tbuckley/cabot-search huggingface dataset:
An analysis of indwelling pleural catheter (IPC) insertions for malignant pleural effusions
Authors: Elaine Reid, Pasupathy Sivasothy, Stefan Marciniak
Journal: European Respiratory Journal (2011)

Introduction: Persistent malignant pleural effusion (MPE) is a common complication of malignant disease. IPCs are a safe effective strategy to relieve dyspnoea, maintain quality of life, reduce hospitalisation and length of hospital stay.

Objective: To describe the use and outcomes of IPCs in management of MPE.

Method: Retrospective analysis of 47 sequential IPC insertions for patients with MPE's in a single centre from May 2009 to February 2011.

Results: 47 IPC insertions for MPE were performed in 44 patients (1 bilateral and 2 repeated procedures)

![Figure][1] 



21 patients had IPC insertion due to trapped lung, 19 patients after failed pleurodesis. Median hospitalisation 2 days for elective admission (IQR 1), 6 days for emergency admission (IQR 2.5). Median survival post insertion, if still insitu at time of death, 35 days (IQR 28); mean 54 days (SD 54.5). Complication rates were low; 2 cases of cellulitis, 2 cases of skin sensitivity to dressing, 1 tube displacement and 1 fracturing of IPC requiring removal. IPCs were removed in 4 patients after auto-pleurodesis. In 4 cases drainage ceased but IPCs were left insitu until end of life. No difference in frequency of auto-pleurodesis in patients who had trapped lung or failed pleurodesis.

Conclusions: IPC's are effective and safe for management of MPE with low complication rates and obvious cost benefit advantage in reduced hospital admissions offering immediate and sustained relief of symptoms.

 [1]: pending:yes
Long-Term Results in Patients With Idiopathic Dilated Cardiomyopathy After Weaning From Left Ventricular Assist Devices
Authors: Michael Dandel, Yuguo Weng, Henryk Siniawski, Evgenij Potapov, Hans B. Lehmkuhl, Roland Hetzer
Journal: Circulation (2005)

Since our first successful left ventricular assist device (LVAD) explantation in a patient with idiopathic dilated cardiomyopathy (IDCM) in 1995, an additional 31 IDCM patients have been weaned in our department. Echocardiographic evaluations during repeated "off-pump" trials were the cornerstone for weaning decisions. After 9 years of experience, we assessed the reliability of our weaning criteria in light of the long-term results.We evaluated all of the IDCM patients who were weaned between March 1995 and March 2004 with regard to preservation of cardiac function without LVAD support and survival after weaning. Additionally, we reviewed our echocardiographic data to assess their predictive value for long-term stability of cardiac function after weaning. The 32 weaned IDCM patients showed a survival rate of 78.3%+/-8.1 at 5 years after LVAD explantation. Heart failure (HF) recurred during the first 3 years after weaning in 31.3%. Only 2 patients died because of HF after weaning; the other patients with HF recurrence were successfully transplanted. Off-pump LV end-diastolic diameter >55 mm and/or LVEF <45% before LVAD removal, as well as history of HF > or =5 years before LVAD implantation, appeared to be major risk factors for early recurrence of HF. Patients without any of these 3 risk factors showed no HF recurrence during the first 3 years after weaning, but at the same time, all of those with at least 2 of these 3 risk factors developed early recurrence of HF. In patients with HF recurrence during the first 3 postweaning years, a significant LVEF decrease already occurred during the first month after weaning, whereas in those with long-term stable cardiac function even at the end of the sixth postweaning month, the LVEF was not different from that before LVAD removal.For selected patients with IDCM, weaning from LVADs is a clinical option with good results over >9 years and should, therefore, be considered in those with cardiac recovery after LVAD implantation. Off-pump echocardiographic data are reliable for the detection of LV recovery and prediction of long-term cardiac stability after weaning.
Hepatic Cytologic and Neoplastic Changes in Mice Given Benzidine Dihydrochloride
Authors: Charles H. Frith, Kenneth Dooley
Journal: JNCI Journal of the National Cancer Institute (1976)

