Biomedical subjects

C Y Hsu

Publications and source records attributed to C Y Hsu.

At least 19 recordsLinked to original sources

PubMed2006

Developing an NLP and IR-based algorithm for analyzing gene-disease relationships.

OBJECTIVES: High-throughput techniques such as cDNA microarray, oligonucleotide arrays, and serial analysis of gene expression (SAGE) have been developed and used to automatically screen huge amounts of gene expression data. However, researchers usually spend lots of time and money on discovering gene-disease relationships by utilizing these techniques. We prototypically implemented an algorithm that can provide some kind of predicted results for biological researchers before they proceed with experiments, and it is very helpful for them to discover gene-disease relationships more efficiently. METHODS: Due to the fast development of computer technology, many information retrieval techniques have been applied to analyze huge digital biomedical databases available worldwide. Therefore we highly expect that we can apply information retrieval (IR) technique to extract useful information for the relationship of specific diseases and genes from MEDLINE articles. Furthermore, we also applied natural language processing (NLP) methods to do the semantic analysis for the relevant articles to discover the relationships between genes and diseases. RESULTS: We have extracted gene symbols from our literature collection according to disease MeSH classifications. We have also built an IR-based retrieval system, "Biomedical Literature Retrieval System (BLRS)" and applied the N-gram model to extract the relationship features which can reveal the relationship between genes and diseases. Finally, a relationship network of a specific disease has been built to represent the gene-disease relationships. CONCLUSIONS: A relationship feature is a functional word that can reveal the relationship between one single gene and a disease. By incorporating many modern IR techniques, we found that BLRS is a very powerful information discovery tool for literature searching. A relationship network which contains the information on gene symbol, relationship feature, and disease MeSH term can provide an integrated view to discover gene-disease relationships.

Algorithms↗

PubMed2005

Amyloid-beta peptide enhances tumor necrosis factor-alpha-induced iNOS through neutral sphingomyelinase/ceramide pathway in oligodendrocytes.

Although accumulating evidence demonstrates that white matter degeneration contributes to pathology in Alzheimer's disease (AD), the underlying mechanisms are unknown. In order to study the roles of the amyloid-beta peptide in inducing oxidative stress damage in white matter of AD, we investigated the effects of amyloid-beta peptide 25-35 (Abeta) on proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha)-induced inducible nitric oxide synthase (iNOS) in cultured oligodendrocytes (OLGs). Although Abeta 25-35 by itself had little effect on iNOS mRNA, protein, and nitrite production, it enhanced TNF-alpha-induced iNOS expression and nitrite generation in OLGs. Abeta, TNF-alpha, or the combination of both, increased neutral sphingomyelinase (nSMase) activity, but not acidic sphingomyelinase (aSMase) activity, leading to ceramide accumulation. Cell permeable C2-ceramide enhanced TNF-alpha-induced iNOS expression and nitrite generation. Moreover, the specific nSMase inhibitor, 3-O-methyl-sphingomyelin (3-OMS), inhibited iNOS expression and nitrite production induced by TNF-alpha or by the combination of TNF-alpha and Abeta. Overexpression of a truncated mutant of nSMase with a dominant negative function inhibited iNOS mRNA production. 3-OMS also inhibited nuclear factor kappaB (NF-kappaB) binding activity induced by TNF-alpha or by the combination of TNF-alpha and Abeta. These results suggest that neutral sphingomyelinase/ceramide pathway is required but may not be sufficient for iNOS expression induced by TNF-alpha and the combination of TNF-alpha and Abeta.

Amyloid beta-Peptides↗

PubMed2005

Infrared thermography to mass-screen suspected SARS patients with fever.

Fever greater than 38 degrees C is a cardinal sign of patients with the severe acute respiratory syndromes (SARS). To reduce the risk of nosocomial cross infections, screening all patients and visitors who visit hospitals and clinics for fever at the entrance of every hospital building has become a standard protocol in Taiwan during the SARS epidemic from mid-April to mid-June 2003. We used a digital infrared thermal imaging (DITI) system (Telesis Spectrum 9000 MB) to conduct mass screening of patients and visitors who entered the hospital to identify those with fever. The DITI system has two components: a sensor head and a PC imaging workstation. The sensor head is an optic-mechanical device which consists of imagining optics for focusing the infrared source information on the infrared detector. The infrared images are further converted into electrical signals, which are then processed for real-time display on the monitor. During the period from April 13 to May 12 2003, 72,327 outpatients and visitors entered Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan. A total of 305 febrile patients (0.42%) was detected by infrared thermography. Among them, three probable SARS patients were identified after thorough studies including contact history, laboratory tests and radiology examinations. The findings suggests that infrared thermography was an effective and reliable tool ideal for mass-screening patients with fever in the initial phase of screening for SARS patients at a busy hospital which sees approximately 3,000 outpatients every weekday during the SARS epidemic.

