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Draft at 4/28/2013 10:45:40 PM

Created By: Timahje Keesee

A1: Long-lasting chemicals(pollution) are eliminating sea turtles.
Q2: Report:(Required*)
A2: Everyone know that our oceans are polluted, with some so filthy that it just looks black. We also know that our aquatic mammals are being poisoned. One species, however, has somehow fallen under the radar. That species is the sea turtle.They have been overlooked for such a long time that they are now on the verge of getting on the endangered animals list. But before we investigate sea turtles, we must first know how they are being poisoned and dying.

80% of the ocean's pollution is caused by land, with agriculture the main contributor. Nearly 12% are because of humans using marine transport. And in South America, 98% of untreated wastewater gets left in the ocean. China dumps 60 million tons of waste into the ocean daily. According to the Ifremer, the French Institute for Exploitation of the Sea, marine pollution cost the worlds economy nearly 12.8 billion dollars in 2006 (Oriental 2011,1,2).

What is marine pollution, exactly? Marine pollution is the result of dumping harmful substances into any part of Earth's oceans. This can be anything from domestic wastes, (sewage, pollutants in runoff water), industrial wastes,(Hydrocarbons, metals, synthetic chemical and organic substances), agricultural wastes,(fertilizers, pesticides). Basically any harmful substances that were thrown into the sea is considered marine pollution (Oriental 2011, 3).

Many assume that because the ocean is so large, the water dilutes and eventually the pollutants go away. Well they assumed incorrectly. The pollutants are still there, and it adds up- little by little, piece by piece. Sure, sea water spreads pollution thin, but its still there. In fact, since the water breaks apart the chemicals into smaller particles, it becomes more concentrated- and even more deadly. (Gaine 2010,9)

Most of the pollution starts from coastal areas, then spreads outward, carried by winds and currents. The only pollution that happens in the middle of ocean are usually accidents, like shipwrecks or oil spills. The bodies of water that are surrounded by land (like the Mediterranean Sea, the Baltic Sea, the Caspian Sea, and the Black Sea) are polluted the most. This is because the oil spills and accidents that happen on those bodies of water spread, and because the volume of water is small, the chemicals fill up the water extremely fast (Oriental 2011,4,5).

Pollution causes the most damage near the coast than out on sea. The water quality can get so bad that it would be impossible to do activities like fishing or leisure activities such as paddle boating. Pollution can harm the economy as well, with the world spending around 12.8 billion dollars, as I stated above. In South Carolina, pesticide pollution wiped out nearly half the fish living there. Dr.Oriental says that-"The 10 billion tons of ballast water poured into the sea every year from one end of the globe to the other introduce species which colonise the environment at the expense of indigenous species. Toxic substances are stored in the fatty tissue of fish, marine mammals and piscivorous birds."(Oriental 2011,6)

Even cars play a role in polluting the ocean. The exhaust that comes out of the back of car pollutes the ocean. No, the smoke does not go directly into the ocean. It collects in the clouds above and eventually comes down in the form of acid rain. Acid rain pollutes the ocean and kills many fish over a period of time. If we cant stop pollution from cars, or at least cut down on the pollution, then the fish population will decrease. (Annenburg 2002,1).

Now, enough of brushing up on your
knowledge of pollution- it's time we get to sea turtles.

From the moment they are born, sea turtles are in danger. As soon as they hatch from their eggs, they must first dig their way out of the earth and onto the surface. This process of hatching and then traveling and swimming out to sea is referred to as swim frenzy. (Booth 2011,1) Then, while evading predators such as crabs and birds, they begin a long migration into the ocean. Only one out of 10 turtles survive into adulthood. (Isreal 2013,1)

The danger starts as soon as the eggs are laid. Predators such as raccoons, crabs, and ants raid the eggs while they are still in the nest. If the eggs hatch, the baby turtles make a nice snack for birds and crabs and many other ocean predators. Then, if the small percentage that make it into the ocean actually survives into adulthood, natural predators are almost non-existent except for the occasional shark attack.(Gaine 2010,2)

Even if they do hatch, theres another danger- not another predator, but artificial lighting. Dr. Gaine says that "Nesting turtles depend on dark, quite beaches to reproduce successfully. Today, these turtles are endangered, in part, because they must compete with tourists, businesses and coastal residents to use the beach. This man-made, coastal development results in artificial lighting on the beach that discourages female sea turtles from nesting. Instead, turtles will choose a less-than-optimal nesting spot, which affects the chances of producing a successful nest. Also, near-shore lighting can cause sea turtle hatchlings to become disoriented when they are born. Instead, they will wander inland where they often die of dehydration, predation, or even from being run over on busy coastal streets".(2010,7)

However, the most dangerous predator a sea turtle will face will most likely be the little piece of plastic in your pocket that you mindlessly and carelessly threw away on the beach, or over a ridge that led into the ocean. Almost 100 million marine mammals each year are killed by plastic debris in the ocean. 80% comes from land, while the other 20% obviously come from the sea, mainly boats littering.

Dr. Gaine says that "Although sea turtles have spiritual or mythological importance in many cultures around the world, this has not prevented humans from consuming their eggs or meat. In many coastal communities, especially in Central America and Asia, sea turtles have provided a source of food. During the nesting season, turtle hunters comb the beaches at night looking for nesting females. Often, they will wait until the female has deposited her eggs to kill her. Then, they take both the eggs and the meat. Additionally, people may use other parts of the turtle for products, including the oil, cartilage, skin and shell. Many countries forbid the taking of eggs, but enforcement is lax, poaching is rampant, and the eggs can often be found for sale in local markets."(Gaine 2010,3)

On top of that, adult sea turtles now have to face a new threat- an extremely toxic one.

