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Angelina's Research Report Edits

Created By: Riley Quijano
Caffeine is a type of stimulant drug that is widely taken across the world. It is mainly characterized as a way to get a quick burst of energy and a sense of alertness, causing many people to consume it early in the morning, mainly in the form of coffee. Caffeine is a psychoactive drug, meaning it has an effect on the nervous system, which causes the brain to function differently. Although it is classified as legally safe by the FDA for being a not-so-lethal psychoactive drug, unlike drugs like cocaine, marijuana, hallucinators, and etc., what effect does caffeine have on organisms other than giving people a wake up call?

It has been proved that animals' locomotion can be affected by caffeine. Some effects of caffeine are not experienced by humans, but humans cannot avoid all of caffeine's effects on the central nervous system (Chawla 2011, 1). The most evident effects of caffeine include a sense of alertness, increased energy, and an increased sense of focus. Although moderate levels of caffeine intake are harmless, high amounts of caffeine intake can result in jitteriness, anxiousness, not being able to sleep, and fast heart palpitations (Chawla 2011, 2). 

The composition of caffeine is similar to that of uric acid (Chawla 2011, 4). Caffeine is mostly found in drinks and some foods. When people think of items with caffeine in it, they will of course think of coffee. In addition to coffee, caffeine is also in tea, energy drinks, chocolate-based drinks, candy bars, and soda. Coffee contains the most caffeine out of these products with 71-220 mg/150 mL (Chawla 2011, 3). 

Neurons in people's brains are constantly working while people are awake and while they work, they produce a byproduct called adenosine. If one's adenosine levels get too high, which is tracked by the nervous system, the body starts to become tired and drowsy in response to this (Purdy 2010, 1). There are adenosine receptors all over the body and in muscle and as quoted by Braun, the author of the book  Buzz: The Science and Lore of Alcohol and Caffeine, "For one thing, the problem with caffeine is that there are adenosine receptors all over the body, including muscles." (Purdy 2010, 7)

Adenosine is impersonated by caffeine, and therefore results in caffeine being accepted by adenosine receptors. The caffeine attaches itself to the receptors and blocks the receptors, which lets stimulants produced by the brain, dopamine and glutamate, to give the person a sense of alertness. Braun describes this behavior as, "Like taking the chaperones out of a high school dance" and in his book, "putting a block of wood under one of the brain's primary brake pedals." (Purdy 2010, 3)

In the same article, the author also explains how the brain starts to become more tolerant towards the effects of caffeine (Purdy 2010, 4). Purdy also states that the tolerance for caffeine starts to develop after a week to twelve days of daily caffeine intake (Purdy 2010, 5). However, one can start to experience symptoms of caffeine withdrawal after around 12 to 24 hours of caffeine consumption also. The body becomes so used to consuming caffeine and living with caffeine that it doesn't seem to know how to function without the presence of caffeine in the system. Purdy lists the withdrawal symptoms as, "Headaches are the nearly universal effect of cutting off caffeine, but depression, fatigue, lethargy, irritability, nausea, and vomiting can be part of your cut-off, too, along with more specific issues, like eye muscle spasms." (Purdy 2011, 6)

 Caffeine is absorbed quickly in the stomach of humans, and finally hits the bloodstream in about 1 to 2 hours. Most bodily tissues absorb caffeine, and that causes it to affect most of a person's body (Braun 2013, 1). Exercise can be affected by caffeine because when someone exercises, they break down a sugar taken from food called glycogen, but caffeine helps slow down the body from draining the glycogen by encouraging the use of fat as a source of energy. Energy can be saved for longer amounts of time this way (Braun 2013, 2). However, contradictory to the previous study mentioned, another study was performed to see how caffeinated drinks can effect performance. Subjects didn't know whether their drink had caffeine in it and only 50% guessed correctly afterwards (Kovacs 1998, 2). The experiment concluded that caffeinated drinks didn't effect cycling performance (Kovacs 1998, 1).

