tbuckley/cabot-search huggingface dataset:
Utility of closed pleural biopsy in a teaching hospital in Singapore
Authors: Hang Siang Wong
Journal: European Respiratory Journal (2012)

Introduction

• The yield of closed pleural biopsy is quoted in most studies to be around 90% for pleural TB and 70% for malignancy.

Objective

• To determine the yield of closed pleural biopsy in our institution and the possible factors affecting the yield.

Methods

• This was a retrospective study. All pleural biopsies done from 1/6/10 till 31/7/11 were included. Inclusion criteria were subjects with lymphocytic exudative pleural effusion who underwent closed pleural biopsy. All closed pleural biopsies were done under ultrasound guidance either by a respiratory trainee or an interventional radiologist.

Results

• A total of 50 subjects underwent closed pleural biopsy. The positive yield of closed pleural biopsy in the cohort was 33/50(66%). Out of the 33 positive yield, 17(51.5%) were pleural TB, 6(18.2%) were malignancy and 10(30.3%) were others. The positive yield of pleural TB was 17/26(65.4%), malignancy 6/13(46.2%) and others 10/11(90.9%). 32/50(64%) pleural biopsies were done by respiratory trainees and 18/50(36%) by interventional radiologists. The positive yield of pleural biopsies done by respiratory trainees was 18/32(56.3%) and by interventional radiologists 15/18(83.3%). No difference in the yield of closed pleural biopsy across the ages from 22 to 94 years old (p=0.85), male versus female (p=0.76), race (p=0.26), respiratory trainees versus interventional radiologist (p=0.067), TB versus malignancy (p=0.312).

Conclusion

• The yield of closed pleural biopsy was lower compared to most studies in other centers. Age, gender, race, operator experience, TB versus malignancy did not show any significant difference in the yield.
In vitro abrogation of acquired tamoxifen resistance using histone deacetylase inhibitors
Authors: M. Beeram, D. Russell, L. DeGraffenreid, J. Freeman
Journal: Journal of Clinical Oncology (2007)

10607 Tamoxifen (TAM) is a highly effective therapy for breast cancer. However, only 60% of estrogen receptor expressing (ER+) breast cancers respond to TAM (40% de-novo resistance). Continuous TAM treatment causes emergence of acquired resistance in these initially- responsive cancers. Strategies that abrogate TAM-resistance are therefore of significant clinical importance. One approach being studied is the use of histone deacetylase (HDAC) inhibitors. These compounds impact tumor biology both at the level of gene transcription and protein stability. In our study, we developed an in vitro model of tamoxifen resistance to test the efficacy of a hydroxamic acid derivative, Trichostatin A (TSA) at modulating breast cancer cell growth both in TAM responsive as well as TAM resistant cells. Forty-eight MCF-7 breast cancer single-cell colonies were isolated from a heterogeneous population, with 16 of the 48 (33%) surviving 4 months of continual growth in charcoal-stripped media with 10 -7 M tamoxifen. ER expression was lost in 9 (56%) and HER-2 expression was acquired in 7 (44%) of the 16 resistant clones. The ER-negative cells demonstrated a concomitant increase in p-Rb, p21 and p27 levels, as well as significant increase in activation of both the PI3K and MAP kinase pathways. These results suggest that alteration of parent cell phenotype is an adaptive event at the transcriptional level, and is a significant mechanism for mediating TAM resistance. Inhibition of growth, by TSA, was studied in both the ER+ and ER- cells, with and without cotreatment with TAM. Cotreatment with TSA effectively blocked the emergence of resistance and prolonged the duration of response to TAM. The molecular mechanisms mediating this enhanced response were studied and focused on the effects of TSA on ER and HER-2 activity and expression. Our results indicate that short term exposure to TSA induces suppression of ER gene transcription, as well as targets ER for protein degradation where as long term exposure shows paradoxical effects at the genomic level. The effects of TSA on acquired HER-2 expression are being studied. These data have important clinical ramifications for the clinical development of HDAC inhibitors for the treatment of breast cancer patients. No significant financial relationships to disclose.
OP08 Evidence for early astrocyte activation, cellular stress and compensatory microglial related transforming growth factor-α responses in bile-duct ligated rats
Authors: G Wright, T Newman, Y Sharifi, N Davis, R Jalan
Journal: Gut (2010)

