Research progress on mechanism of traumatic brain injury promoting fracture healing / 中国修复重建外科杂志

OBJECTIVE@#To summarize the research progress on the mechanism related to traumatic brain injury (TBI) to promote fracture healing, and to provide theoretical basis for clinical treatment of fracture non-union.@*METHODS@#The research literature on TBI to promote fracture healing at home and abroad was reviewed, the role of TBI in fracture healing was summarized from three aspects of nerves, body fluids, and immunity, to explore new ideas for the treatment of fracture non-union.@*RESULTS@#Numerous studies have shown that fracture healing is faster in patients with fracture combined with TBI than in patients with simple fracture. It is found that the expression of various cytokines and hormones in the body fluids of patients with fracture and TBI is significantly higher than that of patients with simple fracture, and the neurofactors released by the nervous system reaches the fracture site through the damaged blood-brain barrier, and the chemotaxis and aggregation of inflammatory cells and inflammatory factors at the fracture end of patients with combined TBI also differs significantly from those of patients with simple fracture. A complex network of humoral, neural, and immunomodulatory networks together promote regeneration of blood vessels at the fracture site, osteoblasts differentiation, and inhibition of osteoclasts activity.@*CONCLUSION@#TBI promotes fracture healing through a complex network of neural, humoral, and immunomodulatory, and can treat fracture non-union by intervening in the perifracture microenvironment.

Induction of brain injury and depression in rats by chronic unpredictable stress associated with the augmentation of nitrosative stress and apoptosis / Inducción de lesión cerebral y depresión en ratas por estrés crónico impredecible asociado con el aumento del estrés nitrosativo y la apoptosis

SUMMARY: Repeated stress is a risk factor for memory impairment and neurological abnormalities in both humans and animals. We sought to investigate the extent of (i) brain tissue injury; (ii) nitrosative and oxidative stress in brain tissue homogenates; (iii) apoptotic and survival biomarkers in brain tissue homogenates; and (iv) immobility and climbing abilities, induced over a period of three weeks by chronic unpredictable stress (CUS). Wistar rats were either left untreated (Control group) or exposed to a variety of unpredictable stressors daily before being sacrificed after 3 weeks (model group). Assessment of depression-like behavior was performed and animals were then culled and harvested brain tissues were stained with basic histological staining and examined under light microscopy. In addition, brain tissue homogenates were prepared and assayed for these parameters; inducible nitric oxide synthase (iNOS), malondialdehyde (MDA), superoxide dismutase (SOD), caspase-3, and B-cell lymphoma 2 (Bcl-2). Histology images showed CUS induced profound damage to the cerebral cortex as demonstrated by severe neuronal damage with shrunken cells, disrupted atrophic nuclei, perineuronal vacuolation and swollen glial cells. CUS also significantly (p<0.05) induced iNOS, MDA, and caspase-3, whereas SOD and Bcl-2 brain tissue levels were inhibited by CUS. In addition, data from the depression-like behavior, forced swimming test showed significant (p<0.05) increase in animal immobility and decrease in climbing ability in the model group of rats. Thus, here we demonstrated a reliable rat model of chronic stress-induced brain injury, which can further be used to investigate beneficial drugs or agents used for a period of three weeks to protect against CUS-induced brain damage.

RESUMEN: El estrés crónico es un factor de riesgo para el deterioro de la memoria y las anomalías neurológicas tanto en humanos como en animales. Intentamos investigar el alcance de lesión del tejido cerebral; (ii) estrés nitrosativo y oxidativo en homogeneizados de tejido cerebral; (iii) biomarcadores apoptóticos y de supervivencia en homogeneizados de tejido cerebral; y (iv) inmovilidad y habilidades de escalada, inducidas durante un período de tres semanas por estrés crónico impredecible (ECI). Se dejaron sin tratamiento (grupo control) ratas Wistar, o se expusieron a una variedad de factores estresantes impredecibles diariamente antes de ser sacrificadas después de 3 semanas (grupo modelo). Se realizó una evaluación del comportamiento similar a la depresión y luego se sacrificaron los animales y se tiñeron los tejidos cerebrales con tinción histológica básica y se examinaron con microscopía óptica. Además, se prepararon homogeneizados de tejido cerebral y se analizaron los siguientes parámetros; óxido nítrico sintasa inducible (iNOS), malondialdehído (MDA), superóxido dismutasa (SOD), caspasa- 3 y linfoma de células B 2 (Bcl-2). Las imágenes histológicas mostraron que el CUS indujo un daño profundo en la corteza cerebral como lo demuestra el daño neuronal severo con células encogidas, núcleos atróficos alterados, vacuolación perineuronal y células gliales inflamadas. ECI también indujo significativamente (p <0,05) iNOS, MDA y caspase-3, mientras que los niveles de tejido cerebral SOD y Bcl-2 fueron inhibidos por ECI. Además, los datos del comportamiento similar a la de- presión, la prueba de natación forzada mostró un aumento significativo (p <0,05) en la inmovilidad animal y una disminución en la capacidad de escalada en el grupo modelo de ratas. Por lo tanto, aquí demostramos un modelo confiable de daño cerebral crónico en rata inducido por el estrés, que se puede utilizar para investigar medicamentos o agentes beneficiosos usados durante un período de tres semanas para proteger el daño cerebral inducido por ECI.

