Which kind of cloning is beneficial ?

Cloning has been a great development for science world ever since, but unfortunately there have been some ethical issues relating to the two specific kind of cloning. One is reproductive cloning. Reproductive cloning is ‘‘a type of cloning which is performed for the purpose of creating a duplicate copy of another organism. It is accomplished using a process called somatic cell nuclear transfer. In 1996, Scottish researchers announced that they had successfully cloned the first mammal, a sheep that came to be known as Dolly. In somatic cell nuclear transfer, scientists extract the nucleus of a somatic cell, a cell which can come from anywhere in the body, and insert it into an egg which has had its nucleus removed. The egg is stimulated, and it begins dividing and growing, developing into an embryo which can be implanted into a gestational surrogate and carried to term.'' The problem with this kind of cloning is that ''some people believe that life begins at conception, and they feel that reproductive cloning is unnatural and that it could potentially violate their religious beliefs. Others are simply perturbed by the idea of being able to clone copies of living organisms, and they wonder about the risks of using cloned animals in the food supply. Psychologists and other people who study development are intrigued by the potential to use reproductive cloning as a test of the famous nature versus nurture debate.'' There are other issues from a scientific perspective. ''Clones appear to have shorter lifespans, leading to concerns about the disadvantages of reproductive cloning. There is also the risk of losing genetic diversity as a result of using cloning, especially in the agricultural industry, where the temptation to use standardized animals is understandably tempting. Like any new scientific development, reproductive cloning was heavily challenged in the scientific community when it first emerged, especially after scandals in which scientists claimed to have cloned animals but actually hadn't.'' 

On the other hand, there is this other cloning called Therapeutic cloning. This cloning is ''cloning which is performed for the purpose of medical treatment. For example, it could theoretically be used to grow a replacement organ, to generate skin for a burn victim, or to create nerve cells for someone suffering from brain damage or a neurological condition. Therapeutic cloning is closely related to reproductive cloning, in which a copy of an organism is produced, but the two have very different end goals.'' In my opinion this kind of cloning has less issues than the other one. At least therapeutic cloning does not change the concept of reproduction. It is also beneficial for the human kind which should be saved. There are a lot of advantages to show that Therapeutic cloning is useful. ''The advantage to therapeutic cloning in medical treatment is that it would allow doctors to grow replacements for missing and damaged body parts for their patients. This would eliminate organ and tissue shortages, ensuring that every patient who required something like a new liver or new kidneys could get what he or she needed. Using cloned body parts would also eliminate the need for immunosuppressive drugs, and reduce the risk of rejection and other problems which are commonly associated with transplants.''

''In addition to being used for conventional transplant medicine, therapeutic cloning has far-reaching potential applications. For example, cloning research on mice has suggested that new nerve cells can be grown with reproductive cloning techniques and used to repair damaged brains, an application which could be useful for people with dementia, Alzheimer's disease, or strokes. Therapeutic cloning could also potentially be used to produce replacement limbs, and in a variety of other therapeutic applications. Using recombinant technology, scientists can even create customized biological material.''

CITATION

http://www.wisegeek.com/what-is-reproductive-cloning.htm

http://www.wisegeek.com/what-is-therapeutic-cloning.htm

                              

Do you think the advances in genetics and what we know about human genetics prove that humans are more similar to each other, or that humans are more different from each other?

              Nowadays, advances in genetics bring us the question of similarity in human race. From the help of the Human Genome Project diseases can be identified, humans’ past generations can be learned and mostly crimes can be solved. While the advances are helping, it also makes us question which is consist of similarity in human race. The Human Genome Project which ‘‘is an international 13-year effort formally begun in October 1990. The project was planned to last 15 years, but rapid technological advances accelerated the completion to 2003. Project goals were to determine the complete sequence of the 3 billion DNA subunits (bases), identify all human genes, and make them accessible for further biological study. As part of the HGP, parallel sequencing was done for selected model organisms such as the bacterium E. coli to help develop the technology and interpret human gene function. The Department of Energy's Human Genome Program and the National Institutes of Health's National Human Genome Research Institute (NHGRI) together sponsored the U.S. Human Genome Project.’’ makes us t understand the difference among people. According to the Project, it indicates that ‘‘there are a very small number of DNA bases which make one person different from any other person in the world. This creates a feeling of unity, of oneness with all people, but even if human genome shows that the small differences which do exist are important ones which give each person his or her uniqueness’’(skin color etc.) , it also creates problems like discrimination and misunderstanding. Are we really same with our uniqueness? In my opinion, small differences create individuality, but do not mean that we are different. We all come from the same family and we all breathe same air with similar organs. Skin color or anything that count as more superior than other is a fallacy. In the past some scientists believe that some human races are more superior than the other ones, but is it a true statement, really? In addition, the Project has brought a lot of issues into societies.  

