Aussie turtles 'ride the EAC' to Peru

Dr Michelle Boyle, of the School of Marine and Tropical Ecology at James Cook University in north Queensland has tracked the migration of Australian born logger-head sea turtles using genetic testing.

“The turtles have been using the east Australian current to travel to the south pacific to the waters off Peru and Chile and return using the Southern Equatorial Current” says Dr Boyle, It is unknown how long the journey takes and how much is active or passive transportation via currents.

To confirm the Pacific Ocean migration theory Dr Boyle used a combination of techniques that focuses on the sea turtles movement in the south pacific. Using tissue and the genetic analysis of the mitochondrial DNA haplotypes showed that South American and East Australian sea turtles shared the same genetic background.

Dr Boyle’s study pushes for the need for international collaborations when developing management and conservation policies.

James- 41781218

links
http://www.abc.net.au/science/articles/2004/03/23/1071046.htm
http://www.abc.net.au/news/stories/2009/03/10/2512564.htm

Feeling a bit stressful? Good for you!

A new finding by researchers from Northwestern University in Evanston has discovered that mild stress can delay aging with the help of several proteins. The anti-aging effect is triggered by a key regulator of a mechanism preventing protein damage caused by stress.

Exposure to stress causing agents triggers a damage limiting mechanism, which is also known as heat shock response, to prevent cell death via restoring the conformation of deformed proteins. In this way, life span of the cell is extended. The researchers have found that the heat shock response in human cell lines is regulated by Sirtuin 1 (SIRT1), an aging-related protein that plays many roles in longevity by several different stress-busting pathways.

In fact, the key component of the heat shock response is a protein known as heat shock factor 1. When a cell is under stress, heat shock factor 1 binds to DNA and initiates production of the protein repair molecules. Nevertheless, excessive protein repair molecules triggers heat shock response to terminate the protein production through an acetyl group, which removes heat shock factor 1 from the DNA strand through binding to it.

On top of that, the researchers have also discovered that acetyl group can be removed by SIRT 1 for continuous production of protein repair molecules. Termination of protein repair molecules is determined by the abundance of these proteins regardless of any unrepaired damage.

A study using calorie-restricted diet as a stress factor tested on mice and dogs has uncovered a possible relationship between stress and life span of the cells tested based on the result of an increase in the levels of SIRT1.

In older cells, the sensitivity of heat shock response declines in response to stress due to a decrease in the amount of SIRT1. With this, the researchers theorize the possibility for SIRT1 to be used as activator of the heat shock response on demand especially in brain cells, as a treatment for neurodegenerative diseases such as Alzheimer’s and Huntington’s disease. Yet, manipulation of SIRT1 in keeping cells in a defensive state also prolongs life span of cancer cells equally.

There is a need for extension studies to be done to validate the co-operation between the heat shock factor 1 and SIRT1 in protecting the cells of whole organisms, not merely the cell lines tested.

Original Article:
Anti-aging: A little stress may keep cells youthful
http://www.sciencenews.org/view/generic/id/41044/title/Anti-aging__A_little_stress_may_keep_cells_youthful
Student ID: 41827394

Gene Therapy, does it really show promise for HIV?

Mengmei Deng
Student number: s4200951
Prac session: P5

The most commonly used treatment for HIV is known as anti-retroviral treatment (ART). This type of treatment shows effectiveness to a certain extent but is very high in cost and toxicity and is impractical to be taken every day for life. In order to solve these problems with ART, three groups of scientists endeavoured to find cure to HIV through the method of gene therapy.

The first group of scientists added a DNA-disrupting molecule, known as zinc fingers nucleases (ZFNs) which will zero in on and disrupt any chosen gene. In this case, the chosen gene is the CCR5 gene which codes for making the HIV door-handle protein. The CD4 cells, which are the cells attacked by HIV viruses, are then extracted from the patient’s blood and added with a harmless virus carrying the genes that code for the ZFNs. The altered CD4 cells produce ZFNs which sabotage the CCR5gene. The ZFNs and the harmless virus are then washed away and the modified cells are injected back to the patient’s body. The engineered cells replicate faster and live longer than the cells that are already infected with HIV, so that the modified cells will eventually become dominant CD4 cells and block HIV from getting into the cells. However, the problem with this method of gene therapy is that it raises the question of whether it is ethical to destroy a HIV patient’s existing immune cells, as the engineered cells won’t work if the existing immune cells are not eliminated.

The second group of scientists aimed to add the gene coding for ribozyme, an enzyme that disrupt HIV replication into the cell so that the HIV replication is inhibited once it gets inside the cell. The scientists extracted CD34 stem cells from the patients with a virus that carries a gene for a ribozyme. This enzyme will be expressed when the cells are injected back into the patients and the replication of HIV is stopped as the enzyme snips up the tat gene, the gene essential for the virus to replicate itself, in any HIV that enters the cell. However, the number of cells with the ribozyme disappeared rather than multiplying over a period of time and the therapy is not as effective as usual ART.

The third group of scientists combined the techniques of the first and second groups. These scientists used viruses to load patients’ blood cells with three genes to defend them from HIV: one prevents the HIV to get into the cell and the other two sabotage the HIV even if it does get into the cell. However, though this method had been applied to a few patients, the patients carried on their usual anti-retroviral treatment while the gene therapy was applied. Therefore, the effectiveness of this method has not yet been finally determined.

All of the three methods of gene therapy proposed by the scientists to cure HIV had its own problems. Though they all showed encouraging signs to the cure of HIV, it is still hard to determine whether gene therapy is the ultimate solution for the disease.

