Attitude of Jordanians towards a new enactment for an opt-out organ donation system: a cross-sectional study.

BACKGROUND: Organ donation entails saving or transforming lives through the provision of organs, either from living donors or deceased individuals. In Jordan, low donation rates are attributed to religious misconceptions, limited education and insufficient awareness of the burden on patients with organ failure. OBJECTIVES: To investigate the attitudes of the Jordanian population towards the practicality and effectiveness of introducing an opt-out organ donation system through legislative measures, with the aim of increasing donation rates. DESIGN: This cross-sectional study used a designed self-administered questionnaire. Data were subsequently analysed using IBM SPSS software. SETTING: The study encompassed all 12 cities located in Jordan. PARTICIPANTS: Data were collected from 1146 Jordanian participants, excluding individuals under the age of 18. RESULTS: Approximately 36.6% reported organ or blood donation while 18.9% participated in awareness campaigns. Many (75.7%) perceived insufficient awareness about the importance of organ donation, and 67.1% noted a scarcity of online donor registration platforms. Only 12.0% of participants discussed organ donation with healthcare providers. As anticipated, only 9.0% were registered donors while 67.7% expressed acceptance of organ donation, with 55.3% willing to enrol in donor programmes. Religion influenced 54.2% of organ donation decisions. There are associations between agreement for a new enactment and prior organ or blood donation or discussions with healthcare providers. However, religion affected willingness to donate organs. Most importantly, refusal to be a donor after death was associated with religion, occupation and awareness levels. CONCLUSION: Despite the population's understanding and support for the concept of organ donation, the willingness towards donating their own organs is limited. To boost organ donation rates and acceptance of the new enactment, we recommend conducting educational campaigns, improving online registration platforms, enhancing healthcare provider engagement, collaborating with religious communities and advocating for supportive policies.

From spreading depolarization to blood-brain barrier dysfunction: navigating traumatic brain injury for novel diagnosis and therapy.

Considerable strides in medical interventions during the acute phase of traumatic brain injury (TBI) have brought improved overall survival rates. However, following TBI, people often face ongoing, persistent and debilitating long-term complications. Here, we review the recent literature to propose possible mechanisms that lead from TBI to long-term complications, focusing particularly on the involvement of a compromised blood-brain barrier (BBB). We discuss evidence for the role of spreading depolarization as a key pathological mechanism associated with microvascular dysfunction and the transformation of astrocytes to an inflammatory phenotype. Finally, we summarize new predictive and diagnostic biomarkers and explore potential therapeutic targets for treating long-term complications of TBI.

Rodent brain extraction and dissection: A comprehensive approach.

The neuroscience is continuously expanding field, and conducting experiments serves as one of the most effective approaches to enhance and broad our understanding of this fascinating field. Most of the lab work in neuroscience involves the use of animal models such as rats and mice for experiments dedicated to monitoring cerebral changes. The study:•Introduces a practical method for brain extraction without perfusion with paraformaldehyde prioritizing brain integrity and avoiding damage.•Offers a detailed, step-by-step dissection guide for different brain regions, including the hippocampus, cerebral cortex, corpus striatum, thalamus, cerebellum, and medial prefrontal cortex, from rodent brains, accompanied by high-resolution images that provide anatomical clarity.•Presents enhanced reliability, precision, and detailed anatomical descriptions.Conclusion: This study has introduced a reliable technique for brain extraction that eliminates the need for paraformaldehyde perfusion. Furthermore, a comprehensive methodology has been presented for extracting different brain regions from rodent brains.

Mitochondrial dysfunction underlies impaired neurovascular coupling following traumatic brain injury.

Traumatic brain injury (TBI) involves an acute injury (primary damage), which may evolve in the hours to days after impact (secondary damage). Seizures and cortical spreading depolarization (CSD) are metabolically demanding processes that may worsen secondary brain injury. Metabolic stress has been associated with mitochondrial dysfunction, including impaired calcium homeostasis, reduced ATP production, and elevated ROS production. However, the association between mitochondrial impairment and vascular function after TBI is poorly understood. Here, we explored this association using a rodent closed head injury model. CSD is associated with neurobehavioral decline after TBI. Craniotomy was performed to elicit CSD via electrical stimulation or to induce seizures via 4-aminopyridine application. We measured vascular dysfunction following CSDs and seizures in TBI animals using laser doppler flowmetry. We observed a more profound reduction in local cortical blood flow in TBI animals compared to healthy controls. CSD resulted in mitochondrial dysfunction and pathological signs of increased oxidative stress adjacent to the vasculature. We explored these findings further using electron microscopy and found that TBI and CSDs resulted in vascular morphological changes and mitochondrial cristae damage in astrocytes, pericytes and endothelial cells. Overall, we provide evidence that CSDs induce mitochondrial dysfunction, impaired cortical blood flow, and neurobehavioral deficits in the setting of TBI.