"Scientists are discovering sea turtles, long ignored by toxicologists who study wildlife, are highly contaminated by industrial chemical and pesticides. No one, however, knows the extent to which sea turtles in the wild are harmed," says Dr. Isreal. "While other ocean creatures, including whales, seals, and some fish, are well-studied, the chemical threats to sea turtles remain under a shell." One of reasons sea turtles might have been ignored or overlooked is that the pollutants in their blood are of a lower magnitude than marine mammal blood. This means that while they are still in danger, they have a less percentage of pollutants in their bloodstream than other marine creatures. (Isreal 2013,2)

And its not only sea turtles who are in danger- not even close. 8 years ago, two photographers- Chris Jordan and Susan Middleton- captured the scene of dead albatrosses on the beach at Midway. their stomachs were split and filled to brim of your everyday average bottle cap, disposable cigarette lighters and plastic bags. Seeing the colorful debris, the birds swooped in and swallowed the bits of plastic. As you should know, no living being on the face of this Earth can digest any small plastic objects. . Eventually, the birds, with their stomach bloated from all the plastic,( which is also non-biodegradable), died. (Bowermaster 2011,1)

With climate change, poaching, accidental snaring and ocean trash, almost all United States of America species of sea turtles are protected by the Endangered Species Act, which makes them even harder to observe and study. One species of U.S. sea turtle was not added to list. That species is the Natator depressus. (Delgado 2011,1) However, though we are limited to what we can observe about sea turtles, we have found that they are vulnerable in their thryroid, ( "The thyroid gland or simply, the thyroid, in vertebrate anatomy, is one of the largest endocrine glands. The thyroid gland is found in the neck, below the thyroid cartilage (which forms the laryngeal prominence, or "Adam's apple"). The isthmus (the bridge between the two lobes of the thyroid) is located inferior to the cricoid cartilage."-Wikipedia.), liver, and neurological damage. (Isreal 2013)

Pollution also plays a role in what the sea turtles eat. There has been research of a disease called fibropapillomas, which is directly linked to pollution in oceans and in near-shore waters. When pollution enters the water, it contaminates and kills aquatic plant life and aquatic animal life which sea turtles normally eat. So now, finding no food, sea turtles are mistakenly ingesting fatal quantities of plastic debris. Though only 0.26% of all plastic ends up in the ocean, that is .026% of the nearly two hundred and sixty million TONS of plastic manufactured each year. Doing the math, that is six million, seven hundred and sixty thousand tons in the ocean.

Climate change also disrupts a turtles life, like Dr. Gaine stated- "Because sea turtles use both marine and terrestrial habits during their life cycles, the affects of climate change are likely to have a devastating impact on these endangered species. Climate change affects nesting beaches. With melting polar ice caps and rising sea levels, beaches are starting to disappear. As the water level begins to rise, the size of nesting beaches decrease. Stronger storms, predicted as a result of increasing temperatures, will continue to erode coastal habitats. Higher temperatures can adversely affect sea turtle gender ratio. Increasing incubation temperatures could result in more female sea turtles, which reduces reproductive opportunities and decreases genetic diversity." (2011,10)

Even beach driving can disturb a turtle, whether it be night or day. Night time driving can disturb nesting females, disorient baby sea turtles trying to find their way into the ocean, and/or crush hatchlings. Tire marks left by cars can extend the time it takes for hatchlings to reach the ocean, therefore making baby sea turtles' chances of being caught by a predator increase. Day time driving can cause sand compaction, resulting in a lowered rate of nesting success. Additionally, beach driving causes erosion, especially during high tide or on narrow beaches.

Now, sea turtles were living the average marine mammal life- they fed, reproduced, hunted, and were hunted. The population was doing pretty good. On top of that, they were living in crystal clear waters- little to no pollution could be found. What i just stated happened over two hundred years ago. With the introduction of machines, we were manufacturing items faster than no one thought possible. However, this came at a price. The introduction of machines also brought pollution. Slowly and slowly this issue became progressively worse. More and more of marine creatures were being put on watch by the Endangered Species Act- however, one creature was suffering. Scientists ignored it for the longest time until there was a very drastic decrease in it's population. That creature is the sea turtle. If we don't do something about this soon, the sea turtle will become dangerously close to becoming extinct.
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Angelina's Paper

Created By: Timahje Keesee
DON'T INDENT                            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 effected 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 MORE IN DEPTH ON THESE SYMPTOMS(Chawla 2011, 2).

The composition of caffeine is similar to that of uric acid BRIEFLY EXPLAIN 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 your brain are constantly working while people are awake and while they work, they produce a byproduct called adenosine. If one's adenosine level's gets 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 result 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 twelve 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 effect most of a person's body (Braun 2013, 1). Exercise can be AFFECTED effected 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 AFFECT effect cycling performance (Kovacs 1998, 1).

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

Caffeine is a pretty powerful psychoactive drug and it has many effects on organisms. It has both positive and negative effects, 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. 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.TOO LITTLE WORDS. HYPERLINKS DON'T WORK. 
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Alex's Paper

Created By: Timahje Keesee
How the brain controls the speech in your body is very complicated and amazing 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. MORE INFO IN THE INTRO

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, communicattion, coordination in work, ect. 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. 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 to twitch a bit and the body. 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 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). 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 coordinate their plucks, bows, or blows to make a group sound the sounds amazing. Such as 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. They have patients say stuff such 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 (Feng et.al 2010, 2).

