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Timajhe's paper

Created By: Sarah Nguyen
(Write more.. and make your your paragraphs into different paragraphs. 
Introduction

Have you ever wondered what it might be like to be immortal? Or maybe you've wonder if there are any possible ways to cure cancer. Some might think that it would take supernatural help to accomplish this. But scientists may have discovered a way that would not be as difficult.(Don't start your sentence with BUT..)  Resetting Neurons has captivated scientists for years. Neurons are nerve cells located in the brain that are the basic components involved in the nervous system. They are specialized cells that transmit impulses through the body. Resetting neurons could potentially cause the brain to revert to a younger age. Scientists are positive that this process can be done based on the discovery of the Immortal Jellyfish. The Immortal Jellyfish resets the neurons in its brain to become sexually mature. It constantly does this and is therefore considered immortal, unless killed by another animal. This discovery and recent research has given scientists hope of finally finding a cure for fatal viruses and diseases that provide a huge probability for the person to die. In this report I will explain what neurons are, how they can help people, and why they can help people who are suffering from illnesses that threaten theiFindings.(What are ifindings?)

Findings
(Don't start your paragraph with "there are a lot of things"...) 
There are a lot of things that are important to first learn about neurons before you can understand how resetting them works. Neurons are nerve cells the are in the brain that are much like other cells, but also different in many ways.  ( this sentence does not make sense..) Some similarities include: a nucleus, cell membrane, mitochondria, golgi bodies, and cytoplasm(Cherry 2011 1, 2) (Don't start your sentences with but..)  But a big difference is that neurons stop growing very shortly after growing and do not go through mitosis. Some types of neurons include sensory neurons, motor neurons, and interneurons. (Cherry 2011 3) Sensory neurons gather information from the sensory receptors found around the body, and it brings it back to the brain. Motor neurons allow the muscles to work by sending information from the brain telling the muscles what movement to make. Interneurons are responsible for communicating information from one neuron to the next. Interneurons are composed of axons and dendrites. The dendrites in neurons receive information from the sensory receptothars(Do you mean Receptors..?)  throughout the body or receive information from other neurons (This sentence doesn't make sense.)  (Don't use the shortcut of information..) This information then travels through the axons in the form of action potential, or an electrical signal. Once the action potential reaches the axon's end, the information (Try to find another word for information..) is transmitted across a synapse to the next neuron's dendrites. Sometimes the jump across the synapse happens extremely fast (Cherry 2011 4, 5, 6, 7 , 8). Other times, neurotransmitters are needed to give the information to the neuron. Neurotransmitters are chemical messengers that are released by the axon to jump the synapse and reach the receptors of the other neuron. Neurotransmitters are important in everyday life. Some important neurotransmitters are Acetylcholine, Endorphins, and Dopamine. Acetylcholine associates with memory, muscle contractions, and learning abilities. Loss of Acetylcholine is usually considered with how most people are diagnosed  Alzheimer's disease. Endorphins are components in emotions and pain perceptions. The body usually releases Endorphins to respond to fear or trauma being triggered. Dopamine is associated with thoughts and most pleasurable feelings. Parkinson's disease is caused by lack of dopamine. Contrastingly, schitzophrenia is caused by excess amounts of dopamine. (Cherry 2011 9, 10) (<Which sentence is this hyperlink suppose to be in?)  The hippocampus is the part of the forebrain which is critical to the formation of memories. It also allows the brain fast (This part is confusing..)  and also easy access to the neocortex for memories that are essential for planning the future and generating creative ideas. Most studies of the hippocampus have been conducted on rodents and gave a rise to the spacial navigation theory (Buzsaki 2011 1). 

Being immortal.(Incomplete thought?..) This idea has become popular ever since humans have worshiped deities.(What are deities?) Thousands of plays, films, and novels have been created based off of the idea of never dying. The questions is, would making people immortal be a good thing? Studies have shown that resetting neurons in the brain greatly increases memory, making connections, and the results of resetting neurons. Diseases such as Cancer, Amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, and Angleman syndrome are considered some of the most lethal diseases. These diseases can attack even the most healthy of individuals.  Due to the results of neurons, these diseases may not effect humans ever again. There is an animal that is adept(adapt?)  towards the process of restoring its own neurons. This animal is called the Turritopsis dorhnii jellyfish or as it is most commonly known as, the Immortal Jellyfish. Most jellyfish die within a year, but this particular jellyfish can live as long as something does not kill it. When the animal is hurt or deprived of food, they attach their body to a stable object and turn into a blob. This is referred to as the polyp stage in which the cells return to their juvenile stage. This process allows cells to serve different functions that differ from those that they served before the animal rebuilds itself. Even though some species of salamanders can grow new arms, legs, or tails, after one has been cut off, the Immortal Jellyfish is the only known animal that can revert to its polyp stage after sexual maturation. Though most people would want to use it on selfish things such as beauty creams or other beauty products, scientists will look forward to finding cures for cancer and other diseases. Even if victims of these diseases just hear of this study, they will gain hope that they will make it through whatever they are going through and also give hope to their families and close friends.(Reword..?)

