摘要
Neck injuries caused by traffic accidents increase by years, timely and effective treatment can greatly reduce the mortality rate. This paper summarized the characteristics, image features, evoked potential detection and serum markers detection of neck injury caused by traffic accidents. Then, the condition of injuries was comprehensively considered and analyzed, and the priorities were correctly judged. The injuries were classified and treated. It is conducive for the attending doctors to carry out precise individualized first aid and surgical treatment for the patients, in order to save lives to the maximum extent, reduce disabilities, and prevent and treat post traumatic stress disorders.
摘要
<p><b>OBJECTIVE</b>Radiation is an important cause of delayed wound healing, and there still exist many questions regarding the patterns and mechanisms of wound healing. This study investigated the characteristics of wound healing after varying doses of local radiation and explored possible causes of the delay in healing caused by radiation.</p><p><b>METHODS</b>A full-thickness dorsal longitudinal skin tissue, 2 cm in diameter, was excised after local irradiation on one side of the back of swine, and the other side was wounded as a control. The size of the wound area was recorded every two days after injury. Pathological changes, proliferating cell nuclear antigen (PCNA, immunohisto- chemistry) and apoptosis levels (TUNEL assay) were measured at different time points after wounding.</p><p><b>RESULTS</b>The course of wound healing can be divided into four phases, namely: the arresting phase, the healing priming phase, the fast healing phase, and the healed phase. Although the total wound healing time was closely correlated to the dose of irradiation (R(2) equal to 0.9758), it was more dependent on the length of the arresting phase (R(2) equal to 0.9903) because once the arresting phase ended, the wound healed at a similar speed regardless of radiation doses. Pathological analysis showed that compared with the control side there were more necrotic tissues, slower epithelial crawling, as well as fewer blood vessels and cellular components in the irradiated side at the arresting phase, while other phases revealed no significant difference concerning these measurements. Immunohistochemistry showed that the irradiated wounds had significantly less PCNA-positive and more TUNEL-positive labeling of cells in the arresting phase than in other phases. Moreover, the changes were positively related to the radiation doses, but there was no obvious difference in cell proliferation or apoptosis among the healing priming phase, fast healing phase or healed phase, whether on the control side or on the irradiated side.</p><p><b>CONCLUSIONS</b>After local irradiation, the length of the arresting phase determines the wound healing time. Increased apoptosis and decreased cell proliferation might be an important reason for the formation of the arresting phase.</p>
Subject(s)
Animals , Apoptosis , Cell Proliferation , Skin , Soft Tissue Injuries , Swine , Wound Healing摘要
<p><b>OBJECTIVE</b>To study the association between decreased ligand binding activity of glucocoid receptor (GR) and heat shock protein 90 (Hsp90), the molecular chaperone of GR, after acute lung injury (ALI) in mice.</p><p><b>METHODS</b>In mouse models of oleic acid-induced ALI, the levels of GR, Hsp90 and Hsp70 were dynamically observed using Western blotting, and the binding capacity and binding affinity of GR assessed with radioligand binding assay.</p><p><b>RESULTS</b>After ALI, pulmonary edema was significantly aggravated in the mice with significantly increased lung body index and lung water ratio. GR increased within 1 h after the injury, but then decreased significantly to the lowest level at 12 h after the injury, and the levels of Hsp90 and Hsp70 was increased obviously and reached the highest at 12 h. Radioligand binding assay showed that the Bmax decreased gradually and Kd value increased, and these changes were consistent with the changes of Hsp90/GR.</p><p><b>CONCLUSION</b>The ligand binding activity of GR is related to the changes of Hsp90 after ALI.</p>
Subject(s)
Animals , Female , Male , Mice , Acute Lung Injury , Metabolism , Binding Sites , HSP70 Heat-Shock Proteins , Metabolism , HSP90 Heat-Shock Proteins , Metabolism , Oleic Acid , Radioligand Assay , Random Allocation , Receptors, Glucocorticoid , Metabolism摘要
Recently, activation of the adenosine A2A receptors has been shown to exert protection against peripheral tissue injuries but aggravation in the central nervous system (CNS) injuries. To explore the different effects of adenosine A2A receptors and try to perform some new treatment strategies for peripheral tissue and CNS traumas, we constructed the mouse models of skin trauma, skin combined radiation-impaired wound and traumatic brain injury (TBI), respectively. Wild type mice and A2A receptor gene knockout mice were both used in the experiments. In skin trauma and combined radiation-impaired wound models, the time of wound healing was observed, while in TBI model, neurological deficit scores, water content in injured brain and glutamate concentration in cerebral spinal fluid (CSF) were detected at 24 h after TBI. The results showed that in skin trauma and combined radiation-impaired wound models, CGS21680 (an agonist of the A2A receptors) promoted while A2A receptor gene knockout delayed the course of skin wound healing. On the contrary, in TBI model, A2A receptor gene knockout, not CGS21680, showed a protective role by inhibition of glutamate release. These data further indicate that promoting glutamate release may account for the different effects of A2A receptor activation in CNS injury and peripheral tissue injury models. These findings may provide some experimental evidence and a new strategy for clinical treatment of peripheral tissue damages by agonists of A2A receptors, while treatment of CNS injuries by antagonists of A2A receptors.
Subject(s)
Animals , Mice , Adenosine , Pharmacology , Brain , Pathology , Brain Injuries , Disease Models, Animal , Glutamic Acid , Cerebrospinal Fluid , Mice, Knockout , Phenethylamines , Pharmacology , Receptor, Adenosine A2A , Genetics , Physiology , Wound Healing摘要
<p><b>OBJECTIVE</b>To establish a mice model with selective inactivation adenosine A2A receptors (A2ARs) in peripheral white blood cells (PWBC).</p><p><b>METHODS</b>A2ARs were selectively inactivated in PWBCs by transplanting bone marrow cells (BMCs) from A2AR knockout (KO) mice into their wild type (WT) littermates after a single total body irradiation of 9.5 Gy or fractionated total body irradiation of 6.2 Gy x 2. The efficiency of reconstitution of bone marrow-derived cells in chimeric mice was assessed.</p><p><b>RESULTS</b>PCR band patterns changed from the recipient pattern (one band of 330 bp) to the donor (two bands of 300 and 330 bp) pattern. Immunohistochemistry analysis showed that 10.21% of cells were A2AR+ in PWBCs in KO--> WT mice, whereas 96.72% of cells were A2AR+ in WT mice. The survival rates of mice irradiated with 6.2 Gy x 2 and transplanted with more than 6 x 10(6) BMCs were about 91%.</p><p><b>CONCLUSION</b>A murine model of selective inactivation adenosine A2A receptors in PWBCs was established successfully.</p>