The administration of benzidine dihydrochloride in water to mice for up to 39 weeks resulted in hemosiderosis of the spleen, focal vacuolization of the transitional epithelium of the urinary bladder, and chronic inflammation and cytologic and neoplastic changes in the liver. Basophilic and acidophilic cytologic foci appeared in the liver as two distinct entities and both appeared preneoplastic. Benign and malignant liver tumors were also seen. Both types of cytologic changes and malignant liver tumors were more common in the female than male mouse.
Predominant Glandular Cholinergic Dysautonomia in Patients With Primary Sjögren's Syndrome
Authors: Richard Imrich, Ilias Alevizos, Lolita Bebris, David S. Goldstein, Courtney S. Holmes, Gabor G. Illei, Nikolay P. Nikolov
Journal: Arthritis & Rheumatology (2015)

Objective The autonomic nervous system (ANS) modulates exocrine gland function. Available data show poor correlation between the degree of function and destruction of the exocrine glands in primary Sjögren's syndrome (SS), suggesting that other mechanisms, such as autonomic dysfunction, may be important in these patients. The aim of this study was to perform a comprehensive analysis of sympathoneural and sympathetic cholinergic function in well‐characterized patients with primary SS. Methods Twenty‐one patients with primary SS (mean ± SEM age 44.2 ± 2.8 years) and 13 healthy control subjects (mean ± SEM age 50.8 ± 1.9 years) were assessed during orthostasis and intravenous injection of edrophonium (10 mg). The postganglionic sympathetic cholinergic system was evaluated by assessing sweat production by means of the Quantitative Sudomotor Axon Reflex Test (QSART). Tests of gastric emptying were used to assess the gastrointestinal ANS in primary SS patients. Results The velocity index and the acceleration index were significantly higher ( P &lt; 0.05) in patients with primary SS as compared to controls, both before and during the orthostatic and edrophonium tests. Findings of other hemodynamic and neurochemical parameters did not differ between primary SS patients and controls during the orthostasis and edrophonium test; however, the edrophonium‐induced saliva increment was lower in primary SS patients ( P = 0.002). Abnormally low sweat production was found in 4 primary SS patients but in none of the controls, as determined by the QSART. Gastric emptying was delayed in 53% of primary SS patients. Conclusion We observed subtle differences in several ANS domains, including the gastrointestinal and sympathocholinergic systems, suggesting the presence of a complex ANS dysfunction in primary SS. The impact was greatest on the exocrine glands, with subtle differences in the cardiac parasympathetic function that were independent of glandular inflammation and atrophy, suggesting an alternative mechanism of disease pathogenesis in primary SS.
Atopy, asthma, and lung function in relation to folate and vitamin B<sub>12</sub> in adults
Authors: B. H. Thuesen, L. L. N. Husemoen, L. Ovesen, T. Jørgensen, M. Fenger, G. Gilderson, A. Linneberg
Journal: Allergy (2010)

To cite this article: Thuesen BH, Husemoen LLN, Ovesen L, Jørgensen T, Fenger M, Gilderson G, Linneberg A. Atopy, asthma, and lung function in relation to folate and vitamin B 12 in adults. Allergy 2010; 65 : 1446–1454. Abstract Background: Recent studies suggested low serum folate and impaired folate metabolism as potential risk factors for development of asthma and atopic disease, but the results are inconsistent. The aim of this study was to investigate the relations of markers of folate and vitamin B 12 (B 12 ) deficiency with different phenotypes of asthma and atopy. Methods: A random sample of 6784 persons from a general population aged 30–60 years participated in a health examination in 1999–2001, and 4516 (66.6%) of those also participated in a follow‐up examination 5 years later. The examinations included spirometry, measurements of serum folate and B 12 , specific IgE to inhalant allergens, total IgE, and genotyping of the MTHFR‐C677T polymorphism – a genetic marker of impaired folate metabolism. Information about dietary intake of folate and B 12 , asthma diagnosis, and airway symptoms was obtained by questionnaires. Results: Low serum folate levels and the TT genotype of the MTHFR‐C677T polymorphism were associated with increased prevalence of self‐reported doctor‐diagnosed asthma [odds ratio (OR) 1.37, 95% confidence interval (CI) 1.05–1.79 and OR 1.52; 95% CI 1.12–2.06, respectively] and attacks of shortness of breath (OR 1.43, 95% CI 1.14–1.79 and OR 1.47; 95% CI: 1.14–1.91, respectively). We found no significant associations with lung function or atopic outcomes. Serum levels of B 12 and dietary intake of folate and B 12 were not associated with asthma or atopy. Conclusions: We found that two objective markers of folate deficiency were associated with self‐reported doctor‐diagnosed asthma and attacks of shortness of breath, but not with lung function or atopy.
The Inheritance of Mental Diseases.
Authors: Abraham Myerson
Journal: JAMA (1925)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Abstract 899: Combination of PI3K and MEK inhibitor chemosensitivity in human tumor explants and cell lines using the Mosaic Blue assay and relationship to biomarkers by immunohistochemistry
Authors: Lisa M. Dauffenbach, Gela C. Sia, Patricia A. Cash, Sherif K. Girees, Ryan S. Lim, Jianping Zheng, Eric P. Olsen, Christopher A. Kerfoot
Journal: Cancer Research (2014)

Abstract The PI3K and MEK pathways promote tumor cell survival through a variety of downstream signals and are commonly explored in cancer research. Many agents are in clinical development and new evidence suggests that a combination of these inhibitors may be required to achieve optimal anti-tumor activity. Twenty-one viable colorectal and non-small cell lung cancer tissue explants with matched formalin-fixed, paraffin embedded (FFPE) tissue and 8 cell lines (A431, AGS, HCT-116, HT-29, MCF-7, MDA-MB-468, MKN45, and T47D) were used for this study. Fresh tissues were disaggregated into single cells and exposed to GDC-0941, a PI3K inhibitor, and AZD6244, a MEK inhibitor, both as single agents and in combination in the Mosaic Blue assay. Combination results were compared to single agent results. Samples were classified as resistant or sensitive. Matched FFPE tissues and cells were stained with the following biomarkers to identify predictive relationships: pAKT, p4EBP1, pPRAS40, ppS6 kinase, pS6 ribosomal protein, pERK, PTEN, cMET, EGFR, HER3, Ki-67, and p53. To assess pharmacodynamics changes, the 8 cell lines were also exposed to 1 concentration of each inhibitor both as single agents and in combination. The cells were fixed and paraffin embedded for IHC staining of the following biomarkers to identify pharmacodynamic relationships: pAKT, p4EBP1, pPRAS40, ppS6 kinase, pS6 ribosomal protein, pEGFR, pHER3, pMET, pERK, and Ki-67. The combination of inhibitors demonstrated additive growth inhibition in the explants and cell lines. The average combination IC50 was more potent than single agents, with greater additivity demonstrated in colorectal cancer compared to lung cancer. Predictive and pharmacodynamic biomarkers were identified with both single agent and combination treatments, and differences were observed between the two inhibitors. In summary, this study demonstrated that the Mosaic Blue assay is a useful tool for classifying sensitive and resistant tumor explants and cell lines and also confirmed that dual targeting of PI3K and MEK pathways is a valuable approach to achieving higher therapeutic activity in vitro. Evaluation of biomarker profiles revealed predictive and pharmacodynamic relationships in this setting. Citation Format: Lisa M. Dauffenbach, Gela C. Sia, Patricia A. Cash, Sherif K. Girees, Ryan S. Lim, Jianping Zheng, Eric P. Olsen, Christopher A. Kerfoot. Combination of PI3K and MEK inhibitor chemosensitivity in human tumor explants and cell lines using the Mosaic Blue assay and relationship to biomarkers by immunohistochemistry. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 899. doi:10.1158/1538-7445.AM2014-899
I Saw the Saw I Said I Saw
Authors: Kathryn Starbuck
Journal: JAMA (2005)

