Altered resting-state connectivity in subjects at ultra-high risk for psychosis: an fMRI study

<p>Abstract</p> <p>Background</p> <p>Individuals at ultra-high risk (UHR) for psychosis have self-disturbances and deficits in social cognition and functioning. Midline default network areas, including the medial prefrontal cortex and posterior cingulate cortex, are implicated in self-referential and social cognitive tasks. Thus, the neural substrates within the default mode network (DMN) have the potential to mediate self-referential and social cognitive information processing in UHR subjects.</p> <p>Methods</p> <p>This study utilized functional magnetic resonance imaging (fMRI) to investigate resting-state DMN and task-related network (TRN) functional connectivity in 19 UHR subjects and 20 matched healthy controls. The bilateral posterior cingulate cortex was selected as a seed region, and the intrinsic organization for all subjects was reconstructed on the basis of fMRI time series correlation.</p> <p>Results</p> <p>Default mode areas included the posterior/anterior cingulate cortices, the medial prefrontal cortex, the lateral parietal cortex, and the inferior temporal region. Task-related network areas included the dorsolateral prefrontal cortex, supplementary motor area, the inferior parietal lobule, and middle temporal cortex. Compared to healthy controls, UHR subjects exhibit hyperconnectivity within the default network regions and reduced anti-correlations (or negative correlations nearer to zero) between the posterior cingulate cortex and task-related areas.</p> <p>Conclusions</p> <p>These findings suggest that abnormal resting-state network activity may be related with the clinical features of UHR subjects. Neurodevelopmental and anatomical alterations of cortical midline structure might underlie altered intrinsic networks in UHR subjects.</p

Highly interconnected ordered mesoporous carbon-carbon nanotube nanocomposites: Pt-free, highly efficient, and durable counter electrodes for dye-sensitized solar cells

We report the preparation of highly interconnected ordered mesoporous carbon-carbon nanotube nanocomposites which show Pt-like dye-sensitized solar cell (DSSC) efficiency and remarkable long-term durability as DSSC counter electrodes.close413

Reduced cortical folding of the anterior cingulate cortex in obsessive-compulsive disorder