References:
“Gene therapy promises one-shot treatment for HIV” from http://www.newscientist.com/article/mg20126964.400-gene-therapy-promises-oneshot-treatment-for-hiv.html?full=true
“Gene therapy for HIV shows promise” from http://www.newscientist.com/article/dn16601-gene-therapy-for-hiv-shows

Selecting and Modifying Bacteria to Solve Environmental Problems

You may think that the only way to stop the pollution of our planet is for everyone to become aware and change our ways. What if we create bacteria that will reduce our impact on the planet through breaking down some of the unwanted pollutants or use it as a sort of catalyst to aid us in creating greener technologies?
One example would be to develop a PET plastic bottle eating bacteria. Despite the fact that PET plastic bottles are so common, it is still doesn’t have cost effective industrial processing. There are bacteria found which lives off the bottles and make it into a more valuable polymer, PHA. Each bacterium eats so much of the PET bottle that they are 24% PHA plastic by volume. These bacteria can be used for further selection in the lab for an even more efficient bottle eating bugs.
Modified bacteria can also be used as a catalyst, the example here is the hydrogen economy. Fuel cell requires expensive platinum catalysts and this can be replaced by bacterium enzyme. The price of enzyme-catalysed cell is more likely to drop than that of the platinum which grows in demand as resources reduce.
These are only two examples; there are much more application where the bacteria can be engineered to do what we want.

Original Article:
How our green technology may rest on bacteria skills
http://www.newscientist.com/article/dn16841-how-our-green-technology-may-rest-on-bacterial-skills.html

A Blog That WON'T Grow on You!

It has long been known that genetics can play a vital role in a person’s susceptibility to cancer growth. In some cases, a poor family history can almost guarantee that they fall victim to the disease. Fortunately, there is now good news regarding melanoma, the deadliest form of skin cancer, coming from America’s National Institute of Health (NIH). Published in Nature Genetics, the study showed that mutations in the parts of the genetic code which are translated into the cancer suppressing enzyme 'matrix metalloproteinase', more commonly known as MMP, were prevalent in many melanomas. Where MMP would normally act as a ‘checking’ enzyme to prevent uncontrolled cell growth, it was found that in 25% of cases this enzyme did not function correctly.

These tumor suppressing genes were originally thought to be over-productive oncogenes, which encourage cell growth, as such they were targeted by medications to be blocked thus reducing levels of MMP. In contrast the opposite would have been more appropriate to instead increase levels of MMP. This may be the reason why those treatments, simply put, did not work. Future medications may seek to improve the function of MMP encoding genes in the hope that the MMP enzyme may be able to slow or even put a stop to melanoma growth.

Rhys-42010081

Source: http://www.biologynews.net/archives/2009/03/29/skin_cancer_study_uncovers_new_tumor_suppressor_gene.html

Gene Which Protects Against Lung Cancer Identified

A recent study by researchers from the University of Nottingham has identified a gene that protects the body from lung cancer. Lung cancer is a preventable disease and smoking cause up to 85% of lung cancer cases in developed countries. The research have shown that a tumour suppressor gene, LIMD1 is responsible in protecting the body from developing lung cancer, paving the way new medical treatments and screening techniques.
A long term smoker of 25 or more cigarettes has 25 times the chances of developing lung cancer compared to a person who never smokes. Lung cancer is caused by the combination of tar and nicotine in smoke. Tar will coat the lungs and spread throughout the breathing system and engulf the respiratory system whereas nicotine, an addictive drug in cigarette will raise heart pressure and heart rate everything you smoke, straining both the blood vessels and heart, thus magnify the chances of heart attack. There are two main types of lung cancer, small cell lung cancer and non-small cell lung cancer. Small cell lung cancer is strongly linked with smoking and occurs in 15% of all lung cancer cases. The research conducted was a joint effort between University of Nottingham researcher team led by Dr Tyson Sharp and US collaborator Dr Greg Longmore and the research direction focus on the loss of LIMD1 gene in relation to lung cancer.
In the research, the University of Nottingham team examined tissues sample from lung cancer patients and compared them with healthy lung tissue. The absence of LIMD1 gene in most of the lung cancer samples when compared to healthy lung tissue indicate that LIMD1 gene has a critical role in protecting the body against lung cancer. In a separate research conducted by US team, mice were tested and those mice without the presence of LIMD1 gene developed lung cancer, thus supporting finding from Dr Sharp research team.
Dr Sharp mentioned that the LIMD1 gene studied in this research is located on part of chromosome 3, called 3p21. Chromosome 3p21 is often removed very early on in the development of lung cancer by toxic chemicals in cigarettes, implying that the inactivation of LIMD1 gene could be a particular important process in early stages of lung cancer development.
Dr Sharp and his team hope to further understand LIMD1 gene and extend the findings to develop a novel prognostic tool for detection of early stage lung cancer.

This article can be found at:
http://www.sciencedaily.com/releases/2008/12/08

Blame the parents

A team of researchers from Tufts School of Medicine in Boston have discovered evidence that offspring may benefit from their parents’ cognitive abilities at the time of conception. Led by Larry Feig, the team bred a group of mice, ‘knockout’ mice, lacking the ras-grf-2 gene which results in defective memory. Half of these knockout mice were exposed to an enriched environment (EE) - a cage with toys, increased social interaction and voluntary exercise - for two weeks before adolescence with the aim to overcome this memory defect.

Both groups of knockout mice were subjected to a fear conditioning memory exercise. This exercise involved placing the mice in a cage in which they soon receive a small electric shock to their feet. Normal mice quickly develop a fear association with the cage and learn to freeze in fear when placed inside. In contrast, knockout mice are unable to form this association and consequently fail to freeze. Carrying out this fear exercise with enriched knockout mice, it was found that they froze when placed in the cage, just as the normal mice. From this it was concluded that the two weeks spent in an EE was sufficient to compensate for their defective memory.

With this information in mind, the research team bred the enriched knockout mice to investigate whether these cognitive benefits could be passed on to offspring. To achieve this, the offspring were raised by unenriched parents to prevent any direct learning from enriched parents and were not exposed to an EE. The offspring then underwent the fear conditioning memory exercise. Most remarkably, the offspring froze when reintroduced to the cage, indicating that they were able to form the normal fear association despite their memory defect and lack of enrichment. This same test was carried out with the offspring of unenriched knockout mice, however, like their parents, they were unable to form any fear association with the electric shock cage.

In addition to these findings, researchers found that it was not sufficient to have an unenriched mother and an enriched father to overcome the memory defect. Also, the cognitive effect was not passed on to a third generation and was only inherited if the offspring were conceived within three months of enrichment.

To explain these results, Feig suggests that the cognitive benefits the enriched mice enjoy is passed on during gestation through epigenetic chemical markers which attach themselves to the embryo’s genes, regulating their expression.

