M*e
2 楼
比如看cctv
谢谢!!!
谢谢!!!
g*e
3 楼
Docker
The Docker Engine container comprises just the application and its
dependencies. It runs as an isolated process in userspace on the host
operating system, sharing the kernel with other containers. Thus, it enjoys
the resource isolation and allocation benefits of VMs but is much more
portable and efficient.
似乎他需要做每个container里面所有bin/lib 和 local OS的衔接,这个不好做吧?比
如linux 里面用fork() exec(), windows里是createProcess(), docker是不是都得安
排好这些?
The Docker Engine container comprises just the application and its
dependencies. It runs as an isolated process in userspace on the host
operating system, sharing the kernel with other containers. Thus, it enjoys
the resource isolation and allocation benefits of VMs but is much more
portable and efficient.
似乎他需要做每个container里面所有bin/lib 和 local OS的衔接,这个不好做吧?比
如linux 里面用fork() exec(), windows里是createProcess(), docker是不是都得安
排好这些?
H*e
4 楼
Wow, on the top list!
Well, I never expect to be on the top list. This reason is that I am not
here very often. Also apologize to those are discussing about the topic and
expect me to give my opinion.
I believe that the previous title regarding to someone retract her paper is
misleading. So it is necessary to clear some issue and have an opportunity
to draw more discussion. Now back to the stem cell issue not the Amy or
Carla although name may be mentioned but please ignore my own personal
opinion on both of them. Also I like to restrict my view on lung and lung
cancer in case that I forget type lung.
1. Lung stem cell?
Is there lung stem cell? Unlike many other tissues, the lung tissue
turnover is very very slow. So once, it has been almost accepted that there
is no stem cells in lung. This is changed until everyone accepted the lung
epithelial injury model: chemical induced lung injury. Specific layer of
epithelial can be “removed” by carcinogen although the mechanism is not
completely understood. So the idea is that there are unclear stem cells: 1)
to join Clara cells recovery the airway and bronchial epithelium; and 2) to
become type II cells and then type I cells to repair alveolar.
Now where is the stem cell population? Carla Kim’s Cell paper found BASCs
and a almost perfect situation to solve it. This is not only the perfect
new type of cells but also perfect location in term of lung anatomy. Her
other works even pointed to the direction that lung cancer is from BASCs.
However, it then became to be too good? There are people arguing the wrong
technology or wrong marker in Carla’s work. There are people who
identified new stem cells with new identity. Then Carla argued back that
others used wrong antibody. (Please forgive me ignore the reference because
it is very easy to find on pubmed!)
Then, partial answer is from Hogan’s work using the transgenic mouse to
track the lineage. The conclusion is that Clara cells in airway and
Bronchial epithelium is self renew population. So Clara cells can to self
repair! Can we call Clara cells stem cells? Or it is just because there
are too many! And beyond our imagine about the “very small number of cells
” in lung?
I said “partial” above. The reason is the unanswered question regarding
to type II cells? Way back to decades ago, text book said type II, like
Clara cells, can repopulate itself. In Carla’s earlier year seminar, she
gave very strong statement that there was no evidence about type II
repopulation. I personally hate any strong statement like Amy’s no
transdifferentiation. However, this is no clear answer!
2. Lung cancer stem cells?
Without mentioning how people using the stem cell marker to search cancer
stem cells, this concept may not be right in lung cancer. Narrow down to
adenocarcinoma since Kras and VEGF models’ major/only consequence. Earlier
work used Tag can reach the same tumor by CCSP or SPC promoter, concluding
that tumor could be from both type II and Clara cells. This seems confirmed
by carcinogen induced AJ mouse tumor (I always wonder why this strain get
tumor but not the common Black strain?) and by EM too. Then people found
that CCSP does not express well in tumor; so a theory is that Clara cells
no longer express CCSP when it become tumor and somehow the gene is shut
down. Then why the transgene remains on? By selection?
So if there is lung cancer stem cell, it should be more than one type, at
least one for typeII tumor and one for Clara tumor. As matter of fact, I
suspect it for long time when I was a strong believer of cancer stem cell.
This seems being answered by Carla’s Cell Stem Cell paper recently that
Kras and EGFR tumor stem cells have different potency and identity (?).
Then are they all from BASCs? Or other common population?
I had done experiment to express Kras or EGFR in either typeII or Clara
cells but found that they all form tumors. An experiment that I designed to
get the answer but generate more question!
3. What is lung cancer origin?
In the above discussion, I more or less touched this issue. By microarray,
there are 6-7 types of NSCLC and, among them, there are at least 3-4
different adenocarcinoma. This is human case. Is mouse same of different?
For many years, I try not to touch this issue because I know I only care
about result and publication. Now this becomes concept issue. I have been
asked for it. I have no answer. But to Kras model, I like to say this only
represent one type of adenocarcinoma. Then what is the origin of Kras lung
cancer in mouse? By histology, I see most tumors in alveolar. So I vote
for typeII cells. Then question is what will happen if someone see a tumor
in bronchial.