Research on whether caffeine affected a newborn baby's weight and fetal growth was set up from 1996 until 1998 (Clausson, et al. 2001, 1). Scientists recruited mothers in Sweden who were pregnant with a single infant (Clausson, et al. 2001, 2). Scientists found that caffeine intake did not have any association with birth weight and fetal growth. Exposure to caffeine did not even affect the mothers when they took in caffeine during their 32nd to 34th weeks of pregnancy, which is towards the end of the last trimester of pregnancy (Clausson, et al. 2001, 3).

In a fairly recent study, it was discovered that caffeine affected bees in a positive way. Scientists set up an experiment where they produced "nectar" with the same amount of sugar, but various levels of caffeine. The caffeine levels ranged from no caffeine at all to about the same amount of caffeine as instant coffee. Scientists also tested whether increasing sugar levels would also contribute to the memory-boosting, but the results were the same as the regular sugar level nectar fluid (Reshanov 2013, 1). Within 24 hours of the experiment, the amount of bees that remembered the nectar tripled and by 72 hours, doubled (Gorman 2013, 1).

This kind of relationship not only benefits the bees, but also the flowers. The flowers are competing with other nectar producing organisms and the caffeine helps them gain more pollinators, which result in more fertilized eggs (Reshanov 2013, 2). However, scientists also found out that high amounts of caffeine can effect the bees negatively. If caffeine levels reach 1mM, the measurement of concentration in a solution, the bees will become less interested in the nectar solute (Reshanov 2013, 3). 

Endogenous glucose production was found to be not affected by caffeine. Endogenous glucose production, abbreviated as EGP, is when the body produces glucose (Battram et al. 2005, 1). The caffeine did affect adrenaline levels, but there was still no affect whatsoever on the EGP levels (Battram et al. 2005, 2). It was concluded that a human's EGP levels are not affected by caffeine, but it was found that dogs' glucose output is affected by caffeine (Battram et al. 2005, 3). 

Caffeine is a pretty powerful psychoactive drug and it has many affects on organisms. It has both positive and negative affects, which can mainly stem from the user of caffeine in many cases. I learned that caffeine doesn't just give people a wake-up call just by consuming it, but that it actually just helps the brain's own stimulate to wake up on it's own by block receptors.(Sentence is difficult to understand) Also, that it can give bees a memory boost, but can also give them different behaviors towards flowers if the caffeine levels are too high. All in all, caffeine is one of natures most complex products, in my opinion. This report is really good but short of the 1800 word requirement.
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Alex's Research Report Edits

Created By: Riley Quijano
How the brain controls the speech in your body is very complicated and amazing and some ways to explain (clarify what you mean by "and some ways to explain")   are the background of the brain and speech relations,   which part of the brain controls speech, the areas of the brain, and some of the many speech disorders and aphasias. (Revise this intro. Provide a hook and split it up in to multiple sentences. This is one big run-on right now)

Researchers have been studying how the brain works and always asked questions about how it even can control speech. Speech is in all creatures for mating calls, communication, coordination in work, etc.(Try to leave out abbreviations like "etc.") The list can go on forever (Miyagawa et.al 2013, 1). It is what is needed for all successful life, as people depend on good speech skills every day (Kerlin et.al 2010, 1). But recently at the University of California San Fransisco, researchers have found through brain neuron during brain surgery where these type of skills come from.(Clarify sentence) Edward Chang, who is a neurosurgeon at the University of California San Fransisco Epilepsy Center and a worker at the University of California, San Fransisco Center for Integrative Neuroscience, said,"Speaking is so fundamental to who we are as humans – nearly all of us learn to speak, but it’s probably the most complex motor activity we do"(Rannals 2013, 3). Now that these studies are able to take place, new information is able to be recorded because before, all information was from the 1940's where they used electric stimulation to get the face and the body to twitch. But now scientists are to have a more advanced brain mapping for future events (Bardi 2013, 4).