Cross Infection↗

PubMed2004

Assessment: transcranial Doppler ultrasonography: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.

OBJECTIVE: To review the use of transcranial Doppler ultrasonography (TCD) and transcranial color-coded sonography (TCCS) for diagnosis. METHODS: The authors searched the literature for evidence of 1) if TCD provides useful information in specific clinical settings; 2) if using this information improves clinical decision making, as reflected by improved patient outcomes; and 3) if TCD is preferable to other diagnostic tests in these clinical situations. RESULTS: TCD is of established value in the screening of children aged 2 to 16 years with sickle cell disease for stroke risk (Type A, Class I) and the detection and monitoring of angiographic vasospasm after spontaneous subarachnoid hemorrhage (Type A, Class I to II). TCD and TCCS provide important information and may have value for detection of intracranial steno-occlusive disease (Type B, Class II to III), vasomotor reactivity testing (Type B, Class II to III), detection of cerebral circulatory arrest/brain death (Type A, Class II), monitoring carotid endarterectomy (Type B, Class II to III), monitoring cerebral thrombolysis (Type B, Class II to III), and monitoring coronary artery bypass graft operations (Type B to C, Class II to III). Contrast-enhanced TCD/TCCS can also provide useful information in right-to-left cardiac/extracardiac shunts (Type A, Class II), intracranial occlusive disease (Type B, Class II to IV), and hemorrhagic cerebrovascular disease (Type B, Class II to IV), although other techniques may be preferable in these settings.

Adolescent↗

PubMed2003

Involvement of nucleophosmin/B23 in TPA-induced megakaryocytic differentiation of K562 cells.

Human myelogenous leukaemia K562 cells were induced to undergo megakaryocytic differentiation by treatment with phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) (20 nM, 24-72 h). The steady-state level of nucleophosmin/B23 mRNA decreased during the TPA-induced differentiation. There was also decrease in the level of cellular nucleophosmin/B23 protein and appearance of its degraded product (25 kDa) during the TPA-induced differentiation. Furthermore, K562/B23 (wild type), K562/D1 (delta280-294) and K562/D2 (delta263-294) cells were less, while K562/D3 (delta244-294) cells were more responsive to TPA-induced differentiation as compared to K562/vector or parental K562 cells. Activation of the ERK/MAPK was observed in parental K562 cells upon TPA treatment (5 nM, 5-30 min). As compared to K562/vector cells, less activation of ERK/MAPK was observed in K562/D2 cells, while ERK/MAPK was highly activated in K562/D3 cells upon TPA treatment. Our results indicate that nucleophosmin/B23 plays an important role in TPA-induced differentiation of K562 cells and the amino acids 244-294 at C-terminal of nucleophosmin/B23 could be an important site for regulation of cellular response to differentiation.

Carcinogens↗

PubMed2003

Dose reconstruction for residents living in buildings with moderate and minor 60Co contamination in rebar.

Previously, we have reconstructed cohort dependent individual doses for residents living in rebar buildings of high 60Co contamination. These reconstructions were carried out using intensively collected TLD data on exposure rates at locations of 1 m height and 1 m x 1 m intersections. The present work deals with dose reconstructions for residents living in rebar buildings of moderate and minor 60Co contamination. Since only limited data on exposure rates from survey meters were available, dose reconstructions were based on these data using interpolations. To utilize such data, we examined them with respect to all factors that influenced the dose uncertainties. The interpolated results were given in terms of contour plots (isodose curves) and compared with corresponding results derived from TLD data and Monte Carlo simulations. The comparison revealed that survey meter data could be used to provide reasonable and conservative estimates of residential doses. By applying the cohort-dependent room occupancy factor and the site-dependent area occupancy factor, we reconstructed cohort dependent individual doses and associated uncertainties. Results of dose reconstructions for all residents living in contaminated rebar buildings were provided to the Atomic Energy Council and health authorities for epidemiologic and medical uses.