Written by student 42019431


Primary reference:
Motluk, Alison. Can experience before conception be passed on?. New Scientist, Feb 7, 2009, pp 12.

For original journal article:
The Journal of Neuroscience, February 4, 2009, 29(5):1496-1502; doi:10.1523/JNEUROSCI.5057-08.2009

Genes Linked to Addiction

The dependency of individuals upon drugs and other stimulants has no doubt increased within society over time. Previously, researchers have had little luck in finding evidence of the origin of such substance addiction. However, recently it has been established that certain genes associated with alcohol addiction are in fact also closely related to dependence of other stimulants such as cocaine, cannabis, heroin, opioids and nicotine. “Addiction researchers have found that several genes are linked with multiple addictions,” states Ming Li, a professor of psychiatry and neurobehavioral sciences. According to these researchers, once they are able to locate the correct genetic variants, they will be able to generate more effective treatments, than those of current use, for individuals suffering from substance addictions. So far, scientists have found specific genomic locations on 11 chromosomes where dependencies of these substances are grouped together. Through the comparison of peaks on these certain chromosomal locations, it has been confirmed that genetic susceptibility to different substances overlaps. With continual genetic advances about the occurrence and vulnerability of substance addictions, knowledge such as this will certainly benefit society in the combat to overcome severe addiction problems, in turn, potentially saving many lives.

http://www.sciencedaily.com/releases/2009/03/090310142912.htm

Danielle Morrison
42051981

Melanoma: Is Oestrogen a Factor?

Does the expression “slip, slop, slap” ring a bell? What about the New South Wales Government’s latest catch phrase, “There’s nothing healthy about a tan”? We are constantly bombarded with messages about the importance of sun protection to prevent the formation of skin cancers. However, new studies suggest that the most deadly form of skin cancer, melanoma could, to some extent, be caused by an alternative risk factor.

MDM2 (murine double minute 2) is a cancer promoting gene (oncogene) present in everyone’s cells. When oestrogen binds to MDM2, production of this gene increases. It has been suggested that the interaction between oestrogen and a genetic variant that can occur in the promoter of the MDM2 gene could significantly increase melanoma risk, thus contributing to a larger prevalence of these cancers in women under the age of 50. Although the binding of MDM2 (without the genetic variant) and oestrogen ‘switches on’ its manufacture; the defect identified in the gene’s promoter causes stronger bonding and increases MDM2 production.

Normally, the tumor suppressing gene, p53 regulates MDM2 levels, and in turn MDM2 regulates p53 levels. In individuals with the genetic defect however, MDM2 is ‘flicked on’ irrespective of p53 levels, leading to suppressed p53 protection from cancerous cell formation.

Oestrogen levels in pre-menopausal women tend to be highest, and it is suggested that women with elevated oestrogen, in combination with the MDM2 variant present a significantly higher melanoma risk.

A recent study by David Polsky and his team of researchers of 227 melanoma cases at the NYU School of Medicine has revealed that this naturally occurring genetic variant was present in over 40 percent of diagnosed female melanoma patients (under 50), thereby providing evidence to support this notion. Polsky is looking to develop a cancer risk model based on hormonal status and genetic factors. Such a test would have significant implications for cancer prevention.

Original Article:

New Risk Factor for Melanoma in Younger Women, Science Daily, viewed 27 March 2009, http://www.sciencedaily.com/releases/2009/03/090324131448.htm
Adapted from materials provided by the NYU Langone Medical Center

References:

Hardcastle, I. R. 2007, Inhibitors of the MDM2-p53 interaction as anticancer drugs, online illustration, Drugs of the Future, viewed 28 March 2009, http://journals.prous.com/journals/servlet/xmlxsl/pk_journals.xml_summary_pr?p_JournalId=2&p_RefId=1131965&p_IsPs=N

Melanoma 2009, online illustration, Wikipedia: The Free Encyclopedia, viewed 28 March 2009, http://en.wikipedia.org/wiki/Melanoma

Melanoma Diagnostics 2009, University of California San Francisco, viewed 28 March 2009, http://www.melanomadiagnostics.com/

Queensland Researchers discover Melanoma gene 2009, online illustration, ABC, viewed 29 March 2009, http://www.abc.net.au/news/stories/2008/05/19/2249091.htm

Skin Cancers 2009, World Health Organization, viewed 28 March 2009, http://www.who.int/uv/faq/skincancer/en/index1.html

Soussi, T 2008, MDM2 and MDM4, The TP53 Website, viewed 28 March 2009, http://p53.free.fr/p53_info/mdm_family.html


Caitlin Swalwell
42008707

Genetics, not the most accurate prediction

As new, amazing discoveries in modern science are made every day, it seems like it is the most reliable source for all information. However, it turns out that currently genetic predictions made about height are still about ten times less accurate than Sir Francis Galton’s method of predicting height which he devised in the Victorian era, in 1886. Genetist, Yurii Aulchenko using a much more complex method of scanning people’s genomes was able to compare the modern method to Galton’s method.

Galton became heavily involved in Hereditary, Historiometry and Eugenics after seeing his cousin, Charles Darwin’s publication, “The Origin of Species”. His method simply, averages the height of a child’s parents and made adjustments on the height based on age and sex. With a correlation made between measured height and this predictor, about 40% of the heights are predicted correctly. Proving to be quite accurate compared to predictions made based on human genotypes.

In order to predict height using genotypes, Aulchenko’s team had to analyse 54 different genetic variants, which were linked to height for 5748 people. These 54 selected genotypes were linked to studies that showed they were mutations in the genetic structure which tall people tended to possess. Yet, based on people who carried these genes, the correlation between their measured height and the prediction with variations based on age and sex; only 4% of the sample was predicted accurately. This draws many questions as the two methods are testing the same thing, generally with the same basic principles. Do we currently know enough about the human genome? Were there enough genotypes picked, deemed to be related to height? The obvious answer is currently, no, as hypothetically if everything was known about the human genome Aulchenko’s method would predict height within 80% variance.

Unfortunately, gaining enough knowledge about the human genome will not be done for many years as most genetic variations do not have much to do with height. This is further complicated, as our genome around 20,000 to 25,000 protein-coding genes with over 3 billion DNA base pairs. For now, Sir Francis Galton’s 123 year old method is still the most accurate for children’s height prediction.

