Reed Richards is probably smarter, no?
I never was an Iron Man fan, tbh.
Yes Richards is and neither am I.
Reed Richards is probably smarter, no?
I never was an Iron Man fan, tbh.
Ok asshole, let's consider these links in the context of your initial assertion: 3D movies will cause long term damage to your eyesight.
Presents no reliable sources. Presents no firm conclusion. Quote: "more research needs to be done before we can conclude that 3D HDTV is safe, even for adults." Given the meat of the article, he could just as easily have concluded, "more research needs to be done before we can conclude that 3D HDTV is harmful for adults.". Also it's an audiophile website, so guaranteed to be 100% pure unfiltered, undiluted, concentrated bullshit.
Says nothing, NOTHING about long-term effects.
This article is about kids. Who gives a fuck about kids?
Quote: "I won't pretend there's any hard evidence that these transient effects could develop into permanent problems."
Says nothing about long-term effects (except for kids, and fuck them). Quote: "found via an online survey." Derp.
Quote: "The Australian branch of Samsung has put out a health risk warning concerning watching 3D TV on its website. Under the headline “Photosensitive Seizure Warning and Other Health Risks”, it sums up the possible dangers of watching 3D." This is 100% cover-your-ass (which is why the warning label appears only on Autralian websites - it's a regulatory issue). No evidence. Says nothing about long term effects.
In conclusion you're either a dishonest piece of worthless shit, or a category-5 full-blown moron. Or both. Die in a fire.
To me, a graphic novel is nothing more than a really long comic book (hence the use of "novel"). It's essentially taking a bunch of comic issues and binding them together.
Can you tell me what was exactly bad about the 3D?
I have to agree on Watchmen. I don't like the whole superhero genre but Watchmen is one of my favorite movies.
I was! I have Iron Man 1, and Tales of Suspense 40... But not 39... Yet. :'(
I honestly didn't know anything about the Iron Man story, much less Tony Stark's character until many years later when the Iron Man flick came out.
Awesome dude, wish I read more of it at the time. :\
http://www.audioholics.com/news/editorials/warning-3d-video-hazardous-to-your-health
http://io9.com/#!5477698/science-proves-3+d-movies-hurt-your-brain
https://www.parentstv.org/PTC/publications/rgcolumns/2010/0428.asp
http://www.slate.com/id/2215265/pagenum/all/
http://www.telegraph.co.uk/technolo...d-video-games-cause-nausea-and-headaches.html
http://www.broadbandtvnews.com/2010/04/23/samsung-issues-3d-health-warning/
Let me know if you need more links. They weren't hard to find & there are dozens more.
I don't watch anything in 3D. 3D movies are a joke & will cause long term problems with your eyesight. I'm actually surprised 3D displays are selling as well as they are. Many of those people will be in for a big surprise in a couple years.
The problem of moving the eyes to fixate a new target in space (or indeed any other movement) entails two separate issues: controlling the amplitude of movement (how far), and controlling the direction of the movement (which way). The amplitude of a saccadic eye movement is encoded by the duration of neuronal activity in the lower motor neurons of the oculomotor nuclei. As shown in Figure 20.6, for instance, neurons in the abducens nucleus fire a burst of action potentials prior to abducting the eye (by
causing the lateral rectus muscle to contract) and are silent when the eye is adducted. The amplitude of the movement is correlated with the duration of the burst of action potentials in the abducens neuron. With each saccade, the abducens neurons reach a new baseline level of discharge that is correlated with the position of the eye in the orbit. The steady baseline level of firing holds the eye in its new position.
Motor neuron activity in relation to saccadic eye movements. The experimental setup is shown on the right. In this example, an abducens lower motor neuron fires a burst of activity (upper trace) that precedes and extends throughout the movement (solid (more...)
The direction of the movement is determined by which eye muscles are activated. Although in principle any given direction of movement could be specified by independently adjusting the activity of individual eye muscles, the complexity of the task would be overwhelming. Instead, the direction of eye movement is controlled by the local circuit neurons in two gaze centers in the reticular formation, each of which is responsible for generating movements along a particular axis. The paramedian pontine reticular formation (PPRF) or horizontal gaze center is a collection of local circuit neurons near the midline in the pons responsible for generating horizontal eye movements (Figure 20.7). The rostral interstitial nucleus or vertical gaze center is located in the rostral part of the
midbrain reticular formation and is responsible for vertical movements. Activation of each gaze center separately results in movements of the eyes along a single axis, either horizontal or vertical. Activation of the gaze centers in concert results in oblique movements whose trajectories are specified by the relative contribution of each center.