There are many studies that are being conducted to test whether it is possible for neurons to forcibly be rest without damaging the individual. The answer is yes.The idea to use neural oscillation, or resetting neurons to an advantage, has been around for years.The brain has an ability to change neurons to adapt to new jobs in less than a second. By using this method, the brain can develop abilities that greatly outweigh those given to us at birth. The plasticity ,or its ability to change when needed,of the nervous system allows it to respond more quickly to physiological changes, enviornmental pressures, and experiences with functional changes that might last long after the events that drew out the neural plasticity are long gone. Plasticity is also present when recovering from movement or speech impairments that occur after injury, while healthy neurons in the brain are redirected to take on new responsibilities to ease the neurologic deficit in the area. This new formation of neurons may lead to new behavior patterns that are maladaptive, or incapable of providing adequate adjustment to the enviornment, and lack repairative and protective benifit. An example would be an amputee, or someone who's had a limb removed, who has serious and long-lasting phantom pain in the absence of a pain stimulus. Phantom pain is pain felt by someone who has recently been amputated. A "phantom limb" is when someone who has had a limb amputated still feels as if it were still there. An example would be someone who has had their foot amputated can still feel as if they can still move their toes around.
(Needs more findings..)?

Conclusion

All in all, the work going into the science of resetting neurons is enough to be able to see it being used to treat patients in a few years time. Families everywhere should look forward to the day when this treatment is available, especially the families of these patients.
I personally am glad that this topic is being studied because of my family members that suffer from lethal illnesses. This was the primary reason why I decided to choose this topic to write this research paper. Even the thought of being able to be cured would help a cancer patient that thought they had no chance of survival. Resetting neurons will play a great role in the future of medical tragedies.
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Jessica D Research Paper

Created By: Sarah Nguyen
(your paper is really good.. barely had edits..) 
"I sleep—for a while—two or three hours—then a dream—no—a nightmare seizes me in its grip . . . I sense it and I know it . . . and I am also aware that somebody is coming up to me, looking at me, running his fingers over me, climbing onto my bed, kneeling on my chest, taking me by the throat and squeezing . . . squeezing . . . with all its might, trying to strangle me. I struggle, but I am tied down by that dreadful feeling of helplessness that paralyzes us in our dreams. I want to cry out—but I can't. I want to move——I can't do it. I try, making terrible, strenuous efforts, gasping for breath, to turn on my side, to throw off this creature who is crushing me and choking me—but I can't! Then, suddenly, I wake up, panic-stricken, covered in sweat. I light a candle. I am alone." - Guy de Maupassant (Cheyne 2013, 7). Recent experiments have shown that activation of the neurotransmitters GABA and glycerine in REM sleep initiates motor atonia, which may still be intact while one is awake. This experience, known as sleep paralysis, can be horrifying. This essay will preview a brief background of sleep paralysis, causes of paralysis, formation of hallucinations, and possible treatments for sleep paralysis.

Background

Sleep Paralysis is a temporary skeletal muscle paralysis that normally occurs when one is waking up, but may also occur as one is falling asleep (Cheyne and Pennycook 2013, 1, Anonymous 2012, 8). Muscle paralysis, or motor atonia, usually lasts a few minutes or even seconds, but one may feel as though they are paralyzed for hours as they are aware of their inability to speak or move. The only muscles able to move are the eyes and any non-voluntary muscles such as the diaphragm (DeGuzman et al. 2010, 5, Sharpless et al. 2011, 2).

Since one's eyes are fully functional (as they are controlled by the cranial nerves), one is aware of their physical surroundings and can often project their dreams into their rooms. Those experiences are called hypnagogic or hypnopompic hallucinations, and occur in an estimated 20 percent of sleep paralysis episodes (Morton 2010, 6, 7). Hypnagogic hallucinations are those that occur as one falls asleep. In contrast, hypnopompic hallucination refer to those that take place as one wakes up (Cheyne 2013, 8). Considering that one feels vulnerable and sees paralysis as abnormal, hallucinations are often realistic and horrific (Anonymous 2012, 9). The hallucinations can be split into 3 categories: intruder, incubus, and vestibular-motor experiences.

"I suddenly could not move.... I heard two distinct voices: One was a demonic woman that said "we should have never let you get away from us"... I struggled and struggled and felt my mouth moving and calling my sister Rose... After what seemed like an eternity, the pressure suddenly left and I got up. I ran downstairs and asked Rose if she could hear me calling her name, she said No" (Anonymous 2007, 1). 

Hallucinations which are visual, auditory, and tactile sensations contribute to strong feelings of the presence of another being in the room, such as the one described in the quote above, are known as intruder experiences (Cheyne and Pennycook 2013, 4). The victim may see a shadowy figure dash across the corner of their eye or may hear faint whispers along with nearing footsteps, but no creature truly invades their privacy.

Though the diaphragm is functioning properly, breathing is automatic and cannot be controlled by a victim of sleep paralysis. This may trick the victim into believing that they are suffocating (Cheyne 2013, 16). Incubus hallucinations involve feelings of intense chest pressure, suffocation, and near death experiences (Cheyne and Pennycook 2013, 5). These experiences are often called "old hag attacks" because one may often see a demonic figure, such as a witch, sitting on one's chest, as described in the quote by Guy de Maussipant (MacKinnon 2013, 2).

Vestbular-motor experiences are much less frightening than intruder and incubus because they focus on one's body instead of the sensed presence of a devilish creature (Cheyne and Girard 2008, 4). Vestibular-motor hallucinations consists of illusory movement experiences (IMEs), and out of body experiences (OBEs). IMEs include feelings of floating, flying, falling and motor hallucinations. Motor hallucinations are those in which believes they moved a limb or even their whole body until they realize that they were paralyzed (Cheyne and Girard 2008, 13). According to an experiment in 2008, are(What is more common?)  more common than OBEs which involve seeing one's body from up above and alienation from one's body  (Cheyne and Girard 2008, 3, 8). 

