scholarly journals Slc4a11 disruption causes duct cell loss and impairs NaCl reabsorption in female mouse submandibular glands

2019 ◽  
Vol 7 (23) ◽  
Author(s):  
Ning‐Yan Yang ◽  
Taro Mukaibo ◽  
Xin Gao ◽  
Ira Kurtz ◽  
James E. Melvin
Keyword(s):  
Female Mouse ◽  
Cell Loss ◽  
Duct Cell ◽  
Submandibular Glands

Proliferative and structural differences between male and female mouse submandibular glands

1993 ◽  
Vol 235 (2) ◽  
pp. 303-311 ◽  
Author(s):  
Yang Chai ◽  
Donna K. Klauser ◽  
Patricia A. Denny ◽  
Paul C. Denny
Keyword(s):  
Female Mouse ◽  
Male And Female ◽  
Submandibular Glands ◽  
Structural Differences

ANDROGENIC ACTION OF GLUCOCORTICOIDS ON THE GRANULAR DUCTS OF MOUSE SUBMANDIBULAR GLANDS

1981 ◽  
Vol 89 (2) ◽  
pp. 267-NP ◽  
Author(s):  
SEIICHI SATO ◽  
SHICHIRO MARUYAMA ◽  
TAKEO AZUMA
Keyword(s):  
Submandibular Gland ◽  
Cell Size ◽  
Androgen Receptors ◽  
Testosterone Propionate ◽  
Duct Cell ◽  
Testicular Feminization ◽  
Submandibular Glands ◽  
Gland Weight ◽  
Duct Cells ◽  
Granular Ducts

The administration of cortisol acetate and dexamethasone to castrated–adrenalectomized mice increased the submandibular gland weight, the granular duct cell size of the gland and the number of androgen-dependent granules detected with the staining for tryptophan in the duct cell. These changes were not as pronounced as when testosterone propionate was given. Similar effects on the duct cells and an increase in androgen-dependent esteroprotease activity of the submandibular glands were observed in castrated mice, but not in mice with testicular feminization which are genetically deficient in androgen receptors. These results suggest that glucocorticoids exert a certain degree of androgenic action on the granular duct cell through androgen receptors when androgens are absent or deficient.

Chemoradiation-Induced Cell Loss in Human Submandibular Glands

2005 ◽  
Vol 115 (6) ◽  
pp. 958-964 ◽  
Author(s):  
Christopher A. Sullivan ◽  
Robert I. Haddad ◽  
Roy B. Tishler ◽  
Anand Mahadevan ◽  
Jeffrey F. Krane
Keyword(s):  
Cell Loss ◽  
Submandibular Glands

Sonographic analysis of rat submandibular glands in experimentally-induced sialadenitis

1999 ◽  
Vol 29 (2) ◽  
pp. 90-96 ◽  
Author(s):  
M Shimizu ◽  
K Tokumori ◽  
M Saitoh ◽  
K Miwa ◽  
K Yoshiura ◽  
...  
Keyword(s):  
Submandibular Glands ◽  
Experimentally Induced

Strahlenwirkung am Normalgewebe

2010 ◽  
Vol 49 (S 01) ◽  
pp. S53-S58 ◽  
Author(s):  
W. Dörr
Keyword(s):  
Radiation Exposure ◽  
Normal Tissue ◽  
Radiation Effects ◽  
A Priori ◽  
Cell Loss ◽  
Turnover Time ◽  
Complete Healing ◽  
Internal Radiotherapy ◽  
Normal Tissues ◽  
Chronic Radiation

SummaryThe curative effectivity of external or internal radiotherapy necessitates exposure of normal tissues with significant radiation doses, and hence must be associated with an accepted rate of side effects. These complications can not a priori be considered as an indication of a too aggressive therapy. Based on the time of first diagnosis, early (acute) and late (chronic) radiation sequelae in normal tissues can be distinguished. Early reactions per definition occur within 90 days after onset of the radiation exposure. They are based on impairment of cell production in turnover tissues, which in face of ongoing cell loss results in hypoplasia and eventually a complete loss of functional cells. The latent time is largely independent of dose and is defined by tissue biology (turnover time). Usually, complete healing of early reactions is observed. Late radiation effects can occur after symptom-free latent times of months to many years, with an inverse dependence of latency on dose. Late normal tissue changes are progressive and usually irreversible. They are based on a complex interaction of damage to various cell populations (organ parenchyma, connective tissue, capillaries), with a contribution from macrophages. Late effects are sensitive for a reduction in dose rate (recovery effects).A number of biologically based strategies for protection of normal tissues or for amelioration of radiation effects was and still is tested in experimental systems, yet, only a small fraction of these approaches has so far been introduced into clinical studies. One advantage of most of the methods is that they may be effective even if the treatment starts way after the end of radiation exposure. For a clinical exploitation, hence, the availability of early indicators for the progression of subclinical damage in the individual patient would be desirable. Moreover, there is need to further investigate the molecular pathogenesis of normal tissue effects in more detail, in order to optimise biology based preventive strategies, as well as to identify the precise mechanisms of already tested approaches (e. g. stem cells).

The identification of diabetes genes mediating β-cell loss and hyperglycemia using positional cloning

2018 ◽  
Author(s):  
TT Cui ◽  
N Hallahan ◽  
W Jonas ◽  
P Gottmann ◽  
M Jähnert ◽  
...  
Keyword(s):  
Positional Cloning ◽  
Cell Loss ◽  
Β Cell

Leucocytes and Thrombosis

1973 ◽  
Vol 30 (01) ◽  
pp. 036-046 ◽  
Author(s):  
D.C Banks ◽  
J.R.A Mitchell
Keyword(s):  
Cell Count ◽  
White Cell Count ◽  
Cell Loss ◽  
White Cell ◽  
Structural Resemblance ◽  
The Masses

SummaryWhen heparinised blood is rotated in a glass flask at 37°C. the white cell count falls and it has been shown that this is due to the adherence and aggregation of polymorphonuclear white cells on the wall of the flask. The masses formed bear a close structural resemblance to thrombi and the mechanisms involved in white cell loss during rotation may therefore increase our knowledge of the thrombotic process.

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