During natural behavior humans continuously adjust their gaze by moving head and eyes, yielding rich dynamics of the retinal input. Sensory coding models, however, typically assume visual input as smooth or a sequence of static images interleaved by volitional gaze shifts. Are these assumptions valid during free exploration behavior in natural environments? We used an innovative technique to simultaneously record gaze and head movements in humans, who freely explored various environments (forest, train station, apartment). Most movements occur along the cardinal axes, and the predominance of vertical or horizontal movements depends on the environment. Eye and head movements co-occur more frequently than their individual statistics predicts under an independence assumption. The majority of co-occurring movements point in opposite directions, consistent with a gaze-stabilizing role of eye movements. Nevertheless, a substantial fraction of eye movements point in the same direction as co-occurring head movements. Even under the very most conservative assumptions, saccadic eye movements alone cannot account for these synergistic movements. Hence nonsaccadic eye movements that interact synergistically with head movements to adjust gaze cannot be neglected in natural visual input. Natural retinal input is continuously dynamic, and cannot be faithfully modeled as a mere sequence of static frames with interleaved large saccades.
Head-fixed camera systems are widely known, but since they are aligned by the head only and not by the eyes they are not able to always look at what the cameraman is looking at, and the image quality is poor if no effort is made to stabilize the camera. Systems like Steadycam, in contrast, focus on image stabilization at the cost of restricting the cameraman in his actions. The prototype of a new mobile head-mounted camera system was developed that is continuously aligned with the orientation of gaze. In doing so, the biological gaze stabilization reflexes are used to keep the video camera stable on target. Applications like movie making through the eyes of an actor or documentary movies for sports and other activities are conceivable. The system was tested by a surgeon who could successfully document his activities
Downbeat nystagmus (DBN) is the most frequent form of acquired persisting fixation nystagmus with different symptoms such as unsteadiness of gait, postural instability, and blurred vision with reduced visual acuity (VA) and oscillopsia. However, different symptomatic therapeutic principles are required, such as 3,4-diaminopyridine and 4-aminopyridine, that effectively suppress DBN. Chlorzoxazone (CHZ) is a nonselective activator of small conductance calcium-activated potassium (SK) channels that modifies the activity of cerebellar Purkinje cells. We evaluated the effects of this agent on DBN in an observational proof-of-concept pilot study.
Methods:
Ten patients received CHZ 500 mg 3 times a day for 1 or 2 weeks. Slow-phase velocity of DBN, VA, postural sway, and the drug9s side effects were evaluated. Recordings were conducted at baseline, 90 minutes after first administration, and after 1 or 2 weeks.
Results:
Mean slow-phase velocity significantly decreased from a baseline of 2.74°/s ± 2.00 to 2.29°/s ± 2.12 (mean ± SD) 90 minutes after first administration and to 2.04°/s ± 2.24 (p < 0.001; post hoc both p = 0.024) after long-term treatment. VA significantly increased and postural sway in posturography showed a tendency to decrease on medication. Fifty percent of patients did not report any side effects. The most common reported side effect was abdominal discomfort and dizziness.
Conclusions:
The treatment with the SK-channel activator CHZ is a potentially new therapeutic agent for the symptomatic treatment of DBN.
Classification of evidence:
This study provides Class IV evidence that CHZ 500 mg 3 times a day may improve eye movements and visual fixation in patients with DBN.