Even after the brief period of extended motor atonia(What is motor atonia?) has worn off, one may suffer from post-episode distress (a lingering feeling of anxiety) (Anonymous 2012, 11). Scientists have uncovered a strong connection between fear and the intensity of the hallucinations to post-episode distress (Cheyne and Pennycook 2013, 13).(I think you should put an example?)?

Sleep paralysis is quite common seeing that over 50 percent of the world population will undergo 1 or more episodes of sleep paralysis (Morton 2010, 1). Even then the experience is seemingly foreign and abnormal. For that reason, people often seek supernatural explanations and describe their hallucinatory incident as encounters with the devil, demons, and even aliens. Different cultures have different explanations for hallucinations. For example, Africans interpreted the episodes as acts of voodoo magic from zombies,while Europeans often believed the evil creatures were witches (MacKinnon 2013, 3, 4). Supernatural beliefs about sleep paralysis date back to 1781 and further on. In 1781, Henry Fuseli painted "the Nightmare" which represents sleep paralysis itself. "The Nightmare" portrays incubus hallucinations as the portrait has a woman lying immobilized and a demon sitting on her chest as though trying to suffocate her (MacKinnon 2013, 1). Though not fully proven, some scientists believe that the vividness of an episode, among other factors, may push forth supernatural beliefs (Cheyne and Pennycook 2013, 15).

Findings

Sleep paralysis and its effects are widely known, but the causes of the episodes have only recently been studied. (You should probably write more for this sentence?)

Sleep remains the primary cause of sleep paralysis. The sleep cycle is divided into 5 stages: 4 of non-rapid eye movement (NREM) and 1 of rapid eye movement (REM). NREM is the period of sleep in which brain waves are slowed as the body regenerates and repairs itself; each of the 4 stages lasts for 5 to 15 minutes for a total of 90 minutes (Johnson 2012, 2, 6). As one drifts into stage 1 of NREM sleep, one experiences a falling sensation which may be followed by an abrupt muscle contraction (Johnson 2012, 3). While in stage 2 (light sleep), the body slowly adjusts to stages 3 and 4 of deep sleep (Johnson 2012, 4). The final stage is a 10 minute period of REM. As the cycle repeats itself, REM periods grow longer. REM is the stage of sleep in which dreams occur and, according to EEG recordings, brain waves are similar in speed to those during wakefulness ( Johnson 2012, 7).

The REM portion of one's sleep is where motor atonia occurs as a result of dreams. Within a dream, one is constantly moving, therefore one's central nervous system (CNS) is sending frequent motor instruction to the body (DeGuzman et al. 2010, 4). In order to prevent a person from reenacting their dream, signals sent from neurons to cells called nerve impulses must be blocked, thus paralyzing the person (Anonymous 2012, 2).

Nerve impulses occur in 5 steps: resting potential, action potential, repolarization, hyperpolarization, and the refractory period. A neuron is  in resting potential when it is polarized. During polarization, the neuron is not stimulated (Wiley 2013, 2). Polarized nerve cells contain potassium with a negative charge on the inside of the cell membrane and sodium with a positive charge on the outside (Wiley 2013, 3). When a stimulus is presented, the neuron's gated channels (channels in the membrane of a neuron that open and close) permits positive sodium ions to enter the cell turning the inside positive. This is called action potential (Wiley 2013, 4). Repolarization comes after the action potential as the cell membrane allows negative potassium ions to exit the cell (Wiley 2013, 5). Hyperpolarization then takes place as there are more potassium ions outside than there are sodium ions inside (Wiley 2013, 6). After the impulse passes through the neuron, potassium ions return inside and sodium ions return outside the cell in the final step called the refractory period (Wiley 2013, 7, 8).

In order for this process to take place, neurotransmitters (chemicals produced within neurons) are necessary to transport the impulse across synapses 
(Cherry 2013, 1, 5). As an inhibitory neurotransmitter, gamma-Aminobutyric acid (GABA) reduces neuron activity by blocking upcoming action potentials therefore stopping impulses (Wiley 2013, 9). The blockade formed by GABA, however, is not enough to paralyze a person. According to Patricia Brooks and John Peever (2012, 8), the inhibitory neurotransmitters glycerin and GABA must both block impulses in order to initiate REM motor atonia. 


Sometimes, GABA and glycerin continue to block nerve impulses even though it is no longer necessary. In other words, REM motor atonia extends into wakefulness therefore creating sleep paralysis episodes (Brooks and Peever 2012, 13).   

Neurologists were able to find the cause of sleep paralysis, but what induces hypnagogic and hypnopompic hallucinations? James Cheyne and Todd Girard (2008, 6) suggest sleeping in the supine position (face up) is a general cause of hallucinations, but what happens within the brain to trigger such vivid experiences?

Though not all scientists agree, the amygdala is fundamental to conjure hallucinations during sleep paralysis. The amygdala (plural form amygdalae) are 2  small, almond-shaped masses of grey matter located inside the brain. The "threatactive vigallince system" as James Cheyne (2013, 3) calls it, is responsible for one's response to intense emotions (including fear) as well as remembering these emotions. Fear is a necessary part in both animal and human development because it allows the organism to detect danger (Cheyne 2013, 5). During sleep, the amygdala is heightened (Morton 2010, 8). As explained above, one feels as though they are defenseless during paralysis thus creating immense  fear within the victim. The amygdala interprets the fear and releases the hormone adrenaline (Takahashi 2008, 4). The abundance of adrenaline increases the heart and respiratory rates (Takahashi 2008, 5). Blood pressure in the brain also increases causing change the the visual and/or auditory cortex, creating a hallucination (Takahashi 2008, 6). In other words, a victim's eyes and/or ears respond to an absent stimulus. Also an effect of fear, the victim's pupils dilate, meaning the pupils widen to let more light in, and allow the person perceive threat (Takahashi 2008, 7).

