in this theory i will suppose the dynamic is represant the 5th dimension this subject require much mathematical and theoratical proving.
i will explain how can consider the dynamic is the 5th dimension .
first the physical fact that the universe
السبت، 18 يوليو 2009
الأربعاء، 15 يوليو 2009
the gene axises theory
we will focouse to prove this theory on the tumer supressor genes and their role in the cells tissues when they will be active and their effect on the other genes and will foucouse the growth factor and their role too this will help us to understand the phisology well genes such p53 and p73 and p63 and rb can tell us much dealthes about their functions not just as tumer supressor genes but other roles in the cell and their effect on the transcription process for the other genes and their role to control the growth process and the cell divisions the genes axises theory can explain the protein arrangement in the cells tissusand the programed steps in the cells
الأحد، 12 يوليو 2009
the genes axises teory
in this blog i will speak just about the genes line or gene axises schemes that indicate the genes line function in the tissues cells we can represant that by diagrams the scheme to indicate the gene role in the tissues cell to explain that we study them in certain cell
السبت، 11 يوليو 2009
the genes axises theory
in the privious blog i wrote much about this theory we can think that this theory may will explain the mechanisim of the tumer supressor genes and the oncagenes these genes play an certain role in the cell their action will be efective in te cell this action it efect the other genes in the same genes line or genes axises genes such p53 will be active in different genes lines as we showed priviously we can understand the relation between these genes as p53 and the other genes like p73 mdm2 p63 etc the tumer supressor genes role in the cell and the relation between them will enable us to understand the genes lines theory the defection in the tumer supressor genes will cause defection in the cell and disorder the other genes functions in the cell that this defacted gene active in it that means the genes line disordered for example when gene p53 will be defected will cause canser and the other active genes in the cell which transformed to cansrous cell will disordered the same thing to the fetal genes in the embryo growth will cause the death to the embryo and will disorder the other genes actions
الجمعة، 10 يوليو 2009
new discovered gene
NIH Scientists Identify Gene for Fatal Childhood Disorder, Niemann-Pick Type C: Finding Points to Critical New Steps in Cholesterol Processing
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Download Adobe ReaderFor release: Thursday, July 10, 1997
Bethesda, MD -- After decades of work, scientists at the National Institutes of Health have identified a gene alteration associated with the fatal childhood cholesterol disorder Niemann-Pick type C (NPC). Learning how the gene functions may lead to the first effective treatment for the disease and to a fundamental new understanding of how cholesterol is processed in the body.
The gene, known as NPC1, is located on human chromosome 18. NPC causes progressive deterioration of the nervous system by blocking the movement of cholesterol within cells. The finding opens the door to improved diagnosis and understanding of this neurological disorder, which is usually fatal by age 25, and to the design of therapies that may correct the underlying problem. The finding also may contribute to the understanding of atherosclerosis, a more common killer associated with cholesterol buildup. Atherosclerosis is an accumulation of fatty tissue inside arteries that blocks blood flow, leading to heart disease and stroke.
"This discovery is an excellent example of how research on rare brain disorders often pays off in other ways," says Zach W. Hall, Ph.D., Director of the National Institute of Neurological Disorders and Stroke (NINDS). "By identifying this gene, we not only take a crucial step forward in understanding this devastating disorder, but also gain insights into problems that affect every one of us."
The NPC1 finding is the first step toward developing a cure for NPC. "This gene reveals a new way that cells handle cholesterol," says Peter G. Pentchev, Ph.D., of NINDS. "It provides a fundamental understanding of a previously undefined pathway of cholesterol metabolism. Like motor mechanics, we have to know what's wrong before we can fix it." Dr. Pentchev and his colleagues at NINDS have studied NPC for almost 20 years. Other key members of the team that identified the human gene include Eugene D. Carstea, Ph.D., formerly of the NINDS; Jill A. Morris, Ph.D., of NINDS; and Danilo A. Tagle, Ph.D., and Melissa A. Rosenfeld, Ph.D., of the National Human Genome Research Institute (NHGRI).
