What will happen if science will develop a theory of consciousness? Negative Ramifications.

For a long time, philosophers and scientists have attempted without success to develop a mind-body theory, a consciousness theory (Tc) to explain the exact relation between the mind and the body, a solution which is based on an assumed connection between consciousness and the activity of the neurophysiological processes in the brain. An important concern of the present paper, then, is to address the question of why, despite the great research effort on the subject, no successful Tc has ever been developed. In response, McGinn (1989) proposes that the human being’s cognitive system is not equipped to solve the problem. The present paper suggests another possible answer: If Tc had been discovered, a number of “negative-ramifications” would have emerged. These ramifications would have interfered with the development of a Tc. The paper discusses these ideas and arguments and finally suggests that it would be helpful to conceive of consciousness as an explanatory concept, which has yet to be explained

Configural and featural processing in humans with congenital prosopagnosia.

Prosopagnosia describes the failure to recognize faces, a deficiency that can be devastating in social interactions. Cases of acquired prosopagnosia have often been described over the last century. In recent years, more and more cases of congenital prosopagnosia (CP) have been reported. In the present study we tried to determine possible cognitive characteristics of this impairment. We used scrambled and blurred images of faces, houses, and sugar bowls to separate featural processing strategies from configural processing strategies. This served to investigate whether congenital prosopagnosia results from process-specific deficiencies, or whether it is a face-specific impairment. Using a delayed matching paradigm, 6 individuals with CP and 6 matched healthy controls indicated whether an intact test stimulus was the same identity as a previously presented scrambled or blurred cue stimulus. Analyses of d´ values indicated that congenital prosopagnosia is a face-specific deficit, but that this shortcoming is particularly pronounced for processing configural facial information

From upright to upside-down presentation: A spatio-temporal ERP study of the parametric effect of rotation on face and house processing

<p>Abstract</p> <p>Background</p> <p>While there is a general agreement that picture-plane inversion is more detrimental to face processing than to other seemingly complex visual objects, the origin of this effect is still largely debatable. Here, we address the question of whether face inversion reflects a quantitative or a qualitative change in processing mode by investigating the pattern of event-related potential (ERP) response changes with picture plane rotation of face and house pictures. Thorough analyses of topographical (Scalp Current Density maps, SCD) and dipole source modeling were also conducted.</p> <p>Results</p> <p>We find that whilst stimulus orientation affected in a similar fashion participants' response latencies to make face and house decisions, only the ERPs in the N170 latency range were modulated by picture plane rotation of faces. The pattern of N170 amplitude and latency enhancement to misrotated faces displayed a curvilinear shape with an almost linear increase for rotations from 0° to 90° and a dip at 112.5° up to 180° rotations. A similar discontinuity function was also described for SCD occipito-temporal and temporal current foci with no topographic distribution changes, suggesting that upright and misrotated faces activated similar brain sources. This was confirmed by dipole source analyses showing the involvement of bilateral sources in the fusiform and middle occipital gyri, the activity of which was differentially affected by face rotation.</p> <p>Conclusion</p> <p>Our N170 findings provide support for both the quantitative and qualitative accounts for face rotation effects. Although the qualitative explanation predicted the curvilinear shape of N170 modulations by face misrotations, topographical and source modeling findings suggest that the same brain regions, and thus the same mechanisms, are probably at work when processing upright and rotated faces. Taken collectively, our results indicate that the same processing mechanisms may be involved across the whole range of face orientations, but would operate in a non-linear fashion. Finally, the response tuning of the N170 to rotated faces extends previous reports and further demonstrates that face inversion affects perceptual analyses of faces, which is reflected within the time range of the N170 component.</p

Diagnosis and management of Silver–Russell syndrome: first international consensus statement