Why this is a concern? I care about this issue from my concern about which
type of cells may act like stem cells then cancer stem cells. But my friend
in carcinogen field told me that this is very important. Smoke carcinogen
can only be metabolized by P450 Cyp2a13, which only is expressed in airway
and bronchial epithelium not alveolar type II cells. The injury is seen in
bronchial. But DNA adduct (I know little about this term) was seen in both
type of cells? To them, they like to know which cell is the targeted cells
that generate mutation. Then I told him both cells can form tumor by
arguing that only 20% NSLC is related to smoke. Practically, I then start
to wonder if I can identify the origin of certain lung cancer I may choose
the right cells to study the initiation stage. Now which cells to choose,
typeII or Clara? So I selected BASCs for some time and realized that these
is no such thing. Then what is my next cell?
4. Stem cell population in cell lines?
I read some comments about the cell lines. It recalled me a manuscript that
I had reviewed. This manuscript, like some of them out there, used the
markers (SCA, CD133, CD166…) to stain MCF7 and SW480 cells for cancer stem
cells. I rejected it because I know that the chromosome number in a plate
of cells vary between 1N to 4N and their identities may vary by some markers
. However, not every reviewer agrees or knows this fact. One has not
problem to find this type of work. Indeed, there is a paper which did all
“stem cell marker” staining on the NCI cells and reported all the
percentage for each stem cell markers. It turns out that some cells has >90
% stem cells and some has <1%. I believe that this is great paper that
gives people the fact and they can choose what to think. To me, a single
cell of cell line can form not only the colony but also tumor without too
much problems and by concept cell line is stem cell. Then, there is no stem
cell because they are all stem cells now. Also different cell lines from
the same cancer can have different identities. Then my guess is that each
individual tumor has its own specific stem cell. Why we work on stem cells?
5. What I am going to do?
Now back to earth, I hate this concept like many senior scientists in the
field but I have to follow it in case that … The other reason that I did
not stop working on “lung cancer stem cells” by using different markers is
the application of specific marker producing a defined population of cancer
cells, which may be more “pure” for other experiment such as microarray
etc. At least, the experiment can be reproduced. Otherwise, using the
primary tumor even Kras mouse, I found the result varies from time to time.
In case that I used the one right marker that people call it stem cell
marker someday, I …
Again, I am not here very often. If there is anything wrong, this is
restricted to BBS discussion or forgive me base on how much I typed tonight.
If you need my help, I do not want to mislead you as I already did to
myself as described above. If you like to have more discussion, I am open
for it but again I am not here very often. Also please no personal attack.
I am not feeling well by mentioning Amy and Clara since we know each other
well.
Well, I never expect to be on the top list. This reason is that I am not
here very often. Also apologize to those are discussing about the topic and
expect me to give my opinion.
I believe that the previous title regarding to someone retract her paper is
misleading. So it is necessary to clear some issue and have an opportunity
to draw more discussion. Now back to the stem cell issue not the Amy or
Carla although name may be mentioned but please ignore my own personal
opinion on both of them. Also I like to restrict my view on lung and lung
cancer in case that I forget type lung.
1. Lung stem cell?
Is there lung stem cell? Unlike many other tissues, the lung tissue
turnover is very very slow. So once, it has been almost accepted that there
is no stem cells in lung. This is changed until everyone accepted the lung
epithelial injury model: chemical induced lung injury. Specific layer of
epithelial can be “removed” by carcinogen although the mechanism is not
completely understood. So the idea is that there are unclear stem cells: 1)
to join Clara cells recovery the airway and bronchial epithelium; and 2) to
become type II cells and then type I cells to repair alveolar.
Now where is the stem cell population? Carla Kim’s Cell paper found BASCs
and a almost perfect situation to solve it. This is not only the perfect
new type of cells but also perfect location in term of lung anatomy. Her
other works even pointed to the direction that lung cancer is from BASCs.
However, it then became to be too good? There are people arguing the wrong
technology or wrong marker in Carla’s work. There are people who
identified new stem cells with new identity. Then Carla argued back that
others used wrong antibody. (Please forgive me ignore the reference because
it is very easy to find on pubmed!)
Then, partial answer is from Hogan’s work using the transgenic mouse to
track the lineage. The conclusion is that Clara cells in airway and
Bronchial epithelium is self renew population. So Clara cells can to self
repair! Can we call Clara cells stem cells? Or it is just because there
are too many! And beyond our imagine about the “very small number of cells
” in lung?
I said “partial” above. The reason is the unanswered question regarding
to type II cells? Way back to decades ago, text book said type II, like
Clara cells, can repopulate itself. In Carla’s earlier year seminar, she
gave very strong statement that there was no evidence about type II
repopulation. I personally hate any strong statement like Amy’s no
transdifferentiation. However, this is no clear answer!
2. Lung cancer stem cells?
Without mentioning how people using the stem cell marker to search cancer
stem cells, this concept may not be right in lung cancer. Narrow down to
adenocarcinoma since Kras and VEGF models’ major/only consequence. Earlier
work used Tag can reach the same tumor by CCSP or SPC promoter, concluding
that tumor could be from both type II and Clara cells. This seems confirmed
by carcinogen induced AJ mouse tumor (I always wonder why this strain get
tumor but not the common Black strain?) and by EM too. Then people found
that CCSP does not express well in tumor; so a theory is that Clara cells
no longer express CCSP when it become tumor and somehow the gene is shut
down. Then why the transgene remains on? By selection?
So if there is lung cancer stem cell, it should be more than one type, at
least one for typeII tumor and one for Clara tumor. As matter of fact, I
suspect it for long time when I was a strong believer of cancer stem cell.