The brain has several areas that are their to help the decipher language and get it back out to respond the conversations that people have every day.the first main area is called the Broca area, which is named after Paul Broca. WHERE IS THE BROCA AREA, OTHER THAN LEFT SIDEPaul Broca is a French Neurologist who had a patient with majoor 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 see why his speech was so messed up. What he found was that the patient's brain, in front of the frontal lobe, his motor cortex was severly damaged which was why he wasn't 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), if someone said 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 area after the German neurologist Carl Wernicke, who had the patient that about the complete oppisite of Paul Broca's patient, because Carl Wernicke's patient ws 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 speak to other people. When Carl Wernicke's patient died, Wernicke performed an autopsy on him and discover that an upper part of the man's temporal lobe, barely behind the auditory cortex, was damaged. So Carl Wernicke said that this part of the brain was brain 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 mix up words that sound alike and or look alike. It is related to as a screwed up "Mental Dictionary" (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, 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, they are able to clearly understand what people are saying. They can also go ahead and speak coherently but with some amount of difficulty. But when it comes to the process of having to go ahead 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 discover during an autopsy of a young patient who died. 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 conducted the autopsy discovered that the angular gyrus is where several speech problems are from. Such Alexia which is the inability to read. And Dyslexia which difficulties with reading. And finally the inability to write which is agraphia (Boeree 2004, 3).

There re 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. Thay also will not be able to carry out commands that people have given to them or even name out objects. Also they cannot go ahead and repeat read or write. And finally repeat out words or phrases people have said to them. 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 (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. The symptoms of Logopenic Progressive Aphasia are slowed speech while normal articulation is taking place. Impaired comprehension of sentence syntax as well as the impaired naming of things. 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 go away that control speech and language. Which is the left (dominant) part of the brain in the frontal temporal and parietal regions. 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 an language disorders. It starts just as a normal degeneration would be with speech and language issues. 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 is 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 are 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).

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 let researchers to believe that to general terms that as the posterior temporal gyrus or Heschi gyrus. The second auditory area is the postero superior portion of the temporal lobe. Which includes most of the middle temporal lobe with it (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 doesn't not get more complicated as the aphasias and speech disorders go on. TOO LITTLE WORDS WITHOUT INTRO/CONCLUSION. GOOD PAPER OVERALL





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Martin's Paper

Created By: Timahje Keesee
  Did you know that around 7.6 people die every year due to cancer? Cancer is the number two cause of mortality worldwide and so far has no cure. Of course, there is therapy available for different cancers but these therapies cause harm to your body in order to destroy cancer cells. And often the therapies can cause more harm and pain than the cancer itself. Recently, leading studies in the past few years have opened the worlds eyes to a new technology with countless possibilities. This new technology is known as nanotechnology. Nanotechnology has become a very popular subject in the scientific field because the more it is looked into, the more researchers find out how this technology can be useful to us. Probably the most popular possibility is its in medicinal purposes which hold the key to treating diseases like cancer. The idea of putting nanotechnology into the use of medicine is already known as nano medicine. Nano medicine is amazing because it offers to treat disease in an atomic level without damaging or doing anything it isn't supposed to to a cell. Just Imagine cancer for example, if all you would need was one shot of nanoparticles to kill tumors and cancer cells more efficiently and with no harm to your body! Therefore, extensive research of nanomedicine has led me to believe that this new technology has the ability to treat cancer and many other diseases more efficiently and more effectively than medicines we use today. GREAT INTRO

Nanotechnology itself is a very interesting topic and is essential to the understanding of nano medicine because nano medicine is based off of nanotechnology. Nanotechnology itself is the manipulation of matter at the atomic level, which is the smallest level possible because we know of nothing smaller than the atom and its parts: neutrons, protons, and electrons (Strickland 2012, 1). Just to give more of an idea of the scale of nanotechnology, it is worked with in the measurement of nanometers (Strickland 2012, 2). A nanometer itself is just a billionth of a regular meter and nano scientists still have to work at a smaller scale because atoms are still smaller than a nanometer (Strickland 2012 3)! By controlling molecules and atoms, you can end up with materials with unique and useful properties such as the nanotube developed by NASA that is 100 times stronger than metal steel and just one sixth of the weight of steel too (Strickland 2012, 4, 8). To do this, scientists work with graphite and make a sheet out of the graphite molecules and then roll them perfectly into a tube and you will get the amazing result of a nanotube(Strickland 2012, 6). Of course nanotechnology doesn't have to be as complicated as making a nanotube. We use nanotechnology in our regular life on a more simple level like simply putting zinc oxide particles into our sunscreen so that they can provide us with a transparent, protective layer on our skin to protect us from the sun (Strickland 2012, 11). It can even be seen as simply snapping LEGO blocks together at an atomic level to make nano particles or nano materials with amazing properties and abilities (Ralph 1996,5).

There is so much information you can get from nanotechnology because it is such a broad and vast topic with so many possibilities and with so much already being done with it. It is a technology that can change the world. With all the possibilities of this technology it can sound ridiculous like something out of a science fiction movie but it is in fact very real and being researched and tested by scientists this day. The most popular possibility of nanotechnology is nano medicine. Although nano medicine is not a possibility but already being worked on and used, it is itself a subject of its own with still countless possibilities and work already being done with it. Some of the possibilities of application of nano medicine can include needle less injectors, insulin pumps, blood pressure monitors, glucose monitoring, and probably the most useful, drug delivery systems(Rouse 2007, 2). Of course there are countless other possibilities out there. The most advanced of nano medicine would involve the use of nano robots to carry out surgery and to repair cells and even replace organelles and other structures(Rouse 2007, 7).