In Reply We reported on an unusual patient who presented in the emergency room with symptoms and signs of an exceptional hBPPV (1): acute spontaneous and spinning vertigo, nausea, vomiting, spontaneous nystagmus, and VOR gain deficit on the right side. After being treated with liberatory maneuvers, the patient was free of symptoms and nystagmus and was released from the emergency unit. This case was special in 4 respects: 1) gravity dependence of spontaneous nystagmus, 2) recovery of the horizontal VOR gain on the affected right side immediately after treatment, 3) asymmetry of VEMP (both cVEMP and oVEMP) to air-conducted sound (ACS) before and 2 days after treatment, and 4) VEMP recovery 30 days after treatment. We hypothesized that the most plausible explanation for all effects is a reversible horizontal canal dysfunction due to the presence of a plug. The Commentary by Curthoys (this issue) on our case report (1) reveals the ongoing controversy surrounding the hypothesis of a canal origin of VEMP to ACS. At the heart of the controversy lies the challenge, which this hypothesis poses to the widely accepted interpretation that VEMP responses to ACS are purely of otolithic origin. The Commentary raised a number of issues related to Luis et al. (1) and Zhu et al. (2). Therefore, this joint reply by the authors of both studies aims to address the concerns inthe Commentary by Curthoys and to clarify several important issues related to the technical aspects of VEMP testing, the time course of VEMP and VOR gain recovery in the reported patient, the observed eye velocity saturation as a possible sign for a canal plug, and to the literature on human and animal VEMP neurophysiology. VEMP TESTING First, the Commentary by Curthoys raised doubts as to whether we met the minimum requirements for interpreting VEMPs to ACS. Both VEMP and audiometry (pure tone and acoustic impedance, i.e., tympanometry with stapedial reflexes) are always evaluated as bundle tests in the lab of the first author. All tests were performed on all occasions from Day 1 on and were unremarkable. The phones were correctly inserted by an experienced otologist under direct viewing conditions with headlight. Nevertheless, as in all cases of absent or asymmetric response, the patient was asked if he could hear the stimulus; the examiner himself heard the stimulus, and the cables were double checked and swapped. A technical failure can therefore be excluded as a possible explanation for the simultaneous absence and recovery of both cVEMP and oVEMP. To avoid redundant information and to keep the article, a Clinical Capsule Report, as short as possible, the information provided was formulated simply: “the neurootological examination was otherwise unremarkable.” ASSOCIATION OF VOR WITH VEMP RECOVERY In view of the apparent dissociation between VOR and VEMP recovery times in the reported patient, the authors of the Commentary raised the issue of a “logical problem” in our conclusion (1). The VOR gain recovered early after treatment, whereas the recovery of both oVEMP and cVEMP was delayed. In our Discussion (1), we emphasized that “this differentially delayed normalization (…) remains to be explained.” Here, we provide the following more detailed considerations: A possible but admittedly speculative explanation might be the residual mild gain asymmetry of 15% (0.81 on the right versus 1.09 on the left) reported for Day 3, that is, 48 hours after the treatment. As can be seen in the eye and head velocity regression diagram in figure 1, this mild gain asymmetry is the result of a right gain deficit occurring only at head velocities above 150 degrees per second. In the Discussion, this was attributed to “continuing changes in biomechanical semicircular canal properties.” It might well be that such a mildly reduced gain is already a sufficient condition to have an effect on the VEMPs. The interpretation in the Commentary that “canal function and VEMPs returned independently” is therefore not supported by the data we presented (1). On the contrary: after complete recovery 80 days after treatment, a second episode with a right geotropic hBBPV, which occurred 8 months later, again showed a mild asymmetry of both VOR gain and cVEMP, which eventually recovered 30 days later. The recovery pattern in the 2 episodes shows that VEMPs and horizontal VOR gain are not independent, as suggested by the Commentary, but that they are associated; whenever the horizontal VOR was even mildly affected, this also had an effect on the VEMPs. What “remains to be explained” in future work is the observation that the association of horizontal VOR with VEMPs does not seem to be a metrical one, that is, the immediate partial recovery of VOR gain after treatment from 0.29 to 0.81 is not reflected in a comparable VEMP recovery. This might be due to a number of mechanisms, for example, a threshold in semicircular canal biomechanics, central compensation, or frequency-dependent differences in response to 500 Hz ACS versus head impulses with a frequency content of 5 Hz. In addition, the 2 episodes are different in that the first event was characterized by an unusual horizontal canal plug and the second event by a more common hBPPV, which might be a reason for the dissociation of oVEMP