Representational Account of Memory: Insights from Aging and Synesthesia

The representational account of memory envisages perception and memory to be on a continuum rather than in discretely divided brain systems [Bussey, T. J., & Saksida, L. M. Memory, perception, and the ventral visual-perirhinal-hippocampal stream: Thinking outside of the boxes. Hippocampus, 17, 898–908, 2007]. We tested this account using a novel between-group design with young grapheme-color synesthetes, older adults, and young controls. We investigated how the disparate sensory-perceptual abilities between these groups translated into associative memory performance for visual stimuli that do not induce synesthesia. ROI analyses of the entire ventral visual stream showed that associative retrieval (a pair-associate retrieved in the absence of a visual stimulus) yielded enhanced activity in young and older adults' visual regions relative to synesthetes, whereas associative recognition (deciding whether a visual stimulus was the correct pair-associate) was characterized by enhanced activity in synesthetes' visual regions relative to older adults. Whole-brain analyses at associative retrieval revealed an effect of age in early visual cortex, with older adults showing enhanced activity relative to synesthetes and young adults. At associative recognition, the group effect was reversed: Synesthetes showed significantly enhanced activity relative to young and older adults in early visual regions. The inverted group effects observed between retrieval and recognition indicate that reduced sensitivity in visual cortex (as in aging) comes with increased activity during top–down retrieval and decreased activity during bottom–up recognition, whereas enhanced sensitivity (as in synesthesia) shows the opposite pattern. Our results provide novel evidence for the direct contribution of perceptual mechanisms to visual associative memory based on the examples of synesthesia and aging

First occurrence of the invasive alien species Polydora cornuta Bosc, 1802 (Polychaeta: Spionidae) on the coast of Greece (Elefsis Bay; Aegean Sea)

The present study reports on the occurrence of two specimens of the alien species Polydora cornutaBosc, 1802, in Elefsis Bay, the Saronikos Gulf (Aegean Sea, eastern Mediterranean). This is the firstrecord of this invasive alien species on the coast of Greece and the second report in the eastern MediterraneanSea after its first finding in Izmir Bay (on the Turkish Aegean coast). This finding enhances its distributionalpattern within the Mediterranea

Treatment outcomes in the inpatient management of severe functional neurological disorder: a retrospective cohort study.

Functional neurological disorder (FND) is a heterogeneous condition; severe forms can be disabling. Multidisciplinary treatment and rehabilitation are recommended for severe FND, but there remains a lack of evidence for its efficacy and lack of understanding of the predictors and components of recovery. We report clinical outcome data for an inpatient cohort with severe FND. Clinical Global Impression Improvement with treatment is the primary outcome measure. Admission and discharge measures (Euroqol quality of life measures, Beck Depression Inventory, Spielberger Trait Anxiety Inventory, Cambridge Depersonalisation Scale, Illness Perception Questionnaire (Revised) and Functional Mobility Scale) are reported as secondary outcomes. We describe an FND cohort (n=52) with chronic illness (mean symptom duration 9.7 years). At admission, there were clinically relevant levels of depression, anxiety and depersonalisation derealisation. At the time of discharge, most (43/52) patients' global condition had improved. Measures of mobility, depression and quality of life also significantly improved while at discharge, symptoms were experienced as more understandable and less distressing than at admission. An admission measure of patient confidence in treatment was predictive of eventual clinical outcome. The most frequent outcome of inpatient rehabilitation is global improvement, even when symptoms are chronic and severe, reflected in measurable changes in both physical and psychological functioning. Significant levels of depersonalisation derealisation seen in this patient group suggest that routine enquiry into such experiences could help personalise FND treatment approaches. Patient confidence in treatment is key in determining clinical outcomes. [Abstract copyright: © Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

