tbuckley/cabot-search huggingface dataset:
Hemangiopericytoma - An extremely rare bronchial tumour, a difficult diagnosis
Authors: Ruxandra Ulmeanu, Ramona Nedelcu, Dalia Manolache, Radu Matache, Dan Ioan Ulmeanu, Andrada Florian, Radu Stoica, Oana Deleanu, Doina Boiculese, Florin Mihaltan
Journal: European Respiratory Journal (2012)

Background:  Hemangiopericytoma is a rare mesenchymal tumor originating from the capillary pericytes (about 1% of vascular tumors). Its primary localization in the lung is extremely rare.   Case presentation:  A 52year old man, smoker(60PY), is diagnosed two months ago-by bronchoscopy and chest CT scan-with the main left bronchus tumor with subsequent negative biopsies. He was admitted to our hospital for reconsideration and clarification endoscopic diagnosis. Encefaloidal endoscopic tumor that stenosis left main bronchus from the begining by 65%, but without bronchial wall infiltration around the tumor.  1.We performed rigid bronchoscopy and “Jet”ventilation with snare electroresection of tumor in three stages.   Histopathological  examination of a biopsy specimens -  non-small carcinoma.   After bronchoscopy intervention, persist only distal total obstruction of left main bronchus.  2. Radical left pneumonectomy with mediastinal lymphadenectomy and intrapericardial approach of vessels is involved.   Macroscopically : white multinodular tumor, 14/10/10cm size, with large foci of necrosis.  Microscopically : malignant hemangiopericytoma    Discussion : Diagnosis of hemangiopericytoma was established after left pneumonectomy. Postoperative chemotherapy that combined carboplatin and taxol were performed.   Conclusion : Hemangiopericytoma is a rare vascular slow-growing tumor with high local recurrence and poor prognosis because the recurrence of disease. Preoperative diagnosis is difficult. Surgical radical excision is the treatment of choice, although the criteria for determining the area of resection have not been established.
A SURVEY OF SEX-CHROMOSOME ABNORMALITIES AMONG 4514 MENTAL DEFECTIVES
Authors: N. Maclean, J.M. Mitchell, D.G. Harnden, Jane Williams, PatriciaA. Jacobs, KarinA. Buckton, A.G. Baikie, W.M. Court Brown, J.A. Mcbride, J.A. Strong, H.G. Close, D.C. Jones
Journal: The Lancet (1962)
Rapid Response Teams—Walk, Don't Run
Authors: Bradford D. Winters, Julius Pham, Peter J. Pronovost
Journal: JAMA (2006)

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
Androgen Receptor Is Targeted to Distinct Subcellular Compartments in Response to Different Therapeutic Antiandrogens
Authors: Hayley C. Whitaker, Sarah Hanrahan, Nick Totty, Simon C. Gamble, Jonathan Waxman, Andrew C. B. Cato, Helen C. Hurst, Charlotte L. Bevan
Journal: Clinical Cancer Research (2004)

Abstract Purpose: Antiandrogens are routinely used in the treatment of prostate cancer. Although they are known to prevent activation of the androgen receptor (AR), little is known about the mechanisms involved. This report represents the first study of the localization of wild-type AR following expression at physiologic relevant levels in prostate cells and treatment with androgen and antiandrogens. Experimental Design: We have characterized a cellular model for prostate cancer using in situ cellular fractionation, proteomics, and confocal microscopy and investigated the effect of antiandrogens in clinical use on the subcellular localization of the AR. Results: Different antiandrogens have diverse effects on the subcellular localization of the AR. Treatment with androgen results in translocation from the cytoplasm to the nucleoplasm, whereas the antiandrogens hydroxyflutamide and bicalutamide lead to reversible association with the nuclear matrix. In contrast, treatment with the antiandrogen cyproterone acetate results in AR association with cytoplasmic membranes and irreversible retention within the cytoplasm. In addition, we demonstrate that AR translocation requires ATP and the cytoskeleton, regardless of ligand. Conclusions: These results reveal that not all antiandrogens work via the same mechanism and suggest that an informed sequential treatment regime may benefit prostate cancer patients. The observed subnuclear and subcytoplasmic associations of the AR suggest new areas of study to investigate the role of the AR in the response and resistance of prostate cancer to antiandrogen therapy.
Depressive Symptoms and Quality of Life in Adolescents With Type 2 Diabetes
Authors: Barbara J. Anderson, Sharon Edelstein, Natalie Walders Abramson, Lorraine E. Levitt Katz, Patrice M. Yasuda, Sylvia J. Lavietes, Paula M. Trief, Sherida E. Tollefsen, Siripoom Vudhipoom McKay, Patricia Kringas, Terri Lynn Casey, Marsha D. Marcus
Journal: Diabetes Care (2011)

