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.

難經上有所謂的 1 脈 10 變,
干支應該是百變以上.

舉例來說:

1.
甲戌, 甲是大樹, 戌是土,
所以單單甲戌就會有痣或胎記.
配合年月日時, 就可以知道長在那裡.

2.
再例, 甲戌日柱, 年上官星,
大概就是家裡的長子或長女.

3.
而甲到了戌月或戌時,
都是向下收斂結果入冬前的準備,
秋木不是結果就是高木,
這可以先看身材與風格.

4.
戌字本身有藏干 3 波段, 丁戊辛,
早上人家問工作感情的事,
如果甲戌帶入 3 波段,
男生先有激情(丁), 再來穩定感情(戊),
最後辛字壓力/小孩進來打第 2 根樁.

.

之前甲戌寫了 4 個變化, 再繼續變下去了

5.
比如說夏天的甲木就需要水,
冬天的甲木就需要火.

所以甲木在天干遇到丙就是開花,
在地支戌土遇到午反而要很小心.

因為有可能夏天寅字 1 出現,
整個地支寅午戌 1 片火海,
地支動, 天干透, 事件就會表象化,
整片森林甲木就因此而燒了起來.

這個會瞬間發生很嚴重的意外,
或生病腎水瞬間熬乾就掛了.

6.
甲木與己土, 己甲己,
甲木左擁右抱, 用情不專.

這個某個程度也是很危險,
因為地支辰戌沖 1 下, 事情爆開,
甲己合土, 甲木變成戊土, 與己土還原成朋友,
戊己異性形成陌路.

7.
見不見之形, 抽不抽之絮.

遇甲等於己, 遇戌等於辰.
寅戌拱午, 午戌推寅.

戌字遇申, 暗拱酉字,
酉字為酒, 為醫, 為骨,
為內心深處不為人知的想法.

8.
甲膽之氣為震木,
所以荷葉, 蒼朮, 升麻, 為清震湯.

甲木受傷, 很容易是頭,
是手指, 是末梢最突出的部分.

.

鐵板數把甲設為 1, 戌集則為 11.

前面玩的方式都是設好 1 個 model 欲求前知:

　不管 8 字抓的演化週期生成次序,
　或斗數抓的斗杓, astrology 抓的太陽系,
　or 卦抓 invariant, 睡覺抓的作夢 ......

都是這類 model, 準與不準, 1 翻 2 瞪眼.

.

鐵板數逆推玩法就像用網子去撈魚,
看設的網子大小與撈法.

比如說同樣甲戌, 逆向出條文,
用歷代名家詩詞替換, 就可以得到底下可能情況:

9.
韓愈: " 洞庭連天 9 疑高, 蛟龍出沒猩鼯號. "

李白: " 為我 1 揮手, 如聽萬壑松. "

王維: " 寒山轉蒼翠, 秋水日潺湲. "

錢起: " 竹憐新雨後, 山愛夕陽時. "

許渾: " 高樹曉還密, 遠山晴更多. "


10.
加上亥字就變成柳宗元的句子,

　" 嶺樹重遮千里目, 江流曲似九迴腸. "

或者大家都很熟悉的,

　" 千山鳥飛絕, 萬徑人蹤滅. "

對應韋應物,

　" 空山松子落, 幽人應未眠. "

-----

木火土太過旺燥, 得拼命找水來調和,
就會出現底下情況:

張旭, " 桃花盡日逐流水, 洞在清谿何處邊. "

.

舉個例子,
直接用李白寫的詩當條文,
來算李白流年:

. 724, 開元 12 年秋天, 24 歲:

　" 峨眉山月半輪秋, 影入平羌江水流,
　　夜發清溪向三峽, 思君不見下渝州. "

. 725, 開元 13 年夏秋之交, 李白 25 歲:

　" 天門中斷楚江開, 碧水東流至此迴,
　　兩岸青山相對出, 孤帆一片日邊來. "

. 725,726, 開元 13,14 年初游金陵, 長干行片段:

　" 郎騎竹馬來, 繞牀弄青梅, 同居長干里, 兩小無嫌猜. "
　" 15 始展眉, 願同塵與灰, 長存抱柱信, 啟上望夫臺. "

. 728, 開元 16 年暮春, 李白 28 歲, 孟浩然 40 歲:

　" 故人西辭黃鶴樓, 煙花 3 月下揚州,
　　孤帆遠影碧山盡, 唯見長江天際流. "

. 開元 22 年, 春遊洛陽:

　" 誰家玉笛暗飛聲, 散入春風滿洛城.
　　此夜曲中聞折柳, 何人不起故園情. "

. 736, 開元 24 年, 36 歲,

　" 君不見黃河之水天上來, 奔流到海不復回,
　　君不見高堂明鏡悲白髮, 朝如青絲暮成雪,
　　
　　人生得意需盡歡, 莫使金樽空對月.
　　天生我材必有用, 千金散盡還復來. "

. 743, 天寶 2 年, 43 歲,

　" 雲想衣裳花想容, 春風拂檻露華濃,
　　若非群玉山頭見, 會向瑤台月下逢. "

. 744, 天寶 3 年正月,

　" 鏡湖流水漾清波, 狂客歸舟逸興多,
　　山陰道士如相見, 應寫黃庭換白鵝. "

. 746, 天寶 5 年, 秋杜甫告別李白,

　" 城邊有古樹, 日夕連秋聲.
　　魯酒不可醉, 齊歌空復情. "

. 747, 天寶 6 年遊金陵,

　" 總為浮雲能蔽日, 長安不見使人愁. "

. 749, 天寶 8 年,

　" 我寄愁心與明月, 隨風直到夜郎西. "

. 753, 754, 天寶 12, 13 年, 53, 54 歲,

　" 眾鳥高飛盡, 孤雲獨去閑,
　　相看 2 不厭, 只有敬亭山. "

. 759, 乾元 2 年 2 月, 59 歲,

　" 朝辭白帝彩雲間, 千里江陵 1 日還,
　　2 岸猿聲啼不盡, 輕舟已過萬重山. "

. 760, 上元元年,

　" 我本楚狂人, 狂歌笑孔丘. "

. 762, 寶應元年, 李白臨終時所作, 62 歲,

　" 大鵬飛兮振 8 裔, 中天催兮力不濟.
　　餘風激兮萬世, 遊扶桑兮挂石袂.
　　後人得之傳此, 仲尼亡兮誰為出涕. "

----

" 棄我去者, 昨日之日不可留.
　亂我心者, 今日之日多煩憂.

　俱懷逸興壯思飛, 欲上青天覽明月.
　抽刀斷水水更流, 舉杯消愁愁更愁. "

這就是以李白詩為條文的鐵板術了