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
Abstract 4011: Single cell transcriptomic analysis identified a potential dormant signature in prostate cancer disseminated tumor cells
Authors: Hung-Ming Lam, Lisly Chéry, Ilsa Coleman, Bryce Lakely, Sandy Larson, Roger Coleman, Julio Aguirre-Ghiso, Jing Xia, Roman Gulati, Peter S. Nelson, Bruce Montgomery, Paul H. Lange, Linda A. Snyder, Robert L. Vessella, Colm Morrissey
Journal: Cancer Research (2014)

Abstract Prostate cancer (PCa) disseminates before radical prostatectomy and can remain in the bone marrow for a prolonged period of time (&amp;gt;10 years) until lethal metastasis develops. These cells are referred to as disseminated tumor cells (DTC). Dormant DTC are resistant to current chemotherapy targeting cell division, therefore understanding the nature of DTC will allow the development of novel drug target to prevent overt cancer metastases. DTC were isolated from the bone marrow aspirates of PCa patients with no evidence of disease (NED, undetectable PSA level after 7-18 years after radical prostatectomy) or advanced diseases (ADV, disease progression after treatment or existing distant metastases). Eighty-five EpCAM+/CD45- individual cells were subjected to microarray gene expression analyses and two populations of cells were identified: erythroid progenitor-like and prostate epithelial cells. We utilized a dual signature method to identify EpCAM+/CD45- cells that are of prostatic origin. Comparison among prostate DTC showed that the DTC population within each patient was heterogeneous. Importantly, comparison between DTC from NED and ADV patients revealed that DTC from NED patients were enriched in a dormancy-associated signature identified in the head and neck squamous cell carcinoma, supporting the dormant nature of DTC from NED patients. Global clustering analysis and Ingenuity Pathway Analysis further identified a potential PCa dormancy signature, and this signature is significantly suppressed in a subpopulation of DTC isolated from ADV patients. We reported a single cell transcriptomic analysis to reveal for the first time clinically heterogeneous DTC population in PCa patients and a dual signature method to identify cells of prostatic origin from erythroid-progenitor cells that harbored the same epithelial (EpCAM) surface marker in the bone marrow. The proposed gene signature associated with PCa dormancy may allow development of possible biomarkers to predict prognosis and therapeutic targets to promote PCa dormancy or prevent dormancy escape. Citation Format: Hung-Ming Lam, Lisly Chéry, Ilsa Coleman, Bryce Lakely, Sandy Larson, Roger Coleman, Julio Aguirre-Ghiso, Jing Xia, Roman Gulati, Peter S. Nelson, Bruce Montgomery, Paul H. Lange, Linda A. Snyder, Robert L. Vessella, Colm Morrissey. Single cell transcriptomic analysis identified a potential dormant signature in prostate cancer disseminated tumor cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4011. doi:10.1158/1538-7445.AM2014-4011
p53 family interacting pathways in carcinogenesis and cellular response to ionizing radiation.
Authors: Jodi L. Johnson, James P. Lagowski, Alexandra Sundberg, Sarah Lawson, Yuangang Liu, Molly Kulesz-Martin
Journal: Cancer Research (2006)

