Сайт massively.com опубликовал обзор того, что ждет игроков в PvP находящегося в разработке дополнения к MMORPG World of Warcraft: Cataclysm от компании Blizzard Entertainment. В частности, было сообщено следующее:
-Акцент в PvP отныне смещается с Арены на поля боев.
-Новое поле боя «Битва за город Гильнеас» (Battle for Gilneas City) появится в игре в день выхода Катаклизма (нарушивший NDA mmo-champion.com успел выложить несколько скриншотов, демонстрирующих локацию где-то в Twilight Highlands, где клан орков Драконьей Пасти cheap nfl jerseys и клан дворфов Громовой Молот сойдутся в жестокой сече.
-Поля боев старой школы Ущелье Песни Войны, Низина Арати и Альтеракская долина претерпят небольшие косметические изменения, отображающие географические изменения всего Азерота Смертокрылом, которые, впрочем, никак не скажутся на их геймплее.
-Рейтинговые поля боев могут стать довольно враждебными для игроков. Blizzard уже заявляла о том, что лучшая PvP-экипировка будет доступна пользователям, нога которых ни разу не ступала на Арену, поэтому именно на полях боев будут собираться самые сильные игроки, представляющие угрозу для казуальных пугов в виде организованных премейдов.
-Премейды подобной силы будут «разрывать» пуги, что может деморализовать игроков, не готовых к уровню такого соперничества.
-Премейды будут повсюду – даже не на рейтинговых полях боя. Команды будут использовать их для тренировки тактик или набора очков Чести, в то время как казуалы могут сильно пострадать из-за этого. Blizzard вряд ли сможет придумать способ, как этого избежать, поэтому игрокам нужно подготовиться к jordans for cheap будущим изменениям.
-Катаклизм станет лучшим временем для того, чтобы наслаждаться полям боев.
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In some patients, mild TBI occurs without an impact to the head, such as after rapid rotational acceleration of the head in restrained occupants during a motor vehicle crash.11 At a neurophysiological level, these mechanical and inertial forces result in the stretching of white matter axons, leading to diffuse axonal injury.12Although axonal disconnection rarely occurs at the time of injury, the rapid stretching of oakley outlet axons causes an unregulated flux in ion concentrations, including an efflux of K+ and influx of Na+ from and into the axon that, in turn, causes an increase in intra axonal Ca2+ concentrations.13, 14 As the concentration of Ca2+ increases, the protease calpain becomes activated, triggering calpain mediated proteolysis of cytoskeletal proteins, which might translate into irreversible axonal pathology.15 An increase in intra axonal Ca2+ concentration stimulates glutamate release and glutamate mediated activation of N methyl D aspartate receptors, resulting in further depolarization cheap oakleys of neurons.16, 17 Increased activity of various membrane pumps to restore the ionic balance leads to increased glucose consumption, depletion of energy stores, Ca2+ influx into mitochondria, impaired oxidative metabolism, and glycolysis with lactate production, which causes acidosis and oedema.In addition to these ionic disturbances, ultrastructural studies of axons show mechanical breakage and buckling of microtubules at the time of injury, which can trigger progressive microtubule disassembly.18 These combined pathological processes result in interruption of axonal transport and accumulation of protein products. This accumulation gives rise to the two classic neuropathological phenotypes of axonal swelling: singular axonal bulbs (previously called retraction balls) and axonal varicosities, which occur as a series of protrusions along individual axons.13, 19 At a critical threshold of axonal swelling, the axons disconnect at the location of the injury (secondary axotomy).16, 17, 20, 21 Neuronal damage consisting of axonal bulbs and swellings is most commonly located in the deep gyri at the interface between the grey and white matter.13, 22 Studies using advanced MRI techniques, such as diffusion tensor imaging, show that the extent of white matter abnormalities after mild TBI correlates with the severity of postconcussion cognitive problems.23, 24, 25Many practicing clinicians have assumed that the axonopathy and metabolic stress in patients with mild TBI is reversed within 1 weeks, because this is when clinical symptoms have most often disappeared.26 However, magnetic resonance spectroscopy findings, electrophysiological data and neuropsychological assessments suggest that patients’ physiological parameters return to baseline after 30 days.27, 28 Moreover, neuropathological analyses indicate that axonopathy might continue for years after TBI.13 Another important consideration affecting the patient’s recovery after mild TBI is their age, since the developing brain seems to be more vulnerable to repeated concussions than is the adult brain,29 owing to differences in the degree of myelination, volume ratio of brain to water, elastic properties, and blood barrier (BBB) integrity.30, 31 This knowledge, in conjunction with available biomechanical, radiological and clinical data,32, 33 should be communicated to parents with the aim of discouraging the participation of children in contact sports that target the head.A form of TBI induced early dementia was first ray ban outlet reported in 1928 among professional boxers, years after their careers had ended.34 Initially termed dementia pugilistica or punch drunk syndrome, the prevalence of this neuropsychiatric manifestation is now estimated at around 20% in former professional boxers.35, 36 These observations aroused great interest in the long term outcomes of nba jerseys sales patients who developed chronic or progressive symptoms after a single episode or repeated episodes of mild TBI.37 Such symptoms can include changes in cognition (memory and executive functioning), mood (depression, apathy and suicidal thoughts), personality and behaviour (poor impulse control and behavioural disinhibition), and movement (including parkinsonism and symptoms of motor neuron dysfunction), which are similar to those described in ex boxers.38 Some investigators have started to describe this constellation of symptoms as chronic traumatic encephalopathy (CTE);39, 40, 41 however, vigorous debate is ongoing among researchers regarding the definition of CTE from both neuropsychiatric and neuropathological perspectives.The brains of cheap Air Jordans former boxers with CTE also display the hallmark pathologies of Alzheimer disease (AD), including neurofibrillary tangles composed of hyperphosphorylated custom jerseys tau and amyloid (A plaques.42, 43 Progressive axonopathy in these patients might underlie the rapid formation of A plaques after TBI.44 The risk factors for CTE in ex boxers are a long career, many bouts, high sparring exposure, many knockouts, poor performance, and being able to tolerate Wholesale Jerseys many blows without being knocked out, all of which are Brittle associated with discount football jerseys cumulative exposure to repetitive brain trauma.40 According to one study, a positive apolipoprotein E status, commonly associated with AD, is a risk factor for CTE in these individuals.36 Similarly, tau and A pathology, as well as TAR DNA binding protein 43 (TDP 43) deposition, have been found in the brains of patients with CTE approximately 10 years after professional participation in contact sports such as American football.45 Notably, neuritic A plaques and neurofibrillary tangles have also been found in patients a few years to four decades after a single episode of moderate or severe TBI.46 However, TDP cheap mlb jerseys 43 deposition was not found in these patients, suggesting that custom jerseys this pathological feature might be used to distinguish patients with CTE due to a single episode of TBI from those with CTE due to repetitive TBI.47Top of pageCurrently available fluid biomarkersCSF biomarkers of acute brain injuryThe cerebrospinal fluid (CSF) is in direct contact with the extracellular matrix in the brain, and its composition reflects biochemical changes that occur in this organ.48 For these reasons, the CSF might be considered an optimal source of biomarkers of brain injury.