Air Pollution, Indoor↗

PubMed2003

Successful treatment with weekly paclitaxel in a patient with recurrent endometrial cancer. A case report.

The best treatment for recurrent endometrial cancer is still uncertain, although weekly paclitaxel has shown some promise in the management of this disease. In this report we present a patient with recurrent endometrial cancer treated with weekly paclitaxel. Serial power Doppler angiography was used to assess the effects of therapy. The response was good, suggesting that recurrent endometrial cancer may be successfully treated with weekly paclitaxel and effectively monitored with power Doppler angiography.

Adenocarcinoma↗

PubMed2002

Amyloid-beta induces Smac release via AP-1/Bim activation in cerebral endothelial cells.

Insoluble fibrils of amyloid-beta peptide (Abeta) are the major component of senile and vascular plaques found in the brains of Alzheimer's disease (AD) patients. Abeta has been implicated in neuronal and vascular degeneration because of its toxicity to neurons and endothelial cells in vitro; some of these cells die with characteristic features of apoptosis. We used primary cultures of murine cerebral endothelial cells (CECs) to explore the mechanisms involved in Abeta-induced cell death. We report here that Abeta(25-35), a cytotoxic fragment of Abeta, induced translocation of the apoptosis regulator termed second-mitochondria-derived activator of caspase (Smac) from the intramembranous compartment of the mitochondria to the cytosol 24 hr after exposure. In addition, we demonstrated that X chromosome-linked inhibitor-of-apoptosis protein (XIAP) coimmunoprecipitated with Smac, suggesting that the two proteins bound to one another subsequent to the release of Smac from the mitochondria. Abeta(25-35) treatment also led to rapid AP-1 activation and subsequent expression of Bim, a member of the BH3-only family of proapoptotic proteins. Bim knockdown using an antisense oligonucleotide strategy suppressed Abeta(25-35)-induced Smac release and resulted in attenuation of CEC death. Furthermore, AP-1 inhibition, with curcumin or c-fos antisense oligonucleotide, reduced bim expression. These results suggest that Abeta activates an apoptotic cascade involving AP-1 DNA binding, subsequent bim induction, followed by Smac release and binding to XIAP, resulting in CEC death.

Amyloid beta-Peptides↗

PubMed2002

Zinc translocation accelerates infarction after mild transient focal ischemia.

Excess release of chelatable zinc (Zn(2+)) from central synaptic vesicles may contribute to the pathogenesis of selective neuronal cell death following transient forebrain ischemia, but a role in neurodegeneration after focal ischemia has not been defined. Adult male Long-Evans rats subjected to middle cerebral artery occlusion (MCAO) for 30 min followed by reperfusion developed delayed cerebral infarction reaching completion 3 days after the insult. One day after the insult, many degenerating cerebral neurons exhibited increased intracellular Zn(2+), and some labeled with the antibody against activated caspase-3. I.c.v. administration of the Zn(2+) chelator, EDTA saturated with equimolar Ca(2+) (CaEDTA), 15 min prior to ischemia attenuated subsequent Zn(2+) translocation into cortical neurons, and reduced infarct volume measured 3 days after ischemia. Although the protective effect of CaEDTA at this endpoint was substantial (about 70% infarct reduction), it was lost when insult severity was increased (from 30 to 60 min MCAO), or when infarct volume was measured at a much later time point (14 days instead of 3 days after ischemia). These data suggest that toxic Zn(2+) translocation, from presynaptic terminals to post-synaptic cell bodies, may accelerate the development of cerebral infarction following mild transient focal ischemia.

Aminoquinolines↗

PubMed2001

Tumor necrosis factor receptor deletion reduces nuclear factor-kappaB activation, cellular inhibitor of apoptosis protein 2 expression, and functional recovery after traumatic spinal cord injury.

