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Home WarZone Selling the Bin Laden Lie
Selling the Bin Laden Lie
FROM THE REAL KILLERS OF 9/11, SELLING THE BIN LADEN "TERROR MYTH"
By Gordon Duff, VT Senior Editor
I pity those who cheered or felt relief at the announced death of Osama bin Laden. It isn't just that the real bin Laden died years ago. It's that Osama bin Laden was never a terrorist in the first place. Nearly a decade of investigation failed to connect bin Laden to 9/11 with a single shred of evidence.
Instead, when that original cover-up, the 9/11 Commission proven categorically to be a "whitewash," to the extent that even Fox News reported it openly, all evidence pointed to the Bush White House and Israeli intelligence services.
https://www.youtube.com/watch?v=tE3pMPObcGU
The undisputed evidence, Building 7, showed that massive explosive devices were planted under the World Trade Center. No newspaper reported this, even when the Fox Network carried the stories on prime time. No mention of this has been made this week. What it proved is that terrorists had nothing to do with 9/11. Simply put, if one building was sabotaged, then all the attacks were staged.
AUSSIES AIN'T BUYIN' IT
The evidence for this, hard evidence, science, testimony, not theory but a very real conspiracy is massive and supported by the majority of Americans. One "conspiracy theory debunker," Jon Fain of ABC, went after Kevin Braken, a political leader in Australia.
77% of Australians in a Herald Sun poll believe that 9/11 is a US government "inside job." That number applies to Americans as well.
Then why is nothing of any of this mentioned now? Why was Obama allowed to ramble on, in what we can prove was an incoherent manner, driveling on about bin Laden and 9/11? Perhaps the most shameful of all is Geraldo Rivera, the Fox News journalist who helped break the story that proved bin Laden was never involved in 9/11. He now rants about bin Laden and ghoulishly celebrates the "mass murderer of 9/11" that he himself helped prove innocent.
Where do you find people like that?
THE ALTERNATIVE MEDIA
When major corporations and "interest groups" based in a small Middle Eastern non-Islamic country managed to gain control over 95% of America's media, destroying the lines between, not only "news" and "entertainment" but "fact" and "fiction" as well, it was the end of any semblance of democracy in America. Democracy is based on public consensus. If someone controls what the public believes and thinks, if the public is continually bombarded with falsehood, there is no basis for democracy.
Simply put, the controlled media, which includes much of the internet as well, is a criminal organization directed at undermining the American government.
PHONY BIN LADEN WATCHING PHONY BIN LADEN
In 2000, when a very real conspiracy rigged a presidential election and the Supreme Court of the United States appointed a president, something well outside its constitutional venue, we started down that "slippery slope" to very real dictatorship. It wasn't long before 9/11 and the two totally unfounded wars, all blamed on the mysterious Osama bin Laden, continually spoken of then as now as the greatest criminal mastermind in world history.
But those who heard his actual words and knew his history know better. Bin Laden worked closely with the United States but eventually became mildly critical of its policies.
"Mildly critical of its policies," yes, this is exactly what I am saying. As close to terrorism as Osama bin Laden ever got were statements that were mildly critical of American policies.
The rest of it, the threats, the terror organizations, we made it all up.
This leaves the real job of supporting the constitution to the alternative media, a group infected by the same people who brought American down in 2000, flush with cash from their entertainment empire, the Washington law firms and public relations agencies and the powerful Israel lobby.
Our investigations of one "patriotic resistance" site found these to be those responsible for paying the bills:
AFIPAC
Alexis de Tocqueville Institution
Allied Pilots Association
American Association of Health Plans
American Association of Political Consultants
American Conservative Union
Americans for Hope, Growth & Opportunity
American Policy Center
American Public Philosophy Institute
Australian Barley Board
Black America's Political Action Committee
Blackwell Corporation
Bruce W. Eberle & Associates
Business Mail Express
Campaign Solutions
Canadian MG Lewis MacKenzie (Ret.)
CapitolWatch
The Carmen Group
Carrying Capacity Network
Citizens for State Power
Collegiate Network[1]
Conservative Political Action Conference
Crown Publishing
Davis, Manafort & Freedman, Inc.
The Honorable Pete DuPont
Employee Benefits Associates
Energy Freedom Alliance
Federalist Society
Flickers Films
Free Enterprise Fund
Free Speech Coalition
Freedom Alliance
Forbes for President 2000
The Galen Institute
Grassfire.org
The Hawthorn Group
Institute for Legal Reform
Institute for Policy Innovation
Institute for Socio-Economic Studies
The Keene Report
The Manhattan Institute
McGuire/Woods Consulting, LLC.
National Audit Defense Network
National Center for Policy Analysis
National Farmers Federation of Australia
National Rifle Association-ILA
News World Communications
Nuclear Energy Institute
The O'Leary/Kamber Report
Playcare Incorporated
PM Consulting Corporation
Prima Publishing
Progress & Freedom Foundation
Public Safety Systems
Republican Majority Coalition
Natan Sharansky
Small Business Survival Committee
Southeastern Legal Foundation
Starboard Response
Stevens & Schriefer
United Seniors Association
Washington Times Foundation
Westinghouse Corporation
The Winston Group
WND Books
Despite the innocent-sounding names, this list includes the very heart of the most anti-American elements in American society. There are 20 groups here far more dangerous than any "bin Laden" and far more dedicated to destroying the United States than "Al Qaeda." For those who find themselves on this "rogues gallery" and were unaware they were financing an extremist group, perhaps, next time, they will look before writing a check to buy "influence."
Along with some innocent and decent on this list are groups dedicated to turning the United States into a feudal slave labor state. These are the folks that rig elections, the folks that wrote the scandalous Patriot Acts and, especially, those responsible for crashing the stock markets, rigging our courts and controlling the news.
This is just one list, there are more. Soon after finding this, the Antisemitic/white supremacist organization they finance began hiding behind offshore proxy servers. It was too late for them. They are now "frozen in time."
THE INDEPENDENT PRESS, BIN LADEN, AND WIKILEAKS
When Julian Assange's relationship with the powerful financial groups that control the media organizations he is now critical of was exposed, early in 2011, it became clear that Wikileaks would never be a reliable source for news. Julian Assange has always been very 'mainstream press' when it comes to terrorism and 9/11.
His close relationship with Israel, the nation most often tied to complicity in 9/11 as a "false flag" conspiracy, seems to have deeply prejudiced him and crippled Wikileaks. It will never be seen as honest or independent as long as it remains dogmatic and joined at the hip with the big news organizations and the Israel lobby.
Far from it, Wikileaks, at heart, always gravitates toward its center, a schizophrenic message that exposes abuses of the United States but strongly supports the extremist policies that led America to its military adventures in Afghanistan and Iraq. Assange seems to love America's use of force, openly advocating war on Iran but hides behind a veneer of controversy through leaking oddly selected documents.
Early on, Assange received considerable support from the independent press. Even later on, some organizations continued supporting him even though his allegiances to money and power became clear. The more guilty Assange seemed, the more some groups supported him.
The result was a positive one, a cleansing of the independent media and the recognition by many that their co-workers, some at least, were not who they seemed. In that sense, Julian Assange was invaluable.
Where Wikileaks demonstrated the weakness of the internet media, primarily organizations that developed around the call for an honest investigation of 9/11, the recent bin Laden episode has been different.
The moment the frozen corpse, the "Osama-sicle" was tossed into the Indian Ocean and the actors came out of the woodwork, bin Laden's family, the spurious videos, the contradictory stories, the independent media or alternative media began to show its maturity and power.
Stories hit that were well written, facts were presented with a care to detail that the corporate press was denied, being tied to a 'dead horse" as it were. The most recent bin Laden's "death" has been an easy target for sure, so farcical that the public has begged for the truth to the point that those who have engaged in honest reporting have been flooded with traffic.
What the bin Laden story has shown us that the mantle has passed to the internet and that quality reporting of real facts is available there. The mantle that has passed to the independent media is that of trust, something the corporate media will never be able to regain.
They depended on Americans forgetting 9/11, for Americans to be so hungry for an attractive lie that they would lap up the crud like a starving dog.
They guessed wrong.
Gordon Duff posted articles on VT from 2008 to 2022. He is a Marine combat veteran of the Vietnam War. A disabled veteran, he worked on veterans and POW issues for decades.
Gordon is an accredited diplomat and is generally accepted as one of the top global intelligence specialists. He manages the world's largest private intelligence organization and regularly consults with governments challenged by security issues.
Duff has traveled extensively, is published around the world, and is a regular guest on TV and radio in more than "several" countries. He is also a trained chef, wine enthusiast, avid motorcyclist, and gunsmith specializing in historical weapons and restoration. Business experience and interests are in energy and defense technology.
Gordon's Archives: 2008-2015
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Was 9/11 attack a false flag operation? (Part II)


Influence in organizations has never been so complex. People from different generations work side by side. People who come from different cultures with different set of values work together. Matrix organizations have dramatically changed the way people work with one another, often with no direct authority and from a remote location. For example, the Purchasing Department employee operating from New Jersey has to influence the head of Food and Beverage in Shanghai regarding which lunch ingredients to purchase for employees in a factory in India.
1. Character. Before all else comes the very basic aspect of character. Is a person trustworthy? Reliable? Cooperative? Does he or she keep agreements and promises? These character traits, amongst others, cannot be faked. The person either develops them over time or does not.
2. Network of active relationships. One obvious way to increase influence throughout an organization is to form a wide, well-developed network of relationships. These networks have to be well-maintained and kept active. The world is becoming more and more interconnected via social media. One's "real" social network, based on face-to-face interactions or direct communication, must expand as well. It will be much easier for the person in New Jersey to influence the person in Shanghai if they have an active, ongoing relationship.
3. Sophisticated influence mindsets and skill-sets. In most cases, the mindsets and skill sets are clearly a competency area that people develop through trial and error, not at school. Fortunately, Barnes & Conti's Exercising Influence model offers a hands-on influence education. Most participants find it challenging to become aware of their existing range of Influence Tactics and learn new ones.
In facilitating this program, I've found that the great majority of managers are heavily biased towards the Expressive Influence Tactics (the ones by which you send your ideas to the other) and have much less experience with the Receptive Influence Tactics (the tactics where you draw out and take in information or ideas). This is especially the case with participants who have an engineering or technical background; these participants may have had little opportunity or encouragement to develop the "Receptive" of their influence portfolio. There are also fields in which the opposite is true. Many managers lack balance in their influence approach and thus miss opportunities to be more effective. A wider range of influence skills and approaches allows access to different people in different situations at different times.
Abraham Maslow once said, "He who has a hammer tends to think every problem is a nail." We can say with confidence that in an era of complexity, a person with command of a wide range of Influence Tactics, Behaviors, and Tools will have a better toolkit and thus, far greater impact on his or her organization and community.
In summary, your ability to influence others depends on all three: what kind of a person you are (character), what kind of relationships you build (network), and the breadth of the influence tactics and behaviors you develop (skills).
If you are interested in increasing your influence skills, check out the virtual Influence Celebration, happening this November.
Aviad Goz is the Chairman of the Momentum Group, Creator and CVO, and N.E.W.S. Navigation.


