Research Progress and Forensic Application of Human Vascular Finite Element Modeling and Biomechanics.

The finite element method (FEM) is a mathematical method for obtaining approximate solutions to a wide variety of engineering problems. With the development of computer technology, it is gradually applied to the study of biomechanics of human body. The application of the combination of FEM and biomechanics in exploring the relationship between vascular injury and disease, and pathological mechanisms will be a technological innovation for traditional forensic medicine. This paper reviews the construction and development of human vascular FEM modeling, and its research progress on the vascular biomechanics. This paper also looks to the application prospects of FEM modeling in forensic pathology.

Brain-specific loss of Abcg1 disturbs cholesterol metabolism and aggravates pyroptosis and neurological deficits after traumatic brain injury.

Based on accumulating evidence, cholesterol metabolism dysfunction has been suggested to contribute to the pathophysiological process of traumatic brain injury (TBI) and lead to neurological deficits. As a key transporter of cholesterol that efflux from cells, the ATP-binding cassette (ABC) transporter family exerts many beneficial effects on central nervous system (CNS) diseases. However, there is no study regarding the effects and mechanisms of ABCG1 on TBI. As expected, TBI resulted in the different time-course changes of cholesterol metabolism-related molecules in the injured cortex. Considering ABCG1 is expressed in neuron and glia post-TBI, we generated nestin-specific Abcg1 knockout (Abcg1-KO) mice using the Cre/loxP recombination system. These Abcg1-KO mice showed reduced plasma high-density lipoprotein cholesterol levels and increased plasma lower-density lipoprotein cholesterol levels under the base condition. After TBI, these Abcg1-KO mice were susceptible to cholesterol metabolism turbulence. Moreover, Abcg1-KO exacerbated TBI-induced pyroptosis, apoptosis, neuronal cell insult, brain edema, neurological deficits, and brain lesion volume. Importantly, we found that treating with retinoid X receptor (RXR, the upstream molecule of ABCG1) agonist, bexarotene, in Abcg1-KO mice partly rescued TBI-induced neuronal damages mentioned above and improved functional deficits versus vehicle-treated group. These data show that, in addition to regulating brain cholesterol metabolism, Abcg1 improves neurological deficits through inhibiting pyroptosis, apoptosis, neuronal cell insult, and brain edema. Moreover, our findings demonstrate that the cerebroprotection of Abcg1 on TBI partly relies on the activation of the RXRalpha/PPARgamma pathway, which provides a potential therapeutic target for treating TBI.

Sleep disorder as a clinical risk factor of major depression: associated with cognitive impairment.

BACKGROUND: This research aims explored the sleep disorder (SD) role in major depressive disorder (MDD), and the SD influencing their cognition. METHODS: 372 MDD patients and 457 healthy controls (HCs) were enrolled. RESULTS: Patients increased a 38.88 times SD risk compared with HCs. In patients, visuospatial/constructional score was lower in SD than non-SD, and PSQI score was negatively associated with visuospatial/constructional score of SD. In SD and non-SD, RBANS scores were lower in MDD than HCs, excepted for visuospatial/constructional in non-SD. CONCLUSION: The SD as a MDD risk factor, has more serious visuospatial/constructional impairment alleviated via improving sleep/depression in patients.

Characteristics of Visual Evoked Potential in Different Parts of Visual Impairment. / 不同部位损伤致视力障碍的视觉诱发电位特征.