Tumor necrosis factor-alpha (TNF-alpha) expression has been documented extensively in animal models of traumatic spinal cord injury (SCI). However, the pathophysiological significance of TNF-alpha expression in the injured cord remains to be delineated. The TNF receptor (TNFR)-nuclear factor-kappaB (NF-kappaB) signal transduction pathway is important for maintaining cell viability. NF-kappaB exerts anti-apoptotic effects via an endogenous caspase inhibitory system mediated by cellular inhibitor of apoptosis protein 2 (c-IAP2). NF-kappaB transactivates c-IAP2 to inhibit caspase-3 activation. Progressive cell death, including morphological and biochemical features suggestive of apoptosis, has been noted after SCI. We explored the effects of TNFR1 or TNFR2 deletion on the apoptotic events downstream of NF-kappaB in relation to SCI pathology and functional recovery. Nuclear proteins from the injured cords of the TNFR1(-/-) mice had a reduced NF-kappaB binding activity compared with the wild-type controls. This decrease in NF-kappaB activation was accompanied by a reduction in c-IAP2 expression and an increase in the active form of caspase-3 protein. After SCI the TNFR1(-/-) mice had greater numbers of apoptotic cells, a larger lesion size, and worse functional recovery than wild-type mice. TNFR2-deficient mice had a similar, although not as pronounced, consequence as the TNFR1(-/-) mice. These findings support the argument that the TNFR-NF-kappaB pathway is beneficial for limiting apoptotic cell death after SCI and that a defective TNFR-NF-kappaB pathway results in a poorer neurological outcome. A worse functional outcome in TNFR(-/-) mice suggests that an endogenous apoptosis inhibitory mechanism mediated by TNFR activation, NF-kappaB, and c-IAP2 may be of pathophysiological importance.

Animals↗

PubMed2001

Glucocorticoid receptor-mediated suppression of activator protein-1 activation and matrix metalloproteinase expression after spinal cord injury.

Post-traumatic inflammatory reaction may contribute to progressive tissue damage after spinal cord injury (SCI). Two key transcription factors, nuclear factor kappaB (NF-kappaB) and activator protein-1 (AP-1), are activated in inflammation. An increase in NF-kappaB binding activity has been shown in the injured spinal cord. We report activation of AP-1 after SCI. Electrophoretic mobility shift assay showed that AP-1 binding activity increased after SCI, starting at 1 hr, peaking at 8 hr, and declining to basal levels by 7 d. Methylprednisolone (MP) is the only therapeutic agent approved by the Food and Drug Administration for treating patients with acute traumatic SCI. MP reduced post-traumatic AP-1 activation. RU486, a glucocorticoid receptor (GR) antagonist, reversed MP inhibition of AP-1 activation. Immunostaining showed an increase in the expression of the Fos-B and c-Jun components of AP-1 in the injured cord. A c-fos antisense oligodeoxynucleotide (ODN) inhibited AP-1, but not NF-kappaB, activation after SCI. AP-1 and NF-kappaB can transactivate genes encoding matrix metalloproteinase-1 (MMP-1) and MMP-9. Western blotting and immunostaining show increased expression of MMP-1 and MMP-9 in the injured cord. MP inhibited MMP-1 and MMP-9 expression after SCI. RU486 reversed this MP effect. The c-fos antisense ODN, however, failed to suppress MMP-1 or MMP-9 expression. These findings demonstrate that MP may suppress post-traumatic inflammatory reaction by inhibiting both the AP-1 and NF-kappaB transcription cascades via a GR mechanism. Expression of inflammatory genes such as MMP-1 and MMP-9 that are transactivated jointly by AP-1 and NF-kappaB may not be suppressed by inhibiting only AP-1 activity.

Animals↗

PubMed2001

Amyloid-beta peptides are cytotoxic to oligodendrocytes.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive dementia. Amyloid-beta peptide (Abeta), a 39-43 amino acid peptide derived from beta-amyloid precursor protein, forms insoluble fibrillar aggregates that have been linked to neuronal and vascular degeneration in AD and cerebral amyloid angiopathy. Here we demonstrate that Abeta 1-40 and a truncated fragment, Abeta 25-35, induced death of oligodendrocytes (OLGs) in vitro in a dose-dependent manner with similar potencies. Abeta-induced OLG death was accompanied by nuclear DNA fragmentation, mitochondrial dysfunction, and cytoskeletal disintegration. Abeta activation of redox-sensitive transcription factors NF-kappaB and AP-1 and antioxidant prevention of Abeta-mediated OLG death suggest that oxidative injury contributes to Abeta cytotoxicity in OLGs. Recent demonstration of Abeta deposition and white matter abnormalities in AD implies a potential pathophysiological role for Abeta-mediated cytotoxicity of OLGs in this neurodegenerative disease.

