Theta synchrony supports Weber–Fechner and Stevens' Laws for error processing,uniting high and low mental processes

Human brain theta rhythm has been related to the operation of a generic mechanism involved in error detection processes of different types (e.g., detecting incorrect motor responses or incorrect arithmetic equations). This theta activity seems to be sensitive to error salience or magnitude, that is, stronger theta activity is found with larger or more deviant errors (e.g., 1+2=8) than with smaller or less deviant ones (e.g., 1+2=4). A time‐frequency decomposition analysis indicated that theta activity is modulated by the magnitude of erroneous information in a nonlinear fashion, which can be characterized using Weber–Fechner's law of logarithmic function and Stevens' law of power function. The present study suggests that the generic mechanisms for error detection and evaluation may share similar fundamental neural schemes with primary cognitive and sensory or perceptual processes, which are directly involved in processing the specific type of input.     

Matefin/SUN-1 is a nuclear envelope receptor for CED-4 during Caenorhabditis elegans apoptosis

In Caenorhabditis elegans, the antiapoptotic protein CED-9 is localized at the mitochondria, where it binds the proapoptotic protein CED-4. Induction of apoptosis begins when the proapoptotic protein EGL-1 is expressed and binds CED-9. The binding of EGL-1 to CED-9 releases CED-4 from CED-9 and causes the activation of the caspase CED-3. Upon its release from CED-9, CED-4 rapidly translocates to the nuclear envelope (NE) in a CED-3-independent manner. However, the identity of the NE receptor for CED-4 and its possible role in the execution of apoptosis has remained unknown. Here, we show that the inner nuclear membrane SUN-domain protein matefin/SUN-1 is the NE receptor for CED-4. Our data demonstrate that matefin/SUN-1 binds CED-4 and is specifically required for CED-4 translocation and maintenance at the NE. The role of matefin/SUN-1 in the execution of apoptosis is further suggested by the significant reduction in the number of apoptotic cells in the organism after matefin/SUN-1 down-regulation by RNAi. The finding that matefin/SUN-1 is required for the execution of apoptosis adds an important link between cytoplasmic and nuclear apoptotic events.     

Infant brains detect arithmetic errors

A current debate is whether increased looking time in infancy is related to violation of expectations. In this study, 6- to 9-month-old infants' brain activity was analyzed during presentation of correct and incorrect solutions to simple arithmetic equations [(e.g., presentation of 1 + 1; one doll on a TV monitor, with another doll added from behind a screen, followed by a solution of 2 (correct) or 1 (incorrect)]. Infants looked longer at incorrect solutions than at correct ones. Event-related potentials, time-locked to the presentation of the solution, also differed between conditions, with greater negative activity for the incorrect solution condition. Spectral analysis showed a similar pattern to that of adults observing correct and incorrect arithmetical equations. These findings show (i) that the brain network involved in error detection can be identified in infancy and (ii) that this network can support an association between looking time and violation of expectations.     

Maternal traces of deep common ancestry and asymmetric gene flow between Pygmy hunter-gatherers and Bantu-speaking farmers

Two groups of populations with completely different lifestyles-the Pygmy hunter-gatherers and the Bantu-speaking farmers-coexist in Central Africa. We investigated the origins of these two groups and the interactions between them, by analyzing mtDNA variation in 1,404 individuals from 20 farming populations and 9 Pygmy populations from Central Africa, with the aim of shedding light on one of the most fascinating cultural transitions in human evolution (the transition from hunting and gathering to agriculture). Our data indicate that this region was colonized gradually, with an initial L1c-rich ancestral population ultimately giving rise to current-day farmers, who display various L1c clades, and to Pygmies, in whom L1c1a is the only surviving clade. Detailed phylogenetic analysis of complete mtDNA sequences for L1c1a showed this clade to be autochthonous to Central Africa, with its most recent branches shared between farmers and Pygmies. Coalescence analyses revealed that these two groups arose through a complex evolutionary process characterized by (i) initial divergence of the ancestors of contemporary Pygmies from an ancestral Central African population no more than approximately 70,000 years ago, (ii) a period of isolation between the two groups, accounting for their phenotypic differences, (iii) long-standing asymmetric maternal gene flow from Pygmies to the ancestors of the farming populations, beginning no more than approximately 40,000 years ago and persisting until a few thousand years ago, and (iv) enrichment of the maternal gene pool of the ancestors of the farming populations by the arrival and/or subsequent demographic expansion of L0a, L2, and L3 carriers.     

Silicone embolism syndrome: a case report, review of the literature, and comparison with fat embolism syndrome

Liquid silicone is an inert material that is utilized for cosmetic procedures by physicians as well as illegally by nonmedical personnel. We present a case report and collated clinical findings of 32 other patients who were hospitalized after illegal silicone injections. Symptoms and signs of the "silicone syndrome" included dyspnea, fever, cough, hemoptysis, chest pain, hypoxia, alveolar hemorrhage, and altered consciousness. Bilateral patchy alveolar infiltrates were present on the chest radiographs, and silicone pulmonary emboli were detected in all the patients. The patients could be divided into two groups based on the initial presentation and clinical outcome. Twenty-seven patients in group 1 presented predominantly with respiratory symptoms, and 93% of patients were discharged home within 3 weeks. Six patients (group 2) presented with severe neurologic findings, and experienced rapid deterioration and 100% mortality. The clinical findings after silicone embolism are very similar to the published reports of fat embolism, including hypoxemia in 92% of patients with silicone embolism (patients with fat embolism, 56 to 96%), dyspnea in 88% of patients (patients with fat embolism, 56 to 75%), fever in 70% of patients (patients with fat embolism, 23 to 67%), alveolar hemorrhage in 64% of patients (patients with fat embolism, 66%), neurologic symptoms in 33% of patients (patients with fat embolism, 22 to 86%), petechiae in 18% of patients (patients with fat embolism, 20 to 50%), chest pain in 15% of patients (patients with fat embolism, 26%), and mortality in 24% of patients (patients with fat embolism, 5 to 20%). The similarities among the mode of injury to the lung, the clinical findings, and the high incidence of alveolar hemorrhage suggest a common pathogenesis of silicone and fat embolism syndromes. We discuss the possibility that the activation of the coagulation system may be important in the development of these clinical syndromes.     

Genetic and environmental risk factors in congenital heart disease functionally converge in protein networks driving heart development

Congenital heart disease (CHD) occurs in ～1% of newborns. CHD arises from many distinct etiologies, ranging from genetic or genomic variation to exposure to teratogens, which elicit diverse cell and molecular responses during cardiac development. To systematically explore the relationships between CHD risk factors and responses, we compiled and integrated comprehensive datasets from studies of CHD in humans and model organisms. We examined two alternative models of potential functional relationships between genes in these datasets: direct convergence, in which CHD risk factors significantly and directly impact the same genes and molecules and functional convergence, in which risk factors significantly impact different molecules that participate in a discrete heart development network. We observed no evidence for direct convergence. In contrast, we show that CHD risk factors functionally converge in protein networks driving the development of specific anatomical structures (e.g., outflow tract, ventricular septum, and atrial septum) that are malformed by CHD. This integrative analysis of CHD risk factors and responses suggests a complex pattern of functional interactions between genomic variation and environmental exposures that modulate critical biological systems during heart development.