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Biomedical subjects

R L Baehner

Publications and source records attributed to R L Baehner.

At least 163 records · Page 9Linked to original sources
PubMed1977

Effect of hyperoxia on superoxide anion and hydrogen peroxide production of polymorphonuclear leucocytes and alveolar macrophages.

Hyperoxia activates superoxide dismutase (SOD) while inactivating catalase and glutathione peroxidase in polymorphonuclear leucocytes (PMN) and alveolar marcophages (AM) obtained from guinea-pigs exposed to 85% oxygen for 90 h. The influence of these altered enzyme activities on the rate of oxygen consumption and release of superoxide anion (O--2) and hydrogen peroxide (H2O2) was investigated. By 18 h O--2 released from resting PMN increased two-fold and remained elevated through the entire periods of the study, whereas H2O2 release and oxygen consumption at the same time points remained normal. At 66 h PMN phagocytizing opsonized zymosan particles released additional quantities of O--2 and H2O2 and consumed significantly more oxygen compared to the usual increase noted at earlier time points. Although oxygen consumption was almost two-fold higher in AM than PMN, phagocytizing AM released three-fold less O--2 and five-fold less H2O2 than did PMN. Furthermore, AM of animals exposed to hyperoxia no longer exhibited enhanced O--2 production upon exposure to opsonized zymosan. Hydrogen peroxide release progressively decreased at rest but progressively increased during phagocytosis of opsonized zymosan during the 90 h exposure to hyperoxia. No changes in oxygen consumption of AM occurred during hyperoxia. The divergent oxidative responses in PMN and AM of guinea-pigs exposed to hyperoxia suggest different biochemical adaptive mechanisms.

Animals↗
PubMed1977

An unusual form of chronic neutropenia in a father and daughter with hypogammaglobulinaemia.

Chronic neutropenia, with an abundance of mature neutrophils in the bone marrow, was discovered in a father and daughter who also had common variable hypogammaglobulinaemia. Under the stress of infection or following the administration of typhoid vaccine, release of neutrophils from the marrow was enhanced sufficiently to abolish neutropenia temporarily. Although their morphology was abnormal, the function of neutrophils in vitro was normal. Thus, the increased susceptibility to infection that characterized these patients appeared to be due primarily to their defect in humoral immunity rather than their neutropenia.

Adult↗
PubMed1977

Mechanisms of microtubule diassembly in vivo: studies in normal and chronic granulomatous disease leucocytes.

Microtubule assembly in human polmorphonuclear leucocytes is a dynamic process that can be initiated by binding of the plant lectin Concanavalin A to surface receptors. Colchicine inhibits lectin-induced microtubule assembly and promotes the movement of Concanavalin A into surface caps. Inhibition of microtubule assembly and enhanced Concanavalin A cap formation also follow treatment of normal leucocytes with two specific glutathione-oxidizing agents, 'diamide' and tertiary butylhydroperoxide. Our objective here was to determine if microtubule inhibition is mediated via glutathione disulphide or via hydrogen peroxide that is generated in Concanavalin A-treated leucocytes and may accumulate when cells are depleted of reduced glutathione. We show that exogenous hydrogen peroxide induces Concanavalin A capping on normal polymorphonuclear leucocytes but only at concentrations that simultaneously oxidize glutathione. We also show that 'diamide' and tertiary butylhydroperoxide cause Concanavalin A cap formation in leucocytes from patients with chronic granulomatous disease. These cells cannot generate significant amounts of superoxide or hydrogen peroxide. Thus, it seems likely that the reversible inhibition of microtubule assembly and function caused by glutathione oxidants requires only increased glutathione disulphide and is not dependent on subsequent accumulation of other metabolites.

Child↗
PubMed1977

Oral manifestations of acute leukemia in children.

Seventy-seven children with acute leukemia were examined. A wide spectrum of oral findings was observed as the consequence of direct leukemic infiltration of tissue, infection resulting from bone marrow and immunosuppression, impaired healing responses, and poor oral hygiene. Guidelines for dental treatment are provided.

Adolescent↗
PubMed1977

Improvement of Chediak-Higashi leukocyte function by cyclic guanosine monophosphate.

The addition of cholinergic agents and cyclic 3'5'-guanosine monophosphate (cGMP) to polymorphonuclear leukocytes in vitro from a patient with Chediak-Higashi syndrome corrected the impaired release of the lysosomal enzyme, beta-glucuronidase, to normal. Coinciding with the improvement in degranulation, the bactericidal capacity was enhanced to normal. Similar concentrations of cholinergic agents potentiated chemotaxis to control values. On the other hand, the phagocytic rate of lipopolysaccharide-coated paraffin-oil droplets was not altered by the cholinergic agents. The improvement in Chediak-Higashi syndrome polymorphonuclear leukocyte function by the addition of cholinergic agents and dibutyryl cGMP suggested disturbed intracellular cyclic nucleotide levels.