Relations of neuropeptide Y and heme oxygenase-1 expressions with fetal brain injury in rats with intrahepatic cholestasis of pregnancy

Abstract Purpose: To investigate the relations of neuropeptide Y (NPY) and heme oxygenase-1 (HO-1) expressions with fetal brain injury in rats with intrahepatic cholestasis of pregnancy (ICP). Methods: Sixty rats pregnant for 15 days were randomly divided into experimental and control groups. The ICP model was established in experimental group. On the 21st day, the blood biochemical test, histopathological examination of pregnant rat liver and fetal brain tissues and immunohistochemical analysis of fetal rat brain tissues were performed. Results: On the 21st day, the alanineaminotransferase, aspartate aminotransferase and total bile acid levels in experimental group were significantly higher than control group (P<0.01). Compared with control group, there was obvious vacuolar degeneration in pregnant rat liver tissue and fetal brain tissue in experimental group. NPY expression in fetal brain tissue was negative in control group and positive in experimental group. HO-1 expression in fetal brain tissue was strongly positive in control group and positive in experimental group. There was significant difference of immunohistochemical staining optical density between two groups (P<0.01). Conclusion: In fetal brain of ICP rats, the NPY expression is increased, and the HO-1 expression is decreased, which may be related to the fetal brain injury.

Thymoquinone reverses learning and memory impairments and brain tissue oxidative damage in hypothyroid juvenile rats / Timoquinona protegeu contra deficiências de aprendizagem e memória e danos nos tecidos cerebrais em ratos hipotireoidais juvenis

ABSTRACT In this study, the effect of thymoquinone (TQ) on propylthiouracil (PTU)-induced memory impairment was investigated in juvenile rats. The rats were grouped into control, Hypo, Hypo-TQ5 and Hypo-TQ10. Propylthiouracil increased latency time in the Morris water maze test and decreased delay in entering the dark compartment in the passive avoidance test. Both 5 mg/kg and 10 mg/kg doses of TQ decreased latency time in the Morris water maze test and increased delay in entering the dark compartment in a passive avoidance test. The PTU also increased malondialdehyde and nitric oxide metabolites in the brain while reduced the thiol content and superoxide dismutase and catalase activities and serum T4 level. Both doses of TQ decreased malondialdehyde and nitric oxide metabolites in the brain while enhanced the thiol content and superoxide dismutase and catalase activities and serum T4 level. The results of the present study showed that TQ protected against PTU-induced memory impairments in rats.

RESUMO Neste estudo, foi investigado o efeito da timoquinona (TQ) contra deficiências de memória induzidas por propiltiouracilo (PTU) em ratos juvenis. Os ratos foram agrupados em grupos: controle, Hypo, Hypo-TQ5, e Hypo-TQ10. O PTU aumentou o tempo de latência no teste do labirinto aquático de Morris (MWM) e diminuiu o atraso para entrar no compartimento escuro no teste de evasão passiva (PA). Ambas as doses de TQ diminuíram o tempo de latência no teste de MWM e aumentaram o atraso para entrar no compartimento escuro no teste de PA. O PTU também aumentou os metabolitos de malondialdeído (MDA) e óxido nítrico (NO) no cérebro, enquanto reduziu o teor de tiol e as atividades de superóxido dismutasa (SOD) e catalasa (CAT) e o nível sérico de T4. Ambas as doses de TQ diminuíram os metabolitos de MDA e de NO no cérebro, aumentaram o conteúdo de tiol e as atividades de SOD e CAT e o nível de T4 no soro. Os resultados do presente estudo mostraram que a TQ protegeu contra deficiências de memória induzidas por PTU em ratos.

