The relationship between cognitive control and lexical conflict resolution in developmental dyslexia.

Previous studies have revealed that cognitive control functions contribute to the resolution of lexical interference. Both cognitive control (CC) deficits and reduced speed of lexical retrieval in Rapid Automatized Naming (RAN) tasks are characteristics of Developmental Dyslexia (DD), but it is still not fully understood how these deficits relate to each other and to reading problems. To examine this question, we tested adolescents with DD (n = 38), poor readers (PR; n = 25) and typical readers (TR; n = 33) matched on age and IQ, on CC functions with Stroop, Stop Signal, Simon, Backward Digit Span and n-back tasks and on lexical retrieval and lexical conflict resolution with RAN of pictures in semantically homogeneous vs. mixed trials. As expected, in the blocked RAN Task DD individuals showed longer naming times and a greater effect of lexical conflict resolution (indexed by difference scores of naming times in the homogeneous and mixed conditions) than TR participants. We also found significant group differences (TR = PR > DD) in CC measures. Naming time was associated with CC, while the lexical interference effect did not show any association with this set of abilities. These findings suggest that DD individuals show impairments in multiple cognitive functions, such as cognitive control, lexical retrieval and lexical conflict resolution. Our results also suggest that CC functions are involved in lexical retrieval, but we have not found evidence for their involvement in lexical conflict resolution processes.

Registered Replication Report: Rand, Greene, and Nowak (2012).

In an anonymous 4-person economic game, participants contributed more money to a common project (i.e., cooperated) when required to decide quickly than when forced to delay their decision (Rand, Greene & Nowak, 2012), a pattern consistent with the social heuristics hypothesis proposed by Rand and colleagues. The results of studies using time pressure have been mixed, with some replication attempts observing similar patterns (e.g., Rand et al., 2014) and others observing null effects (e.g., Tinghög et al., 2013; Verkoeijen & Bouwmeester, 2014). This Registered Replication Report (RRR) assessed the size and variability of the effect of time pressure on cooperative decisions by combining 21 separate, preregistered replications of the critical conditions from Study 7 of the original article (Rand et al., 2012). The primary planned analysis used data from all participants who were randomly assigned to conditions and who met the protocol inclusion criteria (an intent-to-treat approach that included the 65.9% of participants in the time-pressure condition and 7.5% in the forced-delay condition who did not adhere to the time constraints), and we observed a difference in contributions of -0.37 percentage points compared with an 8.6 percentage point difference calculated from the original data. Analyzing the data as the original article did, including data only for participants who complied with the time constraints, the RRR observed a 10.37 percentage point difference in contributions compared with a 15.31 percentage point difference in the original study. In combination, the results of the intent-to-treat analysis and the compliant-only analysis are consistent with the presence of selection biases and the absence of a causal effect of time pressure on cooperation.

Pharmacological stimulation and inhibition of insulin secretion in mouse islets lacking ATP-sensitive K+ channels.

BACKGROUND AND PURPOSE: ATP-sensitive potassium channels (K(ATP) channels) in beta cells are a major target for insulinotropic drugs. Here, we studied the effects of selected stimulatory and inhibitory pharmacological agents in islets lacking K(ATP) channels. EXPERIMENTAL APPROACH: We compared insulin secretion (IS) and cytosolic calcium ([Ca(2+)](c)) changes in islets isolated from control mice and mice lacking sulphonylurea receptor1 (SUR1), and thus K(ATP) channels in their beta cells (Sur1KO). KEY RESULTS: While similarly increasing [Ca(2+)](c) and IS in controls, agents binding to site A (tolbutamide) or site B (meglitinide) of SUR1 were ineffective in Sur1KO islets. Of two non-selective blockers of potassium channels, quinine was inactive, whereas tetraethylammonium was more active in Sur1KO compared with control islets. Phentolamine, efaroxan and alinidine, three imidazolines binding to K(IR)6.2 (pore of K(ATP) channels), stimulated control islets, but only phentolamine retained weaker stimulatory effects on [Ca(2+)](c) and IS in Sur1KO islets. Neither K(ATP) channel opener (diazoxide, pinacidil) inhibited Sur1KO islets. Calcium channel blockers (nimodipine, verapamil) or diphenylhydantoin decreased [Ca(2+)](c) and IS in both types of islets, verapamil and diphenylhydantoin being more efficient in Sur1KO islets. Activation of alpha(2)-adrenoceptors or dopamine receptors strongly inhibited IS while partially (clonidine > dopamine) lowering [Ca(2+)](c) (control > Sur1KO islets). CONCLUSIONS AND IMPLICATIONS: Those drugs retaining effects on IS in islets lacking K(ATP) channels, also affected [Ca(2+)](c), indicating actions on other ionic channels. The greater effects of some inhibitors in Sur1KO than in control islets might be relevant to medical treatment of congenital hyperinsulinism caused by inactivating mutations of K(ATP) channels.

