bluuebunny/crossref_metadata_2025_split huggingface dataset:
A large dumbbell glossopharyngeal schwannoma involving the vagus nerve: a case report and review of the literature
Authors: Zhao Hongyu , Li Xiaodong , Lv Qingjie , Yuan Yuhui , Yu Hongwei 
Published: October 2008

Abstract

Introduction
Schwannoma arising from the glossopharyngeal nerve is a rare intracranial tumor. Fewer than 40 cases have been reported. Accurate pre-operative diagnosis and optimal treatment are still difficult.

Case presentation
We present one case of schwannoma originating from the ninth cranial nerve with palsies of the trigeminal nerve, facial-acoustic nerve complex, and vagus nerve in addition to ninth nerve dysfunction. Magnetic resonance imaging showed tumors located in the cerebellopontine angle with extracranial extension via the jugular foramen, with evident enhancement on post-contrast scan. Surgical management single-staged with the help of gamma knife radiosurgery achieved total removal.

Conclusion
Glossopharyngeal schwannoma is devoid of clinical symptoms and neurological signs. High resolution magnetic resonance imaging may play a key role as an accurate diagnostic tool. A favorable option of approach and appropriate planning of surgical strategy should be the goal of operation for this benign tumor.
Prevalence of depressive symptoms among non insulin treated Greek type 2 diabetic subjects
Authors: Sotiropoulos Alexios , Papazafiropoulou Athanasia , Apostolou Ourania , Kokolaki Anthi , Gikas Aristofanis , Pappas Stavros 
Published: October 2008

Abstract

Background
Depression is common among diabetic subjects. We conducted the present study to estimate the prevalence of depression in subjects with type 2 diabetes (T2D) in Greece.

Methods
The study sample consisted of 320 T2D subjects without overt macrovascular disease attending the diabetes outpatient clinic of our hospital, from June 2007 to December 2007. Depressive symptoms were measured using the 21-item Beck Depression Inventory, modified for use in diabetic subjects.

Results
Of the study subjects 107 (33.4%) reported elevated depressive symptoms. More women than men with diabetes reported symptoms of depression (48.4% vs. 12.7%, P < 0.001). In the female study group, depressive symptoms were correlated with HbA1c (P = 0.04), and duration of diabetes (P = 0.004). In the male study group, univariate linear regression analysis showed no significant relationships between depressive symptoms and the testing variables.

Conclusion
The prevalence of depression in Greek T2D subjects is high. Diabetic female subjects showed increased levels of depressive symptoms compared with male subjects. Independent risk factors of depressive symptoms in diabetic female subjects were diabetes duration and glycemic control.
Dicer regulates Xist promoter methylation in ES cells indirectly through transcriptional control of Dnmt3a
Authors: Nesterova Tatyana B , Popova Bilyana C , Cobb Bradley S , Norton Sara , Senner Claire E , Tang Y Amy , Spruce Thomas , Rodriguez Tristan A , Sado Takashi , Merkenschlager Matthias , Brockdorff Neil 
Published: October 2008

Abstract

Background
X chromosome inactivation is the mechanism used in mammals to achieve dosage compensation of X-linked genes in XX females relative to XY males. Chromosome silencing is triggered in cis by expression of the non-coding RNA Xist. As such, correct regulation of the Xist gene promoter is required to establish appropriate X chromosome activity both in males and females. Studies to date have demonstrated co-transcription of an antisense RNA Tsix and low-level sense transcription prior to onset of X inactivation. The balance of sense and antisense RNA is important in determining the probability that a given Xist allele will be expressed, termed the X inactivation choice, when X inactivation commences.

Results
Here we investigate further the mechanism of Xist promoter regulation. We demonstrate that both sense and antisense transcription modulate Xist promoter DNA methylation in undifferentiated embryonic stem (ES) cells, suggesting a possible mechanistic basis for influencing X chromosome choice. Given the involvement of sense and antisense RNAs in promoter methylation, we investigate a possible role for the RNA interference (RNAi) pathway. We show that the Xist promoter is hypomethylated in ES cells deficient for the essential RNAi enzyme Dicer, but that this effect is probably a secondary consequence of reduced levels of de novo DNA methyltransferases in these cells. Consistent with this we find that Dicer-deficient XY and XX embryos show appropriate Xist expression patterns, indicating that Xist gene regulation has not been perturbed.

