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Evaluating whether someone's behavior is praiseworthy or blameworthy is a fundamental human trait. A seminal study by Hamlin and colleagues in 2007 suggested that the ability to form social evaluations based on third‐party interactions emerges within the first year of life: infants preferred a character who helped, over hindered, another who tried but failed to climb a hill. This sparked a new line of inquiry into the origins of social evaluations; however, replication attempts have yielded mixed results. We present a preregistered, multi‐laboratory, standardized study aimed at replicating infants' preference for Helpers over Hinderers. We intended to (1) provide a precise estimate of the effect size of infants' preference for Helpers over Hinderers, and (2) determine the degree to which preferences are based on social information. Using the ManyBabies framework for big team‐based science, we tested 1018 infants (567 included, 5.5–10.5 months) from 37 labs across five continents. Overall, 49.34% of infants preferred Helpers over Hinderers in the social condition, and 55.85% preferred characters who pushed up, versus down, an inanimate object in the nonsocial condition; neither proportion differed from chance or from each other. This study provides evidence against infants' prosocial preferences in the hill paradigm, suggesting the effect size is weaker, absent, and/or develops later than previously estimated. As the first of its kind, this study serves as a proof‐of‐concept for using active behavioral measures (e.g., manual choice) in large‐scale, multi‐lab projects studying infants. [ABSTRACT FROM AUTHOR]

Two experiments examined 8- and 10-month-old infants' (N = 71) binding of object identity (color) and location information in visual short-term memory (VSTM) using a one-shot change detection task. Building on previous work using the simultaneous streams change detection task, we confirmed that 8- and 10-month-old infants are sensitive to changes in binding between identity and location in VSTM. Further, we demonstrated that infants recognize specifically what changed in these events. Thus, infants' VSTM for binding is robust and can be observed in different procedures and with different stimuli.

Abstract Background Fragile X syndrome (FXS) is the most common cause of inherited intellectual disability and non-idiopathic autism. Individuals with FXS present with a behavioral phenotype of specific and selective deficits in an array of cognitive skills. Disruption of number processing and arithmetic abilities in higher-functioning adults and female adolescents with FXS has been well established. Still, both numerical skills and developmentally antecedent cognitive processes have just begun to be investigated in toddlers with FXS. The goal of the current study was to assess how very young children with FXS respond to ordinal relationships among numerical magnitudes. Methods Infrared eye-tracking was used to explore infants’ novelty recognition during passive viewing of ordinal numerical sequences; t-tests were used to analyze group differences in looking time. Results Ordinal recognition of numerical magnitudes is significantly impaired in young toddlers with FXS. Conclusions This study is the first to experimentally evaluate early number sense and ordinal recognition in toddlers with FXS, and our findings reveal that ordinal recognition of numerical magnitudes is significantly impaired in young toddlers with FXS, suggesting that later arithmetic impairments associated with FXS may have their origins in a developmental impairment of this more basic aspect of numerical cognition.

We assessed visual short-term memory (VSTM) for color in 6- and 8-month-old infants (n = 76) using a one-shot change detection task. In this task, a sample array of two colored squares was visible for 517 ms, followed by a 317-ms retention period and then a 3000-ms test array consisting of one unchanged item and one item in a new color. We tracked gaze at 60 Hz while infants looked at the changed and unchanged items during test. When the two sample items were different colors (Experiment 1), 8-month-old infants exhibited a preference for the changed item, indicating memory for the colors, but 6-month-olds exhibited no evidence of memory. When the two sample items were the same color and did not need to be encoded as separate objects (Experiment 2), 6-month-old infants demonstrated memory. These results show that infants can encode information in VSTM in a single, brief exposure that simulates the timing of a single fixation period in natural scene viewing, and they reveal rapid developmental changes between 6 and 8 months in the ability to store individuated items in VSTM.

When learning object function, infants must detect relations among features--for example, that squeezing is associated with squeaking or that objects with wheels roll. Previously, Perone and Oakes (2006) found 10-month-old infants were sensitive to relations between object appearances and actions, but not to relations between appearances and sounds or actions and sounds. In this article the authors probed the development of infants' attention to feature correlations critical for representing function by testing 8- and 12-month-old infants' (N = 126) sensitivity to such relations. Eight-month-old infants learned individual features but were not sensitive to the relations between those features. Twelve-month-old infants were sensitive to the relation among the features and significantly responded to violations in learned relations between object appearances and actions and between appearances and sounds. Thus, across development, infants become sensitive to an increasing number of relations with age, supporting an information-processing account of the development of object function. (Contains 2 tables and 3 figures.)