and cVEMP between the 2 episodes. A Clinical Capsule Report like ours (1) cannot provide conclusive explanations for all these observations. The observed association and its alternative explanations, however, demonstrate that the rigid assumption of an otolithic origin of VEMP responses as the only possible interpretation for the arguable independence of VOR gain and VEMP recovery does not justify a falsification of our conclusion. The controversy ensuing in both the Commentary and in this reply shows how important it is for the clinical interpretation of ACS-induced VEMPs to clarify these questions in future work. The Commentary continues to cite three publications by Manzari et al. (3–5) in support of the view that a dissociation of VOR gains and bone-conducted vibration induced VEMPs demonstrates the different vestibular origins of the 2 outcomes, with VOR gains reflecting canal and VEMPs reflecting otolith function. The first difficulty that arises from comparing our VEMP results with those of Manzari et al. (3–5) is the difference between stimulation methods: we used ACS (1) and the latter used bone-conducted vibration. The Commentary further claims that “all 59 patients in Manzari et al. (3) had normal horizontal canal function during both vHIT and caloric testing.” However, Manzari et al (3) did not report that All 59 patients were examined with vHIT, but only that “many patients were also tested by video recording of horizontal head impulses,” without specifying how many patients were tested by vHIT and what their VOR gains were. Apparently, only the presence of a corrective saccade was assessed by vHIT and not the gain. From the few vHIT details reported by Manzari et al. (3), it is difficult to compare their results with our quantitative vHIT analysis of VOR gain (1). Apart from VOR gain, another missing detail is head impulse velocity. In figure 1 of our case report (1), VEMP asymmetry on Day 3 was associated with a mild VOR gain asymmetry of 15%, which was unmasked only at head velocities between 150 and 300 degrees per second. Whether the head impulses used by Manzari et al. (3,4) were too slow to unmask such a gain asymmetry is not clear. In the case report on a 4-year-old boy by Manzari et al. (5), head impulse velocity was indeed too slow to unmask even a more pronounced asymmetry. Head velocity on the affected right side reached its peak of about 80 degrees per second at about 90 ms after movement onset (fig. 1). This corresponds to an estimated acceleration of roughly 1,400 degrees per square second, which is well below the accelerations typically used in previous studies on head impulse testing. For example, Aw et al. (6) used accelerations of 3,000 to 4,000 degrees per square second and Schmid-Priscoveanu et al. (7) reported 10,000 degrees per square second, with peak velocities of 250 degrees per second. In contrast, Manzari et al. (5) stimulated with less than a third of this peak velocity, although it is well known that only “rapid, … unlike slow” head movements demonstrate the VOR gain asymmetry “that is expressed by Ewald’s Second Law” (8). Because this law is fundamental to head impulse testing, a possible consequence of ignoring it is a false-negative vHIT outcome, as recently demonstrated by Machner et al. (9) in a patient with unstable gait and oscillopsia after left-side mastoidectomy for cholesteatoma. vHIT outcome in this patient was indeed negative as long as peak head velocities remained below 200 degrees per second. In accordance with Ewald’s Second Law, gain asymmetry was only unmasked with head impulse velocities of 300 degrees per second. Therefore, the dissociation between VEMP and vHIT responses in Manzari et al. (3,5) might be due to false-negative vHIT outcomes. In the case report by Manzari et al. (4), the vHIT results in figure 2A do not support the conclusion in the Commentary that the patient had normal horizontal canal function. On the contrary, the gain on the affected right side (mean = 1.14, SD = 0.08, n = 24) was significantly smaller (p = 7 × 10−9, one-tailed t test) than the gain on the left side (mean = 1.35, SD = 0.08, n = 12). Both gains were above the normative range of 0.78 to 1.1 (8). The gain asymmetry of 8.4% was beyond the range of normal values of less than 5.6% (7). VELOCITY SATURATION BY A CANAL PLUG The most puzzling remark in the Commentary concerns the “final error” that we (1) are said to have made by not citing Manzari et al. (10) as the first to “describe” the velocity saturation. This comment is puzzling because in the whole text there is indeed no description of any velocity saturation. The authors of the Commentary point to a velocity saturation in figure 1, which, however, is characterized by the occurrence of many saccades, by slow phase eye velocities that are difficult to distinguish from saccades and “bump artifacts” (11), by a considerable noise content, by a low image resolution, and by image compression artifacts. A velocity saturation is therefore difficult to detect. Only on the basis of this figure and without the raw data, it is impossible to assess the claim in the Commentary that this figure shows a velocity saturation. If there was a velocity saturation, it went unnoticed. Interestingly, a similar velocity saturation