Collaborating scientists, led by William J. Pavan, Ph.D., of NHGRI, identified the same gene in a mouse model for NPC. The human and mouse gene findings appear in back-to-back reports in the July 11, 1997, issue of the journal Science. , NPC develops when a person receives two altered copies of the gene -- one from each parent. Carriers of the disease, who possess a single copy of the altered gene, sometimes develop subtle abnormalities in cholesterol metabolism. However, they remain healthy, and most do not know they are carriers until they have an affected child. NPC often appears at random in families with no history of the disorder, and it occurs in individuals from many ethnic groups.
Approximately 300 Americans are afflicted with NPC, in which low-density lipoprotein (LDL)-derived cholesterol accumulates in digestive compartments called lysosomes that are found within cells of the brain, liver, spleen, lungs, and bone marrow. LDL is the so-called "bad" cholesterol molecule linked to atherosclerosis. Symptoms of NPC usually appear in early childhood and typically include an enlarged spleen and liver, poor muscle control, impaired eye movements, slurred speech, and dementia. Drugs can control some symptoms of NPC, and laboratory studies suggest that low-cholesterol diets and cholesterol-lowering drugs might be beneficial. However, there is no proven treatment that can slow the course of the disease.
"The identification of this gene, the fruit of a successful partnership between scientists and families, is a significant step in NPC research," says Dr. Tagle, senior author of the human gene paper. "Our search was greatly accelerated by the tools and resources provided by the Human Genome Project. Moreover, our findings shed new light on how cells metabolize cholesterol that may be different from pathways involved in cardiovascular diseases and provide insights on how cholesterol affects brain functions."
The discovery of the NPC1 gene will improve scientific understanding of how cells process and transport cholesterol within the cell. Since the NPC1 gene affects the brain, it also may provide insight about how cholesterol affects brain development and the formation of myelin, a fatty substance that improves transmission of nerve signals.
Although the researchers do not know precisely how it works, the NPC1 protein is similar in structure to several other proteins involved in cholesterol regulation. The protein is also similar to proteins found in yeast and worms, suggesting that it is important for survival because it has remained largely unchanged throughout millions of years of evolution. The protein's presence in these organisms makes them a powerful resource for testing new therapies and learning how the protein works. Inserting copies of the NPC1 gene into cultured skin cells from NPC patients corrects the abnormal cholesterol buildup, suggesting that gene therapy might eventually be able to cure the disease. The first step to successful gene therapy, however, is for scientists to find better ways to insert genes into cells of the brain, where the worst symptoms of NPC arise. It may also be possible to use drugs to reverse the abnormal cholesterol storage.
"Researchers should be able to test new therapies relatively quickly because they already have a mouse model with the mutated gene," says Dr. Pavan, senior author of the mouse gene report. "Usually, scientists must spend time creating animal models with the mutated gene after the human gene is discovered."
The NIH researchers located NPC1 by a combination of approaches, including conventional positional cloning techniques and a strategy using yeast artificial chromosomes (YACs) containing large pieces of human DNA, to narrow the region likely to contain the gene. To date, the researchers have identified eight different NPC1 mutations in nine unrelated NPC families. They hope to link specific mutations to differences in the way the disease manifests itself in particular patients, such as age of onset. "In spite of the wide variety of mutations, the discovery of the gene will now enable the development of genetic tests for prenatal diagnosis and assessment of carrier status in families affected by this devastating disorder," says Dr. Carstea. Dr. Carstea recently left the NINDS, where he headed the gene cloning collaboration, to take up a new post as Director of the Saccomano Research Institute at St. Mary's Hospital, Grand Junction, Colorado.
While 95 percent of the NPC families tested so far have mutations in the NPC1 gene, the disease in some families shows no correlation with chromosome 18. This means there must be a second NPC gene on another chromosome. This gene probably controls another step in the newly identified cholesterol pathway that goes awry in NPC, says Dr. Pentchev. The researchers now plan to focus on locating the second NPC gene and analyzing how different mutations affect the onset and symptoms of the disease.
Researchers from the Czech Republic, France, Israel, New Zealand, Japan, the Netherlands, and several United States institutions contributed to these findings by sharing data and cell lines from affected families. The Niemann-Pick Foundation of the United Kingdom also helped the effort by locating families afflicted with the disorder. The investigators received major financial support for this work from the Ara Parseghian Medical Research Foundation and from the National Niemann-Pick Disease Foundation.