Conclusion
We conclude that Xist promoter methylation prior to the onset of random X chromosome inactivation is influenced by relative levels of sense and antisense transcription but that this probably occurs independent of the RNAi pathway. We discuss the implications for this data in terms of understanding Xist gene regulation and X chromosome choice in random X chromosome inactivation.
Neurocognitive deficits in a patient with small cell lung cancer: a case report
Authors: Hudhud Kanan H , Masood Ashiq , Oh Yun , Hegazi AZ 
Published: October 2008

Abstract

Introduction
The neurocognitive deficits associated with small cell lung cancer include metastasis to brain and paraneoplastic syndrome. The patients are also predisposed to herpes encephalitis due to immunosuppression and chemotherapy.

Case presentation
We report a case of 72 year old female diagnosed with small cell lung cancer started with memory deficits, ataxia, vertigo, and hearing loss. The paraneoplastic work-up returned as anti-Hu antibody positive. The MRI brain showed area of edema and inflammation right medial temporal lobe as well as enhancement in the underlying meningi. Although PCR/HSV of CSF was negative, the patient was empirically treated with IV acyclovir and showed significant improvement and was discharged in good condition.

Conclusion
The case highlights the importance of keeping broad minded approach in treating patients with serious malignant diseases. The case also call attention to the use of empiric therapy in possible life threatening diseases such as Herpes encephalitis
Association between inflammatory mediators and response to inhaled nitric oxide in a model of endotoxin-induced lung injury
Authors: Trachsel Sebastien , Deby-Dupont Ginette , Maurenbrecher Edwige , Nys Monique , Lamy Maurice , Hedenstierna Göran 
Published: October 2008

Abstract
Introduction
Inhaled nitric oxide (INO) allows selective pulmonary vasodilation in acute respiratory distress syndrome and improves PaO2 by redistribution of pulmonary blood flow towards better ventilated parenchyma. One-third of patients are nonresponders to INO, however, and it is difficult to predict who will respond. The aim of the present study was to identify, within a panel of inflammatory mediators released during endotoxin-induced lung injury, specific mediators that are associated with a PaO2 response to INO.

Methods
After animal ethics committee approval, pigs were anesthetized and exposed to 2 hours of endotoxin infusion. Levels of cytokines, prostanoid, leucotriene and endothelin-1 (ET-1) were sampled prior to endotoxin exposure and hourly thereafter. All animals were exposed to 40 ppm INO: 28 animals were exposed at either 4 hours or 6 hours and a subgroup of nine animals was exposed both at 4 hours and 6 hours after onset of endotoxin infusion.

Results
Based on the response to INO, the animals were retrospectively placed into a responder group (increase in PaO2 ≥ 20%) or a nonresponder group. All mediators increased with endotoxin infusion although no significant differences were seen between responders and nonresponders. There was a mean difference in ET-1, however, with lower levels in the nonresponder group than in the responder group, 0.1 pg/ml versus 3.0 pg/ml. Moreover, five animals in the group exposed twice to INO switched from responder to nonresponder and had decreased ET-1 levels (3.0 (2.5 to 7.5) pg/ml versus 0.1 (0.1 to 2.1) pg/ml, P < 0.05). The pulmonary artery pressure and ET-1 level were higher in future responders to INO.

Conclusions
ET-1 may therefore be involved in mediating the response to INO.
Reliability of continuous cardiac output measurement during intra-abdominal hypertension relies on repeated calibrations: an experimental animal study
Authors: Gruenewald Matthias , Renner Jochen , Meybohm Patrick , Höcker Jan , Scholz Jens , Bein Berthold 
Published: October 2008

Abstract
Introduction
Monitoring cardiac output (CO) may allow early detection of haemodynamic instability, aiming to reduce morbidity and mortality in critically ill patients. Continuous cardiac output (CCO) monitoring is recommended in septic or postoperative patients with high incidences of intra-abdominal hypertension (IAH). The aim of the present study was to compare the agreement between three CCO methods and a bolus thermodilution CO technique during acute IAH and volume loading.