This seems being answered by Carla’s Cell Stem Cell paper recently that
Kras and EGFR tumor stem cells have different potency and identity (?).
Then are they all from BASCs? Or other common population?
I had done experiment to express Kras or EGFR in either typeII or Clara
cells but found that they all form tumors. An experiment that I designed to
get the answer but generate more question!
3. What is lung cancer origin?
In the above discussion, I more or less touched this issue. By microarray,
there are 6-7 types of NSCLC and, among them, there are at least 3-4
different adenocarcinoma. This is human case. Is mouse same of different?
For many years, I try not to touch this issue because I know I only care
about result and publication. Now this becomes concept issue. I have been
asked for it. I have no answer. But to Kras model, I like to say this only
represent one type of adenocarcinoma. Then what is the origin of Kras lung
cancer in mouse? By histology, I see most tumors in alveolar. So I vote
for typeII cells. Then question is what will happen if someone see a tumor
in bronchial.
Why this is a concern? I care about this issue from my concern about which
type of cells may act like stem cells then cancer stem cells. But my friend
in carcinogen field told me that this is very important. Smoke carcinogen
can only be metabolized by P450 Cyp2a13, which only is expressed in airway
and bronchial epithelium not alveolar type II cells. The injury is seen in
bronchial. But DNA adduct (I know little about this term) was seen in both
type of cells? To them, they like to know which cell is the targeted cells
that generate mutation. Then I told him both cells can form tumor by
arguing that only 20% NSLC is related to smoke. Practically, I then start
to wonder if I can identify the origin of certain lung cancer I may choose
the right cells to study the initiation stage. Now which cells to choose,
typeII or Clara? So I selected BASCs for some time and realized that these
is no such thing. Then what is my next cell?
4. Stem cell population in cell lines?
I read some comments about the cell lines. It recalled me a manuscript that
I had reviewed. This manuscript, like some of them out there, used the
markers (SCA, CD133, CD166…) to stain MCF7 and SW480 cells for cancer stem
cells. I rejected it because I know that the chromosome number in a plate
of cells vary between 1N to 4N and their identities may vary by some markers
. However, not every reviewer agrees or knows this fact. One has not
problem to find this type of work. Indeed, there is a paper which did all
“stem cell marker” staining on the NCI cells and reported all the
percentage for each stem cell markers. It turns out that some cells has >90
% stem cells and some has <1%. I believe that this is great paper that
gives people the fact and they can choose what to think. To me, a single
cell of cell line can form not only the colony but also tumor without too
much problems and by concept cell line is stem cell. Then, there is no stem
cell because they are all stem cells now. Also different cell lines from
the same cancer can have different identities. Then my guess is that each
individual tumor has its own specific stem cell. Why we work on stem cells?
5. What I am going to do?
Now back to earth, I hate this concept like many senior scientists in the
field but I have to follow it in case that … The other reason that I did
not stop working on “lung cancer stem cells” by using different markers is
the application of specific marker producing a defined population of cancer
cells, which may be more “pure” for other experiment such as microarray
etc. At least, the experiment can be reproduced. Otherwise, using the
primary tumor even Kras mouse, I found the result varies from time to time.
In case that I used the one right marker that people call it stem cell
marker someday, I …
Again, I am not here very often. If there is anything wrong, this is
restricted to BBS discussion or forgive me base on how much I typed tonight.
If you need my help, I do not want to mislead you as I already did to
myself as described above. If you like to have more discussion, I am open
for it but again I am not here very often. Also please no personal attack.
I am not feeling well by mentioning Amy and Clara since we know each other
well.
x*0
5 楼
POSITION SUMMARY
A Senior Scientist who will play a key role in new drug characterization and
analysis using LC/MS in research and development. Major responsibilities
include bioanalytical assay development for drug DMPK studies and peptide/
protein and antibody analysis in support of drug candidate selection,
preclinical and IND-enabling studies
ESSENTIAL FUNCTIONS
- Peptide/protein and antibody analysis using Agilent QTOF
- Developing in vitro DMPK assays using SCIEX QTRAP including metabolic
stability, metabolite profiling, structure elucidation, and CYP450
inhibition assays
- Preclinical bioanalytical assays for PK studies to determine drug
concentration in plasma, urine, and different tissues
- PK calculations and interpretation using Phoenix WinNonlin software
- LC/MS instrument maintenance and trouble shooting
EDUCATION/EXPERIENCE REQUIREMENTS
Ph.D in chemistry with more than 7 years pharmaceutical experience using LC/
MS
REQUIRED COMPETENCIES – KNOWLEDGE, SKILLS, ABILITIES
- Expert in Mass Spectrometry for small molecule and protein analysis