As time goes along, that same question has come along of where in the brain does speech come from. Ever since the late 1600's have scientists been pondering on the thought of where does the speech that is said every day (might wanna take this out) come from (Murphy 2013, 2). The speech in humans is in the left side of the brain. Speech in the human body comes from the sensorimotor cortex. Edward Chang performed three tests on three different patients at the University of California, San Fransisco, the sensorimotor cortex controls the lip, tongue, jaw, and larynx all at once (Bardi et,al 2013, 1). (Need a connection between the two clauses in this sentence) The scientists there said and explained this type of activity as a "split second symphony" because of how in on (?) short second, the sensorimotor cortex controls the lips, tongue, jaw, and the pharynx (Bardi et.al 2013, 2). “These properties may reflect cortical strategies to greatly simplify the complex coordination of articulators in fluent speech,” said Kristofer Bouchard. Another explanation that went along with the explanation of how the sensorimotor cortex is like a split second symphony is how the orchestra has to go ahead and (delete this) coordinate their plucks, bows, or blows to make a group sound the sounds amazing. Such is how that when a person speaks, it causes the lips, tongue, jaw, and pharynx to coordinate together for a clear articulated sound that allows for communication between people (Bardi et.al 2013, 3). When it comes that these scientists have to go ahead and test these patients during brain surgery. (Does not make sense and get rid have "have to go ahead") They have patients say stuff phrases as "I owe you a yo-yo" over many repeated trials(Cai et.al 2011, 1)

When speech comes back, and the brain has to read the words coming through and the process the response, it is the perturbed sensory feedback (Sentence does not make sense) (Feng et.al 2010, 2).

The brain has several areas that are there to help the decipher language and get it back out to respond to the conversations that people have every day. The first main area is called the Broca area, which is named after Paul Broca. Paul Broca is a French Neurologist who had a patient with major speech problems. His patient could only say the word "tan". His patient was a normal person and was able to tell what others were always saying but would not be able to respond. After Paul Broca's patient had passed away, he performed an autopsy on him to go ahead and (delete) see why his speech was so messed up. What he found was that the patient's brain, in front of the frontal lobe (does not fit with rest of sentence), his motor cortex was severely damaged which was why he was not able to speak well. The Broca area is also the area where the deciphering of words is. For example someone with Broca Aphasia (Aphasia is the inability of speech), is told the boy was slapped by the girl, they might think you said that the boy slapped the girl (Boeree 2004, 1)

The next area of the brain is the Wernicke's named area after the German  neurologist Carl Wernicke, who had the patient that  was about the complete opposite  of Paul Broca's patient, because Carl Wernicke's patient was able speak as fine as any other person but when it came to someone speaking to him, he wasn't able to go ahead and (delete) speak to other people. (Run-on sentence) When Carl Wernicke's patient died, Wernicke performed an autopsy on him and discovered that an upper part of the man's temporal lobe, which is located barely behind the auditory cortex, was damaged. So Carl Wernicke said that this part of the brain was brain comprehension.(Speech comprehension?) If someone was to have Wernicke aphasia, they would would do two things. One thing that someone with Wernicke Aphasia would do is if they were asked a question, they would probably answer with something irrational and also something that has poor grammer. Another thing that someone would do if they had Wernicke Aphasia is they would go ahead and (delete) mix up words that sound alike and or look alike. It is related to as a screwed up "Mental Dictionary" (Clarify sentence) (Boeree 2004, 2)

Even though that Broca Aphasia and Wernicke Aphasia sound like they are two separate things, they are actually somewhat connected. They are connected through a set of nerves called the arcuate fascilius. If the arcuate fascilias is damaged, as some people have (not necessary), it will result in a aphasia called Conduction Aphasia. These people are said to have it easier than people that have Broca Aphasia and Wenicke Aphasia. What happens is that those people with Conduction Aphasia are able to clearly understand what people are saying. They can also go ahead and(delete) speak coherently but with some amount of difficulty. But when it comes to the process of having to go ahead(delete) repeat what someone had just said, they are unable to process the information they had just heard.

The last area of the brain is the angular gyrus, which is about halfway between the Wernicke area and the visual cortex. The angular gyrus was discovered during an autopsy of a young patient who died.(Technically redundant because "autopsy" means that the person is dead) The young patient had reading problems, but when the autopsy occurred, they found that his angular gyrus had several problems and abnormalities. The scientists who had gone ahead and (delete) conducted the autopsy discovered that the angular gyrus is where several speech problems are from, such as Alexia, which is the inability to read, Dyslexia which means difficulties with reading, and finally the inability to write which is agraphia (Boeree 2004, 3).