Alzheimer Disease↗

PubMed2001

Delayed glial cell death following wallerian degeneration in white matter tracts after spinal cord dorsal column cordotomy in adult rats.

The devastating consequences of spinal cord injury (SCI) result primarily from damage to long tracts in the spinal white matter. To elucidate the secondary injury processes occurring after SCI, we investigated the relationship between apoptosis and Wallerian degeneration in spinal white matter tracts. In the rat spinal cord, the corticospinal tract (CST) and the dorsal ascending tract (DAT) are separated from each other in the dorsal column and relay information in opposite directions. A dorsal column cordotomy at the eighth thoracic (T8) level simultaneously induces Wallerian degeneration in the CST caudal to and in the DAT rostral to the injury. Using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method, we demonstrate that apoptosis occurred in areas of Wallerian degeneration in both tracts throughout the length of the cord segments studied (from T3 to T12). This delayed cell death, more apparent in the DAT, began at 7 days after injury and peaked at 14 days for the DAT and 28 days for the CST. Although a few TUNEL+ cells, slightly above the noninjury control level, were found in intact areas of both tracts, statistically significant differences in the number of TUNEL+ cells were found between the intact and the lesioned tract segments (CST, F < 0.01; DAT, F < 0.001). Within a particular spinal segment, a mean number of 64 and 939 TUNEL+ cells in the degenerating CST and DAT, respectively, were estimated stereologically at 14 days postinjury. TUNEL+ cells in degenerating tracts outnumber their intact counterparts by 3.8:1 in the CST and 4.1:1 in the DAT, although a statistically significant difference between the two was only found in the DAT at this time point (P < 0.05). Finally, we demonstrated that oligodendrocytes, the myelin-forming cells in the central nervous system, constitute at least a portion of the cells undergoing apoptosis within areas of Wallerian degeneration.

Animals↗

PubMed2001

Ischemic injury and faulty gene transcripts in the brain.

The brain has the highest metabolic rate of all organs and depends predominantly on oxidative metabolism as a source of energy. Oxidative metabolism generates reactive oxygen species, which can damage all cellular components, including protein, lipids and nucleic acids. The processes of DNA repair normally remove spontaneous gene damage with few errors. However, cerebral ischemia followed by reperfusion leads to elevated oxidative stress and damage to genes in brain tissue despite a functional mechanism of DNA repair. These critical events occur at the same time as the expression of immediate early genes, the products of which trans-activate late effector genes that are important for sustaining neuronal viability. These findings open the possibility of applying genetic tools to identify molecular mechanisms of gene repair and to derive new therapies for stroke and brain injury.

Animals↗

PubMed2001

Blood pressure and angiotensin converting enzyme inhibitor use in hypertensive patients with chronic renal insufficiency.

BACKGROUND: Hypertension treatment is important in managing chronic renal insufficiency (CRI). Little is known, however, about the blood pressure (BP) control achieved or the pattern of antihypertensive drug prescription among CRI patients. METHODS: Using computerized medical records, we studied 3,089 adult hypertensive subjects treated at Brigham and Women's Hospital (Boston, MA) from 1990 through 1998. All subjects had at least two serum creatinine measurements 2 years apart, at least two BP readings, and online weight (to estimate Cockcroft-Gault creatinine clearance [CrCl]). RESULTS: The average mean arterial pressure over time (mean MAP) was 103 +/- 9 mm Hg among those with CrCI >60 mL/min, 102 t 9 mm Hg among those with CrCl 41 to 60 mL/min. and 101 +/- 9 mm Hg among those with CrCl 21 to 40 mL/min. There were no significant differences in mean MAP among the different categories of renal function in the multivariate analysis (P = .26 for trend). The proportion of patients with final systolic BP < 160 mm Hg and diastolic BP <90 mm Hg was 68% and did not vary with renal function (P = .68 for trend). The proportion of subjects who were prescribed ACE inhibitors was 38% among those with CrCl >60 mL/min, 36% among those with CrCI 41 to 60 mL/min, and only 27% among those with CrCl 21 to 40 mL/min (P = .003 for trend). CONCLUSIONS: The BP control achieved among hypertensive CRI subjects, although no worse than that among those without CRI, was found to be suboptimal. Patients with CrCl 21 to 40 mL/min were less likely to be prescribed ACE inhibitors than were those with CrCl >60 mL/min. Improvement is needed in the clinical management of these factors that can influence the progression of CRI.