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A hammer toe is a toe that is unnaturally contracted at the joint, forming a claw-like appearance that can cause discomfort and friction, as well as corns and calluses. Hammer toes occur because the tendons and muscles cause irregular pressure against the bone of the toe, forcing it into a bent, cramped position. Hammer toes can be rigid or flexible at the joint; each type requires a different approach for proper treatment.
Hammer toes can occur in any toe. Women are more prone to develop hammer toes because of the shoes worn. They can also be caused by an inherited foot type or stance, such as flat feet or high arches. Injury, ill-fitting shoes, and arthritis can also cause hammertoes to form. Hammer toes also frequently occur in people with poor circulation due to diabetes or other causes. Each toe has a pair of muscles that helps it move and provides stability. When these muscles or the tendons and ligaments that connect them to other muscles and bones are out of balance, the force on the toe shifts, causing it to curl or buckle.
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Neural Plasticity
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Citations 25
Volume 2013, Article ID 908741, 10 pages
The Mechanisms of Movement Control and Time Estimation in Cervical Dystonia Patients
Pavel Filip,1,2 Ovidiu V. Lungu,3,4,5 Daniel J. Shaw,1 Tomas Kasparek,1,6 and Martin Bareš1,2
1Central European Institute of Technology, CEITEC MU, Behavioral and Social Neuroscience Research Group, Masaryk University, 625 00 Brno, Czech Republic
2First Department of Neurology, Faculty of Medicine, Masaryk University and St. Anne's Teaching Hospital, 656 91 Brno, Czech Republic
3Department of Psychiatry, University of Montréal, Montréal, QC, Canada H3C 3T5
4Functional Neuroimaging Unit, Research Center of the Geriatric Institute Affiliated with the University of Montréal, Montréal, QC, Canada H3C 3T5
5Department of Research, Donald Berman Maimonides Geriatric Center, Montréal, QC, Canada H3C 3T5
6Department of Psychiatry, Faculty of Medicine, Masaryk University and St. Teaching Hospital, 625 00 Brno, Czech Republic
Received 6 June 2013; Revised 26 August 2013; Accepted 28 August 2013
Academic Editor: Mario U. Manto
Copyright © 2013 Pavel Filip et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Traditionally, the pathophysiology of cervical dystonia has been regarded mainly in relation to neurochemical abnormities in the basal ganglia. Recently, however, substantial evidence has emerged for cerebellar involvement. While the absence of neurological "cerebellar signs" in most dystonia patients may be considered at least provoking, there are more subtle indications of cerebellar dysfunction in complex, demanding tasks. Specifically, given the role of the cerebellum in the neural representation of time, in the millisecond range, dysfunction to this structure is considered to be of greater importance than dysfunction of the basal ganglia. In the current study, we investigated the performance of cervical dystonia patients on a computer task known to engage the cerebellum, namely, the interception of a moving target with changing parameters (speed, acceleration, and angle) with a simple response (pushing a button). The cervical dystonia patients achieved significantly worse results than a sample of healthy controls. Our results suggest that the cervical dystonia patients are impaired at integrating incoming visual information with motor responses during the prediction of upcoming actions, an impairment we interpret as evidence of cerebellar dysfunction.
Cervical dystonia, the most frequent adult focal dystonia, is a syndrome characterized by involuntary twisting movements of the head, leading ultimately to temporary or constant abnormal postures interfering with voluntary movement [1, 2]. Despite over a century of research since its first description in the literature [3], the pathophysiology of this disease still remains elusive. Aberrant activity in the basal ganglia has been noted repeatedly as the main cause of the sustained cocontraction of opposing agonist and antagonist muscles [2, 4, 5]. Recently, however, the cerebellum—first noted in dystonia pathophysiology over 25 years ago [6]—has received considerable attention [7–9]. Neurophysiological [10] and neuroimaging studies [11], showing increase in gray matter density in cerebellum [12], abnormal cerebellar activation in various tasks [13–15], and increased glucose metabolism in cerebellum [16, 17], clearly demonstrate its involvement in dystonia. Furthermore, an elegant review of 25 secondary cervical dystonia cases connects the pathophysiology of cervical dystonia primarily with cerebellar lesions [18].
For a long time the cerebellum has been associated exclusively with motor functions. Increasingly, though, the cerebellum is implicated in a wide spectrum of different process controls extending far beyond the typical cerebellar domain. These include, for example, attention [19, 20], associative learning [21], motivation control [22], and, most relevant to the present study, time assessment [23–26]. The precise role of the cerebellum in the representation of time and a delineation of basal ganglia function in this respect are still a matter of continuous research [27–29]. To date, there is evidence of two dissociable neural timing systems: an "automatic" system, involving the cerebellum and linked closely to motor networks, is responsible for discrete event timing in the range of milliseconds [28, 30, 31]; a "cognitively controlled" system, comprised of basal ganglia and cortical structures focused on attention and memory requirements, deals instead with events in the range of seconds [29, 32].
In accordance with this distinction, we have shown in previous studies that subjects with severe cerebellar damage [23] or less severe dysfunction of the cerebellum [25] have poorer performance on tasks requiring motor timing at the sub-second level. Interestingly, on the very same task, patients with early stages of Parkinson's disease (PD) did not differ significantly from healthy controls [25]. Since PD is associated strongly with basal ganglia dysfunction, this is consistent with the above-mentioned distinction and other studies focusing on timing in PD [33, 34]. The current study builds on this research by investigating the performance of cervical dystonia patients on this motor-timing task. On the basis of the aforementioned evidence, we assumed some cerebellar dysfunction in our sample of cervical dystonia patients. We hypothesized, therefore, that these patients would perform poorly at this task relative to a healthy control group due to disrupted time estimation in very short intervals.
2. Methods and Materials
2.1. Participants
Thirty healthy individuals (15 males; mean age = 55.5 yrs, SD = 12.6 yrs) and 30 primary cervical dystonia (CD) patients (14 males; mean age = 52.0 yrs, SD = 13.65 yrs) participated in the study. All patients showed only symptoms of pure cervical dystonia—there were no further dystonia signs (for more information see Table 1). The cervical dystonia subjects did not suffer from hand tremor nor abnormal upper-arm posture. Only patients with no shoulder elevation or a slightly elevated shoulder (maximally moderate elevation with 1/3–2/3 possible movement range) participated in the study. All subjects were right-handed. None of the subjects had history of color blindness. According to the Montgomery and Asberg Depression Rating Scale (MADRS), no subjects suffered from clinical depression (mean score = 6.50, SD = 6.85) [35]. Prior to testing, the patients were scored on the Toronto Western Spasmodic Torticollis Rating Scale (mean score = 10.2, SD = 4.64) [36]. The patients were recruited from the Movement Disorders Outpatient Clinic at St. Anne's University Hospital, Brno, Czech Republic. The study was approved by the hospital's Institutional Review Board.
Table 1: Further information about the cervical dystonia patients.
2.2. The Task
The subjects performed the same motor-timing computer task as that employed in our earlier studies [23, 25]. In this task, participants are required to press a key with the dominant hand in order to launch a "projectile" that will intercept a circular green "target" object moving from the left side of the screen toward the upper-right corner (Figure 1). This projectile is launched from the lower-right corner of the screen and travels at a constant speed of 20.0 cm/s on an upward and unchanging trajectory. Participants are instructed to launch the projectile at the optimal time for it to hit the moving target in a prespecified, stationary, and fixed interception zone, positioned in the upper-right corner of the screen (Figure 1(a)). Following a successful interception, or "hit," a small explosion animation is produced as a feedback for the subject (Figure 1(b)). In case of failure, no explosion occurs.
Figure 1: The task and experimental conditions. (a) The main interception task. The green ball moves from the left side of the screen to the interception zone in the upper right corner of the screen (as for the position, corresponding to the pink cross square in Figure 1(c)). The blue "gun" in the lower right corner fires a "projectile" travelling at a constant speed to intercept the green ball. (b) Successful hit. If the ball is intercepted by the projectile, both objects explode. In case of miss, there is no animation. (c) Control condition 1. There is no projectile in this condition. The subject is supposed to press the button at the very moment the green ball reaches the interception zone marked by the cross inside the pink square. If the subject is successful, the ball explodes. (d) Control condition 2: the green ball once again moves from the left side of the screen to the interception area. However, there is no gun/projectile or pink interception square. The subject is supposed to press the button as soon as the ball changes its color from green to red.
On each trial, the green target is launched from the left edge of the screen and travelled towards the fixed interception zone at three possible angles (0°, 15°, and 30°) relative to the horizontal plane of the screen. It travels in three different manners (i.e., constant velocity, deceleration, and acceleration) and at three different speeds (slow, medium, and fast). Ergo, with all possible combinations of these variables (type, speed, and angle), the target can travel in 27 different ways. The green target diameter is 1 cm; the projectile diameter is 0.3 cm. Trials were organized into 12 blocks, each with a pseudorandomized combination of target movement parameters (type, speed, and angle). Each particular movement combination was presented twice on each block, with each block formed by 54 trials (27 combinations × 2 instances). Therefore, each movement combination occurred 24 times (12 blocks × 2 instances) during the whole procedure. The blocks were separated by breaks of 20-second durations. The entire procedure lasted approximately 35 minutes. Before the task, subjects underwent one experimental block as practice. When performing the task, participants were seated 60 cm in front of the 14′′ computer screen. No special amendments or mechanical supports for the head and arms were used. Subjects feeling discomfort or pain during the task were excluded from the final analysis.
