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            ΪʲôҪϽ조༭Ӥ

                        ӡ

ϷƼѧںؽ쵼Ŷû༭
Ͷ԰̲Ӥ𾪡кܶ˻ɣǲڴţ
ϾйԱڻ༭ġڿ˺ؽѧ
ϳʾ֮û٣ȷ༭Ӥˡ
ȻʵȫʧܵģҲǲ˵ġ

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ֵλTϸȶϸıϣӵ塣νӣ
һܹϸȥĵʣ磬вԭˣ
ӾͺTϸϵCCR5ϣTϸԭֵĵطȥԭ塣
CCR5߷ӦҪáCCR5ԼҲĳЩԭֵλ㣬
簬̲

̲һһ֡桱ԼûֳģҪ
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ˣȻͷųİֱ̲Tϸ¸Tϸ
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һֽCD4壬̲ܹʶôʶأǰ
һġСӡЩСӡʵһֵʣаĤ
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ʱ̲ҲûϣֲTϸˡ˵Ļǳ˫ɶԵģһ
Ըףһĸףһ˵CCR5CCR5-32
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Լ10%ȺҲCCR5-32򣬲Ƚ١

㽭ѧһڣһܻ༭Ŀ飬泩˵
û༭̥CCR5޸ĳCCR5-32µӤ
԰̲𣿲Ҳð̲ѧĺؽ
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ȵCCR5򶼱༭ɹˣӣͶ԰̲

ϸؽĻУʵûб༭ɹҪģ
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ɼؽʵȫʧܵģŴѧʧܵʵ
鵱˳ɹʵ鱨ˣȷʵ飬Ҳʵˡ
Ҫ٣ȫԸCCR5-32һģһĻС

ĿǰĻ༭ûô׼ЧȻڶ
׼İе˱༭Ǳ༭Ƿǳģڻ༭֮
Ҫʵɸѡ༭ɹġȻǿԶϸʵ
ֲѡԶ˽ѡ𣿲ܡȻ¶¶ʧܵʵ
ҲԴʧܵʵ鶯𣬶ǲ֪Я
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˵ġ

ң༭˶԰еı༭֮⣬пڱĵط
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ġ

ڶ̥л༭ʱܳе̥ϸĻ
༭ɹе̥ϸĻûб༭ˣĽ͵
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ԣĿǰĻ༭ű༭ѰСǶĿܣ
ûоȷ༭Ӥĵزһ˲ͻŴȥ
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Ƕĳһ͵İ̲еֿܶ͵İ̲еֿ
İ̲ͨTϸϵı壨CXCR4TϸģıCCR5
ûеֿΪûCCR5ʹӴ˶԰̲ߣעԤ
̲Ⱦ˸ȾķաиáȫķԤ
̲ȾȫûбҪͨĶķʽңʹҸȾ˰̲
ҲѲǾ֢ͨҩƿԹ

Ҳһŷ༭ӤһҲûá
Ҫ֤ʮ־׼ҪԸĶĻ׷ڼʱ
洦ûгʱӦϽóȻ༭Ӥؽʵʵʣ
һеˣһϽĿ󵼣һֲļ
ޱҪظĶһҪܵĻȱݡܻ
ȱݵӤӦ׷Ρ

2018.12.11.

ѧ硷2019.1.

㶫ʡ༭Ӥ¼鹫֤ʵ˺ؽȷ
༭ӤһдҲɺؽ
༭Ӥʵ鲻Ҫ˵ΥˣӼϿҲȫʧ
ģμĿաҪô׷ؽķΣûо˵
ϣܹ׷ΣΪֲε鱾Ƿġȥ
12³ҽBuzzFeedɷʱ˵һӮСҽԺЦ
޷⡢زʿҲδȫĺͷգ¼
йѧҵɽһ˺ĳЩйѧڴ¿Ұʽ
ûȤThe couples were taken advantage of, according 
to biochemist Fang Shimin of Chinas New Threads magazine (better 
known by his pen name Fang Zhouzi), an award-winning critic of 
scientific misconduct in that country. He told BuzzFeed News an ethics 
review of the experiment signed off by a small for-profit hospital was 
a joke, and suggested that parents likely couldnt understand the 
consent forms for the experiment. I doubt Dr. He himself fully 
understands the consequences and risks, Shimin said, by email. ...
This case will undoubtedly do further damage to the reputation of 
Chinese scientists, said Shimin of New Threads. It proves that some 
Chinese scientists are indeed doing wild Wild West style research and 
the government has little interest to regulate it. 
https://www.buzzfeednews.com/article/danvergano/gene-edited-babies-chi
na-hiv-ivf ¼ΪйȤҰʽо
㣬Ȼֹۡ2019.1.21.

(XYS20190129)

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                    ԪţҴţ

                          ӡ

ԪֿʳƷˣţ⣬ԪţĿǰֻ
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˹ұ׼ͶصĴԪʳƷ׼ҵļŶ볡ˣõǸڹ
ĴԪʳƷ׼һҵȻԼڹı׼Ԫ
ȻҲƶԼʳƷ׼Ȼ⣬һǰˡй
ýѧǿǿڣģʲôȥƶʳƷ׼Ԫܲ
ʳƷ׼Ǽʶһ׼ߵʲô̶ȣȽϡ
ţ͡ԪţĹʣʵڿʲôΪʲôһ
ϴԪʳƷ׼ۣһͲϴԪʳƷ׼ֻأ

ԪԪţ˵ˣߣʳƷǮͨ
նֶΣǶĵĿ顣Ҫţϣܶ˻
ģĲƷ֪ΪΣԱ׳ճ
ġ˿νԪʳƷ׼ʵֻ֣ġԪ
ţҪľǡġһ۸񣬾ǡġۡˡ
ԪţԪһˡԪ㡱Ԫ
Ԫ漦Ԫ⡱Ԫ򡱡ԪѼ̱꣬
׼顣ҾûӦעᡰԪġֱġ
ˣαظţ㰡ʲôģ

2019.1.26.