Sleep paralysis has no known cure, but it can be treated. Understanding which groups of people are more susceptible to sleep paralysis helps when treating victims.

Possible factors that increase sleep paralysis susceptibility include depression, anxiety, and stress (Cheyne and Pennycook, 14). Antidepressants used to treat these personality disorders have also been found to control the severity of episodes.

Sleep paralysis is a known side effect of narcolepsy, a disorder in which people fall asleep in any given time. Regular ways of coping with narcolepsy has shown positive effects on managing sleep paralysis among narcoleptic patients. Narcolepsy can be controlled by taking regular naps throughout the day, engaging in regular exercise, and enforcing a healthy sleeping pattern (Anonymous 2012, 15).

Studies that show students are more prone to experience these brief episodes than the general population indicate stress and lack of sleep are potential inducers (Sharpless et al. 2011, 3). People should avoid stressful situations and receive the recommended amount of sleep for their age. Ways to improve sleep include creating a comfortable sleep environment, avoiding caffeine intake, and abandoning smoking habits. Regular exercise and healthy eating habits also contribute to more peaceful sleep (Anonymous 2012, 13).

Nationality plays a major role in susceptibility as well. Considering that people of African or Asian origin are more inclined to paralysis than those of Caucasian lineage, they should ensure that other factors that increase sleep paralysis susceptibility do not apply to them (Sharpless et al. 2011, 6). 

Conclusion

In conclusion, sleep paralysis is caused by sleep, hypnagogic and hypnopompic hallucinations are formed by the amygdala, and treatments for sleep paralysis can be found by understanding susceptibility. Prolonged motor atonia created in REM sleep causes sleep paralysis episodes. Fear conjured by the amygdala causes rapid breathing and increased heart rate which forms hallucinations. Regular sleep and a healthy lifestyle are the main treatments for sleep paralysis. 
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Riley's Research Paper

Created By: Sarah Nguyen
(Remember not to indent..) 
Throughout the society, many individuals are under the impression that the primary cause of autism is vaccinations. Even though many believe this to be true, there is no scientific evidence to back up their thoughts, proving their beliefs to be invalid. So,  you may be asking a couple of questions right now such as, "Why is it that so many people have associated autism with vaccinations," or "If vaccinations do not cause autism, then what does?" Numerous scientists would have answered such questions by providing an explanation that involves genetics; however, many are beginning to question how much genetics, which was previously recognized as the only contributing factor to autism, actually affects autism. Instead, these scientists that question the reliability of a genetic answer believe that environmental factors are the sole cause of autism. Many are beginning to believe this because of the sudden dramatic increase in autism rates that has recently occurred. After researching the viewpoints of both sets of scientists, those who believe genetic causes are more influential and those who believe environmental causes are more influential, I have been led to believe that the true contribution to autism is a combination of both genetic factors and environmental factors. In order for one to make their own decision about the real cause, it is important for them to become educated about autism by learning about its background information, its symptoms, and of course, its genetic and environmental influences.

In order for one to make their own decisions about the causes of and begin to comprehend autism (This part doesn't make sense..)  it is important for them to begin by learning the basics: background information such as the chronological history, its different types, and its prevalence in recent years. The chronological history of autism began in 1908 when the term "autism" was first used by a Swiss psychiatrist named Eugen Bleuler. (Anonymous d 2013, 1, Mandal 2013, 1) However, Bleuler's use of this term is not the same as today's usage; instead, Bleuler used "autism" to describe a schizophrenic patient who never interacted with other people and was withdrawn in his own world. (Mandal 2013, 2) Bleuler's usage of his newly formulated word makes sense if dissected to the Greek etymologies; the prefix "autos", translates to "self" in modern English, and "ismos" translates to "action or state of being." So, if these two etymologies are put together, they produce a word, autism, meaning "the state of being absorbed by one's self."  (Anonymous d 2013, 2) Although the term "autism" first showed up in 1908, it was not ever recorded to be used again in an important situation until much later by a child psychiatrist named Leo Kanner, who, in 1943, performed a study involving 11 children. The children that he studied that he called autistic each shared similar features which included having troubles with socially interacting, having the five senses be extra sensitive, having difficulty adjusting to changes in a normal routine, having great memory, and having echolalia, or involuntarily repeating words or phrases said by someone else. (Mandal 2013, 3) So, Kanner was the first to classify individuals who are autistic as we know it today. Even though Kanner's use of the word is what is (Remove what is.)  widely used by society today, autism was not recognized as its own disorder until the 1960's. (Anonymous d 2013, 3) So, the most important events of the chronological history of autism include the first use of the word by Bleuler in 1908, the study performed by Kanner in 1943 that defined autism as its known today, and the recognition of autism being its own disorder in the 1960's.
        
Since the initial discovery of autism, or at least what it is known as today, in 1943, five different kinds have been established. Before one learns about these different kinds, it is first important for them to understand that autism itself is not a single disorder. Instead, autism is a spectrum of disorders that are greatly related because of their core symptoms. (Smith, et. al. 2012, 1) This is why autism's disorders are technically known as "autism spectrum disorders." The five autism spectrum disorders are autistic disorder, Asperger's syndrome, pervasive developmental disorder (PDD), Rett syndrome, and childhood disintegrative disorder. (Anonymous e 2013, 1) Although all of these disorders are all autism spectrum disorders, each one has symptoms that differ in severity.
       