also went unnoticed in a surgical canal plugging (see figure S1 in (11)), which clearly supports our conclusion that this particular velocity profile might be a specific sign of a canal plug. This profile was documented both with search coil and with vHIT. The search coil recording, however, showed a clearer image of this saturation than did the vHIT recording. The difference might be due to the recognized “bump artifact” (11) present in the vHIT device that the authors used. Could the contralateral inhibitory saturation be responsible for the saturation in the eye velocity profile?Evidence from vHIT testing in unilateral vestibular loss after schwannoma surgery contradicts this, as thereis clearly no velocity saturation (see fig. 4 in (11)). The reason for this probably relies on the fact that each contralateral firing cell has its own firing discharge and velocity-firing characteristic. Therefore each would hit the firing rate saturation boundary at 0 Hz at another velocity. vHIT velocity saturation in vestibular neuritis seems unlikely. Instead, for us (1) the most plausible explanation for the saturation of the eye velocity response (and the nystagmus pattern) observed in the reported BPPV patient was the presence of an otoconial canal plug, since such a plug would cause a negative cupular pressure and block endolymph flow, thus modifying the cupular-endolymph biomechanical dynamics. VEMP PHYSIOLOGY Curthoys’ group was the first to specifically examine the neural basis of VEMP testing by studying the responses of vestibular afferents to clinical VEMP stimuli. They reported that sound primarily activated the saccule (12–14) and utricle (15), but not the canals, even at intensities of 80 or 90 dB SL re ABR threshold. These seminal works have been widely cited to support the current saccular theory of cervical VEMP. While the simplicity of the saccular theory has played an important role in the rapid development of the field, it has been challenged by accumulating evidence that shows sound activation of the semicircular canals (for literature review, see (2)). To address the neural basis of sound activation of the vestibular system, which is essential for interpreting clinical VEMP testing results, Zhu and Zhou at the University of Mississippi Medical Center have conducted a series of studies over the past decade to further characterize the responses of the vestibular system to clinical VEMP stimuli in monkeys (16–19) and rats (2,20–23). Their efforts are motivated by 3 aims. The first aim is to develop a quantitative measurement of sound sensitivity of an individual vestibular neuron. This is achieved by computing the cumulative probability of evoking a spike (CPE) that measures how a transient stimulus (e.g., a brief click) induces a change of firing probability of a neuron (24). Instead of simply classifying an afferent as sound sensitive or nonsound sensitive, the CPE analysis provides a quantitative assessment of sound sensitivity of a vestibular neuron. The second aim is to employ the CPE approach to record a large number of vestibular afferents from all the 5 vestibular end organs to test the saccular theory of VEMPs. The third aim is to seek sound parameters that can selectively activate certain vestibular end organs, which will serve as the neural basis of discriminative VEMP testing protocols and interpretation guidelines. Zhu et al., cited by Luis et al. (1) as reference 15 and in the Commentary as reference 2, surveyed the sound sensitivity of over 900 vestibular afferents in anesthetized rats. In addition to activating 81% of irregular otolith afferents, acoustic clicks [80 dB SL re ABR threshold (∼130 dB pSPL)] activate a substantial number of irregular anterior canal afferents (AC, 59%) and horizontal canal afferents (HC, 47%). Among them, ∼50% of sound sensitive AC afferents and ∼20% of sound-sensitive HC afferents are high sound-sensitive afferents (i.e., CPE > 0.5; figs. 2 and 3 in (2)), which are considered to contribute to generating VEMPs. It should be noted that the canal afferents with lower CPE values may also contribute to VEMPs because summation of synchronous activation of a population of sound-sensitive afferents may result in measurable VEMP responses. In addition to the neurophysiologic evidence of sound activation of the canals, a recent intra-axonal recording/labeling study shows that click sensitive afferents innervate the HC and AC cristae as well as the saccular and utricular maculae (22), therefore, providing direct anatomic evidence for sound activation of both the canals andotoliths. Because motoneurons of the sternocleidomastoid muscles (SCM) receive inputs from both the canals and the otoliths (for reviews, (25,26)), these new data suggest that the contribution of canal afferents to VEMPs should not be ruled out in clinical VEMP testing. However, given the distinct physical and geometrical properties of the otoliths and the canals, it is possible to achieve selective activation of a set of vestibular end organs by employing appropriate sound parameters (20,21,27–30). Their ongoing experiments have this aim. The Commentary also mentioned an issue related to identifying the end organ innervated by an otolith afferent. In intact animals, otolith afferents can be