tbuckley/cabot-search huggingface dataset:
Clinical usefulness of PET/CT in initial staging and response evaluation of primary gastric lymphoma
Authors: J. Yi, S. Kim, S. Lee, S. Park, Y. Ko, J. Choi, W. Kim
Journal: Journal of Clinical Oncology (2009)

e19541 Background: Positron emission tomography (PET)/computed tomography (CT) scan has a well-established role in the management of non-Hodgkin's lymphoma (NHL). However, in case of the primary gastric lymphoma, which is the most frequent extranodal NHL, the role of PET/CT scan is still controversial. Methods: We retrospectively analyzed 42 patients with primary gastric lymphoma who underwent PET/CT scans; 32 patients with diffuse large B-cell lymphoma (DLBCL) and 10 patients with extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) were analyzed. The PET/CT scans were compared with clinicopathologic features and the results of CT and endoscopy. After corresponding treatment, response was evaluated by conventional CT scans or PET/CT scans and endoscopy with biopsy Results: Nine patients were up-staged based on the results of their PET/CT scan compared to CT (7 DLBCL, 2 MALT lymphomas) while six patients were down-staged by the PET/CT scan. The high SUVmax group, defined as SUVmax ≥ median value, was significantly associated with an advanced Lugano stage (P &lt; 0.001). Three patients with DLBCL, who showed an initially high SUVmax, died of disease progression. Although not statistically significant, there was a tendency of inferior outcome in the group with high SUVmax. Among 24 patients for whom follow-up PET/CT scan with endoscopy was performed, 11 patients with ulcerative or mucosal lesions showed residual FDG uptake. All of these gastric lesions were grossly and pathologically benign lesions without evidence of lymphoma cells. Conclusions: PET/CT scan can help staging patients with primary gastric lymphoma, and the maximum SUV has possibility to have prognostic value. However, the residual FDG uptake observed during follow-up should be interpreted cautiously in association with the results of endoscopy and multiple gastric biopsies. No significant financial relationships to disclose.
EPID-03MENINGIOANGIOMATOSIS ASSOCIATED WITH MICROCEPHALY AND DEVELOPMENTAL DELAY IN A PEDIATRIC PATIENT
Authors: Kyle Hickman, Karen Fernandez, Sarah Martin, Jane Maksimovic, Julian Lin, Reuben Antony
Journal: Neuro-Oncology (2015)