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           DNA֮ɭɨزΪȷ

                          ӡ

ղķ˹ɭDNA˫ṹķ֮һýҲ׼ȷؽ
DNA֮ɭԭȪ۷ѧʵҵΣԼʮǰ
ڽܲɷʱ˵޹֮ԱȽΪͱȽϵ͡
۵ȻܵɭȵǸȪʵݣ
ǱͷΡһɭļ¼ƬɭƬ˵
ȻǰĹ۵㣬ͱȽϵ֤̲ͣԵĽƽ
Ȱ˵͡Ȫʵ˷ɭÿѧɢ壬
еͷΣϾϵʵұɭФҲ
ȡˡ

ΪȻйȫһˡۿ
ей˶֧֡ͬɭе˵ɭֻ˵֪ʵ
ȴܵ󡱵ȺҲе˵ʹɭĹ۵ϲȷҲӦ
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Ⱥ壬ǰ˼ٸŴȺ壬ˡҲֱ
ܶŴȺ塣ȺŴҪȺö࣬Ϊ
ȺǴӷȺһ֧ݱġΪˡˡּ
ķ಻Ŵѧ壬ôȥоЩȺ֮ĳŴ״
Ҳû塣

ȷЩоֺ˵ƽ̱Ȱ˵͡ǲ˾ƶ˵
ͱȰ˵͡Ϊ̲ܺܺõزһ˵
̵ĸߵͲܻӰ죬ܵصӰ죬ӪȺ
ضӰ쵽̲Խ1932굽1978꣬ƽÿʮ
3㣬ȻΪ˵ÿʮ͵õĽӪ
ƵĽӪ״ᾭõλкܴϵԺ˵ƽ
Ȱ˵ͣǷӳ˺˵ᾭõλձȰ˵֪ʵ
˵˵ͱȰ˵͡

һתˣԽ٣Խš
ۿõܶϡ塢⣬ҲˣǡǡЩ
Ŵѧ֪ٵߣԼŴѧĹϵ
пѧ񣬰ŴѧĹʶΪˡȷʵй
ˡйǺͬġʮǰɭۺ
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ҪΪһѧѧʣй˸㵽Ǯɭ
ѧоԺɭƼġɭӦõйˡ

2019.1.20.

(XYS20190129)

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ԽĿѧº
ҽ˵

ߣݿƴ

201310Ѯǰͬ¸ңҽˣ˲е
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ΪҵӦġҲҪסΪΪѧĿѧ
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(XYS20190129)

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ԺʿM.L. McCabe and Z. DlaminiĵĵαȽ



ǲöǰһάѧα죬˾塣
ҷ˷١ҽṩ¼
ǷºͱԵġ

 Yunping Zhao1,2, Ruwen Wang2, Daiming Fan1* ƽ 
 The molecular mechanisms of esophageal cancer 2006
EXCLI־

ABSTRACT
Esophageal Cancer ranks among the 10˵Dlamini ԭ: the 
ninthmost frequent cancers in the world, and recent evidence shows 
that its incidence is increasing. Prognosis of this disease is poor, 
with an overall 5-year survival rate of less than 10%. Unraveling the 
mechanisms or developing animal models for esophageal carcinoma have 
thus far not been successful. Many genes have been found that are 
believed to play a role in the development of esophageal cancer but 
the underlying mechanism by which this disease develops is still not 
clear. It is believed that esophageal cancer has an intricate 
molecular mechanism of evading apoptosis by the down-regulation of Bax, 
up-regulation of Bcl-2, Bcl- xl and Survivin, mutation of p53 
andalteration in Fas expression. A great deal of research has been 
perxxxxed in order to determine the key genes that initiate and 
promote the growth of esophageal cancer. This review focuses on 
apoptosis and candidate genes linked to the development of esophageal 
cancer, which it is hoped may provide diagnostic and therapeutic tools, 
and potential therapeutic strategies for the management of this 
carcinoma.
Key Words: Human oesophageal cancer; Molecular genetics; Apoptosis 
signaling pathway; Geneomics; Oesphageal cancer therapeutics

M.L. McCabe and Z. DlaminiģMini review
The molecular mechanisms of oesophageal cancer.2005귢
International Immunopharmacology

ABSTRACT
Apoptosis is a process of programmed cell death, which is as 
essential as cell growth, for the maintenance of homeostasis. When 
these processes loose integration such as cancer, then uncontrolled 
cell growth occurs. Cancer of the oesophagus ranks as the ninth most 
common malignancy in the world, and recent evidence shows that its 
incidence is increasing. Prognosis of this disease is poor, with an 
overall 5-year survival rate of less than 10%. Unraveling the 
mechanisms or developing animal models for oesophageal carcinoma have 
thus far not been successful. It is believed that oesophageal cancer 
has an intricate molecular mechanism of evading apoptosis by the down- 
regulation of Bax, up-regulation of Bcl-2, Bcl-xl and Survivin, 
mutation of p53 and alteration in Fas expression. A great deal of 
research has been perxxxxed in order to determine the key genes that 
initiate and promote the growth of oesophageal cancer. This review 
focuses on apoptosis and candidate genes linked to the development of 
oesophageal cancer, which it is hoped may provide diagnostic and 
therapeutic tools, and potential therapeutic strategies for the 
management of this carcinoma.
Key words:  Human oesophageal cancer; Molecular genetics; 
Apoptosis signaling pathway; Geneomics; Oesphageal cancer therapeutics 


¡
Molecular genetics of oesophageal cancer As oesophageal 
carcinogenesis is poorly understood, much research is being carried 
out to understand the precise mechanisms causing the metaplasiaC 
dysplasia sequence of oesophageal carcinoma at a molecular level. It 
is known that tumour suppressor genes, oncogenes, and apoptotic genes 
are involved in the initiation and development of oesophageal cancer, 
but to date no gene directly related to oesophageal cancer has been 
identified . Many candidate genes and their role in the development of 
oesophageal cancer are still to be revealed before a human oesophageal 
carcinogenesis model can be developed. Key tumour related genes and 
their specific role played in the development of oesophageal cancer 
are discussed in more detail.


Dlamini¡
Molecular genetics of oesophageal cancer As oesophageal 
carcinogenesis is poorly understood, much research is being carried 
out to understand the precise mechanisms causing the metaplasiaC 
dysplasia sequence of oesophageal carcinoma at a molecular level. It 
is known that tumour suppressor genes, oncogenes, and apoptotic genes 
are involved in the initiation and development of oesophageal cancer, 
but to date no gene directly related to oesophageal cancer has been 
identified . Many candidate genes and their role in the development of 
oesophageal cancer are still to be revealed before a human oesophageal 
carcinogenesis model can be developed. Key tumour related genes and 
their specific role played in the development of oesophageal cancer 
are discussed in more detail.