Blood Bactericidal Activity↗
PubMed1977

The causes of interstitial pneumonitis in immunocompromised children: an aggressive systematic approach to diagnosis.

A systematic, aggressive approach to the immunocompromised child with interstitial pneumonitis has been used in 24 consecutive patients. Parent and physician awareness of early symptoms and signs had been emphasized. When laboratory data confirmed clinical suspicion, open lung biopsy was done and lung tissue was studied by impression smears, sections, and culture techniques. The etiologic agent was established by stained impression smears within three hours of receipt of tissue in 21 of 24 patients. Eighteen of 24 patients survived. Patients had a poor prognosis if they required ventilatory assistance (five of seven died) or had respiratory symptoms for three days or more prior to biopsy (four of 13 died). Children with solid tumors who had absolute lymphocyte counts less than 500/cu mm, had received chemotherapy and radiotherapy to the chest, and had developed Pneumocystis carinii pneumonitis had a poor outcome (all three died).

Adolescent↗
PubMed1977

Sudden death in an infant from methemoglobinemia after administration of "sweet spirits of nitre".

The administration of "sweet spirits of nitre" (4% ethyl nitrite CH3CH2ONO in 70% ethyl alcohol) was followed by acute methemoglobinemia and severe anoxic metabolic acidosis in infant twins, Methylene blue administration reversed methemoglobinemia in both, but one twin died from the consequences of hypoxemia. Hemoglobin electrophoresis and methemoglobin reductase determinations were normal for age. This medicine is available without prescription and contains the potent oxidant ethyl nitrite. In infants with sudded death or onset of cyanosis, appropriate toxicological and historical information should be obtained.

Death, Sudden↗
PubMed1977

Autooxidation as a basis for altered function by polymorphonuclear leukocytes.

To investigate the possibility that human polymorphonuclear leukocytes (PMN) elaborate sufficient amounts of hydrogen peroxide (H2O2) and other radicals of reduced oxygen to be autotoxic and retard directed cell movement and phagocytosis, the rate of ingestion of opsonized lipopolysaccharide-paraffin oil particles and movement through Nuclepore filters were studied. Ingestion rates were increased under anaerobic conditions and in normal aerobic conditions in the presence of extracellular catalase but not superoxide dismutase (SOD) or scavengers of singlet oxygen or hydroxyl radicals. Conversely, ingestion rates were decreased when cells were exposed to H2O2 or a superoxide anion (O2-)-H2O2 generating system of xanthine-xanthine oxidase. Catalase, but not SOD, prevented the effect and also enhanced the directed movement of PMN in normal aerobic conditions. PMN from volunteers administered 1600 U/day of the membrane lipid antioxidant alpha-tocopherol were hyperphagocytic but killed Staphylococcus aureus 502A less effectively than controls, suggesting that less H2O2 was available to damage PMN or kill bacteria. H2O2-dependent stimulation of the hexose monophosphate shunt, H2O2 release from phaogytizing PMN, and fluoresceinated concanavalin A cap formation promoted by H2O2 damage to microtubules were all diminished, but the release of O2- from phagocytizing PMN was not diminished in the vitamin E group. These results support the hypothesis that directed movement and phagocytosis by PMN are attenuated by autooxidative damage to the cell membrane by endogenously derived H2O2 and that the administration in vivo of vitamin E may prevent this damage by scavenging H2O2.

Aerobiosis↗
PubMed1976

Correction of leukocyte function in Chediak-Higashi syndrome by ascorbate.

Because ascorbate potentiates chemotaxis of normal leukocytes, we examined the effect of ascorbate on polymorphonuclear leukocytes from a patient with the Chediak-Higashi syndrome. Chemotactic migration was 104+/-16 leukocytes per 10 fields (mean+/-S.D.) initially and 258+/-44 (P less than 0.001) after ascorbate, as compared to 182+/-10 in controls. There was no bactericidal activity by 40 minutes in the patient's untreated leukocytes. After ascorbate bactericidal activity of patient and untreated control cells was the same. The addition of ascorbate reduced cAMP levels in the patient's cells from a mean of 34.5 pmoles per 10(7) polymorphonuclear leukocytes to 5.9, as compared to a control value of 3.1+/-1.4. The association of elevated cAMP and impaired function in the polymorphonuclear leukocytes of patients with the Chediak-Higashi syndrome may be related to abnormal microtubular assembly.

