An infrared small target detection model via Gather-Excite attention and normalized Wasserstein distance.

Infrared small target detection (ISTD) is the main research content for defense confrontation, long-range precision strikes and battlefield intelligence reconnaissance. Targets from the aerial view have the characteristics of small size and dim signal. These characteristics affect the performance of traditional detection models. At present, the target detection model based on deep learning has made huge advances. The You Only Look Once (YOLO) series is a classic branch. In this paper, a model with better adaptation capabilities, namely ISTD-YOLOv7, is proposed for infrared small target detection. First, the anchors of YOLOv7 are updated to provide prior. Second, Gather-Excite (GE) attention is embedded in YOLOv7 to exploit feature context and spatial location information. Finally, Normalized Wasserstein Distance (NWD) replaces IoU in the loss function to alleviate the sensitivity of YOLOv7 for location deviations of small targets. Experiments on a standard dataset show that the proposed model has stronger detection performance than YOLOv3, YOLOv5s, SSD, CenterNet, FCOS, YOLOXs, DETR and the baseline model, with a mean Average Precision (mAP) of 98.43%. Moreover, ablation studies indicate the effectiveness of the improved components.

Multilevel thresholding using a modified ant lion optimizer with opposition-based learning for color image segmentation.

Multilevel thresholding has important research value in image segmentation and can effectively solve region analysis problems of complex images. In this paper, Otsu and Kapur's entropy are adopted among thresholding segmentation methods. They are used as the objective functions. When the number of threshold increases, the time complexity increases exponentially. In order to overcome this drawback, a modified ant lion optimizer algorithm based on opposition-based learning (MALO) is proposed to determine the optimum threshold values by the maximization of the objective functions. By introducing the opposition-based learning strategy, the search accuracy and convergence performance are increased. In addition to IEEE CEC 2017 benchmark functions validation, 11 state-of-the-art algorithms are selected for comparison. A series of experiments are conducted to evaluate the segmentation performance of the algorithm. The evaluation metrics include: fitness value, peak signal-to-noise ratio, structural similarity index, feature similarity index, and computational time. The experimental data are analyzed and discussed in details. The experimental results significantly demonstrate that the proposed method is superior over others, which can be considered as a powerful and efficient thresholding technique.

Improved barnacles mating optimizer algorithm for feature selection and support vector machine optimization.

With the rapid development of computer technology, data collection becomes easier, and data object presents more complex. Data analysis method based on machine learning is an important, active, and multi-disciplinarily research field. Support vector machine (SVM) is one of the most powerful and fast classification models. The main challenges SVM faces are the selection of feature subset and the setting of kernel parameters. To improve the performance of SVM, a metaheuristic algorithm is used to optimize them simultaneously. This paper first proposes a novel classification model called IBMO-SVM, which hybridizes an improved barnacle mating optimizer (IBMO) with SVM. Three strategies, including Gaussian mutation, logistic model, and refraction-learning, are used to improve the performance of BMO from different perspectives. Through 23 classical benchmark functions, the impact of control parameters and the effectiveness of introduced strategies are analyzed. The convergence accuracy and stability are the main gains, and exploration and exploitation phases are more properly balanced. We apply IBMO-SVM to 20 real-world datasets, including 4 extremely high-dimensional datasets. Experimental results are compared with 6 state-of-the-art methods in the literature. The final statistical results show that the proposed IBMO-SVM achieves a better performance than the standard BMO-SVM and other compared methods, especially on high-dimensional datasets. In addition, the proposed model also shows significant superiority compared with 4 other classifiers.

Pathological factors contributing to crossed cerebellar diaschisis in cerebral gliomas: a study combining perfusion, diffusion, and structural MR imaging.