Background: Anterior cingulate cortex (ACC) abnormalities have been implicated consistently in the pathophysiology of obsessive-compulsive disorder (OCD), yet it remains unclear whether these abnormalities originated during early neurodevelopment. In this study, we examined the ACC sulcal/gyral patterns to investigate whether neurodevelopmental anomalies of the ACC were present in patients with OCD. We hypothesized that patients with OCD would show reduced cortical folding of the ACC compared with controls. Methods: We used magnetic resonance imaging (MRI) of 169 healthy volunteers and 110 patients with OCD to examine the paracingulate sulcus and cingulate sulcus. We assessed cortical folding patterns according to established classification criteria and constructed 3 categories of paracingulate sulcus morphology according to its presence and anteroposterior extent: "prominent," "present" and "absent." We classified the cingulate sulcus as "interrupted" or "continuous" according to the interruptions in its course. In addition, we evaluated ACC sulcal asymmetry based on interhemispheric comparisons of paracingulate sulcus morphology. Results: Analyses revealed that patients with OCD were significantly less likely than controls to show a well-developed left paracingulate sulcus: 50.0% of patients and 65.1% of controls showed a "prominent" or "present" paracingulate sulcus in the left hemisphere. However, there were no differences in regard to cingulate sulcus continuity, and patients also showed the same leftward ACC sulcal asymmetry as controls. Limitations: Our study was limited by the fact that we obtained the MRI scans from 2 different scanners, and we did not calculate cerebral fissurization as our study was restricted to 1 specific brain region. Moreover, patients and controls differed significantly in terms of sex ratio and IQ, although we controlled these variables as covariates. Conclusion: Our findings imply a subtle deviation in the early neurodevelopment of the ACC in patients with OCD, but the extent to which these anomalies contributed to the pathogenesis of OCD remains unclear. Further studies that link the ACC morphologic anomalies to the pathophysiology of OCD are recommended.This work was supported by Cognitive Neuroscience Program of the Korean Ministry of Science and Technology (M10644020003-08N4402-00310).Jung MH, 2009, PROG NEURO-PSYCHOPH, V33, P605, DOI 10.1016/j.pnpbp.2009.02.017Whittle S, 2009, PSYCHIAT RES-NEUROIM, V172, P68, DOI 10.1016/j.pscychresns.2008.06.005Gu BM, 2008, BRAIN, V131, P155, DOI 10.1093/brain/awm277Fornito A, 2007, ACTA PSYCHIAT SCAND, V116, P467, DOI 10.1111/j.1600-0447.2007.01069.xShin YW, 2007, HUM BRAIN MAPP, V28, P1128, DOI 10.1002/hbm.20338Huster RJ, 2007, NEUROIMAGE, V34, P888, DOI 10.1016/j.neuroimage.2006.10.023De Geus F, 2007, PSYCHIAT CLIN NEUROS, V61, P45, DOI 10.1111/j.1440-1819.2007.01609.xFornito A, 2006, SCHIZOPHR RES, V88, P192, DOI 10.1016/j.schres.2006.06.034Jang JH, 2006, AM J PSYCHIAT, V163, P1202Kim YY, 2006, BRAIN TOPOGR, V18, P201, DOI 10.1007/s10548-006-0269-2Klimkeit EI, 2006, CORTEX, V42, P113Valente AA, 2005, BIOL PSYCHIAT, V58, P479, DOI 10.1016/j.biopsych.2005.04.021Rosenberg DR, 2004, J AM ACAD CHILD PSY, V43, P1146, DOI 10.1097/01.chi.0000132812.44664.2dFornito A, 2004, CEREB CORTEX, V14, P424, DOI 10.1093/cercor/bhh004Shin YW, 2004, PSYCHIAT CLIN NEUROS, V58, P16Yucel M, 2003, BRIT J PSYCHIAT, V182, P518Yucel M, 2002, BIOL PSYCHIAT, V52, P15Lyoo IK, 2001, J CLIN PSYCHIAT, V62, P637Allman JM, 2001, ANN NY ACAD SCI, V935, P107Yucel M, 2001, CEREB CORTEX, V11, P17Bradshaw JL, 2000, BRAIN LANG, V73, P297Bush G, 2000, TRENDS COGN SCI, V4, P215Penalva J, 2000, BIOSENS BIOELECTRON, V15, P99Lohmann G, 1999, CEREB CORTEX, V9, P754Magnotta VA, 1999, CEREB CORTEX, V9, P151Tibbo P, 1999, J PSYCHIATR NEUROSCI, V24, P15Rosenberg DR, 1998, BIOL PSYCHIAT, V43, P623Purcell R, 1998, BIOL PSYCHIAT, V43, P348SAXENA S, 1998, BRIT J PSYCHIAT S, V35, P26FIRST MB, 1998, STRUCTURED CLIN INTESIEGEL S, 1998, NONPARAMETRIC STAT BRauch SL, 1997, J NEUROPSYCH CLIN N, V9, P568Bartley AJ, 1997, BRAIN, V120, P257VanEssen DC, 1997, NATURE, V385, P313Paus T, 1996, CEREB CORTEX, V6, P207FIRST MB, 1996, STRUCTURED CLIN INTEVOGT BA, 1995, J COMP NEUROL, V359, P490DEVINSKY O, 1995, BRAIN, V118, P279ARMSTRONG E, 1995, CEREB CORTEX, V5, P56PAULS DL, 1995, AM J PSYCHIAT, V152, P76KIM JS, 1995, KOREAN J CLIN PSYCHO, V14, P111*AM PSYCH ASS, 1994, DIAGN STAT MAN MENTBAXTER LR, 1992, ARCH GEN PSYCHIAT, V49, P681HUANG CC, 1991, BRAIN DEV-JPN, V13, P27WELKER W, 1990, CEREBRAL CORTEX B, V8, P3DIXON WJ, 1990, BMDP STAT SOFTWARE MHOLLANDER E, 1990, ARCH GEN PSYCHIAT, V47, P27CROW TJ, 1989, ARCH GEN PSYCHIAT, V46, P1145GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1006GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1012SWEDO SE, 1989, ARCH GEN PSYCHIAT, V46, P518RAKIC P, 1988, SCIENCE, V241, P170BEAR D, 1986, ARCH NEUROL-CHICAGO, V43, P598GESCHWIND N, 1985, ARCH NEUROL-CHICAGO, V42, P521FLORHENRY P, 1983, CEREBRAL BASIS PSYCH, P301CHI JG, 1977, ANN NEUROL, V1, P86ANNETT M, 1970, BRIT J PSYCHOL, V61, P303CRICHTONBROWNE J, 1879, BRAIN, V2, P42

