Novel targets for the treatment of ACTH-secreting tumors

2006 ◽  
Vol 114 (08) ◽  
Author(s):  
M Labeur ◽  
M Paez-Pereda ◽  
M Theodoropoulou ◽  
J Stalla ◽  
B Woelfel ◽  
...  
Keyword(s):  
2014 ◽  
Vol 122 (03) ◽  
Author(s):  
UJ Knappe ◽  
C Jaspers ◽  
D Buschsieweke ◽  
R Salbeck ◽  
W Saeger ◽  
...  

1965 ◽  
Vol 48 (4) ◽  
pp. 565-568 ◽  
Author(s):  
W. A. Sullivan ◽  
Jerrold D. Hydovitz ◽  
H. Rosomoff ◽  
T. S. Danowski

ABSTRACT A third episode of Cushing's syndrome developed in an adult male who had undergone subtotal adrenalectomy and then complete hypophysectomy in temporarily successful treatment of two earlier episodes. Judging from necropsy findings, this final recurrence was not the result of incomplete pituitary ablation or regeneration of pituitary remnants. Extrasellar pituitary or other ACTH secreting tissue could not be identified, but the patient's marked melanosis suggested its presence with consequent excesses of ACTH or MSH. However, irrespective of whether such excesses did or did not exist, it is clear that the third episode of Cushing's syndrome resulted from hyperfunction of the small adrenal remnant.


2019 ◽  
Author(s):  
Meenakshi Parsad ◽  
Emily Phisaklea ◽  
Victoria Reay ◽  
Livoon Chong

2007 ◽  
Vol 148 (15) ◽  
pp. 697-702 ◽  
Author(s):  
Marianna Murányi ◽  
Zsombor Lacza

It is now known that astrocytes are not merely supporting cells but they also play an important role in neuronal funcions. Astrocytes tightly ensheat neuronal synapses and regulate the excitation of neurons by uptaking neurotransmitters; reglulate the cerebral blood flow, cerebral fluid volume and extracellular concentrations of ions. They also supply fuel in the form of lactate and provide free radical scavangers such as glutathione for active neurons. These facts indicate that impaired function of astrocytes may lead to neuronal dysfunction. After brain injury (stroke, trauma or tumors) astrocytes are swollen and release active molecules such as glutamate or free radicals resulting in neuronal dysfunction. Thus, investigation of the molecular mechanisms of astrocyte function may reveal novel targets for the development of therapeutic tools in neuronal diseases.


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