One of the main reasons scientists are beginning to believe that environmental factors have the largest influence on autism spectrum disorders, is its rising prevalence in recent years around the world.  (A?) One decade after these disorders were considered  to be their own disorders in the 1960's, they were present in 1 in every 5,000 individuals worldwide, meaning approximately 0.02% of people people were autistic. During the next decade, or more specifically, 1985, autism spectrum disorder rates doubled from that of the previous decade, and 1 in every 2,500 individuals were affected worldwide (0.04%). Then, in 1995, the rates increased five-fold from 1985, and 1 in every 500 individuals were affected (0.2%). As, of 2009 autism rates were extremely high, affecting 1 in every 110 individuals worldwide, meaning about 0.91%. (Anonymous f 2012, 1)  Additionally, the national rates in the United States are drastically higher than the average international rates. In fact, the United States autism(autistic)  rates have increased from affecting less than 3 per 10,000 individuals in the 1970's, to affecting more than 30 per 10,000 individuals in the late 1990's. (Blaxill 2004, 1) Taking into account, all of autism spectrum disorder's important background information such as chronological history, different types, and prevalence in recent years is extremely important for one grasp the concept of what many think is just "autism"  truly is.

For one to fully understand what autism spectrum disorders actually are and what are their affects on individuals, it is crucial  to understand the symptoms. All autism spectrum disorders have three core symptoms; however, depending on the type of disorder, the severity of each of these three symptoms differs. Autism spectrum disorders specifically contain the word "spectrum" because its core symptoms can differ so greatly, being on "one of the spectrum or the other." The three main symptoms of all autism spectrum disorders are difficulty socially interacting with others, issues with communicating verbally and non-verbally, and  having repetitive behaviors or having obsessive interests. (Schoenstadt 2008, 1) First, one with an autism spectrum disorder will encounter difficulties with social interaction such as enormous struggle learning to develop nonverbal skills like eye-to-eye contact, facial expression, and body language. Because of this difficulty with social interaction, the learning process is also made much more difficult, for much less is conceived from whoever is instructing . (Schipul, et. al. 2011, 6) Behavioral studies have proven that procedural learning, learning by performing (practicing)  and perceptual learning, learning by being instructed, were both impaired in those with autism spectrum disorders. (Schipul, et. al. 2011, 7)  Additionally, those with autism spectrum disorders may fail to make friends with those their age and lack empathy, failing to understand the pain and sorrow of others. (Anonymous a 2010, 1) Difficulty with social interaction can be recognized in an individual as early as when they are an infant, for they may be unresponsive to the presence of others or focus so much on one item for long periods of time that they completely exclude everything else around them. (Schoenstadt 2008, 2)
       
Second, one who has an autism spectrum disorder will have problems with communicating verbally and non-verbally. Such problems with communication include complications with just learning to talk, difficulty starting a conversation, struggling to continue a conversation that has already begun, and echolalia, the constant repeating of a word or phrase previously heard. Also, communication is so much of an issue that 40% of individuals with an autism spectrum disorder never speak. (Anonymous a 2010, 2) Furthermore, they have difficulty making sense of what others are thinking or feeling because they are incapable of understanding social clues like tone of voice. (Schoenstadt 2008, 5)   
         
The last core symptom of autism spectrum disorders is repetitive behaviors or obsessive, limited interests.  One limited interest is an unusual focus on a piece of a whole object as opposed to the whole object itself. For example, one with an autism spectrum disorder may direct all of their attention to the wheels of a toy car instead of the actual toy car. Another limited interest is a preoccupation with a certain topic. In addition to limited interests, an individual with an autism spectrum disorder has repetitive behaviors and may need to consistently follow the same routine day after day. (Anonymous a 2010, 3) They may also engage in repetitive motions like rocking and twirling or engage in self-abusive behavior like biting themselves and banging their head against something. (Schoenstadt 2008, 6) In addition to the three core symptoms of autism spectrum disorders, experiencing difficulty socially interacting with others, having issues with communicating verbally and non-verbally, and having repetitive behaviors or having obsessive interests, many individuals have altered sensitivity. For example, most children with an autism spectrum disorder have reduced sensitivity to pain and are very sensitive to sensory stimuli such as sound or touch. (Schoenstadt 2008, 9)
       
Although understanding the symptoms of all autism spectrum disorders in general is extremely important, of equal importance in understanding the variations in symptoms of specific disorders. Overall, there are five of these autism spectrum disorders; these include autistic disorder, Asperger's syndrome, pervasive developmental disorder, Rett syndrome, and childhood disintegrative disorder. Autistic disorder is an autism spectrum disorder that has all three core symptoms: problems with social interactions, problems with communication, and limited interests. (Anonymous e 2013, 2) The second disorder is Asperger's syndrome, which has problems with social interactions, a small struggle with language (communication), and a limited scope of interests. (Anonymous e 2013, 3) One with pervasive developmental disorder, the third disorder, experiences only some of the symptoms of a true autism spectrum disorder, but not all. So, pervasive developmental disorder does not technically fall under the autism spectrum disorder category, but since those who have it cannot be labeled as any of the other four disorders, they are still considered autistic. (Anonymous e 2013, 4) The fourth disorder, Rett syndrome, is known to cause children to start developing normally but then begin to lose communication skills and social skills; then by age one to age four, children start to have repetitive hand movements instead of purposeful use of the hands. (Anonymous e 2013, 5) The final disorder, childhood disintegrative disorder, causes children to develop normally for at least two years, but then they lose two or more of their acquired skills in areas of language, socializing, play, bowel or bladder control, and coordination. (Anonymous e 2013, 6, Anonymous g 2013, 1) All in all, autism spectrum disorders vary greatly in many aspects but always have the same general symptoms.