Effects of dexamethasone on renal and systemic acid-base metabolism

Effects of dexamethasone on renal and systemic acid-base metabolism. We carried out long-term balance studies in adrenalectomized (ADX) dogs to evaluate the effects of small amounts of a glucocorticoid steroid with minimal mineralocorticoid potency (dexamethasone; DEX) on renal and systemic acid-base metabolism under conditions of constant mineralocorticoid replacement and both normal and increased systemic acid loads. We investigated the effects of low and high dosages of dexamethasone (0.2 mg/day [normal-DEX] vs. 0.8 mg/day [high-DEX]) before and during hydrochloric acid feeding (5 mmol/kg/day) in paired studies on ADX dogs (N = 7) maintained on constant mineralocorticoid replacement (deoxycorticosterone, corticosterone, aldosterone). Prior to hydrochloric acid feeding, no differences in plasma acid-base composition were observed between the two dosages despite greater endogenous acid production with the higher dosage of DEX, evidenced by greater rates of both net acid excretion (NAE) and the excretion of urinary anions other than chloride, bicarbonate, and phosphate (urine anion gap). During hydrochloric acid feeding, mean plasma bicarbonate (PHCO3) decreased from 21.2 ± 0.4 to 13.7 ± 0.5 (normal-DEX) and from 21.1 ± 0.4 to 15.8 ± 0.4 mEq/liter (high-DEX). The difference in the decrements in PHCO3 between groups was significant (P < 0.05). With continued hydrochloric acid feeding in both groups, increasing the DEX dosage from 0.2 to 0.8 mg/day in the normal-DEX group resulted in a. significant increase in NAE (ΣΔNAE, +161 mEq, P < 0.02) and in PHCO3 (+3.6 ± 0.5 mEq/liter, P < 0.01) to steady-state levels by day 10, which were values not significantly different from those in high-DEX. The DEX dose-related increase in NAE was greater than the corresponding increase in endogenous acid production estimated from the change in urine anion gap, and was due largely to an increase in ammonium excretion, which, because urine pH did not decrease, could not be attributed to increased intraluminal trapping of ammonia as a result of more acidic tubular fluid. These studies indicate that the severity of hydrochloric acid-induced metabolic acidosis in mineralocorticoid-replete ADX dogs can be mitigated by increasing the dosage of exogenous glucocorticoid and suggest that this acidosis mitigating effect is mediated in part by the increased NAE associated with the stimulation of renal ammonia production. These studies further indicate that the rate of production of fixed acids of metabolism increases with an increased dosage of exogenous glucocorticoid, but that this acidosis-producing effect is more than offset by independent stimulation of renal net acid excretion, such that metabolic acidosis is prevented (basal condition) or if present (hydrochloric acid feeding) is significantly ameliorated.Effets de la dexaméthasone sur le métabolisme acido-basique rénal et systémique. Les études de bilan qui sont rapportées ont été réalisées chez des chiens surrénalectomisés (ADX) pour évaluer les effets de faibles quantités d'un stéroïde glucocorticoïde, ayant une activité minéralocorticoïde faible (dexaméthasone; DEX), sur le métabolisme acido-basique rénal et systémique dans des conditions de traitement substitutif permanent de minéralocorticoïdes et de charge acide soit normale soit élevée. Nous avons étudié les effets de doses de dexaméthasone (0,2 mg/jour; normale-DEX) ou 0,8 mg/jour (élevée-DEX) avant et pendant l'administration d'acide chlorhydrique à raison de 5 mmol/kg/jour dans des études appariées chez des chiens ADX (N = 7) recevant un traitement substitutif par les minéralocorticoïdes (deoxycorticosterone acetate, corticosterone, aldosterone). Avant l'administration d'acide chlorhydrique, il n'y avait pas de différence dans la composition acido-basique du plasma selon les doses de DEX malgré l'augmentation de production endogène d'acide sous l'effet de la dose la plus élevée de DEX, augmentation traduite par une élévation de l'état stationnaire d'excrétion nette d'acide (NAE) et de la somme des débits d'excrétion des anions urinaires autres que le chlore, le bicarbonate et le phosphate (trou anionique urinaire). Au cours de l'administration d'acide chlorhydrique la concentration plasmatique moyenne de bicarbonate (PHCO3) a diminué de 21,2 ± 0,4 à 13,7 ± 0,5 (normale-DEX) et de 21,1 ± 0,4 à 15,8 ± 0,4 mEq/litre (élevée-DEX). La différence des diminutions de bicarbonate était significative (P < 0,05). Au cours de l'administration prolongée d'acide chlorhydrique aux deux groupes l'augmentation de la dose de DEX de 0,2 à 0,8 mg/jour dans le groupe normale-DEX a eu pour résultat une augmentation significative de NAE (ΣΔNAE, +161 mEq, P < 0,02) et de PHCO3 (+ 3,6 ± 0,5 mEq/litre, P < 0,01), jusqu'à de nouveaux états stationnaires, le jour 10, non sigmficativement différents de ceux observés dans le groupe élevée-DEX. L'augmentation de NAE dépendant de la dose de DEX a été plus grande que l'augmentation correspondante de la production endogène d'acide estimée à partir de la modification du trou anionique urinaire, elle était principalement due à une augmentation de l'excrétion d'ammonium qui, du fait que le pH de l'urine n'a pas diminué, ne peut pas être attribuée à une augmentation de la captation intraluminale d'ammonia. Ces résultats indiquent que la sévérité de l'acidose métabolique déterminée par acide chlorhydrique chez les chiens ADX recevant des minéralocorticoïdes peut être atténuée par l'augmentation de la dose de glucocorticoïdes exogènes et suggère que cet effet d'atténuation a pour médiateur partiel l'augmentation de NAE associée à la stimulation de la production rénale d'ammonia. Ces résultats indiquent, de plus, que le débit de production des acides fixes augmente en même temps que la dose de glucocorticoïdes exogènes mais que cet effet de production d'acidose est plus que compensé par la stimulation indépendante de l'excrétion rénale nette d'acide, de telle sorte que l'acidose métabolique est empêchée (conditions basales) ou significativement améliorée au cours de l'administration acide chlorhydrique