reliably identified by their responses to static head tilts because canal afferents do not respond to changes in head orientation with respect to gravity. In animals that undergo surgical procedures for vestibular nerve recording, however, Goldberg and Fernandez (1975) (31) showed that the vertical canal afferents are sensitive to static head tilts because removal of the brain tissue overlying the vestibular nerves and ganglion exposes the bony labyrinth to room temperature. This results in a thermal gradient across the labyrinths, which makes the vertical canals sensitive to gravitational changes. To avoid this ambiguity, it is important to use turntables that provide adequate rotational stimulation to the vertical canals. CONCLUSION In summary, we addressed the arguments of the Commentary in the following points: 1) We have demonstrated that a technical failure can be excluded as a possible explanation for the simultaneous absence and recovery of both cVEMP and oVEMP. Very basic technical aspects, are not the most plausible causes for our findings; 2) vHIT and VEMP responses did not return independently but were associated. Whenever the horizontal VOR was even mildly affected, this also had an effect on VEMPs; 3) To the best of our knowledge vHIT was used for the first time to document a high-frequency VOR hypofunction during BPPV. Moreover, it documented an eye velocity saturation profile as was later demonstrated in a surgical canal plug (11); 4) our case showed that a patient with BPPV might present with spontaneous nystagmus. BPPV must be ruled out in acute vestibular syndrome patients. Not only the direction but also the intensity of the nystagmus position dependency should be tested in every patient with spontaneous nystagmus, just as the vHIT velocity profile; 5) as there is solid and growing evidence of sound canal activation, canal contributions to VEMPs should not be ruled out before the neurophysiologic basis of sound activation of the vestibular system is fully understood. Leonel Luis, M.D. Health Sciences Institute Portuguese Catholic University Clinical Physiology Translational Unit Institute of Molecular Medicine Faculty of Medicine University of Lisbon Lisbon, Portugal [email protected] Hong Zhu, M.D., Ph.D. Departments of Otolaryngology and Communicative Sciences and Neurobiology & Anatomical Sciences University of Mississippi Medical Center Jackson, Mississippi, U.S.A. João Costa, M.D., Ph.D. Clinical Physiology Translational Unit Institute of Molecular Medicine Faculty of Medicine University of Lisbon EMG and Motor Control Unit Neurology Department, Hospital Clinic Universitat de Barcelona, IDIBAPS Barcelona, Spain Josep Valls-Solé, M.D., Ph.D. EMG and Motor Control Unit Neurology Department, Hospital Clinic Universitat de Barcelona, IDIBAPS Barcelona, Spain Thomas Brandt, M.D. German Center for Vertigo and Balance Disorders Ludwig-Maximilians University Munich Munich, Germany Wu Zhou, Ph.D. Departments of Otolaryngology and Communicative Sciences and Neurobiology & Anatomical Sciences University of Mississippi Medical Center Jackson, Mississippi, U.S.A. Erich Schneider, Ph.D. German Center for Vertigo and Balance Disorders Ludwig-Maximilians University Munich, Germany Brandenburg University of Technology, Cottbus Senftenberg, Germany Thomas Brandt is shareholder and Erich Schneider is general manager and shareholder of EyeSeeTec GmbH. All other authors disclose no conflicts of interest. Acknowledgments: The authors thank Judy Benson for critically reading the manuscript. Supported by the German Federal Ministry of Education and Research (Grant 01 EO 0901) and NIH R01DC012060 (HZ), NIH R01DC008585 (WZ) and NIH R01 DC05785 (WZ).
The eye movement component that rotates around the line of sight, i.e., the ocular torsion, is in many aspects different from horizontal and vertical eye movements. While ocular torsion is mediated only by reflexive pathways like the torsional vestibulo-ocular and optokinetic reflexes (TVOR and OKN, respectively), horizontal and vertical components are also subject to intentional control mechanisms that are mediated by the saccadic and the pursuit systems. Dynamic properties of torsional eye movements are also very distinct. While horizontal and vertical VOR components show a gain close to unity and a small neural integration leakage with a time constant around pi=30 s, the TVOR shows a smaller gain of 0.4 and also a greater leakage with pi=2 s. During slow head rotations in roll, the TVOR is even less compensatory. At small stimulation levels the gain drops to a value of 0.2 and proves thus to be nonlinear, i.e., to depend on the stimulus magnitude. In a recent study, we hypothesized that this nonlinearity might be the result of a nonlinear processing of nystagmus quick phases rather than a nonlinearity in direct or integrator TVOR pathways. In the present study, we experimentally tested this hypothesis by measuring ocular torsion responses at different head rotation speeds. In addition to the conventional approach of analyzing slow-phase velocity (SPV) gains, we also analyzed properties of nystagmus quick phases. This method proved to be suitable for determining whether nonlinear processing of nystagmus frequency is responsible for the TVOR nonlinearity.