OBJECTIVES: To study the quantitative and qualitative differences of visual evoked potential (VEP) in monocular visual impairment after different parts of visual pathway injury. METHODS: A total of 91 subjects with monocular visual impairment caused by trauma were selected and divided into intraocular refractive media-injury group (eyeball injury group for short), optic nerve injury group, central nervous system injury and intracranial combined injury group according to the injury cause and anatomical segment. Pattern Reversal visual evoked potential (PR-VEP) P100 peak time and amplitude, Flash visual evoked potential (F-VEP) P2 peak time and amplitude were recorded respectively. SPSS 26.0 software was used to analyze the differences of quantitative (peak time and amplitude) and qualitative indexes (spatial frequency sweep-VEP acuity threshold, and abnormal waveform category and frequency) of the four groups. RESULTS: Compared with healthy eyes, the PR-VEP P100 waveforms of the intraocular eyeball injury group and the F-VEP P2 waveforms of the optic nerve group showed significant differences in prolonged peak time and decreased amplitude in injured eyes (P<0.05). The PR-VEP amplitudes of healthy eyes were lower than those of injured eyes at multiple spatial frequencies in central nervous system injury group and intracranial combined injury group (P<0.05).The amplitude of PR-VEP in patients with visual impairment involving central injury was lower than that in patients with eye injury at multiple spatial frequencies. The frequency of VEP P waveforms reaching the threshold of the intraocular injury group and the optic nerve injury group were siginificantly different from the intracranial combined injury group, respectively(P<0.008 3), and the frequency of abnormal reduction of VEP amplitude of threshold were significantly different from the central nervous system injury group, respectively(P<0.008 3). CONCLUSIONS: VEP can distinguish central injury from peripheral injury, eyeball injury from nerve injury in peripheral injury, but cannot distinguish simple intracranial injury from complex injury, which provides basic data and basis for further research on the location of visual impairment injury.

Application of Immunohistochemistry and Special Staining Technique in Forensic Traumatic Pathology Identification. / å ç–«ç»„ç»‡åŒ–å­¦åŠç‰¹æ®ŠæŸ“è‰²æŠ€æœ¯åœ¨æ³•åŒ»æŸä¼¤ç— ç†å­¦é‰´å®šä¸­çš„åº”ç”¨.

In forensic traumatic pathology practice, immunohistochemistry and special staining technique play an important role in wound age estimation and complications of traumatic complication identification. They even play an important role in the identification of special cases, such as snakebites and insulin killings. This article reviews the application and value of immunohistochemistry and special staining techniques in forensic traumatic pathology based on the cases of forensic practice reported in literature.

Chronic restraint stress exacerbates neurological deficits and disrupts the remodeling of the neurovascular unit in a mouse intracerebral hemorrhage model.

Growing evidences have shown that patients recovering from stroke experience high and unremitting stress. Chronic restraint stress (CRS) has been found to exacerbate neurological impairments in an experimental focal cortical ischemia model. However, there have been no studies reporting the effect and mechanism of CRS on intracerebral hemorrhage (ICH). This study aimed to evaluate the effect of CRS on a mouse ICH model. Adult male C57BL mice were subjected to infusion of collagenase IV (to induce ICH) or saline (for sham) into the left striatum. After ICH, animals were stressed with application of CRS protocol for 21 days. Our results showed that CRS significantly exacerbated neurological deficits (Garcia test, corner turn test, and wire grip test) and the ipsilateral brain atrophy and reduced body weight gain after ICH. Immunofluorescence staining indicated that CRS exerted significant suppressive effects on neuron, astrocyte, vascular endothelial cell and pericyte and excessively activated microglia post ICH. All of the key cellular components mentioned above are involved in the neurovascular unit (NVU) remodeling in the peri-hemorrhagic region after ICH. Western blot results showed that matrix metalloproteinase (MMP)-9 and tight junction (TJ) proteins including zonula occludens-1, occludin and claudin-5 were increased after ICH, but MMP-9 protein was further up-regulated and TJ-related proteins were down-regulated by CRS. In addition, ICH-induced activation of endoplasmic reticulum stress and apoptosis were further strengthened by CRS. Collectively, CRS exacerbates neurological deficits and disrupts the remodeling of the peri-hemorrhagic NVU after ICH, which may be associated with TJ proteins degradation and excessive activation of MMP-9 and endoplasmic reticulum stress-apoptosis.LAY SUMMARYCRS exacerbates neurological deficits and disrupts the remodeling of the NVU in the recovery stage after ICH, which suggest that monitoring chronic stress levels in patients recovering from ICH may merit consideration in the future.