In addition to the experimental condition described above, subjects performed two control conditions. The first (control condition 1 [CC1]) involved instantaneous interception of the moving target comparable to the experimental condition. Participants were required to press the button as soon as the target reached the interception zone, which was marked by a pink crosshair (Figure 1(c)). In this case, subjects were not required to estimate the travel time of the projectile; in other words, this condition tested the ability of the subjects to judge the temporal characteristics of the target under less demanding circumstances. The second control condition (CC2) involved the detection of the target color change. Here, the participants were required to press the button as quickly as possible when the moving target changed color from green to red (Figure 1(d)). The color change occurred randomly along its trajectory. In this condition, we tested simple reaction time that required accurate pursuit of the target along its trajectory but no estimation of target movement. The subjects were shown explicitly the transition from green and red targets in advance and asked if they were able to detect accurately the color change.
2.3. Data Analysis
The variables of interest were the hit ratio (i.e., the number of successful hits relative to the total number of trials) across the different movement combinations (i.e., speed, angle, and type), the total number of hits and early and late errors (i.e., subjects pressing the button before or after the target entered the interception zone), and the response time (RT). In order to use parametric statistical techniques, requiring a normal distribution for the hit ratio (normally a binary variable in each trial), we computed the percentage of hits for each subject and for each trial type in each block, and we then averaged these values across blocks. When comparing the number of hits and early and late errors, we employed nonparametric techniques; namely, we employed the Chi-square test to compare the distribution of early and late errors between the control group and the patient group. Given that the outcome of an individual trial (hit, early error, and late error) may be influenced by the outcome obtained in the previous trial, we performed a trial-by-trial analysis to determine the extent to which subjects were able to use their very last experience (the previous trial) to improve their performance in the current trial. In this case, we used the Chi-square test and the Cramer's and phi coefficient (a correction of Chi-square as a function of the number of cases considered).
The task was designed to produce varying levels of difficulty. Specifically, the individual combinations of variables lead to different time windows where a successful interception was possible (in the range of about 50 to 175 ms); the shorter the time interval to press the button, the more difficult the task; for example, higher target speeds were more difficult to intercept. Therefore, we expected higher hit ratios for trials with wider compared with shorter time windows. The effects of the movement parameter combinations on the hit ratio were assessed using a general linear model analysis (GLM). Finally, we compared the hit ratio between blocks 1–6 and blocks 7–12 to evaluate possible learning effects during the course of the experiment.
All analyses were performed in SPSS (SPSS Inc., Chicago, IL, USA).
In the following analyses, we have excluded the "angle" movement parameter since it had been proven to be of no significant effect on hit ratio or reaction time [23, 25]. We did not notice any fatigue of motor or cognitive nature in the subjects.
3.1. Reaction Time
In the control condition CC2, we found a significant difference in the reaction time to color change between the patient group (mean = 341.84 ms, SD = 57.40) and the healthy group (mean = 288.72 ms, SD = 32.10 [F1,58 = 19.38; ]). As shown in Figure 2(a), this revealed that healthy controls were faster in the task than the patients.
Figure 2: Reaction times. (a) Mean reaction time in the control condition 2: the reaction time of the patients was significantly slower than the reaction time in the control group. (b) Mean reaction times as a function of movement type in two groups: These results show that even if the patient group was generally slower (Figure 2), the reaction time was not affected by other parameters of the moving target (speed, acceleration) in a different way. This finding excludes the eventuality that the differences between the groups in the other main parameters may be due to oculomotor difficulties in the cervical dystonia group [37].
Furthermore, the GLM analysis to determine the main effect of target movement type showed significant interactions between the independent factors (group, type of movement, and speed [F2,116 = 14.24, ]). As Figure 2(b) depicts, reaction times were slower for constant speed than during acceleration or deceleration trials. This interesting finding could point to the fact that changes in color are easier to spot when the target movement is variable, relative to when it is constant. Even if this is seemingly counterintuitive, it is consistent with our previous results when comparing the reaction time to color change in moving and stationary targets [25]. We had found that moving targets are easier and quicker to react to, possibly suggesting that following a moving target increases the attention of the subject resulting in faster responses. There was no interaction effect, however, which indicates that the two groups are affected similarly by the kinematics of the target.
3.2. Hit Ratios
The first control condition (CC1) was designed to eliminate the need of complex estimation depending on the movement types (CC1, see Figure 1). We performed a GLM analysis to compare the patient group with the control group. The dependent variable was the hit ratio, and the independent factors were the group (cervical dystonia patients and healthy controls), movement type (acceleration, deceleration, and constant), and speed (fast, medium, and slow). We observed a significant difference in the hit ratio between the healthy control group (mean = 0.71; SD = 0.04) and the patients (mean = 0.57; SD 0.18; ; see Figure 3). The three-way interaction term was not significant (F4,116 = 1.60, ), however, indicating that the success rate was not affected differentially by the movement type or speed of the target across groups, in contrast to the main task.
Figure 3: Performance in the main task and the control task 1.
In both groups, performance in CC1 was superior to performance in the main task (F1,58 = 54.36; ; see Figure 3). This is an expected result, since the main task is associated with far more complex temporal estimation of target movement parameters. Indeed, even in the control condition, patients had lower hit ratios than healthy individuals (F1,58 = 22.87; ).
A comparison of performance in the first and second half of the task revealed a significant difference in hit ratios in both groups, indicating that the participants improved their performance over time (controls: F1,29 = 5.87; ; patients: F1,29 = 5.27; ). We observed no significant interaction between the two groups (F1,58 = 0.19; ), indicating that performance changed similarly in both patients and healthy controls over time.
Regarding the movement parameters, there was a significant effect of both movement type and speed on the hit ratio in both groups (Figure 4). Overall, the increase in target speed led to a decrease of hit ratio both in healthy (F2,58 = 15.58; ) and in cervical dystonia patients group (F2,58 = 16.28; ). Similarly, the deceleration and constant movements of the target lead to higher hit ratios than when the target was accelerating in both groups (F2,58 = 77.96; for controls, and F2,58 = 77.29; for patients). However, there was also a significant interaction between the speed and type of movement in each group (F4,116 = 54.44; for controls, and F4,116 = 28.72; for patients). This effect indicated that hit ratio was inversely related to speed when target moved with constant and accelerating speed, whereas this effect was reversed for targets with decelerating speeds (Figure 4).
Figure 4: Mean hit ratio as a function of movement type and speed of the target in the main task.
A detailed analysis of the hit rates revealed that the hit ratio distribution in the cervical dystonia group was much wider than that of the healthy controls (Figure 5). Based on this distribution, we classified the patient group into two subgroups according to a threshold set at the lower limit of the healthy group performance: Group 1 with a hit ratio comparable to the healthy controls ( patients), and Group 2 with lower hit ratios ( patients). We analyzed the individual characteristics in both patient subgroups. The parameters we focused on were age, sex, disease severity (TWSTRS score), dystonia clinical presentation (head tremor or deviation), length of the disease, and age at which the disease manifested. None of these factors differed significantly between the groups, however ( ). Taken together, these results imply that the presumed cerebellar deficit in cervical dystonia patients—regardless of severity—leads to worse performance in time estimation in general. In some patients, however, this ability is impaired only slightly relative to the healthy population, while in others the dysfunction manifests as a far greater "disability."
Figure 5: Histogram of hit ratios distributions in the patient group and the control group showing wider distribution curve for the cervical dystonia patients.
3.3. Early and Late Errors
We also examined the distribution of errors to determine the characteristics of unsuccessful reactions, that is, whether the subjects were too early or too late in general to intercept the target. The two types of errors seemed approximately equally distributed in the early and late spectrum in both subject groups (see Figure 6(a)); the ratio of early/late errors was 41.73/58.27% in the cervical dystonia group and 43.84/56.16% in the control group. Nonparametric tests indicate that these two groups differed in the distribution of early and late errors, however, with patients making more late than early errors (Cramer's and phi coefficient = 0.21, ).
Figure 6: Error distribution. (a) Distribution of early and late errors in healthy subjects and cervical dystonia patients. (b) Trial-by-trial distribution of hits and errors: The effect of feedback and the impact of the success rate in the previous trial on the hit ratio and early/late errors distribution. In the graph, the error type distribution is presented as a function of the previous trial result.
3.4. Trial by Trial Adaptation
Figure 6(b) illustrates the distribution of early and late errors according to the performance in the previous trial. We determined whether the feedback from the previous trial had a significant impact on the performance in the current trial. We hypothesized that the subjects could benefit from the outcome of the previous trial by adjusting their motor timing in the current trial. Analyses revealed a significant effect of the preceding trial outcome on the distribution of early and late errors and hits in both the healthy control and patient group (Cramer's and phi coefficient = 0.07, ; and 0.08, , resp.). There were, however, slightly different qualitative outcomes when comparing healthy subjects and cervical dystonia patients. The residual standardized scores indicate that the success in the previous trial increased the hit rate on the current trial and reduced the rate of early errors in both the patient and the control group. By the same token, patients had more late errors and fewer hits in the current trial after a late error in the preceding trial, whereas for the healthy group late errors did not lead to a significant change in hit ratio.