PURPOSE: To investigate imaging features of crossed cerebellar diaschisis (CCD) in cerebral gliomas, and its underlying pathophysiological mechanisms. METHODS: Thirty-three pre-surgical patients with cerebral gliomas and 33 healthy controls underwent arterial spin-labeling, diffusion tensor imaging, and high-resolution T1-weighted imaging using MRI, in order to estimate cerebral blood flow (CBF), white matter integrity, and lesion volume, respectively. Asymmetry indices of CBF in the cerebellum were used for evaluating the level of CCD in the patients. These indices were correlated with clinical variables (lesion size and position, tumor histological grade, and CBF asymmetry) and diffusion tensor imaging parameters (fractional anisotropy and number of fibers in the cortico-ponto-cerebellar pathway and across the cerebral hemispheres), respectively. RESULTS: The patients showed decreased CBF in the cerebellar hemisphere contralateral to the supratentorial tumor, and increased CBF asymmetry in the cerebellum (both P < 0.05). CCD levels in high-grade gliomas were higher than those of low-grade gliomas (P < 0.05). CCD levels were negatively correlated with the size of the supratentorial lesions, and positively correlated with FA asymmetry in the cerebral fibers (both P < 0.05). CONCLUSIONS: CCD in cerebral gliomas was specifically associated with tumor histological grade, lesion size, and white matter impairments in the hemisphere ipsilateral to the tumor. The findings implicated that observing CCD might have potential for assisting grading diagnosis of cerebral gliomas.

Chrysin suppresses proliferation, migration, and invasion in glioblastoma cell lines via mediating the ERK/Nrf2 signaling pathway.

BACKGROUND: Chrysin, an active natural bioflavonoid, has been proven to protect against carcinogenesis. However, the role of chrysin in glioblastoma and the potential molecular mechanisms remain to be elucidated. In our previous study, we found that nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) is highly expressed in a variety of glioblastoma cell lines associated with the mitogen-activated protein kinase (MAPK) pathway. The aim of this study was to evaluate the antitumor effects of chrysin in glioblastoma cells and how chrysin is related to the MAPK/Nrf2 signaling pathway. METHODS: A Cell Counting Kit-8 assay and a plate colony formation assay were performed to evaluate cell proliferation. Cell migration ability was tested by a wound-healing assay. Transwell migration and Matrigel invasion assay were used to test the migration and invasion potential of cells. Nrf2 was knocked down by shRNA transfection. Protein expression was determined by Western blotting and immunofluorescence staining. The in vivo anticancer effect was measured using tumor xenografts in nude mice. RESULTS: Chrysin inhibited the proliferation, migration, and invasion capacity of glioblastoma cells in dose- and time-dependent manners. Mechanistically, chrysin deactivated the Nrf2 signaling pathway by decreasing the translocation of Nrf2 into the nucleus and suppressing the expression of hemeoxygenase-1 (HO-1) and NAD(P)H quinine oxidoreductase-1, meanwhile, Nrf2 shRNA attenuated the anticancer activity of chrysin. Furthermore, chrysin downregulated the protein expression of p-extracellular signal-regulated kinase 1 and 2 (ERK1/2), but did not significantly affect p-JNK and p-P38 expression levels. However, the downregulated level of Nrf2 and the antitumor effect of chrysin in glioblastoma cell lines were partially abrogated by the ERK1/2 signaling inhibitor (U0126). Finally, chrysin inhibited tumor growth in U87 xenografts. CONCLUSION: Our results show that chrysin exerts anticancer activity in glioblastoma cell lines possibly via the ERK/Nrf2 signaling pathway and indicate the potential application of chrysin as a natural sensitizer in chemotherapy.

Hippocampus-associated causal network of structural covariance measuring structural damage progression in temporal lobe epilepsy.