Neurological forms of Gaucher disease, the inherited disorder of β-Glucosylceramidase caused by bi-allelic variants in GBA1, is a progressive disorder which lacks a disease-modifying therapy. Systemic manifestations of disease are effectively treated with enzyme replacement therapy, however, molecules which cross the blood-brain barrier are still under investigation. Clinical trials of such therapeutics require robust, reproducible clinical endpoints to demonstrate efficacy and clear phenotypic definitions to identify suitable patients for inclusion in trials. The single consistent clinical feature in all patients with neuronopathic disease is the presence of a supranuclear saccadic gaze palsy, in the presence of Gaucher disease this finding serves as diagnostic of 'type 3' Gaucher disease.We undertook a study to evaluate saccadic eye movements in Gaucher patients and to assess the role of the EyeSeeCam in measuring saccades. The EyeSeeCam is a video-oculography device which was used to run a protocol of saccade measures. We studied 39 patients with non-neurological Gaucher disease (type 1), 21 patients with type 3 (neurological) disease and a series of 35 healthy controls. Mean saccade parameters were compared across disease subgroups.We confirmed the saccadic abnormality in patients with type 3 Gaucher disease and identified an unexpected subgroup of patients with type 1 Gaucher disease who demonstrated significant saccade parameter abnormalities. These patients also showed subtle neurological findings and shared a GBA1 variant.This striking novel finding of a potentially attenuated type 3 Gaucher phenotype associated with a specific GBA1 variant and detectable saccadic abnormality prompts review of current disease classification. Further, this finding highlights the broad spectrum of neuronopathic Gaucher phenotypes relevant when designing inclusion criteria for clinical trials.
The intensity of downbeat nystagmus (DBN) decreases during the daytime when the head is in upright position.
Objective:
This prospective study investigated whether resting in different head positions (upright, supine, prone) modulates the intensity of DBN after resting.
Methods:
Eye movements of 9 patients with DBN due to cerebellar (n = 2) or unknown etiology (n = 7) were recorded with video-oculography. Mean slow-phase velocities (SPV) of DBN were determined in the upright position before resting at 9 am and then after 2 hours (11 am) and after 4 hours (1 pm) of resting. Whole-body positions during resting were upright, supine, or prone. The effects of all 3 resting positions were assessed on 3 separate days in each patient.
Results:
Before resting (9 am), the average SPV ranged from 3.05 °/s to 3.6 °/s on the separate days of measurement. After resting in an upright position, the average SPV at 11 am and 1 pm was 0.65 °/sec, which was less (p < 0.05) than after resting in supine (2.1 °/sec) or prone (2.22 °/sec) positions.
Conclusion:
DBN measured during the daytime in an upright position becomes minimal after the patient has rested upright. The spontaneous decrease of DBN is less pronounced when patients lie down to rest. This indicates a modulation by otolithic input. We recommend that patients with DBN rest in an upright position during the daytime.
Classification of evidence:
This study provides Class II evidence that for patients with DBN 2 hours of rest in the upright position decreases nystagmus more than 2 hours of rest in the supine or prone positions (relative improvement 79% upright, 33% supine, and 38% prone: p < 0.05).
Medical treatments of a surgeon or a dentist are sometimes documented for teaching, telemedicine, or liability issues using a scene oriented video camera. But the most interesting parts of the scene are often covered by the operators hand or body. The best view to the scene is next to the operators field of view or perfectly: Within his head. Head-mounted scene cameras are used to create this exclusive point of view. Eye tracking systems could be used to emphasize the point of gaze within the scene image. The presented system improves classical eye trackers with an additional gaze-driven camera. The resulting scene image maintains the overall context, while the image from the gaze driven camera acts like a magnifying glass and provides a high-resolution image of the gazed detail using an independent exposure, thus creating a high dynamic range image. We show an application in a real dental treatment scenario.
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