Methods
Ten pigs were anaesthetised and instrumented for haemodynamic measurements. Cardiac output was obtained using CCO by pulse power analysis (PulseCO; LiDCO monitor), using CCO by pulse contour analysis (PCCO; PiCCO monitor) and using CCO by pulmonary artery catheter thermodilution (CCOPAC), and was compared with bolus transcardiopulmonary thermodilution CO (COTCP) at baseline, after fluid loading, at IAH and after an additional fluid loading at IAH. Whereas PulseCO was only calibrated at baseline, PCCO was calibrated at each experimental step.

Results
PulseCO and PCCO underestimated CO, as the overall bias ± standard deviation was 1.0 ± 1.5 l/min and 1.0 ± 1.1 l/min compared with COTCP. A clinically accepted agreement between all of the CCO methods and COTCP was observed only at baseline. Whereas IAH did not influence the CO, increased CO following fluid loading at IAH was only reflected by CCOPAC and COTCP, not by uncalibrated PulseCO and PCCO. After recalibration, PCCO was comparable with COTCP.

Conclusions
The CO obtained by uncalibrated PulseCO and PCCO failed to agree with COTCP during IAH and fluid loading. In the critically ill patient, recalibration of continuous arterial waveform CO methods should be performed after fluid loading or before a major change in therapy is initiated.
Comparative sequence analyses reveal sites of ancestral chromosomal fusions in the Indian muntjac genome
Authors: Tsipouri Vicky , Schueler Mary G , Hu Sufen ,   NISC Comparative Sequencing Program, Dutra Amalia , Pak Evgenia , Riethman Harold , Green Eric D 
Published: October 2008

Abstract
Background
Indian muntjac (Muntiacus muntjak vaginalis) has an extreme mammalian karyotype, with only six and seven chromosomes in the female and male, respectively. Chinese muntjac (Muntiacus reevesi) has a more typical mammalian karyotype, with 46 chromosomes in both sexes. Despite this disparity, the two muntjac species are morphologically similar and can even interbreed to produce viable (albeit sterile) offspring. Previous studies have suggested that a series of telocentric chromosome fusion events involving telomeric and/or satellite repeats led to the extant Indian muntjac karyotype.

Results
We used a comparative mapping and sequencing approach to characterize the sites of ancestral chromosomal fusions in the Indian muntjac genome. Specifically, we screened an Indian muntjac bacterial artificial-chromosome library with a telomere repeat-specific probe. Isolated clones found by fluorescence in situ hybridization to map to interstitial regions on Indian muntjac chromosomes were further characterized, with a subset then subjected to shotgun sequencing. Subsequently, we isolated and sequenced overlapping clones extending from the ends of some of these initial clones; we also generated orthologous sequence from isolated Chinese muntjac clones. The generated Indian muntjac sequence has been analyzed for the juxtaposition of telomeric and satellite repeats and for synteny relationships relative to other mammalian genomes, including the Chinese muntjac.

Conclusions
The generated sequence data and comparative analyses provide a detailed genomic context for seven ancestral chromosome fusion sites in the Indian muntjac genome, which further supports the telocentric fusion model for the events leading to the unusual karyotypic differences among muntjac species.
CD44 promotes progenitor homing into the thymus and T cell maturation
Authors: Rajasagi Mohini , Vitacolonna Mario , Benjak Bojan , Marhaba Rachid , Zöller Margot 
Published: October 2008

AbstractRegain of immunocompetence after myeloablation and bone marrow cell (BMC) reconstitution essentially depends on T progenitor homing into the thymus and intrathymic T cell maturation. CD44 facilitates progenitor homing and settlement in the bone marrow and is known as a T progenitor marker. In search for improving regain of immunocompetence after BMC reconstitution, we explored whether the CD44 standard (CD44 s) and/or variant isoforms CD44v6 and CD44v7 contribute to thymus repopulation and thymocyte maturation. Antibody-blocking studies and cells/mice with a targeted deletion of CD44v6/7 or CD44v7 revealed that CD44s, but not CD44v6 and CD44v7, has a major impact on progenitor cell homing into the thymus. Instead, CD44v6 strengthens apoptosis resistance and expansion of early thymocytes. CD44v6-induced apoptosis resistance, most strong in double-negative (DN) thymocytes, is accompanied by Akt activation. CD44v6-induced proliferation of DN cells proceeds via activation of the MAPK pathway. At later stages of T cell maturation, CD44 acts as an accessory molecule, initiating and supporting TCR/CD3 complex-mediated signal transduction in double-positive and single-positive thymocytes. Thus, CD44 plays a major role in thymus homing. In addition, CD44v6 is important for survival and expansion of early thymocytes. These findings suggest that strengthening CD44v6 expression on lymphoid progenitors could well contribute to accelerated regain of immunocompetence.
Impact of Disease Risk on Efficacy of Matched Related Bone Marrow Transplantation for Pediatric Acute Myeloid Leukemia: The Children's Oncology Group
Authors: Horan John T. , Alonzo Todd A. , Lyman Gary H. , Gerbing Robert B. , Lange Beverly J. , Ravindranath Yaddanapudi , Becton David , Smith Franklin O. , Woods William G. 
Published: October 2008