Salubrinal offers neuroprotection through suppressing endoplasmic reticulum stress, autophagy and apoptosis in a mouse traumatic brain injury model.

Traumatic brain injury (TBI) is a complex injury that can cause severe disabilities and even death. TBI can induce secondary injury cascades, including but not limited to endoplasmic reticulum (ER) stress, apoptosis and autophagy. Although the investigators has previously shown that salubrinal, the selective phosphatase inhibitor of p-eIF2α, ameliorated neurologic deficits in murine TBI model, the neuroprotective mechanisms of salubrinal need further research to warrant the preclinical value. This study was undertaken to characterize the effects of salubrinal on cell death and neurological outcomes following TBI in mice and the potential mechanisms. In the current study, ER stress-related proteins including p-eIF2α, GRP78 and CHOP showed peak expressions both in the cortex and hippocampus from day 2 to day 3 after TBI, indicating ER stress was activated in our TBI model. Immunofluorescence staining showed that CHOP co-located NeuN-positive neuron, GFAP-positive astrocyte, Iba-1-positive microglia, CD31-positive vascular endothelial cell and PDGFR-ß-positive pericyte in the cortex on day 2 after TBI, and these cells mentioned above constitute the neurovascular unit (NVU). We also found TBI-induced plasmalemma permeability, motor dysfunction, spatial learning and memory deficits and brain lesion volume were alleviated by continuous intraperitoneal administration of salubrinal post TBI. To investigate the underlying mechanisms further, we determined that salubrinal suppressed the expression of ER stress, autophagy and apoptosis related proteins on day 2 after TBI. In addition, salubrinal administration decreased the number of CHOP+/TUNEL+ and CHOP+/LC3+ cells on day 2 after TBI, detected by immunofluorescence. In conclusion, these data imply that salubrinal treatment improves morphological and functional outcomes caused by TBI in mice and these neuroprotective effects may be associated with inhibiting apoptosis, at least in part by suppressing ER stress-autophagy pathway.

IL-33/ST2L Signaling Provides Neuroprotection Through Inhibiting Autophagy, Endoplasmic Reticulum Stress, and Apoptosis in a Mouse Model of Traumatic Brain Injury.

Interleukin-33 (IL-33) is a member of the interleukin-1 (IL-1) cytokine family and an extracellular ligand for the orphan IL-1 receptor ST2. Accumulated evidence shows that the IL-33/ST2 axis plays a crucial role in the pathogenesis of central nervous system (CNS) diseases and injury, including traumatic brain injury (TBI). However, the roles and molecular mechanisms of the IL-33/ST2 axis after TBI remain poorly understood. In this study, we investigated the role of IL-33/ST2 signaling in mouse TBI-induced brain edema and neurobehavioral deficits, and further exploited underlying mechanisms, using salubrinal (SAL), the endoplasmic reticulum (ER) stress inhibitor and anti-ST2L. The increase in IL-33 level and the decrease in ST2L level at injured cortex were first observed at 24 h post-TBI. By immunofluorescent double-labeled staining, IL-33 co-localized in GFAP-positive astrocytes, and Olig-2-positive oligodendrocytes, and predominantly presented in their nucleus. Additionally, TBI-induced brain water content, motor function outcome, and spatial learning and memory deficits were alleviated by IL-33 treatment. Moreover, IL-33 and SAL alone, or their combination prevented TBI-induced the increase of IL-1ß and TNF-α levels, suppressed the up-regulation of ER stress, apoptosis and autophagy after TBI. However, anti-ST2L treatment could significantly invert the above effects of IL-33. Together, these data demonstrate that IL-33/ST2 signaling mitigates TBI-induced brain edema, motor function outcome, spatial learning and memory deficits, at least in part, by a mechanism involving suppressing autophagy, ER stress, apoptosis and neuroinflammation.

Estimating the age of Lucilia illustris during the intrapuparial period using two approaches: Morphological changes and differential gene expression.