3.5. Hit Ratio and the Time Window
As previously mentioned, the temporal window within which a successful outcome is possible is an indication of the task difficulty; the longer this time interval, the greater the likelihood that subjects could execute the movement successfully. We computed the correlation between window width and hit ratio for both the healthy control and patient group and then compared these correlation coefficients between them. Figure 7 illustrates the relationship between hit ratio (percentage) and window width (in milliseconds) for both groups. While we obtained a significantly positive correlation coefficient for both groups (a higher hit ratio corresponded to wider window width), we did not find any significant difference between them. In fact, the hit ratios of two groups were affected similarly by the window width indicating that the slopes were similar (F1,536 = 0.411; ; ~20% change in hit ratio for 100 ms window width in each group). Also, there was greater variability among patients: while window width explained 31.7% of the variability in hit ratio among healthy individuals, this factor explained only 19.3% of the variability among patients. This finding may be related to the heterogeneity of the disease manifestation among patients.
Figure 7: The effect of response window width and hit ratio. The relationship between hit ratio (percentage) and window width (milliseconds) for the two groups.
This current study investigated whether patients with cervical dystonia exhibit impaired performance on a motor-timing task known to require cerebellar input. Using a motor-timing computer task, we reveal the following pattern of results: the principal finding is a lower hit ratio of the patients in comparison to the control group in a specific motor-timing task in association with significantly slower reaction time to a simple color change in the dystonia group. On the other hand, the ability to take advantage of the wider time window was comparable in cervical dystonia patients and the control group. Likewise, there was a significant effect of both movement type and speed on the success rate in the control group and cervical dystonia patients not showing a prominent difference between those two groups. Visual-motor integration at the millisecond range, which is believed to be a substantial constituent of cerebellum responsibilities [28, 30, 31], is of crucial importance for success on this task. Although the cerebellum is not noted traditionally as one of the major sources of dystonia development, interest towards this neuronal structure has increased recently [8, 9, 38], with its role in the pathophysiology of the dystonia suggested by animal models [7, 39, 40], imaging studies [11, 41, 42], neurophysiological studies [10], and even secondary cervical dystonia analyses [18, 43]. Our findings demonstrate that the temporal estimation of target parameters and requirements for a quick motor response posed a fundamental problem for the cervical dystonia patients. This is consistent with the notion that the cerebellum may also be affected by this disease.
It remains to be determined whether the cerebellum stands at the very pathophysiology origin of cervical dystonia or it forms only a component of a complex network compensating for dysfunction of other parts of the brain. Nevertheless, our data indicate that cervical dystonia subjects show decreased performance on a task in which the cerebellum has been shown previously to play an essential role [23–25]. Our results are also consistent with the current theories of a discrete event timing network responsible for time interpretation and assessment in the millisecond range, located in cerebellum [28, 30, 31]. The cerebellum is hypothesized to be a major node in timing tasks with noncontinuous movements [44, 45], a function fitting undeniably with the spirit of our task. The cerebellum hosts a vast convergence of mossy fiber inputs [46], and it is known to be involved in the synthesis of information from virtually all brain areas. As such, the cerebellar structure is well situated for complex predictions of an integrative character, providing crucial data for further processing by the cerebral cortex [47, 48].
Of course, the nature of our study makes it impossible to assess complexly the extent of eventual cerebellar dysfunction; this network node is associated with a wide spectrum of functions of which we were interested specifically in only one, that is, movement timing. Performance on other tasks involving cerebellum function, such as attention [19, 20], associative learning [21], and motivation control [22], remains to be investigated. This leaves a window for further research into the association between the cerebellum and dystonia open. In particular, imaging studies of cerebellum connectivity and its eventual functional abnormities in cervical dystonia will be of great importance. Nevertheless, our observation of decreased performance in a timing task in patients with no clear neurological cerebellar signs (e.g. ataxia and dysmetria) could be attributed to abnormal cerebellar activity in dystonia—specifically a gain of cerebellar function similar to epilepsy in the cerebral cortex [39, 49]. This very abnormity might be related closely to cortical excitability disorder in cervical dystonia patients [50], leading possibly to typical cervical dystonia symptoms.
Of course, it would be inappropriate to dismiss completely the contribution from the basal ganglia, which is both an important pathophysiological node with direct connection to dystonia in general and an essential contributor to motor timing. In our previous study, however, dysfunction of the basal ganglia, a structure noted particularly in attention and memory tasks in the range of seconds [29, 32, 51], did not lead to lower performance in our motor-timing task [25]. Patients with Parkinson's disease, despite their hypokinesia, performed at levels comparable to healthy subjects. In contrast, patients with essential tremor and spinocerebellar ataxia, disorders connected with cerebellum dysfunctions, showed comparable problems in time estimation and movement analysis. Moreover, the late error ratio in spinocerebellar ataxia patients was increased in comparison with healthy controls—a trend observed also in cervical dystonia patients. Another important observation in our study is that the cervical dystonia patients and the spinocerebellar ataxia patients, in addition to poor performance, had abnormal timing adjustment.
Furthermore, we should not overlook the possibility that the impaired performance in cervical dystonia patients was caused by oculomotor problems. Should this be true, the distribution of errors should shift in favor of late errors in the cervical dystonia patients. This was not the case, however. Moreover, the increasing speed and acceleration/deceleration posing higher demands for the visuomotor abilities of the subject, that is, the shorter time window, influenced cervical dystonia patients to the same extent as healthy controls. We also observed that the reaction time was not affected by the parameters of the moving target (i.e. speed or acceleration) differently between the two groups. This rejects further the possibility that differences between the groups arise from oculomotor difficulties in the cervical dystonia group.
Lastly, the slight abnormal shoulder posture of some cervical dystonia subjects might be considered to contribute to our pattern of findings. We find this unlikely, however, as the task is designed specifically to minimize the aspect of unnatural posture. Subjects did not use the whole limb or bigger limb segments to intercept the target; they were required merely to push the response button with their finger.
Our results contribute to our understanding of both the role of the cerebellum dystonia pathophysiology and its function in general. A growing body of research in this former area implicates an increasing number of defective neural network nodes in this disease [52, 53], thus challenging the traditional view of dystonia. Indeed, although it is clear that basal ganglia play a significant role in dystonia pathophysiology, our findings pointing to cerebellum dysfunction, together with the results of clinical and animal studies [39, 54, 55], associate dystonia with defective interactions among different components of the motor network rather than the dysfunction of any one node. Standing on the doorstep of the first real complex insight and understanding of cerebellum and the central nervous system itself, backed up by ever-advancing technological possibilities, we cannot afford to overlook this slowly crystallizing role of the cerebellum in the pathophysiology of cervical dystonia.
There are no potential conflict of interests regarding this paper and no financial or personal relationships that might bias this work.
This work was supported by the "CEITEC-Central European Institute of Technology" Project (CZ.1.05/1.1.00/02.0068) from the European Regional Development Fund and by Ministry of Health of the Czech Republic/Ministry of Health's Departmental Research and Development Program III (2010–2015) NT/13437. Ovidiu Lungu is supported by Maimonides Medical Foundation. The authors wish to thank Ivica Husarova, M.D., Eduard Minks, M.D., and Hana Streitova, M.D., for their contribution in referring the patients and useful comments on the paper.
S. Fahn, S. B. Bressman, and C. D. Marsden, "Classification of dystonia," Advances in Neurology, vol. 78, pp. 1–10, 1998. View at Google Scholar · View at Scopus
A. Albanese, K. Bhatia, S. B. Bressman et al., "Phenomenology and classification of dystonia: a consensus update," Movement Disorders, vol. 28, no. 7, pp. 863–873, 2013. View at Publisher · View at Google Scholar
H. Oppenheim, "Uber eine eigenartige kramotkrankheit des kindlichen und jugendlichen alters (dysbasia lordotica progressiva, dystonia musculorum deformans)," Neurologie Centralblatt, vol. 30, pp. 1090–1107, 1911. View at Google Scholar
J. L. Vitek, "Pathophysiology of dystonia: a neuronal model," Movement Disorders, vol. 17, no. 3, pp. S49–S62, 2002. View at Google Scholar · View at Scopus
M. R. DeLong and T. Wichmann, "Circuits and circuit disorders of the basal ganglia," Archives of Neurology, vol. 64, no. 1, pp. 20–24, 2007. View at Publisher · View at Google Scholar · View at Scopus
N. A. Fletcher, R. Stell, A. E. Harding, and C. D. Marsden, "Degenerative cerebellar ataxia and focal dystonia," Movement Disorders, vol. 3, no. 4, pp. 336–342, 1988. View at Google Scholar · View at Scopus
M. Vidailhet, D. Grabli, and E. Roze, "Pathophysiology of dystonia," Current Opinion in Neurology, vol. 22, no. 4, pp. 406–413, 2009. View at Publisher · View at Google Scholar · View at Scopus
A. Sadnicka, B. S. Hoffland, K. P. Bhatia, B. P. van de Warrenburg, and M. J. Edwards, "The cerebellum in dystonia—help or hindrance?" Clinical Neurophysiology, vol. 123, no. 1, pp. 65–70, 2012. View at Publisher · View at Google Scholar · View at Scopus
P. Filip, O. V. Lungu, and M. Bareš, "Dystonia and the cerebellum: a new field of interest in movement disorders?" Clinical Neurophysiology, vol. 124, no. 7, pp. 1269–1276, 2013. View at Publisher · View at Google Scholar
