tbuckley/cabot-search huggingface dataset:
THE THERMAL DEATH-POINT OF TUBERCLE BACILLI IN MILK AND SOME OTHER FLUIDS
Authors: Theobald Smith
Journal: The Journal of Experimental Medicine (1899)

1. Tubercle bacilli when suspended in. distilled water, normal salt solution, bouillon and milk, are destroyed at 60 degrees C. in 15 to 20 minutes. The larger number are destroyed in 5 to 10 minutes. 2. When tubercle bacilli are suspended in milk, the pellicle which forms during the exposure at 60 degrees C. may contain living bacilli after 60 minutes.
A Glycemic Threshold for Diabetic Complications?
Authors: GianCarlo Viberti
Journal: New England Journal of Medicine (1995)

Most physicians accept that hyperglycemia makes an important contribution to the complications of diabetes mellitus involving small and large vessels, but whether hyperglycemia alone is sufficient to explain diabetic vascular disease remains controversial. Epidemiologic evidence suggests that the end-organ response to exposure to diabetes, defined as the duration of hyperglycemia multiplied by its degree, differs in different vascular beds. Given time, retinopathy appears to develop in virtually all patients with insulin-dependent diabetes mellitus (IDDM), but this is not the case for nephropathy or cardiovascular disease.1 The cumulative risk of albuminuria in patients with IDDM is about 35 percent, no matter . . .
Food and the responsibility deal: how the salt reduction strategy was derailed
Authors: Graham A MacGregor, Feng J He, Sonia Pombo-Rodrigues
Journal: BMJ (2015)

The food we eat is now the biggest cause of death and ill health in the UK, owing to the large amounts of salt, saturated fat, and sugars added by the food industry. <b>Graham MacGregor</b>, <b>Feng He</b>, and <b>Sonia Pombo-Rodrigues</b> discuss the Food Standards Agency’s successful salt reduction strategy and how Andrew Lansley and the coalition government’s responsibility deal has stalled its progress. They call for urgent action to protect and improve our nation’s health
Dietary fat modulation of left ventricular ejection fraction in the marmoset due to enhanced filling
Authors: P L McLennan, L R Barnden, T M Bridle, M Y Abeywardena, J S Charnock
Journal: Cardiovascular Research (1992)

Journal Article Dietary fat modulation of left ventricular ejection fraction in the marmoset due to enhanced filling Get access P L McLennan, P L McLennan Correspondence to Dr McLennan. Search for other works by this author on: Oxford Academic PubMed Google Scholar L R Barnden, L R Barnden Search for other works by this author on: Oxford Academic PubMed Google Scholar T M Bridle, T M Bridle Search for other works by this author on: Oxford Academic PubMed Google Scholar M Y Abeywardena, M Y Abeywardena Search for other works by this author on: Oxford Academic PubMed Google Scholar J S Charnock J S Charnock Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 26, Issue 9, September 1992, Pages 871–877, https://doi.org/10.1093/cvr/26.9.871 Published: 01 September 1992 Article history Received: 10 October 1991 Accepted: 06 March 1992 Published: 01 September 1992
New mutations stabilize NOTCH1
Authors: Hema Bashyam
Journal: The Journal of Experimental Medicine (2007)

A leukemia-associated signaling protein accumulates to dangerous levels when its own mutations shield it from degradation. Now, reports from O'Neil et al. (page 1813) and Thompson et al. (page 1825) identify outside forces that also lead to its buildup. Defects in proteasomal targeting, they find, can also trigger leukemia.






Figure 1

Mutant versions of FBW7 from T-ALL patients don't bind NICD.




T cell acute lymphoblastic leukemia (T-ALL) is triggered by mutations in the NOTCH1 receptor. Once activated, this transmembrane protein is clipped to release its intracellular domain (NICD), which then activates the transcription of genes that goad stem cells to become T cells.

Many transformed T cells have too much NICD, as their NOTCH1 proteins carry mutations that protect them from proteasomal degradation. This increase sends many NOTCH1 targets, particularly oncogenes, into overdrive.

The new reports show that NICD levels are also high in some leukemic cell lines that lack NOTCH1 mutations. The defect in these cells lay instead in an enzyme called FBW7, which normally ubiquitinates NOTCH1 so it is recognized by the proteasome. The mutated version, which was also found in some T-ALL patients, failed to bind and ubiquitinate NICD.

