tbuckley/cabot-search huggingface dataset:
Hypercapnia
Authors: Franklin H. Epstein, Steven E. Weinberger, Richard M. Schwartzstein, J. Woodrow Weiss
Journal: New England Journal of Medicine (1989)

HYPERCAPNIA is a well-recognized consequence of a variety of diseases, not only those involving the lungs but also those affecting the neural, muscular, chest-wall, and circulatory components of the respiratory system. In the past 20 years, we have developed a greater appreciation of the way these components interact in the genesis of hypercapnia. The impaired elimination of carbon dioxide that results in hypercapnia reflects not merely abnormal lung function, but rather a complex interaction of abnormalities in respiratory drive, muscle function, and lung function.In this paper, we will first consider the fundamental factors controlling the elimination of carbon dioxide . . .
The unusual cecum
Authors: D. Frager
Journal: JAMA (1984)

<h3>History</h3> A 90-year-old woman was admitted to Montefiore Medical Center with a two-day history of severe right lower quadrant pain associated with nausea and vomiting. The patient's past medical record indicated a history of severe peripheral arterial disease, including bypass surgery, previous myocardial infarction, and right cerebral infarction. Physical examination showed right lower quadrant tenderness without peritoneal signs and a heme-positive stool. A blood examination revealed a hemoglobin level of 11.0 g/dL with hypochromic, microcytic indices. A barium enema study was obtained (Figs 1 and 2); the abnormalities demonstrated involved the cecum and ascending colon and will be described subsequently. <h3>Diagnosis</h3> Ischemic colitis involving the cecum and ascending colon. Figure 2 ("spot" film) demonstrates (1) a mass on the lateral surface of the ascending colon just above the ileocecal valve (black arrow); (2) edematous folds in the cecum (black arrowheads); (3) submucosal polypoid masses on the lateral wall of the
British Journal of Radiology, London
Journal: JAMA (1969)

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
TRUTH AND POETRY CONCERNING URIC ACID. XIII.
Journal: JAMA (1905)

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 328: ADAM17-induced activation of HER receptors mediate resistance to trastuzumab in a subset of moderate HER2-expressing breast cancer cells
Authors: Katharina Feldinger, Vasanthy Vigneswara, Gillian Murphy, Anthony Kong
Journal: Cancer Research (2019)

Abstract Currently anti-HER2 therapies are indicated for HER2-positive breast cancer patients that are IHC3+ or FISH positive. However, there have been studies suggesting that some HER2-negative patients may also respond to these treatments. Previously, our laboratory showed that trastuzumab upregulates ADAM17 and ADAM10 levels; and the resultant ligand release and the activation of HER receptors mediates trastuzumab acquired resistance in HER2-positive breast cancer. The aim of this study is to further understand the mechanisms of response and resistance of HER2 targeting agents such as trastuzumab and neratinib in low and moderate HER2-expressing breast cancer cells. The HER2 expression of a panel of eight breast cell lines was assessed by IHC, FISH, western blot, and qRT-PCR. Using cell viability studies we found that in comparison with high (IHC 3+) and low HER2 expressing (IHC 0 or 1+) breast cancer cells, moderately expressing HER2 (2+) cells showed an intermediate response to trastuzumab and neratinib. Three moderate HER2-expressing breast cancer cell lines (IHC 2+), MDA-MB-361, MDA-MB-453 and HCC1569 were shown to respond to increasing doses of neratinib (with an IC50 less than 30nM). However, increasing doses of trastuzumab (up to 120 μg/ml) was unable to decrease the cell viability of these cells to below 50% of the control. The response to trastuzumab and neratinib correlated with basal ADAM17 but not ADAM10 expression. Trastuzumab treatment led to an upregulation of ADAM17 and the shedding of HER ligands in the media, as well as the phosphorylation of HER members. ADAM17 inhibition, using a specific anti-ADAM17 antibody or knockdown of the protein, decreased activation of HER members as well as downstream markers, correlating with reduced cell viability in moderate HER2-expressing cell lines. In addition, the combination of trastuzumab with neratinib was more effective than either single agent in moderate HER2-expressing cell lines. Thus, ADAM17 may play a key role in the resistance to trastuzumab in moderate HER2-expressing breast cancer cells. Combining trastuzumab with an ADAM17 inhibitor or an irreversible pan-HER inhibitor such as neratinib may be an effective therapeutic strategy for targeting breast cancers with moderate HER2 expressing tumors. Citation Format: Katharina Feldinger, Vasanthy Vigneswara, Gillian Murphy, Anthony Kong. ADAM17-induced activation of HER receptors mediate resistance to trastuzumab in a subset of moderate HER2-expressing breast cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 328.
Excitotoxic Amino Acids And Neuropsychiatric Disorders
Authors: J. Olney
Journal: The Annual Review of Pharmacology and Toxicology (1990)