Expression of Aquaporin 4 in Diffuse Brain Injury of Rats / 法医学杂志

OBJECTIVE@#To observe the expression of aquaporin 4 (AQP4) in diffuse brain injury (DBI) of rats and to explore the corresponding effect of AQP4 for brain edema.@*METHODS@#The rat model of DBI was established using Marmarou's impact-compression trauma model. Brain water content was measured by dry-wet weight method. Blood-brain barrier permeability was evaluated by Evans blue (EB) staining. Immunohistochemical method was used to observe the expression of AQP4.@*RESULTS@#Brain water content increased after 3 h and peaked at 24 h after DBI. Brain EB content significantly increased and peaked at 12 h after DBI. The expression of AQP4 significantly increased after 3 h and peaked at 24 h after DBI, and the number of AQP4 positive astrocytes increased.@*CONCLUSION@#The increment of the permeability of blood-brain barrier and the expression of AQP4 may contribute to the development of brain edema in rat DBI. The change of AQP4 expression in astrocytes may also contribute to determine DBI.

Effect of volume replacement during combined experimental hemorrhagic shock and traumatic brain injury in prostanoids, brain pathology and pupil status / Efeito da reposição volêmica durante o choque hemorrágico combinado com traumatismo craniencefálico sobre prostanóides, patologia cerebral e status pupilar

Traumatic brain injury (TBI) is the main cause of trauma-related deaths. Systemic hypotension and intracranial hypertension causes cerebral ischemia by altering metabolism of prostanoids. We describe prostanoid, pupilar and pathological response during resuscitation with hypertonic saline solution (HSS) in TBI. Method Fifteen dogs were randomized in three groups according to resuscitation after TBI (control group; lactated Ringer’s (LR) group and HSS group), with measurement of thromboxane, prostaglandin, macroscopic and microscopic pathological evaluation and pupil evaluation.Result Concentration of prostaglandin is greater in the cerebral venous blood than in plasma and the opposite happens with concentration of thromboxane. Pathology revealed edema in groups with the exception of group treated with HSS.Discussion and conclusion There is a balance between the concentrations of prostaglandin and thromboxane. HSS prevented the formation of cerebral edema macroscopically detectable. Pupillary reversal occurred earlier in HSS group than in LR group.

O traumatismo cranioencefálico (TCE) é a principal causa de morte relacionada ao trauma. O choque hemorrágico e hipertensão intracraniana causam isquemia cerebral alterando o metabolismo de prostanóides. Neste estudo, relatamos o comportamento dos prostanóides, resposta pupilar e patologia durante a reposição volêmica com solução salina hipertônica (SSH) no TCE. Método Quinze cachorros foram randomizados em três grupos (controle, grupo de Ringer lactato e grupo de SSH) e foram avaliados tromboxane, prostaglandina, avaliação patológica macroscópica e microscópica e status pupilar.Resultado A concentração de prostaglandina é maior no sangue cerebral em comparação ao plasma, e o inverso ocorre com o tromboxane. A patologia revelou edema em todos os grupos, com exceção do grupo tratado com SSH.Discussão e conclusão Existe um equilíbrio entre concentrações cerebrais e plasmáticas de prostaglandina e tromboxane. A SSH protegeu o cérebro da formação de edema pós traumático.

Proteomics analysis after traumatic brain injury in rats: the search for potential biomarkers / Análise proteômica após lesão cerebral traumática em ratos: a busca por biomarcadores

Many studies of protein expression after traumatic brain injury (TBI) have identified biomarkers for diagnosing or determining the prognosis of TBI. In this study, we searched for additional protein markers of TBI using a fluid perfusion impact device to model TBI in S-D rats. Two-dimensional gel electrophoresis and mass spectrometry were used to identify differentially expressed proteins. After proteomic analysis, we detected 405 and 371 protein spots within a pH range of 3-10 from sham-treated and contused brain cortex, respectively. Eighty protein spots were differentially expressed in the two groups and 20 of these proteins were identified. This study validated the established biomarkers of TBI and identified potential biomarkers that could be examined in future work.