In mesial temporal lobe epilepsy (mTLE), the causal relationship of morphometric alterations between hippocampus and the other regions, that is, how the hippocampal atrophy leads to progressive morphometric alterations in the epileptic network regions remains largely unclear. In this study, a causal network of structural covariance (CaSCN) was proposed to map the causal effects of hippocampal atrophy on the network-based morphometric alterations in mTLE. It was hypothesized that if cross-sectional morphometric MRI data could be attributed temporal information, for example, by sequencing the data according to disease progression information, GCA would be a feasible approach for constructing a CaSCN. Based on a large cohort of mTLE patients (n = 108), the hippocampus-associated CaSCN revealed that the hippocampus and the thalamus were prominent nodes exerting causal effects (i.e., GM reduction) on other regions and that the prefrontal cortex and cerebellum were prominent nodes being subject to causal effects. Intriguingly, compensatory increased gray matter volume in the contralateral temporal region and post cingulate cortex were also detected. The method unraveled richer information for mapping network atrophy in mTLE relative to the traditional methods of stage-specific comparisons and structured covariance network. This study provided new evidence on the network spread mechanism in terms of the causal influence of hippocampal atrophy on progressive brain structural alterations in mTLE. Hum Brain Mapp 38:753-766, 2017. © 2016 Wiley Periodicals, Inc.

Acute single dose of ketamine relieves mechanical allodynia and consequent depression-like behaviors in a rat model.

Both chronic pain and depression are debilitating diseases, which often coexist in clinic. However, current analgesics and antidepressants exhibit limited efficacy for this comorbidity. The present study aimed to investigate the effect of ketamine on the comorbidity of inflammatory pain and consequent depression-like behaviors in a rat model established by intraplantar administration of complete Freunds adjuvant (CFA). The mechanical withdrawal threshold, thermal withdrawal latency, open field test, forced swimming test, and sucrose preference test were evaluated after the CFA injection and ketamine treatment. The hippocampus was harvested to determine the levels of interleukin (IL)-6, IL-1ß, indoleamine 2,3-dioxygenase (IDO), kynurenine (KYN), 5-hydroxytryptamine (5-HT), and tryptophan (TRP). The inflammatory pain-induced depression-like behaviors presented on 7days and lasted to at least 14days after the CFA injection. Single dose of ketamine at 20mg/kg relieved both the mechanical allodynia and the associated depression-like behaviors as demonstrated by the attenuated mechanical withdrawal threshold, reduced immobility time in the forced swim test, and increased sucrose preference after ketamine treatment. The total distance had no significant change after the CFA injection or ketamine treatment in the open field test. Simultaneously, ketamine reduced the levels of IL-6, IL-1ß, IDO, and KYN/TRP ratio and increased the 5-HT/TRP ratio in the hippocampus. In conclusion, acute single dose of ketamine can rapidly attenuate mechanical allodynia and consequent depression-like behaviors and down-regulate hippocampal proinflammatory responses and IDO/KYN signal pathway in rats.

Knockdown of retinoblastoma protein may sensitize glioma cells to cisplatin through inhibition of autophagy.

Glioblastoma multiforme (GBM) is one of the deadliest forms of cancer due to its limited sensitivity to chemotherapy and radiotherapy. Cisplatin (CCDP) is a widely used chemotherapeutic agent for tumors, but the agent often results in the development of chemo-resistance. In several cancers, cisplatin resistance is associated with autophagy induction. Here, we found that in glioma cells cisplatin treatment induced autophagy. Our data indicates that the autophagy induction plays a critical role in cisplatin resistance of glioma cells, knockdown of RB inhibited autophagy induced by cisplatin, and inhibition of autophagy improved cisplatin-induced apoptosis. It suggests that a combination of autophagy inhibitors with cisplatin may improve the therapeutic efficiency of cisplatin towards GBM with acquired resistance.

Inhibition of Autophagy by Chloroquine Enhances the Antitumor Efficacy of Sorafenib in Glioblastoma.