J. Liepert, T. Kucinski, O. Tüscher, F. Pawlas, T. Bäumer, and C. Weiller, "Motor cortex excitability after cerebellar infarction," Stroke, vol. 35, no. 11, pp. 2484–2488, 2004. View at Publisher · View at Google Scholar · View at Scopus
M. Obermann, C. Vollrath, A. de Greiff et al., "Sensory disinhibition on passive movement in cervical dystonia," Movement Disorders, vol. 25, no. 15, pp. 2627–2633, 2010. View at Publisher · View at Google Scholar · View at Scopus
B. Draganski, C. Thun-Hohenstein, U. Bogdahn, J. Winkler, and A. May, "'Motor circuit' gray matter changes in idiopathic cervical dystonia," Neurology, vol. 61, no. 9, pp. 1228–1231, 2003. View at Google Scholar · View at Scopus
H. Kadota, Y. Nakajima, M. Miyazaki et al., "An fMRI study of musicians with focal dystonia during tapping tasks," Journal of Neurology, vol. 257, no. 7, pp. 1092–1098, 2010. View at Publisher · View at Google Scholar · View at Scopus
X.-Y. Hu, L. Wang, H. Liu, and S.-Z. Zhang, "Functional magnetic resonance imaging study of writer's cramp," Chinese Medical Journal, vol. 119, no. 15, pp. 1263–1271, 2006. View at Google Scholar · View at Scopus
R. S. Baker, A. H. Andersen, R. J. Morecraft, and C. D. Smith, "A functional magnetic resonance imaging study in patients with benign essential blepharospasm," Journal of Neuro-Ophthalmology, vol. 23, no. 1, pp. 11–15, 2003. View at Publisher · View at Google Scholar · View at Scopus
M. Niethammer, M. Carbon, M. Argyelan, and D. Eidelberg, "Hereditary dystonia as a neurodevelopmental circuit disorder: evidence from neuroimaging," Neurobiology of Disease, vol. 42, no. 2, pp. 202–209, 2011. View at Publisher · View at Google Scholar · View at Scopus
D. Alvarez-Fischer, M. Grundmann, L. Lu et al., "Prolonged generalized dystonia after chronic cerebellar application of kainic acid," Brain Research, vol. 1464, pp. 82–88, 2012. View at Publisher · View at Google Scholar
M. S. LeDoux and K. A. Brand, "Secondary cervical dystonia associated with structural lesions of the central nervous system," Movement Disorders, vol. 18, no. 1, pp. 60–69, 2003. View at Publisher · View at Google Scholar · View at Scopus
E. Perlov, L. Tebarzt van Elst, M. Buechert et al., "H1-MR-spectroscopy of cerebellum in adult attention deficit/hyperactivity disorder," Journal of Psychiatric Research, vol. 44, no. 14, pp. 938–943, 2010. View at Publisher · View at Google Scholar · View at Scopus
J. C. Bledsoe, M. Semrud-Clikeman, and S. R. Pliszka, "Neuroanatomical and neuropsychological correlates of the cerebellum in children with attention-deficit/hyperactivity disorder-combined type," Journal of the American Academy of Child and Adolescent Psychiatry, vol. 50, no. 6, pp. 593–601, 2011. View at Publisher · View at Google Scholar · View at Scopus
D. Timmann, J. Drepper, M. Frings et al., "The human cerebellum contributes to motor, emotional and cognitive associative learning. A review," Cortex, vol. 46, no. 7, pp. 845–857, 2010. View at Publisher · View at Google Scholar · View at Scopus
D. J. Bauer, A. L. Kerr, and R. A. Swain, "Cerebellar dentate nuclei lesions reduce motivation in appetitive operant conditioning and open field exploration," Neurobiology of Learning and Memory, vol. 95, no. 2, pp. 166–175, 2011. View at Publisher · View at Google Scholar · View at Scopus
M. Bares, O. Lungu, T. Liu, T. Waechter, C. M. Gomez, and J. Ashe, "Impaired predictive motor timing in patients with cerebellar disorders," Experimental Brain Research, vol. 180, no. 2, pp. 355–365, 2007. View at Publisher · View at Google Scholar · View at Scopus
M. Bares, O. V. Lungu, T. Liu, T. Waechter, C. M. Gomez, and J. Ashe, "The neural substrate of predictive motor timing in spinocerebellar ataxia," The Cerebellum, vol. 10, no. 2, pp. 233–244, 2011. View at Publisher · View at Google Scholar · View at Scopus
M. Bareš, O. V. Lungu, I. Husárová, and T. Gescheidt, "Predictive motor timing performance dissociates between early diseases of the cerebellum and parkinson's disease," Cerebellum, vol. 9, no. 1, pp. 124–135, 2010. View at Publisher · View at Google Scholar · View at Scopus
I. Husárová, O. V. Lungu, R. Mareček et al., "Functional imaging of the cerebellum and basal ganglia during predictive motor timing in early parkinson's disease," Journal of Neuroimaging, 2011. View at Publisher · View at Google Scholar
D. L. Harrington, R. R. Lee, L. A. Boyd, S. Z. Rapcsak, and R. T. Knight, "Does the representation of time depend on the cerebellum? Effect of cerebellar stroke," Brain, vol. 127, no. 3, pp. 561–574, 2004. View at Publisher · View at Google Scholar · View at Scopus
J. T. Coull, R.-K. Cheng, and W. H. Meck, "Neuroanatomical and neurochemical substrates of timing," Neuropsychopharmacology, vol. 36, no. 1, pp. 3–25, 2011. View at Publisher · View at Google Scholar · View at Scopus
D. L. Harrington, J. L. Zimbelman, S. C. Hinton, and S. M. Rao, "Neural modulation of temporal encoding, maintenance, and decision processes," Cerebral Cortex, vol. 20, no. 6, pp. 1274–1285, 2010. View at Publisher · View at Google Scholar · View at Scopus
G. Koch, M. Oliveri, S. Torriero, S. Salerno, E. L. Gerfo, and C. Caltagirone, "Repetitive TMS of cerebellum interferes with millisecond time processing," Experimental Brain Research, vol. 179, no. 2, pp. 291–299, 2007. View at Publisher · View at Google Scholar · View at Scopus
E. D'Angelo and C. I. de Zeeuw, "Timing and plasticity in the cerebellum: focus on the granular layer," Trends in Neurosciences, vol. 32, no. 1, pp. 30–40, 2009. View at Publisher · View at Google Scholar · View at Scopus
P. A. Lewis and R. C. Miall, "Distinct systems for automatic and cognitively controlled time measurement: evidence from neuroimaging," Current Opinion in Neurobiology, vol. 13, no. 2, pp. 250–255, 2003. View at Publisher · View at Google Scholar · View at Scopus
Q. J. Almeida, J. S. Frank, E. A. Roy, A. E. Patla, and M. S. Jog, "Dopaminergic modulation of timing control and variability in the gait of Parkinson's disease," Movement Disorders, vol. 22, no. 12, pp. 1735–1742, 2007. View at Publisher · View at Google Scholar · View at Scopus
M. Jahanshahi, C. R. G. Jones, J. Zijlmans et al., "Dopaminergic modulation of striato-frontal connectivity during motor timing in Parkinson's disease," Brain, vol. 133, no. 3, pp. 727–745, 2010. View at Publisher · View at Google Scholar · View at Scopus
S. A. Montgomery and M. Asberg, "A new depression scale designed to be sensitive to change," The British Journal of Psychiatry, vol. 134, no. 4, pp. 382–389, 1979. View at Google Scholar · View at Scopus
E. S. Consky and A. E. Lang, "Clinical assessments of patients with cervical dystonia," Neurological Disease and Therapy, vol. 25, p. 211, 1994. View at Google Scholar
M. P. Grant, R. J. Leigh, S. H. Seidman, D. E. Riley, and J. P. Hanna, "Comparison of predictable smooth ocular and combined eye-head tracking behaviour in patients with lesions affecting the brainstem and cerebellum," Brain, vol. 115, no. 5, pp. 1323–1342, 1992. View at Google Scholar · View at Scopus
L. Avanzino and G. Abbruzzese, "How does the cerebellum contribute to the pathophysiology of dystonia?" Basal Ganglia, vol. 2, no. 4, pp. 231–235, 2012. View at Publisher · View at Google Scholar
R. S. Raike, H. A. Jinnah, and E. J. Hess, "Animal models of generalized dystonia," NeuroRx, vol. 2, no. 3, pp. 504–512, 2005. View at Publisher · View at Google Scholar · View at Scopus
H. A. Jinnah, E. J. Hess, M. S. LeDoux, N. Sharma, M. G. Baxter, and M. R. DeLong, "Rodent models for dystonia research: characteristics, evaluation, and utility," Movement Disorders, vol. 20, no. 3, pp. 283–292, 2005. View at Publisher · View at Google Scholar · View at Scopus
M. Carbon, M. F. Ghilardi, M. Argyelan, V. Dhawan, S. B. Bressman, and D. Eidelberg, "Increased cerebellar activation during sequence learning in DYT1 carriers: an equiperformance study," Brain, vol. 131, no. 1, pp. 146–154, 2008. View at Publisher · View at Google Scholar · View at Scopus
R. Opavský, P. Hluštík, P. Otruba, and P. Kaňovský, "Sensorimotor network in cervical dystonia and the effect ofbotulinum toxin treatment: a functional MRI study," Journal of the Neurological Sciences, vol. 306, no. 1, pp. 71–75, 2008. View at Google Scholar
V. C. Extremera, J. Álvarez-Coca, G. A. Rodríguez, J. M. Pérez, J. L. R. de Villanueva, and C. P. Díaz, "Torticollis is a usual symptom in posterior fossa tumors," European Journal of Pediatrics, vol. 167, no. 2, pp. 249–250, 2008. View at Publisher · View at Google Scholar · View at Scopus
R. M. C. Spencer, T. Verstynen, M. Brett, and R. Ivry, "Cerebellar activation during discrete and not continuous timed movements: an fMRI study," NeuroImage, vol. 36, no. 2, pp. 378–387, 2007. View at Publisher · View at Google Scholar · View at Scopus
H. Lorås, H. Sigmundsson, J. B. Talcott, F. Öhberg, and A. K. Stensdotter, "Timing continuous or discontinuous movements across effectors specified by different pacing modalities and intervals," Experimental Brain Research, vol. 220, no. 3-4, pp. 335–347, 2012. View at Publisher · View at Google Scholar
J. R. de Gruijl, P. Bazzigaluppi, M. T. G. de Jeu, and C. I. de Zeeuw, "Climbing fiber burst size and olivary sub-threshold oscillations in a network setting," PLoS Computational Biology, vol. 8, no. 12, Article ID e1002814, 2012. View at Google Scholar
M.-U. Manto, "On the cerebello-cerebral interactions," Cerebellum, vol. 5, no. 4, pp. 286–288, 2006. View at Publisher · View at Google Scholar · View at Scopus
M. Molinari, M. G. Leggio, and M. H. Thaut, "The cerebellum and neural networks for rhythmic sensorimotor synchronization in the human brain," Cerebellum, vol. 6, no. 1, pp. 18–23, 2007. View at Publisher · View at Google Scholar · View at Scopus
D. Eidelberg, J. R. Moeller, A. Antonini et al., "Functional brain networks in DYT1 dystonia," Annals of Neurology, vol. 44, no. 3, pp. 303–312, 1998. View at Publisher · View at Google Scholar · View at Scopus
P. Kaňovský, M. Bareš, H. Streitová, H. Klajblová, P. Daniel, and I. Rektor, "Abnormalities of cortical excitability and cortical inhibition in cervical dystonia: evidence from somatosensory evoked potentials and paired transcranial magnetic stimulation recordings," Journal of Neurology, vol. 250, no. 1, pp. 42–50, 2003. View at Publisher · View at Google Scholar · View at Scopus
J.-C. Dreher and J. Grafman, "The roles of the cerebellum and basal ganglia in timing and error prediction," European Journal of Neuroscience, vol. 16, no. 8, pp. 1609–1619, 2002. View at Publisher · View at Google Scholar · View at Scopus
M. Hallett, "Pathophysiology of dystonia," Journal of Neural Transmission, Supplement, no. 70, pp. 485–488, 2006. View at Google Scholar · View at Scopus
N. Murase, J. C. Rothwell, R. Kaji et al., "Subthreshold low-frequency repetitive transcranial magnetic stimulation over the premotor cortex modulates writer's cramp," Brain, vol. 128, no. 1, pp. 104–115, 2005. View at Publisher · View at Google Scholar · View at Scopus
V. K. Neychev, X. Fan, V. I. Mitev, E. J. Hess, and H. A. Jinnah, "The basal ganglia and cerebellum interact in the expression of dystonic movement," Brain, vol. 131, no. 9, pp. 2499–2509, 2008. View at Publisher · View at Google Scholar · View at Scopus
V. K. Neychev, R. E. Gross, S. Lehéricy, E. J. Hess, and H. A. Jinnah, "The functional neuroanatomy of dystonia," Neurobiology of Disease, vol. 42, no. 2, pp. 185–201, 2011. View at Publisher · View at Google Scholar · View at Scopus

