Tuesday, July 20, 2010

GMOs

What is a GMO?
It stands for Genetically Modified Organism. It is something whose genetic material has been altered in some way using genetic techniques. It gives an organism modified genes.
If I told you some genetically modified products were:
1. A fishy tomato. It is a tomato that is frost resistant. It is created by adding an antifreeze gene from cold-water fish to it. The tomatoes can now grow in cold, frosty conditions and they proved to be successful. This way, tomatoes stay good in harsher conditions and helps farmers gain more profit.


2. Tearless Onion. In Japan they discovered the enzyme that causes tears when an onion is cut. The gene was isolated which controls the production and now can be switched on and off.


3. Blue Strawberries. Dr. Elizabeth Davies and colleagues identified the gene that makes blueberries blue and injected it into the strawberry. The taste is still exactly the same except the berry is now blue.


Which one is the fake GMO?
The fake one turns out to be the blue strawberries. Nothing has been done with those; however, that does mean the fishy tomatoes and the tearless onions are real GMOs that have been created.
Most people will say there really isn’t a need for GMOs. Everything is the best in their natural state without any genes transferred.

•One of the GMOs that I studied more in depth in my class was the BT toxin genes. BT (Bacillus thuringiensis) is a soil bacterium which produces Cry (a protein that is toxic to insects). The toxins are meant to reduce crop losses to plant-eating bugs.
•Corn and cotton carry the Bt Cry gene. There has been a version in potatoes but it is not used anymore because restaurants and other people do not want to purchase transgenic potatoes.
•Risks involved with the GMO are with people who have fragile immune systems and acknowledging that the BT toxin can increase deterioration in the body.

Cloning

Use of human stem cells?
1. Research to gain understanding of complex events in human development
2. Research to test new drugs
3. Treatment or therapy to replace dead or damaged cells

The first animal to successfully cloned was Dolly the sheep


There are two types of cloning:
Reproductive-creating offspring asexually
Therapeutic-creates organs or tissue to cure diseases or treat injuries.

There are two methods in cloning
• Artificial Twinning using embryos (Blastomere Separation)
• Somatic cell nuclear transfer.

Risks Involved:
•High failure rate
•Large Offspring Syndrome (LOS)-Animals cloned are always larger and have to be born C-section usually.
•Abnormal gene expression patterns
•Decrease in length of telomeres

Pros for Cloning
•Production of animals models for disease study
•Production of stem cells
•Produce drugs from transgenetic animals
Agricultural Application
•Produce animals w/desirable traits
•Increase efficiency of livestock production
•Preserve endangered animals

Cons for cloning
•Decline in genetic diversity
•It is taking nature into their own hands
•Religious and moral reasoning
•Physical problems (birth defects)
•Possibility of mental and emotional problems of the clone



Do you think cloning is an acceptable thing to do? Will it ever fully be figured out? It is a complicated process that doesn’t have a high success rate.

Cystic Fibrosis


What is Cystic Fibrosis?
It is an inherited disease affecting the lungs and digestive system.
Mucous clogs the lungs, making it difficult to breath and leads to potential life-threatening infections.
•The disease keeps natural enzymes from helping the body break down food and absorbing the nutrients.
•The most common mutation occurs on the gene DeltaF508.
•People born with the disease typically live to their 30’s or 40’s which has increased significantly since research has been done.


Diagnosis:
•Most people are diagnosed by age two
•Roughly 1,000 new cases come about every year.



Inheritance:
•It is a recessive disease caused by mutation on chromosome 7.
•Heterozygous carriers of the gene with not show any affects. Two mutated genes have to be present for the Cystic Fibrosis to appear.
•Two unaffected parents that are carriers have a 25% chance of having an affected child.

Diagnosing
•Blood tests
•Sweat chloride test is common for determining if a person has cystic fibrosis. High salt level (salty tasting sweat)is a sign of the disease.
•Lung function tests

Symptoms (just a few)
•Slow growth
•May not have bowel movements in the first couple days of life
•Nausea and loss of appetite
•Weight loss
•Coughing/increasing mucous in lungs
•Nasal Congestion
•Sinus pain/pressure
Two people having the same mutation may have different symptoms because CF (Cystic Fibrosis) is influenced greatly by genetic factors.

