Assessment of cochlear synaptopathy by electrocochleography to low frequencies in a preclinical model and human subjects

Cochlear synaptopathy is the loss of synapses between the inner hair cells and the auditory nerve despite survival of sensory hair cells. The findings of extensive cochlear synaptopathy in animals after moderate noise exposures challenged the long-held view that hair cells are the cochlear elements most sensitive to insults that lead to hearing loss. However, cochlear synaptopathy has been difficult to identify in humans. We applied novel algorithms to determine hair cell and neural contributions to electrocochleographic (ECochG) recordings from the round window of animal and human subjects. Gerbils with normal hearing provided training and test sets for a deep learning algorithm to detect the presence of neural responses to low frequency sounds, and an analytic model was used to quantify the proportion of neural and hair cell contributions to the ECochG response. The capacity to detect cochlear synaptopathy was validated in normal hearing and noise-exposed animals by using neurotoxins to reduce or eliminate the neural contributions. When the analytical methods were applied to human surgical subjects with access to the round window, the neural contribution resembled the partial cochlear synaptopathy present after neurotoxin application in animals. This result demonstrates the presence of viable hair cells not connected to auditory nerve fibers in human subjects with substantial hearing loss and indicates that efforts to regenerate nerve fibers may find a ready cochlear substrate for innervation and resumption of function

Splenectomy for splenomegaly and secondary hypersplenism

Splenomegaly and secondary hypersplenism may be associated with acute and chronic infections, autoimmune states, portal hypertension or splenic vein thrombosis, and a number of infiltrative and neoplastic conditions involving the spleen. Our experience and that of others with these various conditions demonstrates that the decision to perform splenectomy should be based on well-defined and often strictly limited indications. Except for idiopathic splenomegaly, the presence and severity of secondary hypersplenism or severely symptomatic splenomegaly should be well documented. In each case, the potential for palliation and known mean duration of expected response must be weighed against the increased morbidity and mortality of splenectomy (as compared to operation for “primary” hypersplenism) . La splénomégalie avec hypersplénisme secondaire relève de multiples causes: infection aigue ou chronique, états autoimmunologiques, hypertension portale, thrombose de la veine splénique, lésions tumorales spléniques. L'expérience de l'auteur qui rejoint celle de nombreux collègues lui permet d'affirmer que les indications de la splénectomie doivent être bien définies et sont strictement limitées. A l'exception de la splénomégalie idiopathique, l'existence et l'intensité de l'hypersplénisme, l'importance des symptomes provoqués par la splénomégalie doivent être aprréciées avec précision. Dans chaque cas le potentiel de la rémission de l'affection et la durée de la rémission doivent être pris en considération en fonction de l'éventuelle morbidité et de l'éventuelle mortalité de la splénectomie (par comparaison avec la splénectomie pour hypersplénisme primaire). Eplenomegalia e hiperesplenismo secundario pueden estar asociados con infecciones agudas y crónicas, estados autoinmunes (síndrome de Felty, lupus eritematoso sistémico), “esplenomegalia congestiva” por hipertensión portal o trombosis de la vena esplénica y con una variedad de entidades de tipo infiltrativo y neoplásico que afectan al bazo (sarcoidosis, enfermedad de Gaucher, varios desórdenes mieloproliferativos y linfomas). Nuestra experiencia, y aquella de otros autores, con tales condiciones demuestra que la decisión de realizar esplenectomía debe estar fundamentada en indicaciones bien definidas y estrictamente limitadas. Excepto en casos de esplenomegalia idiopática, la presencia y severidad del hiperesplenismo secundario o de esplenomegalia severamente sintomática debe ser bien documentada. En cada caso debe determinarse el potencial de paliación y la duración de la respuesta que se espera obtener frente a la incrementada morbilidad y mortalidad de la esplenectomía (en comparación con la operación que se realiza por hiperesplenismo “primario”).Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41318/1/268_2005_Article_BF01655279.pd

First measurement of Ωc0 production in pp collisions at s=13 TeV

The inclusive production of the charm–strange baryon 0 c is measured for the first time via its hadronic √ decay into −π+ at midrapidity (|y| <0.5) in proton–proton (pp) collisions at the centre-of-mass energy s =13 TeV with the ALICE detector at the LHC. The transverse momentum (pT) differential cross section multiplied by the branching ratio is presented in the interval 2 < pT < 12 GeV/c. The pT dependence of the 0 c-baryon production relative to the prompt D0-meson and to the prompt 0 c-baryon production is compared to various models that take different hadronisation mechanisms into consideration. In the measured pT interval, the ratio of the pT-integrated cross sections of 0 c and prompt + c baryons multiplied by the −π+ branching ratio is found to be larger by a factor of about 20 with a significance of about 4σ when compared to e+e− collisions

Elliptic flow of charged particles at midrapidity relative to the spectator plane in Pb–Pb and Xe–Xe collisions

Measurements of the elliptic flow coefficient relative to the collision plane defined by the spectator neutrons v2{ SP} in collisions of Pb ions at center-of-mass energy per nucleon–nucleon pair √ 2.76 TeV and Xe ions at √ sNN = sNN =5.44 TeV are reported. The results are presented for charged particles produced at midrapidity as a function of centrality and transverse momentum for the 5–70% and 0.2–6 GeV/c ranges, respectively. The ratio between v2{ SP} and the elliptic flow coefficient relative to the participant plane v2{4}, estimated using four-particle correlations, deviates by up to 20% from unity depending on centrality. This observation differs strongly from the magnitude of the corresponding eccentricity ratios predicted by the TRENTo and the elliptic power models of initial state fluctuations that are tuned to describe the participant plane anisotropies. The differences can be interpreted as a decorrelation of the neutron spectator plane and the reaction plane because of fragmentation of the remnants from the colliding nuclei, which points to an incompleteness of current models describing the initial state fluctuations. A significant transverse momentum dependence of the ratio v2{ SP}/v2{4} is observed in all but the most central collisions, which may help to understand whether momentum anisotropies at low and intermediate transverse momentum have a common origin in initial state f luctuations. The ratios of v2{ SP} and v2{4} to the corresponding initial state eccentricities for Xe–Xe and Pb–Pb collisions at similar initial entropy density show a difference of (7.0 ±0.9)%with an additional variation of +1.8% when including RHIC data in the TRENTo parameter extraction. These observations provide new experimental constraints for viscous effects in the hydrodynamic modeling of the expanding quark–gluon plasma produced in heavy-ion collisions at the LHC

Luteococcus sanguinis sp. nov., isolated from human blood

An unusual catalase-positive, Gram-positive, coccus-shaped bacterium that originated from a human blood specimen was subjected to a polyphasic taxonomic study. Cell-wall murein and lipid composition analyses indicated that the unknown isolate was a member of the genus Luteococcus. The results of comparative 16S rRNA gene sequence analysis were consistent with chemotaxonomic findings and showed that the unidentified bacterium represents a hitherto unknown sublineage, within the genus Luteococcus that is closely related to, but distinct from, Luteococcus japonicus. On the basis of both phenotypic and phylogenetic evidence, it is proposed that the unknown bacterium from human blood should be classified as Luteococcus sanguinis sp. nov., with the type strain CCUG 33897(T) (=CIP 107216(T))