‘‘Genetic discrimination, The Abortion controversy, Genetic determinism, human freedom, and the gene myth, Genes, sin, crime, and racial discrimination, The gay gene, Stem cells, Cloning, Gene patenting, Somatic therapy versus germ line enhancement. ’’After all those issues being brought up, ‘‘church leaders respond responsibly to new developments in HGP, one thing can be confidently forecast: This affirmation of dignity will become decisive for thinking through the ethical implications of genetic engineering. Promoting dignity is a way of drawing an ethical implication from what the theologian can safely say, namely, that God loves each human being regardless of his or her genetic makeup and, therefore, people should love one another according to this model.’’ This kind of response should be considered as a fair answer. I think that we are all same even if there are different genes that make us an individual. People may overcome these issues with an objective eye so that people should not have to feel abnormal.  Overall, genetics prove that there are small differences among us that define ourselves, and the genes are just used as a tool for human’s health and future that should be protected.

If you want to get some more information about the Project. Here are the websites:

http://www.encyclopedia.com/topic/Human_Genome_Project.aspx

http://www.ornl.gov/sci/techresources/Human_Genome/faq/faqs1.shtml

Additional Citation

Biology book IB Pearson?

Pearson Baccalaureate Biology Standard level for the IB Diploma 

Who should decide? ( KARYOTYPE)

Karyotyping

Karyotyping is a test to examine chromosomes in a sample of cells, which can help identify genetic problems as the cause of a disorder or disease. This test can:

• Count the number of chromosomes
• Look for structural changes in chromosomes

How the Test is Performed

The test can be performed on almost any tissue, including:

• Amniotic fluid
• Blood
• Bone marrow
• Tissue from the organ that develops during pregnancy to feed a growing baby (placenta)

To test amniotic fluid, an amniocentesis is done.

A bone marrow specimen requires a bone marrow biopsy.

The sample is placed into a special dish and allowed to grow in the laboratory. Cells are later taken from the growing sample and stained. The laboratory specialist uses a microscope to examine the size, shape, and number of chromosomes in the cell sample. The stained sample is photographed to provide a karyotype, which shows the arrangement of the chromosomes.

Certain abnormalities can be identified through the number or arrangement of the chromosomes. Chromosomes contain thousands of genes that are stored in DNA, the basic genetic material.

How to Prepare for the Test

There is no special preparation needed.

How the Test Will Feel

How the test will feel depends on whether the sample procedure is having blood drawn (venipuncture), amniocentesis, or bone marrow biopsy.

Why the Test is Performed

This test is usually done to evaluate a couple with a history of miscarriages, or to examine any child or baby who has unusual features or developmental delays that suggest a genetic abnormality.

The bone marrow or blood test can be done to identify the Philadelphia chromosome, which is found in about 85% of people with chronic myelogenous leukemia (CML).

The amniotic fluid test is done to check a developing fetus for chromosome abnormalities.

Normal Results

• Females: 44 autosomes and 2 sex chromosomes (XX), written as 46, XX
• Males: 44 autosomes and 2 sex chromosomes (XY), written as 46, XY

What Abnormal Results Mean

Abnormal results may be due to a genetic syndrome or condition, such as:

• Down syndrome
• Klinefelter syndrome
• Philadelphia chromosome
• Trisomy 18
• Turner syndrome

This list is not all-inclusive.

Additional conditions under which the test may be performed:

• Ambiguous genitalia
• Chronic myelogenous leukemia (CML) or other leukemias
• Developmental delays
• Multiple birth defects

Risks

The risks are related to the procedure used to obtain the specimen.

See:

• Amniocentesis
• Bone marrow biopsy
• Chorionic villus sampling
• Venipuncture

In some cases, an abnormality may occur as the cells as growing in the lab dish. Karyotype tests should be repeated to confirm that an abnormal chromosome problem is actually in the body of the patient.