Purpose There is considerable variation in the use of HLA-matched related bone marrow transplantation (BMT) for the treatment of pediatric patients with newly diagnosed acute myeloid leukemia (AML). Some oncologists have argued that BMT should be offered to most patients in first complete remission (CR). Others have maintained that transplantation in first remission should be reserved for patients with high-risk disease. We performed this study to determine how disease risk influences the efficacy of BMT. Methods We combined data from four cooperative group clinical trials: Pediatric Oncology Group 8821, Children's Cancer Group (CCG) 2891, CCG 2961, and Medical Research Council 10. Using cytogenetics and the percentage of marrow blasts after the first course of chemotherapy, patients were stratified into favorable, intermediate, and poor-risk disease groups. Patients who could not be risk classified were analyzed separately. Outcomes for patients assigned to BMT and for patients assigned to chemotherapy alone were compared. Results The data set included 1,373 pediatric patients with AML in first CR. In the intermediate-risk group, the estimated disease-free survival at 8 years for patients who did not undergo transplantation was 39% ± 5% (2 SE), whereas it was 58% ± 7% for BMT patients. The estimated overall survival for patients who did not undergo transplantation was 51% ± 5%, whereas it was 62% ± 7% for BMT patients. Both differences were significant (P < .01). There were no significant differences for survival in the other two risk groups or in the non–risk-stratified patients. Conclusion Our study indicates that HLA-matched related BMT is an effective treatment for pediatric patients with intermediate-risk AML in first CR.
Primary and Secondary Kinase Genotypes Correlate With the Biological and Clinical Activity of Sunitinib in Imatinib-Resistant Gastrointestinal Stromal Tumor
Authors: Heinrich Michael C. , Maki Robert G. , Corless Christopher L. , Antonescu Cristina R. , Harlow Amy , Griffith Diana , Town Ajia , Mckinley Arin , Ou Wen-Bin , Fletcher Jonathan A. , Fletcher Christopher D.M. , Huang Xin , Cohen Darrel P. , Baum Charles M. , Demetri George D. 
Published: October 2008

PurposeMost gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor α (PDGFRA) kinases, which are imatinib targets. Sunitinib, which targets KIT, PDGFRs, and several other kinases, has demonstrated efficacy in patients with GIST after they experience imatinib failure. We evaluated the impact of primary and secondary kinase genotype on sunitinib activity.Patients and MethodsTumor responses were assessed radiologically in a phase I/II trial of sunitinib in 97 patients with metastatic, imatinib-resistant/intolerant GIST. KIT/PDGFRA mutational status was determined for 78 patients by using tumor specimens obtained before and after prior imatinib therapy. Kinase mutants were biochemically profiled for sunitinib and imatinib sensitivity.ResultsClinical benefit (partial response or stable disease for ≥ 6 months) with sunitinib was observed for the three most common primary GIST genotypes: KIT exon 9 (58%), KIT exon 11 (34%), and wild-type KIT/PDGFRA (56%). Progression-free survival (PFS) was significantly longer for patients with primary KIT exon 9 mutations (P = .0005) or with a wild-type genotype (P = .0356) than for those with KIT exon 11 mutations. The same pattern was observed for overall survival (OS). PFS and OS were longer for patients with secondary KIT exon 13 or 14 mutations (which involve the KIT-adenosine triphosphate binding pocket) than for those with exon 17 or 18 mutations (which involve the KIT activation loop). Biochemical profiling studies confirmed the clinical results.ConclusionThe clinical activity of sunitinib after imatinib failure is significantly influenced by both primary and secondary mutations in the predominant pathogenic kinases, which has implications for optimization of the treatment of patients with GIST.
Body-Mass Index and Progression of Hepatitis B: A Population-Based Cohort Study in Men
Authors: Yu Ming-Whei , Shih Wei-Liang , Lin Chih-Lin , Liu Chun-Jen , Jian Jhih-Wei , Tsai Keh-Sung , Chen Chien-Jen 
Published: October 2008