Over the past two decades, deadly coronaviruses, with the most recent being the severe acute respiratory syndrome-related coronavirus-2 (SARS-CoV-2) 2019 pandemic, have majorly challenged public health. The path for virus invasion into humans and other ...Read More
Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial
Authors: A MENDELOW, B GREGSON, H FERNANDES, G MURRAY, G TEASDALE, D HOPE, A KARIMI, M SHAW, D BARER
Journal: The Lancet (2005)
Lectures on the Experimental Investigation of the Action of Medicines
Authors: T. L. Brunton
Journal: BMJ (1871)

Comparison of thze Eftects of Drugs on differentt Animnals in dzfferent Doses.-Mode of determining the Exact Cause of Symitptoms.-AMode of raising Blood-p ressure.-Modes of counting thle Beats of (lie Heart.-Causes of Quickened Pulse.-DirectStinuzlation of thze Sympathtetic.-Stimulation of Cardiac Ganglia.-Pa}alysis of the Vagus-roots and Fibres, and of its entds in thze Heart.-Ca uses of Slow Pulse.-Irritation of Vagus-roots.-Mode of supplying thle Head and Body withi different kintds of Blood.-IndirectIrritation of Vaguts-roots through the Blood-pressure: mode of lowerinzg and rais- in,g it.
PTH-103 The Management And Assessment Of Incidental Pancreatic Cysts On Computer Tomography In A Non-pancreatic Centre
Authors: S Kadir, U Sheikh, J Iqbal
Journal: Gut (2014)

<h3>Introduction</h3> With increased use and sensitivity of cross sectional imaging more incidental pancreatic cystic lesions are found. Studies have demonstrated a prevalence of 2.5% of cystic pancreatic lesions in asymptomatic patients on MRI and CT scanning. Cystic lesions have a wide variety of radiological appearances and prognostic outcomes. We aimed to review cases found to have incidental pancreatic cysts on CT scanning and ascertain the concordance between CT and EUS and the management of such lesions in a non-pancreatic centre. <h3>Methods</h3> We retrospectively reviewed patients undergoing EUS for pancreatic cystic lesions found on incidentally on CT scan between 2010 and 2012. Twenty-five patients were included. Solid lesions with a cystic component were excluded. <h3>Results</h3> There were 15 female; 10 male. Indications for CT scan included abdominal pain 32%; weight loss 16%; jaundice and suspected stone disease with abnormal USS 16%. In all cases there was no preceding clinical suspicion of pancreatic cysts/disease. Median number of cysts was 1 (1–4); mean size 3 cm (1–11 cm). In 70% of cases the cyst was &gt;3 cm; and &lt;3 cm in 30%. They were located in the HOP 36%; BOP 32%; TOP 16%; NOP 4%; multiple sites 12%. The cyst was aspirated +/- biopsy in 12 (48%) cases, of which in 2 (16%) this changed the CT diagnosis. Final diagnosis was pseudocyst 10 (40%); IPMN 6 (24%); simple cyst 2 (8%); serous cystadenoma 2 (8%); mucinous cystadenoma (MCA) 1 (4%); cystic adenoca 1 (4%); wegeners cyst 1 (4%); renal cyst 1 (4%). In 32% (8 cases), the EUS findings were inconsistent with CT findings, due to IPMN and MCA in the vast majority. Greatest concordance between EUS and CT findings was in the diagnosis of pseudocysts. <h3>Conclusion</h3> Increasing number of asymptomatic pancreatic cysts found incidentally will undoubtedly cause increased referrals to tertiary pancreatic centres. EUS is a better imaging modality with additional benefit of attaining samples. Performing EUS +/- cyst FNA provided an alternative diagnosis to CT in a significant percentage (32%) of patients and helped streamline referrals for tertiary opinion. EUS should be considered in all patients presenting with incidental pancreatic cysts on cross-sectional imaging. This may be performed at the index hospital (if non-pancreatic centre) and should not be restricted to tertiary HPB centres if operator experience and confidence allows. <h3>Disclosure of Interest</h3> None Declared.
Assessment of treatment with panitumumab, cetuximab, and bevacizumab among mCRC patients with wild-type <i>RAS</i> or <i>BRAF</i> treated at community cancer centers in the United States.
Authors: Tamer Garawin, Kimberly Lowe, Michael Anthony Kelsh, Gerry C. Bohac
Journal: Journal of Clinical Oncology (2016)

