Kinematic coordinations capture learning during human-exoskeleton interaction.

Human-exoskeleton interactions have the potential to bring about changes in human behavior for physical rehabilitation or skill augmentation. Despite significant advances in the design and control of these robots, their application to human training remains limited. The key obstacles to the design of such training paradigms are the prediction of human-exoskeleton interaction effects and the selection of interaction control to affect human behavior.

The Role of c-Jun and Autocrine Signaling Loops in the Control of Repair Schwann Cells and Regeneration.

After nerve injury, both Schwann cells and neurons switch to pro-regenerative states. For Schwann cells, this involves reprogramming of myelin and Remak cells to repair Schwann cells that provide the signals and mechanisms needed for the survival of injured neurons, myelin clearance, axonal regeneration and target reinnervation. Because functional repair cells are essential for regeneration, it is unfortunate that their phenotype is not robust.

Comparing Plan Recognition Algorithms Through Standard Plan Libraries.

Plan recognition deals with reasoning about the goals and execution process of an actor, given observations of its actions. It is one of the fundamental problems of AI, applicable to many domains, from user interfaces to cyber-security. Despite the prevalence of these approaches, they lack a standard representation, and have not been compared using a common testbed.

Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun.

After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes significant clinical problems.

Characterising cellular and molecular features of human peripheral nerve degeneration.

Nerve regeneration is a key biological process in those recovering from neural trauma. From animal models it is known that the regenerative capacity of the peripheral nervous system (PNS) relies heavily on the remarkable ability of Schwann cells to undergo a phenotypic shift from a myelinating phenotype to one that is supportive of neural regeneration. In rodents, a great deal is known about the molecules that control this process, such as the transcription factors c-Jun and early growth response protein 2 (EGR2/KROX20), or mark the cells and cellular changes involved, including SOX10 and P75 neurotrophin receptor (p75NTR).

"PhysIt" - A Diagnosis and Troubleshooting Tool for Physiotherapists in Training.

Many physiotherapy treatments begin with a diagnosis process. The patient describes symptoms, upon which the physiotherapist decides which tests to perform until a final diagnosis is reached. The relationships between the anatomical components are too complex to keep in mind and the possible actions are abundant.

Aetna's Compassionate Care Program: Sustained Value for Our Members with Advanced Illness.

In 2004, Aetna, a national health insurer, launched the Aetna Compassionate Care Program (ACCP) targeting members diagnosed with an advanced illness with a view to increase access to palliative care and hospice services. The objective of this study is to evaluate the impact of ACCP on health care utilization and hospice enrollment among enrolled members. This was a retrospective cohort study comparing participants in ACCP to a matched control group using a propensity score method.

Schwann Cell Precursors; Multipotent Glial Cells in Embryonic Nerves.

The cells of the neural crest, often referred to as neural crest stem cells, give rise to a number of sub-lineages, one of which is Schwann cells, the glial cells of peripheral nerves. Crest cells transform to adult Schwann cells through the generation of two well defined intermediate stages, the Schwann cell precursors (SCP) in early embryonic nerves, and immature Schwann cells (iSch) in late embryonic and perinatal nerves. SCP are formed when neural crest cells enter nascent nerves and form intimate relationships with axons, a diagnostic feature of glial cells.

Preventing early-onset group B streptococcal sepsis: is there a role for rescreening near term?

The Centers for Disease Control and Prevention 2010 guidelines recommend group B streptococcus (GBS) screening at 35-37-week gestation to identify women with positive cultures who should receive intrapartum antibiotics and notes that the predictive value of a negative culture declines after 5 weeks. However, despite the lack of evidence, current guidelines do not recommend rescreening for those screened between 35 and 37 weeks. Our objectives were to investigate the rate of conversion from negative to positive results in women rescreened after appropriate screening at 35-37-week gestation and to examine the impact of rescreening on the use of intrapartum antibiotics.

The Success and Failure of the Schwann Cell Response to Nerve Injury.

The remarkable plasticity of Schwann cells allows them to adopt the Remak (non-myelin) and myelin phenotypes, which are specialized to meet the needs of small and large diameter axons, and differ markedly from each other. It also enables Schwann cells initially to mount a strikingly adaptive response to nerve injury and to promote regeneration by converting to a repair-promoting phenotype. These repair cells activate a sequence of supportive functions that engineer myelin clearance, prevent neuronal death, and help axon growth and guidance.

Management Decisions Made by Physician Assistants and Nurse Practitioners in Cutaneous Malignant Melanoma Patients: Impact of a 31-Gene Expression Profile Test.

Importance: The 31 gene-expression profiling test (31-GEP) has been shown to provide useful prognostic information in patients with cutaneous melanoma. The test dichotomizes patients into lower risk (Class 1) or higher risk (Class 2) for melanoma metastasis. Previous studies have demonstrated the clinical utility of the test in impacting dermatologists’ management decisions.