Purpose To determine prospectively whether body-mass index (BMI) is associated with liver-related morbidity and mortality among male hepatitis B virus (HBV) carriers. Patients and Methods We performed a prospective study of 2,903 male HBV surface antigen–positive government employees who were free of cancer at enrollment between 1989 and 1992. Main outcome measures included ultrasonography, biochemical tests, incident hepatocellular carcinoma (HCC), and liver-related death. Results During mean follow-up of 14.7 years, 134 developed HCC and 92 died as a result of liver-related causes. In Cox proportional hazards models adjusting for age, number of visits, diabetes, and use of alcohol and tobacco, the hazard ratios for incident HCC were 1.48 (95% CI, 1.04 to 2.12) in overweight men (BMI between 25.0 and 29.9 kg/m2) and 1.96 (95% CI, 0.72 to 5.38) in obese men (BMI ≥ 30.0 kg/m2), compared with normal-weight men (BMI between 18.5 and 24.9 kg/m2). Liver-related mortality had adjusted hazard ratios of 1.74 (95% CI, 1.15 to 2.65) in overweight men and 1.50 (95% CI, 0.36 to 6.19) in obese men. Excess BMI was also associated with the occurrence of fatty liver and cirrhosis detected by ultrasonography, as well as elevated ALT and γ-glutamyltransferase (GGT) activity during follow-up. The association of BMI with GGT was stronger than with ALT, and elevated GGT activity and cirrhosis were the strongest predictors for incident HCC and liver-related death. Conclusion This longitudinal cohort study indicates that excess body weight is involved in the transition from healthy HBV carrier state to HCC and liver-related death among men.
“BRCAness” Syndrome in Ovarian Cancer: A Case-Control Study Describing the Clinical Features and Outcome of Patients With Epithelial Ovarian Cancer Associated With BRCA1 and BRCA2 Mutations
Authors: Tan David S.P. , Rothermundt Christian , Thomas Karen , Bancroft Elizabeth , Eeles Rosalind , Shanley Susan , Ardern-Jones Audrey , Norman Andrew , Kaye Stanley B. , Gore Martin E. 
Published: October 2008

Purpose We evaluated the clinical impact of germ-line BRCA1/2 mutations in patients with epithelial ovarian cancer (EOC) on responses to first and subsequent lines of chemotherapy, treatment-free interval (TFI) between each line of therapy, and overall survival (OS). Patients and Methods Twenty-two EOC patients with germ-line BRCA1 or BRCA2 mutations (BRCA-positive) were selected from our database and matched (1:2) with 44 nonhereditary EOC controls (defined by no associated personal history of breast cancer and no family history of breast and ovarian cancer or an uninformative BRCA mutation test) for stage, histologic subtype, age, and year of diagnosis. All patients received primary platinum-based chemotherapy. Statistical comparisons included responses after first-, second-, and third-line treatment (χ2/Fisher's exact test) and median OS (Kaplan-Meier method/log-rank test). Results Compared with controls, BRCA-positive patients had higher overall (95.5% v 59.1%; P = .002) and complete response rates (81.8% v 43.2%; P = .004) to first line treatment, higher responses to second and third line platinum-based chemotherapy (second line, 91.7% v 40.9% [P = .004]; third line, 100% v 14.3% [P = .005]) and longer TFIs. A significant improvement in median OS in BRCA-positive patients compared with controls was observed from both time of diagnosis (8.4 v 2.9 years; P < .002) and time of first relapse (5 v 1.6 years; P < .001). BRCA status, stage, and length of first response were independent prognostic factors from time of first relapse. Conclusion BRCA-positive EOC patients have better outcomes than nonhereditary EOC patients. There exists a clinical syndrome of BRCAness that includes serous histology, high response rates to first and subsequent lines of platinum-based treatment, longer TFIs between relapses, and improved OS.