Reduction of prolonged excitatory neuron swelling after spinal cord injury improves locomotor recovery in mice.

Spinal cord injury (SCI) results in acute damage and triggers secondary injury responses with sustained neuronal loss and dysfunction. However, the underlying mechanisms for these delayed neuronal pathologies are not entirely understood. SCI results in the swelling of spinal neurons, but the contribution of cell swelling to neuronal loss and functional deficits after SCI has not been systematically characterized.

General Anesthesia Blocks Pain-Induced Hemorrhage and Locomotor Deficits After Spinal Cord Injury in Rats.

Research has shown that engaging pain (nociceptive) pathways after spinal cord injury (SCI) aggravates secondary injury and undermines locomotor recovery. This is significant because SCI is commonly accompanied by additional tissue damage (polytrauma) that drives nociceptive activity. Cutting communication with the brain by means of a surgical transection, or pharmacologically transecting the cord by slowly infusing a sodium channel blocker (lidocaine) rostral to a thoracic contusion, blocks pain-induced hemorrhage.

Noxious Stimulation Induces Acute Hemorrhage and Impairs Long-Term Recovery after Spinal Cord Injury (SCI) in Female Rats: Evidence Estrous Cycle May Have a Modulatory Effect.

Spinal cord injuries (SCIs) are often the result of traumatic accidents, which also produce multiple other injuries (polytrauma). Nociceptive input from associated injuries has been shown to significantly impair recovery post-SCI. Historically, work in our laboratory has focused exclusively on male animals; however, increasing incidence of SCI in females requires research to determine whether pain (nociceptive) input poses the same risk to their recovery.

Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?

Pain (nociceptive) input soon after spinal cord injury (SCI) expands the area of tissue loss (secondary injury) and impairs long-term recovery. Evidence suggests that nociceptive stimulation has this effect because it promotes acute hemorrhage. Disrupting communication with the brain blocks this effect.

Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics.

Nociceptive input diminishes recovery and increases lesion area after a spinal cord injury (SCI). Recent work has linked these effects to the expansion of hemorrhage at the site of injury. The current article examines whether these adverse effects are linked to a pain-induced rise in blood pressure (BP) and/or flow.

Myocarditis in SARS-CoV-2 negative patients with suspected preceding infection.

SARS-CoV-2 is primarily a respiratory disease; however, there have been multiple reports of associated myocarditis. In our 463 bedded, district general hospital, we noted an influx of young patients with myocarditis shortly after the peak of the outbreak. We report two cases presenting with myocarditis, both of whom tested negative for the virus despite clinical and biochemical evidence of recent infection.

Pharmacological Transection of Brain-Spinal Cord Communication Blocks Pain-Induced Hemorrhage and Locomotor Deficits after Spinal Cord Injury in Rats.

Spinal cord injury (SCI) is often accompanied by additional tissue damage (polytrauma), which engages pain (nociceptive) fibers. Prior research has shown that nociceptive input can increase cell death, expand the area of hemorrhage, and impair long-term recovery. The current study shows that these adverse effects can be blocked by the sodium channel blocker lidocaine applied rostral to a contusion injury.

Learning to promote recovery after spinal cord injury.

The present review explores the concept of learning within the context of neurorehabilitation after spinal cord injury (SCI). The aim of physical therapy and neurorehabilitation is to bring about a lasting change in function-to encourage learning. Traditionally, it was assumed that the adult spinal cord is hardwired-immutable and incapable of learning.

A brief period of moderate noxious stimulation induces hemorrhage and impairs locomotor recovery after spinal cord injury.

Spinal cord injury (SCI) is often accompanied by additional tissue damage (polytrauma) that provides a source of pain input. Our studies suggest that this pain input may be detrimental to long-term recovery. In a rodent model, we have shown that engaging pain (nociceptive) fibers caudal to a lower thoracic contusion SCI impairs recovery of locomotor function and increases tissue loss (secondary injury) and hemorrhage at the site of injury.

Brain-Dependent Processes Fuel Pain-Induced Hemorrhage After Spinal Cord Injury.

Pain (nociceptive) input caudal to a spinal contusion injury can undermine long-term recovery and increase tissue loss (secondary injury). Prior work suggests that nociceptive stimulation has this effect because it fosters the breakdown of the blood-spinal cord barrier (BSCB) at the site of injury, allowing blood to infiltrate the tissue. The present study examined whether these effects impact tissue rostral and caudal to the site of injury.

Engaging pain fibers after a spinal cord injury fosters hemorrhage and expands the area of secondary injury.

In humans, spinal cord injury (SCI) is often accompanied by additional tissue damage (polytrauma) that can engage pain (nociceptive) fibers. Prior work has shown that this nociceptive input can expand the area of tissue damage (secondary injury), undermine behavioral recovery, and enhance the development of chronic pain. Here, it is shown that nociceptive input given a day after a lower thoracic contusion injury in rats enhances the infiltration of red blood cells at the site of injury, producing an area of hemorrhage that expands secondary injury.