BACKGROUND: Meningioangiomatosis is a rare benign lesion of the central nervous system characterized by focal leptomeningeal and meningovascular proliferation most commonly in the frontal and temporal cerebral cortex. Typically meningioangiomatosis presents with seizures and much less commonly headache, visual disturbance, limb weakness and personality change. Genetic mutations in Microcephalin1 (MCPH1) and ASPM (abnormal spindle like microcephaly) cause primary microcephaly and their role in carcinogenesis is being elucidated. CASE REPORT: A boy with global developmental delay due to microcephaly of undetermined etiology and vesicoureteral reflux presented with a new onset generalized tonic clonic seizure. He had a family history of developmental delay in male relatives (maternal uncle and brother) and a family history (maternal) of malignancy in female relatives (breast, mesothelioma, ovarian and uterine cancer). He had large low set ears, prominent jaw and normal testicles. MRI demonstrated a minimally enhancing vascular 1.9 x 1.9 x 1.5 cm lesion in the mesial right inferior frontal lobe predominantly in the superficial cortical gray matter. The lesion had a low intensity T2 signal and dense calcification along the periphery and a central zone of linear vascular enhancement. There was no associated vasogenic edema or any other abnormal MRI findings. The lesion was totally resected under image guidance. Histopathological examination showed meningoendothelial proliferation without atypical features. Intervening neurons immunoreactive with synaptophysin, GFAP and NeuN were seen. The final diagnosis was frontal lobe meningioangiomatosis. Fragile X syndrome testing was negative (FMR gene CGG repeat number: 32) and chromosomal microarray analysis was normal. Follow up MRIs have not demonstrated recurrence of the meningioangiomatosis and he has been seizure free on Levetiracetam/Topiramate therapy. CONCLUSION: We speculate that there is a genetic basis to the microcephaly and meningioangiomatosis in our patient perhaps involving genes in the X chromosome, MPCH1 or ASPM genes. Further testing is warranted.
Identification Of Novel Markers Of Human AML Stem Cells Using High Resolution Proteomics and Transcriptomics
Authors: Simon Raffel, Jenny Hansson, Lutz Christoph, Daniel Klimmeck, Nina Cabezas-Wallscheid, Eike C. Buss, Christian Thiede, Anne Flörcken, Sabrina Hanke, Marco Tinelli, Oliver Bischel, Christoph Rösli, Jörg Westermann, Gerhard Ehninger, Anthony D. Ho, Jeroen Krijgsveld, Andreas Trumpp
Journal: Blood (2013)
THU0632-HPR The Neck Bournemouth Questionnaire, an Item Response Theory Study
Authors: T. Geri, D. Piscitelli, R. Meroni, M. Testa
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background</h3> Several questionnaires on neck pain are usually assumed to be unidimensional as their raw scores are considered interval measures. However, the assumption of unidimensionality requires the questionnaire data to satisfy certain criteria when tested with modern psychometric approaches, such as Item Response Theory. The Neck Bournemouth Questionnaire (NBQ) has already been cross-culturally adapted and validated in Italian on a population of subjects with chronic neck pain (Geri et al., 2014). We examined this scale by means of Rasch analysis an Item Response Theory model in order to provide a disease-specific questionnaire whose scores can be assumed as interval variables and, consequently, legitimately their change scores as meaningful. <h3>Objectives</h3> Validation of the Italian NBQ with Rasch analysis. <h3>Methods</h3> A sample of 161 subjects with chronic neck pain was assessed with the NBQ. The structure of the scale was preliminarily tested with both exploratory and confirmatory factor analyses. Rasch analysis was performed analysing the following features: the goodness of fit of the data to the model, thresholds ordering, unidimensionality, local independence of the items and Differential Item Functioning (DIF) were examined to consider the NBQ an interval scale. Further, the Person Separation Index and the Mean Location of Persons were used, respectively, to assess the internal consistency and the targeting of the scale. <h3>Results</h3> Both the exploratory and confirmatory factor analyses revealed a two factors structure of the NBQ. Factor 1 (item 1, 2, 3, 6) fitted the model (χ<sup>2</sup>=10.65, df 8, <i>p</i>=0.22) after removal of item 7, which had low communalities on exploratory factor analysis and further showed disordered thresholds (Figure). Item 2 presented a marginal uniform Differential Item Functioning across educational level. The Person Separation Index was 0.80 and the Mean Location of Persons was 0.48 (SD=1.02). Factor 2 (Item 4 and 5) fitted the model (χ<sup>2</sup>=3.86, df 4, <i>p</i>=0.42). The Person Separation Index and the Mean Location of Persons of factor 2 were, respectively, 0.77 and -0.71 (SD=1.57). <h3>Conclusions</h3> The NBQ is a useful tool for the assessment of patients with chronic neck pain. The NBQ showed a two factors structure, each factor fitted the Rasch model and therefore works as a unidimensional measure. Using the interval scores of the NBQ may provide meaningful change scores to establish the effectiveness of treatments for chronic neck pain in clinical trials. <h3>References</h3> Geri T, Signori A, Gianola S, Rossettini G, Grenat G, Checchia G, et al. Cross-cultural adaptation and validation of the Neck Bournemouth Questionnaire in the Italian population. Quality of Life Research. 2014. Epub ahead of print 23 September 2014. <h3>Disclosure of Interest</h3> None declared
ENGOT-OV24-NSGO/AVANOVA: Niraparib versus bevacizumab-niraparib combination versus bevacizumab and niraparib as sequential therapy in women with platinum-sensitive epithelial ovarian, fallopian tube, or peritoneal cancer.
Authors: Mansoor Raza Mirza, Christiane Ehlers Mortensen, Elisabeth Avall-Lundqvist, Line Bjorge, Jonathan S. Berek, Jorn Herrstedt, Anne Juul Holm, Tinne Kirkegaard, Johanna Maenpaa
Journal: Journal of Clinical Oncology (2015)