Muitos estudos de expressão proteica após lesão cerebral traumática (LCT) identificam biomarcadores para determinação diagnóstica ou prognóstica do LCT. No presente estudo, foram investigados marcadores proteicos adicionais de LCT, através de um aparelho de impacto no fluxo e perfusão em ratos S-D. Eletroforese bidimensional em gel e espectrometria de massa foram utilizadas para identificar diferentes proteínas expressas. Após a análise proteômica, detectamos marcas de proteínas 405 e 371, com pH variando entre 3-10 no córtex de ratos sham e naqueles com contusão cerebral, respectivamente. Oitenta marcas proteicas foram expressas nos dois grupos e 20 destas proteínas foram identificadas. Este estudo validou o estabelecimento de biomarcadores de LCT e identificou potencial biomarcadores que poderão ser estudados em estudos futuros.

Expression of p35 and p25 after Focal Cerebral Contusion in Rat / 法医学杂志

OBJECTIVE@#To study the expression of p35 and p25 in rat after focal cerebral contusion and to provide experimental data for estimating brain injury time.@*METHODS@#Fifty adult male SD rats were randomly divided into 0 h, 6 h, 12 h, 24 h, 3 d, 5 d, 7 d, 10 d after focal cerebral contusion, control and sham-operated groups (5 rats each group). The focal cerebral contusion rat model was established. The expression of p35 and p25 protein of the damage peripheral zone in brain were detected by HE staining, immunohistochemistry and Western blotting at different injury time.@*RESULTS@#A large number of p35 protein and a small amount of p25 protein were expressed in control group and sham-operated group. After focal cerebral contusion, p35 presented unimodal change with time and p25 presented bimodal changes with time.@*CONCLUSION@#Expression of p35 and p25 showed different regularity with good time correlation, which could help to estimate the brain injury time.

Expression of S100B and GFAP after primary brainstem injury in rat / 法医学杂志

OBJECTIVE@#To study the expression of S100B and glial tibrillory acidic protein (GFAP) atter primary brainstem injury in rat and discuss the changes with brainstern injury time and their mechanism in the injury.@*METHODS@#The brainstem injury animal model was established using the mechanical impacting method. The HE staining, Gless argentaffin staining and SP immunohistochemical method were applied to observe the changes of S100B and GFAP at different injury time. The immunostaining results were measured statistically with imaging analysis technology.@*RESULTS@#A large number of S100B positive cells could be seen in 30 min. Afterward, expression increased gradually with time and peaked up in 24 h, and reversed back the normal in 72h. The GFAP positive cells showed rise continually in 30 min, and reached the peak in 48 h, then started to decrease, but still higher than that in control.@*CONCLUSION@#The expression of S100B and GFAP is correlated with post traumatic intervals after brainstem injury in rat, and may be useful in estimation post traumatic intervals and nerve regeneration.

Mesenteric lymph reperfusion after superior mesenteric artery occlusion shock exacerbates endotoxin translocation in brain

PURPOSE: To determine the role of mesenteric lymph reperfusion (MLR) on endotoxin translocation in brain to discuss the mechanism of brain injury subjected to superior mesenteric artery occlusion (SMAO) shock. METHODS: Twenty-four rats were randomly assigned to MLR, SMAO, MLR+SMAO and sham groups. MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h and then allowing reperfusion for 2 h in the MLR group; SMAO involved clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h in the SMAO group; occlusion of both the SMA and MLD for 1 h was followed by reperfusion for 2 h in the MLR+SMAO group rats. RESULTS: SMAO shock induced severe increased levels of the endotoxin, lipopolysaccharide receptor, lipopolysaccharide-binding protein, intercellular adhesion molecule-1 and tumor necrosis factor-α. Concurrently, MLR after SMAO shock further aggravates these deleterious effects. CONCLUSION: Mesenteric lymph reperfusion exacerbated the endotoxin translocation in brain; thereby increased inflammatory response occurred, suggesting that the intestinal lymph pathway plays an important role in the brain injury after superior mesenteric artery occlusion shock. .