Some other examples of the Implementation of nanotechnology into medicine can include cell repair, drug delivery, and diagnosing of diseases in the body with little to no harm to the body(Tareen 2010, 1). There are many more types of possibilities still for nano medicine of course, but these are the subjects that are being worked on the most currently. These three subjects of nano medicine themselves have the potential to save thousands of lives(Tareen 2010, 6). For the subject of drug delivery in nano medicine, buckyballs and benzene rings are being tested and used to deliver drugs to cancer cells, HIV molecules and even to be used to diagnose patients with diseases(Tareen 2010, 7, 8, 11). The cage like shape of buckyballs for example, allows for other desired molecules to be attached to it so it can make direct and precise contact with another targeted molecule(Tareen 2010, 7). An example of how buckyballs have been used would be in 1991 when Simon Freidman from the university of Kansas made a proteas inhibitor which is a substance that prevents the replication of HIV cells and used buckyballs to deliver the proteas inhibitor to the body(Tareen 2010, 8) The result was that the protease inhibitor attached to HIV sites in the body 50 times better than other molecules thanks to the buckyball(Tareen 2010, 8). However the buckyball can cause harm to the body if it is not closely monitored. Another molecule that is being used in nano medicine is the nano wire developed by researchers at Harvard University(Tareen 2010, 19). This nanowire of course is another nano molecule but has been discovered to be able to detect cancer and therefore can be used to diagnose patients with no harm to their bodies(Tareen 2010, 19). This nanowire has the ability to someday in the future, equip doctors with handheld devices that you can use anywhere to diagnose patients while saving money, time, and therefore allowing hospitals to spend time on more patients in a period of time(Tareen 2010, 20).

Another very promising possibility of nano medicine in the medical field is its potential to treat vascular diseases(Hulpt, Gupta 2010, 1). Because Vascular disease is one of the top highest causes of the mortality of the world, there is much being done to try to treat vascular disease(Hulpt, Gupta 2010, 2). Nano medicine however can offer new ways to effectively treat these diseases by delivering the drugs to the body more efficiently. By using nanotechnology on liposome delivery, nano medicine will be a very likely contributor to the more efficient treatment of vascular disease in the near future(Hulpt, Gupta 2010, 5).

Probably the most popular of all the uses of nano medicine is using it to treat cancer. the way this would work would be by using polymeric micelles, which are nano particles with shells that can carry substances such as drugs to kill cancer cells inside of them(Blanco, et. al. 2013, 1). The implementation of micelles into the treatment of cancer has been reported since the early 1980's(Blanco, et. al. 2013, 8). It is better to deliver drugs used to kill cancer cells by using micelles because since micelles will be carrying the drug inside of them, the drug will not have dissolved in the blood like it normally would if it was directly put into the blood stream. Instead, micelles will be able to carry more concentrated and there for more powerful doses of anti cancer medications more effectively to tumors(Blanco, et. al 2013, 9, 11, 12).The micelles nano particles offer to fight tumor cells efficiently while reducing toxicity of the drug to the patients body and several types are currently going under phase 1/2 of clinical trials to be used in the future(Blanco, et. al 2013, 3)

Gastroenterology is also a very possible place that nano medicine can take a part on in the future. Gastroenterology is a branch of medicine that focuses on the human digestive system and is currently developing nanotechnology to deliver drugs to specific parts of the gastrointestinal tract(Laroui, et. al, 2010, 1, 2). Nano medicine has the ability to find and treat gastrointestinal diseases while reducing the side affects and therefore outperforming the most effective and existing treatments for gastrointestinal disease(Laroui, et. al, 2010, 2,3). The main reason of why nano medicine seems to have a good future in gastroenterology is because it can deliver higher concentrations of medicine to the desired, diseased site without damaging normal cells along the gastrointestinal tract and may be able to pass through the normal digestive processes going on in the gastrointestinal tract(Laroui, et. al, 2010, 9). However, if this medicine is to be used someday, the nano material used to deliver the drugs must be specially designed to still work normally and efficiently in the varying pHs, pressures, and the activity of enzymes undertaking degradation in the gastrointestinal system and this will represent a whole other of development issue by it's self(Laroui, et. al, 2010, 10). Only overtime will the advances of nanotechnology and nano medicine be able to provide us with the nano material with the desired properties to treat gastroenterological diseases more efficiently and with less harm to the patient.

Related to the issue of nano particles and their properties to suit their functions the size of nano particles. This is being studied by nano scientists because the size of these materials greatly effects their properties(Tao, et. al, 2011, 1). Although shape plays an even bigger variable contributing to the properties of a nano particle, the importance of shape has barely begun to come out and not enough is yet known about it(Tao, et. al, 2011, 1, 2). Though a good example of shape properties would be the cylindrically shaped filomicelles(just a type of nano particle) that stay in blood circulation for a period of a week which is much longer compared to spherical shaped filomicelles(tao, et. al, 2011, 2). Particle shape is very less well understood than particle size because shape data has shown to be very profound in the properties of nano particles(Tao, et. al 2011, 4, 5). Nanoscientists have tried to change the size of nano particles by stretching them and have noticed that when they stretch spherical shaped nano particles their properties such as water solubility(Tao, et. al. 2011, 9, 10). In conclusion, the relation of size and shape with a nano particle's properties is a great factor when working with nanotechnology to find the one that can do the job.

