Recycling of Nutrients from Dairy Wastewater by Extremophilic Microalgae with High Ammonia Tolerance.

This study explored the possibility of incorporating extremophilic algal cultivation into dairy wastewater treatment by characterizing a unique algal strain. Results showed that extremophilic microalgae Chlorella vulgaris CA1 newly isolated from dairy wastewater tolerated a high level of ammonia nitrogen (2.7 g/L), which was over 20 times the ammonia nitrogen that regular Chlorella sp. could tolerate. The isolate was mixotrophically cultured in dairy effluent treated by anaerobic digestion (AD) for recycling nutrients and polishing the wastewater. The highest biomass content of 13.3 g/L and protein content of 43.4% were achieved in the culture in AD effluent. Up to 96% of the total nitrogen and 79% of the total phosphorus were removed from the dairy AD effluent. The ability of the algae to tolerate a high level of ammonia nitrogen suggests the potential for direct nutrient recycling from dairy wastewater while producing algal biomass and high value bioproducts.

Blindsight after hemidecortication: visual stimuli in blind hemifield influence anti-saccades directed there.

Patients missing a cortical hemisphere, removed surgically at adulthood, cannot consciously see a visual probe stimulus (P) flashed in their blind contralesional, hemifield. Nevertheless, they have a low-level form of blindsight wherein P can affect the reaction time of a manual response to the appearance of a visual target in their seeing hemifield. This ability is thought to require the pathway from retina-to-ipsilesional superior colliculus (SC) to cortex of the remaining hemisphere (Leh et al., 2006a, 2006b, 2009). Apart from emitting ascending signals, the SC normally sends saccade commands to the brainstem, a function seemingly conserved after hemidecortication because such patients can generate voluntary and accurate saccades bilaterally (Herter and Guitton, 2004). However, they cannot generate goal-directed saccades to P in their blind hemifield. We hypothesized that, in hemidecorticate patients, P might influence anti-saccades directed to the blind hemifield, to the mirror location of a visual cue presented in the seeing hemifield. We used anti-saccades because our patients could scale their anti-saccade amplitudes approximately according to different cue locations, thereby permitting us to control the end point of their anti-saccades to the blind hemifield. We identified in these patients a new form of blindsight wherein unseen P, if properly timed at the anti-saccade goal location in the blind hemifield, reduced the reaction time and improved the accuracy of anti-saccades directed to that general location. We hypothesize that P in the blind hemifield produced low-level signals in the ipsilesional SC that, if appropriately located and timed relative to anti-saccade goal and onset, interacted with anti-saccade motor preparatory activity - produced by descending commands to SC from the remaining hemisphere - so as to modify both anti-saccade reaction time and end point. Our results support normally encoded and functionally useful, but subliminal, signals in the retina-to-ipsilesional SC-to-reticular pathway of hemidecorticate patients.

Ipsilateral head and centring eye movements evoked from monkey premotor cortex.

Recent studies in monkeys have identified a 'polysensory, defensive zone', in the ventral premotor cortex, stimulation of which results in coordinated multisegmental movements reminiscent of those normally produced by animals that react to head-directed threatening stimuli. Here, we describe gaze movements evoked in the head-fixed and head-unrestrained monkey by electrical stimulation of the polysensory zone. Centring eye movements were elicited at all sites and under both conditions. With the head free to move, ipsilateral head movements always accompanied evoked eye movements and carried gaze into a final steady-state position in ipsilateral body space. Our results support the hypothesis that stimulation of the polysensory zone generates avoidance behaviours in which gaze is moved away from a head-directed threatening stimulus.

Evidence for gaze feedback to the cat superior colliculus: discharges reflect gaze trajectory perturbations.

Rapid coordinated eye-head movements, called saccadic gaze shifts, displace the line of sight from one location to another. A critical structure in the gaze control circuitry is the superior colliculus (SC) of the midbrain, which drives gaze saccades by relaying cortical commands to brainstem eye and head motor circuits. We proposed that the SC lies within a gaze feedback loop and generates an error signal specifying gaze position error (GPE), the distance between target and current gaze positions. We investigated this feedback hypothesis in cats by briefly stopping head motion during large ( approximately 50 degrees ) gaze saccades made in the dark. This maneuver interrupted intended gaze saccades and briefly immobilized gaze (a plateau). After brake release, a corrective gaze saccade brought the gaze on goal. In the caudal SC, the firing frequency of a cell gradually increased to a maximum that just preceded the optimal gaze saccade encoded by the position of the cell and then declined back to zero near gaze saccade end. In brake trials, the activity level just preceding a brake-induced plateau continued steadily during the plateau and waned to zero only near the end of the corrective saccade. The duration of neural activity was stretched to reflect the increased time to target acquisition, and firing frequency during a plateau was proportional to the GPE of the plateau. In comparison, in the rostral SC, the duration of saccade-related pauses in fixation cell activity increased as plateau duration increased. The data show that the cat's SC lies in a gaze feedback loop and that it encodes GPE.