- Strong knowledge in DMPK study
- Skillful in bioanalytical assay development
If you feel interested, please contact Sherry via email [email protected]
com
Thanks
A Senior Scientist who will play a key role in new drug characterization and
analysis using LC/MS in research and development. Major responsibilities
include bioanalytical assay development for drug DMPK studies and peptide/
protein and antibody analysis in support of drug candidate selection,
preclinical and IND-enabling studies
ESSENTIAL FUNCTIONS
- Peptide/protein and antibody analysis using Agilent QTOF
- Developing in vitro DMPK assays using SCIEX QTRAP including metabolic
stability, metabolite profiling, structure elucidation, and CYP450
inhibition assays
- Preclinical bioanalytical assays for PK studies to determine drug
concentration in plasma, urine, and different tissues
- PK calculations and interpretation using Phoenix WinNonlin software
- LC/MS instrument maintenance and trouble shooting
EDUCATION/EXPERIENCE REQUIREMENTS
Ph.D in chemistry with more than 7 years pharmaceutical experience using LC/
MS
REQUIRED COMPETENCIES – KNOWLEDGE, SKILLS, ABILITIES
- Expert in Mass Spectrometry for small molecule and protein analysis
- Strong knowledge in DMPK study
- Skillful in bioanalytical assay development
If you feel interested, please contact Sherry via email [email protected]
com
Thanks
f*t
6 楼
做他那个位置的人 要保护的是整个家族 fredo曾经胳膊肘往外拐 不杀可能也什么事都
没有 但是作为教父 要不不做 做就做绝
没有 但是作为教父 要不不做 做就做绝
t*b
7 楼
目前没有,bluray player尽管有些能联网,但没有看到能支持第三方开发的。
z*e
8 楼
就是一个底层的跨平台的container
就认为是没有任何其他类库的一个轻量级的垮os封装
docker的流行充分说明没有多少程序员对于os有兴趣的
底层的东西不是被这个封装就是被那个封装
本质上说,就是程序员不愿意碰这些底层系统软件的缘故
就认为是没有任何其他类库的一个轻量级的垮os封装
docker的流行充分说明没有多少程序员对于os有兴趣的
底层的东西不是被这个封装就是被那个封装
本质上说,就是程序员不愿意碰这些底层系统软件的缘故
h*n
9 楼
great post.
To me, the cellular origin of a specific lung cancer is one of the most
important questions.
When I have time I will discuss more.
To me, the cellular origin of a specific lung cancer is one of the most
important questions.
When I have time I will discuss more.
e*2
10 楼
好地方 尔湾公寓价格均价多少?
and
【在 x**********0 的大作中提到】
: POSITION SUMMARY
: A Senior Scientist who will play a key role in new drug characterization and
: analysis using LC/MS in research and development. Major responsibilities
: include bioanalytical assay development for drug DMPK studies and peptide/
: protein and antibody analysis in support of drug candidate selection,
: preclinical and IND-enabling studies
: ESSENTIAL FUNCTIONS
: - Peptide/protein and antibody analysis using Agilent QTOF
: - Developing in vitro DMPK assays using SCIEX QTRAP including metabolic
: stability, metabolite profiling, structure elucidation, and CYP450
and
【在 x**********0 的大作中提到】
: POSITION SUMMARY
: A Senior Scientist who will play a key role in new drug characterization and
: analysis using LC/MS in research and development. Major responsibilities
: include bioanalytical assay development for drug DMPK studies and peptide/
: protein and antibody analysis in support of drug candidate selection,
: preclinical and IND-enabling studies
: ESSENTIAL FUNCTIONS
: - Peptide/protein and antibody analysis using Agilent QTOF
: - Developing in vitro DMPK assays using SCIEX QTRAP including metabolic
: stability, metabolite profiling, structure elucidation, and CYP450
r*e
13 楼
非常不错的总结!
我也比较支持KRas induced adenocarcinoma是从type2 cell出来的,从histology很容
易看到。
另外ccsp promoter的specificity比较难说,至少ccsp-rtTA的表达在type2 cell。我当
时看某些文献也糊涂了半天。见G&D 2001 15:3249
and
is
opportunity
【在 H*****e 的大作中提到】
: Wow, on the top list!
: Well, I never expect to be on the top list. This reason is that I am not
: here very often. Also apologize to those are discussing about the topic and
: expect me to give my opinion.
: I believe that the previous title regarding to someone retract her paper is
: misleading. So it is necessary to clear some issue and have an opportunity
: to draw more discussion. Now back to the stem cell issue not the Amy or
: Carla although name may be mentioned but please ignore my own personal
: opinion on both of them. Also I like to restrict my view on lung and lung
: cancer in case that I forget type lung.
我也比较支持KRas induced adenocarcinoma是从type2 cell出来的,从histology很容
易看到。
另外ccsp promoter的specificity比较难说,至少ccsp-rtTA的表达在type2 cell。我当
时看某些文献也糊涂了半天。见G&D 2001 15:3249
and
is
opportunity
【在 H*****e 的大作中提到】
: Wow, on the top list!
: Well, I never expect to be on the top list. This reason is that I am not
: here very often. Also apologize to those are discussing about the topic and
: expect me to give my opinion.
: I believe that the previous title regarding to someone retract her paper is
: misleading. So it is necessary to clear some issue and have an opportunity
: to draw more discussion. Now back to the stem cell issue not the Amy or
: Carla although name may be mentioned but please ignore my own personal
: opinion on both of them. Also I like to restrict my view on lung and lung
: cancer in case that I forget type lung.
g*e
15 楼
以及java这种不care平台的语言?
H*e
16 楼
No evidence!
all
all
l*n
18 楼
docker底层只是linux,在windows/mac里是跑在linux虚拟机上的
enjoys
【在 g*********e 的大作中提到】
: Docker
: The Docker Engine container comprises just the application and its
: dependencies. It runs as an isolated process in userspace on the host
: operating system, sharing the kernel with other containers. Thus, it enjoys
: the resource isolation and allocation benefits of VMs but is much more
: portable and efficient.