In conclusion, nano medicine is an extremely promising technology with amazing possibilities for the future that can make medication more efficient and less harmful. This technology has surely not even been fully explored and is bound to have more possibilities in the future. Although we still don't have all of the technology available to us to fully experience all the promises and wonders of nano medicine, it shouldn't be very long before we do because we are rapidly advancing and finding out more about this technology and actually using it. This is why i believe that nano medicine has the ability to treat diseases more effectively and efficiently than current medicine. Nano medicine has the ability to change our world. One step at a time, this technology will be unraveled over time to bring its full potential onto the world and make it a better place to live in for the diseased and for the healthy.  NOT ENOUGH WORDS WITHOUT THE INTRO/CONCLUSION. GREAT PAPER OVERALL
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Buzsaki 2011

Created By: Timahje Keesee
http://www.scholarpedia.org/article/Hippocampus

[1]The hippocampus is a part of the forebrain, located in the medial temporal lobe. It is critical for the formation of those kinds of memories, which can be consciously declared. Due to its self-generated network patterns, newly acquired memories are gradually transferred to neocortical stores through the process of memory consolidation. The hippocampus, as the brain’s search engine also allows a fast and efficient search among the deposited memories in the neocortex, which is a process essential for planning the future and generating creative ideas. Most physiological studies on the hippocampus have been performed in rodents and gave rise to the spatial navigation theory. This, however, does not reflect a species difference. Instead, it appears that neural algorithms, perhaps evolved initially for computing first-order (neighborhood) and higher order (e.g., short-cuts, detours) distances in the physical world, are the same as those used for the navigation in cognitive space during recall and planning. Nearly all hippocampal functions are performed in collaboration with several of its partners, of which the most prominent is the entorhinal cortex, and strongly influenced by subcortical neuromodulators.
Contents [hide]
1 Hippocampal connections constrain functional operations
2 Network patterns of the hippocampus
3 Hippocampal place cells and episode cells
4 Consolidation and transfer of hippocampal memories
5 Other functions and implications
6 References
7 Further reading
8 External links
9 See also
Hippocampal connections constrain functional operations



Figure 2: Main excitatory paths in the entorhinal-hippocampal feedforward loop. Parallel-organized local circuits (gc, granule cells; CA1 and layer 3 entorhinal pyramidal neurons) alternate with varying degrees of recurrent circuits (CA3 and principal cells of layers 5 and 2 of entorhinal cortex). Such organization allows for repeated segregation and integration of information in successively coupled recurrent and parallel circuits, respectively. Main excitatory inputs and outputs from the loop are indicated by arrows. The subicular complex (Sub-c; subiculum, presubiculum and parasubiculum) is another loop between the hippocampus and entorhinal cortex. The main cortical output of the hippocampus is CA1, whereas hippocampal information is routed to subcortical structures largely by way of the subiculum.
The banana-shaped hippocampus can be conceived as an appendage to the neocortex (Fig. 1). By way of its main partner, the entorhinal cortex, it communicates with all parts of the neocortex (Amaral and Lavenex, 2006). Two important principles emerge from such connectivity. First, since the main output target of the hippocampus are the same as its input source, its expected physiological contribution is to modify the connections of its inputs (i.e., circuits in the neocortex). Second, since all parts of the neocortex are represented in the hippocampus in a compressed manner and all neocortical regions can be addressed by the hippocampal-entorhinal output, hippocampal operations in different species largely reflect the nature of neocortical operations. With the large expansion of the neocortex during the mammalian evolution, the relatively small representation of associational areas in the ventral quadrant of the rodent hippocampus has become enlarged in primates (uncus and body; Fig. 1). A consequence of this anatomical organization is that insights about the global function of the hippocampus depend on the portion of the hippocampus being investigated and the species. Studying the physiological pattern of the dorsal hippocampus of the rat (corresponding largely to the tail of the primate hippocampus) gave rise to the cognitive map theory (O’Keefe and Nadel, 1978). In contrast, human studies involving surgical removal of the uncus and body of the hippocampus in drug treatment-resistant cases of epilepsy, such as the famous patient H. M., lead to the conclusion that the hippocampus is responsible for generating personal (autobiographical) or episodic memories (Scoville and Milner, 1957). These conceptual differences therefore should not be viewed as different functions from the viewpoint of the hippocampus (since hippocampal operations remain largely the same across all species and in all parts of the hippocampus). Instead, one may hypothesize that the neural algorithms that evolved initially for the computation of first-order (neighborhood) and higher order (e.g., short-cuts, detours) distances in the physical world are fundamentally the same as those used for navigation in cognitive space and for the computation of relationships among perceived, conceived or imagined items. Making a map requires exploration of the environment by self-referenced (egocentric) dead-reckoning type of navigation, (i.e., the same method as used by Christopher Columbus to discover the New World). Similarly, generation of semantic (i.e., self-independent or allocentric) knowledge requires prior self-referenced episodic experience. For these reasons, it has been hypothesized that the mechanisms underlying dead reckoning navigation and episodic memory ('navigation in cognitive space') are the same. Similarly, the mechanisms that support the cognitive map and semantic knowledge are also identical (Buzsáki, 2006).


Figure 3: Relationship between navigation and memory.
Information in the multisynaptic feedforward loops of the entorhinal-hippocampal system is propelled mainly unidirectionally (Fig. 2). An important feature of this complex circuit is that recurrent excitatory networks are interposed between layers with largely parallel organization. The most extensive recurrent system in the brain is formed by the extensive collaterals of the CA3 neurons. Entorhinal layer 2 and layer 5 axon collaterals are also extensive. The advantage of this alternating pattern type of organization is that in successive layers the neuronal representations can be iteratively segregated (at parallel stages) and integrated (at recursive stages). These operations require time for computation before the results of local processing can be transmitted forward to the next computational stage. The speed of layer-to-layer transfer is controlled by the complex system of inhibitory interneurons. Such control dynamics, often in the form of network oscillations, provide time for local computation and enable the hippocampal system to communicate effectively with various domains of the neocortex in discrete temporal windows. The relatively simple cortical circuitry of the hippocampus has inspired many connectionist theories.
Network patterns of the hippocampus