Glioblastoma multiforme (GBM) is the most aggressive and common brain tumor in adults. Sorafenib, a multi-kinase inhibitor, has been shown to inhibit cell proliferation and induce apoptosis through inhibition of STAT3 signaling in glioblastoma cells and in intracranial gliomas. However, sorafenib also induces cell autophagy. Due to the dual roles of autophagy in tumor cell survival and death, the therapeutic effect of sorafenib on glioblastoma is uncertain. Here, we combined sorafenib treatment in GBM cells (U373 and LN229) and tumors with the autophagy inhibitor chloroquine. We found that blockage of autophagy further inhibited cell proliferation and migration and induced cell apoptosis in vitro and in vivo. These findings suggest the possibility of combination treatment with sorafenib and autophagy inhibitors for GBM.

Functional Connectome before and following Temporal Lobectomy in Mesial Temporal Lobe Epilepsy.

As mesial temporal lobe epilepsy (mTLE) has been recognized as a network disorder, a longitudinal connectome investigation may shed new light on the understanding of the underlying pathophysiology related to distinct surgical outcomes. Resting-state functional MRI data was acquired from mTLE patients before (n = 37) and after (n = 24) anterior temporal lobectomy. According to surgical outcome, patients were classified as seizure-free (SF, n = 14) or non-seizure-free (NSF, n = 10). First, we found higher network resilience to targeted attack on topologically central nodes in the SF group compared to the NSF group, preoperatively. Next, a two-way mixed analysis of variance with between-subject factor 'outcome' (SF vs. NSF) and within-subject factor 'treatment' (pre-operation vs. post-operation) revealed divergent dynamic reorganization in nodal topological characteristics between groups, in the temporoparietal junction and its connection with the ventral prefrontal cortex. We also correlated the network damage score (caused by surgical resection) with postsurgical brain function, and found that the damage score negatively correlated with postoperative global and local parallel information processing. Taken together, dynamic connectomic architecture provides vital information for selecting surgical candidates and for understanding brain recovery mechanisms following epilepsy surgery.

More Severe Extratemporal Damages in Mesial Temporal Lobe Epilepsy With Hippocampal Sclerosis Than That With Other Lesions: A Multimodality MRI Study.

Mesial temporal lobe epilepsy with hippocampal sclerosis (mTLE-HS) presents different clinical presentations from that with other lesions (OL). It is significant to investigate the neural mechanism underlying the different clinical presentations using neuroimaging study.Thirty mTLE patients with mTLE-HS, 30 mTLE patients with other lesions (mTLE-OL), and 30 age- and sex-matched healthy controls were involved. Amplitude of low-frequency fluctuation (ALFF) analysis-based resting-state functional magnetic resonance imaging (fMRI) and voxel-based morphometry (VBM) based morphometric MRI were employed to describing functional and structural imaging alterations in mTLE. Imaging parameters of ALFF and gray matter volume (GMV) were compared among groups and correlated with clinical variables and cognitive scores.For parameter of ALFF, both patient groups of mTLE-HS and mTLE-OL showed decrease in the frontal cortices relative to the healthy controls; mTLE-HS showed more decrease in the prefrontal and brain default regions relative to mTLE-OL. For GMV, both patient groups showed decrease in the frontal cortex, thalamus, and cerebellum; mTLE-HS showed more GMV decrease relative to the mTLE-OL, also mainly in the prefrontal and brain default regions. In both patient groups, the prefrontal regions showed negative correlation between GMV and epilepsy duration.This work revealed distinct alteration patterns of functional and structural brain organizations in mTLEs with different forms. MTLE-HS, despite with smaller lesion size of the pathological focus, presented more severe functional and structural damages in the extratemporal regions than mTLE-OL. The findings provided imaging evidence to support the proposal that mTLE-HS is a special epilepsy syndrome.

Connectome Reorganization Associated With Surgical Outcome in Temporal Lobe Epilepsy.

