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Server time: 2018-02-23, 14:51

King of the Castle - Lopatino (Melee only - OOC Event)
TOMORROW - 2018-02-24 23:00:00 (server time) - Starts in 1 day, 8 hours, 8 minutes

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  2. Dimitris photoshops or screenshots.

    @dimitri - hot.
  3. BeanZ WAR

    179
  4. Random Screenshots

    @dimitri
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    @human142 @LoneFox
  6. Hope you all stay safe <3

    Peace dude, have a good one. Be nice to see ya when ya return.
  7. Hope you all stay safe <3

    Later dude, if you ever need any advice about military life hit me up. o7
  8. Seen this system inconvenience genuine people more than it deters those who intended to abuse alts. -1 from me, don't make it harder.
  9. Waiting to crack a cold one

    It feels good to see people camping out like it's Black Friday to get a beer at our Pub, right @Jean!
  10. Condensed Notebook

    Symptoms mimicking Viral Encephalitis Naegleria fowleri Rabies Viral Encephalitis (including measles and rubella) An inflammation of the brain caused by a virus. An be triggered by microorganisms, bacteria, fungi and parasites Also triggered by enteroviruses herpes simplex virus varicella zoster virus Epstein-Barr virus cytomegalovirus adenovirus rubella measles Murray Valley encephalitis (MVE) virus and Kunjin virus Japanese encephalitis virus. Virus moves to brain, body responds to protect, brain swells Travels via blood or nerve cells to brain and through blood-brain barrier Certain viruses prefer certain areas (herpes – temporal lobe by each ear) Treatment for viral encephalitis Various medicine for various symptoms (pain, vomiting, seizures, fever) Antiviral medicine, intravenously Fluids to prevent dehydration, but not too much as this can worsen cerebral oedema (swelling of the brain). Medications or actions such as induced hypothermia for brain swelling Naegleria fowleri Humans become infected when water containing Naegleria fowleri enters the nose and the ameba migrates to the brain along the olfactory nerve, NOT from drinking water Trophozoites can turn into a temporary, non-feeding, flagellated stage (10-16 µm in length) when stimulated by adverse environmental changes such as a reduced food source. They revert back to the trophozoite stage when favorable conditions return Naegleria fowleri trophozoites are found in cerebrospinal fluid (CSF) and tissue, while flagellated forms are occasionally found in CSF Cysts are not seen in brain tissue When a cyst comes into contact with an inviting host, it sprouts tentacle-like pseudopods and turns into a form known as a trophozoite. Once it’s transformed, the trophozoite heads straight for the host’s central nervous system, following nerve fibers inward in search of the brain. Once it’s burrowed into its host’s brain tissue — usually the olfactory bulbs — N. fowleri sprouts a “sucking apparatus” called an amoebostome and starts chowing down on juicy brain matter. As the amoeba divides, multiplies and moves inward, devouring brain cells as it goes, its hosts can go from uncomfortable to incoherent to unconscious in a matter of hours. miltefosine has shown some promise in combination with some of these other drugs. Miltefosine has shown ameba-killing activity against free-living amebae, including Naegleria fowleri, in the laboratory. Miltefosine has also been used to successfully treat patients infected with Balamuthia and disseminated Acanthamoeba infection Rabies But rabies viruses don’t just settle down anywhere in the brain, they specifically seek out the hippocampus, amygdala and hypothalamus, brain structures that play central roles in memory, fear and emotion. And they don’t just devour brain cells indiscriminately, either; instead, they alter the ways these cells release neurotransmitters like serotonin, GABA, and endogenous opioids. In other words, they turn their hosts’ own brain chemistry against them. In the altered states brought on by a rabies infection, animals often lash out at any nearby living thing, but this may be more out of fear than anger. Human rabies patients become terrified of water and puffs of air, both of which make them flinch and twitch uncontrollably. To date, fewer than 10 people have survived a clinical-stage rabies infection — ever, in history. Many doctors consider the disease untreatable. The better news, though, is that it’s easily preventable with a vaccine. Fighting back In a turnabout, a biochemical self-destruct trigger found in many other types of cells appears to guard the lives of brain cells during an infection with West Nile virus The self-destruct trigger, a protein called RIPK3 (pronounced rip-3), is better known for activating a certain type of cell death during infection or damaging events in other parts of the body. The death of infected cells in this manner is a protective mechanism that helps the body eliminate the infection. During a West Nile virus infection, however, the activation of RIPK3 in brain cells doesn't cause them to die. That's because its signaling within the central nervous system is not the same as in cell types elsewhere in the body. Its brain-specific role implies that there are central nervous system functions for RIPK3 not observed in other tissues. "RIPK3 acts as part of the milieu of signals that support anti-viral inflammation in the brain," RIPK3 responds to the presence of West Nile virus in the brain by placing an order for chemokines Chemokines attract an influx of infection-fighting white blood cells In a different cell type, such as a fibroblast, the entry of a West Nile virus would result in the cell initiating its own demise. Too much interference with RIPK3 in the brain could make it prone to certain viral infections. The rabies virus, transmitted largely through the bites of infected animals, has evolved over thousands of years to hijack nerve cells, which it uses to climb from infected muscle tissue into the brain. That allows it to bypass a major hurdle: the blood-brain barrier, a selective membrane that keeps out most pathogens that travel through the bloodstream. But the barrier also prevents treatments—like cancer drugs—from reaching infected cells, limiting options for patients. Nanoparticle expert Yu Seok Youn and his team have engineered gold particles so that they have the same rodlike shape and size as the virus. The nanoparticle’s shape gives it more surface area than spherical particles, improving the surface protein’s ability to bind with receptors on nerve cells that serve as a gateway to the nervous system. The particles don’t carry any drugs, but the tiny gold rods readily absorb laser light, which heats them up and kills surrounding tissue. To see whether these new particles could be effective against tumors, Youn and his team first injected them into the tail veins of four mice with brain tumors. The nanoparticles quickly traveled to the brain, where they accumulated near the tumor sites. The team then fired a near infrared laser at the nanoparticles, heating them to nearly 50°C. The light harmlessly passed through skin and bone, but heat from the gold particles radiated outward, effectively cooking nearby cancer cells. The treatment greatly reduced the size of the tumors, Youn and his colleagues report this month in Advanced Materials. In another experiment, the researchers used the same treatment on mice with tumor cells that had been injected into their flanks. Tumors on two of the mice disappeared after 7 days, whereas the other tumors shrank to about half their original size. Still uncertain is just how the nanoparticles reached the tumor cells. Youn says they likely traveled the same path as the rabies virus—through the central nervous system.
  11. Personal Notes of Elizabeth Smith