TPS5607 Background: Multiple Phase 1 and 2 clinical studies of PARP inhibitors used as monotherapy to treat patients with recurrent ovarian cancer (ROC) suggest that the agents are active in this population and there is level one evidence that bevacizumab is beneficial In the same population. A phase two randomized study demonstrated that the addition of a PARP inhibitor to an anti-angiogenic drug cediranib improves Progression-free survival (PFS). Our aim is to compare tolerability and efficacy of niraparib alone versus niraparib-bevacizumab combination versus sequential bevacizumab and niraparib. Methods: The ENGOT-OV24-NSGO/AVANOVA study comprises of two parts. Part 1 is a classic phase 1 trial of niraparib and bevacizumab combination. Part 2 is a three-arm, open-label, phase II, 1:1:1 randomized study of niraparib and/or Niraparib-bevacizumab combination against bevacizumab followed by niraparib in women with platinum-sensitive ROC. BRCAmut and or high-grade serous/endometrioid carcinoma patients with platinum-sensitive ROC are eligible. Patients must have disease that is measurable according to RECIST or assessable according to the GCIG CA-125 criteria. Primary objective of phase 1 part is to evaluate the safety and tolerability of bevacizumab-niraparib combination therapy and determine the Recommended Phase 2 Dose (RP2D) of bevacizumab-niraparib. Primary objective of phase 2 part is to obtain preliminary evidence of efficacy of bevacizumab- niraparib combination or sequential therapy or niraparib single agent treatment. Primary end-point is PFS. Secondary end-points include PFS in each group according to trial stratification factors; PFS comparison of sequential versus concomitant bevacizumab and Niraparib; Objective response rate; Disease control rate (DCR); Patient Reported Outcomes (PROs); Time to subsequent chemotherapy and survival. Study status: The study is activated and sites are invited to participate. ClinicalTrials.gov Identifier: NCT02354131 Clinical trial information: NCT02354131.
Lesson of the Week: Dangers of oral fluoroquinolone treatment in community acquired upper respiratory tract infections
Authors: J R Korner, S D Reeves, P A MacGowan
Journal: BMJ (1994)

Journalists working in Kenya, Uganda, and Tanzania presented three papers on the environmental and social consequences of tobacco growing.These were the most exciting and important ofthe conference.For many years the tobacco control community has received fragmentary reports about the deforestation caused by land clearing and tree felling to provide fuel for flue curing in areas where other fuels are unavailable.Many of these reports have been anecdotal and outrageously exaggerated.The three papers, which will be published in Tobacco Control, provided detailed accounts of the extent and consequences of deforestation and of the disruption to social life that tobacco growing causes local communities in these countries.They showed that industry estimations of surviving trees from reforestation projects were utterly fanciful and seem certain to ignite major concerns about the environment, particularly in the West. Price policyDavid Sweanor ofthe Canadian Non-smokers Rights Association presented compelling information on elasticities of demand for tobacco products under different taxation and excise conditions.He argued
Phase I Study of 3-Week Schedule of Irinotecan Combined With Cisplatin in Patients With Advanced Solid Tumors
Authors: Maja J. A. de Jonge, Alex Sparreboom, André S. T. Planting, Maria E. L. van der Burg, Maureen M. de Boer-Dennert, Judith ter Steeg, Christian Jacques, Jaap Verweij
Journal: Journal of Clinical Oncology (2000)

PURPOSE: To assess the feasibility, pharmacokinetic interaction, and possible sequence-dependent effects of the irinotecan/cisplatin combination given every 3 weeks, and to assess the influence of additional granulocyte colony-stimulating factor (G-CSF) on the hematologic toxicity. PATIENTS AND METHODS: Patients who had received no more than one prior combination chemotherapy regimen or two single-agent regimens were entered. Treatment consisted of a 90-minute irinotecan infusion followed by a 3-hour cisplatin infusion on day 1, with cycles repeated once every 3 weeks. After the maximum-tolerated dose was determined, the sequence of administration was reversed. In a separate cohort of six patients, we assessed the effect of G-CSF on the experienced hematologic toxicity and dose-intensity. Irinotecan doses ranged from 175 to 300 mg/m 2 and cisplatin doses ranged from 60 to 80 mg/m 2 . RESULTS: Fifty-two patients entered the study; one was not eligible, and two were not assessable for response. Twenty-five patients were pretreated, and 26 were not. Fifty-one patients received a total of 223 courses. The dose-limiting toxicity was a combination of neutropenic fever, diarrhea, and fatigue at a dose level combining irinotecan 300 mg/m 2 with cisplatin 80 mg/m 2 . Neutropenia was common (grades 3 to 4, 68%). Irinotecan pharmacokinetics were linear over the dose range studied. No sequence-dependent side effects were observed. Tumor responses included three complete responses and eight partial responses. CONCLUSION: For phase II studies, we recommend irinotecan 260 mg/m 2 combined with cisplatin 80 mg/m 2 once every 3 weeks for chemotherapy-naive patients in good physical condition, and irinotecan 200 mg/m 2 combined with cisplatin 80 mg/m 2 for other patients.
Concept of a Pathology Institute
Journal: JAMA (1963)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Ex vivo imaging of active caspase 3 by a FRET-based molecular probe demonstrates the cellular dynamics and localization of the protease in cerebellar granule cells and its regulation by the apoptosis-inhibiting protein survivin
Authors: Laura Lossi, Carolina Cocito, Silvia Alasia, Adalberto Merighi
Journal: Molecular Neurodegeneration (2016)

