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At least 1,783 records · Page 99Linked to original sources
PubMed2003

Role of the bcl-2 gene after contusive spinal cord injury in mice.

OBJECTIVE: Apoptosis is indicated to have an important role in the secondary injury mechanisms of acute spinal cord injury (SCI). The proto-oncogene bcl-2 has been demonstrated to prevent apoptotic cell death in a wide variety of cell types. This study examined the recovery of behavioral function and histopathological variables after controlled-impact SCI in human bcl-2 transgenic (TG) mice and control mice. METHODS: Six bcl-2 TG mice and five control mice were subjected to controlled-impact SCI of moderate severity at T10, with the use of a pneumatic impact device (0.25-mm-deep deformation; impact velocity, 2 m/s). Functional deficits were evaluated at times up to 28 days after SCI, with assessments of hindlimb reflexes and coordinated motor function. The extents of the lesions were histopathologically analyzed and quantified with morphometric measurements. RESULTS: Both control and bcl-2 TG mice exhibited profound deficits immediately after injury, with subsequent gradual symptomatic recovery. The mean functional scores for the control mice were lower than those for the bcl-2 TG mice, although the Mann-Whitney U test revealed no significant differences. The mean lesion volume for the bcl-2 TG mice (mean +/- standard deviation, 2.9 +/- 1.1 x 10(-2) mm(3)) was significantly lower than that for the control mice (5.1 +/- 0.8 x 10(-2) mm(3); unpaired t test, P = 0.0101). Immunohistological analysis of the spinal cords from the bcl-2 TG mice revealed marked expression of Bcl-2 at the injury site and in adjacent regions. CONCLUSION: Our results suggest that overexpression of the bcl-2 gene may play a protective role in neuropathological sequelae after SCI.

Animals↗
PubMed2005

Reduced neuronal injury after treatment with NG-nitro-L-arginine methyl ester (L-NAME) or 2-sulfo-phenyl-N-tert-butyl nitrone (S-PBN) following experimental brain contusion.

OBJECTIVE: Nitric oxide (NO) and oxygen free radicals are implicated in the pathophysiology of traumatic brain injury (TBI). Peroxynitrite formation from NO and superoxide contributes to secondary neuronal injury but the neuroprotective effects of nitric oxide synthase (NOS)-inhibitors have been contradictory. This study was undertaken to examine whether PTtic administration of the (NOS)-inhibitor N-nitro-l-arginine methyl ester (L-NAME), and a combination of L-NAME and the nitrone radical scavenger 2-sulfo-phenyl-N-tert-butyl nitrone (S-PBN) favorable affects neuronal injury in a model of TBI. METHODS: A weight-drop model of TBI was used. The animals received L-NAME, S-PBN or a combination of the drugs 15 minutes prothrombin time (PT) and sacrificed after 24 hours or six days. NOS activity was measured by the conversion of L-[U-C]arginine to L-[U-C]citrulline. Peroxynitrite formation, cellular apoptosis, neuronal degeneration and survival were assessed by nitrotyrosine-, TUNEL-, Fluoro-Jade- and NeuN-stainings. RESULTS: eNOS and nNOS activity was significantly reduced in animals that received L-NAME alone or the combination with S-PBN. iNOS activity or iNOS immunoreactivity was not affected. All treatments significantly reduced neuronal degeneration and nitrotyrosine immunoreactivity at 24 hours and increased neuronal survival at six days PT. No differences were detected between L-NAME and L-NAME + S-PBN groups. CONCLUSION: NO from NOS contributes to secondary neuronal injury in this TBI-model. PTtic treatment does not inhibit early beneficial NO-related effects. L-NAME and S-PBN limit peroxynitrite formation, promoting neuronal survival. The combination of L-NAME and S-PBN was neuroprotective; surprisingly no additive effects were found on nitrotyrosine formation, apoptosis or neuronal survival.

Animals↗
PubMed2005

A mapping study of caspase-3 activation following acute spinal cord contusion in rats.