The effect of meditation on brain structure: cortical thickness mapping and diffusion tensor imaging

A convergent line of neuroscientific evidence suggests that meditation alters the functional and structural plasticity of distributed neural processes underlying attention and emotion. The purpose of this study was to examine the brain structural differences between a well-matched sample of long-term meditators and controls. We employed whole-brain cortical thickness analysis based on magnetic resonance imaging, and diffusion tensor imaging to quantify white matter integrity in the brains of 46 experienced meditators compared with 46 matched meditation-naïve volunteers. Meditators, compared with controls, showed significantly greater cortical thickness in the anterior regions of the brain, located in frontal and temporal areas, including the medial prefrontal cortex, superior frontal cortex, temporal pole and the middle and interior temporal cortices. Significantly thinner cortical thickness was found in the posterior regions of the brain, located in the parietal and occipital areas, including the postcentral cortex, inferior parietal cortex, middle occipital cortex and posterior cingulate cortex. Moreover, in the region adjacent to the medial prefrontal cortex, both higher fractional anisotropy values and greater cortical thickness were observed. Our findings suggest that long-term meditators have structural differences in both gray and white matter

Identification of MYC as an antinecroptotic protein that stifles RIPK1-RIPK3 complex formation

The underlying mechanism of necroptosis in relation to cancer is still unclear. Here, MYC, a potent oncogene, is an antinecroptotic factor that directly suppresses the formation of the RIPK1-RIPK3 complex. Gene set enrichment analyses reveal that the MYC pathway is the most prominently down-regulated signaling pathway during necroptosis. Depletion or deletion of MYC promotes the RIPK1-RIPK3 interaction, thereby stabilizing the RIPK1 and RIPK3 proteins and facilitating necroptosis. Interestingly, MYC binds to RIPK3 in the cytoplasm and inhibits the interaction between RIPK1 and RIPK3 in vitro. Furthermore, MYC-nick, a truncated form that is mainly localized in the cytoplasm, prevented TNF-induced necroptosis. Finally, down-regulation of MYC enhances necroptosis in leukemia cells and suppresses tumor growth in a xenograft model upon treatment with birinapant and emricasan. MYC-mediated suppression of necroptosis is a mechanism of necroptosis resistance in cancer, and approaches targeting MYC to induce necroptosis represent an attractive therapeutic strategy for cancer

Predicting factors of present hepatitis C virus infection among patients positive for the hepatitis C virus antibody

Background/AimsTo identify the predicting factors of present hepatitis C virus (HCV) infection among patients with positivity for antibodies to HCV (anti-HCV).MethodsWe analyzed patients who showed positive enzyme immunoassay (EIA) results and performed an HCV RNA test as a confirmatory test at Kyung Hee University Hospital at Gangdong from June 2006 to July 2012. The features distinguishing the groups with positive and negative HCV RNA results were reviewed.ResultsIn total, 490 patients were included. The results of the HCV RNA test were positive and negative in 228 and 262 patients, respectively. The index value of anti-HCV, mean age, platelet counts, total bilirubin, prothrombin time international normalized ratio, albumin and alanine transaminase (ALT) levels differed significantly between the two groups. On multivariable analysis, an index value of anti-HCV >10 [odds ratio (OR)=397.27, P40 IU/L (OR=3.64, P=0.001), and albumin <3.8 g/dL (OR=2.66, P=0.014) were related to present HCV infection.ConclusionsAlthough EIA is not a quantitative test, considering the anti-HCV titer with ALT and albumin levels may be helpful in predicting present of HCV infection