Figure 4: Two network states of the hippocampus are defined by theta oscillations (~5 sec left) and sharp waves. Recordings from str. radiatum of the left and right hippocampus during exploration (walk, theta) to immobility (still, SPW) transition.
Three major network patterns characterize the temporal dynamics of the hippocampal system: theta oscillations (4–10 Hz), sharp waves and associated ripples (140–200 Hz), and gamma (30–130 Hz) oscillations. These patterns also define states of the hippocampus. The theta state is associated with exploratory (preparatory) movement and REM sleep, while intermittent sharp waves mark immobility, consummatory behaviors, and slow-wave sleep (Fig. 4; MOVIE). These two competing states also largely determine the main direction of information flow, with neocortico-hippocampal transfer taking place mainly during theta oscillations and hippocampo-neocortical transfer during sharp waves. These two states also affect the regularity of gamma oscillations and switching between the states is largely determined by the subcortical neuromodulatory inputs to the hippocampal system.
Gamma frequency oscillations are present in all brain structures where fast inhibition is provided by soma-targeting interneurons (Whittington et al., 1995; Wang and Buzsáki, 1996; Bartos et al.; neural inhibition by Jonas and Buzsáki, 2007). In the simplest case, an interconnected network of basket interneurons can generate sustained gamma oscillations, provided that their depolarization and spiking are secured by some means (such as subcortical neurotransmitters). In the intact brain, gamma oscillations are mainly generated by the interaction between principal cells and interneurons. In both scenarios, the frequency of oscillations is mainly determined by the time course of GABAA receptor–mediated inhibition. Neurons that discharge within the time period of a gamma cycle (10–30 msec) define a cell assembly (Harris et al., 2003). Because the membrane time constant of pyramidal neurons in vivo is also within this temporal range, recruiting neurons into this assembly time window is the most effective mechanism for discharging the downstream postsynaptic neuron(s) on which the assembly members converge (Buzsáki, 2010). Although gamma oscillations can emerge in each hippocampal region, they can be coordinated across regions by either excitatory connections or by long-range interneurons.
The LFP theta oscillation is the result of coherent membrane potential oscillations across neurons in all hippocampal subregions (Buzsáki, 2002). Theta currents derive from multiple sources, including synaptic currents, intrinsic currents of neurons, dendritic Ca2+ spikes, resonance and other voltage-dependent membrane oscillations. The theta rhythm modulation of perisomatic interneurons provides an outward current in somatic layers. The theta rhythm phase therefore biases the power of gamma oscillations, the results of which is a theta-nested gamma burst. Excitatory afferents form active sinks (inward current) at confined dendritic domains of the cytoarchitecturally organized layers of all regions. Since each layer-specific input is complemented by one or more families of interneurons with similar axonal projections, such layer-specific inhibitory dipoles can compete with the excitatory inputs. The resulting rich consortium of theta generators in hippocampal and parahippocampal regions is coordinated by the medial septum and a network of long-range interneurons (Freund and Buzsáki, 1996; Klausberger and Somogyi, 2008). Although theta oscillations are generally coherent throughout the hippocampal system, the momentary power, coherence and phase of theta oscillators can fluctuate significantly in different regions and layers as a function of overt and covert behaviors.
When subcortical modulatory inputs decrease in tone, as it happens in the absence of ambulatory movement and during sleep, theta oscillations are replaced by intermittently occurring, large-amplitude field potentials, or sharp waves (SPWs). SPWs are initiated by the self-organized population bursts of the CA3 pyramidal cells (Buzsáki et al., 1983). The CA3-induced depolarization of CA1 pyramidal cell apical dendrites is reflected by an extracellular negative wave, that is, the SPW, which is most prominent in stratum radiatum. SPWs are associated with fast-field oscillations (140–200 Hz), or ripples, confined to the CA1 pyramidal cell layer (O’Keefe and Nadel, 1978; Buzsáki et al., 1992; fast oscillations by Traub, 2006). In the time window of SPWs, 50,000–100,000 neurons discharge synchronously in the CA3–CA1–subicular complex–entorhinal axis of the rat. The population burst is characterized by a three- to five-fold gain of network excitability in the CA1 region, preparing local circuits for synaptic plasticity and, at the same time, exerting a powerful effect on cortical targets.
Hippocampal place cells and episode cells



Figure 5: Interleaved cell assemblies. A. Three example model neurons (color-coded) with identical oscillation frequency but different phase onset, according to their maximal discharge location. Temporal distance T is the time needed for the rat to run the distance between the peaks of the two place fields (real time). τ , time offset between the two neurons within the theta cycle (theta time). Bottom, the summed activity of the entire population of model neurons (black dashed line) oscillates slower than each transiently active individual neuron (color-coded). B. The phase of the three example neurons with respect to the oscillation of the population is plotted against time. Note that the neuronal spikes phase-precess approximately 360° due to the interference between the oscillatory spiking frequency of the most active neurons and the oscillation frequency of the entire population. Right: spike density for the example neurons. C. Interleaved neuron sequences represent position and distance relationships. The width of the bars indicates firing intensity of the hypothesized assemblies while the theta-time scale temporal (phase) differences between assemblies reflect their respective distance representations. In successive theta cycles, assemblies representing overlapping place fields (P1 to P8) shift together in time and sustain a temporal order relationship with each other so that the assembly that fires on the earliest phase represents a place field whose center the animal traverses first. This "temporal compression" mechanism (Skaggs et al., 1996) allows distances to be translated into time. Approximately, 7±2 assemblies/gamma cycles are present in a given theta period (Bragin et al., 1995; Lisman and Idiart, 1995). A and B, modified after Geisler et al. (2010). C, modified after Dragoi and Buzsáki (2006).
A striking and reliable correlate of firing patterns of hippocampal pyramidal cells is the spatial location of the rat in a given environment, for which reason these cells are known as place cells, discovered by John O'Keefe. (Fig. 6; courtesy of D. Robbe; O’Keefe and Nadel, 1978; Moser et al., 2008). From a physiological perspective, place cells are speed-dependent oscillators, since their oscillation frequency is determined by the animal’s traveling velocity. Every place cell oscillates faster than the ongoing LFP theta, i.e., the extracellular field, which is largely generated by the coherent membrane potential fluctuations of the contributing place cells.