Adult↗

PubMed2001

Building a generic architecture for medical information exchange among healthcare providers.

Due to the inability to exchange clinical information among hospitals, continuity of care cannot be maintained and a tremendous amount of medical resource has been wasted. This paper describes an architecture that would facilitate exchange of clinical information among heterogeneous hospital information systems. It is dubbed 'Medical Information Exchange Center' or MIEC as part of a six-year Health Information Network Project hosted by the Department of Health. MIEC was designed so that it is innovative yet technically feasible today. It is convenient for authorized users yet secure enough so people can trust and has minimal impact to participated hospitals. Authorized users will be able to access information through two web-based interfaces directed to physician and non-physician users respectively. Hospitals are connected through a virtual private network to exchange patient information and users need to obtain a private key from the certificate authority in order to securely connect to MIEC. A pilot project was conducted to demonstrate the feasibility of this architecture and the problems encountered were discussed.

Computer Communication Networks↗

PubMed2001

Development and deployment of a web-based physician order entry system.

The computer-based Physician Order Entry System (POES) has been employed in many clinical institutes in Taiwan. Most of the POES systems are developed in the two-tier client-server architecture, and a large portion of the systems are constructed on a mainframe or even a single PC. The exponential growth of the Internet has had a tremendous impact on our society in recent years. In consideration of the future user interface and system architecture, we have developed a three-tier web-based Physician Order Entry System and successfully deployed it in the Wang-Fang Hospital in Taipei. The system is the first POES based on three-tier and World Wide Web (WWW) in Taiwan. The system provides the Subjective, Objective, Assessment, and Plan (SOAP) structure for the physician to enter subject, object, diagnoses, medicine dosage, treatment and laboratory test request, and prints out the prescription and necessary document. The doctor can also retrieve the patient's medical record on the system. One of the special characteristics of the system is its personalized design. The doctor can define their own diagnosis, medicine and treatment database and any combination of these to facilitate their clinical work. The system has been reviewed since February 1999. The result shows that the clinical procedure has become more efficient, and the chances of omission have been reduced. The system is very stable and the Open Database Connectivity (ODBC) database access did not show any delay in the network. Since we have incorporated many new web-programming techniques, the progress of the techniques will improve the system performance in the future.

Computer Systems↗

PubMed2001

A clinicopathologic study of 81 patients with ependymomas and proposal of diagnostic criteria for anaplastic ependymoma.

Optimal histologic criteria for the classification of and grading of ependymomas, including their anaplastic forms, remain elusive. This is especially true because of the poor correlation of these criteria with clinical outcome. The aim of this study was to identify the histopathologic parameters that could distinguish different prognostic groups of patients with ependymomas. Eighty-one patients with ependymal tumors, including those originally diagnosed ependymomas, anaplastic ependymomas and myxopapillary ependymomas, were enrolled in this study. Thirteen histologic parameters, including hypercellularity, nuclear pleomorphism, mitoses, endothelial proliferation, necrosis, clear cell, thrombi, dystrophic calcification, psammoma bodies, bone, cartilage, Rosenthal fibers and MIB-1 labeling index (LI), were evaluated in each patient and correlated with clinical outcome. We assigned one score for each histopathologic parameter evaluated and used a stepwise selection method with entry model based on the significance of the log-rank statistic to formulate a scoring model. Four parameters were chosen in this process, including mitoses > or = 4/10 hpf (1.7/mm2), hypercellularity, endothelial proliferation and necrosis. The sum of these four parameters (scores) was the histopathologic score of the tumor. The progression-free survival (PFS) and overall survival (OS) of patients with histopathologic scores 0 and 1 were significantly better than those with histopathologic scores 2, 3 and 4 (p < 0.001 and p = 0.005, respectively). Because of the latter finding, we proposed that anaplastic ependymoma could be diagnosed by the presence of any two of the aforementioned four parameters. Multivariate analyses including clinical and histopathologic variables showed that histopathologic score > or = 2 and subtotal resection were the factors related to increased risk of recurrence, while histopathologic score > or = 2 was the only factor related to overall survival. Based on the above findings, we concluded that histopathology is an important prognostic indicator for patients with ependymomas.

Adolescent↗