Uptake and accumulation in vitro of 3H-noradrenaline in adrenergic nerves of human atrium.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to C Sachs.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A technique for the in vitro culture of rheumatoid synovial tissue with (14)C-amino acids and isolation and quantitation of the newly synthesized immunoglobulins has been developed. This technique has been used to compare immunoglobulin synthesis of 12 rheumatoid synovia with that of synovia from nonarthritic patients and with that of normal human lymph nodes and spleen. In addition, the spleen of a patient with Felty's syndrome has also been examined. Immunoglobulin synthesis in rheumatoid synovia has been shown to be quantitatively and qualitatively similar to that of normal human spleen and lymph nodes although somewhat less active than the Felty's syndrome spleen examined. 79% of the immunoglobulin produced in rheumatoid synovia was of the IgG type, whereas IgM comprised 10% and IgA, 11% of the total. Less than 10% of the IgM synthesized was found to be rheumatoid factor. A fraction containing approximately 90% of its radioactivity in the form of IgG has been obtained for further studies.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effects of early surgical lesions of ascending noradrenaline (NA) axons and 6-hydroxydopamine (6-OHDA) induced NA denervation of the spinal cord on the postnatal development of central NA neurons of the rat have been studied using histo- and neurochemical techniques. The lesions were performed during the first week after birth and analyzed at the age of one or two weeks or in the adult stage. Complete unilateral hemisection at the mesencephalic level in the neonatal stage produced marked reductions of the 3H-NA uptake in vitro in the cerebral cortex with concomitant significant increases (+30-50%) of the uptake on the ipsilateral side of the pons-medulla when determined in adulthood. Partial unilateral hemisection, restricted to produce an axotomy of the dorsal NA bundle, led to almost complete NA depletions in the cerebral cortex, while significant NA elevations were found in the mesencephalon (+25-40%), pons-medulla (+15%) and cerebellum (+90%) on the ipsilateral side. In the latter region a significant NA increase (+50%) was also observed in the controlateral side. Regional analysis of the 3H-NA uptake after partial hemisection gave similar results. Intraspinal injection of 6-OHDA on the day of birth resulted consistently in marked NA depletions (-90% or more) in the spinal cord, while the effects on NA in the cerebral cortex varied, being either unaffected or markedly reduced. Animals with unaffected cerebral cortex disclosed a significant NA increase in the pons-medulla only, whereas animals with cortical NA denervation displayed significant increases in endogenous NA levels both in the pons-medulla and the cerebellum. The present results give further support for the "pruning effect" concept explaining the growth response that central NA neurons exhibit after neonatal 6-OHDA treatment systemically or when one axonal branch is damaged neonatally.
A series of cytotoxic oxygenated derivatives of oleic acid, 8-oxo-9, 9-oxo-10, 10-oxo-8-, and 11-oxo-9 trans octadecenoic acid, uniquely found at post-mortem in airway cells of cotton workers, were synthesized and shown to be cytotoxic, i.e., inhibitory of growth for several cell lines, including HL-60 and U-937 promyelocytes and Eagle's KB carcinoma cells. At microM concentrations, the 8- and 11- keto acids: are chemokinetic for human neutrophils; activate production of O2-. and H2O2; stimulate promyelocytes in culture to differentiate into neutrophils; and increase diglyceride metabolism in inflammatory cells. These results indicate that these four monooxygenated fatty acids, which are found in airways of cotton workers and initiate both inflammation and differentiation in vitro, may be etiologic in the abnormal differentiation and inflammation seen in small airways of cotton workers. This abnormal differentiation in bronchi may result from altered diglyceride metabolism with resultant activation of phosphoprotein kinase C initiated by the keto fatty acids.
Following injury or activation in some immune cell lines, elevation of intracellular Ca2+ concentration (Cai2+) is an early and major event that precedes cell death. Agents shown to elevate Cai2+ and to result subsequently in the death of some cells include human immunodeficiency virus (HIV) (in T4+ cells), 25-hydroxy cholesterol, tumor necrosis factor (TNF), cyclosporine, dexamethasone, alpha-interferon, and Ca2+ ionophores. The effects of these agents, both on Cai2+ and on cytotoxicity, are additive. This type of Ca2+-related cytotoxicity may be associated with either accelerated synthesis of triglycerides (TNF), accelerated synthesis of cholesterol ester (25-hydroxy cholesterol), or cholesterol (HIV) and terminally with declining synthesis of structural phospholipid. Agents that can lower Cai2+ (e.g., phorbol esters, diglycerides, lipoproteins [LDL], oleic acid, or serum) under appropriate conditions ameliorate the Ca2+-induced cytotoxicity. Metabolism of other divalent metals, i.e., Zn2+ and Cd2+, also become altered with cell injury, e.g., glucocorticoids elevate Cai2+, but block uptake of Zn2+. These observations support the idea that chronic elevation of Cai2+ by many chemically unrelated agents leads to cell death by creating imbalance both in cell biosynthetic mechanisms--especially in those controlling lipid metabolism--as well as creating imbalances in metabolism of other trace metals, especially Zn2+.
Explore the source record for details and available documents.