Ascorbic Acid↗
PubMed1976

Septicemia and meningitis in children splenectomized for hodgkin's disease.

Retrospective evaluation of the occurrence of septicemia and meningitis in 200 children who had staging laparotomy iwth splenectomy for Hodgkin's disease revealed 20 episodes occurring in 18 children. Symptoms were usually fulminant; only 10 of these patients survived their episode. Infections occurred eight days to three years after splenectomy. Adolescents, as well as younger children, were affected; half were older than 10 years of age. Leukopenia was not a major factor in onset or survival since the average white-cell count was 12,000 in both survivors and children who died. Pneumonococcus accounted for 50 per cent, and streptococcus for 15 per cent of infections; there was one episode each of Haemophilus influenzae and meningococcus; in 25 per cent, no organism was isolated. Predominance of penicillin-sensitive organisms and high mortality suggest that penicillin prophylaxis and the protection offered by bacterial vaccines should be evaluated in children with Hodgkin's disease whose staging laparotomy includes splenectomy.

Adolescent↗
PubMed1976

Favorable prognosis for survival in children with coincident opso-myoclonus and neuroblastoma.

Case reports of 28 neuroblastoma patients who had opso-myoclonus as their presenting feature are reviewed. As compared with the 30%-34% two-year survival rate for the overall population of patients with neuroblastoma, those who exhibited the opso-myoclonus/neuroblastoma combination had a tumor-free two-year survival rate of 89.3%. This excellent prognosis may be explained partially by earlier diagnosis and a higher percentage (71% vs. 33%) of patients with Stage I, II, and IV-S disease in the opso-myoclonus sub-group. However, these factors are not, of themselves, sufficient to explain totally the differences in survival rate since five of seven patients with Stage III-IV disease also exhibited long-term survival. This raises the question as to whether the neurologic dysfunction in these patients is pathogenetically related to an unknown factor (possibly autoimmune) which also controls growth and spread of the tumor.

Child, Preschool↗
PubMed1976

Portal hypertension in infants and children with histiocytosis X.

Histiocytosis X describes a disease characterized by histiocytic infiltration of the reticuloendothelial system, skin, bones, and pituitary gland. The disseminated form frequently occurs in infants and children. Chemotherapy has significantly improved the prognosis in this disorder. Sixty-three per cent of survivors, however, have some residual disability related to fibrosis of tissues previously infiltrated by histiocytes. In instances of liver involvement, healing by fibrosis may result in cirrhosis with portal hypertension and bleeding esophageal varices. Clinical findings include hepatosplenomegaly, jaundice, ascites, hypoalbuminemia, prolonged prothrombin time, and Bromsulphalein retention. Histologic examination of the liver shows a characteristic dense "macronodular" periportal cirrhotic pattern. Three children with portal hypertension and bleeding varices due to healed histiocytosis X were sucessfully managed by portosystemic shunt procedures. Portacaval, mesocaval, and central splenorenal shunts were equally effective in relieving poral hypertension. These children had neither recurrence of bleeding nor evidence of encephalopathy. Two children remain well whereas in one patient a primary hepatoma developed fourteen years posthung and he died of pulmonary metastases. Portosystemic shunt procedures effectively relieve the threat of potentially fatal variceal hemorrhage and improve the opportunity for long-term survival in children with cirrhosis and portal hypertension due to healed histiocytosis X.

Age Factors↗
PubMed1976

Effect of diet on urinary excretion of VMA, HVA, metanephrine, and total free catecholamine in normal preschool children.

Quantitation of the urinary metabolites of catecholamines, including VMA, HVA, and metanephrines, from six normal preschool children was performed during a normal diet, a restricted diet, and a diet with increased amounts of vanilla, vanillin, and phenolic acids. Ingestion of these substances has been suspected of producing elevated values of urinary catecholamines and their metabolites. Urine was collected on the fourth day of each diet in two consecutive 12-hour aliquots, beginning at 8:00 AM. Statistically significant diurnal variation in excretion of all three metabolites and total free catecholamines (epinephrine, norepinephrine, and dopamine) was demonstrated. Diet did not alter exceretion of total free catecholamines or any of the three metabolites. This study suggests that a three-day restricted diet is not necessary prior to screening children for neuroblastoma when using quantitative assay methods and that all screening tests should be performed on a 24-hour urine sample.

Catecholamines↗
PubMed1976

Superoxide dismutase activity in polymorphonuclear leukocytes and alveolar macrophages of protein malnourished rats and guinea pigs.