: 似乎他需要做每个container里面所有bin/lib 和 local OS的衔接,这个不好做吧?比
: 如linux 里面用fork() exec(), windows里是createProcess(), docker是不是都得安
: 排好这些?
enjoys
【在 g*********e 的大作中提到】
: Docker
: The Docker Engine container comprises just the application and its
: dependencies. It runs as an isolated process in userspace on the host
: operating system, sharing the kernel with other containers. Thus, it enjoys
: the resource isolation and allocation benefits of VMs but is much more
: portable and efficient.
: 似乎他需要做每个container里面所有bin/lib 和 local OS的衔接,这个不好做吧?比
: 如linux 里面用fork() exec(), windows里是createProcess(), docker是不是都得安
: 排好这些?
N*m
24 楼
http://en.wikipedia.org/wiki/LXC
enjoys
【在 g*********e 的大作中提到】
: Docker
: The Docker Engine container comprises just the application and its
: dependencies. It runs as an isolated process in userspace on the host
: operating system, sharing the kernel with other containers. Thus, it enjoys
: the resource isolation and allocation benefits of VMs but is much more
: portable and efficient.
: 似乎他需要做每个container里面所有bin/lib 和 local OS的衔接,这个不好做吧?比
: 如linux 里面用fork() exec(), windows里是createProcess(), docker是不是都得安
: 排好这些?
enjoys
【在 g*********e 的大作中提到】
: Docker
: The Docker Engine container comprises just the application and its
: dependencies. It runs as an isolated process in userspace on the host
: operating system, sharing the kernel with other containers. Thus, it enjoys
: the resource isolation and allocation benefits of VMs but is much more
: portable and efficient.
: 似乎他需要做每个container里面所有bin/lib 和 local OS的衔接,这个不好做吧?比
: 如linux 里面用fork() exec(), windows里是createProcess(), docker是不是都得安
: 排好这些?
H*e
25 楼
I was asked a question whether it is meaningful to search the cancer origin
of lung cancer in kras model.
Actually, I found that I have no answer after taking more thought about it
and why I am doing it. So I open it for more discussion:
The promoter driving Kras is SP-C, active in both clara and type II cells.
I get myself into it because of Carla's finding on the stem cells. Since I
could not find the evidence to support stem cells, I then asked myself which
cell can form cancer. Obviously, both can based on literature. So I am
really lost on this project. As for Kras, it is then probably not important
since it may only represents for one out 6-7 human lung adenocarcinoma.
Then am I on it because I am on it?
The only reason that I guess that I like to continue is also from Carla's
work on the Kras and EGFR stem cells, which suggests that different gene
mutation may have different impacts on different cells.
of lung cancer in kras model.
Actually, I found that I have no answer after taking more thought about it
and why I am doing it. So I open it for more discussion:
The promoter driving Kras is SP-C, active in both clara and type II cells.
I get myself into it because of Carla's finding on the stem cells. Since I
could not find the evidence to support stem cells, I then asked myself which
cell can form cancer. Obviously, both can based on literature. So I am
really lost on this project. As for Kras, it is then probably not important
since it may only represents for one out 6-7 human lung adenocarcinoma.
Then am I on it because I am on it?
The only reason that I guess that I like to continue is also from Carla's
work on the Kras and EGFR stem cells, which suggests that different gene
mutation may have different impacts on different cells.
g*a
28 楼
多谢各位解答
我疑惑的就是,mike也是重视家庭的人, 貌似他所作的一切最终目的和他爸一样, 是为
了维持他的家族
所以杀掉fredo有点不合拍
而且之前他其实是放了fredo生路的 ,只是永远不见而已
后来那么煽情的拥抱之后, 竟然又杀掉了他, 这个有点令人费解
可能每天看到fredo, 反而提醒了他很多
我疑惑的就是,mike也是重视家庭的人, 貌似他所作的一切最终目的和他爸一样, 是为
了维持他的家族
所以杀掉fredo有点不合拍
而且之前他其实是放了fredo生路的 ,只是永远不见而已
后来那么煽情的拥抱之后, 竟然又杀掉了他, 这个有点令人费解
可能每天看到fredo, 反而提醒了他很多
a*n
29 楼
主要是cgroup, aufs 和iptables 。docker其实最主要是dockerfile 每一行对应aufs
的管理。这个以前的lxc没有。
的管理。这个以前的lxc没有。
g*a
30 楼
mike的作为和老教父其实一样
为什么老教父家庭和谐, 很成功的样子
而Mike最后有点妻离子散, 很凄凉的感觉?
是时代变了么? 有其他深层原因没有
为什么老教父家庭和谐, 很成功的样子
而Mike最后有点妻离子散, 很凄凉的感觉?
是时代变了么? 有其他深层原因没有
n*r
36 楼
michael杀fredo是fredo要杀michael在先。
g*a
41 楼
多谢
可能是我没问明白
但acidia同学的确解答了我真正的疑问
mike刚知情的时候放了fredo生路, 他只是说fredo来看妈妈的时候通知他, 他好躲开.
没有要杀fredo的迹象
反而后来在connie鼓动下, 在mama葬礼上和fredo拥抱合好, 这之后杀了他.