redpajama_set_name: RedPajamaCommonCrawl


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text:
Mimivirus è un genere virale contenente una sola specie ad oggi identificata cui è stato attribuito il nome Acanthamoeba polyphaga mimivirus (APMV), facente parte della famiglia Mimiviridae.
Nel linguaggio colloquiale, l'APMV è più comunemente definito con la sola denominazione di "Mimivirus".
Fino alla scoperta del più grande Pandoravirus nel 2013, questa specie possedeva il più grande capside fra tutti i virus conosciuti. Il Mimivirus possiede un genoma più esteso e complesso della maggior parte dei virus.

Scoperta
L'APMV venne scoperto in modo del tutto casuale all'interno di una cellula dell'ameba Acanthamoeba polyphaga, dalla quale ha preso il nome, nel 1992 durante delle ricerche sulla malattia del legionario. Il virus venne identificato attraverso la tecnica della colorazione di gram e, per questo, erroneamente classificato come batterio gram-positivo. In conseguenza di ciò venne chiamato "Bradforcocco" poiché l'ameba dalla quale era stato isolato venne raccolta nel distretto di Bradford, in Inghilterra. Nel 2003, ricercatori della Université de la Méditerranée a Marsiglia, Francia, pubblicarono un articolo sulla rivista "Science" nel quale affermarono di aver identificato il microorganismo come un virus.

Il Mimivirus potrebbe essere l'agente eziologico di alcune forme di polmonite; comunque, questa è una ipotesi basata solamente sull'evidenza della formazione di anticorpi diretti contro questo organismo nel sangue di pazienti colpiti da polmonite. Anche se la classificazione di Mimivirus come un agente patogeno è provvisoria, l'evidenza dimostra una nutrita serie di elementi di prova che può causare la polmonite virale.

Classificazione
Mimivirus è stato inserito dalla Commissione Internazionale per la Tassonomia dei Virus nella famiglia Mimiviridae, e fa parte del gruppo I della classificazione di Baltimore.

Mimivirus appartiene al phylum di grandi virus conosciuto come grandi virus nucleo-citoplasmatici a DNA (NCLDV, nome scientifico Nucleocytoviricota). Essi sono tutti virus di grandi dimensioni che mostrano in comune sia caratteristiche molecolari che genomi molto complessi. Il genoma del Mimivirus possiede inoltre circa 21 geni che codificano per omologhi di proteine che sono state ritrovate con un alto grado di conservazione in quasi tutti i NCLDV, e ricerche successive tenderebbero a mostrare che il Mimivirus sia il membro divergente più recente in questo gruppo.

Struttura

Il Mimivirus è il virus più grande conosciuto, con un capside del diametro di 400 nanometri. Filamenti proteici della lunghezza di 100 nanometri dipartono dalla superficie del capside, incrementando il diametro totale del virus a 600 nanometri. Molti testi scientifici considerano questa misura molto approssimata, preferendo includere il diametro più probabile dell'organismo in range compreso fra 400 e 800 nanometri dipendentemente da quanto la lunghezza totale del capside e del virione siano misurate.
Il capside appare esagonale se visto con un microscopio elettronico, quindi si può ragionevolmente supporre che la simmetria del capside stesso sia icosaedrica. Esso non sembra possedere un pericapside, o envelope, suggerendo che il virus non esca dalla cellula ospite per gemmazione ma che invece ne venga liberato in seguito alla lisi della stessa.

Il mimivirus ha in comune con gli altri NCLDV molte caratteristiche morfologiche. Poiché molti virus di questo gruppo presentano un rivestimento (envelope) lipidico interno circondante il "nucleo" interno, i biologi M. Suzanne-Monti ed altri hanno suggerito che anche questo virus possa presentare una struttura analoga, sebbene non sia ancora stata osservata direttamente.
Il denso cuore centrale del virione appare come una regione scura nelle immagini al microscopio elettronico. Il grande genoma del virus risiede completamente in quest'area.

Dalla purificazione dei virioni possono essere isolati molti trascritti di mRNA. Come per altri NCLDV, sono stati riscontrati anche trascritti per la DNA polimerasi, una proteina del capside ed un fattore di trascrizione TFII-simile. Inoltre, tali ricerche hanno mostrato la presenza di tre differenti trascritti di enzimi amminoacil-tRNA sintetasi e quattro molecole sconosciute di RNA tipiche di questo genere di virus. Questi trascritti pre-impacchettati possono essere tradotti in enzimi senza che avvenga una preventiva espressione genica da parte del patrimonio genetico virale e dovrebbero essere necessari per la corretta replicazione del mimivirus. Anche altri virus a DNA, come il citomegalovirus umano e l'Herpesvirus presentano dei trascritti di RNA pre-impacchettati.

Un ceppo di Mimivirus conosciuto come Mamavirus si è rivelato il primo virus al mondo a possedere un suo proprio virus parassita, soprannominato "Sputnik"

Genoma
Il genoma del mimivirus è una molecola lineare e continua di DNA a doppio filamento, contenente 1,2 milioni di coppie di basi. Ciò lo rende il più grande genoma virale mai riscontrato, superando di poco più del doppio il precedente detentore del record, il miovirus "Batteriofago G".
Inoltre, esso è più esteso del genoma di 30 organismi cellulari.
In relazione al suo enorme genoma, il mimivirus possiede all'incirca 911 geni codificanti per proteine, superando decisamente il numero minimo di 4 geni che è richiesto ad un virus per poter completare correttamente il ciclo vitale. Analisi del suo genoma hanno mostrato la presenza di geni mai riscontrati in altri virus, inclusi geni codificanti per le amminoacil-tRNA sintetasi, ed altri che erano precedentemente ritenuti come tipici ed esclusivi degli organismi cellulari. Come altri grandi virus a DNA, il mimivirus contiene molti geni coinvolti nel metabolismo di amminoacidi, zuccheri e lipidi, ma anche altri geni metabolici mai riscontrati in altri virus (M. Suzan-Monti, 2006).
Circa il 90% del genoma virale ha capacità di codificare, mentre il restante 10% sembrerebbe essere semplice DNA non codificante.

Replicazione
Ciò che fa sì che il mimivirus debba essere considerato un virus e non un batterio, è la modalità di replicazione, non autonoma. Lo svolgimento del processo replicativo del mimivirus non è ancora completamente compreso, ma come minimo è noto che il mimivirus si attacca ad un recettore sulla membrana della cellula dell'ameba e dopo di ciò entra all'interno della stessa per endocitosi. Una volta all'interno, inizia una "fase di eclissi", durante la quale il virus sparisce e la cellula appare completamente sana e inalterata.
Dopo circa quattro ore piccoli accumuli proteici possono essere riscontrati in alcune aree della cellula. Otto ore dopo l'infezione molti virioni di mimivirus risultano chiaramente visibili nella cellula. Il citoplasma della cellula continua a riempirsi di virioni appena sintetizzati e circa 24 ore dopo l'infezione iniziale la cellula probabilmente scoppia rilasciando i nuovi mimivirus.

Poco è conosciuto riguardo ai dettagli della replicazione, probabilmente consistente in attacco alla superficie della cellula ed ingresso, rilascio del genoma conservato nel "core", trascrizione, traduzione, assemblaggio e rilascio della progenie virale.
Tuttavia, gli scienziati hanno stabilito le linee generali del processo utilizzando micrografie elettroniche delle cellule infette in vari momenti dopo l'ingresso del virione.
Queste micrografie mostrano che il capside del mimivirus viene assemblato nel nucleo, mentre il DNA acquista un rivestimento interno di membrane lipidiche attraverso gemmazione dalla membrana nucleare, e la presenza di particelle molto simili a quelle prodotte da molti altri virus, compresi tutti gli NCLDV.
Queste particelle sono conosciute in altri virus come "fabbriche virali" e contribuiscono ad un efficiente assemblaggio dei virioni attraverso l'alterazione di vaste aree della cellula ospite.

Implicazioni nella definizione di "vita"
Il mimivirus possiede molte caratteristiche che lo pongono al confine fra viventi e non-viventi. Le sue dimensioni sono analoghe a quelle di molti organismi batterici, come rickettsie e molti altri procarioti, possiede un genoma di dimensioni comparabili a molti procarioti anche non parassiti, che codifica proteine apparentemente inutili per un normale virus  In più, esso contiene geni che codificano per enzimi coinvolti nella sintesi di nucleotidi e amminoacidi, che non sono presenti in molti virus parassiti intracellulari obbligati. Ciò significa che differentemente da questi virus il mimivirus non dipende dal genoma della cellula ospite per l'espletazione dei processi metabolici necessari alla loro produzione. Esso tuttavia non possiede i geni per le proteine ribosomiali e dipende perciò dal suo ospite per sintesi proteica e processi energetici. Questi fattori combinati insieme hanno portato gli scienziati a chiedersi se il mimivirus si possa considerare una forma di vita distinta, appartenente ad un ulteriore dominio oltre ai normali eucarioti, batteri ed archea. Nondimeno, il mimivirus non mostra delle caratteristiche che sono considerate essenziali nella corrente definizione di vita: omeostasi, risposta agli stimoli, crescita e riproduzione nel senso classico o divisione cellulare.