Introduction  Inflammation and ammonia are important mediators in the pathogenesis of hepatic encephalopathy and though the mechanisms are unclear astrocytes are thought to have a central role. Recently Microglia, which also mediate brain inflammation, were implicated in the brain effects of acute liver failure; however their influence in chronic liver disease is unknown.  Aim  The aim of this longitudinal study was to characterise the early brain responses in bile-duct ligated (BDL) rats in the 4-weeks following ligation.  Method  Twenty-four male Sprague-Dawley rats were studied after sham-operation or BDL and sacrificed at either 1-day or, 1-, 2- or 4 weeks post-surgery (n=4/group). Consciousness, brain water content, arterial ammonia, plasma biochemistry and proinflammatory (IL-6, TNF-α and γ-IFN) and antiinflammatory (IL-4 and IL-10) cytokines, were analysed. Immunohistochemical markers of activated microglia (ED1, OX6 and Iba-1), astrocytes (GFAP), inflammatory responses (IL-1s and iNOS), cellular stress (HSP-25) and the predominant antiinflammatory and alternative microglial activation marker TGF-s (using RT-PCR), were also analysed.  Results  Compared to Shams, arterial and brain ammonia (p  Conclusion  Regional astrocyte activation and cellular stress (indicated by increased HSP-25 expression), are early features of BDL. These events are associated with increased brain proinflammatory cytokine production and iNOS expression. This proinflammatory response is not due to obvious microglia activation, but consequent upon activation of astrocytes, possibly related to hyperammonemia and/or associated cell swelling. However, an observed TGF-s response may reflect compensatory antiinflammatory microglial responses, designed to limit the effect of astrocyte activation; with interventions targeting its brain expression potential novel therapies for hepatic encephalopathy.
Insulin Resistance and<i>APOE</i>ε4
Authors: Auriel A. Willette, Christine M. Burns, Barbara B. Bendlin
Journal: JAMA Neurology (2015)

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 Neurology HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Neurology journal
Failure to thrive, interstitial lung disease, and progressive digital necrosis with onset in infancy
Authors: Justin Chia, Fehime Kara Eroglu, Seza Özen, Dicle Orhan, Gina Montealegre-Sanchez, Adriana A. de Jesus, Raphaela Goldbach-Mansky, Edward W. Cowen
Journal: Journal of the American Academy of Dermatology (2015)
Patient may have had a muscular dystrophy or Andersen's syndrome
Authors: P. Jardine
Journal: BMJ (1996)

Janet Lock and Dawn Gallagher are surprised that we mentioned the use of cardioselective P blockers.We did not wish to imply that patients with clear cut active asthma would be given ( blockers but rather wished to point out that many patients with little or no disease at all could be considered for treatment.Many patients are labelled as having asthma but do not in fact have the condition, and we considered our audience to be sufficiently sophisticated to take our point.With regard to methysergide, we mentioned ret- roperitoneal fibrosis to highlight a reasonably well appreciated clinical problem.With regard to
Carbon monoxide decreases interleukin-1β levels in the lung through the induction of pyrin
Authors: Seul-Ki Kim, Yeonsoo Joe, Yingqing Chen, Jinhyun Ryu, Jeong-Hee Lee, Gyeong Jae Cho, Stefan W. Ryter, Hun Taeg Chung
Journal: Cellular and Molecular Immunology (2015)

