捷安特故事 躍上國際舞台！
更新日期:2007/09/27 19:30 記者:記者邱瓊平/台北報導
台灣本土企業的故事將躍上國際舞台！政大商學院今天和加拿大西安大略大學商學院(IVEY)簽約，雙方將合作撰寫台灣的本土個案，並以中、英文等版本推廣至世界各地，預計三年內將完成25份個案，並公開發行，提供學術界和實務界使用，提升台灣本土企業的國際能見度。

政大商學院院長周行一說，不少台灣本土企業在大中華地區經營相當成功，但並沒有廣為人知。他有感而發地指出，在國外的機場常可以看見LG的液晶電視，「台灣也有很好的製造，應該要讓更多人知道。」

周行一提到，加拿大西安大略大學是一所歷史悠久且享譽國際的學府，所屬商學院更被譽為「加拿大的哈佛商學院」，其個案發行量位居世界第二，普及率達到25%，「政大商學院與加拿大IVEY合作是政大歷史性的一刻。」

他進一步表示，政大商學院將與加拿大IVEY共同開發與撰寫中文版與英文版的本土企業個案，讓國外的學者、學生和企業能夠了解台灣本土企業的營運和發展策略，並進行深入研究與提出建議，對台灣本土企業的發展有正面助益。

此外，台灣本土企業個案版權由政大商學院與加拿大IVEY共有，並由雙方教師聯名發表。第一年的五份個案撰寫已針對不同領域與產業進行，其中在企業國際化以「捷安特」為對象；在企業系統資訊化方面則以「寶來集團」為例。

加拿大IVEY教授Paul W.Beamish則說，他七年前的生日收到一台捷安特腳踏車，卻不知道是台灣製造的，相當可惜。這次的台灣行將會搭高鐵前往捷安特工廠參觀。他強調，三年的計畫結束後仍會繼續與政大商學院合作，且透過本土個案撰寫，勢必能提高台灣本土企業的國際曝光度。

引發對舊物新論的感慨 轉貼如下 大都是中藥或是常用的食品


NATURAL COMPOUNDS THAT BENEFICIALLY AFFECT PROSTANOID AND
LEUKOTRIENE SYNTHESIS

Boswellic acid ‧ Boswellic acid inhibited the lipoxygenase pathway, specifically 5-lipoxygenase activity and 5-
HETE production. It also produced anti-inflammatory effects in animals. The IC50 for 5-
lipoxygenase was 1.5 to 33 μM. The effects of boswellic acid on lipoxygenase appeared to be
independent of any antioxidant activity.

CAPE and bee propolis ‧ Propolis has a history of use as an anti-inflammatory agent. Oral administration of propolis
extract (at 240 mg/kg) significantly suppressed prostaglandin and leukotriene generation by
mouse macrophages in vivo and suppressed the lipoxygenase pathway during inflammation.
The equivalent human dose is about 2.3 grams per day. Of its constituents, caffeic acid
phenethyl ester (CAPE) was the most potent inhibitor.
‧ CAPE inhibited 5-lipoxygenase at an IC of about 8 μM.
‧ Oral administration (about 45 mg/kg) of CAPE inhibited leukotriene synthesis in the colon and
liver of rats treated with a tumor-promoting agent.
‧ At 9 μM, CAPE suppressed production of PGE in stimulated human skin cells, and at
concentrations above 35 μM it inhibited COX-2 activity. An intraperitoneal dose of 30 mg/kg
inhibited PGE production in rats, and an intraperitoneal dose of 100 mg/kg reduced COX-2
expression. The equivalent human oral doses are about 1.1 and 3.6 grams, respectively.

Curcumin ‧ Curcumin inhibited 5-lipoxygenase, 12-lipoxygenase, and cyclooxygenase in vitro. Its effect on
lipoxygenases may be due in part to its antioxidant activity.
‧ Oral administration of approximately 170 mg/kg of curcumin inhibited synthesis of various
leukotrienes in rat liver and colon cells. In vitro, it inhibited leukotriene production in these
cells by an average of 28% at 10 μM and 64% at 50 μM.
‧ In stimulated mouse skin cells, curcumin (at 3 μM) decreased the production of 5-HETE and 8-
HETE by 40% and PGE production by 42%.
‧ Curcumin inhibited 5-HETE production at an IC50 between 3 and 10 μM.
‧ Curcumin inhibited COX-2 expression in epithelial cells at 10 to 20 μM.

EPA and DHA ‧ EPA inhibited leukotriene B synthesis in rat lung macrophages at an IC50 of about 2 μM. Low
concentrations of EPA may compete with arachidonic acid as a phospholipase A2 (PLA 2 )
substrate. PLA 2 is the enzyme that releases fatty acids for the synthesis of eicosanoids.
‧ EPA reduced the ability of rat macrophages to produce 5-HETE in vitro.
‧ EPA (at 1 μM) inhibited COX-2 activity in human mast cells in vitro.
‧ DHA (at 4% in diet) partially suppressed the growth of human breast cancer cells in mice and
reduced angiogenesis. Inhibition of angiogenesis appeared due to reduced PGE 2 and 12- and 15-
HETE synthesis. The equivalent human dose is about 46 grams per day.
‧ Oral administration of fish oil (at 18% of diet) inhibited COX-1 and COX-2 synthesis in
chemically induced breast cancers in rats by 28% and 36%, respectively.
‧ Fish oil administration (at 20% of diet) reduced COX-2 expression in chemically induced colon
tumors and in colon tissue in rats. COX-1 expression was not affected.

