EFFECT OF CAROTID SINUS STIMULATION ON THE ELECTROCARDIOGRAMS OF CLINICALLY NORMAL INDIVIDUALS

1957 ◽  
Vol 1 (3) ◽  
pp. 209-211
Author(s):  
G. H. HEIDORN ◽  
A. P. MCNAMARA
Blood ◽  
1983 ◽  
Vol 61 (3) ◽  
pp. 449-455 ◽  
Author(s):  
SJ Knox ◽  
BR Greenberg ◽  
RW Anderson ◽  
LS Rosenblatt

Abstract Tritiated thymidine incorporation in a whole blood lymphocyte stimulation test (LST) and lymphocyte colony formation (CFU-L) from whole blood were measured following in vitro x-irradiation. Lymphocytes from patients with myelodysplastic disorders, acute nonlymphocytic leukemia, and patients at increased risk for leukemia because of their primary disease and/or cytotoxic therapy were found to be significantly more sensitive to in vitro x-irradiation than lymphocytes from clinically normal individuals. Cloning efficiencies and mitogenic responsiveness of patient lymphocytes were significantly depressed as compared to normal values. Using monoclonal antibodies to specific surface markers, quantitative abnormalities in lymphocytic subpopulations from myelodysplastic patients also were observed. These findings are suggestive of a defect at the T-cell level that may directly or indirectly affect hematopoiesis.


1964 ◽  
Vol 207 (4) ◽  
pp. 777-781 ◽  
Author(s):  
J. E. Kendrick ◽  
Kenneth A. Turner

Reducing body temperature in dogs to 24 C caused a small reduction in the size of the carotid sinus depressor response. Along with this reduction the response also became more gradual at the lower body temperatures. Systematic studies demonstrated that the more gradual nature of the response appeared to result from changes in the vascular smooth muscle. Depression of the nervous elements of the baroreceptor reflex arc during hypothermia was not evident. The response to carotid sinus stimulation in the warm, perfused hindlimb was essentially unchanged by cooling the body to 24 C. Local cooling of the perfused hindleg did not reduce the size but did result in a more gradual response.


1998 ◽  
Vol 31 ◽  
pp. 37
Author(s):  
R. Krol ◽  
S. Saksena ◽  
A. Prakash ◽  
G. Krol ◽  
P. Default ◽  
...  

2003 ◽  
Vol 90 (3) ◽  
pp. 391-394 ◽  
Author(s):  
S.S. Choi ◽  
Y.-J. Lim ◽  
J.-H. Bahk ◽  
S.-H. Do ◽  
B.-M. Ham

2020 ◽  
Vol 52 (06) ◽  
pp. 421-426
Author(s):  
Celso E. Gomez-Sanchez ◽  
Elise P. Gomez-Sanchez ◽  
Koshiro Nishimoto

AbstractThe CYP11B2 enzyme is the terminal enzyme in the biosynthesis of aldosterone. Immunohistochemistry using antibodies against CYP11B2 defines cells of the adrenal ZG that synthesize aldosterone. CYP11B2 expression is normally stimulated by angiotensin II, but becomes autonomous in primary hyperaldosteronism, in most cases driven by recently discovered somatic mutations of ion channels or pumps. Cells expressing CYP11B2 in young normal humans form a continuous band beneath the adrenal capsule; in older individuals they form discrete clusters, aldosterone-producing cell clusters (APCC), surrounded by non-aldosterone producing cells in the outer layer of the adrenal gland. Aldosterone-producing adenomas may exhibit a uniform or heterogeneous expression of CYP11B2. APCC frequently persist in the adrenal with an aldosterone-producing adenoma suggesting autonomous CYP11B2 expression in these cells as well. This was confirmed by finding known mutations that drive aldosterone production in adenomas in the APCC of clinically normal people. Unilateral aldosteronism may also be due to multiple CYP11B2-expressing nodules of various sizes or a continuous band of hyperplastic ZG cells expressing CYP11B2. Use of CYP11B2 antibodies to identify areas for sequencing has greatly facilitated the detection of aldosterone-driving mutations.


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