There are many aphasias and speech disorders. Another aphasia is the Global Aphasia. It happens when both the Broca area and the Wernicke area are both damaged. What happens to those that have been diagnosed with global aphasia is that they are affected with speech problems in both language and speech.  They can only say a few words and phrases at most and understand a few phrases and words. They also will not be able to carry out commands that people have given to them or even name objects. Also they cannot go ahead and (delete) repeat read or write.(Confusing sentence) And finally repeat out words or phrases people have said to them.(Does not make sense) Hence the reason, Global Aphasia, because it affects both of the major speech areas of the brains, and its symptoms are most of the other aphasias (Does not make sense) (Anonymous 2013,1)

Another aphasia is Logopenic Progressive Aphasia. What happens is that when the angular gyrus in the temporal lobe and inferior parietal lobe can lead to Logogpenic Progressive Aphasia. (Does not make sense) The symptom of Logopenic Progressive Aphasia is slowed speech while normal articulation is taking place. Impaired comprehension of sentence syntax as well as the impaired naming of things. (Fragment / Does not make sense) Logopenic Progressive Aphasia is hypothesized to be somehow connected to Alzheimer's (Anonymous 2013, 2)

Primary Progressive Aphasia is another aphasia. What happens in the brain is that all parts of the brain start to go ahead and (delete) go away that control speech and language. Which is the left (dominant) part of the brain in the frontal temporal and parietal regions. (Does not make sense) The thing that is different about Primary Progressive Aphasia is that it gradually gets worse and worse and it starts with simple speech problems such as normal speech and language disorders. It starts just as a normal degeneration would be with speech and language issues.(Does not make sense) What ends up happening is slowly more aphasias and speech disorders. The speech disorders it develops are progressive non-fluent aphasia, semantic dementia, and Logopenic Progressive Aphasia. It comes from a group of underlying diseases. But mostly Alzheimer's or Frontotemporal Lobar Degeneration (Anonymous 2013, 3)

Another Aphasia is Transcortical Motor Aphasia, which is when  the communication between the Broca Area and the pre-motor or Supplementary motor area is cut off. Since the Wernicke's Area and the Arcuate Facicillius are ok, people with Transcortical Motor Aphasia have good repetition skills, but cuts off the link between the Broca's area and the basal ganglia and or thalamus. In the basal ganglia and thalamus have some sort of pre-motor function along with it. Damage could end up causing symptoms that will affect the link in between the Broca Area and limbic system which is involved in memory, speech, and language. Since that Transcortical Motor Aphasia does not affect aphasia, repetition does not affect grammar and articulation is normal. Someone with Transcortical  Motor Aphasia will have a big problem organizing a response in the event of a question. If someone with Transcortical Motor phasia was asked something  like why are you in the hospital, they would not be able to answer it. They will be able to answer what their home town is or yes or no questions. Those with Transcortical Motor Aphasia can not answer questions well. But will have good to fair articulation. And good to excellent audio comprehension (McCaffery 2013, 1). (Revise fragments throughout this whole paragraph, and define scientific terms. Currently difficult to understand)

The final Aphasia I will present is Auditory Aphasia. It results from damage to the Temporal Lobe which includes part or all six different corticl areas on the internal part of the cortex. Studies led researchers to believe that to general terms that as the posterior temporal gyrus or Heschi gyrus. (Does not make sense) The second auditory area is the posterior superior portion of the temporal lobe, which includes most of the middle temporal lobe. (Anonymous 2013, 1)

The brain is a very complex part of the body as is, but when it comes to speech, the brain contolling the speech of  the human body and its disorders, it does not get more complicated as the aphasias and speech disorders go on. (Conclusion should be longer.)
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Daylen's Research Report Edits

Created By: Riley Quijano
                            Imagine a world where all problems within your DNA could be solved with simple operations. Where diseases would be near nonexistent, and rare and useful materials could be salvage with ease. (Sentence should be clarified)  By using protein modifications and genetic engineering, scientists plan to accomplish these type of things. Scientists plan to use these methods to modify crops, create goat milk, repair proteins in DNA, and find ways to extract materials with more ease. Scientists are also trying to use these methods to create a more sustainable way of living.