     
In order for one to make their final decision of whether autism spectrum disorders mainly come from genetic influences or environmental influences, it is vital for them to examine studies performed that seek the main cause. Studies performed that seek the main cause of autism spectrum disorders through genetics have identified copy number variants (CNV's), microscopic deletions or duplications in the DNA, as the main cause of autism. (Morrow, et. al. 2008, 5) De novo CNV's are microscopic deletions or duplications in offspring that resulted from mutations in gametes of the parents. (Anonymous b 2012, 4) De novo CNV's have been credited with causing autism spectrum disorders for two reasons. First, de novo CNV's are very prevalent in autism spectrum disorder patients, being seen in 8% of their genes as opposed to only 2% in non-autistic genes. De novo CNV's are also credited because they commonly show up in genes such as CHD8, SCN2A, KATNAL2, and NTNG1 and mutate them.  (Mitchell 2012, 5) Although the name of these genes sounds complex, understanding the function of them is rather simple. These genes code for proteins involved in brain functions, such as growing nerves and making physical connections in the brain. (Mitchell 2012, 6) So, if any of these proteins were coded for incorrectly because of the de novo CNV, it is obvious as to why they would lead to struggle in activities involving the brain like socializing and communication, two core symptoms; however, even though a connection has been noticed, how the specific de novo CNV's observed in these genes directly cause autism spectrum disorder symptoms is still not very clear. (Mitchell 2012, 7) Additionally, only a handful of CNV's have been linked with autism spectrum disorders, but there is a possibility that hundreds or even thousands of mutated genes that actually are linked. (Mitchell 2012, 8)
       
There are two factors which increase the prevalence of CNV's in offspring, and therefore, can lead to autism spectrum disorders. First, the prevalence of de novo CNV's in an offspring are increased as the age of father is increased because sperm mutations are more likely to occur. In fact, studies performed suggest that fathers over the age of forty are five times more likely to have a child with autism. (Mitchell 2012, 2) The reason that paternal age, the age of the father, affects the chance of a sperm mutation is because sperm cells continue to divide in men throughout their lifetime, and as a result, the chance of mutation increases. (Mitchell 2012, 3) Second, the chances of CNV's in an offspring is increased if the offspring's parents share ancestors. (Morrow, et. al. 2008, 1) As of now, these are the only genetic relations which have been scientifically proven to be linked with autism spectrum disorders.
       
Just like there are studies focused on the genetic links to autism spectrum, there are studies focused on environmental links to autism. First, however, it is important to understand the truth about one of the most misunderstood "causes" of autism spectrum disorders: vaccinations. Many individuals believe that vaccinations cause children to develop autism spectrum disorders because of a preservative it contains called thimerosal, which contains a mercury. (Gelman 2013, 1) Individuals believed too much of the chemical in too short of a time-frame could potentially impact brain development. (Gelman 2013, 2) However, research has proven that babies excrete thimerosal too quickly for it to build in in dangerous amounts, and thimerosal was removed by most vaccines in 2001; therefore, there should be no question of whether or not vaccines cause autism spectrum disorders now. (Gelman 2013, 3, 5) Possible factors that cause autism spectrum disorders are maternal birth abroad (28% increase), diabetes during pregnancy (100% increase), uterine bleeding during pregnancy(81% increase), and exposure to toxic chemicals.(Gardener, et. al. 2008, 5, 6, 12) Maternal birth abroad is thought to be associated with autism spectrum disorders because a woman born in another country may not be immune to common infections of the country she gives birth in, and as a result, she may contract an infection that increases her child's risk for autism. (Gardener, et. al. 2008, 15) Diabetes and uterine bleeding during pregenancy is thought to have lasting autistic consequences of offspring because it causes a large hormonal imbalances and deprives oxygen in fetuses. (Gardener, et. al. 2008, 17, 20) Last, exposure to toxic chemicals increases the risk of autism spectrum disorders either because the chemicals' toxicity directly injures the brain or the chemicals' makeup negatively alters genetic sequencing. (Landrigan 2012, 11) All environmental exposures have the largest possibility to affect autism during unique "windows of vulnerability" that only occur during certain stages of embryonic and fetal life. (Landrigan 2012, 7)  After learning about the genetic and environmental causes of autism, one can concoct what they believe is the ultimate cause of autism spectrum disorders.

Altogether, autism spectrum disorders are disorders which have unique background information, a wide spectrum of symptoms, and genetic and environmental influences. Regardless of the common belief that these disorders can be caused by vaccinations, scientific studies have proven otherwise. Because this belief has proven to be false, scientists have moved on to studying actual environmental and genetic factors of autism. From this evidence, one can decide for themselves if autism spectrum disorders are caused primarily by genetics, primarily by the environment, or a combination of both.