Carbon monoxide (CO) can act as an anti-inflammatory effector in mouse models of lung injury and disease, through the downregulation of pro-inflammatory cytokines production, though the underlying mechanisms remain unclear. The nucleotide-binding oligomerization domain-, leucine-rich region-, and pyrin domain-containing-3 (NLRP3) inflammasome is a protein complex that regulates the maturation and secretion of pro-inflammatory cytokines, including interleukin-1β (IL-1β). In this report, we show that the CO-releasing molecule (CORM-2) can stimulate the expression of pyrin, a negative regulator of the NLRP3 inflammasome. CORM-2 increased the transcription of pyrin in the human leukemic cell line (THP-1) in the absence and presence of lipopolysaccharide (LPS). In THP-1 cells, CORM-2 treatment dose-dependently reduced the activation of caspase-1 and the secretion of IL-1β, and increased the levels of IL-10, in response to LPS and adenosine 5'-triphosphate (ATP), an NLRP3 inflammasome activation model. Genetic interference of IL-10 by small interfering RNA (siRNA) reduced the effectiveness of CORM-2 in inhibiting IL-1β production and in inducing pyrin expression. Genetic interference of pyrin by siRNA increased IL-1β production in response to LPS and ATP, and reversed CORM-2-dependent inhibition of caspase-1 activation. CO inhalation (250 ppm) in vivo increased the expression of pyrin and IL-10 in lung and spleen, and decreased the levels of IL-1β induced by LPS. Consistent with the induction of pyrin and IL-10, and the downregulation of lung IL-1β production, CO provided protection in a model of acute lung injury induced by intranasal LPS administration. These results provide a novel mechanism underlying the anti-inflammatory effects of CO, involving the IL-10-dependent upregulation of pyrin expression.
Reductions in virological failure and drug resistance to antiretroviral therapy in Chinese patients associated with lamivudine-based regimens, 2003–12: a cross-sectional study
Authors: Hui Xing, Yuhua Ruan, Jenny H Hsi, Wei Kan, Lingjie Liao, Xuebing Leng, Jing Wang, Cui He, Yiming Shao
Journal: The Lancet (2015)
Anaphylactic and anaphylactoid reactions to chemotherapy: outcomes and safety of rapid intravenous and intraperitoneal desensitizations in 413 cases
Authors: M. C. Castells, N. M. Tennant, D. E. Sloane, F. I. Hsu, S. T. Berlin, S. M. Campos, U. A. Matulonis
Journal: Journal of Clinical Oncology (2008)

5526 Background: Hypersensitivity reactions to chemotherapeutic drugs, including monoclonal antibodies, often require that the provoking medication be discontinued, thus raising a dilemma for the caregiver: further use could precipitate a severe, even fatal, allergic reaction upon re-exposure, but alternative drugs may be poorly tolerated or much less effective compared to the preferred agent. To address this difficulty, we have developed a standardized rapid desensitization protocol for achieving temporary tolerization to drug allergens. In this study, we evaluate the safety and efficacy of this protocol. Methods: Ninety-eight patients who developed hypersensitivity reactions in response to treatment with carboplatin, cisplatin, oxaliplatin, paclitaxel, pegylated doxorubicin, adriamycin, or rituximab received rapid desensitization to these agents. A standardized 12-step protocol was used, with treatment applied intravenously or intraperitoneally. Initial desensitizations occurred in the Medical Intensive Care Unit, while most subsequent infusions took place in an outpatient setting. Safety and efficacy of the protocol were assessed by review of treatment records. Results: Of the 413 desensitizations performed, 94% induced mild or no reactions. No life-threatening HSRs or deaths occurred during the procedure, and all patients received their full target dose. Most reactions occurred during the first desensitization. Reactions were most commonly reported at the last step of the protocol. Desensitization infusions via the intravenous and intraperitoneal routes were equally effective. Conclusions: Our standardized 12-step protocol for rapid drug desensitization is safe and effective and should be the standard of care in treating patients who develop hypersensitivity reactions to chemotherapeutic drugs, including monoclonal antibodies. No significant financial relationships to disclose.
New Strategies in Bladder Cancer: A Second Coming for Immunotherapy
Authors: Ali Ghasemzadeh, Trinity J. Bivalacqua, Noah M. Hahn, Charles G. Drake
Journal: Clinical Cancer Research (2015)

Abstract Urothelial bladder cancer (UBC) remains one of the most common and deadly cancers worldwide, and platinum-based chemotherapy, which has been the standard-of-care in metastatic bladder cancer, has had limited success in improving outcomes for patients. The recent development and translation of therapeutic strategies aimed at harnessing the immune system have led to durable and prolonged survival for patients with several different cancers, including UBC. In this review, we discuss new findings in bladder cancer immunotherapy, including recent successes with immune checkpoint blockade. We also discuss therapeutic cancer vaccines and highlight several additional immunotherapy modalities in early stages of development. Clin Cancer Res; 22(4); 793–801. ©2015 AACR.
The High Risk of Low Distal Flow
Authors: James F. Meschia
Journal: JAMA Neurology (2015)