Considerations

Chemotherapy may cause chromosome breaks that affect normal karotyping results.

See also: Mosaicism

Your doctor may also order other tests that go together with a karyotype:

• Telomere studies -- look at the ends of the chromosomes
• Microarray -- looks at small changes in the chromosomes
• Fluorescent in situ hybridisation (FISH) -- looks for small mistakes such as deletions in the chromosomes

Alternative Names

Chromosome analysis

As you see the explanation below, you may think that it is a lot of work and has own risks which should be considered carefully by a pregnant women who will be the one gets injured. On the other hand, this analysis can prevent health problems before baby is born. Someone has to decide whether they will do the analysis or not. This person or people should be the future parents not the doctors, but women who is older 35 should definitely take doctor’s opinion because at that age women’s eggs’ quality decrease and the body gets old so there is more chance to have the abnormality in baby’s chromosomes. For younger women out there should decide themselves with their doctor’s opinion, but not letting them decide on the decision.

            Suppose you’ve already taken the test and you found out that your child had a chromosomal abnormality, what would you do? If you don’t know, let me answer it. In my case I would determine the kind of abnormality that my child would have and then see how would affect my child’s life. Finally I would consider abortion if I’m at the early stage of the pregnancy and the abnormality would completely change baby’s life in the wrong direction.

CITATION

http://www.nlm.nih.gov/medlineplus/ency/article/003935.htm

Is the case of sickle-cell anemia/malaria an example of correlation with causation OR correlation without causation?

Before I answer the question, I want to define the two terms in the question. Here they are:  Sickle cell anemia: A disease in which poorly formed red blood cells cannot bind correctly to oxygen, resulting in low iron, blood clotting, and joint pain. Malaria: A sometimes-fatal disease transferred to humans by mosquitoes, infecting the bloodstream. These two terms are related with each other in a way that the question is brought to a discussion. Therefore my answer to the question is that sickle-cell anemia/malaria is an example of correlation with causation. Because a human who has sickle-cell anemia cells most likely to have an immunity for malaria. The reason behind the immunity is that malaria can't enter these cells. This explains the correlation. About the causation is that there is no such possibility that a person who has sickle-cell anemia has immunity for malaria where area doesn't include malaria. In addition these traits are not inherited from our parents. With the genetic trait (from one parent) you don't get anemia but you do get partial immunity to malaria. With the same trait from both parents you get sickle-cell anemia and sickle cell trait is a gene inherited from one parent which gives partial immunity to malaria and but is unlikely to develop into sickle-cell anemia.  

Finally, the reasons that are mentioned show why it is an example of correlation with causation. 
Extra Information 

Natural Selection: Uncovering Mechanisms of Evolutionary Adaptation to Infectious Disease

By: Pardis C. Sabeti M.D., D.Phil. (Harvard University, Cambridge, MA) © 2008 Nature Education 

Citation: Sabeti, P. (2008) Natural selection: uncovering mechanisms of evolutionary adaptation to infectious disease. Nature Education 1(1)

The evolutionary link between sickle-cell trait and malaria resistance showed that humans can and do adapt. But are the “bugs” that make us sick evolving as well?

In the 1940s, J. B. S. Haldane observed that many red blood cell disorders, such as sickle-cell anemia and various thalassemias, were prominent in tropical regions where malaria was endemic (Haldane, 1949; Figure 1). Haldane hypothesized that these disorders had become common in these regions because natural selection had acted to increase the prevalence of traits that protect individuals from malaria. Just a few years later, Haldane's so-called "malaria hypothesis" was confirmed by researcher A. C. Allison, who demonstrated that the geographical distribution of the sickle-cell mutation in the beta hemoglobin gene (HBB) was limited to Africa and correlated with malaria endemicity. Allison further noted that individuals who carried the sickle-celltrait were resistant to malaria (Allison, 1954).

Allison's confirmation of Haldane's hypothesis provided the first elucidated example of human adaptation since natural selection had been proposed a century earlier. Today, this and other demonstrations of natural selection help point researchers toward biological mechanisms of resistance to infectious disease. Moreover, such examples also shed light on the ways in which pathogens rapidly evolve to remain agents of human morbidity and mortality.