¡
(3) p16INK4a and p15INK4b 
Two tumor suppressor genes are localized at 9p21, Which has been 
shown to undergo hemizygous or homozygous deletion in a variety of 
tumor types. These two genes encode two cyclin dependent kinase (CDK) 
inhibitors which negatively regulate the cell from G1-S phase in 
proliferating cells, contributing to active pRb maintenance (Morgan D, 
1995). During the G1-S phase p16INK4a binds and inhibits CDK4/6 
activity (Retnisdottir et al., 1997), and p15INK4b binds to cyclin 
D-dependent kinase and prevents p27 association(Kunisaki et al., 2004). 
p27 then binds to E-CDK2 complex, blocking the cell cycle at the G1-S 
boundary, risking cells to abnormally proliferate (Kunisaki et al., 
2004). Aberrant methylation of p16INK4a has been found to be a key 
feature in human carcino-genesis, and although aberrant methylation of 
83 
p15INK4b also occurs it is found to occur less frequently in human 
esophageal cancer in Lixian county, China (Xing et al., 1999). A 
common feature of p15INK4b is homozygous deletion, which also takes 
place in p16INK4a.

Dlamini¡
3.4. p16INK4a and p15INK4b
These are tumor suppressor genes and are localized to 9p21. This 
region has been shown to undergo hemizygous or homozygous deletion in 
a variety of tumour types. These two genes encode two cyclin dependent 
kinase (CDK) inhibitors which negatively regulates the cell from G1-S 
phase in proliferating cells, contributing to active pRb maintenance. 
During the G1-S phase p16INK4a binds and inhibits CDK4/6 activity , 
and p15INK4b binds to cyclin D-dependent kinase and prevents p27 
association then binds to E-CDK2 complex, blocking the cell cycle at 
the G1-S boundary, risking cells to abnormally proliferate. Aberrant 
methylation of p16INK4a has been found to be a key feature in human 
carcinogenesis and although aberrant methylation of p15INK4b also 
occurs it is found to occur less frequently in human oesophageal 
cancer in Lixian, China . A common feature of p15INK4b is homozygous 
deletion, which also takes place in p16INK4a.


¡
Angiogenesis
Angiogenesis is the development of new blood vessels, which 
provide blood and nutrient supply to tumors to survive. Once the tumor 
is stable, it can then invade neighbouring cells leading to metastasis. 
In esophageal cancer cells the increased expression of vascular 
endothelial growth factors (VEGFs) stimulates endothelial 
proliferation and migration. Increased expression of VEGFs and VEGFRs 
(receptors) were detected in metaplastic tissues of the lower 
esophagus but not in normal esophageal epithelium, indicating 
sustained neovascular development early in Barretts carcinogenesis 

Dlamini¡
Angiogenesis
Angiogenesis is the development of new blood vessels, which 
provide blood and nutrient supply to tumours to survive. Once the 
tumour is stable, it can then invade neighbouring cells leading to 
metastasis. In oesophageal cancer cells the increased expression of 
vascular endothelial growth factors (VEGFs) stimulates endothelial 
proliferation and migration. Increased expression of VEGFs and VEGFRs 
(receptors) were detected in metaplastic tissues of the lower 
oesophagus but not in normal oesophageal epithelium, indicating 
sustained neovascular development early in Barrett's carcinogenesis 


¡
Invasion and metastasis 
Invasion and metastasis of esophageal cancer is poorly understood. 
The cellCcell adhesion molecules (CAMs) hold cells together, and 
believed to play an important role in metastasis of the cancer cell. 
h-Catenin has been found to play a role in squamous esophageal cancer 
cells, by its cellCcell adhesion ****function and interactions with 
the cytoskeleton and cadherin junctions of cells. h-Catenin has been 
implicated in the transcription of oncogenes such as c-myc, c-jun and 
cyclin D1, which are oncogenes frequently active in esophageal cancer 
cells. The APC gene product targets h-catenin for degradation and 
prevents h-catenin dependent degradation. Increased h-catenin 
dependent transcription due to hcatenin binding to Fz receptors, 
mutations in h-catenin, APC, and increased h-catenin expression due to 
Fz receptor mutations, have all been found in adenocarcinomas and 
squamous esophageal carcinomas. It is therefore believed that 
down-regulation of hcatenin expression by antisense technology could 
be an effective treatment for esophageal cancer.

Dlamini¡
Invasion and metastasis
Invasion and metastasis of oesophageal cancer is poorly understood. 
The cellC cell adhesion molecules (CAMs) hold cells together, and 
believed to play an important role in metastasis of the cancer cell. 
-Catenin has been found to play a role in squamous oesophageal 
cancer cells, by its cellCcell adhesion function and interactions 
with the cytoskeleton and cadherin junctions of cells. -Catenin has 
been implicated in the tranxxxxion of oncogenes such as c-myc, c-jun 
and cyclin D1, which are oncogenes frequently active in oesophageal 
cancer cells. The APC gene product targets -catenin for degradation 
and prevents -catenin dependent degradation. Increased -catenin 
dependent tranxxxxion due to - catenin binding to Fz receptors, 
mutations in -catenin, APC, and increased - catenin expression due 
to Fz receptor mutations, have all been found in adenocarcinomas and 
squamous oesophageal carcinomas. It is therefore believed that 
down-regulation of -catenin expression by antisense technology could 
be an effective treatment for oesophageal cancer.

