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Biomedical subjects

R K Root

Publications and source records attributed to R K Root.

83 records · Page 5Linked to original sources
PubMed1970

Leukocytic function in hypogammaglobulinemia.

The phagocytic, bactericidal, and metabolic capabilities of circulating blood leukocytes from three adults (two males, one female) with hypogammaglobulinemia and recurrent pneumonia, chronic sinusitis, and intestinal giardiasis were studied. These functions were found to be normal when leukocytes from the patients were incubated in media containing normal human serum. Phagocytosis of Staphylococcus albus and polystyrene balls by both patient and normal leukocytes was diminished when the cells were incubated in hypogammaglobulinemic plasma. A similar defect in opsonization by patient plasma was also noted for pneumococci, Escherichia coli and variably with Staphylococcus aureus. Both patient and normal sera had equivalent levels of heat-labile S. albus opsonins; normal serum, however, contained heat-stable S. albus-specific absorbable opsonins in significantly greater quantities to account for its superior opsonic capacity. The addition of commercial gamma globulin or purified IgG to hypogammaglobulinemic sera restored full S. albus opsonic activity. The relevancy of these observations to the impaired host defenses in these patients will be discussed.

Agammaglobulinemia↗
PubMed1968

Pathogenetic mechanisms in experimental immune fever.

When rabbits sensitized to human serum albumin (HSA) are challenged intravenously with specific antigen, fever develops and two transferable pyrogens can be demonstrated in the circulation. The first appears prior to the development of fever and has properties consistent with soluble antigen-antibody complexes. These have been shown to be pyrogenic when prepared in vitro and to produce a state of febrile tolerance when repeatedly administered. The second pyrogen, demonstrable during fever in donor rabbits, appears to be similar to endogenous pyrogen described in other experimental fevers. It is postulated that the formation of antigen-antibody complexes constitutes an important initial phase of the febrile reaction in this type of immune fever.

Anaphylaxis↗
PubMed1966

Studies on the effect of experimental nonketotic diabetes mellitus on antibacterial defense. I. Demonstration of a defect in phagocytosis.

Chronically diabetic nonketotic rats were shown to be more susceptible to experimental Type 25 pneumococcal pneumonia than nondiabetic rats. The cumulative mortality in the diabetic group was significantly higher at infecting doses of 10(3), 10(4), 10(5), and 10(6) organisms, and the LD(50) was less than one twentieth of that for the nondiabetic group. More than ten times as many viable pneumococci were found in the pneumonic lesions of the diabetic animals at 24 and 36 hr as were present in the lesions of the nondiabetic controls, and serial histologic studies revealed that phagocytosis was strikingly depressed in the alveolar exudates of the diabetic animals. The diabetic state was also found to cause a similar depression of in vivo phagocytosis in preformed peritoneal exudates. The results of in vitro experiments indicated that the principal defect in the diabetic animals resided in their serum rather than in their polymorphonuclear leukocytes. The depressive factor in the serum was identified as the abnormally high concentration of glucose. Since equivalent molar concentrations of unmetabolized sugars added to normal serum caused a similar depression of phagocytosis, it was tentatively concluded that the action of the glucose on the leukocytes was primarily osmotic. The sensitivity of the granulocytes to the glucose effect, however, depended upon the conditions of the phagocytic test. Only when the pneumococci were encapsulated and the leukocytes derived from inflammatory exudates were crowded together, as in vivo, was the depressive action of the glucose clearly demonstrable.

Animals↗
PubMedDate not supplied

Effect of microaggregate blood filtration on granulocyte concentrates in vitro.

To determine the effect of transfusing granulocyte concentrates through microaggregate blood filters, granulocytes prepared with a cell processor were passed through screen and depth microaggregate filters. Pre- and postfiltration evaluations were made of total granulocyte count, levels of muramidase, granulocyte viability, motility, phagocytosis, bactericidal activity, and hydrogen peroxide-forming capacity. Compared to prefiltration levels, a significant (p less than 0.05) decrease in postfiltration granulocyte counts was seen for all the depth filters studied but not for the standard 170 microns (control) or the 40 microns screen filter. For the various tests of granulocyte function evaluated prefiltration, no significant postfiltration differences (p greater than 0.05) were seen for any of the filters studied. Screen microaggregate filters retained only 1 to 3 percent of granulocytes contained in the concentrates, and thus appear satisfactory for use in clinical transfusions. The large percentage of neutrophils retained by the depth filters (20-62%), however, precludes their use for transfusion of granulocyte concentrates.