"Because of the dedication of the researchers and generous donations from people all over the world, we have been able to accomplish the isolation of the gene responsible for NPC. This was our first goal when we started the Ara Parseghian Medical Research Foundation two and a half years ago," says Ara Parseghian, former head football coach at the University of Notre Dame in Indiana. Coach Parseghian's three youngest grandchildren suffer from NPC. His grandson, Michael, died this past March, four days before his tenth birthday. Michael's two sisters suffer from various stages of the disorder. "We have the ball, now we have to make it down the field and into the end zone. We can only win this fight by finding out why the gene acts the way it does. And finally, we want to achieve the ultimate victory - a cure for NPC. This is a race against time to save all children afflicted with this terrible disease," says Coach Parseghian.
The NINDS and the NHGRI are part of the National Institutes of Health located in Bethesda, Maryland. NINDS is the nation's leading supporter of research on the brain and nervous system and a lead agency in the Congressionally designated Decade of the Brain. The NHGRI is a major partner in the Human Genome Project, an international research effort to map the estimated 50,000-100,000 genes and read the complete set of genetic instructions encoded in human DNA.
Carstea, E.D.; Morris, J.A.; et. al. "The Niemann-Pick C gene: Homology to other mediators of cholesterol homeostasis." Science, Vol. 277, July 11, 1997, pp. 229-231.
Loftus, S.K.; Morris, J.A.; et. al. "Murine model of Niemann-Pick C1: Mutation in a cholesterol homeostasis gene." Science, Vol. 277, July 11, 1997, pp. 232-235.
Gu, J.Z.; Carstea, E.D.; et. al. "Substantial narrowing of the Niemann-Pick C candidate interval by yeast artificial chromosome complementation." Proceedings of the National Academy of Science of the United States of America, Vol. 94, July 1997, pp. 7378-7383.
Date Last Modified: Tuesday, March 08, 2005
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
National Institute of Neurological Disorders and Stroke
Home | About NINDS | Disorders A - Z | Research Funding | News From NINDS | Find People | Training | Research | American Reinvestment and Recovery Act
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Skip secondary menuHome
Disorders A - Z
News From NINDS
Press ReleasesNews Articles
Funding News
Events
Calendar of Events
Proceedings
Congressional
Testimony
Research Funding
Training & Career Awards
Research Programs
Find People
About NINDS
Email this page
Print-friendly version
Download Adobe ReaderFor release: Thursday, July 10, 1997
Bethesda, MD -- After decades of work, scientists at the National Institutes of Health have identified a gene alteration associated with the fatal childhood cholesterol disorder Niemann-Pick type C (NPC). Learning how the gene functions may lead to the first effective treatment for the disease and to a fundamental new understanding of how cholesterol is processed in the body.
The gene, known as NPC1, is located on human chromosome 18. NPC causes progressive deterioration of the nervous system by blocking the movement of cholesterol within cells. The finding opens the door to improved diagnosis and understanding of this neurological disorder, which is usually fatal by age 25, and to the design of therapies that may correct the underlying problem. The finding also may contribute to the understanding of atherosclerosis, a more common killer associated with cholesterol buildup. Atherosclerosis is an accumulation of fatty tissue inside arteries that blocks blood flow, leading to heart disease and stroke.
"This discovery is an excellent example of how research on rare brain disorders often pays off in other ways," says Zach W. Hall, Ph.D., Director of the National Institute of Neurological Disorders and Stroke (NINDS). "By identifying this gene, we not only take a crucial step forward in understanding this devastating disorder, but also gain insights into problems that affect every one of us."
The NPC1 finding is the first step toward developing a cure for NPC. "This gene reveals a new way that cells handle cholesterol," says Peter G. Pentchev, Ph.D., of NINDS. "It provides a fundamental understanding of a previously undefined pathway of cholesterol metabolism. Like motor mechanics, we have to know what's wrong before we can fix it." Dr. Pentchev and his colleagues at NINDS have studied NPC for almost 20 years. Other key members of the team that identified the human gene include Eugene D. Carstea, Ph.D., formerly of the NINDS; Jill A. Morris, Ph.D., of NINDS; and Danilo A. Tagle, Ph.D., and Melissa A. Rosenfeld, Ph.D., of the National Human Genome Research Institute (NHGRI).