OBJECTIVE The study objective was to examine the prevalence of depressive symptoms and relationships to quality of life and demographics in the Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) study’s large, ethnically diverse youth with type 2 diabetes. RESEARCH DESIGN AND METHODS A total of 704 youth with type 2 diabetes &amp;lt;2 years’ duration, aged 10–17 years, and BMI ≥85th percentile completed depressive symptoms and quality of life measures. RESULTS Some 14.8% reported clinically significant depressive symptoms, and older girls had significantly higher rates than older boys. CONCLUSIONS Rates of significant depressive symptoms were similar to those of healthy adolescents and lower than those of teens with type 1 diabetes. Elevated depressive symptoms, particularly in older girls, suggest clinicians assess vulnerability.
Brian Gerard Haggart
Authors: A. H. L. d. C. F. O'Connor
Journal: BMJ (2014)

Brian Gerard Haggart was a consultant general surgeon at Walton and Fazakerley hospitals in Liverpool. He was born the eldest of three children in Walton, Liverpool. He had two younger, twin sisters, Shirley and Pauline. They were from a modest background; their father worked for Reece’s Dairy in Liverpool. Brian was educated at St Francis De Sales Junior School and then by the Jesuits at St Francis Xavier School, which he attended from 1939 to 1946. This period included a brief evacuation to north Wales during the second world war. While he was there, the diet consisted mostly of rabbit, ensuring a lifelong aversion to this particular delicacy.

A visit to hospital to have his appendix removed as an early teenager convinced him that surgery was his vocation, and he gained a place to study medicine at Liverpool …
Importance of antineutrophil cytoplasmic antibodies in primary sclerosing cholangitis and ulcerative colitis: prevalence, titre, and IgG subclass.
Authors: D S Bansi, K A Fleming, R W Chapman
Journal: Gut (1996)

Antineutrophil cytoplasmic antibodies (ANCA) have been reported in up to 87% of patients with primary sclerosing cholangitis with or without ulcerative colitis (PSC +/- UC) and in 68% of those with UC only. Compared with other liver and diarrhoeal diseases, ANCA have high specificity for PSC (+/- UC) and UC only. This study aimed to determine the prevalence and significance of ANCA in these two diseases and whether the ANCA titre or IgG subclass, or both, could distinguish between PSC + UC and UC only. Subjects included 63 patients with PSC, 85 with UC, 17 with coeliac disease, and 10 with dermatitis herpeteformis and 36 normal subjects. ANCA was detected using the immunoalkaline phosphatase method. The IgG subclass of ANCA was determined in 27 PSC + UC and 30 UC only patients using a panel of mouse monoclonal antibodies specific for the IgG subclasses. At a serum dilution of 1:5, ANCA had a diagnostic sensitivity of 65% for all PSC and 45% for UC only. For PSC + UC the sensitivity was 70% at 1:5 (p = 0.004 v UC only). At 1:50, the sensitivity values were 54% and 25% respectively for PSC + UC and UC only (p = 0.0006). In PSC, ANCA positivity was significantly associated with extensive involvement of the biliary tree but not with other clinical parameters. In UC only, the median disease duration was significantly greater in ANCA positive patients. The PSC + UC ANCA showed increased IgG3 compared with UC only ANCA (p &lt; 0.05), together with increased IgG2 and IgG4 (p = NS). ANCA is a diagnostic marker in PSC and UC. While the higher titres and different IgG subclass distribution of ANCA in PSC + UC patients compared with those with UC only may reflect differences in underlying immune regulation, determination of the ANCA titre and IgG subclass is unlikely to have a role in distinguishing between PSC + UC and UC only ANCA. Future identification of the antigen(s) for ANCA should allow the development of a more sensitive and specific test for the diagnosis of these two conditions and also determine if ANCA is associated with UC or PSC.
Randomized phase II study of two intercalated combinations of eribulin mesylate and erlotinib in patients with previously treated advanced non-small-cell lung cancer
Authors: T.S. Mok, S.L. Geater, N. Iannotti, S. Thongprasert, A. Spira, D. Smith, V. Lee, W.T. Lim, L. Reyderman, B. Wang, P. Gopalakrishna, F. Garzon, L. Xu, C. Reynolds
Journal: Annals of Oncology (2014)
Identification of Hibernating Myocardium With Quantitative Intravenous Myocardial Contrast Echocardiography
Authors: Sarah Shimoni, Nikolaos G. Frangogiannis, Constadina J. Aggeli, Kesavan Shan, Mario S. Verani, Miguel A. Quinones, Rafael Espada, George V. Letsou, Gerald M. Lawrie, William L. Winters, Michael J. Reardon, William A. Zoghbi
Journal: Circulation (2003)