    Fever and High BP, Pulse Anytime you get a fever, your body is working to fight off an infection. Fever raises your temperature, speeds up your heart rate and raises your blood pressure levels. This increased blood pressure is due to "vasoconstriction"– a narrowing of blood vessels. An increase in your heart rate can also occur during other kinds of bacterial or viral infection, including bronchitis, pneumonia and strep throat. This happens in response to your heart's extra oxygen demands, so your system can fight off the infection. A heart-rate increase can also raise your blood pressure. Dehydration from fever or infection can raise your blood pressure, too. High blood pressure can cause non trauma related bleeding in the brain Viral encephalitis Viral encephalitis is an inflammation of the brain caused by a virus. Some viral diseases, such as measles and rubella, can also progress to involve inflammation of the brain. Other micro-organisms, such as bacteria, fungi and parasites, are capable of triggering encephalitis, but viruses – particularly the group known as enteroviruses – are the leading cause. Once inside the blood, the viruses migrate to the brain where they start to multiply. The body notices the invasion and mounts an immune system response. This causes the brain to swell. The combination of infection and immune response creates the typical symptoms of viral encephalitis. The most serious potential complication from viral encephalitis is permanent brain damage. Viruses that can cause encephalitis Some of the viruses that are capable of causing encephalitis include: enteroviruses – such as coxsackievirus, poliovirus and echovirus herpes simplex virus varicella zoster virus Epstein-Barr virus cytomegalovirus adenovirus rubella measles Murray Valley encephalitis (MVE) virus and Kunjin virus Japanese encephalitis virus. Modes of transmission of viruses Viruses spread by different means, and some are more infectious than others. Some of the modes of viral transmission include: coughs or sneezes from an infected person that release airborne viruses, which are then inhaled by others infected insects (such as mosquitoes or ticks) and animals, which can transfer some viruses directly into the bloodstream via their bite eating contaminated food or drink the transfer of some viruses can occur through touching an infected person there is evidence to suggest that some cases of viral encephalitis are caused by a dormant viral infection (such as herpes simplex virus) becoming active again. Infection and the immune system response Once viruses have gained access to the bloodstream, they can multiply and spread to other parts of the body, including to the spinal cord and brain (the central nervous system). Access to the brain is by blood or nerves. After breaching the blood–brain barrier, the viruses slip inside brain cells. This disrupts, damages and ultimately ruptures the infected brain cells. Certain viruses have a preference for different areas of the brain. For example, the herpes simplex virus likes to target the temporal lobes located near each ear. The cells of the immune system rush to the brain and start attacking the viruses. This causes the characteristic brain swelling (cerebral oedema). Both the infection and the attempts of the body to fight the infection are responsible for the symptoms of viral encephalitis Treatment for viral encephalitis Unlike bacteria, viruses are difficult to treat. Antiviral medications only work on a limited number of viruses. Treatment aims to reduce the severity of the symptoms and may include: hospitalisation antiviral medication, given intravenously, if the virus is known to be susceptible to treatment with antiviral medication (such as the herpes simplex virus) intravenous administration of medications to help reduce brain swelling pain-relieving medication medication to prevent vomiting medication to prevent seizures (anticonvulsant) medication to reduce fever, such as paracetamol fluids to prevent dehydration, but not too much as this can worsen cerebral oedema (swelling of the brain). Hemorrhagic Stroke Hemorrhagic stroke is the less common type. It happens when a blood vessel breaks and bleeds into the brain. Subarachnoid hemorrhage — Bleeding from a damaged blood vessel causes blood to accumulate at the surface of the brain. Blood fills a portion of the space between the brain and the skull, and it mixes with the cerebrospinal fluid that cushions the brain and spinal cord. As blood flows into the cerebral spinal fluid, it increases pressure on the brain, which causes an immediate headache. In the days immediately following the bleeding, chemical irritation from clotted blood around the brain can cause brain arteries that are near to this area to go into spasm. Artery spasms can damage brain tissue. Most often, a subarachnoid hemorrhage happens because of a leaking saccular aneurysm (a sack-like bulge in the wall of an artery), but it also can occur because of leakage from an arteriovenous malformation. Intracerebral hemorrhage — Bleeding occurs from a broken blood vessel within the brain. Some things that increase your risk for this kind of hemorrhage are high blood pressure (hypertension), heavy alcohol use, advanced age and the use of cocaine or amphetamines. A mechanical ventilator frequently is used to hyperventilate the stroke patient because this can lead to a lower, safer pressure. The sugar mannitol, which sometimes is used as a medicine, pulls brain fluid into the bloodstream, also lowering intracranial pressure. If necessary, a surgeon will cut the skull bone (with a small drilled hole called a "burr hole," or with a larger surgery) to decrease the compression of the