e15067 Background: There is limited observational data on the use of RAS test results and treatment patterns with chemotherapy and biologics among metastatic colorectal cancer (mCRC) patients. Our objective was to use real world data to evaluate the treatment sequences of mCRC patients who have wild-type RAS (KRAS, NRAS), or BRAF and who are treated at community cancer clinics within the United States (U.S.). Methods: The sample included 536 patients in the Oncology Services Comprehensive Electronic Records (OSCER) database who were diagnosed with mCRC between 1/1/2011 and 8/31/2015. All patients had available treatment data and were confirmed to have wild-type RAS or BRAF. Patients were stratified into mutually-exclusive categories based on 1st line treatment with chemotherapy in combination with either bevacizumab (Bmab), cetuximab (Cmab), panitumumab (Pmab), a combination of Pmab, Cmab or Bmab, or no biologics. Descriptive statistics were used to summarize the data. Results: The demographics of the sample were as follows: mean age 67 years (standard deviation = 12), 55% male, 70% White, and 50% with ECOG value of zero. The use of Bmab, Cmab, or Pmab in combination with chemotherapy in 1st line treatment was follows: Bmab only (n = 270, 50%), Cmab only (n = 81, 15%), Pmab only (n = 28, 5%), and a combination of either Bmab, Cmab and/or Pmab (n = 6, 1%). No biologics were administered to 151 (28%) of the sample in 1st line. There were no statistically significant differences in age, gender, race, insurance type, region of the U.S. or ECOG status at mCRC diagnosis across the 1st line treatment categories. Of the 385 patients who received a biologic in 1st line, 94 (24%) of those who survived and selected to continue treatment received a biologic in 2nd line. Of these 94 patients, 25 (27%) of those who survived and selected to continue treatment also received a biologic in 3rd line. Conclusions: Bmab was the most commonly-used biologic among mCRC patients with wild-type RAS or BRAF in this descriptive study.Future research is needed to better understand what factors impact treatment decisions among mCRC patients.
THE INTERNAL TEMPERATURE OF THE BODY
Journal: JAMA (1933)

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
BOOK REVIEWS
Authors: D. F. BAJORIN
Journal: JNCI Journal of the National Cancer Institute (1988)

Journal Article BOOK REVIEWS Get access Pointers to Cancer Prognosis. Basil A. Stoll, ed. Dordrecht, The Netherlands: Nijhoff, 1987, 368 pp. $106. (U.S. distributor: Kluwer, Norwell, MA) DEAN F. BAJORIN DEAN F. BAJORIN Memorial Sloan-Kettering Cancer Center1275 York Avenue New York, NY 10021 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 80, Issue 2, 16 March 1988, Page 136, https://doi.org/10.1093/jnci/80.2.136-a Published: 16 March 1988
Abstract 2968: Postmortem Genetic Testing of the GPD1-L-Encoded Glycerol-3-Phosphate Dehydrogenase 1-Like Protein in Sudden Infant Death Syndrome
Authors: David W Van Norstrand, Carmen R Valdivia, David J Tester, Kazuo Ueda, Barry London, Jonathan C Makielski, Michael J Ackerman
Journal: Circulation (2007)

Introduction: Approximately 10 – 15% of sudden infant death syndrome (SIDS) may be caused by cardiac channelopathies including Brugada syndrome (BrS). Type 1 BrS (BrS1), due to mutations in the SCN5A-encoded sodium channel, accounts for approximately 20% of BrS. Recently, a novel mutation in glycerol-3-phosphate dehydrogenase 1-like (GPD1-L) disrupted trafficking of SCN5A in a multi-generational family with BrS. We hypothesized that mutations in GPD1-L may be responsible for some cases of SIDS. Methods: Using DHPLC and direct DNA sequencing, we performed comprehensive open reading frame/splice site mutational analysis of GPD1-L on genomic DNA extracted from necropsy tissue of 228 anonymous cases of SIDS (86 females, 142 males, average age = 3 + 2 months, range 6 hours to 12 months). Results: Three putative, SIDS-associated GPD1-L missense mutations, E83K, I124V, and R273C, were discovered in a three-month-old white male, a five-week-old white female, and a one-month-old white male, respectively. All mutations occurred in highly conserved residues and were absent in 600 reference alleles. Compared to wild type GPD1-L, GPD1-L mutations co-expressed with SCN5A in heterologous HEK cells produced a 60% reduction in peak sodium current density (p&lt;0.004). Adenovirus-mediated gene transfer of the E83K-GPD1-L mutation into neonatal mouse myocytes markedly attenuated the sodium current as well (p&lt;0.01). These decreases in current density are consistent with sodium channel loss-of-function diseases like BrS. Conclusion: This study is the first to report mutations in GPD1-L as a pathogenic cause for a small subset (~1%) of SIDS via a secondary loss-of-function mechanism whereby perturbations in GPD1-L precipitate a marked decrease in the peak sodium current and a potentially lethal, BrS-like pro-arrhythmic substrate.
Association of hGrb10 Genetic Variations With Type 2 Diabetes in Caucasian Subjects
Authors: Rosa Di Paola, Ester Ciociola, Watip Boonyasrisawat, David Nolan, Jill Duffy, Giuseppe Miscio, Carmela Cisternino, Grazia Fini, Vittorio Tassi, Alessandro Doria, Vincenzo Trischitta
Journal: Diabetes Care (2006)
ON ARSENIC-EATING
Authors: W. B. Kesteven
Journal: BMJ (1856)

