The Ontology for Biomedical Investigations

The Ontology for Biomedical Investigations (OBI) is an ontology that provides terms with precisely defined meanings to describe all aspects of how investigations in the biological and medical domains are conducted. OBI re-uses ontologies that provide a representation of biomedical knowledge from the Open Biological and Biomedical Ontologies (OBO) project and adds the ability to describe how this knowledge was derived. We here describe the state of OBI and several applications that are using it, such as adding semantic expressivity to existing databases, building data entry forms, and enabling interoperability between knowledge resources. OBI covers all phases of the investigation process, such as planning, execution and reporting. It represents information and material entities that participate in these processes, as well as roles and functions. Prior to OBI, it was not possible to use a single internally consistent resource that could be applied to multiple types of experiments for these applications. OBI has made this possible by creating terms for entities involved in biological and medical investigations and by importing parts of other biomedical ontologies such as GO, Chemical Entities of Biological Interest (ChEBI) and Phenotype Attribute and Trait Ontology (PATO) without altering their meaning. OBI is being used in a wide range of projects covering genomics, multi-omics, immunology, and catalogs of services. OBI has also spawned other ontologies (Information Artifact Ontology) and methods for importing parts of ontologies (Minimum information to reference an external ontology term (MIREOT)). The OBI project is an open cross-disciplinary collaborative effort, encompassing multiple research communities from around the globe. To date, OBI has created 2366 classes and 40 relations along with textual and formal definitions. The OBI Consortium maintains a web resource (http://obi-ontology.org) providing details on the people, policies, and issues being addressed in association with OBI. The current release of OBI is available at http://purl.obolibrary.org/obo/obi.owl

Human motion simulation and action corpus

Acquisition of large scale good quality training samples is becoming a major issue in machine learning based human motion analysis. This paper presents a method to simulate continuous gross human body motion with the intention to establish a human motion corpus for learning and recognition. The simulation is achieved by a temporal-spatialtemporal decomposition of human motion into actions, joint actions and actionlets based on the human kinematic model. The actionlet models the primitive moving phase of a joint and represents the muscle movement governed by kinesiological principles. Joint actions and body actions are constructed from actionlets through constrained concatenation and synchronization. Methods for concatenation and synchronization are proposed in this paper. An action corpus with small number of action vocabularies is created to verify the feasibility of the proposed method

Simulation of human motion for learning and recognition

Acquisition of good quality training samples is becoming a major issue in machine learning based human motion analysis. This paper presents a method to simulate human body motion with the intention to establish a human motion corpus for learning and recognition. The simulation is achieved by a unique temporal-spatial-temporal decomposition of human body motion into actions, joint actions and actionlets based on the human kinematic model. The actionlet models the primitive moving phase of a joint and can be simulated based on the kinesiological study. A joint action is formed by proper concatenation of actionlets and an action is a group of synchronized joint actions. Methods for concatenation and synchronization are proposed in this paper for realistic simulation of human motion. Results on simulating ”running” verifies the feasibility of the proposed method

Structure and magnetic properties of Ni50Mn35In15 thin film

Thin film of Ni50Mn35In15 Heusler alloy was prepared on MgO(001) substrate by epitaxial growth in an ultra-high vacuum (UHV) chamber by a Pulsed Laser Deposition (PLD) method. The epitaxial growth process was monitored by in situ reflection high energy electron diffraction (RHEED) and the structure of the film was checked by ex situ X-ray diffraction (XRD), which indicates that high quality Ni50Mn35In15 single crystal film with a face-centered-cubic (fcc) structure could be stabilized on MgO(001). Magnetic property measurement was also conducted at various temperatures by using physical property measurement system (PPMS). A significant exchange bias was observed for Ni50Mn35In15 film, and the strength of the exchange bias field (HEB ) increases with the decrease of temperature. Such a behavior can be ascribed to the fact that the interfacial spin interaction between ferromagnetic (FM) and antiferromagnetic (AFM) cluster is enhanced with the decrease of temperature

Rab26 restricts insulin secretion via sequestering Synaptotagmin-1.

Rab26 is known to regulate multiple membrane trafficking events, but its role in insulin secretion in pancreatic β cells remains unclear despite it was first identified in the pancreas. In this study, we generated Rab26-/- mice through CRISPR/Cas9 technique. Surprisingly, insulin levels in the blood of the Rab26-/- mice do not decrease upon glucose stimulation but conversely increase. Deficiency of Rab26 promotes insulin secretion, which was independently verified by Rab26 knockdown in pancreatic insulinoma cells. Conversely, overexpression of Rab26 suppresses insulin secretion in both insulinoma cell lines and isolated mouse islets. Islets overexpressing Rab26, upon transplantation, also failed to restore glucose homeostasis in type 1 diabetic mice. Immunofluorescence microscopy revealed that overexpression of Rab26 results in clustering of insulin granules. GST-pulldown experiments reveal that Rab26 interacts with synaptotagmin-1 (Syt1) through directly binding to its C2A domain, which interfering with the interaction between Syt1 and SNAP25, and consequently inhibiting the exocytosis of newcomer insulin granules revealed by TIRF microscopy. Our results suggest that Rab26 serves as a negative regulator of insulin secretion, via suppressing insulin granule fusion with plasma membrane through sequestering Syt1