Lucilia illustris (Meigen, 1826) (Diptera: Calliphoridae) is a cosmopolitan species of fly that has forensic and medical significance. However, there is no relevant study regarding the determination of the age of this species during the intrapuparial period. In this study, we investigated the changes in both morphology and differential gene expression during intrapuparial development, with an aim to estimate the age of L. illustris during the intrapuparial stage. The overall intrapuparial morphological changes of L. illustris were divided into 12 substages. Structures such as the compound eyes, mouthparts, antennae, thorax, legs, wings, and abdomen, each capable of indicating age during the intrapuparial stage, were observed in detail, and the developmental progression of each of these structures was divided into six to eight stages. We recorded the time range over which each substage or structure appeared. The differential expression of the three genes 15_2, actin, and tbp previously identified for predicting the timing of intrapuparial development was measured during L. illustris metamorphosis. The expression of these genes was quantified by real-time PCR, and the results revealed that these genes can be used to estimate the age of L. illustris during the intrapuparial period, as they exhibit regular changes and temperature dependence. This study provides an important basis for estimating the minimum postmortem interval (PMImin) in forensic entomology according to changes in intrapuparial development and differential gene expression. Furthermore, combination of the two approaches can generate a more precise PMImin than either approach alone.

Insect succession on remains of human and animals in Shenzhen, China.

Most forensic entomological succession studies have been carried out using pig or rabbit carcasses; however, there have been few studies on the differences between insect succession patterns on human cadavers and on animal carcasses. In order to clarify the differences between decomposition and insect succession patterns of human cadavers and animal carcasses, one 49.5kg human cadaver, two large pig carcasses (45 and 48kg), two small pig carcasses (23 and 25kg) and two rabbit carcasses (both 1.75kg) were placed in the same field conditions in Shenzhen, China for a comparative study on August, 2013. The results indicated that: (1) The duration from fresh to skeletonization is in order of human cadaver>large pig carcasses>small pig carcasses>rabbit carcasses; (2) insect assemblages (including developmental stages) are more complex on larger carcasses, in order of human cadaver=large pig carcasses>small pig carcasses>rabbit carcasses; (3) the developmental rates of the same forensically important fly species on all carcasses are consistent; (4) all identified species of Calliphoridae can complete development of one generation on human cadaver, and both large and small pig carcasses, while on rabbit carcasses, only a subset of the Calliphoridae species can finish development of one generation; (5) beetles can generate offspring on human cadaver, and both large and small pig carcasses, while they do not generate offspring on rabbit carcasses. This study provides useful comparative data for decomposition and insect succession pattern of human cadaver with animal carcasses.

IL-33 Exerts Neuroprotective Effect in Mice Intracerebral Hemorrhage Model Through Suppressing Inflammation/Apoptotic/Autophagic Pathway.

Interleukin-33 (IL-33) is a recently identified member of the IL-1 family that exerts biologic functions by binding to a heterodimer composed of IL-1 receptor-related protein ST2L and IL-1RAcP. However, the role of IL-33 and whether IL-33 accounts for inflammation, apoptotic, and autophagic neuropathology after intracerebral hemorrhage (ICH) are not clear. Here, we established a mouse ICH model in this study, to determine the role of IL-33 and explore the underlying mechanism. Male mice were subjected to an infusion of type IV collagenase/saline into the left striatum to induce ICH/sham model. IL-33, soluble ST2 (sST2), or saline were also administered by a single intracerebroventricular (i.c.v.) injection, respectively. The results showed that the expression level of IL-33 markedly decreased within 6 h and reached the valleys at 6 and 72 h after ICH vs. sham group. In parallel, ST2L (a transmembrane form receptor of IL-33) significantly increased within 6 h and reached the peaks at 6 h and 24 h after ICH vs. sham group. In addition, administration of IL-33 alleviated cerebral water contents, reduced the number of PI- and TUNEL-positive cells, and improved neurological function after ICH. Moreover, IL-33 treatment apparently suppressed the expression of pro-inflammation cytokines IL-1ß and TNF-α, evidently increased Bcl-2 but decreased cleaved-caspase-3, and obviously decreased the levels of autophagy-associated proteins LC3-II and Beclin-1 but maintained P62 at high level after ICH. On the contrary, treatment with sST2, a decoy receptor of IL-33, exacerbated ICH-induced brain damage and neurological dysfunction by promoting apoptosis, and enhancing autophagic activity. In conclusion, IL-33 provides neuroprotection through suppressing inflammation, apoptotic, and autophagic activation in collagenase-induced ICH model.