Note

Bibliografia
 Raoult D, Audic S, Robert C, Abergel C, Renesto P, Ogata H, La Scola B, Suzan M, Claverie JM. The 1.2-megabase genome sequence of Mimivirus. Science. 2004 Nov 19;306(5700):1344-50. PMID 15486256
 Ghedin, Elodie, and Claverie, J-M, 2005, "Mimivirus relatives in the Sargasso sea," Virology Journal 2:62.
 Peplow, Mark, 2004, "Giant virus qualifies as 'living organism'," News@Nature, doi:10.1038/
 Press Release: Mimivirus: discovery of a giant virus, Paris, 28 marzo, 2003.
 New Scientist, Issue 2544, 25 March 2006.

 Highfield, Roger, "The Bradford bug that may be a new life form, " Daily Telegraph, 15 October 2004.

Voci correlate
Grandi virus nucleo-citoplasmatici a DNA

Altri progetti

Collegamenti esterni

Grandi virus nucleo-citoplasmatici a DNA

redpajama_set_name: RedPajamaWikipedia


text:
Calonectria indusiata is a fungal plant pathogen with several hosts.

Infected plants
See:
 List of azalea diseases
 List of foliage plant diseases (Palmae)
 List of rhododendron diseases
 List of tea diseases

References

External links

Fungal plant pathogens and diseases
Tea diseases
Ornamental plant pathogens and diseases
Nectriaceae
Fungi described in 2002


text:
STATE: NC's Juniper Level Botanic Garden opens two weekends in July – free to all
Published 3:34 pm Tuesday, July 13, 2021
Juniper Level Botanic Garden, a $7.5 million gift to NC State University, will open two weekends this summer, July 16-18 and July 23-25. Hours are 8 a.m.-5 p.m. Friday and Saturday and 1-5 p.m. Sunday. There is no entry fee. For GPS directions, input 9241 Sauls Road, Raleigh.
"Two open garden weekends are scheduled each season," said founder and benefactor Tony Avent. "When our endowment at the university is fully funded, that will allow us to open full-time as a public garden and a sister to JC Raulston Arboretum.
"The Gardening boom of 2020 continues prominently into 2021. There's an almost unprecedented plant shortage in America, especially for long-production time plants like trees and shrubs. In many box stores, where 60 percent of Americans buy their plants, there's a major shortage. Retailers that do not propagate plants are struggling to get a wide range of plants. We are fortunate because we propagate most things here, but it's still tough for us to keep up with demand.
"We'll be giving away pads of prickly pear cactus to our visitors at our Summer Open Garden. I've always been fascinated with cacti, so we now have over 150 different kinds of prickly pear cactus – probably the largest collection in the world. Since we reign them in annually, we're giving cactus pads to our visitors. You can plant them at home and enjoy them. The flower colors range the spectrum of the rainbow, and Native Americans have used the prickly pear cactus as a food crop for years.
"They're so many amazing plants blooming in the summer, and the pollinator activity is incredible. That's when all the insects and birds are gathering nectar, which they need to survive. If you want a lot of pollinator activity in your garden in the summertime, you need plants that have a burst of flowers.
"Adults and children are invited to come to Open Garden Days and learn more about insects from our entomologist Bill Reynolds. Bill used to be with the Museum of Natural Science; he's down to earth, loves nature, and enjoys talking with children. Bill's an insect collector who's also an expert on cicadas, which are very much in the news."
Established in 1988 south of downtown Raleigh, the not-for-profit Juniper Level Botanic Garden has grown into a 28-acre conservation and inspiration garden whose mission is to discover, grow, study, propagate and share the world's flora.
"Currently, we have just over 27,000 different kinds of plants," explained Avent. "That makes our botanic garden one of the top five collections in the United States."
Fundraising efforts for Juniper Level Botanic Garden operate under the auspices of The Endowment Fund of North Carolina State University, a 501(c)3 non-profit. Donors receive an official receipt for contributions to the fund.


text:
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redpajama_set_name: RedPajamaGithub


> I started some tracing in task #1515 (Mochendi, Botswana). I opened a tile (#30) with all roads and many buildings already in place, all somewhat offset from the Bing imagery. Between them they were very consistent, so I figured it would make more sense to align the image than move alle the existing features. This I did and traced the missing buildings to the realigned image.
> Now this tile is pretty consistent in itself but not to the adjoining areas. So what next?
> Can someone check the georeferencing of the Bing image? Or should the whole content be moved to fit to the current imagery? I did not check the whole area, but many roads seem to be similarly offset and many buildings aligned to the current Bing imagery.


As cleanroom professionals, we're all aware of the importance of implementing an efficient goods transfer procedure. But what happens to products once inside the cleanroom?
A transport trolley can bring numerous benefits to cleanroom operatives and to the overall cleanliness level of the cleanroom.
It's of vital importance to keep products clean once inside a cleanroom. A clearing trolley can reduce the transfer of contamination by eliminating the need for touching products repeatedly when transporting them within the cleanroom.
Humans are a large potential source of contamination, so operatives should do what they can to reduce movement and speed when inside a clean environment. A trolley can reduce back and forth trips from the working area to materials transfer, not only reducing contamination, but also boosting productivity.
Trolleys do the carrying for you, so there will be less strain on operatives arms and backs when having to transport a lot of material.
A material which is easy to clean and compatible with the cleaning agents used, such as stainless steel.
Shelves which have a raised profile edge to prevent items falling off.
Curled edges for ease of cleaning and to prevent gloves snagging.
Perfectly welded seams for a stable hold and reduced particle retention.
Smooth castors with the option to lock them when in position for safety.
Noise dampening shelves, to prevent loud rattles when moving.
See our range of clearing and transport trolleys. Hurry for a discount on a limited number of trolleys.


text:
The El Paso Open was a golf tournament on the Ben Hogan Tour. It ran from 1990 to 1991. It was played at Coronado Country Club in El Paso, Texas.

In 1991 the winner earned $25,000.

Winners

Former Korn Ferry Tour events
Golf in Texas
Sports in El Paso, Texas
Recurring sporting events established in 1990
Recurring sporting events disestablished in 1991


Lately my self esteem has been so low, it's becoming a joke! It is really affecting my every day life, and i hate it! I've tryed so much, and i cannot stop myself from getting depressed, and i just cry. What can be done about low self-esteem? It doesn't help that i have social anxiety, and i feel completely usless and so insignificant to everyone else.
What can be done about low self-esteem?The cure for low self esteem is good, solid accomplishment.
How do you expect to have respect for yourself if you don't do something worthy of respect?
Find a task that is hard to do and do it.
Find a thing that is good to do and do it.
Esteem whether from yourself or from others is something that is earned by your deeds.
If you have done nothing, lately, worthy of respect, well, you ain't no fool. You won't respect yourself.
i my self have had issues with my low self esteem since i can remember, and i have slowly worked some of it away, not totaly but alot of it. and there are times that i still feel like i am the most worthless person in the world. it takes time. and trying to get over it is not easy and it is differnt for every one. for me it was mostly about my looks, and my intelegence. i started to get over it when i had a freind (not a family member cause of corse they are biased) tell me that i was beautiful, i told him he was lieing to me. and he said something that i will never forget. "when you get home look at your self in the mirror as if you were a stranger seeing you for the first time, and then you will see how beautiful you are" so i did, i cleared my mind and looked through some one elses eyes at my self and i realized that i was pretty. i still do it some times, not always with the same result, but alot of times i feel that i am still pretty. my intellegence problem was alittle harder, finding out that i had dyslexia was a big starter for me, and then finnaly getting a B gpa helped abit, i was always good at learning, it was the homework that i had a problem with, and when i got to college i did my best to excel. the last college i went to i graduated with perfect attendace (somthing that i had never been able to do before) and i almost made honors, (i didnt make it cause of my terrible math) it didnt matter the fact was that i came close like .5 of a point and that was good enough for me to realize that i could do it.
i did have a large stroke to my ego latly, over the weekend a guy that i had a huge crush on me contacted me, and he told me how he regreted not asking me out, this was a big thing for me, i always felt that he didnt really like me or find me attractive. and now i know other wise.
FGM, sweetie, all I can say is that you are a beautiful woman inside and out. And you know I have no reason to lie to you, or that I say things just to make you feel better.
We have known each other for quite a while now, I promise you that you are a wonderful person with so much to give. You are so smart, so talented and you have this urge inside you to give and help others.
First of all, you should be proud of yourself that you WANT to do something with your life, and that you WANT to be productful. Many people could have used the SA excuse as a means to get away with working and being a productful member of socity. But you are not like that. You are trying to battle this SA and you dream of one day walking out there and making your goals come true. I admire that about you.
Second, there just comes a time where you have to look straight towards your demons' face and say "enough!". You take control of your self esteem. Dont let anyone else control it, not even those voices in your mind that tell you that you are ugly or not good enough. It is very difficult, I have gone through it myself (you know it ;)), but it must be done. You have to really knock out that low self esteem shell that surrounds you, in order to grow out of it and like yourself and be true to yourself. Relay on your friends for this. Friends are wonderful sources of strength. Believe us when we tell you that you ARE beautiful, that you ARE great, that you ARE worth it. We have no reason to lie to you. Draw strength from your kids who look up at you with admiration and unconditional love.
Whenever you feel this yicky feeling of low self esteem taking over you, just fight it. Say no, even outloud -- Yell it. You dont have to start believing that you are Miss Universe or some Model and that you are Miss Perfect. All you have to learn is to accept that this is who you are and the way you are -- And that its perfectly ok to be this way, look this way and just be who you are.
And just remember, you are wonderful. I dont pick my pod partner lightly! And coming to think of it, I only have ONE pod partner in the whole world -- YOU!
Remember the motto: Morr & FGM -- Two Freaks In A Pod!
Anyway - I am working with way through it.
Also - excersice makes me feel better - like taking my dog for a walk. I like Kayaking too ... so being outdoors helps me.
I know how hard it is to have low self esteem and the effect that it has on your life.
Hope that you feel better and find a way to gain more confidence.
I used to be at that point as well, and possibly half an inch of going overboard to the "other side."
After spending some time by myself and thinking about my life, I went through some transformation.
Take some time to yourself and analyze your life. Is there something (a person, place or thing) in your environment that is negative? What do you think makes you sad? What is it that you want to do in your life? Only you have the answer.
After my self-analysis, I have learned is that it's all in your mind. You have the power to control your life and do what you want. Don't spend your time doing nothing, but take the time you need to learn more about yourself and what YOU want to do and discover your desires in life. These words and the words of others may sound foreign, but if you try little by little with just changing your environment or controlling what things you encounter around you (like what you hear and see - avoiding negative things), you will see progress. I am just stating what worked for me and how I changed my life around.
Remember to laugh and play! Live your life to the fullest!
Sorry for the long post, thanks for listening!
stop taking yourself so damn seriously.