VAST illustrates many of the challenges of developing interventional therapy for this patient population. During a median follow-up of 3 years, 12% of the patients in the stenting group and 7% of those in the medical group developed stroke in the symptomatic vertebral arterial territory. The VAST investigators estimated that, with this cumulative absolute rate of stroke events in the medical group, 9500 patients would have to be randomized in a future trial to provide compelling evidence of a 20% reduction in risk. With this in mind, it may be more productive—indeed, perhaps necessary—to reserve the development of interventional therapy for higher-risk populations. It may be useful for future trials to focus on providing treatment for patients sooner after their qualifying event. In VAST, only one-third of the medical group was enrolled within 14 days of their qualifying event.
Pertuzumab in the Treatment of HER2<sup>+</sup>Breast Cancer
Authors: Komal Jhaveri, Francisco J. Esteva
Journal: Journal of the National Comprehensive Cancer Network (2014)

Pertuzumab, a humanized monoclonal antibody and the first in the class of agents called the HER2 dimerization inhibitors, impairs the ability of HER2 to bind to other members of the HER family. It has a unique and complimentary mechanism of action compared with trastuzumab, and the combination has resulted in the enhanced blockade of the HER signaling pathway. When pertuzumab was used in combination with docetaxel and trastuzumab in the first-line treatment of metastatic HER2+ breast cancer, it led to an overall survival benefit. Pertuzumab has therefore been approved by the FDA and is currently used as a standard of care for this indication. It is also the first agent in oncology to receive accelerated FDA approval in the neoadjuvant setting. Randomized trials showed that the addition of pertuzumab to trastuzumab-based chemotherapy improves pathologic complete response rates in HER2+ early-stage breast cancer. A randomized phase III clinical trial with disease-free survival as the primary end point is evaluating the safety and efficacy of pertuzumab in the adjuvant setting. This article describes the preclinical data, synthesizes available data from phase I-III clinical trials of pertuzumab in early stage and metastatic settings, and puts them into perspective with current treatment recommendations and future research developments.
Implications of Including Do-Not-Resuscitate Status in Hospital Mortality Measures
Authors: Leora I. Horwitz
Journal: JAMA Internal Medicine (2015)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Internal Medicine journal
The value of miR221 and miR222 as a biomarker in non small cell lung cancer
Authors: Yasemin Musteri Oltulu, Ender Coskunpinar, Engin Aynaci, Pinar Yildiz, Ilhan Yaylim
Journal: European Respiratory Journal (2014)

Aim of the study is investigate of expression levels of serum specific miRNA221 and miRNA222 as a biomarker in NSCLC.Thirty-two NSCLC cases and 30 healthy control cases that were diagnosed at Yedikule Chest Diseases and Chest Surgery, Training and Research Hospital were included in this study. In the study were used RT-PCR based miRNA (miR-qRT-PCR) detection methods. In NSCLC patients in accordance with control, miR221 and miR222 are expressed 1.46 and 1.63-fold, respectively, and while the difference of expression is statistically significant for miR221 (p:0.0001), significant difference did not be detected for miR222 (p:0.08)  Keywords:NSCLC, biomarker, gene expression, miR221, miR222.
The Innate Immune Receptor PGRP-LC Controls Presynaptic Homeostatic Plasticity
Authors: Nathan Harris, Daniel J. Braiser, Dion K. Dickman, Richard D. Fetter, Amy Tong, Graeme W. Davis
Journal: Neuron (2015)