Simplified diagram of synaptic circuitry responsible for horizontal movements of the eyes to the right. Activation of local circuit neurons in the right horizontal gaze center (the PPRF; orange) leads to increased activity of lower motor neurons (red (more...)
An example of how the PPRF works with the abducens and oculomotor nuclei to generate a horizontal saccade to the right is shown in Figure 20.7. Neurons in the PPRF innervate cells in the abducens nucleus on the same side of the brain. There are,
however, two types of neurons in the abducens nucleus. One type is a lower motor neuron that innervates the lateral rectus muscle on the same side. The other type, called internuclear neurons, sends their axons across the midline and ascends in a fiber tract called the medial longitudinal fasciculus, terminating in the portion of the oculomotor nucleus that contains lower motor neurons innervating the medial rectus muscle. As a result of this arrangement, activation of PPRF neurons on the right side of the brainstem causes horizontal movements of both eyes to the right; the converse is of course true for the PPRF neurons in the left half of the brainstem.
Neurons in the PPRF also send axons to the medullary reticular formation, where they contact inhibitory local circuit neurons. These local circuit neurons, in turn, project to the contralateral abducens nucleus, where they terminate on lower motor neurons and internuclear neurons. In consequence, activation of neurons in the PPRF on the right results in a reduction in the activity of the lower motor neurons whose muscles would oppose movements of the eyes to the right. This inhibition of antagonists resembles the strategy used by local circuit neurons in the spinal cord to control limb muscle antagonists (see Chapter 16).
Although saccades can occur in complete darkness, they are often elicited when something attracts attention and the observer directs the foveas toward the stimulus. How then is sensory information about the location of a target in space transformed into an appropriate pattern of activity in the horizontal and vertical gaze centers? Two structures that project to the gaze centers are demonstrably important for the initiation and accurate targeting of saccadic eye movements: the superior colliculus of the midbrain, and a region of the frontal lobe that lies just rostral to premotor cortex, known as the frontal eye field (Brodmann's area 8). Upper motor neurons in both of these structures, each of which contains a topographical motor map, discharge immediately prior to saccades. Thus, activation of a particular site in the superior colliculus or in the frontal eye field produces saccadic eye movements in a specified direction and for a specified distance that is independent of the initial position of the eyes in the orbit. The direction and distance are always the same for a given stimulation site, changing systematically when different sites are activated.
Both the superior colliculus and the frontal eye field also contain cells that respond to visual stimuli; however, the relation between the sensory and motor responses of individual cells is better understood for the superior colliculus. An orderly map of visual space is established by the termination of retinal axons within the superior colliculus (see Chapter 12), and this sensory map is in register with the motor map that generates eye movements. Thus, neurons in a particular region of the superior colliculus are activated by the presentation of visual stimuli in a limited region of visual space. This activation leads to the generation of a saccade that moves the eye by an amount just sufficient to align the foveas with the region of visual space that provided the stimulation (Figure 20.8).
Figure 20.8
Evidence for sensory motor transformation obtained from electrical recording and stimulation in the superior colliculus. (A) Surface views of the superior colliculus illustrating the location of eight separate electrode recording and stimulation sites. (more...)
Neurons in the superior colliculus also respond to auditory and somatic stimuli. Indeed, the location in space for these other modalities also is mapped in register with the motor map in the colliculus. Topographically organized maps of auditory space and of the body surface in the superior colliculus can therefore orient the eyes (and the head) in response to a variety of different sensory stimuli. This registration of the sensory and motor maps in the colliculus illustrates an important principle of topographical maps in the motor system, namely to provide an efficient mechanism for sensory motor transformations (Box B).
Box B
Sensory Motor Integration in the Superior Colliculus. The superior colliculus is a laminated structure in which the differences between the layers provide clues about how sensory and motor maps interact to produce appropriate movements. As discussed in (more...)