Most kids are normal until they reach their adolescence or adulthood.
They are encouraged to participate in activities as normal until the disease catches up to them and they become disabled.

Population Genetics
About 1 in 2,500-3,500 newborn Caucasian Americans has this disease.
The genetic disorder can’t be prevented.
Some treatments can delay death including:
•Antibiotics
•Chest physical therapy
•Exercise
•Lung problems/possible transplant

Fragile X-Syndrome

Got that name because of its fragile appearance on the x-chromosome
Discovered in 1910 by Thomas Morgan
•It is the most common type of mental retardation inherited
•Normal life span for people who inherit the mutation
•Severity can range but it is typically more severe in males than females
•Anxiety and unstable mood with autistic behaviors


Inheritance
•X-linked recessive
•FMRI is mutated from too many copies of CGG in DNA. When repeats occur too much, FMRP (connects the nerve cells) doesn’t function.

•CGG normal repeats is 6-45 times
• Pre-mutation is 55-200 times
• Full mutation is 200-800 times.



CURE
•There is no cure. Genetic counseling is an option before getting pregnant. Speech and development therapies are available to make a person the most normal.

Percentages
1:2000 males 1:800 male carriers
1:4000 females 1:250 female carriers

Duchene Muscular Dystrophy- discovered in 1861

It is an inherited disorder that involves muscle weakness that continually worsens.

Symptoms-Usually appear early on in childhood.
• Progressive muscle weakness •Belly sticks out due to weak muscles
•Ability to walk worsens •Thin weak thighs
•Motor skills impaired •Starts to affect breathing and heart.
•Skeletal deformities

Life Expectancy is found to be teens to mid thirties

Diagnosis
Gene testing shows errors on Xp21

Gene Mutation
Lack of dystrophin protein
DMD is located on x-chromosome on Xp21 locus
It is an x-linked recessive gene. Boys are generally the ones affected.

Complications
•Congestive heart failure(rare)
•Deformities
•Irregular heart beat(rare)
•Mental impairment

Prevention and Treatment
•No cure
•Use steroids to treat
•Exercise helps and braces when they can’t walk as well. Physical therapy helps.

Familial Hypercholesterolemia-found on chromosome 19

It is a condition passed down through families when a person has high levels of “bad” cholesterol (LDL) in the bloodstream beginning at birth. It can cause heart attacks early on in life.



It is only necessary to get the abnormal gene from one parent in order to receive the disease. If a child is homozygous (received the gene from both parents) it is much more severe.


•Discovered in 1938 as Autosomal Dominant.
•There are high cholesterol levels. Chest pains and leads to heart disease.
•Increases risk of heart attack. Men=40-50 yrs old. Women=50-65 yrs old (if heterozygous)
•If homozygous then heart attacks are possible around 20-30 yrs old.
•If homozygous, LCL receptors remove cholesterol from blood but if a person is homozygous then they don’t really work
• PCR testing can be done to find out if a person has the disease.

•It is not a very common disease (heterozygous-one in 500 people).You can’t prevent the gene; however, you can prolong from getting a heart attack. Liver transplant is a possibility to help or have agents which help lower cholesterol levels.


Treatment
•Proper diet-decrease fat intake to less than 30% of the total calories each day.
•Exercise
•Medications
•Drug Therapy
•Possible surgery (liver transplant)

Phenulketonuria(PKU)-Autosomal Recessive

It is a rare condition when a baby is born without the ability to properly break down an amino acid called phenylalanine.

•there is a mutation in a gene which codes for the enzyme (PAH)
•It is found on chromosome 12
It is a recessive allele so therefore a person must have two copies of the allele in order to be affected by the disease.


Prognosis
•All states test for the disease within first two weeks of birth (Guthrie test & HPLC test)
•It occurs every 1 in 15,000 births.

Symptoms (if un-treated)
Mental retardation, seizures (if you don’t follow the diet)

Treatment-requires a diet low in phenylalanine
“diet for life”
Foods high in phenylalanine
-eggs, fish, seafood, milk, aspartame, sweeteners, meats
Mothers that are carriers should be on the diet while pregnant.
•Take supplements to replace nutrients
•As long as the diet is followed, development and life expectancy is normal.