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Mechanisms for platelet hyperactivit...

The University of Manitoba (Canada).

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Mechanisms for platelet hyperactivity and abnormal calcium homeostasis in diabetes mellitus.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Mechanisms for platelet hyperactivity and abnormal calcium homeostasis in diabetes mellitus./
Author:	Li, Yun.
Description:	210 p.
Notes:	Adviser: Ratna Bose.
Contained By:	Dissertation Abstracts International58-11B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NQ23626
ISBN:	0612236269

Mechanisms for platelet hyperactivity and abnormal calcium homeostasis in diabetes mellitus.
Li, Yun.

Mechanisms for platelet hyperactivity and abnormal calcium homeostasis in diabetes mellitus. - 210 p.

Adviser: Ratna Bose.

Thesis (Ph.D.)--The University of Manitoba (Canada), 1997.

The overall objective of this thesis is to determine the mechanisms responsible for platelet hyperactivity in diabetes mellitus.

ISBN: 0612236269Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Mechanisms for platelet hyperactivity and abnormal calcium homeostasis in diabetes mellitus.
LDR:04715nam 2200337 a 45 001 938680
005 20110512
008 110512s1997 eng d
020 $a 0612236269
035 $a (UnM)AAINQ23626
035 $a AAINQ23626
040 $a UnM $c UnM
100 1 $a Li, Yun. $3 1262653
245 1 0 $a Mechanisms for platelet hyperactivity and abnormal calcium homeostasis in diabetes mellitus.
300 $a 210 p.
500 $a Adviser: Ratna Bose.
500 $a Source: Dissertation Abstracts International, Volume: 58-11, Section: B, page: 5904.
502 $a Thesis (Ph.D.)--The University of Manitoba (Canada), 1997.
520 $a The overall objective of this thesis is to determine the mechanisms responsible for platelet hyperactivity in diabetes mellitus.
520 $a The first part of the study was designed to investigate whether platelet Ca$\sp{2+}$ homeostasis is deranged in diabetes and thus may be responsible for platelet hyperactivity. Platelets were obtained from a group of metabolically uncontrolled diabetic patients and from a group of normal healthy subjects. HbA$\rm\sb{1c}$ level was used as an index of chronic glycemic control. Both the basal cytosolic Ca$\sp{2+}$ concentration and agonist (thrombin and collagen)-stimulated $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}$ responses were enhanced in platelets from diabetic patients. The contents of Ca$\sp{2+}$ in the platelet intracellular store (DTS) and the ability to release Ca$\sp{2+}$ from DTS after thrombin stimulation did not differ in these 2 groups of subjects. The sequestration or extrusion processes of cytosolic Ca$\sp{2+}$ were impaired in platelets from diabetics.
520 $a The purpose of the second part of the study was to determine the possible mechanisms for abnormal platelet calcium homeostasis in diabetes, mainly focusing on the plasma membrane Na$\sp+$-Ca$\sp{2+}$ exchanger. The existence and physiological role of the Na$\sp+$-Ca$\sp{2+}$ exchanger in platelets from normal subjects was investigated. The specificity of the Na$\sp+$-Ca$\sp{2+}$ exchange blocker CBDMB (an amiloride analogue) in intact platelets was found to inhibit the Na$\sp+$-Ca$\sp{2+}$ exchanger, and have no effect on the Na$\sp+$-H$\sp+$ exchanger at $\mu $m concentrations. In platelets from normal subjects, the Na$\sp+$-Ca$\sp{2+}$ exchanger works in the forward mode in the resting state and after thrombin stimulation, however following collagen stimulation the Na$\sp+$-Ca$\sp{2+}$ exchanger works in the reverse mode.
520 $a In the second series of experiments, sensitivity to CBDMB was utilized to study the direction and activity of the Na$\sp+$-Ca$\sp{2+}$ exchanger in intact platelets. In normal subjects, CBDMB increased resting $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}$ whereas in diabetes, CBDMB had no effect on resting $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}.$ After thrombin activation, CBDMB increased the second phase of the thrombin-induced $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}$ response in normals. In platelets from diabetics, CBDMB decreased the thrombin-induced $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}$ response. In platelets from normal subjects, CBDMB decreased the collagen-stimulated $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}$ response. In diabetics the decrease in $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}$ following CBDMB in collagen-activated platelets was enhanced. In diabetes the direction and activity of the Na$\sp+$-Ca$\sp{2+}$ exchanger are altered.
520 $a The third part of the study evaluated the direct effect of hyperglycemia on platelets in vitro. High glucose (43 mM) had no acute effect on thrombin and collagen-induced increases in $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}$ or on aggregation. When the PRP (platelet rich plasma) was incubated in high glucose at 37$\sp\circ $c for 24 hrs, several differences were observed when compared to platelets incubated in 5 mM Glucose. PRP with EDTA as the anticoagulant, was divided into 3 groups: control (5 mM D-glucose medium); high mannitol (5mM D-Glucose + 40 mM Mannitol, as an osmotic control) and high glucose (45mM D-Glucose). In the high glucose group the first peak and second phase of thrombin-induced $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}$ were increased. The enhanced second phase was inhibited by CBDMB. In addition, the collagen-stimulated $\rm\lbrack Ca\sp{2+}\rbrack\sb{i}$ response and aggregation were increased in the high glucose group. (Abstract shortened by UMI.)
590 $a School code: 0303.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Health Sciences, Pathology. $3 1017854
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0419
690 $a 0433
690 $a 0571
710 2 0 $a The University of Manitoba (Canada). $3 1249364
773 0 $t Dissertation Abstracts International $g 58-11B.
790 $a 0303
790 1 0 $a Bose, Ratna, $e advisor
791 $a Ph.D.
792 $a 1997
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NQ23626