Figure 6: Spiking activity of a CA1 pyramidal neuron (place cell) during maze behavior illustrates combination of rate and temporal coding. A short segment of local field potential and spikes (vertical ticks) are shown for a single trial. The neuron consistently fires at the T junction of the maze. The discharges over multiple trials are converted to a tuning curve or 'place map' (left); intensity of firing is illustrated by colors. Listening to the neuron's firing illustrates its rhythmic nature. The rhythm of the neuron is faster (approximately 9 Hz) than the frequency of the simultaneous local field potential theta oscillation (approximately 8.5 Hz), resulting in a phase interference (or 'phase precession', O'Keefe and Recce, 1993), as illustrated by the dots on the theta cycle. When the rat enters the field the neuron discharges on the peak of the theta cycle. When it reaches the place field center it fires the most spikes at the trough of the theta cycle. When it leaves the center the spike continues to shift to earlier phases. The precise spike timing of individual hippocampal neurons relative to the reference population activity is an illustration of temporal coding. (Movie)
The paradox of how a slower population theta is generated by place cells, each of which oscillates faster than the population mean, can be explained as follows. The activity of place cells is modulated by a Gaussian function of the animal's position and by the theta frequency oscillation (Fig. 5; Burgess et al., 2007; Geisler et al., 2010). The place fields of sequentially active place cells can overlap and their temporal relationships are governed by a compression rule: within the theta cycle, the spike timing sequence of neurons predicts the upcoming sequence of locations in the path of the rat, with larger time lags representing larger distances (O’Keefe and Recce, 1993; Skaggs et al., 1996; Dragoi and Buzsáki, 2006). Because of the time lags between the spikes of the transiently oscillating neurons, the oscillation frequency of their population output, also reflected by the local LFP, is slower than the mean of the oscillating frequencies of the constituent neurons. The tripartite relationship between LFP theta frequency fθ , the oscillation frequency of single neurons f0 and the distance-related, theta time-scale temporal lags of spikes (time compressed sequences) has important consequences on the assembly organization of hippocampal neurons. First, the difference in oscillation frequency between the population (fθ) and active single neurons generates an interference pattern, known as phase precession of place cells (O’Keefe and Recce, 1993) so that the distance traveled from the beginning of the place field can be instantly inferred from the theta phase of place cell spikes (Fig. 5). Second, the slope of the phase precession defines the size of the place field. Third, the field size (i.e., the lifetime of activity) is inversely related to the oscillation frequency of the neuron. In sum, neurons which oscillate faster have smaller place fields and display steeper phase-precession slopes, as it is the case in the septal portion of the hippocampus, compared to neurons in more caudal (temporal) parts, which oscillate slower, have larger place fields and less steep phase-precession slopes (Maurer et al., 2005). The dynamic local adjustment of these interdependent parameters is responsible for the globally coherent theta oscillation in the hippocampal system (Geisler et al., 2010).
The bidirectional dynamic relationship between single neurons and their population product has important functional consequences. First, despite the variable running speed of the rat, place cells continue to represent the same positions and distances in a given environment. Second, the duration of the theta cycle (120–150 msec in the rat) sets a natural upper limit of distance coding by theta-scale time lags (~50 cm for neurons in the dorsal hippocampus). The behavioral consequence of this constraint is that objects and locations > 50 cm ahead of the rat are initially less distinguishable, but as the animal approaches, they are progressively better resolved by the interleaved cell assemblies. Third, the number of cell assemblies that can nest in a given theta period (5 to 9, as reflected by the number of gamma cycles/theta; Bragin et al., 1995), determines the spatial resolution of distance representation. A consequence of the limited number of theta-nested assemblies is that distance resolution scales with the size of the environment; temporal lags that represent fine spatial resolution in small enclosures correspond to coarser distance representations in larger environments.
Although our current understanding of the dynamics of hippocampal networks derives largely from experiments carried out in spatial tasks, it is important to recognize that the above physiological mechanisms do not necessarily reflect the imposition of environmental stimuli on hippocampal neurons (Eichenbaum and Cohen, 1993; McNaughton et al., 1996). In fact, all of the above-described patterns can emerge by internal mechanisms, without a reliance on external cues or reafferent body signals (Pastalkova et al., 2008; Gelbard-Sagiv et al., 2008). Conceptualizing locations as discrete items, the temporal compression mechanism can limit the attention span and the register capacity of the memory buffer of the gamma-nested theta-cycle to 5 to 9 items (Lisman and Idiart, 1995). Due to the compression mechanism, the spatiotemporal resolution of an episodic recall is high for the conditions/context that surround a recalled event, whereas the relationships among items representing the far past or far future, relative to the recalled event, are progressively less resolved. However, as the content of the recall moves forward in perceived time, subsequent events gain high contextual resolution. The compression dynamic can also allow that not only adjacent but more distant assemblies are linked, as long as they consistently co-occur in the same theta cycles. These higher order connections, in turn, can provide a substrate for alternative combinations of different assembly sequences, mechanisms necessary e.g., for solving detour and transitive inference problems (Muller et al., 1996) and for higher-order associations of items in episodic memory (Polyn and Kahana, 2008).
Consolidation and transfer of hippocampal memories