This Consensus Statement summarizes recommendations for clinical diagnosis, investigation and management of patients with Silver–Russell syndrome (SRS), an imprinting disorder that causes prenatal and postnatal growth retardation. Considerable overlap exists between the care of individuals born small for gestational age and those with SRS. However, many specific management issues exist and evidence from controlled trials remains limited. SRS is primarily a clinical diagnosis; however, molecular testing enables confirmation of the clinical diagnosis and defines the subtype. A 'normal' result from a molecular test does not exclude the diagnosis of SRS. The management of children with SRS requires an experienced, multidisciplinary approach. Specific issues include growth failure, severe feeding difficulties, gastrointestinal problems, hypoglycaemia, body asymmetry, scoliosis, motor and speech delay and psychosocial challenges. An early emphasis on adequate nutritional status is important, with awareness that rapid postnatal weight gain might lead to subsequent increased risk of metabolic disorders. The benefits of treating patients with SRS with growth hormone include improved body composition, motor development and appetite, reduced risk of hypoglycaemia and increased height. Clinicians should be aware of possible premature adrenarche, fairly early and rapid central puberty and insulin resistance. Treatment with gonadotropin-releasing hormone analogues can delay progression of central puberty and preserve adult height potential. Long-term follow up is essential to determine the natural history and optimal management in adulthood

Analysis of large versus small dogs reveals three genes on the canine X chromosome associated with body weight, muscling and back fat thickness

International audienceDomestic dog breeds display significant diversity in both body mass and skeletal size, resulting from intensive selective pressure during the formation and maintenance of modern breeds. While previous studies focused on the identification of alleles that contribute to small skeletal size, little is known about the underlying genetics controlling large size. We first performed a genome-wide association study (GWAS) using the Illumina Canine HD 170,000 single nucleotide polymorphism (SNP) array which compared 165 large-breed dogs from 19 breeds (defined as having a Standard Breed Weight (SBW) >41 kg [90 lb]) to 690 dogs from 69 small breeds (SBW ≤41 kg). We identified two loci on the canine X chromosome that were strongly associated with large body size at 82–84 megabases (Mb) and 101–104 Mb. Analyses of whole genome sequencing (WGS) data from 163 dogs revealed two indels in the Insulin Receptor Substrate 4 (IRS4) gene at 82.2 Mb and two additional mutations, one SNP and one deletion of a single codon, in Immunoglobulin Superfamily member 1 gene (IGSF1) at 102.3 Mb. IRS4 and IGSF1 are members of the GH/IGF1 and thyroid pathways whose roles include determination of body size. We also found one highly associated SNP in the 5’UTR of Acyl-CoA Synthetase Long-chain family member 4 (ACSL4) at 82.9 Mb, a gene which controls the traits of muscling and back fat thickness. We show by analysis of sequencing data from 26 wolves and 959 dogs representing 102 domestic dog breeds that skeletal size and body mass in large dog breeds are strongly associated with variants within IRS4, ACSL4 and IGSF1

Beneficial effect of antibodies against β- secretase cleavage site of APP on Alzheimer's-like pathology in triple-transgenic mice.

The toxicity of amyloid β and tau, the two hallmark proteins in Alzheimer's disease (AD), has been extensively studied individually. Recently new data suggest their possible interactions and synergistic effects in the disease. In this study, we investigate the ability of antibodies against the β secretase cleavage site on APP, named BBS1, to affect tau pathology, besides their well established effect on intracellular Aβ and amyloid load. For this purpose we treated the triple transgenic mice model of AD (3x Tg-AD) with mAb BBS1 intracerebroventricularly, using mini osmotic pumps for one month. The experimental data demonstrated reduction in total and phosphorylated tau levels, explained by significant reduction in GSK3β which phosphorylates tau on sites recognized by antibodies against PHF1 and AT-8. The treatment increased the cognitive capabilities and reduced the brain inflammation levels which accompany AD pathology. The data showing that tau pathology was significantly reduced by BBS1 antibodies suggest a close interaction between tau and Aβ in the development of AD, and may serve as an efficient novel immunotherapy against both hallmarks of this disease

BBS1 reduced levels of total tau, phosphorylated tau and GSK3β.

<p>Reduced levels of total tau and phophorylated tau in mice treated with mAb BBS1 may be mediated by reduced levels of GSK3β. (<b>A</b>) Total tau levels were quantified using tau 5 antibody in immunoblot. (<b>B</b>) Levels of phosphorylated tau at S199/S202/T205 positions were quantified using AT8 antibody. Scale bar is 500 µm. (<b>C</b>) Levels of paired helical filaments of tau phosphorylated at S396/S404 positions were quantified using PHF1 antibody in immunoblot analysis. (<b>D</b>) GSK3β levels were quantified by immunoblot analysis.</p