Collaborating scientists, led by William J. Pavan, Ph.D., of NHGRI, identified the same gene in a mouse model for NPC. The human and mouse gene findings appear in back-to-back reports in the July 11, 1997, issue of the journal Science. , NPC develops when a person receives two altered copies of the gene -- one from each parent. Carriers of the disease, who possess a single copy of the altered gene, sometimes develop subtle abnormalities in cholesterol metabolism. However, they remain healthy, and most do not know they are carriers until they have an affected child. NPC often appears at random in families with no history of the disorder, and it occurs in individuals from many ethnic groups.
Approximately 300 Americans are afflicted with NPC, in which low-density lipoprotein (LDL)-derived cholesterol accumulates in digestive compartments called lysosomes that are found within cells of the brain, liver, spleen, lungs, and bone marrow. LDL is the so-called "bad" cholesterol molecule linked to atherosclerosis. Symptoms of NPC usually appear in early childhood and typically include an enlarged spleen and liver, poor muscle control, impaired eye movements, slurred speech, and dementia. Drugs can control some symptoms of NPC, and laboratory studies suggest that low-cholesterol diets and cholesterol-lowering drugs might be beneficial. However, there is no proven treatment that can slow the course of the disease.
"The identification of this gene, the fruit of a successful partnership between scientists and families, is a significant step in NPC research," says Dr. Tagle, senior author of the human gene paper. "Our search was greatly accelerated by the tools and resources provided by the Human Genome Project. Moreover, our findings shed new light on how cells metabolize cholesterol that may be different from pathways involved in cardiovascular diseases and provide insights on how cholesterol affects brain functions."
The discovery of the NPC1 gene will improve scientific understanding of how cells process and transport cholesterol within the cell. Since the NPC1 gene affects the brain, it also may provide insight about how cholesterol affects brain development and the formation of myelin, a fatty substance that improves transmission of nerve signals.
Although the researchers do not know precisely how it works, the NPC1 protein is similar in structure to several other proteins involved in cholesterol regulation. The protein is also similar to proteins found in yeast and worms, suggesting that it is important for survival because it has remained largely unchanged throughout millions of years of evolution. The protein's presence in these organisms makes them a powerful resource for testing new therapies and learning how the protein works. Inserting copies of the NPC1 gene into cultured skin cells from NPC patients corrects the abnormal cholesterol buildup, suggesting that gene therapy might eventually be able to cure the disease. The first step to successful gene therapy, however, is for scientists to find better ways to insert genes into cells of the brain, where the worst symptoms of NPC arise. It may also be possible to use drugs to reverse the abnormal cholesterol storage.
"Researchers should be able to test new therapies relatively quickly because they already have a mouse model with the mutated gene," says Dr. Pavan, senior author of the mouse gene report. "Usually, scientists must spend time creating animal models with the mutated gene after the human gene is discovered."
The NIH researchers located NPC1 by a combination of approaches, including conventional positional cloning techniques and a strategy using yeast artificial chromosomes (YACs) containing large pieces of human DNA, to narrow the region likely to contain the gene. To date, the researchers have identified eight different NPC1 mutations in nine unrelated NPC families. They hope to link specific mutations to differences in the way the disease manifests itself in particular patients, such as age of onset. "In spite of the wide variety of mutations, the discovery of the gene will now enable the development of genetic tests for prenatal diagnosis and assessment of carrier status in families affected by this devastating disorder," says Dr. Carstea. Dr. Carstea recently left the NINDS, where he headed the gene cloning collaboration, to take up a new post as Director of the Saccomano Research Institute at St. Mary's Hospital, Grand Junction, Colorado.
While 95 percent of the NPC families tested so far have mutations in the NPC1 gene, the disease in some families shows no correlation with chromosome 18. This means there must be a second NPC gene on another chromosome. This gene probably controls another step in the newly identified cholesterol pathway that goes awry in NPC, says Dr. Pentchev. The researchers now plan to focus on locating the second NPC gene and analyzing how different mutations affect the onset and symptoms of the disease.