Apoptosis takes place in naturally occurring neuronal death, but also in aging, neurodegenerative disorders, and traumatic brain injuries. Caspase 3 (Casp3) is the most important effector protease in apoptosis: being inactive inside the cell, it undergoes enzymatic cleavage and - hence - activation once the apoptotic cascade is triggered. Immunological techniques with antibodies against cleaved Casp3 (cCasp3) or assays with colorimetric/fluorogenic substrates are commonly in use, but they do not allow to directly follow the dynamics of activation in alive neurons that may be committed to die. By combined biolistic transfection, confocal microscopy, and fluorescence resonance energy transfer (FRET), we have implemented a methodology to dynamically monitor Casp3 activation in organotypic cerebellar slices from postnatal mice. After transfection with pSCAT3 FRET probes, we measured the ratio of the emissions of the donor/acceptor pair (ECFPem/Venusem) in fixed or alive cultures. In so doing, we i. discriminated the cellular compartment(s) of enzyme activation (nucleus, perikaryon, neurites); ii. demonstrated that Casp3 was constitutively active in the granule cells; iii. followed the fluctuations of ECFPem/Venusem, and its response to 25 mM KCl depolarization, or to increased intracellular Ca++ after NMDA (1 mM), kainic acid (1 mM), or A23187 (100–200 μM). The specificity of the active pSCAT3-DEVD probe was confirmed with RNA interference and after inhibition of Casp3 with Ac-DEVD-CMK (100 μM), as both sets of experiments brought ECFPem/Venusem to the values recorded with the control probe pSCAT3-DEVG. After double-transfection with pSCAT3-DEVD + pHcRed1-C1-survivin, we also showed a 44–56 % reduction of basal Casp3 activity in cells overexpressing survivin, a protein-member of the family of apoptosis inhibitors, with augmented survival (2.82 folds). Survivin-rescued cells were sensitive to 5 mM H2O2 oxidative stress but died without intervention of Casp3. This ex vivo FRET-based methodology provides quantitative information on the functional and histological dynamics of Casp3 activation in individual neurons at a cell level resolution. Not only it can be combined with experimental manipulation of the apoptotic machinery inside the cell, but offers several advantages over existing protocols for monitoring apoptosis in live mammalian neurons, and has potential to be transferred in vivo. Due to the pivotal role of Casp3 in apoptosis, our approach is relevant for a better comprehension of molecular neurodegeneration in the normal and pathological brain.
GW26-e4477 Safety and Efficacy of using a single transRAdial MAC guiding catheter for coronary angiograPhy and Intervention in patients with STE-MyocarDial infarction (RAPID)
Authors: Jincheng Guo, Wenming Chen, Guozhong Wang, Rong Xu, Zijing Liu, Shunjin Gan, Libin Zhang
Journal: Journal of the American College of Cardiology (2015)
Effect of family history on lung cancer outcomes
Authors: A. Ganti, F. R. Loberiza, A. Kessinger
Journal: Journal of Clinical Oncology (2007)