Expression of CaMK II delta in cerebral cortex following traumatic brain injury / 法医学杂志

OBJECTIVE@#To observe the time-course expression of calcium-calmodulin dependent protein kinase II delta (CaMK II delta) in cerebral cortex after traumatic brain injury (TBI).@*METHODS@#The TBI rat model was established. The expression of CaMK II delta in cerebral cortex around injured area was tested by Western blotting and immunohistochemical staining.@*RESULTS@#Western blotting revealed expression of CaMK II delta in normal rat brain cortex. It gradually increased after TBI, peaked after 3 days, and then returned to normal level. The result of immunohistochemical staining was consistent with that of Western blotting.@*CONCLUSION@#The expression of CaMK II delta around injured area after TBI increased initially and then decreased. It could be used as a new indicator for wound age determination following TBI.

Cerebral hemodynamics: concepts of clinical importance / Hemodinâmica encefálica: conceitos de importância clínica

Cerebral hemodynamics and metabolism are frequently impaired in a wide range of neurological diseases, including traumatic brain injury and stroke, with several pathophysiological mechanisms of injury. The resultant uncoupling of cerebral blood flow and metabolism can trigger secondary brain lesions, particularly in early phases, consequently worsening the patient's outcome. Cerebral blood flow regulation is influenced by blood gas content, blood viscosity, body temperature, cardiac output, altitude, cerebrovascular autoregulation, and neurovascular coupling, mediated by chemical agents such as nitric oxide (NO), carbon monoxide (CO), eicosanoid products, oxygen-derived free radicals, endothelins, K+, H+, and adenosine. A better understanding of these factors is valuable for the management of neurocritical care patients. The assessment of both cerebral hemodynamics and metabolism in the acute phase of neurocritical care conditions may contribute to a more effective planning of therapeutic strategies for reducing secondary brain lesions. In this review, the authors have discussed concepts of cerebral hemodynamics, considering aspects of clinical importance.

Alterações hemodinâmicas e metabólicas do encéfalo ocorrem frequentemente em diversas doenças neurológicas, principalmente em condições de traumatismo cranioencefálico e acidente vascular encefálico, com vários mecanismos patofisiológicos lesionais. O desacoplamento resultante do fluxo sanguíneo e do metabolismo encefálico pode resultar em lesões encefálicas secundárias, principalmente nas primeiras fases, e, consequentemente, no agravamento do desfecho neurológico dos pacientes. Diversos fatores influenciam o fluxo sanguíneo encefálico, entre eles, a concentração sanguínea de gases, viscosidade sanguínea, temperatura corpórea, débito cardíaco, altitude, autorregulação cerebrovascular e acoplamento neurovascular, que é mediado por óxido nítrico (ON), monóxido de carbono (CO), eicosanoides, radicais livres derivados do oxigênio, endotelinas, potássio, íons hidrogênio e adenosinas. Melhor compreensão destes fatores é fundamental para o manejo clínico dos pacientes neurológicos críticos. A avaliação hemodinâmica e metabólica do encéfalo nas lesões encefálicas agudas pode contribuir para o planejamento de estratégias de redução das lesões encefálicas secundárias. Nesta revisão, os autores discutiram princípios da hemodinâmica encefálica, considerando os aspectos de importância clínica.

Aquaporin 9 in rat brain after severe traumatic brain injury / Aquaporina 9 em cérebro de rato após traumatismo cerebral grave

OBJECTIVE: To reveal the expression and possible roles of aquaporin 9 (AQP9) in rat brain, after severe traumatic brain injury (TBI). METHODS: Brain water content (BWC), tetrazolium chloride staining, Evans blue staining, immunohistochemistry (IHC), immunofluorescence (IF), western blot, and real-time polymerase chain reaction were used. RESULTS: The BWC reached the first and second (highest) peaks at 6 and 72 hours, and the blood brain barrier (BBB) was severely destroyed at six hours after the TBI. The worst brain ischemia occurred at 72 hours after TBI. Widespread AQP9-positive astrocytes and neurons in the hypothalamus were detected by means of IHC and IF after TBI. The abundance of AQP9 and its mRNA increased after TBI and reached two peaks at 6 and 72 hours, respectively, after TBI. CONCLUSIONS: Increased AQP9 might contribute to clearance of excess water and lactate in the early stage of TBI. Widespread AQP9-positive astrocytes might help lactate move into neurons and result in cellular brain edema in the later stage of TBI. AQP9-positive neurons suggest that AQP9 plays a role in energy balance after TBI.