Blood↗
PubMedDate not supplied

Unusually high occurrence of drug reactions with nafcillin.

Five patients seen during a two-month period who developed untoward systemic reactions following high dose intravenous administration of nafcillin are described. Recovery was complete upon discontinuation of the drug. The clustering of these cases and the high incidence (5 of 5) of side effects are highly unusual, and suggest that the frequency of nafcillin reactions might be higher than previously suspected.

Adult↗
PubMedDate not supplied

Paraquat suicide in a young woman: results of therapy directed against the superoxide radical.

The clinical course of a young woman following two separate suicide attempts using the herbicide paraquat is reported. The patient survived an intramuscular injection of paraquat almost asymptomatically, but later exhibited a typical fatal course with fulminant proliferative pulmonary fibrosis after an intravenous injection. Fibrosis and death occurred despite a therapeutic regimen based upon a known action of paraquat, the generation of superoxide (O(2)[unk]), using superoxide dismutase, α-tocopherol, and ascorbic acid in conjunction with forced diuresis and prednisone. While treatment failed explanations for the failure of therapy in this case and current therapeutic alternatives are discussed so that they may be considered when future cases are encountered.

Adult↗
PubMedDate not supplied

Glucose-6-phosphate dehydrogenase deficiency and infection: a study of hospitalized patients in Iran.

The Mediterranean variant of glucose-6-phosphate dehydrogenase (G6PD) is functionally deficient and found in a variety of cell types of affected individuals, including both erythocytes and neutrophils. To determine if the presence of this sex-linked gene is associated to any degree with the occurrence of severe bacterial infection, a study of hospitalized male patients in Iran was undertaken. As determined by erythrocyte assay, allele prevalence in male patients with infection was 22% vs. 12% in a patient group matched for the absence of other risk factors for infection and 6% in a second group who had additional risk factors for infection. When the control and patient groups were considered together the difference between the frequency of G6PD deficiency (10.2%) was significantly different from that found in the infected patients (p less than .05). Furthermore, the mean age of infected patients with G6PD deficiency was significantly less than that of infected patients without G6PD deficiency or non-infected control groups. These data suggest that host defenses may be altered in G6PD deficiency so that bacterial infections are more severe. Alternatively, G6PD deficiency and infection might represent concomittant risk factors which lead to hospitalization during bacterial infection. Potential mechanisms by which host defenses might be altered in G6PD deficiency are discussed.

Adult↗
PubMedDate not supplied

Enhanced killing of penicillin-treated gram-positive cocci by human granulocytes: role of bacterial autolysins, catalase, and granulocyte oxidative pathways.

Staphylococci pretreated with subminimal inhibitory concentrations (subMIC) of cell-wall active antibiotics exhibit increased susceptibility to killing by human polymorphonuclear leukocytes (PMNs), even when phagosome information is impaired by the mold metabolite, cytochalasin B. To investigate the role of specific bacterial factors in the process, studies were carried out with organisms lacking catalase (streptococci) or cell-wall autolytic enzymes and compared to findings with Staphylococcus aureus 502A. Neutrophil factors were studied using inhibitors, oxygen radical scavengers, myeloperoxidase (MPO)-deficient PMNs, or PMNs from a patient with chronic granulomatous disease (CGD). Documentation of the enhanced susceptibility of the streptococcal strains to killing by PMNs following subMIC penicillin pretreatment required the use of cytochalasin B. Enhancement of killing occurred independent of the presence or absence of bacterial autolysins or catalase. SubMIC penicillin pretreatment of S. pneumoniae R36A specifically promoted the susceptibility of these organisms to killing by myeloperoxidase (MPO)-mediated mechanisms (enhancement lost using MPO-deficient or azide-treated cells). Factors other than MPO or toxic oxygen products generated by the PMN respiratory burst are responsible for enhanced killing of penicillin-pretreated S. aureus 502A (enhancement preserved using MPO-deficient, azide-treated, or chronic granulomatous disease patient cells). These studies define methods to study the interaction of antimicrobial agents and PMNs in the killing of microorganisms. They also demonstrate that penicillin treatment can change the susceptibility of gram-positive cocci to the action of specific PMN microbicidal mechanisms. The mechanism of the enhancement appears to be bacterial strain-dependent and not predictable by bacterial autolysin or catalase activity.

Acatalasia↗