IL-33 Provides Neuroprotection through Suppressing Apoptotic, Autophagic and NF-κB-Mediated Inflammatory Pathways in a Rat Model of Recurrent Neonatal Seizure.

Interleukin-33 (IL-33) is a novel identified chromatin-associated cytokine of IL-1 family cytokines. It signals through a heterodimer comprised of ST2L and IL-1RAcp, and plays a crucial role in many diseases. However, very little is known about the role and underlying intricate mechanisms of IL-33 in recurrent neonatal seizure (RNS). To determine whether IL-33 plays an important regulatory role, we established a neonatal seizure model in this study. Rats were subjected to recurrent seizures induced by inhaling volatile flurothyl. Recombinant IL-33 or PBS were also administered by intraperitoneally (IP) before surgery, respectively. Here, our current results indicated that RNS contributed to a significant reduction in IL-33 and its specific receptor (ST2L) expressions in cortex. While, in hippocampus, RNS induced an increase in IL-33 and ST2L evidently, compared with Sham group. After injection with IL-33, however, a remarkable increase in total IL-33 was detected both in brain cortex and hippocampus. In addition, IL-33 was mainly co-localized in the nuclear of GFAP+ astrocytes and the cytoplasm of the Iba-1+ microglia and IL-33+/NeuN+ merged cells. In parallel, ST2L was expressed mainly in the membrane of GFAP+ astrocytes, Iba-1+ microglia and NeuN+ neurons, respectively. Furthermore, administration of IL-33 improved RNS-induced behavioral deficits, promoted bodyweight gain, and ameliorated spatial learning and memory ability. Moreover, IL-33 pretreatment blocked the activation of NF-κB, resisted inflammatory cytokines IL-1ß and TNF-α increase, as well as suppressed apoptosis and autophagy activation after RNS. Collectively, IL-33 provides potential neuroprotection through suppressing apoptosis, autophagy and at least in part by NF-κB-mediated inflammatory pathways after RNS.

Dynamin-related protein 1 (Drp1) mediating mitophagy contributes to the pathophysiology of nervous system diseases and brain injury.

As the main source of energy (celluar ATP) in eukaryotic cells, mitochondria are involved in cellular physiology and pathology. The balance of mitochondrial dynamic, fission and fusion regulated by quality control mechanisms, provides a guarantee for maintaining mitochondrial function, even celluar function. Worn out mitochondria would be removed through mitophagy which is regulated by autophagy related proteins and mitochondrial membrane proteins. Drp1, dynamic-related protein 1, is regarded as one of the most important proteins to evaluate mitochondrial fission mediating mitophagy in neurodegenerative diseases (eg. Alzheimer's, Parkinson's, Huntington's, amyotrophic lateral sclerosis) and heart failure. Recent studies have focused on the roles of Drp1 in ischemia-induced mitophagy in the hippocampal CA3 region, and traumatic brain injury (TBI)-induced cell death together with functional deficits. However, the exact mechanisms have not been well characterized. In this review, we will discuss and clarify the role of Drp1 and mitophagy in nervous system diseases and brain injury therein, with a special emphasis on their molecular mechanisms mediating mitochondrial dynamics and mitophagy.

Development of the green bottle fly Lucilia illustris at constant temperatures.

