Photoinduced Switch of a DNA/RNA Inactive Molecule into a Classical Intercalator

2005 ◽  
Vol 127 (4) ◽  
pp. 1074-1075 ◽  
Author(s):  
Kristina Starčević ◽  
Grace Karminski-Zamola ◽  
Ivo Piantanida ◽  
Mladen Žinić ◽  
Lidija Šuman ◽  
...  
Keyword(s):  
Inactive Molecule

scholarly journals Gigantomastia and Macroprolactinemia Responding to Cabergoline Treatment: A Case Report and Minireview of the Literature

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Fatma Dilek Dellal ◽  
Didem Ozdemir ◽  
Cevdet Aydin ◽  
Gulfem Kaya ◽  
Reyhan Ersoy ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Case Report ◽  
Medical Treatment ◽  
High Molecular Weight ◽  
Surgical Therapy ◽  
Surgical Approach ◽  
Breast Tissue ◽  
Surgical Intervention ◽  
Laboratory Examination ◽  
Inactive Molecule

Background. Macroprolactinemia is defined as predominance of high molecular weight prolactin forms in the circulation. Although macroprolactin is considered as a biologically inactive molecule, some authorities suggest treatment in symptomatic cases. Gigantomastia is defined as excess breast tissue and most cases in the literature were treated by surgical intervention.Case. A 44-year-old woman was admitted to our clinic with gigantomastia and galactorrhea. The patient had a demand for surgical therapy. In laboratory examination, she had hyperprolactinemia and macroprolactinemia. Pituitary imaging revealed 6 mm microadenoma in right side of the hypophysis. Since she was symptomatic, cabergolin treatment was started. Macroprolactin became negative, breast circumference decreased significantly, and galactorrhea resolved after treatment.Conclusion. Gigantomastia might be the presenting symptom in patients with macroprolactinemia. In these patients medical treatment with cabergoline may be used initially as an alternative to surgical approach.

Hereditary Angio-Oedema: Its Pathogenesis and Management

1980 ◽  
Vol 25 (3) ◽  
pp. 187-195 ◽  
Author(s):  
Z. Ballogh ◽  
K. Whaley
Keyword(s):  
Clinical Features ◽  
Therapeutic Approach ◽  
Inactive Molecule ◽  
Genetically Determined

Hereditary angio-oedema is a genetically-determined disease. Usually the disease is due to a deficiency of CĪ inhibitor or less commonly to the production of a functionally inactive molecule. The pathogenesis and clinical features of the disease are reviewed, and discussed in relation to the homeostatic role of CĪ inhibitor. Finally the therapeutic approach to the disease is described and the scientific bases for the newer therapeutic regimes discussed.

scholarly journals IL-12 p40 homodimer, the so-called biologically inactive molecule, induces nitric oxide synthase in microglia via IL-12Rβ1

Glia ◽  
2009 ◽  
Vol 57 (14) ◽  
pp. 1553-1565 ◽  
Author(s):  
Malabendu Jana ◽  
Subhajit Dasgupta ◽  
Utpal Pal ◽  
Kalipada Pahan
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inactive Molecule ◽  
Oxide Synthase

Accumulation of Pyruvate in Phenylhydrazine-Treated Avian Red Blood Cells

1957 ◽  
Vol 190 (3) ◽  
pp. 543-550 ◽  
Author(s):  
William F. Geber ◽  
H. H. Rostorfer
Keyword(s):  
Blood Cells ◽  
Ferric Iron ◽  
Anaerobic Conditions ◽  
Oxygen Capacity ◽  
Avian Erythrocytes ◽  
Avian Erythrocyte ◽  
Methemoglobin Formation ◽  
Inactive Molecule ◽  
Metabolic Reduction

Loss in oxygen capacity which occurs when avian erythrocytes are treated in vitro with phenylhydrazine is completely or partially restored (depending on the initial concentration of phenylhydrazine) on incubation of the cells for 1 hour in the presence of glucose or lactate under anaerobic conditions. Restoration in oxygen capacity is always accompanied by a proportional accumulation of pyruvate (the proportion differs for each substrate) which bears the same relationship to the gain in oxygen capacity as that found for the metabolic reduction of methemoglobin by the avian erythrocyte. However under aerobic conditions pyruvate continued to accumulate after all measurable oxygen capacity restoration (methemoglobin reduction) ceased. This is taken as evidence that in the presence of oxygen either methemoglobin formation continues in the treated cell, after all phenylhydrazine is destroyed or washed out, or that some other ferric iron compound is reduced which will not augment oxygen capacity. At the higher concentrations of phenylhydrazine used not all the oxygen capacity initially lost is restored on incubation even under anaerobic conditions. This inactive molecule is thought to be verdoglobin.

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