OBJETIVO: Revelar a expressão e os possíveis papéis da aquaporina 9 (AQP9) no cérebro de ratos após lesão cerebral traumática (LCT) grave. MÉTODOS: Foram utilizados: determinação do conteúdo cerebral de água, corante cloreto de tetrazólio, corante azul de Evans, imunoistoquímica (IHQ), imunofluorescência (IF), western blot e PCR em tempo real. RESULTADOS: O conteúdo cerebral de água alcançou o primeiro e o segundo (o mais alto) picos após 6 e 72 horas. A função da barreira hematoencefálica se mostrou muito prejudicada após 6 horas da LCT. A pior isquemia cerebral ocorreu após 72 horas da LCT. Astrócitos AQP9 positivos e neurônios no hipotálamo foram detectados difusamente pela IHQ e IF após LCT. A abundância de AQP9 e de sua mRNA aumentou após LCT e alcançou dois picos após 6 e 72 horas, respectivamente, da LCT. CONCLUSÕES: AQP9 aumentada pode contribuir para a eliminação de água e lactato em excesso na fase precoce da LCT. Astrócitos difusamente localizados AQP9 positivos podem ajudar a entrada do lactato nos neurônios, promovendo edema cerebral celular na fase tardia da LCT. Neurônios AQP9 positivos sugerem que AQP9 tem um papel no equilíbrio energético após LCT.

Increased Expression of EMMPRIN and VEGF in the Rat Brain after Gamma Irradiation

The extracellular matrix metalloproteinase inducer (EMMPRIN) has been known to play a key regulatory role in pathological angiogenesis. A elevated activation of vascular endothelial growth factor (VEGF) following radiation injury has been shown to mediate blood-brain barrier (BBB) breakdown. However, the roles of EMMPRIN and VEGF in radiation-induced brain injury after gamma knife surgery (GKS) are not clearly understood. In this study, we investigated EMMPRIN changes in a rat model of radiation injury following GKS and examined potential associations between EMMPRIN and VEGF expression. Adult male rats were subjected to cerebral radiation injury by GKS under anesthesia. We found that EMMPRIN and VEGF expression were markedly upregulated in the target area at 8-12 weeks after GKS compared with the control group by western blot, immunohistochemistry, and RT-PCR analysis. Immunofluorescent double staining demonstrated that EMMPRIN signals colocalized with caspase-3 and VEGF-positive cells. Our data also demonstrated that increased EMMPRIN expression was correlated with increased VEGF levels in a temporal manner. This is the first study to show that EMMPRIN and VEGF may play a role in radiation injuries of the central nervous system after GKS.

Occult orbito-cranial penetrating injury by pencil: Role of beta tracer protein as a marker for cerebrospinal fluid leakage.

Orbito-cranial foreign bodies present a treacherous situation that can escape detection. The only evidence of these foreign bodies may be the entry wound in the form of a small lid laceration. A two-year-old boy presented with right upper lid laceration following a fall two hours back. Analysis of the fluid around the wound revealed a beta-tracer protein (beta-TP) value of 33.5 mg/l suggestive of cerebrospinal fluid (CSF). Three-dimensional computed tomography (CT) scan revealed a foreign body measuring 4.2 cm × 0.8 cm passing from the orbital roof to the frontal lobe. The foreign body tract was explored through the eyelid laceration and a broken pencil was removed followed by dural patch graft. The patient developed no ocular or intracranial complications. Beta-TP, a highly specific marker of CSF is routinely used in screening patients of neurosurgery and otolaryngology with CSF leaks, however, its use has never been reported in ophthalmic literature based on an online PubMed search.

Expression of microtubule associated protein-2 mRNA after cerebral contusion / 法医学杂志

OBJECTIVE@#To explore the mRNA expression of microtubule associated protein-2 (MAP-2) after cerebral contusion, and to investigate its relationship with post-injury interval in a rat model of cerebral contusion.@*METHODS@#Based on Feeney's model of cerebral contusion, the time-dependent changes of MAP-2 mRNA were detected by real-time PCR method in different groups.@*RESULTS@#MAP-2 mRNA showed a lower expression in the brain of the control group. The expression of MAP-2 mRNA decreased 1 h post-injury, and reached the lowest level at 6 h, and the expression of MAP-2 mRNA gradually increased in the focus of the cerebral contusion from 12h to 14d after contusion, which kept a high level up to 14 d post-injury.@*CONCLUSION@#The time-dependent changes of MAP-2 mRNA expression may be a new method for estimating the wound age of cerebral contusion in forensic practice.