Pain Input After Spinal Cord Injury (SCI) Undermines Long-Term Recovery and Engages Signal Pathways That Promote Cell Death.

Pain (nociceptive) input caudal to a spinal contusion injury increases tissue loss and impairs long-term recovery. It was hypothesized that noxious stimulation has this effect because it engages unmyelinated pain (C) fibers that produce a state of over-excitation in central pathways. The present article explored this issue by assessing the effect of capsaicin, which activates C-fibers that express the transient receptor potential vanilloid receptor-1 (TRPV1).

Carer-related research and knowledge: Findings from a scoping review.

The review discussed in this paper provides a unique synthesis of evidence and knowledge about carers. The authors adopted a scoping review methodology drawing on a wide range of material from many different sources published between 2000 and 2016. It offers key insights into what we know and how we know it; reinforces and expands evidence about carers' profile; shows knowledge is uneven, e.

Plastome sequences and exploration of tree-space help to resolve the phylogeny of riceflowers (Thymelaeaceae: Pimelea).

Data sets comprising small numbers of genetic markers are not always able to resolve phylogenetic relationships. This has frequently been the case in molecular systematic studies of plants, with many analyses being based on sequence data from only two or three chloroplast genes. An example of this comes from the riceflowers Pimelea Banks & Sol.

Men's health and communities of practice in Australia.

Purpose The purpose of this paper is to examine the social opportunities for Aboriginal and Torres Strait Islander men created through Men's Groups/Sheds across urban, regional and remote areas of Australia. Men's Sheds are a safe space, resembling a work-shop setting or backyard shed, where men are encouraged to socialise and participate in health promotion, informal learning and engage in meaningful tasks both individually and at the community level. Design/methodology/approach Explore five case study sites through Wenger's (1998) active communities of practice (CoP).

Molecular systematics and biogeography of Logania R.Br. (Loganiaceae).

The angiosperm genus Logania R.Br. (Loganiaceae) is endemic to the mainland of Australia.

A molecular phylogeny of the Lepidozia generic complex supports re-circumscription of the Lepidozioideae.

Five molecular markers (chloroplast rbcL and trnL-trnF, mitochondrial nad5-nad4, and nuclear ITS1 and ITS2) were used to investigate membership of the Lepidoziaceae, subfamily Lepidozioideae and relationships between its constituent species. The Lepidozioideae (comprising Lepidozia, Telaranea, Kurzia, Sprucella, Psiloclada) are polyphyletic as are two of its five constituent genera (Telaranea and Kurzia). We find strong support for a monophyletic lineage comprising Lepidozia, Sprucella (nested within Lepidozia), and part of Telaranea.

Disorders of sex development-when and how to tell the patient.

Physicians and other providers are often confronted with difficult decisions in the area of disclosure. This article examines a hypothetical situation relevant to the practice of pediatric endocrinology. The parents of a child with a disorder of sex development (DSD) wish the physician to treat their child, but without revealing key medical information to the child.

A multi-locus molecular phylogeny of the Lepidoziaceae: laying the foundations for a stable classification.

The Lepidoziaceae, with over 700 species in 30 genera, is one of the largest leafy liverwort families. Despite receiving considerable attention, the composition of subfamilies and genera remains unsatisfactorily resolved. In this study, 10 loci (one nuclear 26S, two mitochondrial nad1 and rps3, and seven chloroplast atpB, psbA, psbT-psbH, rbcL, rps4, trnG and trnL-trnF) are used to estimate the phylogeny of 93 species of Lepidoziaceae.

Update on pediatric bone health.

Osteoporosis has long been considered a health problem unique to older adults. Children and adolescents with chronic illness, primary bone disease, or poor nutrition, however, are also predisposed to impaired skeletal health. The present review discusses normal skeletal development, risk factors for low bone mineral density, and prevention and treatment strategies that can help optimize bone health in the pediatric population.

Pediatric dual-energy X-ray absorptiometry: technique, interpretation, and clinical applications.

This article reviews the dual-energy x-ray absorptiometry (DXA) technique, its interpretation, and clinical applications with emphasis on the considerations unique to pediatrics. Specifically, the use of DXA in children requires the radiologist to be a "clinical pathologist," monitoring the technical aspects of the DXA acquisition, a "statistician" knowledgeable in the concepts of Z-scores and least significant changes, and a "bone specialist," aware of the DXA findings in a large number of clinical diseases, providing the referring clinician with a meaningful context for the numeric result obtained with DXA.

Pediatric DXA: clinical applications.

Normal bone mineral accrual requires adequate dietary intake of calcium, vitamin D and other nutrients; hepatic and renal activation of vitamin D; normal hormone levels (thyroid, parathyroid, reproductive and growth hormones); and neuromuscular functioning with sufficient stress upon the skeleton to induce bone deposition. The presence of genetic or acquired diseases and the therapies that are used to treat them can also impact bone health. Since the introduction of clinical DXA in pediatrics in the early 1990s, there has been considerable investigation into the causes of low bone mineral density (BMD) in children.