References

http://www.newscientist.com/article/dn16698-victorian-rule-of-thumb-beats-genetic-prediction.html
http://scienceblogs.com/geneticfuture/2009/03/predicting_height_the_victoria.php
http://www.galtoninstitute.org.uk/Newsletters/GINL9912/francis_galton.htm
http://www.galton.org/
http://www.genome.gov/Pages/Education/AllAbouttheHumanGenomeProject/GuidetoYourGenome07.pdf

By Student Number: 42016092

One protein mediates damage from high-fructose diet

High fructose diets can cause a number of serious disorders with the metabolic system, these metabolic disorders include , fatty liver disease and insulin resistance, which has been related to type 2 diabetes.

I have found an article stating that these disease are only present within a person with a high fructose diet when a certain protein within the liver is also present. This protein is called PGC-1 beta . studies on mice with a high fructose diet have shown that by knocking out or removing this protein found in the liver , can prevent or even reverse some of the damage that is associated with a high fructose diet. But there is a problem getting rid of PGC-1 beta in mice that ate a regular diet actually caused insulin resistance. The researchers believe that this discovery will eventually lead to the prevention of insulin resistance.

The article can be found at http://www.sciencenews.org/view/generic/id/41381/title/One_protein_mediates_damage_from_high-fructose_diet

Dan Mumford
42060778

Stem cell breakthrough: Monitoring the on switch

A team of American researchers have managed to create a “switch” that turns on muscle stem cells, causing growth and regeneration in a living mammal. This breakthrough in genetic engineering could lead to a genetic drug that allows humans to grow new muscle cells, replacing those that are damaged, infected, or just not functioning properly.

The discovery was made when they were breeding a special type of mice with a gene called ‘Cre.’ When this gene was activated, it triggers mutations in the muscle stem cells of the mice. What is amazing is that this gene can be activated by a certain drug. Thus, the scientists have found a ‘switch,’ which gives them the power to turn on the process of muscle growth and recovery. The research team used fluorescent techniques to see the stem cells and find out exactly where muscle tissues were being made. They were able to learn a lot about how muscles tissues were developed from their stem cells.

Charles Keller, M.D., assistant professor at the University of Texas Health Science Center, explains: "We hope that the genetically-engineered mouse models we developed will help scientists and clinicians better understand how to make muscle stem cells regenerate muscle tissue."

The team also uncovered a new way to look at how tumours start and progress in muscle cells. By activating certain tumour-causing mutations, the scientists were able to gain valuable insight into the origins of muscle tumours.

"For our own work on childhood muscle cancers, we also hope to understand how tumors start and progress, and to develop therapies that are less toxic than chemotherapy," said a senior researcher at the University of Texas Health Science Center.

This discovery gives researchers a new way to study muscle cancers and other diseases. It is also a step towards the goal of one day being able to use stem cells to repair wounded and diseased patients.

Article from: http://www.biologynews.net/archives/2009/03/30/stem_cell_breakthrough_monitoring_the_on_switch_that_turns_stem_cells_into_muscle.html

Student ID: 42041768

How do metabolism and body clock related?

Scientists have found the explanation of how the biological body clock corresponds to metabolism and aging related health problems. The finding was contributed by researchers at Washington university of Medicine in St. Louis and Northwestern University. They studied on mice and conclude the weakening of circadian rhythm with age could contribute to age related problems, such as insulin resistance and type 2 diabetes.

Circadian rhythm is commonly known as our body clock. This rhythm is associated with certain hormone production, such as insulin and melatonin. Insulin is normally secreted peak at daytime in order to control the blood sugar level at proper range; whereas melatonin a hormone that controls circadian rhythm by telling the body it’s time to sleep, and its level is usually low during daytime and high at night. Early research has pinpoint that the interfering of melatonin can led to metabolic complications. The new research has linked a gene called SIRT 1 that controls circadian rhythm also plays a significant role in regulate the cellular energy flow.

An enzyme protein SIRT 1 controls the cellular regulation. It manages the body response to nutrition, when the cell energy levels are detected below normal, a signal coenzyme called NAD+ (nicotinamide adenine dinucleotide) is sent to a key protein NAMPT (nicotinamide phosphoribosyltransferase) which activate the cell energy exchange system, and move the energy to where it is required. This mechanism balances aging and metabolism in our body. This finding suggests sleep and healthy diet may help or rebuilt this balance and prevent a range of health problems from diabetes to obesity.

Joe Bass an associated professor of neurobiology and physiology at Northwestern University and colleagues experimented on laboratory mice. These mice’s circadian rhythm was disrupted under controlled condition of light and dark (by placing them in complete darkness for 48 hours). And the results showed that in the control group NDA level changed which means the circadian rhythm continuously function even in complete darkness. However, in mutant animal the NAD level was not changed.
"Seeing this striking abnormality in the NAD levels was like discovering the cause of a disease in a patient after running a blood test," said Bass, "The pathway that controls NAD is tied to the clock at the most intricate level. This shows a direct connection -- changes in the clock influence NAD."
They have conclude that the NAD rhythm was linked to the body clock, and the clock genes SIRT1 directly interact with a biochemical process that produces NAD.
"Perturbing the NAD pathway does affect the clock," said Bass. "It does go in both directions."
Coenzyme NAD+ is required for enzyme SIRT 1 to function, suggesting that SIRT1 activity increased and decreased along with NAD oscillation in the mice. The researchers then determined the feedback cycle is driven by NAD.
“We showed that this feedback cycle is driven by NAD. Because NAD levels reflect nutrition and energy levels, NAD’s link to the circadian and aging mechanisms makes them sensitive to the nutritional status of the organism,” said one of the lead authors, Dr. Shin-ichiro Imai, Washington University School of Medicine in St. Louis.