(XYS20190129)

˿(www.xys.org)(newxys.com)(xys10.dxiong.com)

ȴѧѼЭŻݻƭȡʡⲹ

ߣС֣

ҶԡձʿȴѧѼЭŻݻƭȡʡ
һЩ䣺

Ѽ۶ĳҲڻȴѧѧԺ飬ɼǳѴкҪ󲿷
οʦ©⣬۸ԾӴѧҵѼѧԺԺݰ
Ŷȥ̨ͬʱҲűѧԺսʦΪķͬŵ
ְΪȻƸսʦɹýְƣ

ӱУоϣѼְȨ˵оǰ
ѱƱҵУΪһ߷:

Tight focusing of femtosecond radially polarized light pulses 
through a dielectric interface: Pu, Haosen; . Journal of the 
Optical Society of American A-OPTICS IMAGE SCIENCE AND VISIONVol.32 
(9), P1717-1722, SEP 1 2015

ұǸʦѧҵģȻʦ211Уǡˡ
֪ơһֱʦԺУĸʿѼ۴ձѧ
ѧʿĳƺţٵϸʦҵаڶΪʦ
ԺУߣ

http://paee.fjnu.edu.cn/d2/ec/c3111a53996/page.htm

Ѽ12굱Ժȱʧ£̱˽ңŲѧԺƽѡ
ѧƽ辭ѼЧ޴ϣҲͬΪʦҵȴѧͼıϴ
ǿԲϢ飬ȴѧŻһͰɣ

(XYS20190129)

˿(www.xys.org)(newxys.com)(xys10.dxiong.com)

ɵơԪ

ߣܺ

һ£ɵơһƺǴԪԷģԪġм 
ţԴΪʲôôɵأ˹֮֮ô
ҲԸɡ

ޡɵơ˵Ǹۼͼֻ㡰ʱװơΪʱ
վδߣһֻҲûΪûΪϺթƭ̫
ˣ15һ࣬һ١йټý˸߲
Яֵƣļŵˡƨ¶ѷȴ
еĺκһ׮⣬ˣˡ
ôأԪţ⣬ȻѣҪ

ЧӦ֪ģ˵һֻطһ³򣬾Ȼ
Ǹطһ硣˼˵ֻô棬˵
չĽԳʼмΪеԡ⻰ʲô˼أԴԪ
ۼʧΪԪۼ֮ʧܣΪƭ̫
ˣйټýЯʵ磬ֱӵ´Ԫһ
ؼëԪԼʧܹڰټýЯʣɼû
Ϊνļ˭˭ŶӵҲϰԵġţơ
ѡԼãһţ⣬ýЯʵֹˣ
ˡǸ˭ʲô˼Լֻй֪
Ҳţİɣǣ¡Ԫţֻţ
ơţҪֻˣôᡰءԣޡɵ
ơַˣھԼ뿪˷ҪƵġ

ޡɵơ˵ļΪʲôô߼ۣһԭ۸ļ
ģ۾ĵڶĵ
شͳƨΪڶͼһԼΪļӦ
Ϊ۶磬300Ԫ󼦡Ҳ
ΪļӦΪ۶⣬ġ300ԪһֻϺļ𣿡
ԼΪļӦΪ۶ź塰ΪʲôͶֻ300Ԫ
ļԼΪļΪۺԩ

ޡɵơ㲻֪ǼҲ300Ԫһֻ
۵һ㣬ұ֤Ҫ٣ڡϺļ
ǶθɣѵϺв15թƭͿԸթƭһΣ
쳯ʱͨйթƭҲթƭĹŽͼ˵ʲ
ôǷµծҪģ⡪û!



м ţ

Ԫ  2019-01-23 02:14:10

Ϻ̲һЩԳý ų ҥԵġ
죬ų ˣԪţ⣬˵ţ͵˵

2017꣬ԪʳƷ˾ţһֻ300Ԫͼ
ġΪʲôôɵأΪվƣļƬûPã
һ¡ȷϺ̲15Ƿթƭϰʧǧڣ
ֲ֪ףֻʱװƣʲôʱϰǮˣٴţ˵
ôء

ʱվδߣһֻҲûûз󣬵ΪǴԪ
йټý˸߲ЯҥƣѼŵˡڴ
ԺЩֽŶӵգŪżġ

ôΪʲôһֻ300ԪΪʲôô߼ۣش£

1:۸ǼԼģ۾ְѹصġ

2:ͼһ

3:300Ԫ󼦣൱ϺиԺϺ
һԺ

4:ðɣ300ԪһֻϺļ

5Ϊһ̺ţʮƷ۸һʮԪԪƷеǣΪʲô
Ͷֻ300Ԫļ

ԣʱƨ¶ѷȴеĺΪ
ǶѧΪеˣͬĵˡԪ

˽Ҵת漯ŵľѣҴԷΪ׵Ȧ
͵˰©˰ţҴϺӺ鴺åթƭſӺǮѪ
ǮĳоǰͲϣûйԡûе
ĿϡΪ¼Ƭ͵Ӱκһ׮⣬
Ǽˣôأ

з紵ݶǽУԪţȻѣ


ų ý壬Ϻϰձթƭƨҷţ
ϰϷãǲҽֻװƣϰɱǲұ
ƹϺ̲ѾǶˡ

Ҳû˵ţⰡ

ӵڷһ

Ϻ15թƭĽͼ

(XYS20190129)

˿(www.xys.org)(newxys.com)(xys10.dxiong.com)

Ȼӿ˷ת֪٣Ϊ

оԱ֣Щ˵ķתʿԿѧ֪֮٣Ϊ֪
ࡣǶ֪ʶĴ˸㷺ȺתʳƷķԡ

ֻ֧ǷתʳƷ

һо֣һˡת̬ԽˣͨѧҲԽͣ
ȴΪԼ֪ʶˮƽܸߡ

ΪˡתȺ塱֪٣ΪǶࡷо
ѧ÷Уʢٴѧʥ·˹ϦǴѧ
ô׶ѧͬɣسɹշڡȻ-ΪNature 
Human Behaviourϡ

Ȼ-Ϊ20171ߣڶѧڿȻ־
ӿѧȻѧΪеĶо

оĵһߡѧоԱաѶͺ2017
飨֪ʶĴΪʲôǴδ˼The Knowledge 
IllusionᵽǼѧһ֡ҪһЩѧʶ
۵㣬뱣֤ȱһ֪ʶ

ͨг2500ܷߵĵзоԱ֣
Щ˵ķתʿԿѧ֪֮٣Ϊ֪ࡣǶ֪ʶ
Ĵ˸㷺ȺתʳƷķԡ

оеĵһ飬ڵ1000ˡܷȱʼ
ǶתʳƷķԳ̶Ⱥ͵ǳ̶ȡֵעǣ90.82%ܷ߱
˶תʳƷ̶ͬȵķԣ93.01%ܷ߱˲̶ͬȵĵǡ
ܷ߳ǶתʳƷ⣬ΪΪ֪ʶˮƽ
׼ܷҪһǷɵĿѧԣԿ͹۵
ǵ֪ʶˮƽ