Chronic protein insufficiency in utero was achieved by feeding to rat dams an 8% protein diet beginning before breeding and continuing until weaning. Thereafter, the in utero malnourished pups were fed the 8% protein diet. Superoxide dismutase (SOD), an enzyme which protects against superoxide radical, was quantitated in pellet and supernatant of polymorphonuclear leukocytes (PMN) and alveolar macrophages (AM). The AM of rats malnourished in utero contained 1.7 times as much protein and 3 times as much total SOD activity as the AM of control rats. In PMN of these rats, the amount of protein and SOD activity was the same. Significantly larger number of Streptococcus mutans were located from the dental plaque of the in utero malnourished rats. AM isolated from female guinea pigs fed a 9% protein diet from weaning at 11 days of age contained 1.5 times as much protein and twice as much SOD activity as AM from normal guinea pigs. However their PMN contained smaller amounts of total protein and SOD activity. The malnourished guinea pigs had a mammary gland infection and a prolonged conjunctival infection following inoculation with Guinea Pig Inclusion Conjunctivitis indicating that these animals were more susceptible to these infections. The increase in total SOD activity and in the total amount of protein in AM suggests that chronic protein insufficiency leads to susceptibility to infection and to macrophage activation but has no similar effects on PMN.

Animals↗
PubMed1976

Distribution of T and B lymphocytes in lymphoid tissue of infants and children.

Normal lymphoid tissue from children undergoing elective surgery was examined for T and B lymphocyte distribution. Although established for peripheral blood and bone marrow, T and B lymphocyte distributions have not been previously reported for lymph nodes, appendix, thymus, and spleen tissues in children. Thymus-dependent T cells were determined by the sheep erythrocyte rosette technique, and thymus-independent B cells were determined by the fluorescent labeling of surface immunoglobulins A (IgA), G (IgG), and M (IgM). Fifty percent of lymph node cells were either T or B cells; 65% of these cells were T lymphocytes, whereas 58% of B cells were of the IgM subclass. Less than half of the appendix cells were either T or B cells; 47% of these were T lymphocytes, and the remainder B lymphocytes had subclass distribution similar to that of lymph nodes but different from peripheral blood and bone marrow where B cells bearing IgG predominate. Thymus tissue contained 43% T cells and less than 1% B cells, but the spleen was composed largely of B cells, predominantly of the IgM type. Lymphoid tissue from nine children with either inflammatory or neoplastic diseases were studied and included for contrast. This paper establishes relative distribution values for T and B lymphocytes in normal lymphoid tissue and points out the potential use of this technique to quantitate deviations from normal in certain inflammatory and neoplastic diseases.

Adolescent↗
PubMed1976

The alteration of superoxide dismutase, catalase, glutathione peroxidase, and NAD(P)H cytochrome c reductase in guinea pig polymorphonuclear leukocytes and alveolar macrophages during hyperoxia.

Superoxide dismutase, catalase, glutathione peroxidase and NAD(P)H cytochrome c reductase were quantitated in polymorphonuclear leukocytes (PMN) and alveolar macrophages (AM) obtained from guinea pigs exposed up to 90 h to 85% oxygen. PMN and AM were sonicated and separated into a 16,000-g pellet, a 100,000-g pellet, and a 100,00-g supernate. Superoxide dismutase activity increased in both cells within 18 h, persisted for 66 h and decreased by 90 h. The highest rate of increase was in the 100,000-g pellet containing 3.4% of total enzyme activity in PMN but 28% in AM. The enzyme induction in PMN and AM was partially inhibited by daily intracardiac injections of 50 mg/kg actinomycin D. During oxygen exposure, catalase activity in PMN and AM decreased to 60% of its original activity, and gluthathione peroxidase was reduced in PMN to 60% and in AM to 20% of control values. Although NAD(P)H cytochrome c reductase decreased to 50% in PMN, no change was noted in AM. Upon exposure to superoxide anion, purified catalase, the glutathione peroxidase of the 100,000-g supernate, NADH, and NADPH cytochrome c reductases of the 16,000-g pellet decreased to 66+/-5%, 72+/-4%, 52+/-8%, and 40+/-9%, respectively, of their original activity. This inactivation was prevented by 0.1 mg superoxide dismutase. These in vitro observations could explain the decreased catalase and glutathione peroxidase activity demonstrated in vivo that may lead to an intracellular accumulation of hydrogen peroxide. Increased hydrogen peroxide concentrations have been found to inactivate superoxide dismutase thus impairing the first defense mechanism against superoxide anion.

Animals↗