There are currently no data on the accuracy of intravenous myocardial contrast echocardiography (MCE) in detecting myocardial hibernation in man and its comparative accuracy to dobutamine echocardiography (DE) or thallium 201 (Tl(201)) scintigraphy.Twenty patients with coronary artery disease and ventricular dysfunction underwent MCE 1 to 5 days before bypass surgery and repeat echocardiography at 3 to 4 months. Patients also underwent DE (n=18) and rest-redistribution Tl(201) tomography (n=16) before revascularization. MCE was performed using continuous Optison infusion (12 to 16 cc/h) with intermittent pulse inversion harmonics and incremental triggering (1:1 to 1:8). Myocardial contrast intensity (MCI) replenishment curves were constructed to derive quantitative MCE indices of blood velocity and flow. Recovery of function occurred in 38% of dysfunctional segments. MCE parameters of perfusion in hibernating myocardium were similar to segments with normal function and higher than dysfunctional myocardium without recovery of function (P<0.001). The best MCE parameter for predicting functional recovery was Peak MCIxbeta, an index of myocardial blood flow (area under the curve, 0.83). MCE parameters were higher in segments with contractile reserve and Tl(201) uptake > or =60% (P<0.05) and identified viable segments without contractile reserve by DE. The sensitivity of Peak MCIxbeta >1.5 dB/s for recovery of function was 90% and was similar to Tl(201) scintigraphy (92%) and any contractile reserve (80%); specificity was higher than for Tl(201) and DE (63%, 45%, and 54%, respectively; P<0.05).MCE with intravenous contrast identifies myocardial hibernation in humans. Prediction of viable myocardium with MCE is best using quantification of myocardial blood flow and provides improved accuracy compared with DE and Tl(201) scintigraphy.
Cumulative Incidence of Secondary Neoplasms as a First Event After Childhood Acute Lymphoblastic Leukemia
Authors: Nobuko Hijiya, Melissa M. Hudson, Shelly Lensing, Margie Zacher, Mihaela Onciu, Fred G. Behm, Bassem I. Razzouk, Raul C. Ribeiro, Jeffrey E. Rubnitz, John T. Sandlund, Gaston K. Rivera, William E. Evans, Mary V. Relling, Ching-Hon Pui
Journal: JAMA (2007)

Little is known about the incidence of secondary neoplasms after 15 to 20 years in children and adolescents who were treated for acute lymphoblastic leukemia.To investigate the cumulative incidence of secondary neoplasms in pediatric patients treated for acute lymphoblastic leukemia over 30 years and to characterize late-occurring tumors.Retrospective study of 2169 patients with acute lymphoblastic leukemia treated between 1962 and 1998 at St Jude Children's Research Hospital, Memphis, Tenn, who achieved complete remission and had a median follow-up time of 18.7 years (range, 2.4-41.3 years).Cumulative incidences of secondary neoplasms in first remission and standard incidence ratios of observed rates compared with rates of cancer development in the general US population.Secondary neoplasms developed as the first event in 123 patients and comprised 46 myeloid malignancies, 3 lymphomas, 14 basal cell carcinomas, 16 other carcinomas, 6 sarcomas, 16 meningiomas, and 22 other brain tumors. The cumulative incidence of secondary neoplasm was 4.17% (SE, 0.46%) at 15 years and increased substantially after 20 years, reaching 10.85% (SE, 1.27%) at 30 years. When meningiomas and basal cell carcinomas were excluded, the overall cumulative incidence was 3.99% (SE, 0.44%) at 15 years and 6.27% (SE, 0.83%) at 30 years, representing a 13.5-fold increase in overall risk compared with the general population. The cumulative incidence of each tumor type at 30 years was 2.19% (SE, 0.32%) for myeloid malignancy, 0.17% (SE, 0.10%) for lymphoma, 3.00% (SE, 0.59%) for brain tumor, 4.91% (SE, 1.04%) for carcinoma, and 0.57% (SE, 0.37%) for sarcoma.The cumulative incidence of secondary neoplasms increases steadily over 30 years after treatment of acute lymphoblastic leukemia. Although the majority of the late-occurring secondary neoplasms are low-grade tumors, the increase in incidence of more aggressive malignant neoplasms is significantly higher than expected in the general population. These results suggest that lifelong follow-up of acute lymphoblastic leukemia survivors is needed to ascertain the full impact of treatment and other leukemia-related factors on secondary neoplasm development.
Circulating Brain-Derived Neurotrophic Factor Concentration Is Downregulated by Intralipid/Heparin Infusion or High-Fat Meal in Young Healthy Male Subjects
Authors: Monika Karczewska-Kupczewska, Irina Kowalska, Agnieszka Nikołajuk, Agnieszka Adamska, Magdalena Zielińska, Natalia Kamińska, Elżbieta Otziomek, Maria Górska, Marek Strczkowski
Journal: Diabetes Care (2011)