To identify the distinct pattern of anatomical network reorganization in surgically refractory mesial temporal lobe epilepsy (MTLE) patients using a longitudinal design. We collected longitudinal diffusion-weighted images of 19 MTLE patients before and after anterior temporal lobectomy. Patients were classified as seizure-free (SF) or nonseizure-free (NSF) at least 1 year after surgery. We constructed whole-brain anatomical networks derived from white matter tractography and evaluated network connectivity measures by graph theoretical analysis. The reorganization trajectories of network measures in SF and NSF patients were investigated by two-way mixed analysis of variance, with factors "group" (SF vs NSF) and "treatment" (presurgery vs postsurgery). Widespread brain structures showed opposite reorganization trajectories in FS and NSF groups (interaction effect). Most of them showed group difference before surgery and then converge after surgery, suggesting that surgery remodeled these structures into a similar status. Conversly, contralateral amygdala-planum-temporale and thalamic-parietal tracts showed higher connectivity strength in NSF than in SF patients after surgery, indicating maladaptive neuroplastic responses to surgery in NSF patients. Our findings suggest that surgical outcomes are associated not only with the preoperative pattern of anatomical connectivity, but also with connectome reconfiguration following surgery. The reorganization of contralateral temporal lobe and corticothalamic tracts may be particularly important for seizure control in MTLE.

Tert-butylhydroquinone Ameliorates Early Brain Injury After Experimental Subarachnoid Hemorrhage in Mice by Enhancing Nrf2-Independent Autophagy.

Evidence has shown that the activation of the autophagy pathway after experimental subarachnoid hemorrhage (SAH) protects against neuronal damage. Tert-butylhydroquinone (tBHQ), a commonly used nuclear factor erythroid 2-related factor 2 (Nrf2) activator, was found to significantly enhance autophagy activation. The aim of this study was to explore the effect of tBHQ treatment on early stage brain injury at 24 h after SAH. The results showed that tBHQ treatment failed to stimulate an effective anti-oxidative effect at 24 h after the SAH operation, but succeeded in ameliorating early brain injury, including alleviated brain edema, BBB disruption, neuronal degeneration and neurological deficits. Further exploration found that tBHQ treatment significantly increased the expression of Beclin-1 and the ratio of microtubule-associated protein 1 light chain 3 (LC3)-II to LC3-I, suggesting that autophagy was enhanced after tBHQ treatment. Moreover, tBHQ treatment restored Bcl-2 and Bax expression and reduced caspase-3 cleavage, suggesting the protective effect of tBHQ treatment in ameliorating brain injury after SAH. Furthermore, tBHQ enhanced autophagy activation, decreased neuronal degeneration and improved the neurological score after SAH in Nrf2-deficient mice. Taken together, these findings suggest that tBHQ treatment exerts neuro-protective effects against EBI following SAH by enhancing Nrf2-independent autophagy. Therefore, tBHQ is a promising therapeutic agent against EBI following SAH.

Brain iron redistribution in mesial temporal lobe epilepsy: a susceptibility-weighted magnetic resonance imaging study.

BACKGROUND: The roles of iron in epilepsy and its pathophysiological significance are poorly understood, especially whether iron levels are abnormal in subcortcal structures. This study aims to demonstrate whole-brain iron alterations and its clinical relevancies in mesial temporal lobe epilepsy (mTLE) in vivo, using susceptibility-weighted magnetic resonance imaging (SWI). METHODS: We studied 62 patients with mTLE and 62 healthy controls. Brain iron concentration was quantified using SWI phase values. Voxel-wise analysis was carried out to compare iron levels between mTLE and controls, and to assess the relationship between altered iron concentration and clinical parameters in mTLE. RESULTS: Patients with mTLE showed decreases of iron levels in the subcortical structures such as substantia nigra, red nucleus, and basal ganglia. Conversely, iron levels were decreased in the cortex. Subcortical iron levels were negatively correlated to those in the cortex. Moreover, cortical and basal ganglia iron levels were related to clinical variables including epilepsy duration, age at seizures onset, and histories of precipitating factors. CONCLUSIONS: Our SWI findings suggest a redistribution of iron between subcortical and cortical structures in mTLE. The degree of redistribution is affected by both progression of epilepsy and precipitating factors. Investigation on brain iron redistribution offers new insights into the pathogenesis of mTLE, and may be a potential biomarker for monitoring the clinical progression of epilepsy.