In conclusion, new research has determined the level of SIRT 1 and NAD+ are closely associated, and this is how circadian rhythm related to metabolism. The finding of this relationship may lead innovative ways to treat aging metabolic disorders in the future.
“Our study establishes a detailed scheme linking metabolism and aging to the circadian rhythm. This opens the door to new avenues for treating age-related disorders and ways to restore a healthy daily circadian rhythm. It could also yield new interventions to alleviate metabolic disorders such as obesity and diabetes,” said Imai.
Main article:
http://silverscorpio.com/how-the-body-clock-controls-metabolism-and-ageing/
Same article published by different authors:
http://www.sciencedaily.com/releases/2009/03/090312140840.htm
http://esciencenews.com/articles/2009/03/19/compound.key.coordinator.clock.and.metabolism
http://www.sciam.com/blog/60-second-science/post.cfm?id=link-between-body-clock-and-metabol-2009-03-19
Related articles:
http://www.sciencedaily.com/releases/2008/12/081207133817.htm
http://esciencenews.com/articles/2008/12/07/body.clock.linked.diabetes.and.high.blood.sugar.new.study
http://www.sciencedaily.com/releases/2009/03/090325142513.htm

Picture source from http://www.sciam.com/blog/60-second-science/post.cfm?id=link-between-body-clock-and-metabol-2009-03-19

'ADVANCES IN HUMAN CLONING- Where is Science? Where might it go?'

This article as the title exposes is about the modern day advances in human cloning. The article tracks a five day week of Dr. Emily Senay. It is based on a TV show which attempts to produce the perfect baby, using science the process of cloning a human being. On Monday she takes the decision to produce a baby from cloning. On Tuesday she researches for what she has to do in order to perfectly clone her human being. On the Wednesday she speaks to Michael West of Advanced Cell Technology. Whose work is based on cloning human embryos to study the stem cells they contain. On Thursday she meets with bioethicist Gregory Stock and discusses possibilities and probabilities of "germline engineering", which is the "manipulation of the genetics of egg or sperm (our 'germinal' cells) to modify future generations." On Friday she discovers that couples who are treated for IVF (intro-virto fertilisation) are given the opportunity to have their embryos screened in attempt to prematurely detect any genetic defect to their possible upcoming child. The article finishes up on Friday where Dr. Emily Senay is still on the pursuit of being able to clone the perfect human baby.

The International Hapmap Project

Since the human genome was first mapped in 1995 the field of genomics has boomed, and, like the spread of a good idea, it has invariably led to an increased flurry of similar investigative projects in Genomics. Of these, the International Hapmap Project is possibly the most exciting. Commencing in 2003 the project aimed to develop a haplotype (haploid genotype) map of the human genome. 

Such information is valuable in understanding human genetic variation. Among other things, it provides a resource for understanding how our genes influence health and the onset of disease. The information produced by the International Hapmap Project is made freely available to scientists accross the globe. In October 2007 Phase 2 of the data collection process was completed and the final phase 3 was made available in February this year. In the coming years the data collected as a result of the project will surely prove invaluable in the understanding and treatment of disease. However, ethical issues have been raised in regard to the project, with particular concern over the possibility of missuse of information.

Further information about the project can be found at http://www.hapmap.org/. For an overview of the ethical issues encompassing the project visit http://www.hapmap.org/downloads/HapMapEthics.pdf. For a critique of the project see Terwilliger JD and Hiekkalinna T (2006). An utter refutation of the 'Fundamental Theorem of the HapMap' European Journal of Human Genetics 14, 426–437

Genes may time loss of virginity

Sexual precociousness is in our genes, new research suggests. A unique study of twins separated at birth finds a genetic link to the age at which a person first engages in sexual intercourse. The study was conducted with 48 pairs of twins separated at birth and 23 individuals. By having a large group to test, the researchers were able to rule out some factors that may have affected the results. Factors such as upbringing and social wellbeing cannot be cast aside though.

As far as results though, the team of researchers found that genes could only explain about a third of the differences in participants' age at first intercourse - which was, on average, 19 years old. In comparison, almost 80% of height variations in a population can be explained by genes alone. The team could also not rule out the effect of conservative mores which might delay the teen's first sexual experience. There was also another factor that could have had an effect on results. For example, the team found that female participants who felt unfulfiled in their home life and unhappy were more likely to have sex at a younger age. The team has also admitted that the study, and studies like it, could cause scientists to overestimate the effect of genes.

Other studies have found a gene encoding a receptor for the neurotransmitter dopamine is associated with age at first intercourse. This version DRD4 is also linked to impulsive, risk taking behaviour. Yet unlike other risky behaviours, such as drug use or reckless driving, sex serves an essential biological function. Most of our evolutionary past sexual behaviour hasn't been risk taking. It has been about reproduction and success of the species as a whole.

Sources:
http://www.newscientist.com/article/dn16876-genes-may-time-loss-of-virginity.html

Journal reference: Personality and Individual Differences (DOI: 10.1016/j.paid.2009.02.010)

42053396

FIshy physics - Evolution under water

We all know that light is made up of a rainbow of colours to form the plain white light we see. The deep ocean seems blue to us because water molecules tend to absorb certain wavelength of light(in this case red light is absorbed) when photons go through it.

Biologists have discovered that this process affects the natural selection and evolution of fishes in Lave Victoria, Africa. The physics of light had in fact led to speciation. The cichild species,living in Lake Victoria, have evolved and specific vision tuned to suit the environment they live in. Remember that natural selection always favours traits which excel in a local environment. Picture a murky lake image...

Fish that live in shallow water and deep water portray a variation in habits and nature. Hypothetically,due to the things fish in shallow water see, they are able to prey on other organisms and avoid predators at the same time in a region of water near shore. This is where their reigning zone is. The opposite is true too in deep water regions for fishes that stay there. This is where the genetic variation lies : shallow water fish have higher sensitivity to blue light; deep water fish have higher sensitivity to red light. Now we see the rift in the population and how simple it is created even without allopatric speciation. However,this divergence is further amplified by the sexual selection. As mentioned, shallow water fish would only do well near shore line and would suffer the alienation of other deep water fish when mating partners are chose. Highly beleived that, fishes living in the deep regions are unlikely to possess an optimal sensetivity to blue colouration. Thus, leaving the "blue" fishes alone and selecting the "red" fishes.

The occurrance of natural selection is everywhere and keeps the evolution of all living organisms in an ever-changing state. Futhermore,the introduction of human activity would nonetheless be a crucial factor to ourenvironment and biodiversity. If this prolonges, divergance of species would be unavoidable and a species might eventually seperate to form two entirely different species.