我就是疑问这个
【在 n**********r 的大作中提到】
: 。。。。。。
: 我已经回答了。
: 第二集开头在nevada的家里开完party后,两个刺客朝michael的卧室开枪,试图杀死
: michael和他的老婆,这个是Fredo被Hyman Roth收买干出来的事情。michael后来查清
: 后当然要干掉fredo,而且fredo在古巴拒绝michael的一起上飞机的请求也印证了他心
: 里有鬼。
可能是我没问明白
但acidia同学的确解答了我真正的疑问
mike刚知情的时候放了fredo生路, 他只是说fredo来看妈妈的时候通知他, 他好躲开.
没有要杀fredo的迹象
反而后来在connie鼓动下, 在mama葬礼上和fredo拥抱合好, 这之后杀了他.
我就是疑问这个
【在 n**********r 的大作中提到】
: 。。。。。。
: 我已经回答了。
: 第二集开头在nevada的家里开完party后,两个刺客朝michael的卧室开枪,试图杀死
: michael和他的老婆,这个是Fredo被Hyman Roth收买干出来的事情。michael后来查清
: 后当然要干掉fredo,而且fredo在古巴拒绝michael的一起上飞机的请求也印证了他心
: 里有鬼。
c*e
42 楼
mike在葬礼上和fredo拥抱的那一段有个镜头是他抱着fredo,和他的保镖有个眼神的交
流。那个眼神感觉就是他给的go-ahead. 所以我觉得那个拥抱并不是mike原谅fredo,他只是
在给大家做戏,就像第一集里面他要选在给connie的儿子做教父的那个时刻来暗杀其他
家族的头。
流。那个眼神感觉就是他给的go-ahead. 所以我觉得那个拥抱并不是mike原谅fredo,他只是
在给大家做戏,就像第一集里面他要选在给connie的儿子做教父的那个时刻来暗杀其他
家族的头。
n*r
44 楼
让michael下定决心杀fredo的事情是他们两个人在nevada湖边小屋里面的对话。因为
michael对fredo很了解,这个人软弱,无能,爱bang waitress,当年在las vegas就被
外人当狗使唤。michael在谈话之前还幻想fredo只是糊涂笨蛋上了roth的当,没想到
fredo说出他是大哥,他也要在家族里说话算数的话,这个就使得fredo成为了暗杀
michael事件的主谋之一,如果fredo有了杀害michael的想法并且付诸实施,虽然没成
功,但是在michael立足未稳的时候肯定要解决这个心腹大患。至于留着他一条命,只
是渲染michael还是有一些人情味的。这种事情在历史上屡见不鲜,具体请参考明史和
近现代史。呵呵。
.
【在 g****a 的大作中提到】
: 多谢
: 可能是我没问明白
: 但acidia同学的确解答了我真正的疑问
: mike刚知情的时候放了fredo生路, 他只是说fredo来看妈妈的时候通知他, 他好躲开.
: 没有要杀fredo的迹象
: 反而后来在connie鼓动下, 在mama葬礼上和fredo拥抱合好, 这之后杀了他.
: 我就是疑问这个
michael对fredo很了解,这个人软弱,无能,爱bang waitress,当年在las vegas就被
外人当狗使唤。michael在谈话之前还幻想fredo只是糊涂笨蛋上了roth的当,没想到
fredo说出他是大哥,他也要在家族里说话算数的话,这个就使得fredo成为了暗杀
michael事件的主谋之一,如果fredo有了杀害michael的想法并且付诸实施,虽然没成
功,但是在michael立足未稳的时候肯定要解决这个心腹大患。至于留着他一条命,只
是渲染michael还是有一些人情味的。这种事情在历史上屡见不鲜,具体请参考明史和
近现代史。呵呵。
.
【在 g****a 的大作中提到】
: 多谢
: 可能是我没问明白
: 但acidia同学的确解答了我真正的疑问
: mike刚知情的时候放了fredo生路, 他只是说fredo来看妈妈的时候通知他, 他好躲开.
: 没有要杀fredo的迹象
: 反而后来在connie鼓动下, 在mama葬礼上和fredo拥抱合好, 这之后杀了他.
: 我就是疑问这个
g*a
45 楼
这个情节的确很像我们的历史, 所以很真实啊. 虽然软弱无能,但fredo也不甘心被mike
压着
第一集里的Mike真太牛了
立即成为我的偶像
【在 n**********r 的大作中提到】
: 让michael下定决心杀fredo的事情是他们两个人在nevada湖边小屋里面的对话。因为
: michael对fredo很了解,这个人软弱,无能,爱bang waitress,当年在las vegas就被
: 外人当狗使唤。michael在谈话之前还幻想fredo只是糊涂笨蛋上了roth的当,没想到
: fredo说出他是大哥,他也要在家族里说话算数的话,这个就使得fredo成为了暗杀
: michael事件的主谋之一,如果fredo有了杀害michael的想法并且付诸实施,虽然没成
: 功,但是在michael立足未稳的时候肯定要解决这个心腹大患。至于留着他一条命,只
: 是渲染michael还是有一些人情味的。这种事情在历史上屡见不鲜,具体请参考明史和
: 近现代史。呵呵。
:
: .
