbors an alanine-leucine at which pro-rGH is cleaved to remove the 26 amino acid signal peptide.
Patients with acute nonlymphocytic leukemia were randomized to receive remission induction therapy consisting of seven days of cytosine arabinoside and three days of daunorubicin ("7 + 3") or to receive the same regimen intensified by either the addition of 6-thioguanine or by extension of the administration of cytosine arabinoside to ten days. Additionally, all patients were randomized to receive or not to receive cotrimoxazole antibacterial prophylaxis during the remission induction phase. Neither an increase in intensity of chemotherapy nor the antibacterial prophylaxis increased the remission rate above the 53% for patients treated with the standard "7 + 3" regimen. The second part of this study addressed the issue of the utility of long-term maintenance chemotherapy. To this end, patients were randomized to discontinue all treatment after 8 months of maintenance chemotherapy or to continue maintenance therapy for a total of 3 years. Although there was a transient increase in the relapse rate for patients who discontinued therapy, the proportion of long-term remitters was identical in the two patient groups. Additionally, there is a suggestion of a survival advantage for patients randomized to discontinue all therapy at 8 months.
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The effect of bacterial endotoxins E. coli 0111:B4 or S. minnesota and platelet activating factor (1-0-alkyl-2-acetyl-SN-glycero-3-phosphorylcholine) on platelet aggregation in native whole blood (NWB) were evaluated by impedance aggregometry. In the absence of anticoagulants the patterns of impedance changes associated with aggregation were distinct from those of clotting. Both E. coli 0111:B4 and S. minnesota endotoxins shortened the time to clot formation, but impedance changes suggestive of accelerated platelet aggregation were minimal or absent. In contrast, PAF caused an increased impedance, with oscillations characteristic of aggregation, which in some instances was superseded by the smooth impedance change associated with clotting. E. coli 0111:B4 endotoxin blocked aggregation and delayed the onset of clotting after PAF, whereas S. minnesota endotoxin accelerated platelet aggregation by PAF in ten of thirteen experiments. Incubation of E. coli 0111:B4 endotoxin and PAF markedly enhanced aggregation by PAF, whereas the effect of S. minnesota was variable. Although E. coli 0111:B4 and S. minnesota endotoxins accelerated clotting but not platelet aggregation of human NWB in vitro, their interaction with PAF is complex, depending on the type of endotoxin and individual reactivity. The findings suggest that endotoxin could interact with PAF to significantly augment possible hemorrhagic and/or thrombotic complications of septic shock in humans.
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Platelet aggregation was analyzed during normal pregnancy by evaluation of the same patient cohort (n = 19) on two separate prenatal visits and at 4 weeks post partum. To analyze platelet aggregation five different parameters were evaluated in platelet-rich plasma and whole blood (by impedance aggregometry) with the use of four different aggregating agents: adenosine diphosphate, collagen, sodium arachidonate, and epinephrine. Plasma levels of beta-thromboglobulin, thromboxane B2, and 1,6-keto-prostaglandin F1 alpha were also analyzed. Platelet counts rose 19% after delivery. Plasma levels of beta-thromboglobulin and thromboxane B2 were not significantly changed during the two antepartum visits, but B-thromboglobulin levels were modestly elevated post partum. Levels of 1,6-keto-prostaglandin F1 alpha decreased significantly from a mean of 125 pg/ml before delivery to 50 pg/ml post partum. All antepartum parameters on whole blood aggregation that were significantly different from postpartum values showed enhanced antepartum reactivity. In platelet-rich plasma, pregnancy was associated with greater platelet reactivity except for two variables, time to half-maximal aggregation for epinephrine and the extent of aggregation by collagen, both noted during the first antepartum evaluation. When the patient cohort of 19 was subdivided according to smoking status, all aggregation parameters of significance (p less than 0.05) demonstrated increased platelet reactivity during pregnancy compared with postpartum values. Smoking women accounted for a disproportionate number of significantly enhanced reactivity (seven variables versus three).