By 41952559 (zckry)



Reference link :
http://evolution.berkeley.edu/evolibrary/news/090301_cichlidspeciation
(Video included)

Head Lice Resistance

Head lice have become resistant to many of the original brands of head lice treatment and are currently continuing to become resistant to many of the available treatments. This has become a major problem amongst primary schools, with many schools and parents not knowing what to do. In many cases, schools have been giving the wrong advice, advice in which parents also wholly believe in. This is the idea of treating the children every night or few days until the lice are gone.
This is actually incorrect advice, as treating this often gives lice a better chance to build resistance against these products. Reports of resistant lice have become more frequent, especially those who are chronically infected and have been treated many times with the same or similar products. In the US, it has been found that some lice have become totally resistant to permethrin, the ingredient used to kill lice.
Resistance happens over multiple attempts to kill the lice. After a treatment, there may be a few lice that were for one reason or another able to survive. When these then reproduce, the new lice will most likely carry this trait. Over multiple generations and treatments this will continue, until you have strongly resistant lice.
Human head lice co-evolved with us, so it comes as no surprise that they are building a resistance against treatments designed to kill them.

Cause of Alzheimer’s May Also Be the Cure

Scientists from the Carol Besta National Neurological Institute have found that a newly discovered gene mutation, thought to be the cause of Alzheimer’s disease when inherited from both parents, may give protection from the disease when only one copy is inherited. Mutations in the Amyloid beta (A4) precursor protein (APP), which is responsible for providing instructions for making the amyloid precursor protein, a protein located in many tissues and organs including the brain and stem cell and thought to be important in the binding of cells and proteins, have long been considered a possible cause of Alzheimer’s disease. Mutations in the amyloid precursor protein cause the protein to stick together and block neurons from communicating with one another. These “clumps” have been found to underlie the some of the symptoms of Alzheimer’s such as memory and speech difficulties. Scientists now however have discovered the presence of a single inherited mutation of APP may in fact prevent the onset of the disease.

Fabrizio Tagliavini, a neurologist at the Carol Besta Institute, and his team uncovered the mutation in a person who showed signs of early-onset Alzheimer’s but who lacked mutations in other genes associated with the inherited form of the disease. The 44-year-old man with two copies of the mutated APP gene first showed signs of Alzheimer’s in his mid-thirties and his younger sister, also with two copies of the mutated APP gene also showed signs of cognitive problems, however his relatives with a single copy of the mutation seem to be protected from the disease. When normal and mutant forms of the protein were mixed, the team found the mixture clumped far less often than the mutant protein or normal protein alone. This could explain why the patient’s relatives with a single mutation showed no signs of the disease.

Using this new information Tagliavini and his team have already found that a mutant protein, only six units long, is enough to keep the proteins from forming clumps. Tagliavini admits the potential therapy will need much more work and testing, however this kind of smaller protein has a better chance of travelling from blood vessels across the blood-brain barrier and into the brain then previously seen therapies. Whatever happens, this newly discovered APP mutation will change how researchers thing about the genetics of the disease as the first recessive mutation seen in Alzheimer’s disease to date.

Reference List:
Callaway, J 2009, “Paradoxical gene causes and protects against Alzheimer’s” New Scientist http://www.newscientist.com/article/dn16750-paradoxical-gene-causes-and-protects-against-alzheimers.html
Genetics Home Reference, Amyloid Beta (A4) Precursor Protein: http://ghr.nlm.nih.gov/gene=app
Alzheimer Solutions, Genetic Factors http://alzheimersolutions.stores.yahoo.net/geneticfactors.html
Adams, A 2008, “Genes Can Cause Alzheimer’s Disease” Genetic Health http://www.genetichealth.com/alz_genetics_of_alzheimers_disease.shtml

Student ID: 24036803

Caution: Cancer therapy may backfire!

Cancer is society’s silent killer. We never know when it will strike, and when it does, it’s absolutely deadly. What’s unfortunate is that a potential drug for curing cancer is said to be able to trigger more than half of all cancers. This potentially fatal side effect has been discovered by the researchers from Johns Hopkins by studying demethylating drugs. It is a known fact that a method called hypermethylation makes cancerous cells in the body by disrupting key biological functions. Hypermethylation occurs by increasing the amount of chemical bonds on cancer promoting genes. The method called demethylation causes the reverse reaction – cleaving off all the extra bonds formed on the genes. However, as this research has found, patients using drugs which cause this demethylation reaction may be at risk for acquiring tumours. This ultimately tells us that gene activity can be affected by factors other than actual change in the genetic code. Normally, mutagens and other cancer-causing organisms alter protein making pathways by mutating the genetic code. However, as hypermethylation shows, adding extra bonds – and by this, without altering the DNA code – to a “genetic’s on-off switch” or conversely, “ungluing” bonds of the gene may cause cancer. These processes are called epigenetic changes.

To test this theory, the researchers from Johns Hopkins gathered cells from oral tissues and treated them with demethylating drug 5 – azacytidine and observed the amount of genes that were activated by the drug. The results showed that a grand total of “106 genes specific to head and neck cancer… were activated by the demethylation process…” And according to Dr. Califano, the head researcher, “some of the genes regulate growth, others metabolize sugars and some have already been linked to cancer development.” Another interesting development there was a connection between the 106 activated genes in the cells. A gene called BORIS was present in all, coordinating certain proteins and telling them to activate certain genes through the demethylation process, hence signaling the spread of cancer.

Therefore, the epigenetic changes that occur in genes are just as effective as gene mutations when it comes to creating cancer. Epigenetic changes also induce inappropriate activation of cancer-promoting genes, hence processes such as hypermethylation needs to be prevented quickly using effective treatment. More thorough research needs to be done to make demethylating drugs safe for patients to use. Thus, in order to successfully use demethylation therapies, we need a BORIS blocking chemical so that the cancerous side effect can be prevented within cancer patients.

By 42047135

References:

Science Daily LLC 2009, 'Genetic Changes Outside Nuclear DNA Suspected To Trigger More Than Half Of All Cancers', Science Daily, March 30, [Online], Available: http://www.sciencedaily.com/releases/2009/03/090324101759.htm [2009, March 30].

