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Biomedical subjects

J B Jones

Publications and source records attributed to J B Jones.

At least 127 records · Page 7Linked to original sources

Calcium, phosphorus, and magnesium contents of human milk during early lactation.

Early milk samples from 102 American mothers were examined for Ca, P, and Mg contents in relation to stage of lactation, intake of prenatal mineral supplements, maternal age, parity, and previous history of lactation. A total of 415 samples were collected at three stages of lactation: early transitional (4-7 days postpartum); transitional (10-14 days postpartum); and mature (30-45 days postpartum). No diurnal variations in element concentrations were observed in representative samples of late evening (PM) and early morning (AM) feedings collected during the transitional and mature stages. The mean concentrations for the major elements were highest in early transitional milk and in some cases decreased significantly (p less than 0.05) as lactation progressed. Ca, P, and Mg contents (means +/- SEM) were 26.3 +/- 0.6, 14.6 +/- 0.4, 5.3 +/- 0.1 mg/100 g in early transitional milk and 26.2 +/- 0.5, 13.3 +/- 0.3, and 5.0 +/- 0.1 in mature milk, respectively. Increasing uniformity in the elemental content of milk was noted among the mothers as lactation became established. No significant relationship was found between intake of dietary supplements containing Ca and Mg and levels of these elements in milk. Also, no significant correlations were found between maternal age, parity, or previous history of lactation and the elemental content of milk. From these data, it was estimated that fully breast-fed infants would receive approximately 33, 18, and 6.5 mg/kg/day of Ca, P, and Mg, respectively, during the neonatal period.

Calcium↗

Cyclic Hematopoiesis: animal models.

The four existing animal models of cyclic hematopoiesis are briefly described. The unusual erythropoietin (Ep) responses of the W/Wv mouse, the Sl/Sld mouse, and cyclic hematopoietic dog are reviewed. The facts reviewed indicate that the bone marrow itself is capable of influencing regulatory events of hematopoiesis.

Anemia↗

Canine cyclic haematopoiesis: bone marrow adherent cell influence of CFU-C formation.

Canine cyclic haematopoiesis (CH) appears to be a multipotential stem cell defect, possibly due to an intrinsic marrow defect. The in vitro adherent marrow cells of the cyclic haematopoietic (CH) dog were cultured as underlayers beneath normal dog nonadherent marrow cells. The marrow granulocyte-committed colony forming units (CFU-C0 of the normal dog nonadherent cells were cyclically influenced by the CH adherent cell underlayers. The CH adherent cells collected on the ninth or tenth day following the onset of neutropenia did not stimulate CFU-C formation while those collected on the sixth day stimulated as many as 108 colonies. The CH adherent cells collected on other cycle days supported increased CFU-C formation with the exception of cycle day 3 which inconsistently stimulated growth. These data show that the CH marrow in vitro adherent cells alternately stimulate and inhibit in vitro granulopoiesis of normal dog marrows.

Animals↗

Production of presumptive humoral haematopoietic regulators in canine cyclic haematopoiesis.

Conditioned media (CM) were prepared according to previously published techniques from the bone marrow of dogs with cyclic haematopoiesis (CH). CM prepared from day 9 marrows inhibited mouse bone marrow CFU-s proliferation rate while CM from day 10 marrows were stimulatory and also contained an erythroid stimulating factor which appeared to be erythropoietin. In addition a highly significant trend from CM containing CFU-s inhibitory materials to media with CFU-s stimulatory activity was observed through cycles day 1 to 8. These studies further support the concept that CH is due to a defect in factors controlling stem cell proliferation and suggest that a major event occurs in CH dog marrow on days 9 and/or 10 of the cycle.

Animals↗

Increase in the serum macrophage migration inhibitory activity and lysozyme in dogs affected with cyclic hematopoiesis.