During a 2 1/2-year period, 1131 patients with suspected pulmonary embolism had ventilation-perfusion lung scans; 150 of these patients also underwent pulmonary angiography. In a retrospective study, these 150 patients were re-evaluated using the reference criteria of Biello and Alderson, with 62% read as indeterminate. Twenty patients who had chronic obstructive pulmonary disease with retention of Xe-133 in greater than 50% of the lung fields without corresponding radiographic abnormality were included. Ventilation/perfusion matches and mismatches could be correctly determined in 15 of these patients. These 15 of 20 studies could be correctly reclassified as low-probability, while the other five remained indeterminate. With increasing intervals between ventilation/perfusion lung imaging and the onset of symptoms, the percentage of patients with proven pulmonary emboli correctly diagnosed as high probability continuously decreased, and the percentage of studies read as indeterminate constantly increased. Serial chest radiographs suggested that the development of infiltrates in the region of the embolus convert high-probability ventilation/perfusion scans to indeterminate.
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Twenty-eight peritoneovenous shunts were placed to relieve ascites in 26 patients with a variety of underlying malignancies. Nine of the patients had documented liver metastases and hyperbilirubinemia. Severe thrombocytopenia with laboratory evidence of disseminated intravascular coagulation (DIC) occurred in four of these nine patients following shunt placement. Relative or absolute thrombocytopenia was also commonly observed in this series. Other complications included pulmonary edema, ventricular tachycardia, culture-negative fever, pneumonia, and late shunt occlusion. Good palliation, with relief of abdominal pain or respiratory compromise, was achieved in 57% of these patients. Our experience suggests that DIC following peritoneovenous shunts in patients with malignancy may be more common than previously reported, although not as frequent as the incidence of DIC associated with shunt placement for cirrhotic ascites. Platelet aggregation or Factor X activation by ascitic fluid and failure of the liver to inactivate activated clotting factors may play a role in this coagulopathy. Because of the risk of potentially fatal DIC, palliative peritoneovenous shunts should be considered with caution in patients with liver metastases and hyperbilirubinemia.
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Two young adults with myeloproliferative disease had recurrent thrombotic episodes, which were life threatening or associated with a risk of serious disability. Both patients were treated for arterial occlusive disease, and treatment in one instance reversed spastic paraplegia. During a subsequent two-year period of observation, they have remained symptom free. During that time they have been treated with aspirin, and platelet counts have been maintained at one million/mm3 or less.
The expression of differentiation-associated surface antigens by the clonogenic leukemic cells from 20 patients with acute myeloblastic leukemia (AML) was studied with a panel of seven cytotoxic monoclonal antibodies (anti-Ia, -MY9, -PM-81, -AML-2-23, -Mol, -Mo2, and -MY3). The surface antigen phenotypes of the clonogenic cells were compared with the phenotypes of the whole leukemic cell population, and with the phenotypes of normal hematopoietic progenitor cells. In each case the clonogenic leukemic cells were found within a distinct subpopulation that was less "differentiated" than the total cell population. Clonogenic leukemic cells from different patients could be divided into three phenotype groups. In the first group (7 of 20 cases), the clonogenic cells expressed surface antigens characteristic of the normal multipotent colony-forming cell (Ia, MY9). These cases tended to have "undifferentiated" (FAB M1) morphology, and the total cell population generally lacked expression of "late" monocyte antigens such as MY3 and Mo2. A second group (seven cases) of clonogenic cells expressed surface antigens characteristic of an "early" (day 14) colony-forming unit granulocyte-monocyte (CFU-GM), and a third group (six cases) was characteristic of a "late" (day 7) CFU-GM. The cases in these latter two groups tended to have myelomonocytic (FAB M4) morphology and to express monocyte surface antigens. These results suggest that the clonogenic cells are a distinct subpopulation in all cases of AML, and may be derived from normal hematopoietic progenitor cells at multiple points in the differentiation pathway. The results further support the possibility that selected monoclonal antibodies have the potential to purge leukemic clonogenic cells from bone marrow in some AML patients without eliminating critical normal progenitor cells.