Management of hydrocephalus secondary to pineal region tumors.

BACKGROUND: Hydrocephalus is often secondary to pineal region tumors. Hydrocephalus can lead to high intracranial pressure, which in turn results in disturbance of consciousness, cerebral hernia, and even death. Hydrocephalus management is important in the treatment of pineal region tumors. It is still controversial regarding to when and how to treat hydrocephalus secondary to pineal region tumors. The objective of this study is to investigate the management of hydrocephalus secondary to pineal region tumors. METHODS: We retrospectively analyzed records for 51 patients admitted to the department of Neurosurgery, Jinling Hospital from April 1997 to September 2010 with hydrocephalus secondary to pineal region tumors treated through occipital transtentorial approach. RESULTS: Preoperative ventricular drainage was performed on one patient, and ventriculoperitoneal shunts were performed on two patients. Intraoperative ventriculocisternal shunts were performed on 35 patients (the remission rate was 88.6%), no treatments on 15 patients (the remission rate was 46.7%), and ventricular drainages on three patients. VP shunts were performed on 12 patients with no remission after the operation. CONCLUSION: Pineal region tumors resection usually should be performed before shunting, unless there is an acute obstructive hydrocephalus. The posterior third ventricle should be opened after tumor resection. Intraoperative third ventriculostomy and ventriculocisternal shunt are reliable ways to manage hydrocephalus secondary to pineal region tumors.

Zinc as mediator of ubiquitin conjugation following traumatic brain injury.

Previous studies have shown that pathological zinc accumulation and deposition of ubiquitinated protein aggregates are commonly detected in many acute neural injuries, such as trauma, epilepsy and ischemia. However, the underlying mechanisms are poorly understood. Here we assessed the effect of zinc on ubiquitin conjugation and subsequent neurodegeration following traumatic brain injury (TBI). First, we found that scavenging endogenous Zn(2+) reduced trauma-induced ubiquitin conjugation and protected neurons from TBI insults in rat hippocampus. Second, we detected both zinc accumulation and increased ubiquitin conjugated protein following brain trauma in human cortical neurons. Our previous study has shown that zinc can induce ubiquitin conjugation in cultured hippocampal neurons. All these findings indicate that alterations in Zn(2+) homeostasis may impair the protein degradation pathway and ultimately cause neuronal injury following traumatic brain injury.

The involvement of Nrf2-ARE pathway in regulation of apoptosis in human glioblastoma cell U251.

OBJECTIVES: NF-E2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway plays anti-apoptotic role in normal tissue and tumor. But the role of Nrf2 in apoptosis in glioma is still unknown. Here, we established this experiment to elucidate how Nrf2-ARE pathway participates in apoptosis in human glioblastoma cell U251. METHODS: Two plasmids, pEGFP-Nrf2 and Si-Nrf2, were transfected to up- or downregulate the expression of Nrf2 in U251. After transfection, the apoptosis rate, expression of heme oxygenase-1 (HO-1), Bcl-2, Bax, caspases 3, 9 and activity of caspases 3, 9 were detected. RESULTS: After increasing expression of Nrf2, the apoptosis rate was reduced accompanied with upregulated expression of HO-1, Bcl-2/Bax, decreased expression and activity of caspases 3, 9. After decreasing expression of Nrf2, the apoptosis rate was enhanced accompanied with downregulated expression of HO-1, Bcl-2/Bax, increased expression and activity of caspases 3, 9. DISCUSSION: Our findings suggest that Nrf2 participates in the regulation of apoptosis in U251 through HO-1 and the 'intrinsic' apoptotic pathway.

Impairments of thalamic nuclei in idiopathic generalized epilepsy revealed by a study combining morphological and functional connectivity MRI.

