ALBERT

Description: A bstract : The Colón platform, located in the Bocas del Toro region of Panama, was studied as a near-modern analog for buried reefal platforms. The platform has an areal extent of ~ 90 km 2 and formed in a convergent tectonic setting (backarc) under a tropical climatic regime. The attached platform formed as part of a discontinuously rimmed shelf along the Caribbean side of the Isthmus of Panama and consisted of mixed carbonates and siliciclastics. Based on field relations and strontium-isotope stratigraphy, three depositional sequences were identified in the near-surface deposits of the uplifted platform. A Miocene to late Pliocene lithic sandstone unit (sequence 1, Old Bank Formation) forms the foundation of the platform. Coral-rich limestone and coral-rich siliciclastic units were deposited during both the late Pliocene (sequence 2, Isla Colón Formation) and early Pleistocene (sequence 3, Urracá Formation). In sequences 2 and 3 the sediment composition and fauna show distinct differences between the windward and leeward sides of the platform, with the main lithologic variable being the amount of siliciclastic sediment that was admixed with the biogenic carbonate sediments. The siliciclastic deposits (mud rich) in sequences 2 and 3 exhibit lower permeability and relatively minor diagenetic modification, and they lack major karst features. Conversely, the more carbonate-rich deposits are well cemented and strongly affected by meteoric dissolution and karstification. This facies-selective dissolution occurred when middle Pleistocene regional uplift exposed the platform to a tropical climate with high rainfall. Earthquakes and associated uplift of the platform over the past ~ 1 Myr intensely fractured the limestone. Fracture porosity has contributed to rapid infiltration of meteoric water and pervasive dissolution that resulted in numerous vertical sinks as well as an extensive network of horizontal conduits. A large, incised channel feature connects several of the pre-existing caves and conduits. The Colón platform limestone is a product of an equatorial humid carbonate system and is of size similar to platforms of Oligo-Miocene age near Malaysia (Sarawak), Indonesia, and farther north in the South China Sea.

Description: Millions of people worldwide suffer from diseases that lead to paralysis through disruption of signal pathways between the brain and the muscles. Neuroprosthetic devices are designed to restore lost function and could be used to form an electronic 'neural bypass' to circumvent disconnected pathways in the nervous system. It has previously been shown that intracortically recorded signals can be decoded to extract information related to motion, allowing non-human primates and paralysed humans to control computers and robotic arms through imagined movements. In non-human primates, these types of signal have also been used to drive activation of chemically paralysed arm muscles. Here we show that intracortically recorded signals can be linked in real-time to muscle activation to restore movement in a paralysed human. We used a chronically implanted intracortical microelectrode array to record multiunit activity from the motor cortex in a study participant with quadriplegia from cervical spinal cord injury. We applied machine-learning algorithms to decode the neuronal activity and control activation of the participant's forearm muscles through a custom-built high-resolution neuromuscular electrical stimulation system. The system provided isolated finger movements and the participant achieved continuous cortical control of six different wrist and hand motions. Furthermore, he was able to use the system to complete functional tasks relevant to daily living. Clinical assessment showed that, when using the system, his motor impairment improved from the fifth to the sixth cervical (C5-C6) to the seventh cervical to first thoracic (C7-T1) level unilaterally, conferring on him the critical abilities to grasp, manipulate, and release objects. This is the first demonstration to our knowledge of successful control of muscle activation using intracortically recorded signals in a paralysed human. These results have significant implications in advancing neuroprosthetic technology for people worldwide living with the effects of paralysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bouton, Chad E -- Shaikhouni, Ammar -- Annetta, Nicholas V -- Bockbrader, Marcia A -- Friedenberg, David A -- Nielson, Dylan M -- Sharma, Gaurav -- Sederberg, Per B -- Glenn, Bradley C -- Mysiw, W Jerry -- Morgan, Austin G -- Deogaonkar, Milind -- Rezai, Ali R -- England -- Nature. 2016 Apr 13;533(7602):247-50. doi: 10.1038/nature17435.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Devices and Neuromodulation, Battelle Memorial Institute, 505 King Avenue, Columbus, Ohio 43201, USA. ; Center for Neuromodulation, The Ohio State University, Columbus, Ohio 43210, USA. ; Department of Neurological Surgery, The Ohio State University, Columbus, Ohio 43210, USA. ; Department of Physical Medicine and Rehabilitation, The Ohio State University, Columbus, Ohio 43210, USA. ; Advanced Analytics and Health Research, Battelle Memorial Institute, 505 King Avenue, Columbus, Ohio 43201, USA. ; Department of Psychology, The Ohio State University, Columbus, Ohio 43210, USA. ; Energy Systems, Battelle Memorial Institute, 505 King Avenue, Columbus, Ohio 43201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27074513" target="_blank"〉PubMed〈/a〉

Description: Mutations in the GJB2 gene, which encodes the gap junction protein connexin 26 (Cx26), are the primary cause of hereditary prelingual hearing impairment. Here, the p.Cys169Tyr missense mutation of Cx26 (Cx26C169Y), previously classified as a polymorphism, has been identified as causative of severe hearing loss in two Qatari families. We have analyzed the effect of this mutation using a combination of confocal immunofluorescence microscopy and molecular dynamics simulations. At the cellular level, our results show that the mutant protein fails to form junctional channels in HeLa transfectants despite being correctly targeted to the plasma membrane. At the molecular level, this effect can be accounted for by disruption of the disulfide bridge that Cys169 forms with Cys64 in the wild-type structure (Cx26WT). The lack of the disulfide bridge in the Cx26C169Y protein causes a spatial rearrangement of two important residues, Asn176 and Thr177. In the Cx26WT protein, these residues play a crucial role in the intra-molecular interactions that permit the formation of an intercellular channel by the head-to-head docking of two opposing hemichannels resident in the plasma membrane of adjacent cells. Our results elucidate the molecular pathogenesis of hereditary hearing loss due to the connexin mutation and facilitate the understanding of its role in both healthy and affected individuals.