Cyclic neutropenia (CN) is an inherited disease known to occur in both humans and Gray Collie dogs. In dogs, the disease is characterized by a profound and cyclic decrease in circulating granulocytes at 12-day intervals. Other formed elements of the blood also show cyclic changes and thus the disease is also called cyclic hematopoiesis (CH). In this study, daily serum levels of lysozyme and a factor with macrophage migration inhibitory (MIF) activity were assayed. Both MIF activity and lysozyme levels were elevated more than 2-fold and fluctuated cyclically in CH dogs during the 12-day cycle: CH dogs CH 490 and CH 491, had 32.7 +/- 16.8% and 35.9 +/- 18.3% migration inhibitory activity, respectively, as compared to 15.1 +/- 1.4% in normal dog N 492; CH 490 and CH 491 had 78.7 +/- 43.7 units and 86.9 +/- 58.7 units of lysozyme, respectively, as compared to 33.4 +/- 1.7 units in N 492. The change of MIF activity tended to precede that of lysozyme activity in CH dogs. Furthermore, MIF levels and monocyte counts correlated significantly during the 12-day neutropenia cycle (CH 490, r = 0.677, P less than 0.001; CH 491, r = 0.583, P less than 0.01).

Agranulocytosis↗

Canine cyclic hematopoiesis: blood gas and 2,3-diphosphoglyceric acid studies.

Cyclic hematopoiesis in gray Collies was first described in 1967. These dogs are anemic in comparison with the healthy littermates, and their erythropoiesis is abnormal. Although the basic disorder appears to be an as yet unidentified abnormality of hematopoietic progenitor cells, an inherent difference in responses to blood gas control mechanisms remains as a possible cause. In a study of these mechanisms in dogs with cyclic hematopoiesis, the P50 and 2,3-diphosphoglyceric acid concentrations were increased. Differences in pH, PCO2, PO2, and oxygen saturation were not observed.

2,3-Diphosphoglycerate↗

Cyclic hematopoiesis: etiological concepts. Clinical research update.

The cellular elements of the blood are normally maintained in a remarkable steady state. However, in human patients with cyclic neutropenia and in a putative animal model--canine cyclic hematopoiesis--the formed elements oscillate with constant regularity. The clocklike precision of the cycles implies a strong regulatory control failure. Since an understanding of the pathogenesis of these events could enhance our perception of normal and abnormal regulatory mechanisms, we have undertaken briefly to review current concepts regarding the possible etiologies of cyclic hematopoiesis.

Agranulocytosis↗

Selenium-dependent and selenium-independent formate dehydrogenases of Methanococcus vannielii. Separation of the two forms and characterization of the purified selenium-independent form.

Anaerobic oxidation of formate by Methanococcus vannielii is catalyzed by two readily separable formate dehydrogenases. One of these is a 105,000-dalton protein that contains molybdenum, iron, and acid-labile sulfide, but not selenium. The other is a high molecular weight complex composed of selenoporotein and molybdo-iron sulfur protein subunits. Selenium occurs in this selenoenzyme in the chemical form of selenocysteine residues. M. vannielii cells from selenium-deficient media contain the 105,000-dalton formate dehydrogenase. Marked stimulation of growth by selenite supplementation is correlated with the simultaneous appearance in the cells of the high molecular weight selenoprotein . enzyme complex. The latter is the predominant form in cells from media additionally supplemented with tungstate. Under these conditions partial replacement of molybdenum with tungsten appears to occur. Both formate dehydrogenases are maximally active at pH 8.5 to 9.2 and at 60 degrees C and are extremely oxygen-sensitive. They utilize as electron acceptors 8-hydroxy-5-deazaflavin, FMN, FAD, and viologen and tetrazolium dyes.

Aldehyde Oxidoreductases↗

Cyclic neutropenia. A tale of two brothers and their family.

A family history encompassing four generations is presented. Definite cyclic neutropenia has been noted in two generations. In one member, the symptoms abated as she grew older. One 12-year-old member died of clostridial septicemia secondary to gangrene of the terminal ileum. At autopsy he was found to have amyloidosis. A trial of lithium carbonate therapy was carried out in a 7-year-old male but a positive hematologic response was not obtained.