The functional relationship between the frontal eye field and the superior colliculus in controlling eye movements is similar to that between the motor cortex and the red nucleus in the control of limb movements (see Chapter 17). The frontal eye field projects to the superior colliculus, and the superior colliculus projects to the PPRF on the contralateral side (Figure 20.9). (It also projects to
the vertical gaze center, but for simplicity the discussion here is limited to the PPRF.) The frontal eye field can thus control eye movements by activating selected populations of superior colliculus neurons. This cortical area also projects directly to the contralateral PPRF; as a result, the frontal eye field can also control eye movements independently of the superior colliculus. The parallel inputs to the PPRF from the frontal eye field and superior colliculus are reflected in the deficits that result from damage to these structures. Injury to the frontal eye field results in an inability to make saccades to the contralateral side and a deviation of the eyes to the side of the lesion. These effects are transient, however; in monkeys with experimentally induced lesions of this cortical region, recovery is virtually complete in two to four weeks. Lesions of the superior colliculus change the accuracy, frequency, and velocity of saccades; yet saccades still occur, and the deficits also improve with time. These results suggest that the frontal eye fields and the superior colliculus provide complementary pathways for the control of saccades. Moreover, one of these structures appears to be able to compensate (at least partially) for the loss of the other. In support of this interpretation, combined lesions of the frontal eye field and the superior colliculus produce a dramatic and permanent loss in the ability to make saccadic eye movements.
Figure 20.9
The relationship of the frontal eye field in the right cerebral hemisphere (Brodmann's area 8) to the superior colliculus and the horizontal gaze center (PPRF). There are two routes by which the frontal eye field can influence eye movements in humans: (more...)
These observations do not, however, imply that the frontal eye fields and the superior colliculus have the same functions. Superior colliculus lesions produce a permanent deficit in the ability to perform very short latency reflex-like eye movements called express saccades. The express saccades are evidently mediated by direct pathways to the superior colliculus from the retina or visual cortex that can access the upper motor neurons in the colliculus without extensive, and more time-consuming, processing in the frontal cortex (see Box B). In contrast, frontal eye field lesions produce permanent deficits in the ability to make saccades that are not guided by an external target. For example, patients (or monkeys) with a lesion in the frontal eye fields cannot voluntarily direct their eyes away from a stimulus in the visual field, a type of eye movement called an antisaccade. Such lesions also eliminate the ability to make a saccade to the remembered location of a target that is no longer visible.
Finally, the frontal eye fields are essential for systematically scanning the visual field to locate an object of interest within an array of distracting objects (see Figure 20.1). Figure 20.10 shows the responses of a frontal eye field neuron during a visual task in which a
monkey was required to foveate a target located within an arrray of distracting objects. This frontal eye field neuron discharges at different levels to the same stimulus, depending on whether the stimulus is the target of the saccade or a distractor, and on the location of the distractor relative to the actual target. For example, the differences between the middle and the left and right traces in Figure 20.10 demonstrate that the response to the distractor is much reduced if it is located close to the target in the visual field.
Results such as these suggest that lateral interactions within the frontal eye fields enhance the neuronal responses to stimuli that will be selected as saccade targets, and that such interactions suppress the responses to uninteresting and potentially distracting stimuli. These sorts of interactions presumably reduce the occurrence of unwanted saccades to distracting stimuli in the visual field
Saw it at midnight in IMAX 3D, only cost me 4 bucks so I thought I'd see it in 3D. The 3D was terrible and honestly takes away from what is a rather entertaining movie. The whole time I was like "fuck I should have just seen this in IMAX, the 3D is ruining the experience for me". So, pretty good action movie with a really quick pace.
I saw this in 3D last night.
The 3D was very subtle in this movie, not sure wtf the OP is talking about. did not see it in Imax though, just the Real3D thing.
thought the movie was really good as well, enjoyed every part of it. the way he interacted when he got to earth was hilarious.
I lol'd when he threw down the cup in the diner - "I'll have another!" :awe:
Saw it at midnight in IMAX 3D, only cost me 4 bucks so I thought I'd see it in 3D. The 3D was terrible and honestly takes away from what is a rather entertaining movie. The whole time I was like "fuck I should have just seen this in IMAX, the 3D is ruining the experience for me". So, pretty good action movie with a really quick pace. If you try to get TO into it you'll probably find yourself going "but wtf?", so don't it's a goddamn Marvel Comic Book movie.
I saw it in IMAX 3D. Same opinion. Would have been better in 2D. All movies need to follow the Avatar "Real3D" line of thinking if they want to do their movies in 3D. I saw Avatar in 3D in both Real3D and IMAX - Real3D was far better imo. That and most of the stuff in Thor wasn't really 3D-ish anyway.
Also, I really enjoyed the movie. Great ending after the titles, too! :awe: