Keldysh Space Control of Charge Dynamics in a Strongly Driven Mott Insulator.

The fate of a Mott insulator under strong low frequency optical driving conditions is a fundamental problem in quantum many-body dynamics. Using ultrafast broadband optical spectroscopy, we measured the transient electronic structure and charge dynamics of an off-resonantly pumped Mott insulator Ca_{2}RuO_{4}. We observe coherent bandwidth renormalization and nonlinear doublon-holon pair production occurring in rapid succession within a sub-100-fs pump pulse duration. By sweeping the electric field amplitude, we demonstrate continuous bandwidth tuning and a Keldysh crossover from a multiphoton absorption to quantum tunneling dominated pair production regime. Our results provide a procedure to control coherent and nonlinear heating processes in Mott insulators, facilitating the discovery of novel out-of-equilibrium phenomena in strongly correlated systems.

Direct Observation of Coherent Longitudinal and Shear Acoustic Phonons in TaAs Using Ultrafast X-Ray Diffraction.

Using femtosecond time-resolved x-ray diffraction, we investigated optically excited coherent acoustic phonons in the Weyl semimetal TaAs. The low symmetry of the (112) surface probed in our experiment enables the simultaneous excitation of longitudinal and shear acoustic modes, whose dispersion closely matches our simulations. We observed an asymmetry in the spectral line shape of the longitudinal mode that is notably absent from the shear mode, suggesting a time-dependent frequency chirp that is likely driven by photoinduced carrier diffusion. We argue on the basis of symmetry that these acoustic deformations can transiently alter the electronic structure near the Weyl points and support this with model calculations. Our study underscores the benefit of using off-axis crystal orientations when optically exciting acoustic deformations in topological semimetals, allowing one to transiently change their crystal and electronic structures.

Revealing charge carrier dynamics and transport in Te-doped GaAsSb and GaAsSbN nanowires by correlating ultrafast terahertz spectroscopy and optoelectronic characterization.

Recent advances in the growth of III-V semiconductor nanowires (NWs) hold great promise for nanoscale optoelectronic device applications. It is established that a small amount of nitrogen (N) incorporation in III-V semiconductor NWs can effectively red-shift their wavelength of operation and tailor their electronic properties for specific applications. However, understanding the impact of N incorporation on non-equilibrium charge carrier dynamics and transport in semiconducting NWs is critical in achieving efficient semiconducting NW devices. In this work, ultrafast optical pump-terahertz probe spectroscopy has been used to study non-equilibrium carrier dynamics and transport in Te-doped GaAsSb and dilute nitride GaAsSbN NWs, with the goal of correlating these results with electrical characterization of their equilibrium photo-response under bias and low-frequency noise characteristics. Nitrogen incorporation in GaAsSb NWs led to a significant increase in the carrier scattering rate, resulting in a severe reduction in carrier mobility. Carrier recombination lifetimes of 33 ± 1 picoseconds (ps) and 147 ± 3 ps in GaAsSbN and GaAsSb NWs, respectively, were measured. The reduction in the carrier lifetime and photoinduced optical conductivities are due to the presence of N-induced defects, leading to deterioration in the electrical and optical characteristics of dilute nitride NWs relative to the non-nitride NWs. Finally, we observed a very fast rise time of âˆ¼2 ps for both NW materials, directly impacting their potential use as high-speed photodetectors.

Charge-Spin Correlation in van der Waals Antiferromagnet NiPS_{3}.

Strong charge-spin coupling is found in a layered transition-metal trichalcogenide NiPS_{3}, a van der Waals antiferromagnet, from studies of the electronic structure using several experimental and theoretical tools: spectroscopic ellipsometry, x-ray absorption, photoemission spectroscopy, and density functional calculations. NiPS_{3} displays an anomalous shift in the optical spectral weight at the magnetic ordering temperature, reflecting strong coupling between the electronic and magnetic structures. X-ray absorption, photoemission, and optical spectra support a self-doped ground state in NiPS_{3}. Our work demonstrates that layered transition-metal trichalcogenide magnets are useful candidates for the study of correlated-electron physics in two-dimensional magnetic materials.

Regulation of Caveolin-1 Expression Determines Early Brain Edema After Experimental Focal Cerebral Ischemia.

BACKGROUND AND PURPOSE: Most patients with cerebral infarction die of brain edema because of the breakdown of the blood-brain barrier (BBB) in ischemic tissue. Caveolins (a group of proteins) are key modulators of vascular permeability; however, a direct role of caveolin-1 (Cav-1) in the regulation of BBB permeability during ischemic injury has yet to be identified. METHODS: Cav-1 expression was measured by immunoblotting after photothrombotic ischemia. A direct functional role of Cav-1 in cerebral edema and BBB permeability during cerebral ischemia was investigated by genetic manipulation (gene disruption and re-expression) of Cav-1 protein expression in mice. RESULTS: There was a significant correlation between the extent of BBB disruption and the Cav-1 expression. In Cav-1-deficient (Cav-1(-/-)) mice, the extent of BBB disruption after cerebral ischemia was increased compared with wild-type (Cav-1(+/+)) mice, whereas the increase in cerebral edema volume was ameliorated by lentiviral-mediated re-expression of Cav-1. Furthermore, Cav-1(-/-) mice had significantly higher degradation of tight junction proteins and proteolytic activity of matrix metalloproteinase than Cav-1(+/+) mice. Conversely, re-expression of Cav-1 in Cav-1(-/-) mice restored tight junction protein expression and reduced matrix metalloproteinase proteolytic activity. CONCLUSIONS: These results indicate that Cav-1 is a critical determinant of BBB permeability. Strategies for regulating Cav-1 represent a novel therapeutic approach to controlling BBB disruption and subsequent neurological deterioration during cerebral ischemia.

Treatment of mallet fracture using a percutaneous fixation technique with an 18-gauge needle.

The purpose of this paper is to introduce a simple and intuitive treatment method using an 18-gauge needle for mallet fractures that involve more than one-third of the articular surface. We performed a retrospective review of 17 patients who underwent closed reduction using an 18-gauge needle with transfixation of Kirschner wire between March 2007 and October 2013. According to the Wehbe and Schneider classification, 15 cases were type IB, 1 was type IIB, and 1 was type IIC. The mean size of bony fragments at the time of injury was 53 percent of the articular surface of the distal phalanx. According to Crawford's criteria, 6 of 17 patients had an excellent result, 9 had a good result and 2 had fair results. Our method of percutaneous reduction using an 18-gauge needle with transfixation of Kirschner wire is minimally invasive and is useful for the fixation of mallet fractures.

Neuron type-specific optogenetic stimulation for differential stroke recovery in chronic capsular infarct.

Cortical neuromodulation (CNM) is widely used to promote recovery after stroke. Despite the beneficial results of CNM, the roles played by different neuron types in the effects of current CNM techniques are unable to be differentiated. Our aim was to use selective optogenetic cortical stimulation to explore how different subpopulations of neuronal cells contribute to poststroke recovery. We transduced the sensory-parietal cortex (SPC) of rats with CamKII-ChR2 (pyramidal neurons), PV-ChR2 (parvalbumin-expressing inhibitory neurons), or hSyn-ChR2 (pan-neuronal population) before inducing photothrombotic capsular infarct lesions. We found that selective stimulation of inhibitory neurons resulted in significantly greater motor recovery than stimulation of excitatory neurons or the pan-neuronal population. Furthermore, 2-deoxy-2-[18F] fluoro-D-glucose microPET (FDG-microPET) imaging revealed a significant reduction in cortical diaschisis and activation of the corticostriatal neural circuit, which were correlated with behavioral recovery in the PV-ChR2 group. The spatial pattern of brain-derived neurotrophic factor (BDNF) expression was evident in the stimulated cortex and underlying cortico-subcortical circuit. Our results indicate that the plasticity of inhibitory neurons is crucial for functional recovery after capsular infarct. Modifying CNM parameters to potentiate the stimulation of inhibitory neurons could improve poststroke outcomes.

Development of an anti-tauopathy mucosal vaccine specifically targeting pathologic conformers.

Alzheimer's disease (AD) and related tauopathies are associated with pathological tau protein aggregation, which plays an important role in neurofibrillary degeneration and dementia. Targeted immunotherapy to eliminate pathological tau aggregates is known to improve cognitive deficits in AD animal models. The tau repeat domain (TauRD) plays a pivotal role in tau-microtubule interactions and is critically involved in the aggregation of hyperphosphorylated tau proteins. Because TauRD forms the structural core of tau aggregates, the development of immunotherapies that selectively target TauRD-induced pathological aggregates holds great promise for the modulation of tauopathies. In this study, we generated recombinant TauRD polypeptide that form neurofibrillary tangle-like structures and evaluated TauRD-specific immune responses following intranasal immunization in combination with the mucosal adjuvant FlaB. In BALB/C mice, repeated immunizations at one-week intervals induced robust TauRD-specific antibody responses in a TLR5-dependent manner. Notably, the resulting antiserum recognized only the aggregated form of TauRD, while ignoring monomeric TauRD. The antiserum effectively inhibited TauRD filament formation and promoted the phagocytic degradation of TauRD aggregate fragments by microglia. The antiserum also specifically recognized pathological tau conformers in the human AD brain. Based on these results, we engineered a built-in flagellin-adjuvanted TauRD (FlaB-TauRD) vaccine and tested its efficacy in a P301S transgenic mouse model. Mucosal immunization with FlaB-TauRD improved quality of life, as indicated by the amelioration of memory deficits, and alleviated tauopathy progression. Notably, the survival of the vaccinated mice was dramatically extended. In conclusion, we developed a mucosal vaccine that exclusively targets pathological tau conformers and prevents disease progression.

Bilateral perisylvian ulegyria: an under-recognized, surgically remediable epileptic syndrome.

PURPOSE: Interest in the association of epilepsy and pseudobulbar palsy was rekindled since the identification through magnetic resonance imaging (MRI) of bilateral perisylvian polymicrogyria (PMG). Seizures are often intractable, but resective epilepsy surgery has not been recommended. However, a similar clinical picture can be encountered in patients with bilateral perisylvian destructive lesions, which fit the description of ulegyria (ULG). We report a series of patients with epilepsy and pseudobulbar palsy due to bilateral perisylvian ULG (BP-ULG), show that hippocampal sclerosis (HS) is often associated and highlight the fact that in this entity, unlike in malformative bilateral perisylvian PMG, seizures may be surgically treated. METHODS: The motor, cognitive, epileptologic, and imaging features of 12 patients with perisylvian ULG followed at three institutions are described. For patients with refractory seizures, we detail extracranial and intracranial electrographic recordings, surgical strategies, histopathologic analyses of the resected tissue, and outcome of surgical treatment. Descriptive statistics were used for quantitative and categorical variables. Student's t-test was used to compare means, and a p < 0.05 was considered significant. KEY FINDINGS: Pseudobulbar palsy and mental retardation were present in all patients with symmetrical BP-ULG. Five had refractory seizures. There was no relationship between the severity of the pseudobulbar palsy or of the mental retardation and the degree of seizure control with medication. The five patients in whom seizures were refractory to medication had significantly earlier age of onset and longer duration of epilepsy (p < 0.05). Dual pathology with associated unilateral HS was present in four. One patient with dual pathology had a temporolimbic electroclinical picture and had an anterior temporal lobectomy (ATL) based upon noninvasive evaluation. The other four had ictal semiology suggesting involvement of both temporolimbic and perisylvian cortex. Intracranial electroencephalography (EEG) showed concomitant seizure onset in the anterior temporal region and in the ipsilateral ULG in three of the four with dual pathology and in the ulegyric cortex in the one without HS. Resection guided by a combination of semiology, MRI, and extra and intracranial EEG led to complete seizure control in two and almost complete seizure control (Engel class II) in two other patients. The only surgical failure was an isolated ATL in a patient with dual pathology, and concomitant seizure onset in both lesions according to semiology and intracranial EEG. SIGNIFICANCE: Our findings suggest that BP-ULG mimics the clinical features of bilateral perisylvian PMG. In patients with refractory seizures, recognition of this entity should lead to consideration of resective surgery despite the bilateral ULG.

Prognostic significance of neuronal marker expression in glioblastomas.

PURPOSE: Glioblastomas are the most malignant tumors of central nervous system neoplasms and are well known for their biological heterogeneity. Contrary to the putative hypothesis of purely glial differentiation in glioblastomas, they often demonstrate immunopositivity for neuronal markers. However, the significance of their neuronal marker expression is still controversial. To evaluate the prognostic implication of neuronal expression in glioblastoma, this study investigated the expression of neuronal markers in a large series of glioblastoma patients in terms of patient survival rate. METHODS: Expression of synaptophysin, neurofilament protein, and NeuN was explored using immunohistochemistry in 88 cases of glioblastoma. Clinicopathological variables as well as patients' survival data were compared according to the immunopositivity of cases. RESULTS: Sixty-one of the 88 tumors (69.3 %) were positive for at least one neuronal marker. Synaptophysin positivity was observed in 43 cases (48.9 %). Neurofilament protein and NeuN were positive in 38 (43.2 %) and 42 cases (47.7 %), respectively. There was no statistically significant difference in overall survival and progression-free survival in association with neuronal marker expression. However, gross total removal or combined radiotherapy and chemotherapy significantly prolonged survival (P=0.041 and 0.044). Cox's proportional hazard model revealed that NeuN expression was the independent prognostic factors in progression-free survival (P=0.012). CONCLUSIONS: Although the correlation of neuronal marker expression and clinical outcome in glioblastoma is of considerable interest, the presented data support the limited prognostic value of neuronal marker expression in glioblastoma.

Tumour-infiltrating T-cell subpopulations in glioblastomas.

This study was designed to determine the incidence and prognostic value of various populations of tumour-infiltrating T cells in glioblastomas. We also evaluated the difference in T-cell populations after conventional treatment. Sixty-seven patients with glioblastomas underwent surgery between 2003 and April 2009. Immunohistochemical staining was performed for CD3, CD4, CD8 and FoxP3, and the average number and percentage of positive cells were calculated. In eight patients, the average number of subpopulations was compared between the specimens obtained during the first and second operations. Age, gender, Karnofsky performance status, Radiation Therapy Oncology Group-recursive partitioning analysis (RTOG-RPA) classes, extent of removal, treatment modality, O-6-methylguanine-DNA methyltransferase (MGMT) methylation status and immunopositivity for CD4, CD8 and FoxP3 were analyzed as prognostic factors. There was an average of 12.8 ± 1.8 CD31 T cells, 1.5 ± 0.5 CD41 T cells, 6.8 ± 1.3 CD81 T cells and 0.6 ± 0.2 FoxP3 cells. The percentage of positive T-cell subpopulations was 89.6%, 22.4%, 77.6% and 34.3% for CD3, CD4, CD8 and FoxP3, respectively. In eight patients, there was no difference in the subpopulations between the first and second operations. The median progression-free survival was 7.0 months (95% CI, 5.2-8.9 months) and the overall survival was 14.8 months (95% CI, 11-18.7 months). Univariate analysis showed a statistically significant difference in progression-free survival for CD8 (p = 0.02) and overall survival for RTOG-RPA classes (p = 0.003), the extent of removal (p = 0.01) and MGMT promoter methylation status (p = 0.005). Based on multivariate analysis, RTOG-RPA classes were significantly associated with longer overall survival. The intratumoural immune response occurred frequently in glioblastomas and there was a consistent response, even after conventional treatment. There was a statistically significant difference in progression-free survival for CD81 T cells in immunologically privileged central nervous system.

High Entropy Oxide Relaxor Ferroelectrics.

Relaxor ferroelectrics are important in technological applications due to strong electromechanical response, energy storage capacity, electrocaloric effect, and pyroelectric energy conversion properties. Current efforts to discover and design materials in this class generally rely on substitutional doping as slight changes to local compositional order can significantly affect the Curie temperature, morphotropic phase boundary, and electromechanical responses. In this work, we demonstrate that moving to the strong limit of compositional complexity in an ABO3 perovskite allows stabilization of relaxor responses that do not rely on a single narrow phase transition region. Entropy-assisted synthesis approaches are utilized to synthesize single-crystal Ba(Ti0.2Sn0.2Zr0.2Hf0.2Nb0.2)O3 [Ba(5B)O] films. The high levels of configurational disorder present in this system are found to influence dielectric relaxation, phase transitions, nanopolar domain formation, and Curie temperature. Temperature-dependent dielectric, Raman spectroscopy, and second-harmonic generation measurements reveal multiple phase transitions, a high Curie temperature of 570 K, and the relaxor ferroelectric nature of Ba(5B)O films. The first-principles theory calculations are used to predict possible combinations of cations to design relaxor ferroelectrics and quantify the relative feasibility of synthesizing these highly disordered single-phase perovskite systems. The ability to stabilize single-phase perovskites with various cations on the B-sites offers possibilities for designing high-performance relaxor ferroelectric materials for piezoelectric, pyroelectric, and electrocaloric applications.

Association of a synonymous GAT3 polymorphism with antiepileptic drug pharmacoresistance.

It would be likely that the genetic variants of the GTA3 gene encoding GAT-3, an astrocytic GABA transporter, may alter gamma-aminobutyric acid (GABA) neurotransmission in the synaptic cleft in the epileptic brain and cause antiepileptic drugs (AEDs) pharmacoresistance. A candidate gene association analysis with fine mapping was performed to dissect the genetic contributions of GAT3 to AEDs pharmacoresistance. Two independent case sample sets were recruited (Samples 1 and 2), and each set was divided into two groups (drug-resistant and drug-responsive) according to the treatment outcomes with AEDs. Sample1 (n=400) was used for the initial exploratory stage of the study and sample 2 (n=435) was used for confirmation of the genetic association in the replication stage of the study. A GAT3 polymorphism (GAT3 c.1572 C>T, rs2272400) was nominally associated with AEDs pharmacoresistance (P(CC) vs P(CT/TT)=0.012, P(allelic)=0.01). The odds ratio (OR) for AED pharmacoresistance was 1.6 (95% confidence interval (CI), 1.11-2.24; P=0.01) in the additive models of inheritance. The statistical significance remained after we adjusted for a confounding factor, the etiology of epilepsy, at 0.012 (adjusted OR: 1.73, 95% CI: 1.13-2.67) and used Bonferroni's correction for multiple comparisons at 0.048. Importantly, the positive association of c.1572 T was reproduced in the replication stage (P(allelic)=0.037, joint P-value of the replication=0.001). The results suggest that GAT3 c.1572T may be one of the contributing factors with a modest effect on AEDs pharmacoresistance in the epileptic brain, shed light on a better understanding of the underlying mechanisms and serve as an impetus for new avenues of treatment for AEDs pharmacoresistance.

Evidence for epistatic interactions in antiepileptic drug resistance.

To investigate the epistatic interactions involved in antiepileptic drug (AED) resistance, 26 coding single-nucleotide polymorphisms (SNPs) were selected from 16 candidate genes. A total of 200 patients with drug-resistant localization-related epilepsy and 200 patients with drug-responsive localization-related epilepsy were genotyped individually for the SNPs. Rather than using the traditional parametric statistical method, a new statistical method, multifactor dimensionality reduction (MDR), was used to determine whether gene-gene interactions increase the risk of AED resistance. The MDR method indicated that a combination of four SNPs (rs12658835 and rs35166395 from GABRA1, rs2228622 from EAAT3 and rs2304725 from GAT3) was the best model for predicting susceptibility to AED resistance with a statistically significant testing accuracy of 0.625 (P < 0.001) and cross-validation consistency of 10/10. This best model had an odds ratio of 3.68 with a significant 95% confidence interval of 2.32-5.85 (P < 0.0001). Our results may provide meaningful information on the mechanism underlying AED resistance and, to the best of our knowledge, this is the first report of evidence for gene-gene interactions underlying AED resistance.

Sinonasal teratocarcinosarcoma with rhabdoid features.

Sinonasal teratocarcinosarcoma (SNTCS) is a very rare tumor developed in the nasal cavity and paranasal sinuses. The rhabdoid phenotype represents an aggressive biological behavior, but the rhabdoid feature has hitherto not been reported in cases of SNTCS. A 46-year-old man complained of a 1-month history of left-sided nasal obstruction. Computed tomography scan and magnetic resonance imaging showed a tumor mass involving the left nasal cavity, ethmoid sinus, and ethmoid bone with extension to the left frontal lobe of the brain. A gross total resection of the mass was performed and postoperative radiation therapy administered. Seven weeks later, several recurring masses were detected in the left frontotemporal lobe of the brain. A gross total resection of the mass was performed and postoperative chemotherapy administered. Histopathologically, the tumor showed benign and malignant epithelial, mesenchymal, neural, and immature elements. In addition, diffuse sheets of rhabdoid cells were immunopositive for vimentin, nestin, neuron-specific enolase, and INI1. Ultrastructurally, rhabdoid cells showed paranuclear aggregates and whorls of intermediate filaments with a 9-10 nm diameter. In conclusion, we report first case of rhabdoid features in SNTCS. The present case showed an advanced stage and early recurrence; the rhabdoid component was probably responsible for this aggressive behavior.

Promoter methylation status of hMLH1, hMSH2, and MGMT genes in colorectal cancer associated with adenoma-carcinoma sequence.

PURPOSE: Epigenetic silencing of the DNA mismatch repair genes has been poorly described in colorectal carcinomas showing the classic adenoma-carcinoma pathway of carcinogenesis. The aim of this study was to investigate the methylation status of MutL homolog 1 (hMLH1), MutS homolog 2 (hMSH2), and O-6-methylguanine-DNA methyltransferase (MGMT) in a series of colorectal carcinomas that contain both adenomas and carcinomas. METHODS: Promoter methylation of hMLH1, hMSH2, and MGMT was evaluated in normal mucosa, adenoma, and carcinoma samples from 112 colorectal cancer patients. Methylation was assessed by bisulfite modification and methylation-specific PCR. Expression of the gene products was also examined by immunohistochemistry. RESULTS: Of the 112 adenomas, methylation was detected for hMLH1 (2, 1.8%), hMSH2 (9, 8.0%), and MGMT (38, 33.9%). In the carcinoma samples, methylation was seen in hMLH1 (2, 1.8%), hMSH2 (15, 13.4%), and MGMT (53, 47.3%). In normal mucosa, hMSH2 (6, 5.4%) and MGMT (12, 10.7%) were methylated, whereas hMLH1 was not. Immunohistochemical analysis revealed abnormal hMLH1 (14, 12.5%), hMSH2 (11, 9.8%), and MGMT (53, 47.3%) expression with a significant correlation between aberrant MGMT methylation and a loss of MGMT expression. CONCLUSIONS: These data suggest that CpG island methylation in hMSH2 and MGMT, but not hMLH1, is closely related to carcinogenesis in colorectal carcinomas presenting with a conventional adenoma-carcinoma sequence. Therefore, the detection of hMSH2 and MGMT methylation may have clinical significance in the evaluation of colon cancer patients and in tumor-specific management of the disease.

The presence of stem cell marker-expressing cells is not prognostically significant in glioblastomas.

Glioblastoma is one of the most frequent primary brain tumors and is characterized by aggressive clinical behavior and biologic heterogeneity. To evaluate the prognostic implication of cancer stem cell markers in glioblastoma, the expression of these markers was investigated in a large series of glioblastoma patients in relation to the survival rate. This series includes 88 cases of glioblastoma that were diagnosed at the Chonnam University Hwasun Hospital from 2004 to 2009. The expression of newly established stem cell markers (nestin, CD133 and CD15) was detected using immunohistochemical analysis. The presence of immunopositive tumor cells was evaluated and interpreted in comparison with the patients' survival data. The expression of nestin was high in 60 cases (68.2%). CD133 and CD15 were positive in 52 cases (59.1%) and 40 cases (45.5%), respectively. No statistically significant difference in patient survival according to stem cell marker expression was observed (P > 0.05). However, gross total resection or combined radiation therapy and chemotherapy significantly prolonged survival (P = 0.04 and P = 0.04). Cox's proportional hazards model showed that the gross total resection and combined radiation therapy and chemotherapy were independent prognostic factors. Although the correlation of stem cell marker expression with clinical outcome in glioma is of considerable interest, the data do not support their prognostic value in glioblastoma. Identification of the key cells in the glioblastoma population in the context of clinical outcomes will provide insight into the mechanism of brain tumorigenesis and will be of paramount importance in determining therapeutically appropriate targets.

Nogo-A expression in oligodendroglial tumors.

Nogo-A belongs to the reticulon protein family and is expressed in the inner and outer loops of myelin sheaths of oligodendrocytes. We analyzed the patterns of Nogo-A expression in human gliomas in an effort to identify a useful marker for the characterization of oligodendroglial tumors. We determined the expression of Nogo-A in a panel of 58 astrocytic and oligodendroglial tumors using immunohistochemistry and compared the expression of Nogo-A with Olig-2, a recently identified marker for oligodendrogliomas. To localize Nogo-A expression, immunofluorescent staining was performed using other glial markers (MAP-2 and GFAP). We also confirmed the overexpression of the Nogo-A protein in 53 astrocytic and oligodendroglial tumors using Western blot analysis. Based on immunohistochemical analysis, Nogo-A and Olig-2 had specificity in the detection of oligodendroglial tumors from astrocytic tumors (P=0.001). The level of Nogo-A staining was highly correlated with Olig-2 (P=0.001). The sensitivity and specificity of Nogo-A for oligodendroglial tumors was 86.9% and 57.1%, respectively. Nogo-A expression overlapped that of other oligodendroglial markers, but with different patterns of expression. Western blot analysis revealed that Nogo-A is predominantly expressed in 85.7% of oligodendroglioma cells and 93.7% of anaplastic oligodendroglioma cells. Like other oligodendroglial markers, Nogo-A is highly expressed in oligodendroglial tumors; however, it does not serve as a definite marker specific for oligodendroglial tumors.

Increased expression of L-amino acid transporters in balloon cells of tuberous sclerosis.

OBJECTS: Tuberous sclerosis complex (TSC) is a dysgenetic syndrome involved in multiple organs, and the pathognomonic cortical tuber act as an epileptic substrate. The amino acid transport system L (LAT) is a major nutrient transport system, and LAT1 is highly expressed in malignant tumors to support tumor cell growth. To study the life-long epilepsy from the cortical tuber, the expression of LAT1 in balloon cells and dysplastic neurons of the cortical tuber is investigated. MATERIALS AND METHODS: LAT1 expression was investigated by LAT1 mRNA using reverse transcription-polymerase chain reaction and immunohistochemical staining with anti-human LAT1 antibody in nine patients with TSC and three control brains. CONCLUSION: LAT1 mRNA was detectable only in fresh-frozen tissues of TSC, and it was upregulated in the cortical tuber lesion. While the LAT1 immunopositivity of control brains was limited in the capillary endothelial cells in the gray matter, increased LAT1 immunopositivity was noted in balloon cells of the cortical tubers in addition to the capillary endothelial cells as shown in control brains. Linear and strong immunopositivity along the cell membrane and cytoplasm of the balloon cells, and weakly granular immunopositivity in their cytoplasm were noted. Increased expression of LAT1 in the balloon cells is important for the active transport of large neutral amino acids into the balloon cells, and that the biologic process may play an important role in the active protein synthesis with metabolic maintenance of balloon cells in cortical tubers of patients with TSC.

Congenital pigment synthesizing melanoma of the scalp.

The pigment synthesizing melanoma, so-called animal type melanoma, is a rare variant of melanoma that is characterized by prominent melanin production and an unpredictable prognosis. Congenital onset of this melanoma is exceedingly rare. A 2-month-old Korean girl had a black nodule and a satellite black macule on the scalp which were noticed at birth. She received a surgical resection 3 months later because of rapidly growing lesions and the histopathologic features of a pigment synthesizing melanoma. Two months later, she returned with cervical area swelling, and the excised multiple lymph nodes showed metastatic malignant melanoma. The exact origin and pathogenesis of congenital pigment synthesizing melanoma is different from the more common forms of melanoma and remains poorly understood.