оʹõĿѧۺҿѧᣨNSFŷ޵
飨EurobameterʹõĲ⣬аУӱԭС
ͨûл򣬶תСȵȡ

ʾһ˿͹۵֪ʶˮƽΪԼ֪ʶˮƽĲ죬һ
ˡת̬ȵļ˳̶ȣͳƽϳԡ衰ת
˳̶ȷΧΪ0-70Ϊȫԣ7Ϊǳԣת̶4.77
µʱͳϿԷ֣͹۵֪ʶˮƽһжϵ֪ʶˮƽ
һµġһˡתļ˳̶Ϊֵ7ʱ򣬿͹۵֪ʶˮ
ƽжԼ֪ʶˮƽĲһ¡оת
ϣڼ߶ԣ֪Խ٣ԽΪԼԽࡣ

תⲻͬʵǷͬ仯ϣǵ֪Ҫ
Ӱ졣ͳƽı߱߷
ѧʶ

ڶ͵¹Ϊڵһ飬
һͬĳʽѡ540ˡ500˺519
¹˽е顣սһĽһ¡һͳ
Ľǣšת̬ȵĸˣһԼ֪ʶˮƽߣ
ʱ۵֪Ϳ͹۽֮ĲͱˡȻһ
ת̬Խˣ͹۵֪ʶˮƽԽ͡ŷ޹ңһ۲


Ӣ׶ѧUniversity of Readingϵʦ׶ķµ»
Graham ODwyerΪѶͺչ۲쵽֪ƫܻ
ƣһǡرϢһЩϢ
ЩеͻģôھܾЩϢһ
ЧӦthe Backfire EffectһϢ
ԭĿΥǷ˸ԭϢע
BackfireһͨΪʵ䷴

Ϊʲôô˾ܾŽۣΪ
ͯк µ»ʾҲӰ쵽йȫůıۣ
øѡ

ݴѧά˹УUC Davis2014һоʾǳ
ţ򡢼ȼݼ70%90%תÿ
90ֻݼУ95%ʳúתɷֵϡ

֯WHOתʳƷĻӦתʳƷİȫ
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ΪӪԵضɷ֣嵼ȶԣ༭ص
ӪЧԼܵµκЧӦ

WHOᵽĿǰϣг򵽵תʳƷͨȫ
̫ܶཡɷա⣬תʳѻ׼Ĺͨ
ʳôʳƷཡûӰ졣Ӧԭ򣬳Ӧðȫṹ
ȷתʳƷȫĻ

ܿѧһΪתʳƷǰȫģһ۵⵽˹ڵļ
ԡԴ90תʳƷķչͰŹڵĻɡ
͵ǡƤоģPew Research Center2015һ飬
37%ΪתʳƷһǰȫģ57%ΪʳתʳƷǲȫ
ġˣѧͨƶǸıתʳƷ̬ȡ

һоķ֣ܶԿѧߵĽʽشӰ졣Ϊ
һֱΪڴ򣬶Կѧ̬ȵķǽиĽ
ƺɹ

ѶͺΪһоȺΪѾ˽Щ
ǲܽҪ취ʶ֪ʶϵĲࡣ

ıǵ뷨ҪԸȥԼ֪Ķо
ĵڶߡѧ÷Уʿ˹أNicholas Light
ʾûһͨܺʹǴɷϿѧĹʶ

ҿѧŷ޵Ŀѧ֪ʶˮƽ

ҿѧԹڿѧʮ⣨⣬Ϊ
⣩

1.ķǳȡ

2.½ʼƶҽһֱƶ

3.ǵ̫ת̫ŵת

4.еķ䶼ġ

5.ӱԭС

6.ԭǼ

7.Դһαը

8.ӤŮɸ׵Ļ

9.ؼɱϸҲɱ

10.ǽ˵࣬Ǵڶַչġ

ο𰸣

1.ȷѧҹƣغ˵¶ȳ5538϶ȣӽ̫¶ȡ

2.ȷ鹹ѧרо½Сĵؿǰγɵ㲢
ƶġ̫ƽĵݣؿǰ
ÿƶ5ס

3.̫תǻʶ

4.Ȼ޴ڣر̫СˮֲҲ
䣬㽶зֵһּҲзԡ

5.ȷԶ繹ԭӺĵӺӴ

6.󡣼⼯еǹⲨ

7.ȷǹԴѵĽ֮ͣһܶ޴ĵ㿪
ʼͣǽ쿴ϵǺͺǡһ¼Ϊը
ϸϽӦñΪ͡

8.ȷԱȾɫЯһҪôX(Ů)Ⱦɫ
ҪôY()Ⱦɫ塣ĸȿĸXȾɫϣ
;ӤԱ

9.󡣿ֻɱϸɱ

10.ȷȥһԻʯͻĸо֤ˣ
֣̬

ŷ޵Թ֪ʶˮƽʮ⣨ΪǷ⣩

1. ڻеͷ¾ܼⱦǷۺۺ
Ͳ

2. ¡Ļԭȫͬ

3. ơƻѾƵĽĸɻɵġ

4. Ļгһͬ

5. ʳתˮһ˵ĻҲܷı䡣

6. ̥ϸпܷˡ

7. ༭ĶͨһЩ

8. ͨķѲ򣬶תѺ

9. ϸĹ붯ֲĲͬ

10. ܰѶֲֲС

ο𰸣

1-4. ȷ

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7-10. 

Դ

(XYS20190129)

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غϼ2582019.1.6-10.