Highlights•A conserved innate immune receptor, PGRP, is necessary for presynaptic homeostasis•The PGRP-LCx isoform is necessary in motoneurons for presynaptic homeostasis•PGRP-LC controls the homeostatic modulation of the release-ready vesicle pool•PGRP-LC genetically interacts with RIM and MultiplexinSummaryIt is now appreciated that the brain is immunologically active. Highly conserved innate immune signaling responds to pathogen invasion and injury and promotes structural refinement of neural circuitry. However, it remains generally unknown whether innate immune signaling has a function during the day-to-day regulation of neural function in the absence of pathogens and irrespective of cellular damage or developmental change. Here we show that an innate immune receptor, a member of the peptidoglycan pattern recognition receptor family (PGRP-LC), is required for the induction and sustained expression of homeostatic synaptic plasticity. This receptor functions presynaptically, controlling the homeostatic modulation of the readily releasable pool of synaptic vesicles following inhibition of postsynaptic glutamate receptor function. Thus, PGRP-LC is a candidate receptor for retrograde, trans-synaptic signaling, a novel activity for innate immune signaling and the first known function of a PGRP-type receptor in the nervous system of any organism.
Small cell lung cancer in never-smokers
Authors: María Torres-Durán, Alberto Ruano-Ravina, Karl T. Kelsey, Isaura Parente-Lamelas, Mariano Provencio, Virginia Leiro-Fernández, José Abal-Arca, Carmen Montero-Martínez, Iria Vidal-Garcia, Carolina Pena, Olalla Castro-Añón, Antonio Golpe-Gómez, Cristina Martínez, Rosirys Guzmán-Taveras, María José Mejuto-Martí, Alberto Fernández-Villar, Juan Miguel Barros-Dios
Journal: European Respiratory Journal (2015)

Our aim was to describe the characteristics of a case-series of never-smoker small cell lung cancer (SCLC) cases.Cases of SCLC were selected from a prospective, multicenter, hospital-based case-control study performed in Spain. Participants were never-smokers older than 30 years with an anatomo-pathological confirmation of primary lung cancer. We collected clinical and epidemiological variables according to the study's protocol.We included 19 SCLC cases, 18 females (94.7%), median age 75 years (interquartile range (IQR) 70-80 years). Median residential radon concentration was 195 Bq·m(-3) (IQR 130-229 Bq·m(-3)). 10 patients had limited disease and nine had extended disease. Median survival was 242 days (IQR 94-496 days); 1- and 2-year survival were 36.8% and 17.6%, respectively. Survival was much higher for individuals with limited disease than for those with extended disease (median 336 versus 235 days; 1-year survival 50% versus 22.2% and 2-year survival 27% versus 0%, respectively). Performance status at diagnosis was closely related to survival.SCLC is an infrequent, highly aggressive disease in never-smokers. Survival is poor, even for limited disease. Age at diagnosis in SCLC is higher than that observed for never-smokers with adenocarcinoma. Residential radon exposure is higher than the action levels recommended by the World Health Organization.
Self-Expanding Stents for Malignant Dysphagia
Authors: W D B Clements, L R Johnston, E Mcllwrath Mrcrad, R A J Spence, J McGuigan
Journal: Journal of the Royal Society of Medicine (1996)

Self-expanding metallic stents have been employed successfully for vascular, urethral, and biliary strictures. In a prospective study we examined the efficacy of the 16 mm Wallstent for palliation of malignant dysphagia. Eight patients with severe dysphagia due to advanced primary (four) or secondary (four) oesophageal malignant disease were recruited and nine Wallstents were inserted (one patient required two). Dysphagia was reduced in all but one patient, who died after oesophageal perforation; a second patient had a self-limiting bout of haematemesis. Two patients required subsequent treatment for tumour ingrowth but five had no further palliative therapy from stent insertion to time of death. With careful patient selection and skillful application, a 16 mm self-expanding metal endoprosthesis affords effective palliation in malignant oesophageal obstruction.
Allogeneic Hematopoietic Stem Cell Transplantation For Severe Neuromyelitis Optica
Authors: Raffaella Greco, Attilio Bondanza, Luca Vago, Lucia Moiola, Paolo Rossi, Roberto Furlan, Gianvito Martino, Marta Radaelli, Vittorio Martinelli, Maria Rosaria Carbone, Maria Teresa Lupo Stanghellini, Andrea Assanelli, Massimo Bernardi, Consuelo Corti, Jacopo Peccatori, Chiara Bonini, Paolo Vezzulli, Andrea Falini, Fabio Ciceri, Giancarlo Comi
Journal: Blood (2013)