Lucilia illustris (Meigen 1826) (Diptera: Calliphoridae) is a cosmopolitan species that commonly colonizes carcasses and occasionally acts as parasites of humans or livestock, making it an insect of significant importance in forensic, medical, and veterinary entomology. However, only a few studies have documented the development of L. illustris. Here, we studied the developmental duration and larval body length changes of L. illustris under nine constant temperatures ranging from 15.0 to 35.0°C. Using these results, we generated an isomorphen diagram, thermal summation model, and isomegalen diagram for L. illustris. Simulation equations of the variation in the larval body length with time after hatching and variation in time after hatching with the body length were also obtained. L. illustris could complete its life cycle in 15.0-32.5°C, while its development was incomplete at 35.0°C, where the pupae failed to transform into adults. The development duration was 955.5±16.9, 625.7±16.9, 509.3±18.3, 410.0±17.0, 346.7±12.2, 290.2±6.7, 257.1±8.9, and 234.8±3.2h at 15.0, 17.5, 20.0, 22.5, 25.0, 27.5, 30.0, and 32.5°C, respectively. The developmental threshold temperature and thermal constant were 9.30±0.19°C and 5367.2±98.3°Ch, respectively. These results provide an important basis for the use of L. illustris development-based estimation of the minimum postmortem interval (PMImin) in forensic entomology.

Glucocorticoid treatment inhibits intracerebral hemorrhage­induced inflammation by targeting the microRNA­155/SOCS­1 signaling pathway.

Intracerebral hemorrhage (ICH) results in inflammation, and glucocorticoids have been proven to be effective inhibitors of ICH­induced inflammation. However, the precise underlying mechanisms of ICH­induced inflammation and glucocorticoid function remain largely undefined. Using a mouse ICH model, the present study demonstrated that the short non­coding RNA molecule microRNA­155 (miR­155) is involved in the inflammatory process initiated by ICH in mice. Increased mRNA expression levels of miR­155, as well as the pro­inflammatory cytokines interferon­ß (IFN­ß), tumor necrosis factor­α (TNF­α) and interleukin­6 (IL­6), were observed in vivo following ICH. By contrast, the expression level of suppressor of cytokine signaling 1 (SOCS­1) protein was reduced in the ICH group compared with control mice. Similar results were observed in vitro using astrocytes, the primary effector cells in ICH. Compared with wild type astrocytes, astrocytes overexpressing miR­155 exhibited significant inhibition of SOCS­1 protein expression levels. These results suggest that miR­155 contributes to the development of ICH­induced inflammation in mice by downregulating SOCS­1 protein expression levels and promoting pro­inflammatory cytokine (IFN­ß, TNF­α and IL­6) production. Expression levels of miR­155 and pro­inflammatory cytokines in the ICH group were significantly decreased following dexamethasone administration. This suggests that glucocorticoids attenuate ICH­induced inflammation by targeting the miR­155/SOCS­1 signaling pathway in mice. In conclusion, the results of the present study demonstrated that the miR­155/SOCS­1 signaling pathway is required for ICH­induced inflammation, and glucocorticoids inhibit this process by targeting the miR­155/SOCS­1 signaling pathway.

Mitochondrial division inhibitor 1 (Mdivi-1) offers neuroprotection through diminishing cell death and improving functional outcome in a mouse model of traumatic brain injury.

Mitochondria dysfunction, an enormous potential crisis, has attracted increasing attention. Disturbed regulation of mitochondrial dynamics, the balance of mitochondrial fusion and fission, has been implicated in neurodegenerative diseases, such as Parkinson׳s disease and cerebral ischemia/reperfusion. However the role of mitochondrial dynamics in traumatic brain injury (TBI) has not been illuminated. The aim of the present study was to investigate the role of Mdivi-1, a small molecule inhibitor of a key mitochondrial fission protein dynamin-related protein 1 (Drp1), in TBI-induced cell death and functional outcome deficits. Protein expression of Drp1 was first investigated. Outcome parameters consist of motor test, Morris water maze, brain edema and lesion volume. Cell death was detected by propidium iodide (PI) labeling, and mitochondrial morphology was assessed using transmission electron microscopy. In addition, the expression of apoptosis-related proteins cytochrome c (cyt-c) and caspase-3 was investigated. Our findings showed that up-regulation of Drp1 expression started at 1h post-TBI and peaked at 24 h, but inhibition of Drp1 by Mdivi-1 significantly alleviated TBI-induced behavioral deficits and brain edema, reduced morphological change of mitochondria, and decreased TBI-induced cell death together with lesion volume. Moreover, treatment with Mdivi-1 remarkably inhibited TBI-induced the release of cyt-c from mitochondria to cytoplasm, and activation of caspase-3 at 24 h after TBI. Taken together, these data imply that inhibition of Drp1 may help attenuate TBI-induced functional outcome and cell death through maintaining normal mitochondrial morphology and inhibiting activation of apoptosis.