Adolescent↗

Cyclic neutropenia. Review of clinical manifestations and management.

Human cyclic neutropenia probably represents a rare group of heterogeneous disorders. The disorder most frequently starts in infancy or childhood. During the neutropenic episodes, the most common symptoms are fever and oral ulceration. However, dental and skin manifestations are frequent and require special attention. While the disease is usually benign and the symptoms may ameliorate as the patient grows older, 15 deaths related to neutropenia have been recorded. While many modalities of treatment have been suggested, none have proved to be universally efficacious. Study of cyclic neutropenia may provide insight into the normal control of granulopoiesis and into the genesis of biological rhythms.

Adrenal Cortex Hormones↗

Experimental parvovirus infection in dogs.

Five eight week old dogs were inoculated orally and intranasally with cell culture origin canine parvovirus. Three dogs became depressed and anorectic and developed a mild (one dog) to severe diarrhea five days postinfection. The remaining dogs had subclinical infections but developed a lymphopenia followed by a transient lymphocytosis. The ill dogs developed mild (one dog) to severe neutropenia and a moderate lymphopenia. One died nine days postinfection. Recovery was associated with cessation of viral excretion and with lymphocytosis and antibody production. Two of three dogs challenged intragastrically developed mild clinical signs and a moderate panleukopenia four to eight days postinfection. The pathological changes of the experimental disease were very similar to that of spontaneous disease. Bone marrow changes included a severe granulocytic and mild erythroid depletion. The pathogenesis of canine parvovirus infection is discussed.

Administration, Intranasal↗

Reconstitution of a formate-NADP+ oxidoreductase from formate dehydrogenase and a 5-deazaflavin-linked NADP+ reductase isolated from Methanococcus vannielii.

The formate-dependent reduction of NADP+ by extracts of Methanococcus vannielii is catalyzed by a coupled system consisting of formate dehydrogenase, a 5-deazaflavin cofactor, and 5-deazaflavin-dependent NADP+ reductase. All three components were purified from crude extracts of M. vannielii. Recombination of these components reconstituted the formate-NADP+ oxidoreductase system. The formate dehydrogenase also can utilize FAD, FMN, and a number of artificial dyes as electron acceptors, but these do not replace the 5-deazaflavin cofactor in the coupled enzyme system. The reduced form of 5-deazaflavin binds readily to the NADP+ reductase apoprotein and is not dissociated by ammonium sulfate treatment at neutral pH under anaerobic conditions. This electron transfer cofactor from M. vannielii is identical in many of its properties to the 5-deazaflavin isolated from other methane-producing bacteria.

Aldehyde Oxidoreductases↗

Ultrastructural studies on the evolution of amyloidosis in the cyclic hematopoietic (CH) dog.

Electron microscopy studies were made on tissues of cyclic hematopoietic (CH) dogs of various ages presenting a high incidence of spontaneous amyloidosis. The distribution and morphologic characteristics of amyloidosis in this animal model closely correspond to the secondary and familial forms of the disease in humans. Plasma cells and, particularly, macrophages presented marked changes during the evolution of amyloid deposition. Residual bodies in the macrophages contained abundant cell debris, a result of both endocytic and autophagocytic activities. Intracellular amyloid fibrils were not observed by conventional electron microscopy. A few reticular cells contained intracytoplasmic fibrils which were morphologically different from amyloid. There was no correlation between the amount of intracellular fibrils and the size of the extracellular amyloid deposits. On the contrary, a temporal association between the magnitude of the amyloid deposits and cytoplasmic changes in the macrophages at sequential stages of the evolution of the disease was evident. It is suggested that the hematopoietic defect in the CH dog could play an important role in the production of amyloidosis, making this animal an excellent experimental model for studies of that disease.

Amyloidosis↗