By using scientific and anonymous resource information, I personally feel that autism spectrum disorders are caused by a combination of environmental and genetic factors. Some cases, I believe, are caused primarily by copy number variants, a genetic influence. After examining researches, I feel that cases would only be entirely genetic if an old paternal age was involved or parents both had recently shared ancestry. I also feel cases would only be entirely environmental if the fetus who later develops an autism spectrum disorder was deprived of oxygen in some form or was exposed to a toxic substance . For the remaining cases, I feel environmental factors, such as the chemical make up of a substance, interact with the genetic make up of an individual and cause the genes to become mutated. I believe these mutated genes then incorrectly code for essential proteins, leading one to suffer from symptoms of autism spectrum disorders.   
 (PS: this was really good..)
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Anonymous 2A 2013

Created By: Sarah Nguyen
http://www.britishskinfoundation.org.uk/SkinInformation/AtoZofSkindisease/Melanoma.aspx

Melanoma

What is a melanoma?

Cutaneous malignant melanoma is a cancer of the pigment cells of the skin.  If it is treated early, the outlook is usually good.  It is not contagious.

The word ‘melanoma’ comes from the Greek word ‘melas’, meaning black.  Melanin is the dark pigment that gives the skin its natural colour.  Melanin is made in the skin by pigment cells called melanocytes.  After our skin is exposed to sunlight, the melanocytes make more melanin, and so the skin becomes darker.

[1] Melanocytes sometimes grow together in harmless groups or clusters, which are known as moles.  Most people have between 10 and 50 moles and often they are darker than the surrounding skin. Melanomas can come up in or near to a mole, but can also appear on skin that looks quite normal. They develop when the skin pigment cells (melanocytes) become cancerous and multiply in an uncontrolled way. They can then invade the skin around them and may also spread to other areas such as the lymph nodes, liver and lungs.

What causes melanoma?

The most important preventable cause is exposure to too much ultraviolet light in sunlight, especially during the first 20 years of life.  There is lots of evidence linking melanoma to this, and melanomas are especially common in white-skinned people who live in sunny countries.  The use of artificial sources of ultraviolet light, such as sun beds, also raises the risk of getting a melanoma.

Some people are more likely to get a melanoma than others:

[2] People who burn easily in the sun are particularly at risk.  Melanoma occurs most often in fair-skinned people who tan poorly.  Often they have blond or red hair, blue or green eyes, and freckle easily.  Melanomas are less common in dark-skinned people.  
Past episodes of severe sunburn, often with blisters, and particularly in childhood, increase the risk of developing a melanoma. However, not all melanomas are due to sun exposure, and some appear in areas that are normally kept covered.  
People with many (more than 50) ordinary moles, or with a very large dark hairy birthmark, have a higher than average chance of getting a melanoma. 
Some people have many unusual (atypical) moles (known as ‘dysplastic naevi’).  They tend to be larger than ordinary moles, to be present in large numbers, and to have irregular edges or colour patterns.  The tendency to have these ‘dysplastic naevi’ can run in families and carries an increased risk of getting a melanoma. 
The risk is raised if another family member has had a melanoma. 
People who have already had one melanoma are at an increased risk of getting another one. 
People with a damaged immune system (e.g. as a result of an HIV infection or taking immunosuppressive drugs, perhaps after an organ transplant) have an increased chance of getting a melanoma
.  


Are melanomas hereditary?

About 1 in 10 of people with a melanoma have family members who have also had one.  There are several reasons for this.  Fair skin is inherited; dysplastic naevi can run in families, as can a tendency to have large numbers of ordinary moles.

What are the symptoms of melanoma?

Melanomas may not cause any symptoms at all, but tingling or itching may occur at an early stage.  Some melanomas start as minor changes in the size, shape or colour of an existing mole (see below): others begin as a dark area that can look like a new mole.  Later on a melanoma may feel hard and lumpy, and bleed, ooze or crust up.

 [3] What does a melanoma look like?
All melanomas do not look the same, and there are several different types.  The ABCD system (below) tells you some of the things to look out for. 
A melanoma may show one or more of the following features:
Asymmetry – the two halves of the area differ in their shape.
Border – the edges of the area may be irregular or blurred, and sometimes show notches. 
Colour – this may be uneven. Different shades of black, brown and pink may be seen. 
Diameter - most melanomas are at least 6 mm. in diameter.
Melanomas can appear on any part of the skin but they are most common in men on the body, and in women on the legs.


How is a melanoma diagnosed?

If you are at all worried about changes in a mole, or about a new area of pigmentation appearing on your skin, you should see your family doctor.  The ABCD changes listed above can sometimes be found in completely harmless conditions, and your doctor will often be able to put your mind at rest quickly.   However, if there is still any doubt, your doctor will usually refer you to a specialist (a dermatologist or a surgeon with a special interest in pigmented lesions) who will examine the area, perhaps with a special instrument (a dermatoscope), and decide whether it needs to be removed.  The only way in which the diagnosis of a melanoma can be made firmly is by looking at the suspected area under microscope in the laboratory.  

If the mole needs to be examined further, the whole of the suspicious area will then be removed under a local anaesthetic (an excision biopsy) and sent to the laboratory to be examined. If the area is too large to remove easily, a sample of it (a biopsy) will be taken.  If a melanoma is found, the biopsy specimen will provide valuable information about its type and depth that will help to plan the next step in treatment.

Can a melanoma be cured?

Yes: three quarters of the people who have a melanoma removed will have no further problems.  However it is crucial for a melanoma to be removed as early as possible - before it has had time to spread deep into the skin or to other parts of the body. The thinner the melanoma is when it is removed; the better is the survival rate.  This is why a doctor should examine anyone with a suspicious mole or blemish as soon as possible.  In a small minority of people the melanoma may have spread but further surgery or chemotherapy can often help to control this. 