压着
第一集里的Mike真太牛了
立即成为我的偶像
【在 n**********r 的大作中提到】
: 让michael下定决心杀fredo的事情是他们两个人在nevada湖边小屋里面的对话。因为
: michael对fredo很了解,这个人软弱,无能,爱bang waitress,当年在las vegas就被
: 外人当狗使唤。michael在谈话之前还幻想fredo只是糊涂笨蛋上了roth的当,没想到
: fredo说出他是大哥,他也要在家族里说话算数的话,这个就使得fredo成为了暗杀
: michael事件的主谋之一,如果fredo有了杀害michael的想法并且付诸实施,虽然没成
: 功,但是在michael立足未稳的时候肯定要解决这个心腹大患。至于留着他一条命,只
: 是渲染michael还是有一些人情味的。这种事情在历史上屡见不鲜,具体请参考明史和
: 近现代史。呵呵。
:
: .
a*a
46 楼
你解读过度了, Fredo 说 " I didnt know it was a hit"
Fredo根本没想过杀Mike,只是想证明自己能做一些事情
【在 n**********r 的大作中提到】
: 让michael下定决心杀fredo的事情是他们两个人在nevada湖边小屋里面的对话。因为
: michael对fredo很了解,这个人软弱,无能,爱bang waitress,当年在las vegas就被
: 外人当狗使唤。michael在谈话之前还幻想fredo只是糊涂笨蛋上了roth的当,没想到
: fredo说出他是大哥,他也要在家族里说话算数的话,这个就使得fredo成为了暗杀
: michael事件的主谋之一,如果fredo有了杀害michael的想法并且付诸实施,虽然没成
: 功,但是在michael立足未稳的时候肯定要解决这个心腹大患。至于留着他一条命,只
: 是渲染michael还是有一些人情味的。这种事情在历史上屡见不鲜,具体请参考明史和
: 近现代史。呵呵。
:
: .
g*a
54 楼
fredo拉开窗帘
和刺客里应外合
见刺客无法逃脱, 又杀掉灭口
所以mike已开始就知道敌人有内线
请问这样了fredo还没有要伤害mike的意思?
和刺客里应外合
见刺客无法逃脱, 又杀掉灭口
所以mike已开始就知道敌人有内线
请问这样了fredo还没有要伤害mike的意思?
g*n
56 楼
Taken care of me!" You're my kid brother and you take care of me! Did you
ever think about that, did you ever once think about that? Send Fredo off to
do this, send Fredo off to do that! Let Fredo to take care of some Mickey
Mouse night club somewhere! Send Fredo to pick somebody up at the airport! I
'm your older brother, Mike, and I was stepped over!
【在 n**********r 的大作中提到】
: 记错了,i'm your older brother!
ever think about that, did you ever once think about that? Send Fredo off to
do this, send Fredo off to do that! Let Fredo to take care of some Mickey
Mouse night club somewhere! Send Fredo to pick somebody up at the airport! I
'm your older brother, Mike, and I was stepped over!
【在 n**********r 的大作中提到】
: 记错了,i'm your older brother!
S*A
57 楼
在 Michael 这个位置是一定要杀的 Fredo 的。
这个时规矩,不然老大 show weak, 性命不保。
我记得第一集 Michael 问过老教父的,老教父
说过叛徒一定要杀的,不然没法树立威信,鼓励
类似的事情再发生。第一集里面 Michael 的姐夫
就是这么被干掉的。是同样的两难,因为 Michael
的姐姐会恨一辈子的。
我隐约记得老教父说过,叛徒就算不杀掉,叛徒会
一直惦记自己害过老大,整天惶惶不安,不能像以前
那么衷心。有点什么矛盾就容易被外人利用。
Michael 最大的悲剧在于他娶了个美国老婆。他娶
的意大利老婆被炸死了。意大利老婆对家族绝对支持,
生很多儿子来继承家业。美国老婆看到势头不对,连
肚子里的都 abort 掉了。Michael 后继无人,附近
众叛亲离,这才Michael 是最悲凉的。老教父有个
意大利的老婆,后代里有 Michael 这样的杰出青年。
到 Michael 老了就算什么都没有了。
这个时规矩,不然老大 show weak, 性命不保。
我记得第一集 Michael 问过老教父的,老教父
说过叛徒一定要杀的,不然没法树立威信,鼓励
类似的事情再发生。第一集里面 Michael 的姐夫
就是这么被干掉的。是同样的两难,因为 Michael
的姐姐会恨一辈子的。
我隐约记得老教父说过,叛徒就算不杀掉,叛徒会
一直惦记自己害过老大,整天惶惶不安,不能像以前
那么衷心。有点什么矛盾就容易被外人利用。
Michael 最大的悲剧在于他娶了个美国老婆。他娶
的意大利老婆被炸死了。意大利老婆对家族绝对支持,
生很多儿子来继承家业。美国老婆看到势头不对,连
肚子里的都 abort 掉了。Michael 后继无人,附近
众叛亲离,这才Michael 是最悲凉的。老教父有个
意大利的老婆,后代里有 Michael 这样的杰出青年。
到 Michael 老了就算什么都没有了。
p*a
58 楼
nima, so true
a great wife is #1 important thing for a man to be sucessful
i don't understand, he gets so much money, no need to worry "can't afford to
raise".
should just have 10 babies.