brain tissue. In some cases, surgery is necessary to remove a large portion of the clot after a hemorrhage, but in most patients, the body eventually reabsorbs the clotted blood on its own. Neurological parasites Toxoplasma gondii T. gondii’s life begins in cat feces, where its eggs (known as “oocytes” or “egg cells”) wait to be picked up by carriers like rats. Once they’re safe and warm in the guts of their temporary hosts, the oocytes morph into tachyzoites, the unassuming little blobs that can really do some damage. Those tachyzoites migrate into their hosts’ muscles, eyes and brains, where they can remain hidden for decades without doing much of anything. But when the moment comes to strike, the little T. gondii tachyzoites alter their hosts’ brain chemistry. Infected rats actually become sexually aroused by the smell of cats, and leap fearlessly into their claws, where they die and release the tachyzoites back into the cats, allowing the egg-laying cycle to start anew. Some researchers estimate that as much as 30 percent of the people on earth — more than two billion of us — are carrying little T. gondii tachyzoites around in our brains right now. Another paper, published in the journal Proceedings of the Royal Society B, argued that in areas with high T. gondii infection rates, these tiny parasites could cumulatively alter the behavioral patterns of entire cultures. Infected parents, researchers found, have a 30 percent chance of passing the parasite on to their children Most healthy people recover from toxoplasmosis without treatment. Persons who are ill can be treated with a combination of drugs such as pyrimethamine and sulfadiazine, plus folinic acid. Naegleria fowleri Humans become infected when water containing Naegleria fowleri enters the nose and the ameba migrates to the brain along the olfactory nerve 2,3. People do not become infected from drinking contaminated water. Symptoms start 1-9 days (median 5 days) after swimming or other nasal exposure to Naegleria-containing water. People die 1-18 days (median 5 days) after symptoms begin 4. PAM is difficult to detect because the disease progresses rapidly so that diagnosis is usually made after death N. fowleri can spend long spans of time just hanging around as a cyst, a little armored ball that can survive cold, heat, and dry conditions. When a cyst comes into contact with an inviting host, it sprouts tentacle-like pseudopods and turns into a form known as a trophozoite. Once it’s transformed, the trophozoite heads straight for the host’s central nervous system, following nerve fibers inward in search of the brain. Once it’s burrowed into its host’s brain tissue — usually the olfactory bulbs — N. fowleri sprouts a “sucking apparatus” called an amoebostome and starts chowing down on juicy brain matter. As the amoeba divides, multiplies and moves inward, devouring brain cells as it goes, its hosts can go from uncomfortable to incoherent to unconscious in a matter of hours. The symptoms start subtly, with alterations in tastes and smells, and maybe some fever and stiffness. But over the next few days, as N. fowleri burrows deeper into the brain’s cognitive structures, victims start feeling confused, have trouble paying attention, and begin to hallucinate. Next come seizures and unconsciousness, as the brain loses all control. Two weeks later, the victim’s most likely perishes — although one man in Taiwan managed to stick it out for a grueling 25 days before his nervous system finally gave out. Although N. fowleri infections are rare in the extreme — worldwide historical totals number only in the hundreds — they’re almost always fatal, and tricky to catch and treat before they spiral out of control. a 12-year-old girl, was diagnosed with PAM approximately 30 hours after becoming ill and was started on the recommended treatment within 36 hours. She also received the investigational drug miltefosine, and her brain swelling was aggressively managed with treatments that included therapeutic hypothermia (cooling the body below normal body temperature). This patient made a full neurologic recovery and returned to school. Her recovery has been attributed to early diagnosis and treatment and novel therapeutics including miltefosine and hypothermia 7. Recently an investigational breast cancer and anti-leishmania drug, miltefosine 8, has shown some promise in combination with some of these other drugs. Miltefosine has shown ameba-killing activity against free-living amebae, including Naegleria fowleri, in the laboratory 9, 10,. Miltefosine has also been used to successfully treat patients infected with Balamuthia 11 and disseminated Acanthamoeba infection Rabies This bullet-shaped virus — so small and sneaky that it often escapes detection by the immune system — doesn’t need much of an invitation to dive into a new host; a simple puncture wound will do it. Once it’s inside the host’s bloodstream, it quickly starts taking over cells, transforming them into rabies factories that churn out thousands of copies of the virus. As the attackers grow in number, they make their way to the host’s central nervous system, and head for the brain. But rabies viruses don’t just settle down anywhere in the brain, they specifically seek out the hippocampus, amygdala and hypothalamus, brain structures that play central roles in memory, fear and emotion. And they don’t just devour brain cells indiscriminately, either; instead, they alter the ways these cells release neurotransmitters like serotonin, GABA, and endogenous opioids. In other words, they turn their hosts’ own brain chemistry against them. In the altered states brought on by a rabies infection, animals often lash out at any nearby living