5183   A global view of all three p53 family members (p53, p63, and p73) is needed to understand their interacting roles in tumor development and response to ionizing radiation (IR). We found that keratinocytes with reduced p73 protein expression were radioresistant  in vitro  and produced squamous cell carcinoma (SCC)  in vivo  even in the presence of wild type p53. We investigated p53 family functions in genetically related mouse keratinocytes; precancerous 03C (IR sensitive control), 03C si-p73 (siRNA knock-down of p73 in precancerous cells), and malignant 03R (IR resistant, producing SCC), based upon our observations of reduction of p63 and dramatic loss of p73 proteins upon spontaneous conversion of 03C precursor cells to 03R malignant cells. Compared to the IR sensitive controls, the malignant 03R cells exhibited reduced p53 family member DNA binding to  p21  and  noxa  probes, a lack of p21 or Noxa mRNA induction, failure to arrest in G1, and a lack of normal apoptotic response following treatment with IR. Like the 03R cells, the 03C si-p73 cells were resistant to IR  in vitro , and produced SCC  in vivo . Further, the DNA binding capabilities of p63 protein isoforms but not p53 protein were altered after p73 knock-down in the 03C si-p73 cells. We observed reduced DNA binding of lower molecular weight p63 protein isoforms in the absence of p73, and a loss of p53 target gene induction in response to IR, in spite of p53 DNA binding. This suggests a cooperative interaction between p53 family members, specifically that p73 protein is required for p53 family-dependent cellular response to IR. We will test which specific p73 isoforms are required for the coordinated p53 family response to IR using stable transfection of each p73 isoform into keratinocyte lines heterozygous or null for p63 and/or p73. Insight regarding p53 family members’ roles in tumor suppression and the etiology of radiation response in epithelial cancer could suggest new therapeutic approaches to IR radiation-resistant human solid tumors of epithelia. Supported by NCI CA98893, OHSU Cancer Institute CA69533, Medical Research Foundation of Oregon and the Tartar Trust Fellowship.
Changing prognosis for babies of less than 28 weeks' gestation in the north of England between 1983 and 1994
Authors: W. Tin, U. Wariyar, E. Hey
Journal: BMJ (1997)

<h3>Abstract</h3> <b>Objective:</b> To investigate the changing prognosis for babies of less than 28 weeks9 gestation. <b>Design:</b> A prospective, collaborative, population based survey. <b>Setting:</b> The former Northern Regional Health Authority. <b>Subjects:</b> All the births between 1983 and 1994 at 22 to 27 completed weeks9 gestation to women normally resident in the region. <b>Main outcome measures:</b> Miscarriage, stillbirth, death in the first year of life, and disability in survivors. <b>Results:</b> There were 479 070 registered births in the study period. No baby of 22 weeks9 gestation survived; only eight (4%) of the 197 babies of 23 weeks who were alive at the onset of labour survived for a year–a proportion that did not change during the study period. Survival among other babies of less than 28 weeks improved progressively between 1983-6 and 1991-4, but administration of artificial surfactant to babies requiring ventilation from mid-1990 was associated with further improvement in survival only in those over 25 weeks9 gestation. Babies of 24 weeks required three times as much high dependency care per survivor as babies of 27 weeks (76 <i>v</i> 26 days). The rate of severe disability in the one year survivors of less than 26 weeks9 gestation (30/123; 24%) was similar to that seen in the sampled survivors of 26 and 27 weeks (29/108; 27%); the proportion disabled did not change significantly during the study period. All the children born in 1983, 1987, and 1991 were later reassessed in greater detail: 10% (13/136) seemed destined for a continuing life of total dependency. <b>Conclusions:</b> Gestation, if accurately assessed, can give a woman facing very preterm delivery a clear indication of the prognosis for her baby and help her judge the appropriateness of accepting obstetric intervention and sustained perinatal support. <h3>Key messages</h3> Survival in babies of 24-27 completed weeks of gestation has improved in the past 12 years The proportion of survivors with severe disability (25%) has not changed The survival (viability) of babies born before 24 weeks9 gestation (about 4%) has not changed, and most survivors are severely disabled One in 10 of all survivors has a disability so profound that he or she is never likely to become independently mobile or to communicate effectively with others Gestation, if accurately assessed, can help women facing very preterm delivery (and their attendants) to assess the likely prognosis for the baby at the onset of labour