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G S Cho

Publications and source records attributed to G S Cho.

5 recordsLinked to original sources
PubMed1998

Collection and transfusion of blood and blood components in the United States, 1994.

BACKGROUND: Collections and transfusions of blood in the United States in 1994 were measured and compared with those in 1992. STUDY DESIGN AND METHODS: Completed survey questionnaires were returned by all 147 regional blood centers, 1340 American Association of Blood Banks (AABB) member hospitals, and 523 non-AABB hospitals. Statistical tests verified the representativeness of the sample. RESULTS: The United States domestic blood supply in 1994 (13,340,000 units) was 3.3 percent less than in 1992. It included allogeneic blood (11,773,000 units), autologous blood (1,013,000 units), and directed donations (334,000 units). Of these, 432,000 units were rejected on testing, 11,107,000 units were transfused to 3,398,000 patients, and 1,801,000 units were discarded or unaccounted for. Platelet transfusions amounted to 7,866,000 units. Compared with the totals for 1992, transfusions of single-donor platelets (714,000 packs or 4,284,000 units) increased by 17.6 percent, while transfusions of platelet concentrates (3,582,000 units) fell by 23.6 percent. Fresh-frozen plasma transfusions (2,621,000 units) increased by 16.2 percent over the number for 1992. CONCLUSIONS: The US blood collection rate in 1994 was 74.6 units per 1000 population of donor age, the lowest recorded level since 1971. The US RBC transfusion rate in 1994 was 42.8 units per 1000 population, about the same as 1979. Transfusions of single-donor platelets, 16.5 units per 1000 population, exceeded transfusions of platelet concentrate (13.8/1000) for the first time. Plasma transfusions were 10.1 units per 1000 population. The US blood supply in 1994 was adequate to meet patient demands.

Blood Banks↗
PubMed1996

Influence of 17- alpha-estradiol on catecholamine secretion from the perfused rat adrenal gland.

OBJECTIVES: It has been known that adrenal corticosteroids influence the expression of adrenomedullary catecholamine-synthetizing enzymes and also suppress the emission of axonal-like processes in cultured chromaffin cells. In the present study, it was attempted to investigate the effect of 17-alpha-estradiol on catecholamine (CA) secretion evoked by acetylcholine (ACh). DMPP. McN-A-343, excess K+ and Bay-K-8644 from the isolated perfused rat adrenal gland. METHODS: Mature male Sprague-Dawley rats were anesthetized with ether. The adrenal gland was isolated by the method of WaKade. A cannula used for perfusion of the adrenal gland was inserted into the distal end of the renal vein. The adrenal gland, along with ligated blood vessels and the cannula, was carefully removed from the animal and placed on a platform of a leucite chamber. RESULTS: The perfusion of 17-alpha-estradiol (1-100 uM) into an adrenal vein for 20 min produced relatively dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM). DMPP (100 uM for 2 min). McN-A-343 (100 uM for 2 min) and Bay-K-8644 (10 uM for 4 min), while it did not affect the CA secretory effect of high K+ (56 mM). Also, in the presence of 17-beta-estradiol. CA secretion of ACh. DMPP and McN-A-343, without any effect on excess K(+)-evoked CA sectretion was depressed. However, in adrenal glands pre-loaded with 17-alpha-estradiol (10 uM) plus tamoxifen (2 uM), which is known to be a selective antagonist of estrogen receptors (for 20 min). CA secretory responses evoked by ACh. DMPP and McN-A-343 were condiderably recovered as compared to that of 17-alpha-estradiol only, but excess K(+)-induced CA secretion was not affected. However, pre-treatment with 17-alpha-estradiol in the presence of meclopramide (dopaminergic antagonist) did not affect the secretory effect of CA evoked by ACh. DMPP, McN-A-343 and high potassium. CONCLUSIONS: These results suggest that 17-alpha-estradiol causes the marked inhibition of CA secretion evoked by cholinergic receptor stimulation, but not that by excess K+, indicating strongly that this effect may be mediated by inhibiting the influx of extracellular calcium into the rat adrenomedullary chromaffin cells through the activation of inhibitory estrogen receptors, and it also plays a modulatory role in regulating CA secretion.

Adrenal Glands↗