[Research Progress of Event-related Potential in Mild Cognitive Impairment].

Mild cognitive impairment caused by craniocerebral trauma is the key points and difficulties in judicial authentication. This article has comparative analysis of each mode of event-related potential (classical Oddball, Eriksen flanker task and so on), which can provide a more objective method for such craniocerebral trauma cases in clinical forensic judicial authentication.

[Expression of Zonula Occludens-1 in Cerebral Cortex Following Traumatic Brain Injury].

OBJECTIVE: To observe the time-course expression of zonula occludens-1 (ZO-1) in cerebral cortex after traumatic brain injury (TBI). METHODS: The TBI model of mouse was established. The mice were divided in 1 h, 3 h, 6 h, 12 h, 24 h, 3 d, 7 d after TBI, sham and control groups. The permeability of the blood brain barrier was evaluated by measuring the extravasation of Evans blue (EB) dye. The expression of ZO-1 in cerebral cortex in the injured area was detected by Western blotting and immunohistochemistry. RESULTS: The extravasation of EB dye of injured cortex gradually increased from 1 h, peaked at 1-3 d and approximately decreased to normal at 7 d after TBI. Western blotting revealed that the expression of ZO-1 gradually decreased after 1 h, was at the lowest at 1-3 d, and then significantly increased after 7 d but was still lower than that of normal and sham groups. The result of immunohistochemistry showed that ZO-1 had strong expression in vessel of normal cortex, gradually decreased after TBI, and almost disappeared at 3 d after TBI and gradually recovered to normal level later. CONCLUSION: The expression of ZO-1 in the injured cortex after TBI initially decreases and then increases. The negative correlation between ZO-1 expression and EB extravasation after TBI could be used as a new indicator for wound age estimation.

Mismatch negativity, social cognition, and functional outcomes in patients after traumatic brain injury.

Mismatch negativity is generated automatically, and is an early monitoring indicator of neuronal integrity impairment and functional abnormality in patients with brain injury, leading to decline of cognitive function. Antipsychotic medication cannot affect mismatch negativity. The present study aimed to explore the relationships of mismatch negativity with neurocognition, daily life and social functional outcomes in patients after brain injury. Twelve patients with traumatic brain injury and 12 healthy controls were recruited in this study. We examined neurocognition with the Wechsler Adult Intelligence Scale-Revised China, and daily and social functional outcomes with the Activity of Daily Living Scale and Social Disability Screening Schedule, respectively. Mismatch negativity was analyzed from electroencephalogram recording. The results showed that mismatch negativity amplitudes decreased in patients with traumatic brain injury compared with healthy controls. Mismatch negativity amplitude was negatively correlated with measurements of neurocognition and positively correlated with functional outcomes in patients after traumatic brain injury. Further, the most significant positive correlations were found between mismatch negativity in the fronto-central region and measures of functional outcomes. The most significant positive correlations were also found between mismatch negativity at the FCz electrode and daily living function. Mismatch negativity amplitudes were extremely positively associated with Social Disability Screening Schedule scores at the Fz electrode in brain injury patients. These experimental findings suggest that mismatch negativity might efficiently reflect functional outcomes in patients after traumatic brain injury.

[Expression of CaMK II delta in cerebral cortex following traumatic brain injury].

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.