best remedy is iodide of potassium joined with sarsaparilla, good diet, and keeping the patient if possible during con- aleseoe in the open air.If it be necessary to vary the treatment, cod-liver oil, or quinine, will be found the best medicines.MIJSCELLIEA.Amongst a few excerpta minora of more or less interest in the hospitals this month, is a new form of &Cra8eur, by M.Heurteloup, from which great things are expected.A cu- rious and very rare case of fracture of the astragalus was seen at St. Mary's.Several cases also unfortunately of " hospital gangrene" at various hospitals, the best remedy for wbich seeims to be the irrigatiou of cold water recom- mended by Mr. COCK.This experienced surgeon states he has tried almost every mode of cure, but the irrigation plan alone has not disappointed him.The disease is said to be as prevalent in some English provincial hospitals as it has bece m London.A case of ovarian cyst where we recently saw Ixii of tincture of iodine injected, has ended fatally.A more promising case has been mentioned as baving occurred at Cheltenham.In resections of the knee joint there is no- thinog new, in two cases of diseased knee not very dis- similar.Mr. URE, in one, amputated; Mr. SOUTI, in the other, excised-both are doing very well.The chief want is pure air, as at Jersey or Afargate.A new instrument of much power has been constructed and exhibited by the instrument-maker at St. George's Hospital, for breaking large calculi (as a nutcracker alimost), when the stonie is too large to be extracted through the incision in the pros- tate.The object is a practical one.K.erigiai IInnuniratinn .
Reply to Hiten D. Patel and Mohamad E. Allaf's Letter to the Editor re: Maxine Sun, Andreas Becker, Zhe Tian, et al. Management of Localized Kidney Cancer: Calculating Cancer-specific Mortality and Competing Risks of Death for Surgery and Nonsurgical Management. Eur Urol. In press. http://dx.doi.org/10.1016/j.eururo.2013.03.034
Authors: Maxine Sun, Pierre I. Karakiewicz, Quoc-Dien Trinh
Journal: European Urology (2013)
<i>LRIG1</i> amplification in breast cancer
Authors: I. Ljuslinder, B. Malmer, M. Thomasson, I. Golovleva, K. Grankvist, T. Höckenström, S. Emdin, Y. Jonsson, H. Hedman, R. Henriksson
Journal: Journal of Clinical Oncology (2004)

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Implications diagnostiques et thérapeutiques de la résection endoscopique muqueuse pour les adénocarcinomes œsophagiens classés T2 en échoendoscopie
Journal: Endoscopy (2017)

Le stade T2 en échoendoscopie, qui correspond à l’invasion de la musculaire propre, est plus difficile à porter avec un risque de surestimation ( + + + ) ou de sous-estimation. En cas de surestimation, cela peut faire récuser à tort le patient pour une résection endoscopique et lui faire proposer une chirurgie éventuellement précédée d’une radiochimiothérapie. Cette étude bicentrique hollandaise a pour but de comparer le stade histologique final avec le stade échoendoscopique, puis d’évaluer les possibilités de résection endoscopique.
A New Journal—Survey of Immunologic Research
Journal: JNCI Journal of the National Cancer Institute (1982)

Journal Article A New Journal—Survey of Immunologic Research Get access JNCI: Journal of the National Cancer Institute, Volume 68, Issue 6, June 1982, Page 1044, https://doi.org/10.1093/jnci/68.6.1044 Published: 01 June 1982
DIATHERMY IN THE HOME
Journal: JAMA (1941)

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