Figure 1: Worldwide distribution of malaria

The worldwide distribution of Plasmodium falciparum malaria in 2003.

© 2004 Nature Publishing Group Hartl, D. The origin of malaria: mixed messages from genetic diversity.Nature Reviews Microbiology 2, 16. Used with permission. All rights reserved. 

Selection for Malaria Resistance: A Closer Look

Since Allison and Haldane's work, the action of natural selection on genetic resistance to malaria has been shown in a multitude of contexts (Kwiatkowski, 2005). Indeed, the sickle-cell variant (i.e., the HbS allele) has been identified in four distinct genetic backgrounds in different African populations, suggesting that the same mutation arose independently several times through convergent evolution. Beyond HbS, other distinct mutations in the HBB gene have generated the HbC and HbE alleles, which arose and spread in Africa and in Southeast Asia, respectively.

The various HBB alleles aren't alone in offering protection against malaria, however. The geographic distributions of several other red blood cell disorders, including a-thalassemia, G6PD deficiency, and ovalocytosis, correlate to malaria endemicity, and the diseases also are linked to malaria resistance. An even more striking worldwide geographical difference exists for a mutation in the Duffy antigen gene (FY), which encodes a membraneprotein used by the Plasmodium vivax malaria parasite to enter red blood cells. This mutation disrupts the protein, thus conferring protection against P. vivax malaria, and it occurs at a prevalence of 100% throughout most of sub-Saharan Africa yet is virtually absent outside of Africa. Moreover, throughconvergent evolution, an independent mutation in FY that decreases this gene's expression has also become prevalent in Southeast Asia.

So, why has malaria exerted such strong selective pressure? Scientists now know the answer. Malaria is arguably one of the human population's oldest diseases and greatest causes of morbidity and mortality. Research indicates that the malaria-causing parasite Plasmodium falciparum has occurred in human populations for approximately 100,000 years, with a large population expansion in the last 10,000 years as human populations began to move into settlements (Hartl, 2004). P. falciparum, together with the other malaria species, P. vivax, P. malariae, and P. ovale, infects hundreds of millions of people worldwide each year, and kills more than 1 million children annually (World Health Organization, 2000). Because this disease is so devastating, humans have had to evolve adaptive traits to survive in the face of this infectious condition over the past few millennia (Kwiatkowski, 2005).

Broader Implications of Natural Selection for Investigating Infectious Disease

While malaria is the best-understood example of an infectious disease that has driven human evolution, numerous other infectious diseases have also acted in human populations over generations, thus allowing resistance alleles to emerge and spread over time (Diamond, 2005). Based on historical records from the last millennium, these diseases might include smallpox in ancient Europe and in Native American populations, as well as cholera, tuberculosis, and bubonic plague in Europe. Many diseases in Africa have likely been endemic for even longer, such as numerous diarrheal diseases, yellow fever, and Lassa hemorrhagic fever.

Today, with access to heretofore unprecedented data sets for the study of human genetic variation, researchers can exploit the genetic signatures of natural selection using novel analytical methods. In this way, they can identify genetic variants conferring resistance to infectious diseases that have spread through human populations over time. These studies will help elucidate natural mechanisms of defense and perhaps uncover novel evolutionary pressures. Moreover, the same tools that have revolutionized the study of natural selection in humans will also make unprecedented studies of pathogens possible.

Investigating the signatures of natural selection can help elucidate the evolutionary adaptations that have allowed humans to withstand some of our most complex and challenging selective agents. In particular, researchers can look for variants that might be readily detected in genetic association studies; for distinctive, detectable patterns of genetic variation in the human genome; and for clues as to how pathogens themselves evolve so rapidly.

Searching for Variants via Association Studies

By driving highly protective variants to high prevalence, natural selection produces variants that might be readily detected in genetic association studies to help elucidate the biological basis of disease resistance. The classic examples of host genetic factors that play a role in resistance to malaria, such as HbS, are some of the strongest and most robust signals of genetic susceptibility to infectious disease (Hill, 2006). This is because natural selection acts to increase the prevalence of highly advantageous alleles, over time generating common resistance alleles of especially strong effect. For example, a study of genetic susceptibility of HbS in the Gambia detected a significant level of protection using just 315 cases and 583 controls (Ackerman et al., 2005). By studying other ancient selective pressures in which common resistance alleles of strong effect are acting, scientists may have the power to detect a genetic association even with small sample sizes.