text:
package main

import (
	"flag"
	"fmt"

	"github.com/golang/glog"
	"golang.org/x/net/context"
	"google.golang.org/grpc"

	lspb "github.com/ghasemloo/libraryservice/proto"
)

var (
	addr      = flag.String("addr", "localhost:9000", "LibraryService server address")
	bookID    = flag.String("book_id", "0134190564", "The ISBN of the book")
	bookTitle = flag.String("title", "The Go Programming Language", "The title of the book")
)

func main() {
	flag.Parse()
	glog.Info("LibraryService client")
	ctx := context.Background()

	// Set up a connection to the server.
	conn, err := grpc.Dial(*addr, grpc.WithInsecure())
	if err != nil {
		glog.Exitf("Failed to connect: %v", err)
	}
	defer conn.Close()

	// Create a LibraryService client.
	c := lspb.NewLibraryServiceClient(conn)

	// Contact the server and create a book.
	createReq := &lspb.CreateBookRequest{
		BookId: *bookID,
		Book: &lspb.Book{
			Title: *bookTitle,
		},
	}
	book, err := c.CreateBook(ctx, createReq)
	if err != nil {
		glog.Exitf("CreateBook(%+v) failed: %v", createReq, err)
	}
	fmt.Printf("Created book: %+v\n", book)

	// Contact the server to check that the book is created.
	getReq := &lspb.GetBookRequest{
		Name: book.GetName(),
	}
	book, err = c.GetBook(ctx, getReq)
	if err != nil {
		glog.Exitf("GetBook(%+v) failed: %v", createReq, err)
	}
	fmt.Printf("Got book: %+v\n", book)
}


CLEAN CARFAX!! ONE OWNER!! CERTIFIED PRE-OWNED!! ONLY 6,276 MILES!! REMOTE START!! HEATED SEATS!! HEATED STEERING WHEEL!! BLIND SPOT DETECTION!! LANE DEPARTURE WARNING!! FORWARD COLLISION WARNING!! ADAPTIVE CRUISE CONTROL!! PRO-PILOT ASSIST!! LEATHER!! NAVIGATION!! SUNROOF!! BACKUP CAMERA!! PARKING SENSORS!! BLUETOOTH!! SATELLITE RADIO!! USB/AUX JACK!! POWER SEATS!! DUAL AUTOMATIC CLIMATE CONTROL!! KEYLESS ENTRY!! PUSH BUTTON START!! HOMELINK!! AUTOMATIC HEADLIGHTS!! FOG LIGHTS!!*Stop By Today *Stop by Fred Beans Nissan of Flemington located at 172 Route 202, Flemington, NJ 08822 for a quick visit and a great vehicle!
We make every effort to provide accurate information, but you must verify the information on this page before purchasing. The MSRP price listed is a reference only. All sale prices include freight, dealer prep, any applicable factory rebates & equipment discount packages, coupons, bonus cash and Fred Beans discount. Rebates may be in lieu of special financing, lease and some other offers. Not all customers may qualify. Manufacturers rebates are subject to change. Prior deals excluded. Exclusions may apply. Tax, license & document fees cost extra. Fred Beans' is not responsible for typographical errors." MPG estimates on this website are EPA estimates; your actual mileage may vary. For used vehicles, MPG estimates are EPA estimates for the vehicle when it was new. The EPA periodically modifies its MPG calculation methodology; all MPG estimates are based on the methodology in effect when the vehicles were new (please see the "Fuel Economy" portion of the EPA's website for details, including a MPG recalculation tool). The features and options listed are for the new 2019 Nissan Altima and may not apply to this specific vehicle. Tax, title, license (unless itemized above) are extra. Not available with special finance, lease and some other offers.
This Used Gun Metallic 2019 Nissan Altima 2.5 SL Sedan with a 2.5 L engine and 1-Speed CVT w/OD transmission is for sale at Fred Beans Chevrolet in Doylestown, PA. Contact us online or give us a call at (267) 327-4178 to have your questions answered or obtain a price quote for this vehicle. Fred Beans Chevrolet is happy to serve all Philadelphia and Bucks County residents from our Doylestown new and used car dealership.


text:
Путифигари () — коммуна в Италии, располагается в регионе Сардиния, в провинции Сассари.

Население составляет 732 человека (2008 г.), плотность населения составляет 14 чел./км². Занимает площадь 53 км². Почтовый индекс — 7040. Телефонный код — 079.

Покровительницей коммуны почитается Пресвятая Богородица (Nostra Signora de s'Ena Frisca), празднование в третье воскресение мая.

Демография
Динамика населения:

Администрация коммуны
 Официальный сайт:

Ссылки

 Национальный институт статистики
 Национальный институт статистики


Based on trust, customers rely on East Africa Recovery Experts for recovery services for their mobile phones. Recovery is possible on most Android and Apple Phones. Ie Iphones, Ipads, HTC, LG, Samsung, Infinix, Techno and more.
Solid State Drives can suffer some of the same causes of data loss as traditional hard drives. However, our engineers have an in depth industry leading toolkit designed to offer customers a higher success rate and quicker data retrieval turnaround.
We offer the forensic analysis of Laptops, Desktops, smartphones, tablets and other portable devices, retrieval of deleted data, text messages, call logs, documents, mobile browser history, etc.
provides a cloud based backup and recovery solution that provides SMEs, Private Companies, Government Institution and even Individuals with offsite backup services through an internet connection.


text:
Wi-Fi® is critical to national resilience in the face of COVID-19
December 15, 2020 by Dr. Raul Katz
The COVID-19 pandemic has proven to be a fundamental challenge on a global scale. Our socioeconomic systems have been strained as a result, forcing entire societies to reexamine social practices and production systems that have often been in place for decades, if not centuries. These changes have caused a global economic recession worse than the 2008-2009 financial crisis. Fortunately, the International Monetary Fund (IMF) predicts recovery to begin in 2021.
In a new paper by Telecom Advisory Services, we explore the impact of technology – specifically Wi-Fi® – under pandemic conditions. Additionally, in another study we have demonstrated that digital technology can mitigate the socioeconomic disruption presented by COVID-19, and that countries with highly developed digital infrastructures can reduce the pandemic's long-term, negative economic impact by more than half.
While the social and economic effects of the pandemic have been analyzed in detail, Wi-Fi's impact on the economy during this time of crisis has not been studied. However, many regions have reported huge jumps in Wi-Fi and Wi-Fi-based applications use as people worldwide move toward working and learning from home.
According to ASSIA, Wi-Fi activity increased and stabilized at approximately 82 percent higher than in pre-pandemic conditions. Users are doing more on Wi-Fi than ever before, and Wi-Fi has been shown to fulfill a critical contribution in several areas, including:
User benefits for accessing free Wi-Fi networks in public locations, including Wi-Fi buses
Consumer savings in cellular service when using home internet
Broadband coverage expansion in rural and isolated areas
Enterprise savings in using Wi-Fi for IoT, AR/VR, and other innovative applications
Wi-Fi is one of the most pervasive telecommunications technologies used today and represents a critical component of every country's digital infrastructure. Unsurprisingly, we have found that Wi-Fi networks are a significant contributor to national resilience in the face of the COVID-19 pandemic.
In approaching our analysis, Telecom Advisory Services wanted to better understand how Wi-Fi has contributed to economies around the world and demonstrate its significance under pandemic conditions. My team and I collected empirical evidence that underlines the value of Wi-Fi when it comes to mitigating the negative effects of pandemics, and we examined in detail how Wi-Fi has helped improve the socioeconomic resilience of countries around the globe. We found that Wi-Fi has been crucial in three specific use cases that have become critical in a time of social distancing measures: distance learning, telecommuting, and telepresence.
Distance learning: Even when students are physically in school, many studies have linked better educational outcomes to those with computer and internet access. Conditions resulting from the COVID-19 pandemic proved that Wi-Fi is critical to enabling remote learning, and in many cases becomes the only link existing between the student and the teacher.
Telecommuting: Wi-Fi is the key technology enabling telecommuting, and enterprises have supported enabling employees to work from home where possible—at times by purchasing upgraded equipment or better internet plans. Traffic measurement statistics show that now an average day's Wi-Fi traffic is similar to pre-pandemic holiday season traffic.
Telepresence: In general, telepresence has enabled people to stay safely at home but still have worldly experiences. Telemedicine and virtual events have drastically increased, but an area of focus we found very important is in elderly care. Delivery of virtual reality platforms and applications has helped mitigate the isolation of the elderly. Institutions introducing a blend of entertainment and therapy through VR can help memory care patients improve attention span and give better quality of life to seniors feeling isolated during stay-at-home orders.
Overall, Telecom Advisory Services has found that the global pandemic highlights Wi-Fi's role as a critical component of every country's digital infrastructure, making Wi-Fi networks a key factor in any nation's efforts to recover from the impacts of the COVID-19 pandemic, and potentially other large-scale crises.
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Dr. Raul Katz
Telecom Advisory Services, LLC
Dr. Katz is currently Director of Business Strategy Research at the Columbia Institute for Tele-Information, Visiting Professor at the Universidad de San Andrés (Argentina) and President of Telecom Advisory Services, LLC (URL: www.teleadvs.com). He has been working in the telecommunications and digital industries for over 35 years
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