For Picture:

'Tackling a hard-to-treat childhood cancer by targeting epigenetic changes' 2008, e! Science News, November 3, [Online], Available: http://esciencenews.com/articles/2008/11/03/tackling.a.hard.treat.childhood.cancer.targeting.epigenetic.changes [2009, March 30].

Additional Information:

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004961

Humanity finds a new ally in a distant distant cousin

Researchers are now using sea urchins to study and understand diseases like Cancer, Alzheimer’s, Parkinson’s, muscular dystrophy and infertility. Surprising these small, spiky invertebrates share 7000 genes with humans. When the genes of Sea Urchins and Humans are compared a fair few of the amino acid sequences are perfect matches.

Cristina Calestani, a developmental geneticist at University of Central Florida in Orlando states "You really need a relatively simple system in order to study, but still, also you want it to be complex enough and closer enough to vertebrate in order to use this information". These creatures are one of the few invertebrates that share more genes with humans than fruit flies and worms. As a result, researchers are able to create large amounts of material. Once a complete map of the Sea urchin’s DNA is done, researches will be able to have a greater understanding on genes; and how to combat and even prevent them.

Another fact on Sea Urchins is that they can live up to 100 years, and have a strong immune system. Human’s are born with innate immunity and acquire more over time. Urchin’s however only have innate immunity, however 10 to 20 times more than humans. There is the hope that studying the urchins will result in a new set of antiviral and antibiotic compounds to fight various infectious diseases.

Student no. 41303469

http://www.sciencedaily.com/videos/2007/0304-sea_urchins_reveal_medical_mysteries.htm

Cloning 'resurrects' dead and frozen mice

The idea of resurrecting the woolly mammoth may no longer be science fiction according to the results of a study at the National Academy of Sciences. In the experiment healthy cloned mice were cloned successfully from dead mice cells which had been frozen for 16years. This research could be incredibly useful for the maintenance of genetic diversity of endangered species as they could be saved by simply throwing the dead animal in the freezer and cloned later.
The researchers took a nucleus from one of the cells in the dead mouse’s tissue which had been frozen and thawed. The nucleus was then injected into a mouse cell which had had its nucleus removed. This resulted in an embryo which is used to create embryonic stem cells capable of making every cell in the mouse’s body. Clones were then produced by injecting the nuclei of these cells into other eggs.
Whilst this technique was successful for the mice it will be much more difficult although not impossible to clone extinct animals. This is because the extinct animals such as woolly mammoths have been frozen and thawed several times causing far more damage to the nucleus of their cells than those of the mice. With more research however, it is now believed that resurrecting the ancient animals will be possible.

From New Scientist Article: “Cloning 'resurrects' long-dead mice” 03 November 2008 by Rachel Nowak
Journal reference: Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.0806166105

Improved Antibiotic: Genes For Synthesizing Thiostrepton Identified

At the Georgia Institue of Technology, researchers have made a very significant breakthrough. They have discovered the genes used for the synthesis of Thiostrepton. Thiostrepton is an antibiotic and is naturally produced by certain bacteria. The researchers identified the gene cluster responsible for producing thiostrepton. Thiostrepton is derived from a gentically encoded peptide that undergoes nineteen different modifications. It is rare to find such a complicated process occuring. To add to that, this whole 19 stage process can be carried out by a single-cell bacterium, one of the most basic forms of life.

Wendy Kelly, one of the main researchers involved stated that the discovery, "was a combination of DNA sequencing, bioinformatic analysis of the encoded proteins and biochemical characterization." Despite the complexity of the process, the researchers found that the antibiotic resulted from a process controlled by the ribosome, making it a good target for genetic manipulation.

The antiobiotic is already a very powerful tool against the very dangerous MRSA (methicillin-resistant Staphylococcus aureus) and vancomycin-resistant enterococci. However the major impediment involving the drug is that it is not water soluble, limiting its applications. The researchers aim to put in subsititutions into the genetic machinery that could make it more water solube. Once this is achieved, the drug could be used for the development of a new class of antibiotics. New antiobiotics are needed as resistance and pathogens (like MRSA) are developing. This antibiotic could become extremely important in the near future.

Actual article: http://www.sciencedaily.com/releases/2009/03/090323161123.htm

Swedish scientists discover new cell-division machinery in acid-dwelling microorganism

Actual article:
ARTICLE: Swedish scientists discover new cell-division machinery in acid-dwelling microorganism Date2008-11-07
http://cordis.europa.eu/search/index.cfm?fuseaction=news.document&N_RCN=30075

Before late last year, the division mechanisms of the ‘extremophile’, Crenarchaeota were not explicitly identified. However, this changed dramatically after a discovery by Swedish scientists was made into the proteins required for its cell division. The scientists were able to isolate a certain species of Crenarchaeota from Yellowstone National park in the US that lives in high temperatures and acidic environments, allowing them to attain the required information. They found that a gene complex is activated immediately before cell division with protein products that constrict the cell to form two daughter cells that are unlike previously known proteins related to cell division in bacterial or prokaryotic machineries. The proteins (known as Cdv proteins) however, showed similarities to proteinaceous sorting complexes in eukaryotes. It can be deducted from this that there was possibly a shared origin for the development of these machineries.
This discovery not only increases knowledge of the cell biology of these ‘extremophiles’, but also reveals cell division machinery similarities with more complex organisms. This provides insight into the evolutionary history of these ‘extremophiles’ and eukaryotes, the possible origin of life in hot environments and evidence for the possibility of life in extreme environments on other planets.

Genetic Change Prevents Nicotine Binding

Smoking is the largest single preventable cause of death and disease worldwide. In Australia, in 1998, 15% of all deaths were from smoking related illnesses (1). Smoking behaviour is influenced by several factors such as nicotine dependence, genetic factors and psychosocial factors. Nicotine causes short-term increases in blood pressure, heart rate and the flow of blood from the heart. It takes approximately seven seconds for the substance to reach the brain after inhalation. Nicotine addiction begins with high-affinity binding of nicotine to acetylcholine receptors in the brain.