OBJECTIVE: Neuroimaging evidence suggested that the thalamic nuclei may play different roles in the progress of idiopathic generalized epilepsy (IGE). This study aimed to demonstrate the alterations in morphometry and functional connectivity in the thalamic nuclei in IGE. METHODS: Fifty-two patients with IGE characterized by generalized tonic-clonic seizures and 67 healthy controls were involved in the study. The three-dimensional high-resolution T1-weighted MRI data were acquired for voxel-based morphometry (VBM) analysis, and resting-state blood-oxygenation level functional MRI data were acquired for functional connectivity analysis. The thalamic nuclei of bilateral medial dorsal nucleus (MDN) and pulvinar, as detected with decreased gray matter volumes in patients with IGE through VBM analysis, were selected as seed regions for functional connectivity analysis. RESULTS: Different alteration patterns were found in functional connectivity of the thalamic nuclei with decreased gray matter volumes in IGE. Seeding at the MDN, decreased connectivity in the bilateral orbital frontal cortex, caudate nucleus, putamen and amygdala were found in the patients (P<0.05 with correction). However, seeding at the pulvinar, no significant alteration of functional connectivity was found in the patients (P<0.05 with correction). CONCLUSIONS: Some specific impairment of thalamic nuclei in IGE was identified using morphological and functional connectivity MRI approaches. These findings may strongly support the different involvement of the thalamocortical networks in IGE.

The expression of PGC-1α in the mice brain after traumatic brain injury.

BACKGROUND: Peroxisome proliferator activated receptor γ co-activator-1α (PGC-1α) is a transcriptional co-activator that co-ordinately regulates genes required for mitochondrial biogenesis and is a key contributor to the up-regulation of antioxidant activities in response to oxidative stress. The expression pattern of PGC-1α after traumatic brain injury (TBI) has not been studied. MATERIALS AND METHODS: Ninety male ICR mice (28-32 g) were randomly assigned to six groups: sham, 3, 6, 12, 24 and 48 hours after TBI. PGC-1α mRNA levels in mice brain were detected by reverse-transcriptase polymerase chain reaction and its nuclear protein levels by Western blot from 3-48 hours after TBI. PGC-1α distribution in the cerebral cortex after TBI was investigated by immunohistochemistry. MAIN OUTCOMES AND RESULTS: The PGC-1α mRNA level significantly increased from 3 hours after TBI, peaked at 6 hours and gradually decreased from 12 to 48 hours. The nuclear PGC-1α protein level increased from 6 to 24 hours after TBI and decreased at 48 hours after TBI. Increased PGC-1α immunostaining was detected in the neurons of the cerebral cortex at 12 hours after TBI. CONCLUSION: PGC-1α may play an important role in the brain after TBI.

[Resting functional MRI with default mode-based functional connectivity analysis for localization of epileptic activity].

OBJECTIVE: Using the functional connectivity analysis based on the underlying neurophysiological characteristic that epileptic discharges can induce change of brain default mode, to develop a technique for epileptogenic localization using functional MRI (fMRI) without simultaneous electroencephalography (EEG). METHODS: A data-driven method that jointly employed independent component analysis and functional connectivity analysis was used for the resting functional MRI data analysis of 12 focal epileptic patients. The independent components were ranged according to the coefficients of the negative correlation between independent component time course and the signal temporal course in the region of posterior cingulate cortex. The results were comparatively studied with simultaneous EEG-fMRI. RESULTS: In the 10 successful results from 12 patients underwent EEG-fMRI examination, the outcomes of eight subjects were concordant with pathological foci. While the results of all 10 patients processed by data-driven method were concordant with pathological foci, besides the other patients who failed to perform EEG-fMRI examination. Meanwhile, the default mode was well mapped in all patients. CONCLUSIONS: The default mode-based functional connectivity analysis can localize the epileptogenic foci effectively without simultaneous EEG, besides to detect the default mode of epileptic patients.