In contrast, no single highly protective variant for emergent diseases like HIV and tuberculosis (in Africa) would have had time to spread. For these diseases, resistance appears to be modulated by many rare genetic variants, most with modest protective effect, and genetic studies require extremely large sample sizes (Hill, 2006). This is likely not a biological but, rather, a historical difference. Indeed, hundreds of structural and regulatory mutations exist in HBB, such as HbS, HbE, or HbC, but in populations under malaria selective pressure, a single highly protective variant will often dominate (Kwiatkowski, 2005). Moreover, many variants nearby on the chromosome will rise in prevalence in the population through genetic hitchhiking, such that other nearby linked alleles can serve as proxies for the underlying causal allele in genetic association studies, further enhancing researchers' ability to detect an association. Thus, natural selection may produce important genetic resistance loci that can more easily be detected in association studies.

Searching for Patterns of Variation

As genetic variants conferring resistance to infectious diseases spread through human populations over time through natural selection, they leave distinctive, detectable patterns of genetic variation in the human genome. These signals of selection can uncover novel resistance alleles or even novel evolutionary pressures. Also, as previously mentioned, as advantageous alleles under positive selection rise in prevalence, variants at nearby locations on the same chromosome (linked alleles) also rise in prevalence. Such genetic hitchhiking leads to a "selective sweep" that alters the typical pattern of genetic variation in the region. Selective sweeps produce numerous detectable signals of selection (Nielsen, 2005; Sabeti et al., 2006). As tests for selection have been applied to newly available genetic variation data across the human genome, many of the top signals of selection that have been identified have been at genes and alleles known to be involved with malaria susceptibility, including HBB, FY, CD36, and HLA. These signals were identified in just 90 individuals randomly chosen from the population, and they could have been identified without prior knowledge of a specific variant orselective advantage.

Surveys of natural selection can not only identify new resistance variants for known selective pressures, but they can also potentially uncover previously unrecognized selective pressures. For example, in a genome survey of the Yoruba people of Nigeria, two of the top signals of selection were at genes (LARGE and DMD) biologically linked to the Lassa hemorrhagic fever virus (Sabeti et al., 2007). While little studied, Lassa virus in fact infects many millions of West Africans, and based on oral records and epidemiology, it is likely to be an ancient disease (Richmond & Baglole, 2003). Researchers have documented that in several affected West African populations, between 50% and 90% of individuals are resistant to the virus, suggesting that protective alleles emerged at some point (McCormick & Fisher-Hoch, 2002). This finding could open new avenues for research and shine light on other important pathogens in human history.

Searching for Clues about Pathogen Evolution

The same tools that revolutionized the study of natural selection in humans are now making unprecedented studies of pathogens possible, allowing scientists to better understand how these organisms rapidly evolve to remain agents of human morbidity and mortality. Pathogens are perhaps the most intriguing of all the forces shaping humans. They have had a tremendous impact on our evolution, and they, themselves, evolve over time. The great effect that pathogens have exerted on the human genome is demonstrated by positive selection for traits such as sickle-cell hemoglobin (Sabeti et al., 2006). Natural human defenses have similarly exerted strong pressures on the genomes of pathogens, as has the use of drugs and vaccines (Volkmanet al., 2007). By studying genetic diversity in pathogens, researchers can examine how they have evolved to avoid human immune defenses and therapeutics. Furthermore, scientists can investigate in real time the evolutionary consequences of new vaccines and drugs, with the goal of developing better intervention strategies.

Future Endeavors

Investigation of the links between natural selection and disease resistance has revealed some of the forces that have shaped our species, and the findings of these studies have direct implications for human health. However, research thus far represents just a first glimpse of a vast new landscape. In the years to come, new technologies and analytic methods will enable researchers to learn even more about the genetic basis of evolutionary adaptations that have allowed humans to withstand a wide variety of complex and challenging selective agents.

CITATION

http://wiki.answers.com/Q/What_is_the_connection_between_sickle_cell_anemia_and_malaria

http://www.pbs.org/wgbh/evolution/library/glossary/glossary.html#sickle_cell_anemia
http://www.nature.com/scitable/topicpage/natural-selection-uncovering-mechanisms-of-evolutionary-adaptation-34539