OBJECTIVE Insulin resistance and type 2 diabetes are associated with an increased risk of neurodegenerative diseases. Brain-derived neurotrophic factor (BDNF) regulates neuronal differentiation and synaptic plasticity, and its decreased levels are supposed to play a role in the pathogenesis of Alzheimer’s disease and other disorders. The aim of the current study was to estimate the effects of hyperinsulinemia and serum free fatty acids (FFA) elevation on circulating BDNF concentration in humans. RESEARCH DESIGN AND METHODS We studied 18 healthy male subjects (mean age 25.6 ± 3.0 years; mean BMI 26.6 ± 4.8 kg/m2). Serum and plasma BDNF concentration was measured in the baseline state and in the 120 and 360 min of euglycemic hyperinsulinemic clamp with or without intralipid/heparin infusion. Furthermore, plasma BDNF was measured in 20 male subjects (mean age 22.7 ± 2.3 years; mean BMI 24.9 ± 1.5 kg/m2) 360 min after a high-fat meal. RESULTS Insulin sensitivity was reduced by ∼40% after 6 h of intralipid/heparin infusion (P &amp;lt; 0.001). During both clamps, serum and plasma BDNF followed the same pattern. Hyperinsulinemia had no effect on circulating BDNF. Raising FFA had no effect on circulating BDNF in 120 min; however, it resulted in a significant decrease by 43% in serum and by 35% in plasma BDNF after 360 min (P = 0.005 and 0.006, respectively). High-fat meal also resulted in a decrease by 27.8% in plasma BDNF (P = 0.04). CONCLUSIONS Our data show that raising FFA decreases circulating BDNF. This might indicate a potential link between FFA-induced insulin resistance and neurodegenerative disorders.
A tree reconstruction method that is economical in the number of pairwise comparisons used.
Authors: J Hein
Journal: Molecular Biology and Evolution (1989)

A fast method for reconstructing phylogenies from distance data is presented. The method is economical in the number of pairwise comparisons needed. It can be combined with a new phylogenetic alignment procedure to yield an algorithm that gives a complete history of a set of homologous sequences. The method is applicable to very large distance matrices. An auxiliary program was developed that simplifies large phylogenies without ignoring biologically essential features. A set of 213 globins from vertebrates, plants, and Vitreoscilla (a prokaryote) were analyzed using this method.
Protopine, a novel microtubule stabilizing agent, caused mitotic arrest and subsequent apoptosis in hormone-refractory prostate cancer cells.
Authors: Chun-Han Chen, Cho-Hwa Liao, Shiow-Lin Pan, Jih-Hwa Guh, Che-Ming Teng
Journal: Clinical Cancer Research (2007)