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ڴԪ־ļ£״οͨ͹ܣһ֮4600
ͣ˵־ҲһԪǮȻҪȥԺҡթ衱ֻһԪ
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׬4600ԪǮ̫׬˰ɡ


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4600ͣ4600Ԫ־ֻ1Ԫĺٰɡϵͳõһ
Ͷ5Ԫ200ԪΪ1ԪҪֶá

Charles Zhang
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ܴ׬Ǯ治ס


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׵úܣǰѧèͷӥСʴ𡱵ʱ־ͺüȥ
Ҫ˺üٿǮء

WINSTON
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һµѡԱھưݽʱ໰գܴķ粨
ǰݽҲͬ໰йˡ
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߷Ժٽ˹25״ûܳͥ1999˽᳦
κˣ2009ٰҲκˡˤ߹ǣʱֵڷ
85ˣϣͦꡣ
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ǿڼ߻˵мǰͳ˵ýˣ
ǺûεʱȻеǰͳ˵Ǵû˵
ǵ£ҲԽǡ
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ݲݳϻ磬ְһǰµϡʵ
ھɽɽģǰٻϼңСʱϲݳֻ
ȥһΡǼ󡢱صûѡ
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˭˵³Ѹŵ㣿˵³Ѹܾŵ
ѧίԱϯ˹˵˵ίԱǰ䷢³Ѹ˹ĺնͨ
ũȥ³Ѹܾˡ³Ѹľܾڻţܾ
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Фӥڵ۹ֵܶòƴԪ
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ϼ
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8ǰµϼݳʱŵ280ԪĲ֣
Ʋְݳ140Ԫӯ࣬ڶԸս
ľݳܻȰ
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ȥǴԪ갡һΪöǰˡ˵д꣬
ꡭˡ
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¡ڻҺ𣿡
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Ƕβ㣨ͳơ㡱йģ
һ$32˵ǵβǽ㣨ĳβݽ㣩һ$0.31
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2018̼ŷ3.4%Ǽ״ӡЭʱĳ
ŵǵ2025̼ŷű200526%28%дտڿˡ
յͳĶǼȫůȫѡ
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쵱ʱڵνϴ塱ʵԡǲ֪ܲ
һǺķҡ
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ʥǸһºøĭƷǼݵһôġ
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ͨŽչԭվѡίԱϯŵصʦύͥĲ͸
¶ŵԱṩڲݡӦǴվѡίԱ
ǿ֤ˣǰһֱ˵ŵرָصĶ뾺ѡ֮
ǰ£¿Ǿѡڼ䷢ġ
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Աңų£ʲз⡢С
ҪеĽǮеĻÿеĴ̹еĿŲеİѳ
ˣеȡ֧еĳԾȼãϣʱ衣
Ա֮ı蹤ԱòǮܶ˾벡ٴȥˡ
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Ҽֵ¼188
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˵ҰǹɵģֹݾԮҪ
żݶݱ֮һϣܶ¶ɸ׳ˡ
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ҽʦΰԼŵĹΪθʹҩ
ӵĽ᳦Ϊθʪȣҩù
Լ֣вҽ
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jim
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Ͻһ㡣
ѣҽڣӵĲȷϣ˵Ķǵֱ
᳦
ǣȻҽܣβУԤҽѧ˿ֹδ
Ѳĵһ


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 Jan 10
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ֱǽ᳦һֱ֣ͽ᳦ͨϳƽ᳦ֱҽʦĶ
ӵĽ᳦ֱ˵ҽҩҩԳģһ°



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¡Ŀµķ˨
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ʽܡʢٴձݣչ˾аģϷ¥
ҹ԰ϵͳڼ䱾Ӧúҹ԰һرաΪ˲Ӱ
ݿ¥羰Ųš
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ҵ콭Ƭװĵ߶˶ˣ컹ϡ

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ӾơһҪɶ˰׷һ£˭Ϊ֪ʧ
ȴҸ6Ԫһ¸
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 Jan 9
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һϳĺעͣʹ˵ǲο飬Ȼ
ԡرǳעͲ֣ԭֻһɫľӣû
ţҲԡ""񣿡
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 Jan 9
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ʱ̫ãΪʷãʽ꣬FDAֳ
ֹͣʳƷ顣ȫ۵ʳƷҲҪӰˡ
ŵһǹҹ԰û๤ɨеĹҹ԰ˣе
ԸɨԱμɨҹ԰󣬰͸˰׹
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 Jan 10
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˵ɺϡ1958һTrackdownƬӾһдյ
̾ĩռҪ쵼ǽܱ硣
ھдձɱ
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 Jan 10
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ҽʦνҽƣΪˡԡ顱ҽˮƽ
ԼϡҩšΪ˺ҽ
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 Jan 10
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ͣڽ20죬ʹ¼ˡԱڰ׹
ſʾߺǹôջؼЪš˵Ա
ڶǲнˮڰ참ͳһֱôȥǲеġ
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 Jan 10
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ͣڣ׹ҲӰ죬Ƿˮ˾5ԪˮѡݷɣǷ
30Զˮ60Կˮ˾Ҹ׹ˮ׹
ڿյģԱܶ඼ؼЪˡֶŵʱ򣬰׹
һùʵʵϰ油һ˹
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¡տˮܲܺȣ
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 Jan 10
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йѴգҷйںܶ෽Ҫȿֵе
ࡣΪйʵԶԶҪ׶Ը
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 Jan 10
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ŦԼʱΪʲôѡ̬ɡá̬
ơ̬ϲ̬˵Ψһ֪֮С
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Simon a LiberalChinese
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@LibrealChinese
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﷽ʦϣƽйĸ﷨εɣСޡ
˵ǣ˵ĵδؾѣûбҪȥĶ
֣ϾĸѾ޴ˡΪԼĴ飬ԸЭ
Ȼֵþ壬ȴδʵܶаȨ֪Ҫ


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 Jan 11
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㡢źӱ̬ñ̬ˣ챻Ԫҥˣ
ȥǺˡйΪʲôĸôԭ֮һǷ
ֵαԸ̫ࡣ

Simon a LiberalChinese
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˵ﲻͬĹ۵㡣Ҳ˵
궼йעҲͬĺܶšΪƷͨ
վȨսҶС޶ת̬б
ԷԺ


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 Jan 11
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еװӣȰ汾˺ͼ˱̬ʹԪҪ
˵αԸԩ𣿶Ը˵ֻҪĳ
Ϊͨڡ£˵Ȩ

Simon a LiberalChinese
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@LibrealChinese
 Jan 11
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ŻӦ˵Ƿ֧˵ȨҵȻ֧ͨˡ
Ĵ׷εʦ󻯵޴ͨˣһ
սĿǰԵȨס䣬
ҾþбȨҲȫ˵Ʒͼ


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αԸѵҵס͵䣬ҺҼ˾͸
̬Ԫ裿ԸҲ


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 Jan 11
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û־й˵źͺӵ


