Multi-messenger observations of a binary neutron star merger

On 2017 August 17 a binary neutron star coalescence candidate (later designated GW170817) with merger time 12:41:04 UTC was observed through gravitational waves by the Advanced LIGO and Advanced Virgo detectors. The Fermi Gamma-ray Burst Monitor independently detected a gamma-ray burst (GRB 170817A) with a time delay of ~1.7 s with respect to the merger time. From the gravitational-wave signal, the source was initially localized to a sky region of 31 deg2 at a luminosity distance of 40+8-8 Mpc and with component masses consistent with neutron stars. The component masses were later measured to be in the range 0.86 to 2.26 Mo. An extensive observing campaign was launched across the electromagnetic spectrum leading to the discovery of a bright optical transient (SSS17a, now with the IAU identification of AT 2017gfo) in NGC 4993 (at ~40 Mpc) less than 11 hours after the merger by the One- Meter, Two Hemisphere (1M2H) team using the 1 m Swope Telescope. The optical transient was independently detected by multiple teams within an hour. Subsequent observations targeted the object and its environment. Early ultraviolet observations revealed a blue transient that faded within 48 hours. Optical and infrared observations showed a redward evolution over ~10 days. Following early non-detections, X-ray and radio emission were discovered at the transient’s position ~9 and ~16 days, respectively, after the merger. Both the X-ray and radio emission likely arise from a physical process that is distinct from the one that generates the UV/optical/near-infrared emission. No ultra-high-energy gamma-rays and no neutrino candidates consistent with the source were found in follow-up searches. These observations support the hypothesis that GW170817 was produced by the merger of two neutron stars in NGC4993 followed by a short gamma-ray burst (GRB 170817A) and a kilonova/macronova powered by the radioactive decay of r-process nuclei synthesized in the ejecta

Variation in Human Cytochrome P-450 Drug-Metabolism Genes: A Gateway to the Understanding of Plasmodium vivax Relapses (vol 11, e0160172, 2016)

[This corrects the article DOI: 10.1371/journal.pone.0160172.]

Variation in Human Cytochrome P-450 Drug-Metabolism Genes: A Gateway to the Understanding of Plasmodium vivax Relapses

Although Plasmodium vivax relapses are classically associated with hypnozoite activation, it has been proposed that a proportion of these cases are due to primaquine (PQ) treatment failure caused by polymorphisms in cytochrome P-450 2D6 (CYP2D6). Here, we present evidence that CYP2D6 polymorphisms are implicated in PQ failure, which was reinforced by findings in genetically similar parasites, and may explain a number of vivax relapses. Using a computational approach, these polymorphisms were predicted to affect the activity of CYP2D6 through changes in the structural stability that could lead to disruption of the PQ-enzyme interactions. Furthermore, because PQ is co-administered with chloroquine (CQ), we investigated whether CQ-impaired metabolism by cytochrome P-450 2C8 (CYP2C8) could also contribute to vivax recurrences. Our results show that CYP2C8-mutated patients frequently relapsed early (<42 days) and had a higher proportion of genetically similar parasites, suggesting the possibility of recrudescence due to CQ therapeutic failure. These results highlight the importance of pharmacogenetic studies as a tool to monitor the efficacy of antimalarial therapy

Balance and motor coordination are not fully developed in 7 years old blind children Coordenação motora e equilíbrio não são totalmente desenvolvidos em crianças cegas com 7 anos de idade

Visually impaired children show difficulties in recognizing their own bodies, objects around then and the spatial parameters that are essential for independent movement. This study analyzes the neuro-psychomotor development of a group of congenitally visually impaired children as compared to children with normal sight. We have evaluated two groups of seven-year-olds by means of neurological evolution examination (NEE). The group studied comprised 20 blind children and the control group comprised 20 children with normal sight, and they were paired up according to age and gender. In some tests, the blind children were guided by touch. The visually impaired children performed worse in tests evaluating balance and appendage coordination compared to normal sighted children (p< 0.001), and this suggests that visual deficiency impairs children's neuro-psychomotor development.<br>As crianças portadoras de deficiência visual possuem dificuldades em conhecer seu próprio corpo, objetos a sua volta e parâmetros espaciais imprescindíveis para locomoção independente. Este trabalho analisa o desenvolvimento neuropsicomotor de um grupo de crianças com deficiência visual congênita em comparação a crianças com visão normal. Avaliamos dois grupos de crianças de sete anos de idade, através do exame neurológico evolutivo (ENE). O grupo estudado era constituído de 20 crianças cegas e o grupo controle constituído de 20 crianças com visão normal, pareadas por idade e sexo. Em algumas provas, as crianças cegas foram instruídas pelo tato. As crianças portadoras de deficiência visual tiveram pior desempenho nas provas que avaliaram o equilíbrio e coordenação apendicular, quando comparadas às crianças com visão normal (p< 0,001), sugerindo que o déficit visual compromete o desenvolvimento neuropsicomotor da criança