【在 S*A 的大作中提到】
: 在 Michael 这个位置是一定要杀的 Fredo 的。
: 这个时规矩,不然老大 show weak, 性命不保。
: 我记得第一集 Michael 问过老教父的,老教父
: 说过叛徒一定要杀的,不然没法树立威信,鼓励
: 类似的事情再发生。第一集里面 Michael 的姐夫
: 就是这么被干掉的。是同样的两难,因为 Michael
: 的姐姐会恨一辈子的。
: 我隐约记得老教父说过,叛徒就算不杀掉,叛徒会
: 一直惦记自己害过老大,整天惶惶不安,不能像以前
: 那么衷心。有点什么矛盾就容易被外人利用。
a great wife is #1 important thing for a man to be sucessful
i don't understand, he gets so much money, no need to worry "can't afford to
raise".
should just have 10 babies.
【在 S*A 的大作中提到】
: 在 Michael 这个位置是一定要杀的 Fredo 的。
: 这个时规矩,不然老大 show weak, 性命不保。
: 我记得第一集 Michael 问过老教父的,老教父
: 说过叛徒一定要杀的,不然没法树立威信,鼓励
: 类似的事情再发生。第一集里面 Michael 的姐夫
: 就是这么被干掉的。是同样的两难,因为 Michael
: 的姐姐会恨一辈子的。
: 我隐约记得老教父说过,叛徒就算不杀掉,叛徒会
: 一直惦记自己害过老大,整天惶惶不安,不能像以前
: 那么衷心。有点什么矛盾就容易被外人利用。
n*0
60 楼
你愿意做Micheal么?
他过得快乐么?
他有选择么?
他过得快乐么?
他有选择么?
l*a
68 楼
前一阵子,不知道是不是《to kill the Irishman》的作者,
点过犹太黑帮和西西里黑帮的区别。说意大利人是真正的信奉天下
唯我独尊。干掉对手从来是business的一部分。这里根本没什么
信任可言。犹太人尼,就比较抱团。言下之意,greene 能搞掉
克里夫兰的意大利黑帮-也跟黑帮本来内部倾轧有关。
有个有争议的说法,今天的美国的治安每下愈况-有人就缅怀过去
黑帮统治street的时候-至少没有现在黑鬼/老莫横行街头的烂剧。
老板的儿子也不是好当的。现代的长子就是老爸的期望过高,为了
报答老爸,殚精竭虑做企业,加班,半夜车祸,横死。老郑的另外
一个儿子自杀,贿赂案败露. 何况黑帮?
貌似,现在的富二代,不可同日而语了?
【在 n*********0 的大作中提到】
: 嗯,醒握天下权,醉卧美人膝。
: 男人终极梦想。
: 可是另一面,是生活在 paranoia 里。有片刻安宁么?妻离子散,兄弟相残。很悲剧。
b*n
69 楼
其实如果大家看过原著,这个问题在书的最后,借黑根的嘴解释的很清楚。
“还有一些事情,我也要对你直话直说。老头子死后,迈克尔被定为杀害对象。你可知
道是谁定的吗?是忒希奥。因此,忒希奥必须杀掉。卡罗,也必须杀掉。因为背叛行为
是不
可宽容的。迈克尔本来也可能宽容这种行为,但是,凡是犯了这种错误的人,都绝不会
宽容
自己。他们始终心怀鬼胎,因此他们始终是危险的。迈克尔也实在喜欢忒希奥;迈克尔
也真
心爱他妹妹。但是,要是让忒希奥和卡罗这两人造遥法外,那他就等于对你、对他的孩
子、
对他的全家、对我和我的家庭,推卸责任。这两个家伙对咱们大家,对咱们大家的生命
,都
是一颗定时炸弹。”
“还有一些事情,我也要对你直话直说。老头子死后,迈克尔被定为杀害对象。你可知
道是谁定的吗?是忒希奥。因此,忒希奥必须杀掉。卡罗,也必须杀掉。因为背叛行为
是不
可宽容的。迈克尔本来也可能宽容这种行为,但是,凡是犯了这种错误的人,都绝不会
宽容
自己。他们始终心怀鬼胎,因此他们始终是危险的。迈克尔也实在喜欢忒希奥;迈克尔
也真
心爱他妹妹。但是,要是让忒希奥和卡罗这两人造遥法外,那他就等于对你、对他的孩
子、
对他的全家、对我和我的家庭,推卸责任。这两个家伙对咱们大家,对咱们大家的生命
,都
是一颗定时炸弹。”
j*e
70 楼
我现在看到有人划独木船,就会想到Fredo被干掉了,可见那三个高潮镜头还是蛮成
功的。
功的。
相关阅读
求高人指点美国的化工原材料信息求审稿呀,关于fuel cell, polymer morphology, Nafion想买点 pdCpA,paper help bao zi thanks天天做化学试验会短命求paper:http://iopscience.iop.org/0957-0233/12/5/309/pdf/e10509.pdf包子求 文章O-1 PP Approved求问水基聚氨酯合成的综述文章化学人留在美国的女士居多fresh 化学/环境毒理PHD求工作听说国内生物本科可以直接考试MATCH北美住院医了把教授肛门塞上手榴弹有没有人考国American Association of Bioanalysis 的Technologist license?求实习推荐(半导体氧化物,光电转化)平时大家如何健身?读过多的书 只会让人颓废paper help, thx在中国学IT的新移民朋友半年就找到专业工作了纳米新杂志?