On the feedback control of orienting gaze shifts made with eye and head movements.

Combined eye-head movements are routinely used to orient the visual axis (gaze) rapidly in space. The gaze control system can be modeled using a feedback system in which an internally created instantaneous gaze position error signal equivalent to the distance between the target and the current gaze position is used to drive brainstem eye and head motor circuits. The visual axis is driven until this gaze position error (GPE) is zero. The neural structure of the feedback system is discussed here. The midbrain's superior colliculus (SC) is implicated in gaze control but its 'location' in the feedback circuitry is debated. Our moving hill hypothesis proposed that the SC is within the feedback loop and that GPE is encoded topographically by a moving locus of activity on the motor map. In cat, fixation neurons of the superior colliculus encode GPE, which supports this model. Our preliminary evidence in both monkey and cat shows that neurons on the motor map respond to and encode, at very short latency, gaze shift perturbations. This further supports the hypothesis that the SC is within the gaze feedback loop.

Superior colliculus encodes distance to target, not saccade amplitude, in multi-step gaze shifts.

The superior colliculus (SC) is important for generating coordinated eye-head gaze saccades. Its deeper layers contain a retinotopically organized motor map in which each site is thought to encode a specific gaze saccade vector. Here we show that this fundamental assumption in current models of collicular function does not hold true during horizontal multi-step gaze shifts in darkness that are directed to a goal and composed of a sequence of gaze saccades separated by periods of steady fixation. At the start of a multi-step gaze shift in cats, neural activity on the SC's map was located caudally to encode the overall amplitude of the gaze displacement, not the first saccade in the sequence. As the gaze shift progressed, the locus of activity moved to encode the error between the goal and the current gaze position. Contrary to common belief, the locus of activity never encoded gaze saccade amplitude, except for the last saccade in the sequence.

In multiple-step gaze shifts: omnipause (OPNs) and collicular fixation neurons encode gaze position error; OPNs gate saccades.

The superior colliculus (SC), via its projections to the pons, is a critical structure for driving rapid orienting movements of the visual axis, called gaze saccades, composed of coordinated eye-head movements. The SC contains a motor map that encodes small saccade vectors rostrally and large ones caudally. A zone in the rostral pole may have a different function. It contains superior colliculus fixation neurons (SCFNs) with probable projections to omnipause neurons (OPNs) of the pons. SCFNs and OPNs discharge tonically during visual fixation and pause during single-step gaze saccades. The OPN tonic discharge inhibits saccades and its cessation (pause) permits saccade generation. We have proposed that SCFNs control the OPN discharge. We compared the discharges of SCFNs and OPNs recorded while cats oriented horizontally, to the left and right, in the dark to a remembered target. Cats used multiple-step gaze shifts composed of a series of small gaze saccades, of variable amplitude and number, separated by periods of variable duration (plateaus) in which gaze was immobile or moving at low velocity (<25 degrees /s). Just after contralaterally (ipsilaterally) presented targets, the firing frequency of SCFNs decreased to almost zero (remained constant at background). As multiple-step gaze shifts progressed in either direction in the dark, these activity levels prevailed until the distance between gaze and target [gaze position error (GPE)] reached approximately 16 degrees. At this point, firing frequency gradually increased, without saccade-related pauses, until a maximum was reached when gaze arrived on target location (GPE = 0 degrees). SCFN firing frequency encoded GPE; activity was not correlated to characteristics or occurrence of gaze saccades. By comparison, after target presentation to left or right, OPN activity remained steady at pretarget background until first gaze saccade onset, during which activity paused. During the first plateau, activity resumed at a level lower than background and continued at this level during subsequent plateaus until GPE approximately 8 degrees was reached. As GPE decreased further, tonic activity during plateaus gradually increased until a maximum (greater than background) was reached when gaze was on goal (GPE = 0 degrees). OPNs, like SCFNs, encoded GPE, but they paused during every gaze saccade, thereby revealing, unlike for SCFNs, strong coupling to motor events. The firing frequency increase in SCFNs as GPE decreased, irrespective of trajectory characteristics, implies these cells get feedback on GPE, which they may communicate to OPNs. We hypothesize that at the end of a gaze-step sequence, impulses from SCFNs onto OPNs may suppress further movements away from the target.