Cyclooxygenase-1 (Cox-1) contributes to gastric defense of healthy tissue, but the role in the protection of the gastric epithelium after minor, acute damage has been difficult to study in vivo. Using 710-nm two-photon light absorption to create microscopic gastric damage in anesthetized mice with the gastric mucosal surface surgically exposed and perfused on the microscope stage, the acute response of surface cells to injury could be monitored using in vivo microscopy within seconds after injury. Using exogenous (C1-NERF) and endogenous fluorophores, extracellular pH and cell death were monitored in real time during the entire damage and repair cycle. Two-photon damage was initiated by scanning ~200 [micro][m.sup.2] of gastric surface cells with high laser intensity, causing rapid bleaching of NAD(P)H fluorescence in optically targeted cells. In both Cox-[1.sup.+/-] and Cox-[1.sup.-/-] mice, a similar initial damage area expanded to include bystander epithelial cells over the next 2-5 min, with larger maximal damage noted in Cox-[1.sup.-/-] mice. The maximal damage size seen in Cox-[1.sup.-/-] mice could be reduced by exogenous dimethyl-[PGE.sub.2]. All damaged cells exfoliated, and the underlying epithelium was coincidently repaired over a time interval that was briefer in Cox-[1.sup.+/-] (12 [+ or -] 2 min, n = 12) than in Cox-[1.sup.-/-] (24 [+ or -] 4 min, n = 14) mice. Directly after damage, pH increased transiently in the juxtamucosal layer (maximal at 3-6 min). A smaller peak pH change was noted in Cox-[1.sup.-/-] mice ([DELTA]pH = 0.3 [+ or -] 0.04) than in Cox-[1.sup.+/-] mice ([DELTA]pH = 0.6 [+ or -] 0.2). Recovery to normal surface pH took longer in Cox-[1.sup.-/-] mice (27 [+ or -] 5 min) than in Cox-[1.sup.+/-] mice (12 [+ or -] 1 min). In conclusion, constitutive loss of Cox-1 leaves the gastric mucosa more prone to damage and slowed repair of microlesions. autofluorescence; photodamage; laser scanning microscopy; two-photon microscopy; reduced nicotinamide adenine dinucleotide; surface pH; cyclooxygenase

Cell-death programs executed in the pancreas under pathological conditions remain largely undetermined, although the severity of experimental pancreatitis has been found to depend on the ratio of apoptosis to necrosis. We have defined mechanisms by which apoptosis is induced in pancreatic acinar cells by the oxidant stressor menadione. Real-time monitoring of initiator caspase activity showed that caspase-9 (66% of cells) and caspase-8 (15% of cells) were activated within 30 min of menadione administration, but no activation of caspase-2, -10, or -12 was detected. Interestingly, when caspase-9 activation was inhibited, activation of caspase-8 was increased. Half-maximum activation ([t.sub.0.5]) of caspase-9 occurred within ~2 min and was identified at or in close proximity to mitochondria, whereas [t.sub.0.5] for caspase-8 occurred within ~26 min of menadione application and was distributed homogeneously throughout cells. Caspase-9 but not caspase-8 activation was blocked completely by the calcium chelator BAPTA or bongkrekic acid, an inhibitor of the mitochondrial permeability transition pore. In contrast, caspase-8 but not caspase-9 activation was blocked by the destruction of lysosomes (preincubation with Gly-Phe [beta]-naphthylamide, a cathepsin C substrate), loss of lysosomal acidity (bafilomycin A1), or inhibition of cathepsin L or D. Using pepstatin A-BODIPY FL conjugate, we confirmed translocation of cathepsin D out of lysosomes in response to menadione. We conclude that the oxidative stressor menadione induces two independent apoptotic pathways within pancreatic acinar cells: the classical mitochondrial calcium-dependent pathway that is initiated rapidly in the majority of cells, and a slower, caspase-8-mediated pathway that depends on the lysosomal activities of cathepsins and is used when the caspase-9 pathway is disabled. pancreas; acinar cells; menadione doi:10.1152/ajpgi.00103.2007

Gastric secretion of hydrochloric acid requires protons and chloride, yet the mechanisms and regulation of gastric chloride secretion remain unclear. We developed an in vivo technique to simultaneously measure acid/base and chloride secretion into the gastric lumen of anesthetized rats. The cannulated stomach lumen was perfused with weakly pH-buffered chloride-free solution containing a chloride-sensitive fluorophore [5 [micro]M N-(ethoxycarbonylmethyl)-6-methoxyquinolinium bromide (MQAE)]. Gastric acid and chloride secretion was detected in gastric effluents by 1) flow-through pH electrode and 2) MQAE fluorescence. Gastric effluent was also collected at 1-min intervals for independent determination of chloride amount by chloridometer. In all conditions, both optical and chemical determinations of chloride report similar amounts of secreted chloride. During luminal perfusion with pH 5 solution, net acid and chloride secretion into the lumen was observed. Pentagastrin stimulated both secretions. In contrast, proton pump inhibition (omeprazole) caused alkalinization of the gastric effluent, but chloride secretion was not diminished. During luminal pH 3 perfusion, net alkali secretion was observed, and chloride secretion at luminal pH 3 was greater than pH 5. When tissue is pretreated with omeprazole at luminal pH 3, the addition of prostaglandin E2 synchronously stimulates both alkali and chloride secretion. Results suggest that both acid and alkali secretions are separately coupled with chloride secretion. proton pump, fluorescence, rat, stomach gastric luminal pH