Flavonoids ‧ As a group, flavonoids inhibit the cyclooxygenase and lipoxygenase pathways and also the
activity of other enzymes involved with arachidonic acid metabolism, such as phospholipase A2 .
Enzyme inhibition has been reported for quercetin, luteolin, and apigenin. Although the potency
varies for different enzymes under different conditions, inhibition is generally in the low
micromolar range. Through inhibition of these and other enzymes, topical and intraperitoneal
administration of flavonoids decreased the inflammatory response in rodents. In in-vitro studies,
genistein, apigenin, and quercetin all inhibited COX-2 activity at concentrations below 40 μM
(often below 15 μM).
‧ EGCG inhibited leukotriene LTB 4 release from stimulated rat peritoneal cells at concentrations
above 10 μM. EGCG was the most potent of the green tea catechins.

Garlic ‧ Inhibited the cyclooxygenase and lipoxygenase pathways of eicosanoid production.

Glutathione-enhancing agents ‧ Cellular redox may modulate arachidonic acid metabolism, and in some studies prostaglandin
synthesis was inhibited by normal concentrations of intracellular glutathione.
A number of antioxidants, including vitamin C, are able to increase intracellular glutathione levels.

Melatonin ‧ Melatonin (at 100 nM) markedly downregulated the expression of the 5-lipoxygenase gene in
human B lymphocyte; it appears to affect the gene via its ability to bind to retinoid nuclear
receptors.
‧ Melatonin inhibited linoleic acid (omega-6 fatty acid) uptake and eicosanoid metabolism by liver
cancer cells at physiologic concentrations (1 nM) in vivo. Tumor growth was also inhibited.

NF-κB Inhibitors ‧ NF-κB activity can affect the expression of cyclooxygenase genes. In many cases, PGE 2
production by macrophages may be dependent on NF-κB activation. Thus, NF-κB inhibitors
may reduce eicosanoid production. For example, melatonin inhibited 5-lipoxygenase production
in vitro.

Parthenolide ‧ Inhibited 5-lipoxygenase activity at an IC50 of 20 to 200 μM in rat and human leukocytes.
‧ Inhibited 5-lipoxygenase activity at an IC50 of 33 μM in human platelets.
‧ Inhibited COX-2 activity at an IC50 of 0.8 μM.

PTK inhibitors ‧ PTK activity may mediate the activation of phospholipase A2 , which releases arachidonic acid
from the plasma membrane for use in the production of prostanoids and leukotrienes. This has
been demonstrated for genistein, which inhibited PGE2 production (IC50 = 20 μM) and
leukotriene LTC4 production.
‧ Genistein inhibited leukotriene LTB4 production by stimulated leukocytes.
‧ Genistein (at 37 μM) completely inhibited leukotriene production in leukemia cells.
‧ Genistein inhibited the activities of LTB4 once it was produced. This leukotriene appears to
require PTK activity to exert its effect.

Resveratrol ‧ Inhibited 5-HETE production in human and rat leukocytes at an IC50 of 3 to 9 μM.
‧ Inhibited 5-lipoxygenase activity in human leukocytes at an IC50 of 48 μM.
‧ Inhibited COX-2 activity in human breast cells at concentrations above 2.5 μM.
‧ Inhibited COX-1 activity at an IC50 of 15 μM but did not affect COX-2 activity.

Vitamin E ‧ Oral administration of vitamin E decreased production of 5-HETE by rat leukocytes.
‧ In vitamin E deficient rats, increased macrophage 5-HETE production was observed.
‧ Vitamin E inhibited phospholipase A2 activity both in vitro and in vivo.





NATURAL COMPOUNDS THAT INHIBIT MAST CELL GRANULATION IN VITRO
Eleutherococcus senticosus ‧ Fractions of this herb strongly inhibited histamine release from rat mast cells in a concentration-dependent manner. The most active fraction was 6,800 times stronger than disodium cromoglycate, a successful flavonoid-like antiallergy drug.

Flavonoids ‧ Genistein inhibited histamine release from mast cells at concentrations of 10 to 100 μM.
‧ Luteolin inhibited histamine release in human basophils exposed to tumor-promoting agents. The IC50
was about 15 μM.
‧ Apigenin inhibited histamine release in human basophils and rat mast cells exposed to tumor-promoting
agents. The IC50 was about 35 μM.
‧ Quercetin, luteolin, and apigenin inhibited mast cell degranulation at IC50 s of less than 10 μM. Some
in-vitro studies suggested that quercetin was the most effective of these flavonoids.
‧ Proanthocyanidins reduced histamine levels in blood vessel tissue in vitro.
‧ EGCG inhibited histamine release from stimulated rat peritoneal cells in vitro at concentrations above 10
μM.
‧ EGCG inhibited histamine release from rat basophilic leukemia cells at 100 μM.

Vitamin C ‧ Oral administration of vitamin C (at 2 grams per day) reduced blood histamine levels by 38% in healthy humans. A similar effect was seen in guinea pigs.