Unlabelled: Traumatic brain injury (TBI) or brain surgery may cause extensive loss of cerebral parenchyma. However, no strategy for reconstruction has been clinically effective. Our previous study had shown that self-assembling peptide nanofiber scaffold (SAPNS) can bridge the injured spinal cord, elicit axon regeneration, and eventually promote locomotor functional recovery. In the present study we investigated the effect of SAPNS for the reconstruction of acutely injured brain. The lesion cavity of the injured cortex was filled with SAPNS or saline immediately after surgically induced TBI, and the rats were killed 2 days, 2 weeks, or 6 weeks after the surgery for histology, immunohistochemistry, and TUNEL studies. Saline treatment in the control animals resulted in a large cavity in the injured brain, whereas no cavity of any significant size was found in the SAPNS-treated animals. Around the lesion site in control animals were many macrophages (ED1 positive) but few TUNEL-positive cells, indicating that the TBI caused secondary tissue loss mainly by means of necrosis, not apoptosis. In the SAPNS-treated animals the graft of SAPNS integrated well with the host tissue with no obvious gaps. Moreover, there were fewer astrocytes (GFAP positive) and macrophages (ED1 positive) around the lesion site in the SAPNS-treated animals than were found in the controls. Thus, SAPNS may help to reconstruct the acutely injured brain and reduce the glial reaction and inflammation in the surrounding brain tissue.
From The Clinical Editor: Self-assembling peptide nanofiber scaffold (SAPNS) was reported earlier to bridge the injured spinal cord, elicit axon regeneration, and promote locomotor recovery. In this study the effect of SAPNS for the reconstruction of acutely injured brain was investigated. In SAPNS-treated animals the graft integrated well with the host tissue with no obvious gaps. SAPNS may help to reconstruct the acutely injured brain and reduced the glial reaction and inflammation in the surrounding brain tissue.
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http://dx.doi.org/10.1016/j.nano.2008.12.001 | DOI Listing |
J Physiol
January 2025
Vascular Physiology Laboratory, Group of Research and Innovation in Vascular Health, Department of Basic Sciences, Faculty of Basic Sciences, Universidad del Bío-Bío, Chillán, Chile.
Ischaemic stroke is a leading cause of death and disability. Circulating extracellular vesicles (EVs) post-stroke may help brain endothelial cells (BECs) counter ischaemic injury. However data on how EVs from ischaemic stroke patients, considering injury severity, affect these cells are limited.
View Article and Find Full Text PDFCureus
December 2024
Department of Rehabilitation, Tokyo University of Technology, Tokyo, JPN.
Introduction: On-road tests are considered the gold standard for evaluating real-world driving skills. However, their reliability and validity remain inadequately established, particularly under varying legal and road conditions across countries.
Aim: This study investigates the discriminant validity of the closed-course version of the Standardized On-Road Assessment for Drivers (SOAD) in Japan.
Neurobiol Pain
December 2024
School of Medical Sciences [Neuroscience], and the Brain & Mind Centre, The University of Sydney, NSW, 2006, Australia.
Chronic neuropathic pain is a debilitating condition that results from damage to the nervous system. Current treatments are largely ineffective, with limited understanding of the underlying mechanisms hindering development of effective treatments. Preclinical models of neuropathic pain have revealed that non-neural changes are important for the development of neuropathic pain, although these data are derived almost exclusively from post-mortem histological analyses.
View Article and Find Full Text PDFStem Cell Res Ther
January 2025
Department of Physiology, University of Seville, Seville, Spain.
Introduction: Neural stem cells from the subventricular zone (SVZ) neurogenic niche provide neurons that integrate in the olfactory bulb circuitry. However, in response to cortical injuries, the neurogenic activity of the SVZ is significantly altered, leading to increased number of neuroblasts with a modified migration pattern that leads cells towards the site of injury. Despite the increased neurogenesis and migration, many newly generated neurons fail to survive or functionally integrate into the cortical circuitry.
View Article and Find Full Text PDFChin Med
January 2025
Yunnan Key Laboratory of Integrated Traditional Chinese and Western Medicine for Chronic Disease in Prevention and Treatment, Key Laboratory of Acupuncture and Massage for Treatment of Encephalopathy, College of Acupuncture, Tuina and Rehabilitation, Yunnan University of Traditional Chinese Medicine, Kunming, China.
Objective: Electroacupuncture has been shown to play a neuroprotective role following ischemic stroke, but the underlying mechanism remains poorly understood. Ferroptosis has been shown to play a key role in the injury process. In the present study, we wanted to explore whether electroacupuncture could inhibit ferroptosis by promoting nuclear factor erythroid-2-related factor 2 (Nrf2) nuclear translocation.
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