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Knowledge of the number of people present in a catchment is fundamental for the assessment of spatio-temporal trends in wastewater-based epidemiology (WBE). Accurately estimating the number of people connected to wastewater catchments is challenging however, because populations are dynamic. Methods used to estimate population size can significantly influence the calculation and interpretation of population-normalised wastewater data (PNWD). This paper systematically reviews the reporting of population data in 339 WBE studies. Studies were evaluated based on their reporting of population size, the source of population data, the population calculation methods, and the uncertainties in population estimates. Most papers reported population size (96 %) and the source of population data (60 %). Fewer studies reported the uncertainties in their population data (50 %) and the methods used to calculate these estimates (28 %). This is relevant because different methods have unique strengths and limitations which can affect the accuracy of PNWD. Only 64 studies (19 %) reported all four components of population data. The reporting of population data has remained consistent in the past decade. Based on the findings, we recommend generalised reporting criteria for population data in WBE. As WBE is further mainstreamed and applied, the clear and comprehensive reporting of population data will only become increasingly important., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

pH transitions occur in hydroxyapatite (HAP) columns that are subject to step changes in salt concentration, which have been shown to be controlled by proton exchange on the HAP surface. The pH temporarily decreases before gradually returning to the feed value when the salt concentration increases, potentially compromising the stability of the HAP when either the magnitude or duration of the pH drop is excessive. The opposite happens when the salt concentration decreases. In this work we address the effects of several key variables: the flow rate, the particle size, the use of salt gradients instead of steps, the use of different co-buffers, the surface area of the HAP, and the use of a slightly alkaline wash prior to increasing the salt concentration. Flow rate and particle size were found to have virtually no effect, demonstrating that the pH transitions are equilibrium rather than kinetically driven. Salt gradients resulted in smaller pH drops compared to steps since the exchanged protons are diluted over the gradient volume. MES and histidine used as co-buffers were effective at reducing the duration of the pH transitions but did not affect their magnitude. The same result was found when comparing HAP samples with different surface areas, with the lower surface area HAP yielding much shorter duration but similar pH drops and rises. Finally, washing the HAP column with a pH 7.5 buffer prior to the salt step was found to dramatically reduce the subsequent pH drop. In general, there was good agreement between these results and predictions based on our previously developed model., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Saccades are rapid shifts of gaze that normally place the line of sight on a desired target with a single smooth movement. A number of disease states have been shown to result in saccadic movements that are fragmented, but still end near target position after a multi-step sequence of saccades. Among these disorders are Parkinson's disease and late-onset Tay-Sachs disease (LOTS). We have recently shown that normal human subjects and monkeys also make some two-step saccadic responses in cognitively difficult, choice response tasks. In monkeys we have been able to record neuronal responses as the animals performed a visually guided, choice saccade task. We compared the activity of neurons in the superior colliculus (SC) and the cortical frontal eye field (FEF) during the majority of trials that were accomplished with single-step saccades with those completed with two-step saccades. Several differences in discharge pattern aligned on the first saccade were uncovered. Neurons in the rostral and caudal SC were not modulated at the time of the first saccade, but a class of FEF neurons showed a burst of activity before the first saccade. If these neurons are among those known to project to the saccade generator in the brainstem, they could trigger the onset of a saccade before the remaining machinery in the saccade generator had sufficient activity to sustain the saccade. Overall the results suggest that a delicate balance of triggering and sustaining inputs are required to produce normal single-step saccades. These neural results may also help to clarify the pathology present when fragmented saccades occur in various disease states.

Saccades normally place the eye on target with one smooth movement. In late-onset Tay-Sachs (LOTS), intrasaccadic transient decelerations occur that may result from (1) premature omnipause neuron (OPN) re-activation due to malfunction of the latch circuit that inhibits OPNs for the duration of the saccade or (2) premature inhibitory burst neuron (IBN) activation due to fastigial nucleus (FN) dysregulation by the dorsal cerebellar vermis. Neuroanatomic analysis of a LOTS brain was performed. Purkinje cells were absent and gliosis of the granular cell layer was present in the dorsal cerebellar vermis. Deep cerebellar nuclei contained large inclusions. IBNs were present with small inclusions. The sample did not contain the complete OPN region; however, neurons in the OPN region contained massive inclusions. Pathologic findings suggest that premature OPN re-activation and/or inappropriate firing of IBNs may be responsible for interrupted saccades in LOTS. Cerebellar clinical dysfunction, lack of saccadic slowing, and significant loss of cerebellar cells suggest that the second cause is more likely.

In late-onset Tay-Sachs disease (LOTS), saccades are interrupted by one or more transient decelerations. Some saccades reaccelerate and continue on before eye velocity reaches zero, even in darkness. Intervals between successive decelerations are not regularly spaced. Peak decelerations of horizontal and vertical components of oblique saccades in LOTS is more synchronous than those in control subjects. We hypothesize that these decelerations are caused by dysregulation of the fastigial nuclei (FN) of the cerebellum, which fire brain stem inhibitory burst neurons (IBNs).

This article reviews the current state of knowledge of the primate smooth-pursuit system. The emphasis is on the neuronal mechanisms and pathways that control pursuit eye movements in the monkey. The review covers the neuronal structures believed to be involved in pursuit generation from striate cortex to the final premotoneuron structures in the brainstem. Information gathered from physiological and anatomical work is stressed.