(should make a topic sentence to start off paragraph) Protein engineering is the act of changing the protein to something that is desired, rather than not (Kumar 2012 1). By doing this scientists are able to create new types of proteins. Researchers are able to use this branch of science to make materials with new strengths and abilities (anonymous a 2013 1). Through this, scientists are able to create materials that do not show up in the outside environment (anonymous a 2013 2). Genetic engineering is not that much different from protein engineering. It is the art of modifying genes in living organisms. They do this by adding genes from other animals modified to the scientists specifications (anonymous b 2003 1). Because of the use of genetic modification, the new DNA becomes a part of the animal and will be passed down to its offspring(Moulton 2004 1). There are over two hundred modifications created to date that have real uses in the cells of animals and plants (MacCoss?? et.al. June 2002 1).

There are a few steps scientists must follow in order to successfully complete the process of protein engineering. The first is identification. Researchers must identify the protein that must be changed. The next is characterization. Researchers must isolate and characterize the protein biochemically. The function of the protein and the relationship between the structure and the function of the protein is discovered. Researchers must then decide what type of protein modification should be attempted. Last, scientists and researchers must incorporate the changes into the desired protein (Kumar 2012 3). There are a number of techniques researchers can do to recover the DNA. Some of them are DNA sequencing, site-directed mutagenesis and DNA shuffling (Phillips 26 March 2007 1). (Explain each of these processes)

Much like in protein engineering, implementers must follow steps in order to do it correctly.(Clarify who these implementers are) The implementer must first take the desired chromosome from the DNA and add "sticky ends" onto the new chromosome and the receiving DNA. The DNA piece is then inserted into a vector to transfer the receiving chromosome. (This process needs to be explained more clearly Currently difficult to follow) The vector usually used is a plasmid, which is a circular molecule of DNA found in the cytoplasm of bacteria that bonds with the desired DNA fragment. Once that is completed, the plasmids must reproduce when the host cell does, which will create what is called a gene library. To find the desired DNA, scientists screen the mixture and use gel electrophoresis. This uses a positively charged grid to attract the negative charged DNA fragments. Radioactive or fluorescent probes are then added to produce visible bands. Once the steps have been completed the DNA is ready for commercial use (Moulton 2004 1).

One of the many ways to use genetic engineering is to take the spider silk gene and transfer it into goat's DNA (?). They take the gene and insert it into a goat egg. When the baby goat is born and it lactates, there is spider silk in addition to the normal milk. To extract the spider silk, they take every spider fibre and spool it on a reel. These people have discovered that the spider's silk can be used to repair ligaments, can become a type of elastic, and can be inserted into the body without worry of inflammation (Rutherford 14 January 2012 1). Other uses for spider silk include bullet proof clothing, ligament repair, (ligament repair is listed twice) bandages, Kevlar replacement, ropes, nets, parachutes, rust free panels on boats and planes, bio-friendly water bottles, and new lightweight clothing. These are only a few of the many possibilities of spider silk (anonymous c 2013 1).

One of the many materials that protein modifications have been able to create are immunotoxins. Immunotoxins are described as "the conjugates of cell binding antibody or antigens, covalently bound to a plant or a bacterial toxin"-(anonymous d 2009 3). This helps patients treated with it because the antibody part of the immunotoxin finds cells that need to be killed and the toxin part of it actually does the killing part. ("Part" is repeated many times in this sentence) These immunotoxins are also used for research on tumor cells and how immunotoxins effect them (anonymous d 2009 3).