Craniotomy for acute monitoring of pial vessels in the rodent brain.

A growing awareness for vascular contribution to pathogenesis of brain diseases increases the need for techniques that allow high-resolution imaging and quantification of changes in function and structure of cerebral microvessels. Cerebral vessels are very sensitive structures, making them vulnerable for injury. In addition, they are uniquely characterized with the blood-brain barrier, and an extra caution is required during procedures that involve engagement of cerebral vessels (i.e., craniotomy). Using state of the art facilities, including 3D intravital microscope, we describe here in details:•The steps and equipment required for drilling a craniotomy and removing of the dura, while keeping brain parenchyma and vessels intact. This enables long duration of live and direct monitoring of pial vessels and imaging of BBB permeability.•We present the craniotomy procedure that relevant and compatible with imaging pial vessels and monitoring the blood-brain barrier in small rodents.

Concussion susceptibility is mediated by spreading depolarization-induced neurovascular dysfunction.

The mechanisms underlying the complications of mild traumatic brain injury, including post-concussion syndrome, post-impact catastrophic death, and delayed neurodegeneration remain poorly understood. This limited pathophysiological understanding has hindered the development of diagnostic and prognostic biomarkers and has prevented the advancement of treatments for the sequelae of mild traumatic brain injury. We aimed to characterize the early electrophysiological and neurovascular alterations following repetitive mild traumatic brain injury and sought to identify new targets for the diagnosis and treatment of individuals at risk of severe post-impact complications. We combined behavioural, electrophysiological, molecular, and neuroimaging techniques in a rodent model of repetitive mild traumatic brain injury. In humans, we used dynamic contrast-enhanced MRI to quantify blood-brain barrier dysfunction after exposure to sport-related concussive mild traumatic brain injury. Rats could clearly be classified based on their susceptibility to neurological complications, including life-threatening outcomes, following repetitive injury. Susceptible animals showed greater neurological complications and had higher levels of blood-brain barrier dysfunction, transforming growth factor ß (TGFß) signalling, and neuroinflammation compared to resilient animals. Cortical spreading depolarizations were the most common electrophysiological events immediately following mild traumatic brain injury and were associated with longer recovery from impact. Triggering cortical spreading depolarizations in mild traumatic brain injured rats (but not in controls) induced blood-brain barrier dysfunction. Treatment with a selective TGFß receptor inhibitor prevented blood-brain barrier opening and reduced injury complications. Consistent with the rodent model, blood-brain barrier dysfunction was found in a subset of human athletes following concussive mild traumatic brain injury. We provide evidence that cortical spreading depolarization, blood-brain barrier dysfunction, and pro-inflammatory TGFß signalling are associated with severe, potentially life-threatening outcomes following repetitive mild traumatic brain injury. Diagnostic-coupled targeting of TGFß signalling may be a novel strategy in treating mild traumatic brain injury.

Brainstem and Cortical Spreading Depolarization in a Closed Head Injury Rat Model.

Traumatic brain injury (TBI) is the leading cause of death in young individuals, and is a major health concern that often leads to long-lasting complications. However, the electrophysiological events that occur immediately after traumatic brain injury, and may underlie impact outcomes, have not been fully elucidated. To investigate the electrophysiological events that immediately follow traumatic brain injury, a weight-drop model of traumatic brain injury was used in rats pre-implanted with epidural and intracerebral electrodes. Electrophysiological (near-direct current) recordings and simultaneous alternating current recordings of brain activity were started within seconds following impact. Cortical spreading depolarization (SD) and SD-induced spreading depression occurred in approximately 50% of mild and severe impacts. SD was recorded within three minutes after injury in either one or both brain hemispheres. Electrographic seizures were rare. While both TBI- and electrically induced SDs resulted in elevated oxidative stress, TBI-exposed brains showed a reduced antioxidant defense. In severe TBI, brainstem SD could be recorded in addition to cortical SD, but this did not lead to the death of the animals. Severe impact, however, led to immediate death in 24% of animals, and was electrocorticographically characterized by non-spreading depression (NSD) of activity followed by terminal SD in both cortex and brainstem.