Morphometric and Morphological Study of Human Placenta in Hypertensive Females of West U. P. India

Author(s):  
Chetna Thakur ◽  
Tejendra Singh ◽  
Bhawani Shankar ◽  
Shikha Sharma ◽  
G. S. Bindra
2019 ◽  
Vol 5 (2) ◽  
pp. 1-4
Author(s):  
K.M. Parmar ◽  
◽  
Hetal Vaishnani ◽  
G.V. Shah ◽  
◽  
...  

Author(s):  
Susan B.G. Debaene ◽  
John S. Gardner ◽  
Phil S. Allen

The coleorhiza is a nonvascular sheath that encloses the embryonic radicle in Poaceae, and is generally the first tissue to emerge during germination. Delicate hairlike extensions develop from some coleorhiza cells prior to radicle emergence. Similar to root hairs, coleorhiza hairs are extremely sensitive to desiccation and are damaged by exposure to negative water potentials. The coleorhiza of Lolium perenne is somewhat spherical when first visible, after which a knob forms at a right angle to the caryopsis due to inner pressure from the elongating radicle. This knob increases in length until the radicle finally punctures the coleorhiza. Standard fixation procedures cause severe desiccation of coleorhiza cells and hairs, making morphological study of the coleorhiza difficult. This study was conducted to determine a more successful process for coleorhiza preservation.


2017 ◽  
Vol 77 (04) ◽  
pp. 379-395
Author(s):  
K Mayer-Pickel ◽  
M Gruber ◽  
B Hirschmugl ◽  
U Lang ◽  
M Cervar-Zivkovic ◽  
...  

1985 ◽  
Vol 54 (02) ◽  
pp. 431-437 ◽  
Author(s):  
M J Dembélé-Duchesne ◽  
A Laghchim Lahlou ◽  
H Thaler-Dao ◽  
A Crastes de Paulet

SummaryHuman placental cytosol inhibits platelet aggregation induced by high doses of collagen. The aim of this study was to investigate whether this anti-aggregating activity was caused only by the presence of various activities already described in the placenta (an ADP-consuming enzyme, a fatty acid cyclooxygenase inhibitor, and a thromboxane synthetase inhibitor) or whether another factor was present.Heating the cytosol at 50° C for 6 min destroyed the inhibitor of collagen-induced aggregation. ADPase and the AA pathway inhibitors were not modified by this treatment. We therefore show the presence of an additional anti-aggregating factor: it is destroyed by heating at 50° C.We also tested for the presence of an inhibitor of AA release in the placental cytosol using three different methods (rabbit platelets in PRP, washed rabbit platelets, and NRK fibroblasts) but no inhibition could be evidenced.We conclude that this new anti-aggregating factor, which is probably a protein, acts neither through AA release inhibition nor AA cascade inhibition.


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