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û͵ûУԱ̬ͲαԸ߼


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 Jan 10
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йЭġйŻǣʳ뾫ϸ˵й
Э˾ϸ°׼ŵˡ
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ʱ֮Ľִֻͨôͬӳ
ƬģʱҪ˵йӢŵĵӰҲҪ
ӢӳʱӰӳ϶ͼƬӣƽ
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hellodo
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 Jan 10
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Ϸ߼©ȫ԰ѽƬ˵أȻһͳһ
ʱ䡣


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ˣΪڣĺƬӲӳȫͬӳ


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йϸ׼˾תƷֽڡ˵ԪӮˣҳ
ӡֹת
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 Jan 11
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˵û˵Ҫī縶ǡʵھѡʱ
˵200Σ̨˵ʮΣһڱī縶
50-100Ԫǵļƻ顣ľѡŵҷϣֻҪ
žУ
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 Jan 11
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йЭĹٷ˺šйΪάն̵棬˵ն
Ⱦ°жΪҥԡԼɢҥŻˣŻ
СͳԺóǡƭй
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 Jan 11
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ݡҽʦνҽҽԺ֢ȥԳƽҽΪ
˿ҽҽýֿʼһִáҽʦһ
˵κ˹¡ҽҩκ˹𣿡
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 Jan 11
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ӦðѡҽʦĲҲҽ
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 Jan 11
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йũ󸱽ڷ־ġԭաЦࣺӪѧVα
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 Jan 11
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ץйһǲˣһǻΪڲܼ
ΰǲҲҪץ
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 Jan 11
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2018й֢ռ֢21%֢ռ簩֢
24%ҽû
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Tan, Ziming
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ѽй˿ڴԼ˿ڵ24%ð֢ӦҲѽͳ
Ӧ˿ڻĸɣ


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 Jan 12
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й˿ռ18.5%㴴5.5%

Tan, Ziming
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@gztzm
 Jan 12
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ٶȰٿƵĺҲҵݣҲ±˵ǣ˿77ڣ
й˿14.2ڣԼ٣

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 Jan 13
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ͼҽû壬Ϊձͼйߣԭ
ǰй仯̫ء


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õֻۿͼձݣˬǲǣ


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 Jan 11
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ͣڽ22죬˼¼ԺͨؿԺ
ύǴղͬ⣬ȫԼյĴˡ
ܷû涨ķʽְôȨһ˾ͿòԺֹͣת
Ҳεı׶ˡӦøĳԺͨķԶ
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 Jan 11
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ڷѧ֮һԭȪʵɭڼ¼Ƭ
ۣȪʵҷǴÿѧ֧ƫ
ƺţжĹϵɭҪȥйϡȫְѧˣ
˵ġ̵ܶ͡й˷׷׵
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Sig2017
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@SigCZ75
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֤ݺͳѧ˵мŵѧｱѧ


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 Jan 11
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ǵ߼мй˵ŵйǲҲ
ͣ 

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ĿǰķһЩѧͷϿñӣʵ
ѧϽƺûĿѧ֤Ϊʲôû˸ȥһ
ʵ飬֤ȷʵûйϵأ


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 Jan 12
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Ŵѧһ֪͸ҶûĿѧ֤йľ
֪͸ȴΪߣɭŸȥйϡ

Ping Lu
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 Jan 12
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޹ءҪĿ£Ҹָ·ѡ

topsailgao
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ллҿ¡Ϊﷸһ߼߸
֮ĸֲ죨òƶȵȣһѧͳ
ʵ֪ⷽǻЩʵȻҲܲƫŴѧ
Է֮ϵⲢ֤αЩܴڵʵ


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 Jan 12
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ûŴѧϵ̸ʲô̡Щй߶ǣ
Ϊҷ߼أԴ

Ford
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Ĳμתҽѧᣬ20ǰ¶ڱΪʲôܴҡ
ڵĵ˵Լġΰ񷽡أ@fangshimin
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 Jan 12
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ѧ齻ǮͿȥμӵģֲ뱨档ڱʮǰȥʥǸ
ķԺңһֱû״ȻҾͷSLAPPˡ


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 Jan 12
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2016깲͵ͳѡ˳ѡۣʴգòī
һ80ڡ100ڻ120Ԫʵ֧ƱҪô֧ǽ
ãգһǿ֧Ʊģǽָ10ߣһƬڴ
˵Ҵû˵Ҫī翪֧Ʊ֧ǽáۻһƬ
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 Jan 12
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ý׷ױܼ⵽źˣѡרҡ
˵Ҫش𡱣ѧ֪ôشƵġŦԼʱıǣ
ȻԼ⵽źôĻѧҶԴΨһͬĿǣ
ЩźźܿܲС󱨵йֻС
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 Jan 12
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ΪôѸپͰΰ߿ˣû˵Ҫƶزץ
ˡ
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 Jan 12
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¡ҽҩΰ̲𣿡
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 Jan 12
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ڳｨǻĿ10Ԫֻﵽ2ǧԪ30˾
ڵŵﲻĿ˿ڳվ˵ѿ˻ءվ
ţ˵һҾ10Ԫǻˣ˴Ϊ棬ɽ
ꡣҲ룬ɶʱô󷽡
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 Jan 12
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ͨԳɴ˳ʷղ2007ڸõء5ǧԳ
˳300˳ԳֶױʻӺд
֣Сѧˮƽִ׻дɣӿд
ںӺҵİ¼22СѪõ塷10ƪ

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 Jan 12
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2018˲Ž̵ıΪ35%45˲Ž̵ıѽӽһ롣
òһˣ󲿷˾ͲŽˡ
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Michael Chen
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@Michael801127
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ʮԺſʼŽأʦ


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 Jan 12
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1990Ẕ̌8%200114%201220%201835%ǲǾ
˿˱ԽԽߣһӽȴΪϽ


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 Jan 12
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԰һ˫Ь桱1980Ԫ溬˶˰һ£
Ьǰͱع⡢ˡѷƵġЬ桱һ˫ʮ
Ԫ
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 Jan 13
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ϼ
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 Jan 13
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39.66%ð֢22.03%ڰ֢Ů37.65%ð֢18.76%
֢Ҳ˵һҵ֢߻ᱻйûݣ
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Tan, Ziming
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@gztzm
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 Jan 13
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ǰٶһЩҵ֢68%й37%
ٰ90%й73%ǰٰ99%й54%