Spinal cord injury (SCI) initiates a cascade of biochemical changes that results in necrotic and apoptotic cell death. There is evidence that caspase-3 activation and apoptotic cell death occur within hours after SCI. However, the time course and cellular localization of activated caspase-3 has not been examined. Such information is essential because caspase-3-independent apoptotic pathways do exist. In this experiment, we describe the distribution of and cell types containing activated caspase-3 at 4 hr, 1 day, 2 days, 4 days, and 8 days following SCI in rats. Numerous caspase-3-positive cells were observed at 4 hr and 1 day postinjury and colocalized most often with CC1, a marker for oligodendroglia. Both markers disappeared near the injury epicenter over the next several days. Activated caspase-3 was again present in the injured spinal cord on postoperative day 8, which coincided with a reemergence of CC1-positive cells. Many of these CC1-positive cells again colocalized activated caspase-3. NeuN-positive neurons of the dorsal horn were occasionally immunopositive for activated caspase-3 at early time points. OX42-positive microglia/macrophages rarely contained activated caspase-3. The results indicate a biphasic pattern of caspase-3 activation during the first 8 days postinjury, suggesting that at least two mechanisms activate caspase-3 following SCI. This time-course study provides a framework for investigating and understanding the different signaling events contributing to this biphasic pattern of caspase-3 activation.

Acute Disease↗
PubMed2005

Role of granulocyte-macrophage colony-stimulating factor in preventing apoptosis and improving functional outcome in experimental spinal cord contusion injury.

OBJECT: Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a potent hemopoietic cytokine that stimulates stem cell proliferation in the bone marrow and inhibits apoptotic cell death in leukocytes. Its effects in the central nervous system, however, are still unclear. The present study was undertaken to determine if GM-CSF can rescue neuronal cells from apoptosis and improve neurological function in a spinal cord injury (SCI) model. METHODS: To study the effect of GM-CSF on apoptotic neuronal death, the authors used a staurosporine-induced neuronal death model in an N2A cell line (in vitro) and in a rat SCI model (in vivo). The N2A cells were preincubated with GM-CSF for 60 minutes before being exposed to staurosporine for 24 hours. To inhibit GM-CSF, N2A cells were pretreated with antibodies against the GM-CSF receptor for 60 minutes. Clip compression was,used to induce SCI. Animals were treated with daily doses of GM-CSF (20 microg/day) for 5 days. The number of apoptotic cells in the spinal cord and neurological improvements were assessed. Pretreatment with GM-CSF was found to protect N2A cells significantly from apoptosis, and neutralizing antibodies for the GM-CSF receptors inhibited the rescuing effect of GM-CSF on apoptosis. In the rat SCI model, neurological function improved significantly in the GM-CSF-treated group compared with controls treated with phosphate-buffered saline. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling staining showed that GM-CSF administration reduced apoptosis in the injured spinal cord. CONCLUSIONS: Treatment of SCI with GM-CSF showed beneficial effects. Neuronal protection against apoptosis is viewed as a likely mechanism underlying the therapeutic effect of GM-CSF in SCI.

Animals↗
PubMed1976

[Perimetric diagnosis of chiasmal injury after contusion of skull and brain (author's transl)].

After a discussion of the pathomechanism of skull trauma by a blow leading to chiasmal lesion, frontobasal injuries of the skull are considered; it is shown that typical defects of the visual field resulting from chiasmal damage can be revealed not only in cases of serious industrial or traffic accidents with brain concussion and skull base fracture, but also following minor injuries without unconsciousness and radiologically visible bone fractures.

Adolescent↗
PubMed1976

[Laryngeo-tracheal contusion caused by a seat belt].

The authors report cases of laryngo-tracheal rupture due to seat belts. They analyse the mechanisms, the clinical and radiological signs of these lesions. Although these lesions are rare, they should be recognised by medical teams when called to treat injured patients. It is, in fact, at this level that emergency treatment must be carried out, although difficult, this alone permits one to save a certain number of injured patients from asphyxia.

Adult↗
PubMedDate not supplied

[Bronchial stenosis secondary to severe thoracic contusion. Comment on 2 cases].

Two cases with complete bronchial stenosis of the mainstem bronchus secondary to thoracic blunt trauma are presented. One patient had hemoneumothorax on the left side, the other one had bilateral hemothorax. Both were initially treated with drainage by thoracostomy tube with partial resolution of the thoracic bloody pleural collection. Later, the two patients developed complete atelectasis of the lung, one on the left side and the other one in the right; this later case was subject to lung decortication. The fiberopticbronchoscopy showed a complete occlusion of the mainstem bronchus in both patients. A bronchoplasty with sleeve resection of the stenotic segment was performed; the lumen of the bronchus was preserved by an end-to-end suture with separate stitchs of Vycryl 0000. Both cases remain without bronchopulmonary pathology after 4 years of follow-up of bronchoplasty. In cases of blunt thoracic trauma, it is important to consider the possibility of bronchial rupture. The importance of bronchoscopic diagnosis and surgical treatment is stressed.

Accidents, Traffic↗