By all means, nicotine should paralyze us or even kill us, explains Dennis Dougherty, a Professor of Chemistry at Caltech. Nicotine binds to a receptor in the brain’s neurons, a type of acetylcholine receptor which is also found in many muscle cells. When nicotine binds to these acetylcholine receptors, it increases the levels of several neurotransmitters. If nicotine could bind with these muscle cells, it would cause the muscles to contract with such force that the response could potentially be lethal. Fortunately this is not the case, but still leaves many asking, “Why not?”

It seems to be due to a slight tweaking in the structures of the acetylcholine receptors in the muscle cells and the ones present in brain cells. The shape of the receptors and the way in which chemicals bind and contort to fit into the receptor is determined by a variety of weak chemical interactions. Possibly the most important interaction for the binding of acetylcholine to the acetylcholine receptors in muscles, is the cation-π interaction. In this interaction, a positively charged ion and an electron-rich π system come together. This interaction also happens in brain cells, however, nicotine can make the exact same kind of strong cation-π interaction that acetylcholine makes in both brain and muscle cells.

A strong hydrogen bond is made in the brain’s acetylcholine receptors unlike the receptors in muscle cells which have weak hydrogen bonding. The difference in the binding potency is caused by a single point mutation that occurs in the receptors near the key tryptophan amino acid that produces the cation-π interaction. “This one mutation means that, in the brain, nicotine can cozy up to this one particular tryptophan much more closely than it can in muscle cells,” Doherty explains, “and this is what allows the nicotine to make the strong cation-π interaction.” (2)
“We expected the nicotine’s charge would cause it to do the same thing, to have the same sort of strong interaction that acetylcholine has,” Dougherty states. “But we found that it didn’t.” (3)
So this explains why smoking doesn’t paralyze us, since the nicotine can’t get into the muscle’s acetylcholine receptors, it therefore can’t cause muscle contractions.

As well as solving a chemical mystery in nicotine addictions these findings may one day lead to better drugs to combat nicotine addiction and other neurological disorders such as Alzheimer’s disease, schizophrenia, epilepsy, autism and many more. It may even aid in developing a better drug than nicotine to produce the same enhancements of cognition, increase attention and without being addictive and toxic.

(1) http://www.abs.gov.au/ausstats/abs@.nsf/mf/4831.0.55.001 (28/03/09)

(2)(3) http://www.sciencedaily.com/releases/2009/03)0903232161121.htm (27/03/09)

http://www.americanheart.org/presenter.jhtml?identifier=4753 (29/03/09)

42024006

Dyslexia, a genetic probem?

Four independent studies from the United States, Germany, and England implicate two genes in fostering dyslexia. The genes contribute to early brain development.

Dyslexia, a learning disorder that afflicts at least 5 percent of elementary school children, is characterized by difficulties in perceiving sounds within words, spelling and reading problems, and troubles with written and oral expression.
Both of the newly implicated genes normally trigger production of proteins that assist neurons in migrating to appropriate destinations during brain formation. Each gene lies in a section of chromosome 6 that previous studies linked to dyslexia.
"Genetic testing for susceptibility to dyslexia is a realistic possibility in the future," says pediatrician Jeffrey R. Gruen of Yale University School of Medicine in New Haven, Conn.
A team led by Gruen found that variants of a gene known as DCDC2 frequently occur in individuals diagnosed with a serious reading disability but not in their immediate-family members who don't have a reading problem. The researchers studied 536 parents and siblings in 153 families, each of which contained at least one person with severe difficulties reading and spelling.

The new findings appear in an upcoming Proceedings of the National Academy of Sciences.
Gruen's group examined the DNA sequence within the crucial chromosome-6 region. DNA alterations specific to reading disability appeared only in DCDC2.
The gene's precise function remains unclear. After injecting neurons of rat embryos with a substance that inhibits DCDC2 activity, the investigators found that, as the animals' brains grew, those neurons migrated shorter distances than corresponding cells in healthy rat embryos did.
In laboratory tests on preserved human-brain tissue, Gruen's team observed high concentrations of DCDC2's protein products in areas that brain-scan studies had identified as active during both fluent and poor reading http://www.sciencenews.org/articles/20050430/bob9.asp).
A group led by geneticist Juha Kere of the Karolinska Institute in Stockholm has also found a strong association between variations within DCDC2 and severe dyslexia, as indicated by a pronounced spelling disorder. The team's study, slated to appear in the American Journal of Human Genetics, included 111 German families.
A pair of studies, both conducted in England, link dyslexia to variants of a second gene in the same chromosome-6 region. Laboratory tests indicate that this gene, KIAA0319, also influences early stages of neurons' migration.
A group led by psychologist Julie Williams of Cardiff University reported that specific variations of KIAA0319 frequently appeared in 223 youngsters with dyslexia but not in 273 children without reading problems. The scientists found no association between DCDC2 and dyslexia. They published their findings in the April American Journal of Human Genetics.
A comparably large study just completed by University of Oxford researchers has independently confirmed those results, Oxford geneticist Anthony P. Monaco told Science News.
In contrast, the U.S. and German studies uncovered no role for KIAA0319 in dyslexia. Differences among the populations with dyslexia that were studied or in criteria for diagnosing it may account for the divergent genetic results, Gruen says.
Several genes on chromosome 6 and elsewhere in the genome probably contribute to dyslexia, comments neuroscientist Guinevere Eden of Georgetown University in Washington, D.C. The involvement of DCDC2 and KIAA0319, with their role in brain development, makes sense in light of the subtle disruptions of neural activity that accompany dyslexia, Eden says.

References:
Cope, N. . . . and J. Williams. 2005. Strong evidence that KIAA0319 on chromosome 6p is a susceptibility gene for developmental dyslexia. American Journal of Human Genetics 76(April):581-591. Available at http://www.journals.uchicago.edu/AJHG/journal/issues/v76n4/42045/42045.html.

Further Readings:
Bower, B. 2005. Read all about it. Science News 167(April 30):280-281. Available at http://www.sciencenews.org/articles/20050430/bob9.asp.
______. 2003. Dyslexia's DNA clue: Gene takes stage in learning disorder. Science News 164(Aug. 30):131. Available at http://www.sciencenews.org/articles/20030830/fob1.asp.