JeffCT
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ܳԾ˵ð֢ıô󣿽40%˻ð֢й۲
Ĳܴ


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 Jan 13
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Ϊе˴󲿷ֶû

һ
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۲ȷ֢˿ڼ򻺽ಡ򲡡
һϵԭԣ18%ڰ֢ƶϳһ


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 Jan 13
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֢ڼΪԭǴҪġ֢68%
ûҵ֢ʮݣĴǵ61%Ӧࡣ
Ϊʮ껹ܸĸжߣ˵дԼһ뱻ˣô
ˣ


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 Jan 13
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β
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 Jan 13
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¡ʯٳԵġɵʲô
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zhicheng wang
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׶ۿümitڸƼƷҲ˵ûУ
Ҳú𾪣ЩڶҸŹˣôͻȻƼ𱣽Ʒ



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Ǽҹ˾˼ŵߵأMITʲô


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¶Ĵաշأʢʱ˵׹ڶû׼
ң˵ңûе¡ʵϣڰ׹ûˣʣ
ˡ
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 Jan 13
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ԱųƻʳƷţ
첻ʣһӳҪȼõˡ53%baqŹﴨպ͹
͵Ա29%Այ۾ʣ29%ˡаһЩũ
òǱʾƲҲִ֧սǡ
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 Jan 13
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ָҽƴѧУӱԺʿŶӷıͼƬٺ
ĻͼƬԭѴ浵Լҿȴרǹ
ſƺñͼƬ֤ݣ˵Ҵ١ôԺʿż
ѵƪľдģ
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 Jan 14
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ղȻ𳵵֣أҰˣת
ǽУԭǽѧȻ𳵽СͷȻ𳵾Ұ𣬰ѽˮ
;Ȼϵˡ˵ǴȥʮﴦҰĵطǨ
ġ
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 Jan 14
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ԤꡣӡʥǸûġ
ˮ㣬괺ֻǰҰʢƬǰ괺ĵģ
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Wei Wang
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@WeiWang8964
 Jan 14
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ʲôλãꡣ


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Diamond Valley Lake


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 Jan 14
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ƪʥǸĶ˺ܶʣѧӢĺòϡ
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 Jan 14
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ɶǰӼߡ¾֤־ͬ־˵ơȡ桱ֵ
أƭǻ׷׵ޣǲҥٰʵ
Ϊơ
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 Jan 14
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ɭΪ͵⵽ѧıӣ֪ʶ
ӡȴҪ֤ǻģֻ˵ĸİʹΪ
ɭѧĹʣʹ󲿷й˶ͬɭ۵㣬ô
绤Ҳ̫˰ɣҿ֪ʶӡߡ༭ǵǻ
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؈NACKRHLOIPSN-4-1
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˵˱óͲ֡ΪƼ㵽ϣ
ˣӺˡûβȷ


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 Jan 15
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˵㲻˵϶Ȼ߼֤
͡


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 Jan 14
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£ڳһڡйԺʿٹȻ߼ˡ
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 Jan 14
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ǰٰʽ͵ԭΪȡǰԿԭ
ɸֵǰٰˣ֪ʶӡȴܽȡɸ
˹ƣӶ˲ѷʵʣ
ΪӰ֢ߡ༭ǻİɡ
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 Jan 14
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Ƶġ롱黳ˣȻֱֻƭǮһʡ
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 Jan 14
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½Ǯ̨ǣǰǾƷ׬Ǯ־ӱ
ָа׬ǮܾǻзȨ
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 Jan 14
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Ž24죬׹ʦԱؼЪˡҪô
أѲգϲĿ͡
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 Jan 14
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ôΪԺ15꣬ݺΪߣȻ󱻸
̡Ժĸô˸ߡ
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 Jan 14
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ƬĵãӦõýĿԽСչ硷
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 Jan 15
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й̵Ǹô2012ڷڼô16£ʱ
ô󷨹ٶ˵ҪҲǻǱץġ˳2014
й4ȥ1115꣬ߺȥ12·Ѹ
ٿ̡ͥԺô󷨹ٸöԶ˵ҪҲйץġ
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Lai Xingtao
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@Lai_x_t
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Ϸ治˵ʵ֤һڼôҲǼ
ԺҲҪģΪһоƫᣬЩ֤ûвɡ


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 Jan 15
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Ӧ־ʿ٣һ̣ټN̡
־ʿֵ屻ߺͼԺ


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 Jan 15
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տ͹羿ģ촨նֳ˵300
ԲμӹĴѧھ˵ҳȥ˴Լ1000
췢˵һСʱڳԵһǧ
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Frank Wang
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@fxw2k
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ȻһЩ鲻ִ֧գΪ˰ʡǮҪ֧һ¡


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 Jan 15
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ɵֱʧټʮԪȻܸ˴ʡһٹ
Ǯ


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 Jan 15
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Ͱ̫Фѵ˸С⡱ģأ
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 Jan 15
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ýҽԺáΡ9ǰָˡ
¡й˰Ρ
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 Jan 15
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ŷк׶԰бҵѧϰɼŮк
׶԰СѧѧϰɼŮȽϽӽϳкúܿҪԭ
кСʱȽĸܽעѧϰഺںͬѧӰ죬
ΪûӺš
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 Jan 15
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ըǿ4ϲ˻ҪԼÿ俾ųԣ
ÿըը
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 Jan 15
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һݼɳΪɳܼʣҪ
ʲôɳ
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Eddie Cheng
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@realEddieCheng
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µ񡰴񳵡Ҫˡôͬǵ
ǮΪʲôûгǮһҴֱͧ͵ӭǵļô
Դϲʡȴĥѡ鷳
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 Jan 15
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߼ЩԽҪֽ֧˰ӵԼסһ
ģκ͸˵ΣοԼδԸȥô


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Ϊ롶λԼλ鶨顷ģ

HHG
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ֻӦԱȻڣ


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 Jan 16
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ȨϹȨԹ涨ĻȨЩûԵĴӦú˳
ϹƷ񷨰


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 Jan 15
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ĵ鷢֣ԽǷתʳƷˣտѧ֪ʶŴѧ֪ʶԽ٣
ԽԼתʳƷоĽǣ˷תʳƷ˶
٣ȴΪԼࡣȻйҲġ
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