Palytoxin evokes reversible spreading depolarization in the locust CNS.

Spreading depolarization (SD) describes the near-complete depolarization of central nervous system (CNS) neural cells as a consequence of chemical, electrical, or metabolic perturbations. It is well established as the central mechanism underlying insect coma and various mammalian neurological dysfunctions. Despite significant progress in our understanding, the question remains: which cation channel, if any, generates SD in the CNS? Previously, we speculated that the sodium-potassium ATPase (NKA) might function as a large-conductance ion channel to initiate SD in insects, potentially mediated by a palytoxin (PLTX)-like endogenous activator.

Association of the COVID-19 pandemic on stroke admissions and treatment globally: a systematic review.

Objectives: The COVID-19 pandemic has highlighted insufficiencies and gaps within healthcare systems globally. In most countries, including high-income countries, healthcare facilities were over-run and occupied with too few resources beyond capacity. We carried out a systematic review with a primary aim to identify the influence of the COVID-19 pandemic on the presentation and treatment of stroke globally in populations≥65 years of age.

Motor patterning, ion regulation and spreading depolarization during CNS shutdown induced by experimental anoxia in Locusta migratoria.

Anoxia induces a reversible coma in insects. Coma onset is triggered by the arrest of mechanisms responsible for maintaining membrane ion homeostasis in the CNS, resulting in a wave of neuronal and glial depolarization known as spreading depolarization (SD). Different methods of anoxia influence the behavioural response but their effects on SD are unknown.

Inhibition of ATP-sensitive potassium channels exacerbates anoxic coma in .

Under extreme environmental conditions, many insects enter a protective coma associated with a spreading depolarization (SD) of neurons and glia in the central nervous system (CNS). Recovery depends on the restoration of ion gradients by mechanisms that are not well understood. We investigated the effects of glybenclamide, an ATP-sensitive K (K) channel inhibitor, and pinacidil, a K activator, on the mechanisms involved in anoxic coma induction and recovery in .

Role of adenosine in functional recovery following anoxic coma in Locusta migratoria.

When exposed to prolonged anoxia insects enter a reversible coma during which neural and muscular systems temporarily shut down. Nervous system shut down is a result of spreading depolarization throughout neurons and glial cells. Upon return to normoxia, recovery occurs following the restoration of ion gradients.

Discussion of "Protocolized warfarin reversal with 4-factor prothrombin complex concentrate versus 3-factor prothrombin complex concentrate with recombinant factor VIIa".

Introduction: Life-threatening bleeding is the most feared complication of warfarin therapy. Rapid anticoagulant reversal via replacement of vitamin K dependent clotting factors is essential for hemostasis.

Methods: A retrospective cohort study of warfarin-treated patients experiencing a life-threatening bleed treated with a warfarin reversal protocol comprised of 4F PCC (post-implementation group) and those who received the prior reversal protocol of 3F PCC and rFVIIa (pre-implementation group) was performed.

Prolonged use of extracorporeal membrane oxygenation as a rescue modality following traumatic brain injury.

A 21-year-old male trauma patient presented after a motor vehicle crash, witnessed massive aspiration and sustained traumatic brain injury. On postinjury day 3, the patient progressed to adult respiratory distress syndrome (ARDS) refractory to all conventional therapies, prompting the use of extracorporeal membrane oxygenation (ECMO). After 5 days of ECMO support and 3 thrombosed oxygenators, systemic anticoagulation was initiated.