thing, but this may be more out of fear than anger. Human rabies patients become terrified of water and puffs of air, both of which make them flinch and twitch uncontrollably. To date, fewer than 10 people have survived a clinical-stage rabies infection — ever, in history. Many doctors consider the disease untreatable. The better news, though, is that it’s easily preventable with a vaccine. Brain fights West Nile Virus in unexpected way In a turnabout, a biochemical self-destruct trigger found in many other types of cells appears to guard the lives of brain cells during an infection with West Nile virus The self-destruct trigger, a protein called RIPK3 (pronounced rip-3), is better known for activating a certain type of cell death during infection or damaging events in other parts of the body. The death of infected cells in this manner is a protective mechanism that helps the body eliminate the infection. During a West Nile virus infection, however, the activation of RIPK3 in brain cells doesn't cause them to die. That's because its signaling within the central nervous system is not the same as in cell types elsewhere in the body. Its brain-specific role implies that there are central nervous system functions for RIPK3 not observed in other tissues. "RIPK3 acts as part of the milieu of signals that support anti-viral inflammation in the brain," RIPK3 responds to the presence of West Nile virus in the brain by placing an order for chemokines Daniels explained that these chemicals underlie a successful ousting of West Nile virus. Chemokines attract an influx of infection-fighting white blood cells. These efforts contribute to the clearance of the virus from the brain, but not by directly stopping replacement virus from reproducing within brain cells. Instead, the brain tissue undergoes a kind of inflammation that restricts the West Nile virus infection. In a different cell type, such as a fibroblast, the entry of a West Nile virus would result in the cell initiating its own demise. Too much interference with RIPK3 in the brain could make it prone to certain viral infections. How to stop brain cancer—with rabies The rabies virus, which kills tens of thousands of people a year, has a rare ability to enter nerve cells and use them as a conduit to infect brain tissue The rabies virus, transmitted largely through the bites of infected animals, has evolved over thousands of years to hijack nerve cells, which it uses to climb from infected muscle tissue into the brain. That allows it to bypass a major hurdle: the blood-brain barrier, a selective membrane that keeps out most pathogens that travel through the bloodstream. But the barrier also prevents treatments—like cancer drugs—from reaching infected cells, limiting options for patients. Already, researchers have packaged cancer-fighting drugs into nanoparticles coated with part of a rabies surface protein that lets the virus slip into the central nervous system Nanoparticle expert Yu Seok Youn and his team have engineered gold particles so that they have the same rodlike shape and size as the virus. The nanoparticle’s shape gives it more surface area than spherical particles, improving the surface protein’s ability to bind with receptors on nerve cells that serve as a gateway to the nervous system. The particles don’t carry any drugs, but the tiny gold rods readily absorb laser light, which heats them up and kills surrounding tissue. To see whether these new particles could be effective against tumors, Youn and his team first injected them into the tail veins of four mice with brain tumors. The nanoparticles quickly traveled to the brain, where they accumulated near the tumor sites. The team then fired a near infrared laser at the nanoparticles, heating them to nearly 50°C. The light harmlessly passed through skin and bone, but heat from the gold particles radiated outward, effectively cooking nearby cancer cells. The treatment greatly reduced the size of the tumors, Youn and his colleagues report this month in Advanced Materials. In another experiment, the researchers used the same treatment on mice with tumor cells that had been injected into their flanks. Tumors on two of the mice disappeared after 7 days, whereas the other tumors shrank to about half their original size. Still uncertain is just how the nanoparticles reached the tumor cells. Youn says they likely traveled the same path as the rabies virus—through the central nervous system. Zika virus kills brain cancer stem cells In collaboration with co-senior authors Diamond and Milan G. Chheda, MD, of Washington University School of Medicine, and Jeremy N. Rich, MD, of UC San Diego, Zhu tested whether the virus could kill stem cells in glioblastomas removed from patients at diagnosis. They infected tumors with one of two strains of Zika virus. Both strains spread through the tumors, infecting and killing the cancer stem cells while largely avoiding other tumor cells. The findings suggest that Zika infection and chemotherapy-radiation treatment have complementary effects. The standard treatment kills the bulk of the tumor cells but often leaves the stem cells intact to regenerate the tumor. Zika virus attacks the stem cells but bypasses the greater part of the tumor.
  12. Not really a big deal is it?? i mean sometimes, just sometimes i wish it was shorter just for the fact that my character really pisses me off alot lol and i like a break, But then i miss her. literally cannot win!
  13. No. Why? Reasons stated above already
  14. Nah i honestly have never seen that problem i change character then and then often when i switch group its good as its now its allow people to do more stuff not more strict rules
  15. Today
  16. BeanZ WAR