Figure 7: Time-compressed off-line replay of learned neural patterns. Replay of waking assembly sequences during sleep. Smoothed place fields (colored lines) of 8 place cells during runs from left to right on a track (average of 30 trials). Vertical bars mark the positions of the normalized peaks of the smoothed fields. Non-uniform time axis below shows time within average lap when above positions were passed. Bottom panels, three SPW-R-related sequences from slow wave sleep after the waking session. Note similar sequences during SPW-Rs and run. Note also difference in timescale. Bar = 50 ms. Modified after Lee and Wilson (2002).
Learning an episode typically requires only a single exposure. After an experience, the memory trace either disappears or consolidates into a long-term form. It has been hypothesized that the theta-SPW switch supports a two-stage memory mechanism with a rapid acquisition stage during theta oscillations, followed by repeated reactivation of acquired information during post-experience SPWs (Buzsáki, 1989).
SPWs represent the most synchronous assembly pattern in the mammalian brain, characterized by a three- to five-fold gain of network excitability, creating short time windows for efficient transfer of hippocampal information to the neocortex. Both place cell sequences and the distances between the place fields experienced during exploration are reflected in the temporal structure of neuronal sequences during SPW (Fig. 7; Wilson and McNaughton, 1994; Lee and Wilson, 2002; Dupret et al., 2010), and their selective elimination after learning interferes with memory consolidation (Girardeau et al., 2009). In the waking animal, SPW-related sequences can be replayed in either a forward manner, typically prior to initiating a journey, or in a reverse order after reaching the goal (Foster et al., 2006; Diba and Buzsáki, 2007). This bidirectional re-enactment of temporal sequences may also contribute to the establishment of higher-order associations in episodic memory. Generating windows of high excitability states for teaching the neocortex comes with a price. A slight perturbation of the balance between inhibition and excitation can lead to interictal spikes and seizures. The highly excitable SPWs explain why the hippocampus is the most seizure-prone structure in the brain. Impairment of any of the multiple temporal dynamics can underlie diseases such as schizophrenia and Alzheimer's disease.
Other functions and implications

This overview is meant to be a progress report of our current knowledge of hippocampal dynamics, embedded in a hypothetical framework. I recognize that not all observations fit this framework and acknowledge the many other or related viewpoints, advanced by outstanding colleagues. Hippocampus-like structures are also present in reptiles and birds, and potentially serve navigation functions (http://en.wikipedia.org/wiki/Evolution_of_the_Hippocampus). Granule cells are the specialty neuron of the hippocampus, not present in the neocortex. Granule cells are generated postnatally (Bayer and Altman, 1974; Gage, 2000) and involved in a multitude of functions (Scharfmann, 2007). Revealing the physiological roles of granule cells is, therefore, a key step for understanding hippocampal computation. Furthermore, while this entry focuses on hippocampal-neocortical interactions, the hippocampus also exerts a critical effect on its downstream targets, such as the hypothalamus and basal ganglia, mostly by way of the subiculum.
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Treble 2011

Created By: Timahje Keesee
http://greenanswers.com/news/256367/fountain-youth-immortal-jellyfish-spans-oceans

[1]The concept of immortality has long captivated man. The novel idea of starting-over, beginning anew, and wiping the slate clean for eternity has become the obsession of scientists and the inspiration for countless beauty campaigns. Novels, plays, and films imagine the outcome of attaining immortality. But for the Turritopsis dohrnii jellyfish species, the notion of true rejuvenation isn’t unattainable—it’s routine.

Most jellyfish have a lifespan of hours or months, but Turritopsis dohrnii, dubbed the “immortal jellyfish,” breaks the norm. In many ways, Turritopsis dohrnii are similar to most jellyfish. They have the same umbrella shaped body and flowing tentacles. They grow from polyps, asexually reproduce to form many jellyfish and sexually reproduce at maturity. As the lifecycle ends there for most jellyfish species, for Turritopsis dohrnii, it has only begun. When a Turritopsis dohrnii is deprived of ample nutrition or physically injured, the animal becomes, simply, a blob. [2]The damaged jellyfish attaches its fragile body to a stable object and its cells revert to their juvenile stage. The process of transdifferentiation allows cells to be used for different functions than they previously served as the animal rebuilds itself. The jellyfish goes back to its polyp stage and then grows into its full mature stage again. This process repeats as needed for survival.

[3]While some species of salamanders can grow new limbs (arms, legs, tails) after one has been amputated, these jellyfish are the only animal known that can revert to its polyp stage after sexual maturation. These 4-millimeter creatures are the only immortal animals known to man.

Discovered in 1883, the Turritopsis dohrni’s regenerative capacity was recently realized in the 1990s. Today, genetically identical Turritopsis dohrni have invaded tropical and cooler waters, adapting with ease to the environment. Though the species originated in the Caribbean ocean, swarms of these jellyfish are found worldwide. Scientists speculate that the jellyfish glom onto ships in their cyst state and are transported to faraway oceans, populating the seas with these undying creatures. These animals are only susceptible to death by contracting a disease in their polyp stage or by being prayed upon.

But as these jellyfish continually replicate, fears are arising concerning the ever-booming population. Found off the shores of Spain, Japan, Panama and the Caribbean, these jellyfish may overrun the oceans. Scientists only recently discovered the presence of these immortal jellyfish after the species was well established, highlighting the inconspicuous spread of the species. Scientists have emphasized how difficult it is to detect the presence of these jellyfish until a full swam of them hits the sea. Now, the question remains if the immortal jellyfish population needs to be monitored to prevent an aquatic imbalance and how their presence will affect the existing ocean habitat.

[4]As far as applying this discovery for human benefit, scientists insist that the information they obtain will not work toward advancing beauty creams or other products. Instead, the focus is on cancer. They suspect that these jellyfish have an unparalleled cellular repair mechanism and cancer is spawned from rogue cells. Understanding these jellyfish’s regenerative abilities may shed light upon the cancer epidemic that plagues so many people.
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