With the threat of peak oil around the corner, scientists have been searching for an alternative to oil and other petroleum resources. They believe that through genetic engineering they can create a ecofriendly biofuel that can be more sustainable for the planet. They believe this will be a much better alternative to much more costly oil products. Scientists have been searching into algae and seaweed related bio fuels for decades. Microalgae specifically have been at the front part of scientists' minds as a possible resource for bio fuel. One of the reasons scientists are so focused on the sea related bio fuel options is the ability to not have to take portions of the harvest of corn and soy beans for bio fuel use. Sea related plants can also be used year round where as crops can usually only be harvested annually (Radakovits 10 April 2). From the plants, they specifically want to use the carbohydrates. Using carbohydrates leaves several types of bio fuels to be used including ethanol, butanol, and methane (Radakovits 10 April 2). Others plan to do this by changing the plant's cell wall to make a more rapid breakdown into the bio fuel ethanol. (Clarify the relationship between the breakdown of the cell wall and the production of ethanol. A little hard to understand) Nevertheless many people still believe, no mater how it is done, that it is a national priority even though scientists are still very far from tapping into the true potential of using genetic engineering to increase the use of bio fuels (Rao May 2008 2).

With the global population rising faster than ever before, scientists have been getting worried about how much longer the earth will remain sustainable for all of the people's needs. Through the process of protein engineering, they believe they can solve some of the food related problems. Scientists believe they can modify plants so that they can grow outside of where they normally can (Rao May 2008 3). Scientists observed that when crops go through a large drought,or experience extra high temperatures, there is a severe drop in crop harvesting(Rao May 2008 4, Yang et.al. 22 March 2010 1).Scientists believed this could be caused by impaired photosynthetic efficiency due to a lack of catalytically competent Rubisco at high temperatures.(Define Rubisco) It is known that Rubisco is regulated by Rubisco activase, which is inhibited at temperature less than 45°C. After testing a hypothesis that increasing the thermal stability of Rubisco activase can lead to increased photosynthetic activity at elevated temperatures, it was discovered that instead of targeting Rubisco, it would be better to do protein engineering on Rubisco activase to keep plants surviving at higher temperatures (Rao May 2008 4).

Recently, there have been discoveries on possible cancer cures by using genetic engineering. Scientists took blood samples from 17 patients. They then took a special type of cell, called a T-cell. They genetically modified them to kill cancer cells. The scientists and doctors then injected them back into each patient with the hope that they would multiply and kill the cancer cells (Nilsson 31 August 2006 1). The doctors had then discovered that after one month, the tumors throughout Mr. Origer's body had shrunk by 50%. (Who is Mr. Origer) Then after 18 months, they had declared him to be cancer free. Only him and another, however, lived, and the other 15 patients had died from the cancer (Nilsson 31 August 2006 2). Scientists warn that this is not a fool proof cancer treatment. They fear that because the killer T-Cells could attack normal body tissue with the same receptors as the cancer cells, they could slowly destroy someone's body (Nilsson 31 August 2006 3). In addition to this treatment, others are thinking of a program where pieces of DNA go into your cells and, based on 5 criteria, decide if it is a cancer cell. If it is a cancer cell, then that DNA will destroy the cancerous cell. If, however, there is no cancer, then the DNA will just mover on to another cell (Rutherford 14 January 20122).

Another way genetic engineering can help people with getting around Earth's hurdles is the genetically modified banana.(Revise this sentence) In Uganda, bananas are a very important crop. Scientists wanted to take the gene of resistance to certain diseases and insert it into the DNA of the edible bananas. The disease that is the main source of losing banana crops is called the black leaf streak disease. It is estimated that the people of Uganda lose 50% of their crops every year due to this disease. Scientsists were able to combine the genes to create a black leaf streak disease immune banana, which is now being distributed in Uganda (Mestel 12 July 2012 1). Scientists theorize that the reason that plants, such as the wild banana, are immune to these diseases is that they are in the wild, constantly being attacked by bugs, fungus, and others (Mestel 12 July 2012 2).

Clearly, through much examination I have shown you how genetic and protein engineering are able to assist people and help make the Earth a more sustainable environment. Genetic engineering can be used to make bio fuels out of sea plants, can be used to make disease immune bananas, create new door for the cure to cancer, and create new and easier ways to get spider silk. Protein engineering can be used to create immunotoxins to help someone's body fight disease and create more places to farm.