Shortcomings of current models of glucose-induced insulin secretion.

Glucose-induced insulin secretion by pancreatic beta-cells is generally schematized by a 'consensus model' that involves the following sequence of events: acceleration of glucose metabolism, closure of ATP-sensitive potassium channels (K(ATP) channels) in the plasma membrane, depolarization, influx of Ca(2+) through voltage-dependent calcium channels and a rise in cytosolic-free Ca(2+) concentration that induces exocytosis of insulin-containing granules. This model adequately depicts the essential triggering pathway but is incomplete. In this article, we first make a case for a model of dual regulation in which a metabolic amplifying pathway is also activated by glucose and augments the secretory response to the triggering Ca(2+) signal under physiological conditions. We next discuss experimental evidence, largely but not exclusively obtained from beta-cells lacking K(ATP) channels, which indicates that these channels are not the only possible transducers of glucose effects on the triggering Ca(2+)signal. We finally address the identity of the widely neglected background inward current (Cl(-) efflux vs. Na(+) or Ca(2+) influx through voltage-independent channels) that is necessary to cause beta-cell depolarization when glucose closes K(ATP) channels. More attention should be paid to the possibility that some components of this background current are influenced by glucose metabolism and have their place in a model of glucose-induced insulin secretion.

A centriole-free Drosophila cell line. A high voltage EM study.

The problem of the absence of centrioles in cells of the 1182-4 line of Drosophila melanogaster has been reexamined with high voltage electron microscopy. A hypotonic treatment of the cells before fixation allowed a clear recognition of centrioles in 1 micron thick sections. Three different approaches were used to determine the presence of absence of centrioles in a Kc control cell line and in the 1182-4D cell line. 1) 1500 random 0.5 micron thick sections representing the equivalent of 60 whole cells of the 1182-4D line show no centrioles. In contrast, nearly all centrioles of the Kc cells were detected by this examination. 2) In a blind test 10 grids with either Kc or 1182-4D cells were correctly identified by the operator. In Kc cells, 4 to 6 diplosomes were observed by grid square on about 300 cell profiles, while no centrioles were seen in the sections of 1182-4D cells. 3) Complete serial sections 1 micron thick of whole 1182-4D cells were screened for presence or absence of centriole. No centriole was seen in any section. We conclude that these Drosophila 1182-4D cells, which have been maintained in culture for several years, are free of centrioles.

Gap junctions between germ and somatic cells in the testis of the moth, Anagasta Küehniella (Insecta: Lepidoptera).

Heterocellular gap junctions were demonstrated in germ cysts of the moth Anagasta Küehniella (Lepidoptera). They conjoin peripheral germ cells of a cyst and cells of their envelope. Their morphology differs according to the developmental stage of the germ cell involved. While gap junctional profiles are flat in cysts of gonia, in cysts of early spermatocytes they appear as button-like structures, the germ cell indenting the corresponding cyst cell. In cysts of late spermatocytes and of young spermatids, they are very numerous and often located at the extremity of conical protrusions of the germ cell. On the germ cell side, cytoplasmic microfilaments are associated with the junctional differentiation. Gap junctions are observed as being pinched off from the surface of the spermatids and, correspondingly, gap vesicles are found in the cyst cells. This, together with the fact that gap junctions are not found at later stages of development, suggests that internalization of the gap junctions might take place before elongations of the spermatids. The potential importance of these germ-somatic cell gap junctions is evaluated in light of recent physiological findings obtained by other authors on the oocyte-cumulus system and also in relation with some particularities in the development of the male germ cells in Lepidoptera.

Uptake of horseradish peroxydase by the testis of locusta migratoria during the last larval instar; relation with variations of ecdysteroid levels in haemolymph.

By using horseradish peroxydase (HRP) as a tracer, it is shown that the gonial region of the locust testis is an "open" compartment which is almost always freely penetrated by the tracer. During the last larval instar, however, the penetration of HRP decreases and ceases at the time when high levels of ecdysteroids are detected in the haemolymph by radioimmunoassay. A cause and effect relationship between tracer uptake and hormonal level could not be demonstrated by the experiments carried out up to now. From ultrastructural observations of the testis, it is concluded that the temporary isolation of the gonial compartment is not based upon any morphological structure which could act as a barrier. Penetration of the macromolecule is considered as the expression of an active uptake by the testis and the short period of nonpenetrability as a state of inertia whose significance remains to be discovered.

[Variations in the permeability of the testicular follicle of Locusta migratoria migratorioides (Orthoptera) during the last larval instar]. / Variations de perméabilité du follicule testiculaire chez le Criquet Locusta migratoria migratorioïdes (Orthoptére) au cours du dernier stade larvaire

Variations of the testicular permeability are demonstrated in Locusta migratoria by using tracers such as iron-containing particles of protein. The testicular region containing spermatids is never penetrated by the tracers in contrast to the apical region containing gonia and young spermatocytes. Permeability of this compartment shows variations during the intermoult.