7711 Background: Risk factors for development of lung cancer includes a family history of the disease, especially if younger and multiple family members are affected. The effect of family history on lung cancer outcomes is unknown. A study was conducted to investigate this question. Methods: The following data were abstracted from the medical records of patients with lung cancer seen in the Medical Oncology clinic by one of the authors (AK, AG) between 1999 and 2006: age, gender, smoking history, family history, stage, treatment and survival. χ 2 test and Wilcoxon test were used for univariate comparisons based on family history of lung cancer. Cox Proportional Hazards regression analysis was used to evaluate the adjusted risk of death by family history. Univariate probability of survival was computed using Kaplan Meier estimate and compared using the log rank test. Results: Two hundred and eighty-nine of the 560 patients studied (51%) were male and 519 (93%) had a smoking history. Median age at diagnosis was 63 years (range: 16 - 89 yrs). Of the 148 patients (26%) with a family history of lung cancer, 115 had an affected first degree relative. The histology of the patients’ malignancy was: adenocarcinoma - 227 (41%), squamous cell - 103 (18%), small cell - 93 (17%) and other non-small cell carcinoma - 137 (24%). There was no effect of family history on histology or stage at diagnosis. Median survival in patients with a family history was 53 months compared to 58 months in patients without such a history (p = 0.06). On multivariate analysis, after adjusting for age, histology, stage at diagnosis, and smoking history, patients with a family history of lung cancer had a relative risk of death of 1.65 (95% CI: 1.07 - 2.56) (p = 0.02) compared to those without a family history ( Table ). This risk was especially increased in those who had an affected first degree relative (RR: 1.72; 95% CI: 1.08 - 2.75, p = 0.02). Conclusions: Lung cancer patients who have a first degree relative with lung cancer appear to have a worse outcome than those without a family history of lung cancer. No significant financial relationships to disclose. [Table: see text]
A population code with added grandmothers?
Authors: Malcolm P. Young, Stefano Panzeri, Robert Robertson
Journal: Behavioral and Brain Sciences (2000)

Page's “localist” code, a population code with occasional, maximally firing elements, does not seem to us usefully or testably different from sparse population coding. Some of the evidence adduced by Page for his proposal is not actually evidence for it, and coding by maximal firing is challenged by lower firing observed in neuronal responses to natural stimuli.
Transforming Growth Factor-β Limits Secretion of Lumican by Activated Stellate Cells within Primary Pancreatic Adenocarcinoma Tumors
Authors: Ya'an Kang, David Roife, Yeonju Lee, Hailong Lv, Rei Suzuki, Jianhua Ling, Mayrim V. Rios Perez, Xinqun Li, BingBing Dai, Michael Pratt, Mark J. Truty, Deyali Chatterjee, Huamin Wang, Ryan M. Thomas, Yu Wang, Eugene J. Koay, Paul J. Chiao, Matthew H. Katz, Jason B. Fleming
Journal: Clinical Cancer Research (2016)

Pancreatic ductal adenocarcinoma (PDAC) is lethal cancer whose primary tumor is characterized by dense composition of cancer cells, stromal cells, and extracellular matrix (ECM) composed largely of collagen. Within the PDAC tumor microenvironment, activated pancreatic stellate cells (PSC) are the dominant stromal cell type and responsible for collagen deposition. Lumican is a secreted proteoglycan that regulates collagen fibril assembly. We have previously identified that the presence of lumican in the ECM surrounding PDAC cells is associated with improved patient outcome after multimodal therapy and surgical removal of localized PDAC.Lumican expression in PDAC from 27 patients was determined by IHC and quantitatively analyzed for colocalization with PSCs. In vitro studies examined the molecular mechanisms of lumican transcription and secretion from PSCs (HPSCs and HPaSteC), and cell adhesion and migration assays examined the effect of lumican on PSCs in a collagen-rich environment.Here we identify PSCs as a significant source of extracellular lumican production through quantitative IHC analysis. We demonstrate that the cytokine, TGF-β, negatively regulates lumican gene transcription within HPSCs through its canonical signaling pathway and binding of SMAD4 to novel SBEs identified within the promoter region. In addition, we found that the ability of HPSCs to produce and secrete extracellular lumican significantly enhances HPSCs adhesion and mobility on collagen.Our results demonstrate that activated pancreatic stellate cells within PDAC secrete lumican under the negative control of TGF-β; once secreted, the extracellular lumican enhances stellate cell adhesion and mobility in a collagen-rich environment. Clin Cancer Res; 22(19); 4934-46. ©2016 AACR.