For information about available treatments please visit this page on the website of the British Association of Dermatologists

 
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Anonymous 2013 2B

Created By: Sarah Nguyen
http://www.cancer.net/cancer-types/familial-malignant-melanoma


What is familial malignant melanoma?

Cancer begins when normal cells begin to change and grow uncontrollably forming a lesion called a tumor. A tumor can be benign (noncancerous) or malignant (cancerous, meaning it can spread to other parts of the body).

 [1] Familial malignant melanoma is a term usually referring to families in which two or more first-degree relatives (parent, sibling, or child) have a type of skin cancer called melanoma. Overall, about 8% of people newly diagnosed with melanoma have a first-degree relative with melanoma. A much smaller percentage, about 1%, have three or more close relatives with melanoma.Familial melanoma is a genetic condition. This means that the risk of melanoma can be passed from generation to generation in a family. To date, two genes have been linked to familial melanoma; 

Dysplastic nevi are large, flat, irregular, asymmetric, variably pigmented moles. They occur primarily on sun-exposed skin, but they also occur in areas that are not exposed to the sun. Individuals in melanoma-prone families frequently have these moles. The moles must be monitored very carefully for any change in size, shape, and color to watch for cancer. In the United States, the average age when melanoma is diagnosed in people with familial melanoma is in the 30s; the average age when melanoma is diagnosed in the general population is in the 50s.

What causes familial melanoma?

they are called CDKN2A and CDK4. A mutation (alteration) in one of these genes gives a person an increased risk of melanoma. However, alterations in these two genes only account for a small percentage of familial melanoma.

CDKN2A is unusual because it affects two separate proteins that have different functions; one is called p16, and one is called p14ARF. Both CDKN2A and CDK4 play important roles in controlling when cells divide. Studies of families with mutations in CDKN2A from Europe, North America, and Australia have shown that the risk of melanoma varies by geographic area. The reasons for these differences are not fully understood. There may be differences in the amount of sun they receive, other individual or genetic differences, or a combination of these factors.

Within melanoma-prone families with known genetic mutations dysplastic nevi and sun exposure are independent risk factors for melanoma. There is also growing evidence that variations in another gene, MC1R, alter the risk of melanoma, both in individuals with CDKN2A mutations and in individuals without CDKN2A mutations. MC1R is important in regulating pigment; variations have been associated with freckling and red hair.

Other inherited genes are associated with an increased risk of melanoma. For instance, Xeroderma pigmentosum (XP) is a rare disorder in which patients have a defect in a gene needed for repair of ultraviolet radiation (sunlight) induced DNA damage. Patients with XP have an extremely high rate of skin cancer, including melanoma. The hereditary breast cancer gene, BRCA2, is also associated with a risk of melanoma. Scientists believe that there are other genes not yet identified that also increase the risk of melanoma. Learn more about the genetics of melanoma. Research is ongoing to learn more about familial melanoma.

How is familial melanoma susceptibility inherited?

Normally, every cell has two copies of each gene: one inherited from the mother and one inherited from the father. Familial melanoma susceptibility follows an autosomal dominant inheritance pattern, in which case a mutation happens in only one copy of the gene. This means that a parent with a gene mutation may pass along a copy of his or her normal gene or a copy of the gene with the mutation. Therefore, a child who has a parent with a mutation has a 50% chance of inheriting that mutation. A brother, sister, or parent of a person who has a mutation also has a 50% chance of having the same mutation.

How common is familial melanoma?

Most cases of melanoma are sporadic (occur by chance). The number of people who have an inherited risk of melanoma is unknown, but the number is thought to be low. It is estimated that about 8% of people with melanoma have a first-degree relative with melanoma and that only 1% to 2% of people with melanoma have two or more close relatives with melanoma.

How is familial melanoma diagnosed?

Familial melanoma is suspected when two or more close relatives have invasive melanomas (melanoma that has spread). In areas of higher sun exposure, like the southern United States or Australia, the frequency of sporadic melanoma is higher, so familial melanoma is not diagnosed unless three or more close relatives have invasive melanoma. Familial melanoma may also be suspected if a single family member has multiple melanomas.
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Uong A 2010

Created By: Sarah Nguyen
http://www.ncbi.nlm.nih.gov/pubmed/19795394


Abstract
 [1] Melanocytes are pigment-producing cells in the skin of humans and other vertebrates. A number of genes involved in melanocyte development and vertebrate pigmentation have been characterized, largely through studies of a diversity of pigment mutations in a variety of species. Embryonic development of the melanocyte initiates with cell fate specification in the neural crest, which is then followed by cell migration and niche localization. Many genes involved in melanocyte development have also been implicated in the development of melanoma, an aggressive and fatal form of skin cancer that originates in the melanocyte. [2] Although early stage melanomas that have not spread to the lymph nodes can be excised with little risk of recurrence, patients diagnosed with metastatic melanoma have a high mortality rate due to the resistance of most tumors to radiotherapy and chemotherapy. Transformed melanocytes that develop into melanomas proliferate abnormally and often begin to grow radially in the skin. Vertical growth can then follow this radial growth, leading to an invasion through the basement membrane into the underlying dermis and subsequent metastasis. It is still unclear, however, how a normal melanocyte becomes a melanoma cell, and how melanoma utilizes the properties of the normal melanocyte and its progenitors in its progression. The goal of this mini-review is to highlight the role of melanocyte developmental pathways in melanoma, and to discuss recent studies and tools being used to illuminate this connection
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