Through our lives it has only gotten tougher.(Consider making first sentence of this paragraph a little stronger) The world is changing around us and our resources continue to dwindle more and more. How would you like to solve these problems? You can. Genetic and protein engineering can and are improving our lives and our sustainability. All you have to do is think of what needs to be done.
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Gelman, 2013

Created By: Riley Quijano

In the late 1990s, [1] some researchers started raising concerns over the amount of thimerosal -- a mercury-containing preservative -- found in many children's vaccines. Although thimerosal had been used as an anti-contamination agent for decades, until 1991 the diphtheria-tetanus-pertussis (DTaP) vaccination was the only thimerosal-containing shot recommended for infants and children. The hypothesis: As more thimerosal-containing vaccines like hepatitis B and Hib were added to the recommended schedule, [2] researchers worried that babies were receiving too much of the chemical in too short a timeframe, which could potentially impact brain development.
To understand more about thimerosal safety, a brief chemistry/history lesson is in order. [3] Thimerosal was removed from most vaccines by 2001 because researchers worried that children were being exposed to too-high levels from receiving multiple vaccinations in a short timeframe.

[4] But this decision was based on what levels were considered safe for methyl mercury -- the kind in fish, which is structurally very different from the ethyl mercury found in thimerosal. Although scientists suspected that thimerosal was much safer than methyl mercury, they decided to remove it anyway, just to be super-careful.

[5] Now, new research published in the journal Pediatrics shows that babies excrete thimerosal too quickly for it to build up to dangerous amounts. In the study, researchers tested the blood mercury levels of Argentinean babies after they received routine childhood vaccinations (thimerosal is still used as a vaccine preservative there). They found that infants expel thimerosal about 10 times faster than fish mercury -- so rapidly that it can't accumulate in the body between vaccine doses.

"This study helps to debunk a crucial basis of the autism-vaccines theory, which held that babies were getting so many thimerosal-containing shots that the chemical would build up in the bloodstream and eventually cross over to the brain, where it could theoretically impact development," says study author Michael Pichichero, MD, a professor of microbiology/immunology and pediatrics at the University of Rochester Medical Center. "But thimerosal leaves babies' bodies way too quickly for that to happen, which just adds more proof that this theory is extremely unlikely."

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Mitchell, 2012

Created By: Riley Quijano
A trio of papers in this week’s Nature identifies mutations causing autism in four new genes, demonstrate the importance of de novo mutations in the etiology of this disorder and suggest that there may be 1,000 or more genes in which high-risk, autism-causing mutations can occur.

These studies provide an explanation for what seems like a paradox: on the one hand, twin studies show that autism is very strongly genetic (identical twins are much more likely to share a diagnosis than fraternal twins) – on the other, many cases are sporadic, with no one else in the family affected. How can the condition be “genetic” but not always run in the family? The explanation is that many cases are caused by new mutations – ones that arise in the germline of the parents. (This is similar to conditions like Down syndrome). The studies reported in Nature are trying to find those mutations and see which genes are affected.

They are only possible because of the tremendous advances in our ability to sequence DNA. The first genome cost three billion dollars to sequence and took ten years – we can do one now for a couple thousand dollars in a few days. That means you can scan through the entire genome in any affected individual for mutated genes. The problem is we each carry hundreds of such mutations, making it difficult to recognise the ones that are really causing disease.

The solution is to sequence the DNA of large numbers of people with the same condition and see if the same genes pop up multiple times. That is what these studies aimed to do, with samples of a couple hundred patients each. They also concentrated on families where autism was present in only one child and looked specifically for mutations in that child that were not carried by either parent – so-called de novo mutations, that arise in the generation of sperm or eggs. These are the easiest to detect because they are likely to be the most severe. (Mutations with very severe effects are unlikely to be passed on because the people who carry them are far less likely to have children).