Mecanismos de lesão cerebral no traumatismo cranioencefálico: [revisão] / The pathophysiological mechanisms following traumatic brain injury: [review]

O traumatismo cranioencefálico (TCE) é a principal causa de morte e sequela em crianças e adultos jovens nos países industrializados ocidentais. A lesão encefálica definitiva que se estabelece após o TCE é o resultado de mecanismos fisiopatológicos que se iniciam com o acidente e estendem-se por dias ou semanas. As lesões encefálicas no TCE podem ser classificadas em difusas e focais. Esses dois mecanismos costumam associar-se em um mesmo paciente, embora, geralmente exista o predomínio de um tipo. O conhecimento dos mecanismos fisiopatológicos da lesão cerebral no traumatismo cranioencefálico é fundamental para o estabelecimento de medidas terapêuticas clínicas e cirúrgicas. Neste artigo, realizamos uma revisão crítica da literatura sobre os princípios fisiopatológicos da lesão cerebral no paciente com traumatismo cranioencefálico.

Traumatic brain injury is the main cause of death and disability in children and adults in Western Countries. The definitive brain injury is a consequence of pathophysiological mechanisms that begin at the moment of an accident and may extend for days or weeks. Traumatic brain injury may be classified as diffuse or focal. These two mechanisms are commonly associated in a patient, however one is generally predominant. Therefore knowledge of the pathophysiological mechanisms of brain injury in head trauma is important to establish the therapeutic, clinical and surgical measures. In this paper the authors present a critical review of the literature on the pathophysiological principles of traumatic brain injury.

Recent advances of NF-kappaB in nervous system injury / 法医学杂志

Diagnosis of nervous system injury is one of the most difficult issues in medical-legal practice. Nowadays, the activation of NF-kappaB has been studied by many researchers in order to find objective evidence and indicators to calculate the injury time and to diagnose the severity of brain injury for forensic practice. It was reviewed that the advances and problems of NF-kappaB and its correlation with nervous system injury and diseases, such as cerebral ischemia, traumatic brain injury, Alzheimer's disease and amyotrophic lateral sclerosis.

The expression of NGF after rat diffuse axonal injury / 法医学杂志

OBJECTIVE@#To study the expression of nerve growth factor (NGF) in diffuse axonal injury (DAI) in rat.@*METHODS@#Eighty SD rats were used and samples were taken at 1 h, 3 h, 6 h, 12 h, 24 h, 48 h, 3 d, and 7 d after brain injury. The expressions of NGF in cerebral cortex, thalamus, cerebellum, and hippocampus were studied with immunohistochemistry and compared with normal group and sham operation group.@*RESULTS@#Low expression of NGF was observed in normal group and sham operation group. The expression of NGF increased 1 h after injury, peaked at 12 h, and returned to basal level at day 7.@*CONCLUSION@#NGF is involved in repair of DAI. The changes of NGF expression following DAI may be applied to estimate the post-injury time interval of the brain in forensic medicine.

Change in tissue thromboplastin content of brain following trauma.

BACKGROUND: Tissue thromboplastin (TTP) is an integral membrane protein contributing to coagulopathy after trauma of brain, which is a rich source of TTP. AIMS: A study was undertaken to establish the TTP content of various areas of normal brain and estimate the changes in TTP activity of brain in response to varying degrees of trauma. MATERIALS AND METHODS: Samples from different areas of brain of ten cadavers were used as controls and they were compared with contused brain tissue obtained after surgery in 25 head injury (HI) patients of varying severity. RESULTS: In the study group, the TTP activity of the frontal, parietal, and temporal lobes after HI was significantly raised in contrast to that of the control group. The TTP activity was also significantly higher in the severe HI patients than those having moderate HI. The mode of injury and the time lapse after HI had no significant bearing on the TTP activity. Subjects above 40 years of age demonstrated a higher mean TTP activity after HI, though it was not statistically significant. CONCLUSION: The study provides quantitative data on TTP activity of normal brain and highlights the role of TTP in coagulopathy following HI through its increased activity after HI, more so in the severe HI group.