Hormone-Mediated Intercellular Calcium Signalling in an Insect Salivary Gland – Pathways and Mechanisms

2003 ◽  
pp. 119-130 ◽  
Author(s):  
Bernhard Zimmermann ◽  
Bernd Walz
Keyword(s):  
Salivary Gland ◽  
Calcium Signalling

scholarly journals Calcium signalling in salivary gland physiology and dysfunction

2015 ◽  
Vol 594 (11) ◽  
pp. 2813-2824 ◽  
Author(s):  
Indu S. Ambudkar
Keyword(s):  
Salivary Gland ◽  
Calcium Signalling

ATP-induced calcium signalling in acinar cells of the submandibular salivary gland

2005 ◽  
Vol 37 (5-6) ◽  
pp. 345-352
Author(s):  
N. V. Fedirko ◽  
O. V. Kopach ◽  
N. V. Voitenko ◽  
P. G. Kostyuk
Keyword(s):  
Salivary Gland ◽  
Calcium Signalling ◽  
Acinar Cells ◽  
Submandibular Salivary Gland

Endotoxin Alteration of the Mucopolysaccharide Blood Vessel Coating in Rats

1974 ◽  
Vol 32 ◽  
pp. 148-149
Author(s):  
D. E. Philpott ◽  
A. Takahashi
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Salivary Gland ◽  
Carotid Artery ◽  
Basement Membrane ◽  
Coronary Vessels ◽  
Ruthenium Red ◽  
E Coli ◽  
Old Rats ◽  
The Brain

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.

Electron Beam-Induced Mass Loss in Freeze-Dried Tissue and Protein Samples

1985 ◽  
Vol 43 ◽  
pp. 470-471
Author(s):  
M.E. Cantino ◽  
M.K. Goddard ◽  
L.E. Wilkinson ◽  
D.E. Johnson
Keyword(s):  
Electron Beam ◽  
Salivary Gland ◽  
Mass Loss ◽  
Counting Rate ◽  
Dose Dependence ◽  
X Ray ◽  
Large Samples ◽  
Freeze Dried ◽  
Muscle Homogenate ◽  
Large Muscle

Quantification in biological x-ray microanalysis depends on accurate evaluation of mass loss. Although several studies have addressed the problem of electron beam induced mass loss from organic samples (eg., 1,2). uncertainty persists as to the dose dependence, the extent of loss, the elemental constituents affected, and the variation in loss for different materials and tissues. in the work described here, we used x-ray counting rate changes to measure mass loss in albumin (used as a quantification standard), salivary gland, and muscle.In order to measure mass loss at low doses (10-4 coul/cm2 ) large samples were needed. While freeze-dried salivary gland sections of the required dimensions were available, muscle sections of this size were difficult to obtain. To simulate large muscle sections, frog or rat muscle homogenate was injected between formvar films which were then stretched over slot grids and freeze-dried. Albumin samples were prepared by a similar procedure. using a solution of bovine serum albumin in water. Samples were irradiated in the STEM mode of a JEOL 100C.

Inositol lipids and TRPC channel activation

2007 ◽  
Vol 74 ◽  
pp. 37-45 ◽  
Author(s):  
James W. Putney
Keyword(s):  
Plasma Membrane ◽  
Phospholipase C ◽  
Transient Receptor Potential ◽  
Calcium Signalling ◽  
Receptor Potential ◽  
Breakdown Product ◽  
Channel Activation ◽  
Inositol Lipids ◽  
Transient Receptor ◽  
Secondary Mechanism

The original hypothesis put forth by Bob Michell in his seminal 1975 review held that inositol lipid breakdown was involved in the activation of plasma membrane calcium channels or ‘gates’. Subsequently, it was demonstrated that while the interposition of inositol lipid breakdown upstream of calcium signalling was correct, it was predominantly the release of Ca2+ that was activated, through the formation of Ins(1,4,5)P3. Ca2+ entry across the plasma membrane involved a secondary mechanism signalled in an unknown manner by depletion of intracellular Ca2+ stores. In recent years, however, additional non-store-operated mechanisms for Ca2+ entry have emerged. In many instances, these pathways involve homologues of the Drosophila trp (transient receptor potential) gene. In mammalian systems there are seven members of the TRP superfamily, designated TRPC1–TRPC7, which appear to be reasonably close structural and functional homologues of Drosophila TRP. Although these channels can sometimes function as store-operated channels, in the majority of instances they function as channels more directly linked to phospholipase C activity. Three members of this family, TRPC3, 6 and 7, are activated by the phosphoinositide breakdown product, diacylglycerol. Two others, TRPC4 and 5, are also activated as a consequence of phospholipase C activity, although the precise substrate or product molecules involved are still unclear. Thus the TRPCs represent a family of ion channels that are directly activated by inositol lipid breakdown, confirming Bob Michell's original prediction 30 years ago.

Sialadenoma papilliferum of the bronchus: rare tracheobronchial tumor of salivary gland type

Pneumologie ◽  
2011 ◽  
Vol 65 (S 01) ◽  
Author(s):  
RF Falkenstern-Ge ◽  
G Ott ◽  
G Friedel ◽  
H Markmann ◽  
J Kalla ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Sialadenoma Papilliferum ◽  
Gland Type

Outcomes of Transoral Robotic Surgery for Parapharyngeal Space Salivary Gland Neoplasms

2015 ◽  
Vol 76 (S 01) ◽  
Author(s):  
Christopher Rassekh ◽  
Gregory Weinstein ◽  
Laurie Loevner ◽  
Ara Chalian ◽  
Bert O'Malley
Keyword(s):  
Salivary Gland ◽  
Robotic Surgery ◽  
Parapharyngeal Space ◽  
Transoral Robotic Surgery ◽  
Salivary Gland Neoplasms

Sonoelastographic modalities in the evaluation of salivary gland disease

2016 ◽  
Vol 37 (S 01) ◽  
Author(s):  
B Hofauer ◽  
N Mansour ◽  
M Bas ◽  
K Stock ◽  
A Knopf
Keyword(s):  
Salivary Gland ◽  
Salivary Gland Disease
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