257 research outputs found

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

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    <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

    Robotic pylorus preserving pancreaticoduodenectomy with mini-laparotomy reconstruction in patient with ampullary adenoma

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    Robotic surgical system provides many unique advantages which might compensate the limitations of usual laparoscopic surgery. By using robotic surgical system, we performed robot-assisted laparoscopic pancreaticoduodenectomy (PD). A Sixty-two year old female patient with an ampullary mass underwent robot assisted PD due to imcomplete treatment of endoscopic ampullectomy. The removal of specimen and reconstruction were performed through small upper midline skin incision. Robot working time was about 8 hours, and blood loss was about 800 ml without blood transfusion. She returned to an oral diet on postoperative day 3. Grade B pancreatic leak was noted during the postoperative period, but was successfully managed by conservative management alone. We successfully performed da Vinci-assisted laparoscopic PD, and robot surgical system provided three-dimensional stable visualization and wrist-like motion of instrument facilitated complex operative procedures. More experiences are necessary to address real role of robot in far advanced laparoscopic pancreatic surgery

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

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    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

    Syringocystadenocarcinoma Papilliferum: A Case Report

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    Syringocystadenocarcinoma papilliferum (SCACP) is a rare form of adenocarcinoma of the skin. This is the malignant counterpart of syringocystadenoma papilliferum (SCAP) and usually develops on the scalp in a long-standing lesion identified clinically as SCAP. We describe a 65-yr-old Korean man with a nodule on the right supra-pubic area with a 2-yr duration. Histologically this tumor had a similar overall configuration as in SCAP, but the tumor was asymmetric and poorly circumscribed, extending into the deep dermis and showed cytologic atypia. The tumor cells showed positive reaction to GCDFP-15, but negative reaction to CEA and HMFG-1. We established the diagnosis of SCACP in the patient, and a wide excision was performed to remove the tumor. The patient has been well without relapse or metastasis for 2 yr
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