    178
    • G19RP
    •   
    • LouieRP

    Louie’s great tales when he returns from Greece.

    1. JimRP

      JimRP

      When he returns from Greece?

      rofl

      ok

    2. Josei

      Josei

      Is he going to live there?

  17. It's always good to come up with new ideas! And even more so to share them, while some people may not agree you may find that there are some who do agree. Sadly, in this case, we already have had pushback when it comes to the time of the Character CD's and had to adjust them. To increase the length of the cool down would not incite people to play, what if they got stuck on a character they disliked, or had no current story, or what have you? We want people to be able to explore different aspects of characters as they can and a longer cool down will sort of prevent this. Though we appreciate you sharing your ideas!
  18. I don't see people swapping characters that often as it is, unless they're making new, unrelated characters to anyone and anything, OR playing event characters. 24 hours is fine. So issa nah from me.
  19. Hope you all stay safe <3

    I'll never forget the time you- Nah.. fuck that, I'm over it. Adieu Galaxy, I miss your soundboard. You redeemed yourself pretty damn well as opposed to when you first started here.
  20. Ok well first that is metagaming and you are breaking the rules if you use that OOC info IC. Secondly as long as YOU ARE NOT BREAKING THE RULES, I don't see how the current system is flawed. It allows people to play different styles of character and not let things get stale.
  21. Absolutely not. It would just encourage people to play less, imho. We already had to lower the CD before because of complaints. It used to be 48 hours. Even that was too long.
  22. So I know this probably will get alot of hate. But I think there should be longer cool downs for character switching. As I know there are many people who switch in between characters everyday. Because for me it gets confusing when you hear the same voice on a different person knowing that this is their other character that isn't it your group. I think also the cool downs would help so people that do play as different characters can have more time developing that character. For example: Say I create a new character to kind get away from everything. I can just switch characters within 24 hours to back to my other character that is in a group. And using 2 characters can lead to metagaming in someways like: If one of my characters knows where a base is then I switch to my other one. I wouldn't know IC but OOC I know where it is and I can use that to go to that base. What I think the cool down time should be anywhere from like 3 days to 7 days.
  23. Random Screenshots

    Sure, I'll look into it. @LoneFox
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