Neural crest Notch/Rbpj signaling regulates olfactory gliogenesis and neuronal migration.

The neural crest-derived ensheathing glial cells of the olfactory nerve (OECs) are unique in spanning both the peripheral and central nervous systems: they ensheathe bundles of axons projecting from olfactory receptor neurons in the nasal epithelium to their targets in the olfactory bulb. OECs are clinically relevant as a promising autologous cell transplantation therapy for promoting central nervous system repair. They are also important for fertility, being required for the migration of embryonic gonadotropin-releasing hormone (GnRH) neurons from the olfactory placode along terminal nerve axons to the medial forebrain, which they enter caudal to the olfactory bulbs.

Isolation of Schwann Cell Precursors from Rodents.

Schwann cell precursors are the first defined stage in the generation of Schwann cells from the neural crest and represent the glial cell of embryonic nerves. Highly pure cultures of these cells can be obtained by enzymatic dissociation of nerves dissected from the limbs of 14- or 12-day-old rat and mouse embryos, respectively. Since Schwann cell precursors, unlike Schwann cells, are acutely dependent on axonal signals for survival, they require addition of trophic factors, typically β-neuregulin-1, for maintenance in cell culture.

Graded Elevation of c-Jun in Schwann Cells : Gene Dosage Determines Effects on Development, Remyelination, Tumorigenesis, and Hypomyelination.

Schwann cell c-Jun is implicated in adaptive and maladaptive functions in peripheral nerves. In injured nerves, this transcription factor promotes the repair Schwann cell phenotype and regeneration and promotes Schwann-cell-mediated neurotrophic support in models of peripheral neuropathies. However, c-Jun is associated with tumor formation in some systems, potentially suppresses myelin genes, and has been implicated in demyelinating neuropathies.

Changes in the Coding and Non-coding Transcriptome and DNA Methylome that Define the Schwann Cell Repair Phenotype after Nerve Injury.

Repair Schwann cells play a critical role in orchestrating nerve repair after injury, but the cellular and molecular processes that generate them are poorly understood. Here, we perform a combined whole-genome, coding and non-coding RNA and CpG methylation study following nerve injury. We show that genes involved in the epithelial-mesenchymal transition are enriched in repair cells, and we identify several long non-coding RNAs in Schwann cells.

STAT3 Controls the Long-Term Survival and Phenotype of Repair Schwann Cells during Nerve Regeneration.

After nerve injury, Schwann cells convert to a phenotype specialized to promote repair. But during the slow process of axonal regrowth, these repair Schwann cells gradually lose their regeneration-supportive features and eventually die. Although this is a key reason for the frequent regeneration failures in humans, the transcriptional mechanisms that control long-term survival and phenotype of repair cells have not been studied, and the molecular signaling underlying their decline is obscure.

The repair Schwann cell and its function in regenerating nerves.

Nerve injury triggers the conversion of myelin and non-myelin (Remak) Schwann cells to a cell phenotype specialized to promote repair. Distal to damage, these repair Schwann cells provide the necessary signals and spatial cues for the survival of injured neurons, axonal regeneration and target reinnervation. The conversion to repair Schwann cells involves de-differentiation together with alternative differentiation, or activation, a combination that is typical of cell type conversions often referred to as (direct or lineage) reprogramming.

The Role of Cell Plasticity in Tissue Repair: Adaptive Cellular Reprogramming.

It is becoming clear that a radical change of cell identity of differentiated cells in vivo, triggered by injury or other adversity, provides an essential route to recovery for many different mammalian tissues. This process, which we term adaptive cellular reprogramming, promotes regeneration in one of two ways: by providing a transient class of repair cells or by directly replacing cells lost during tissue damage. Controlling adaptive changes in cell fate in vivo in order to promote the body's own cell therapy, particularly by pharmacology rather than genetics, is likely to become an increasingly active area of future work.

Schwann cell autophagy, myelinophagy, initiates myelin clearance from injured nerves.

Although Schwann cell myelin breakdown is the universal outcome of a remarkably wide range of conditions that cause disease or injury to peripheral nerves, the cellular and molecular mechanisms that make Schwann cell-mediated myelin digestion possible have not been established. We report that Schwann cells degrade myelin after injury by a novel form of selective autophagy, myelinophagy. Autophagy was up-regulated by myelinating Schwann cells after nerve injury, myelin debris was present in autophagosomes, and pharmacological and genetic inhibition of autophagy impaired myelin clearance.

Schwann Cells: Development and Role in Nerve Repair.

Schwann cells develop from the neural crest in a well-defined sequence of events. This involves the formation of the Schwann cell precursor and immature Schwann cells, followed by the generation of the myelin and nonmyelin (Remak) cells of mature nerves. This review describes the signals that control the embryonic phase of this process and the organogenesis of peripheral nerves.