B42   Prostate cancer is the second leading cause of cancer death in men. Because microtubule-stablizing agents, such as docetaxel which has been approved by the Food and Drug Administration for advanced prostate cancer, might have the therapeutic potential, we examined the anticancer effect of protopine in metastatic hormone-refractory prostate cancer PC-3 cells. Protopine is an isoquinoline alkaloid which is common in the plants of  Papaveraceae ,  Fumariaceae  and other families. Protopine exhibited anti-proliferative effect on PC-3 cells in a concentration-dependent manner with a GI 50  of 13.02 ± 1.70 μM as evaluated by sulforhodamine B assay. FACScan flow cytometric analysis revealed that protopine caused cell cycle accumulation at G2/M phase and subsequent at subG1 phase. Meanwhile, protopine activated cyclin-dependent kinase 1 (CDK1) through down-regulation of Tyr15 phosphorylation and up-regulation of Thr161 phosphorylation as well as induction of cyclin B1. By the immunofluorescence microscopy and tubulin polymerization assay, protopine concentration-dependently promoted tubulin polymerization. Furthermore, protopine induced massive apoptotic cell death as detected by TdT-mediated dUTP Nick-End Labeling (TUNEL) assay and oligonucleosomal DNA fragmentation. Protopine increased Bcl-2 and Mcl-1 phosphorylation and eventually caspase-3 activation following PARP cleavage. Overall, this is the first report to demonstrate that protopine stabilized microtubule organization leading to mitotic arrest and subsequent apoptosis in metastatic hormone-refractory prostate cancer PC-3 cell line.
Clinical Heterogeneity in Monogenic Diabetes Caused by Mutations in the Glucokinase Gene (GCK-MODY)
Authors: Antonio L. Cuesta-Muñoz, Tiinamaija Tuomi, Nadia Cobo-Vuilleumier, Hanna Koskela, Stella Odili, Amanda Stride, Carol Buettger, Timo Otonkoski, Philippe Froguel, Joseph Grimsby, Maria Garcia-Gimeno, Franz M. Matschinsky
Journal: Diabetes Care (2009)

OBJECTIVE To evaluate the heterogeneity in the clinical expression in a family with glucokinase mature-onset diabetes of the young (GCK-MODY). RESEARCH DESIGN AND METHODS Members (three generations) of the same family presented either with overt neonatal hyperglycemia, marked postprandial hyperglycemia, or glucosuria. Homeostasis model assessment of insulin resistance (HOMAIR) and insulinogenic and disposition indexes were calculated. Oral glucose tolerance test (OGTT) results in the GCK mutation carriers from this family were compared with those from other subjects with GCK mutations in the same codon (GCK261), with other missense and other types of GCK mutations in different codons from the European MODY Consortium database (GCKm). RESULTS Mutation G261R was found in the GCK gene. During the OGTT, glucose (P = 0.02) and insulin (P = 0.009) response at 2 h as well as at the 2-h glucose increment (GCK261 versus other missense GCK mutations, P = 0.003) were significantly higher in GCK261 than in GCKm carriers. CONCLUSIONS Differing from other GCKm carriers, the glucose and insulin response to oral glucose was significantly higher in GCK261 carriers, indicating clinical heterogeneity in GCK-MODY.
Sustained pharmacological inhibition of δPKC protects against hypertensive encephalopathy through prevention of blood-brain barrier breakdown in rats
Authors: Xin Qi, Koichi Inagaki, Raymond A. Sobel, Daria Mochly-Rosen
Journal: Journal of Clinical Investigation (2007)

Hypertensive encephalopathy is a potentially fatal condition associated with cerebral edema and the breakdown of the blood-brain barrier (BBB). The molecular pathways leading to this condition, however, are unknown. We determined the role of deltaPKC, which is thought to regulate microvascular permeability, in the development of hypertensive encephalopathy using deltaV1-1 - a selective peptide inhibitor of deltaPKC. As a model of hypertensive encephalopathy, Dahl salt-sensitive rats were fed an 8% high-salt diet from 6 weeks of age and then were infused s.c. with saline, control TAT peptide, or deltaV1-1 using osmotic minipumps. The mortality rate and the behavioral symptoms of hypertensive encephalopathy decreased significantly in the deltaV1-1-treated group relative to the control-treated group, and BBB permeability was reduced by more than 60%. Treatment with deltaV1-1 was also associated with decreased deltaPKC accumulation in capillary endothelial cells and in the endfeet of capillary astrocytes, which suggests decreased microvasculature disruption. Treatment with deltaV1-1 prevented hypertension-induced tight junction disruption associated with BBB breakdown, which suggests that deltaPKC may specifically act to dysregulate tight junction components. Together, these results suggest that deltaPKC plays a role in the development of hypertension-induced encephalopathy and may be a therapeutic target for the prevention of BBB disruption.