Researchers from the Czech Republic, France, Israel, New Zealand, Japan, the Netherlands, and several United States institutions contributed to these findings by sharing data and cell lines from affected families. The Niemann-Pick Foundation of the United Kingdom also helped the effort by locating families afflicted with the disorder. The investigators received major financial support for this work from the Ara Parseghian Medical Research Foundation and from the National Niemann-Pick Disease Foundation.
"Because of the dedication of the researchers and generous donations from people all over the world, we have been able to accomplish the isolation of the gene responsible for NPC. This was our first goal when we started the Ara Parseghian Medical Research Foundation two and a half years ago," says Ara Parseghian, former head football coach at the University of Notre Dame in Indiana. Coach Parseghian's three youngest grandchildren suffer from NPC. His grandson, Michael, died this past March, four days before his tenth birthday. Michael's two sisters suffer from various stages of the disorder. "We have the ball, now we have to make it down the field and into the end zone. We can only win this fight by finding out why the gene acts the way it does. And finally, we want to achieve the ultimate victory - a cure for NPC. This is a race against time to save all children afflicted with this terrible disease," says Coach Parseghian.
The NINDS and the NHGRI are part of the National Institutes of Health located in Bethesda, Maryland. NINDS is the nation's leading supporter of research on the brain and nervous system and a lead agency in the Congressionally designated Decade of the Brain. The NHGRI is a major partner in the Human Genome Project, an international research effort to map the estimated 50,000-100,000 genes and read the complete set of genetic instructions encoded in human DNA.
Carstea, E.D.; Morris, J.A.; et. al. "The Niemann-Pick C gene: Homology to other mediators of cholesterol homeostasis." Science, Vol. 277, July 11, 1997, pp. 229-231.
Loftus, S.K.; Morris, J.A.; et. al. "Murine model of Niemann-Pick C1: Mutation in a cholesterol homeostasis gene." Science, Vol. 277, July 11, 1997, pp. 232-235.
Gu, J.Z.; Carstea, E.D.; et. al. "Substantial narrowing of the Niemann-Pick C candidate interval by yeast artificial chromosome complementation." Proceedings of the National Academy of Science of the United States of America, Vol. 94, July 1997, pp. 7378-7383.
Date Last Modified: Tuesday, March 08, 2005
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
National Institute of Neurological Disorders and Stroke
Home | About NINDS | Disorders A - Z | Research Funding | News From NINDS | Find People | Training | Research | American Reinvestment and Recovery Act
Careers@NINDS | FOIA (NIH) | Accessibility Policy | Contact Us | Privacy Statement
new theory about genetics
i would like to speak about this theory i will show some points about this theory
1- every gene doesnot do it function seprably or single it does it function in the group of the active gene in the cell.
2-the genes group which active in the cell named gene
s lines or genes axises.
3-for every tissues cell their genes lines.
4-the gene it does its function in genes line or genes axises depending on its sequences and its codons
5- the cells diffrentation depend on the development of the genes lines.
6- the genes lines development means that whenever genes line be activated will setup new cells conndations to activate new genes line
7-the growth aging and degenarating are controlled by
the genes line
8-the molcular signals that the gene sends them are efecting relatively on the gene line that this gene is active in it these signals such the protien transcriepts or mRNA represants the genes code and the genes lines code for all active gene in the cell represant the genes line or(genes axises) codes which set up to new genes line in cell difrentation.
9-the genes line activated depending the cells environment conditions and other genes activation.
10-the genes line or genes axises consist of sub lines
11- the stem cell represant one of the genes lines or axises theory evideness
1- every gene doesnot do it function seprably or single it does it function in the group of the active gene in the cell.
2-the genes group which active in the cell named gene
s lines or genes axises.
3-for every tissues cell their genes lines.
4-the gene it does its function in genes line or genes axises depending on its sequences and its codons
5- the cells diffrentation depend on the development of the genes lines.
6- the genes lines development means that whenever genes line be activated will setup new cells conndations to activate new genes line
7-the growth aging and degenarating are controlled by
the genes line
8-the molcular signals that the gene sends them are efecting relatively on the gene line that this gene is active in it these signals such the protien transcriepts or mRNA represants the genes code and the genes lines code for all active gene in the cell represant the genes line or(genes axises) codes which set up to new genes line in cell difrentation.