[1] There is already strong evidence that de novo mutations play an important role in the etiology of autism – first, de novo copy number variants (deletions or duplications of chunks of chromosomes) appear at a significantly higher rate in autism patients compared to controls (in 8% of patients compared to 2% of controls). [2] Second, it has been known for a while that the risk of autism increases with paternal age – that is, older fathers are more likely to have a child with autism. (Initial studies suggested the risk was up to five-fold greater in fathers over forty – these figures have been revised downwards with increasing sample sizes, but the effect remains very significant, with risk increasing monotonically with paternal age). This is also true of schizophrenia and, in fact, of dominant Mendelian disorders in general (those caused by single mutations). [3] The reason is that the germ cells generating sperm in men continue to divide throughout their lifetime, leading to an increased chance of a mutation having happened as time goes on.

The three studies in Nature were looking for a different class of mutation – point mutations or changes in single DNA bases. [4]They each provide a list of genes with de novo mutations found in specific patients. Several of these showed a mutation in more than one (unrelated) patient, providing strong evidence that these mutations are likely to be causing autism in those patients. [5] The genes with multiple hits include CHD8, SCN2A, KATNAL2 and NTNG1. Mutations in the last of these, NTNG1, were only found in two patients but have been previously implicated as a rare cause of Rett syndrome. [6] This gene encodes the protein Netrin-G1, which is involved in the guidance of growing nerves and the specification of neuronal connections. CHD8 is a chromatin-remodeling factor and is involved in Wnt signaling, a major neurodevelopmental pathway, as well as interacting with p53, which controls cell growth and division. SCN2A encodes a sodium channel subunit; mutations in this gene are involved in a variety of epilepsies. Not much is known about KATNAL2, except by homology – it is related to proteins katanin and spastin, which sever microtubules – mutations in spastin are associated with hereditary spastic paraplegia. [7] How the specific mutations observed in these genes cause the symptoms of autism in these patients (or contribute to them) is not clear – these discoveries are just a starting point, but they will greatly aid the quest to understand the biological basis of this disorder.

[8] The fact that these studies only got a few repeat hits also means that there are probably many hundreds or even thousands of genes that can cause autism when mutated (if there were only a small number, we would see more repeat hits). Some of these will be among the other genes on the lists provided by these studies and will no doubt be recognisable as more patients are sequenced. Interestingly, many of the genes on the lists are involved in aspects of nervous system development or function and encode proteins that interact closely with each other – this makes it more likely that they are really involved.

These studies reinforce the fact that autism is not one disorder - not clinically and not genetically either. Like intellectual disability or epilepsy or many other conditions, it can be caused by mutations in any of a very large number of genes. The ones we know about so far make up around 30% of cases – these new studies add to that list and also show how far we have to go to complete it.

We should recognise too that the picture will also get more complex – in many cases there may be more than one mutation involved in causing the disease. De novo mutations are likely to be the most severe class and thus most likely to cause disease with high penetrance themselves. But many inherited mutations may cause autism only in combination with one or a few other mutations.

These complexities will emerge over time, but for now we can aim to recognise the simpler cases where a mutation in a particular gene is clearly implicated. Each new gene discovered means that the fraction of cases we can assign to a specific cause increases. As we learn more about the biology of each case, those genetic diagnoses will have important implications for prognosis, treatment and reproductive decisions. We can aim to diagnose and treat the underlying cause in each patient and not just the symptoms.
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Anonymous g, 2013

Created By: Riley Quijano

Children with childhood disintegrative disorder typically show a [1]dramatic loss of previously acquired skills in two or more of the following areas:

  • Language, including a severe decline in the ability to speak and have a conversation
  • Social skills, including significant difficulty relating to and interacting with others
  • Play, including a loss of interest in imaginary play and in a variety of games and activities
  • Motor skills, including a dramatic decline in the ability to walk, climb, grasp objects and perform other movements
  • Bowel or bladder control, including frequent accidents in a child who was previously toilet trained

Loss of developmental milestones may occur abruptly over the course of days to weeks or gradually over an extended period of time.

When to see a doctor
Children typically develop at their own pace, but any loss of developmental milestones is cause for concern. If your child has suddenly lost previously acquired language, social, motor, play, thinking (cognitive) or self-help skills, such as toilet training and feeding, contact your doctor. In addition, if you suspect that your child has gradually shown a loss in any area of development, talk with your doctor.

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