Reliability of sensory predictions determines the experience of self-agency

This study examines the neurocognitive mechanisms underlying the sense of agency, that is, the experience of causing and controlling events in our environment. Specifically, we tested the hypothesis that the sense of agency depends on an optimal integration of different anticipatory signals, generated by motor and nonmotor systems. An established marker of pre-reflective agency experience is the suppression of cortical responses to actively generated feedback as compared to passively observed feedback, which was measured here by event-related potentials (ERPs). Sensory expectations based on motor-related and unrelated signals were induced by varying the probabilistic contingency between action and feedback, and by priming the feedback prior to the action. Moreover, simultaneous conscious agency judgments were assessed. A reduction of visual N1 response was found to self- as compared to externally generated feedback. In addition, the N1 was modulated by accurate anticipations based on prime stimuli, independent of the precision of motor predictions. Conscious agency judgments, in contrast, were enhanced by prime stimuli only in situations where no precise motor predictions of the action feedback were available. These results indicate that anticipatory signals arising from motor and nonmotor systems are integrated differently depending on the level of agency processing. Our findings suggest that, at a pre-reflective level, the brain's agency system relies on both embodied signals and nonmotor sensory expectations. At higher cognitive levels, motor and nonmotor cues are weighted differently depending on their relative reliability in a given context, thereby providing a basis for robust agentive self-awareness.     

Detection of fecal shedding of rotavirus vaccine in infants following their first dose of pentavalent rotavirus vaccine

Studies on rotavirus vaccine shedding and its potential transmission within households including immunocompromised individuals are needed to better define the potential risks and benefits of vaccination. We examined fecal shedding of pentavalent rotavirus vaccine (RV5) for 9 days following the first dose of vaccine in infants between 6 and 12 weeks of age. Rotavirus antigen was detected by enzyme immunoassay (EIA), and vaccine-type rotavirus was identified by nucleotide sequencing based on genetic relatedness to the RV5 VP6 gene. Stool from 22 (21.4%) of 103 children contained rotavirus antigen-positive specimens on ≥1 post-vaccination days. Rotavirus antigen was detected as early as post-vaccination day 3 and as late as day 9, with peak numbers of shedding on post-vaccination days 6 through 8. Vaccine-type rotavirus was detected in all 50 antigen-positive specimens and 8 of 8 antigen-negative specimens. Nine (75%) of 12 EIA-positive and 1 EIA-negative samples tested culture-positive for vaccine-type rotavirus. Fecal shedding of rotavirus vaccine virus after the first dose of RV5 occurred over a wide range of post-vaccination days not previously studied. These findings will help better define the potential for horizontal transmission of vaccine virus among immunocompromised household contacts of vaccinated infants for future studies.     

Surveillance and molecular characterization of rotavirus strains circulating in Manipur,North-Eastern India: Increasing prevalence of emerging G12 strains

To determine the frequency and genotypes of rotavirus strains, samples were collected from children hospitalized with acute diarrhea at the Regional Institute of Medical Sciences, Manipur. The globally common genotypes G1P[8] and G2P[4] constituted 58% of the total positive strains, while 3% and 8% strains were emerging genotypes, G9P[6] and G12P[6]. This is the first report of genotype G12 in Manipur. The G12 strains clustered with lineage III strains and had >98% identity with corresponding rotaviruses from Bangladesh, Thailand and the USA. Other uncommon G–P combinations including G4P[4], G4P[6], G10P[6] and G9P[19], along with a few strains that could not be typed were also found. The VP7 genes of G4 and G10 strains clustered with porcine and bovine strains, indicating possible zoonotic transmission. High frequency (36–62%) of rotavirus infection and predominance of G1P[8] and G2P[4] among children with acute diarrhea emphasized the need for implementation of currently available vaccines to reduce the burden of rotavirus induced diarrhea in India.     

Ursache einer Contusio bulbi

A 21-year-old man presented in the emergency department with noticeable deterioration of vision and a feeling of pressure in the right eye. He stated that he had injured his eye when a shot was fired while cleaning a blank cartridge pistol. Ultrasound examination revealed no evidence of intravitreal hemorrhage or detachment of the retina. Examination by computed tomography did not reveal the presence of a foreign body. The severely reduced visual acuity could most likely be attributed to a traumatic cataract. An in-depth psychiatric examination of the anamnesis revealed that the patient had deliberately injured himself with the weapon. The severe traumatic eye injury was the result of an unrecognized hebephrenic schizophrenia.     

Evidence from recombinant bunyavirus studies that the M RNA gene products elicit neutralizing antibodies

Homologous virus genetic recombination has been demonstrated for snowshoe hare (SSH), La Crosse (LAC), Tahyna (TAH), Lumbo (LUM), and Trivittatus (TVT) viruses, members of the California (CAL) serogroup of bunyaviruses, as well as for Guaroa (GRO) virus, a member of the Bunyamwera serogroup. No heterologous virus genetic recombination has been obtained between GRO and LAC, SSH, TAH, or TVT viruses, although recombination has been demonstrated between TAH and LAC, SSH, or TVT viruses, as well as between LAC and TVT or SSH viruses. Not all the dual temperature sensitive (ts) mutant virus coinfections (e.g., the reciprocal crosses to those that gave recombinants), yielded the expected recombinant viruses. This paradox is discussed in relation to the conditions necessary to produce recombinant viruses. Eight new recombinant viruses (TAH/LAC/TAH, TAH/LAC/LAC, LAC/TAH/LAC, LAC/TAH/TAH, TVT/LAC/TVT, TVT/TAH/TVT, SSH/TAH/TAH, and SSH/TAH/SSH) have been characterized. Plaque reduction neutralization tests have been performed with seven of these eight viruses, and four recombinant bunyaviruses obtained previously (i.e. SSH/LAC/LAC, SSH/LAC/SSH, SSH/SSH/LAC, and LAC/LAC/SSH). The results obtained using antisera raised against prototype TAH, TVT, SSH, or LAC viruses indicate that one or both of the bunyavirus M RNA gene products (i.e., their glycoproteins G1 and G2) specify the antigenic determinants recognized in the neutralization test.     

Effect of the competitive NMDA antagonist, CGP 40 116, and a low dose of l-Dopa on the motor activity deficit of MPTP-treated mice

Three experiments were performed to investigate the effects of combining the active D-stereoisomer of CGP 37 849, i.e. the glutamatergic antagonist, CGP 40 116, with l-dopa, in mice that had undergone treatment with the neurotoxin, MPTP. In the first experiment, the decreased motor activity in MPTP-treated mice was alleviated by the administration of a low dose of l-dopa (5mg/kg, s.c.) together with a low dose of CGP 40 116 (30μg/kg). This dose was inactive in the control (saline-treated) mice. The highest dose of CGP 40 116 used (3000μg/kg) stimulated activity in the control mice. In Experiment 2, the inactive L-stereoisomer, i.e., CGP 40 117, was found to be inactive at doses (3 and 30μg/kg) effective with CGP 40 116. The effects of CGP 40 116 and l-dopa on the 24-h activity of mice tested under either day-night or night-day conditions, were more marked and longer lasting in the night-day condition. Taken together, the results from all three experiments show that CGP 40 116 in a dose range of 1-30μg/kg in combination with l-dopa (5mg/kg, s.c.) alleviated the reduced motor activity in MPTP-treated mice whereas higher doses of CGP 40 116 (100, 300, or 3000μg/kg) or lower doses (0.1 and 0.3μg/kg) were without effect. These experiments are interpreted as support for current views on glutamatergic-dopaminergic interactions in Parkinsonism and offer further evidence for the MPTP mouse model of the disease.