9-the genes line activated depending the cells environment conditions and other genes activation.
10-the genes line or genes axises consist of sub lines
11- the stem cell represant one of the genes lines or axises theory evideness
الأربعاء، 8 يوليو 2009
the genes axises
in this blog we can speak more about the prvious subject (the gene axises)we said in the privious blog that the genes are coding the cell information and will limit its line (the direction of defrentation and development the genes are classified into groups these groups set up there some the other and represant the lines of genes function each group depend on the prvious genes group functions for example in plants the soot formed first the root genes will set up the other genes axises which are the leaf genes the scond step of the plant forming then the trucks genes will be activated depending on the privious genes axises (the root genes axises and the leaf genes axises)
الثلاثاء، 7 يوليو 2009
the stem cells and the genes axises
the stem cells can be considered as the way that explain the genes axises when we folow the stem cell development we will find the genes instructions play an important role to direct the cell to be in one line the genes which will be active in the stem cell will control its development to form tissue or organe in the embryo growth for example the stem cell which forms the hand tissues it folowed the genes codes and instructions these genes that activated in this cell represent the genes axises in this cell the gene will not be activated randomly it will depend on other genes activation this series is the basic in the development of baitic cells there some important example to this concept (gene axises)such the tumer supressor genes and the tumri genes the genes axises regulates the genome it represent the sub maps in the general map (the genome)
الاثنين، 6 يوليو 2009
the gene lines or gene axises theory
in this blog i decided to explain more the gene series theory this theory explain the way that genes form the embryo cells this depend on new concept i can name it the genes lines the gene lines or gene axises that start the codes of the tissues cells it they control the forming steps cells the stem cells in my opinion good evideness to thhis theory as i said in pravious blog the gene lines will start first depending on pravious gene line to start then will set up to new gene lines
الجمعة، 3 يوليو 2009
the genes serries
in the beginning iwould like to say that the genes represant the structuresof the life the genes do not start it function randomly they depend on other gene function to start its function for example i will try to explain the embrioligical formation it start from the crossing and forming zigute the genes which be active will make good environment to enable other genes to start their function to begin new series this lead to embrio development to form new cells to make tissues it will continue and make the stem cells we can understand that in the steps of the embrio growth this is easy wards to describe my new theory the gene seris
الخميس، 2 يوليو 2009
اعرف جيناتك
لقد فكرت كثيرا في البداية التي يتوجب علي ان ابداء بها في ما اعتبره جزء من البحث العلمي في البداية اود ان اعرف ما هي الجينات الجينات هي تسلسلات من الاحماض النووية المسوؤلة عن تحديد المواصفات البايلوجية الكاملة لكل كائن حي يمتلك الانسان مايقارب 30 الف الى 40 الف جينة سوف اقوم بذكر وتصنيف جزء يسير منها في مدونات لاحقة الجينات تقع على مواقع محددة وثابتة على الكروموسومات قد تكون هذه مجرد مقتطفات يسيرة عن موضوع متشعب ودقيق الجينات هي المسؤولة بدرجة كبيرة عن تكويننا وامراضنا وواشكالنا تتالف الاحماض النووية التي تكون الجينات من اربع رموز هذه الرموز هي عبارة عن جزيئات عضوية تعرف بالنيوكليوتيدات تتالف النيوكليوتيدات من سكر رايبوز و فوسفات و قواعد نايتروجينة هي الادنيت والثايمين للدنا او اليوراسيل للرنا والجواينين والسايتوسين كما تتالف الجينات (تسلسات الدنا ) من الاحماض الاميتة التي ساذكرها في مدونة لاحقة هذه مقدمة بسيطة للحديث عتن الجبنات مرفقة بصورة
الجينات
لقد فكرت كثيرا في البداية التي يتوجب علي ان ابداء بها في ما اعتبره جزء من البحث العلمي في البداية اود ان اعرف ما هي الجينات الجينات هي تسلسلات من الاحماض الامينية ال
الاثنين، 29 يونيو 2009
الأحد، 28 يونيو 2009
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