Thompson et al. also found that the dysfunctional FBW7 did not bind some of its other targets, such as c-Myc and cyclin-E—oncogenes that are turned on by NICD. This failure might account for the resistance of these cell lines to antileukemia drugs that prevent NOTCH1 receptor cleavage.
Man and Dolphin
Authors: Joel Shilling
Journal: JAMA (1961)

This narration is based on the prediction that within the next decade or two man will establish vocal communication with another species. This species will be highly intelligent and will most likely be an aquatic animal.<i>Man and Dolphin</i>is a basic handbook for those adventurers in science who can foresee the possibility of interspecies communication. It is a comprehensive outline of the work already undertaken and the research that must be done to establish this contact. The possible implications of this study and of interspecies communication are related in a somewhat humorous vein. Three appendices offer a wealth of information about the dolphin; various animals are compared to the dolphin in regard to brain size, ratio of brain weight to body weight, and inborn intelligence of the species. The book is written on a more or less philisophical plane and, although a bit repititious in places, it is a
A CASE OF PRIMARY (?) LARYNGEAL DIPHTHERIA, TREATED WITH BEHRING'S ANTITOXIN.
Authors: EDWIN J. KUH
Journal: JAMA (1894)

ment of service would be that of preventive medicine.In May 1863, I began on a small scale, and under many discouragements from my friends, the con¬ struction of the first Turkish bath.Not having any model from which to work, the process was neces¬ sarily slow, and much time was consumed in experi¬ ments, not alone with the bath itself, but also upon myself, friends and patients, in testing its practical workings.It was not until October 6 of that year that it was opened to the public.On that day but one bather came and he had left his home, without letting his wife know where he had gone.It was not till four days after that four bathers came.One of
Antiviral therapy of patients with decompensated cirrhosis to prevent recurrence of hepatitis C after liver transplantation
Authors: Xavier Forns, Montserrat Garcı́a-Retortillo, Trinidad Serrano, Anna Feliu, Francisco Suarez, Manuel de la Mata, Juan Carlos Garcı́a-Valdecasas, Miquel Navasa, Antoni Rimola, Juan Rodés
Journal: Journal of Hepatology (2003)
Surgical Anatomy of the Heart.
Authors: P. D Ridley
Journal: Cardiovascular Research (1992)

Journal Article Surgical Anatomy of the Heart. Get access Paul D Ridley Paul D Ridley Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 26, Issue 8, August 1992, Page 816b, https://doi.org/10.1093/cvr/26.8.816b Published: 01 August 1992
The course of acute myocardial infarction. Feasibility of early discharge of the uncomplicated patient.
Authors: J F McNeer, A G Wallace, G S Wagner, C F Starmer, R A Rosati
Journal: Circulation (1975)

This report represents our experience with 522 consecutive patients with acute myocardial infarction admitted directly to the Duke Coronary Care Unit. Fifty items of information were used to characterize the patients, their hospital course and follow-up. Serious complications included death, ventricular tachycardia or fibrillation, second- or third-degree heart block, pulmonary edema, cardiogenic shock, persistent sinus tachycardia or hypotension, atrial flutter or fibrillation, and extension of infarction. Forty-nine percent of the patients (252 of 522) experienced a serious complication. All patients who experienced any serious complications had at least one of the above during the first four days of hospitalization. Patients who survived through day 4 were subgrouped on the basis of the occurrence (complicated) or lack of occurrence (uncomplicated) of the above on day 5. Complicated patients had a subsequent hospital mortality of 14% and an incidence of late serious complications of 51%. Patients who were uncomplicated through day 4 had a subsequent hospital mortality of zero and an incidence of late serious complications of zero. These data suggest that it would be feasible and ethically justified to conduct a prospective clinical trial of early discharge (7th day) in patients who meet the above criteria for uncomplicated. The potential economic savings through earlier discharge in uncomplicated patients are of major significance.
Dissociation of end systole from end ejection in patients with long-term mitral regurgitation.
Authors: M E Brickner, M R Starling
Journal: Circulation (1990)

To determine whether left ventricular (LV) end systole and end ejection uncouple in patients with long-term mitral regurgitation, 59 patients (22 control patients with atypical chest pain, 21 patients with aortic regurgitation, and 16 patients with mitral regurgitation) were studied with micromanometer LV catheters and radionuclide angiograms. End systole was defined as the time of occurrence (Tmax) of the maximum time-varying elastance (Emax), and end ejection was defined as the time of occurrence of minimum ventricular volume (minV) and zero systolic flow as approximated by the aortic dicrotic notch (Aodi). The temporal relation between end systole and end ejection in the control patients was Tmax (331 +/- 42 [SD] msec), minV (336 +/- 36 msec), and then, zero systolic flow (355 +/- 23 msec). This temporal relation was maintained in the patients with aortic regurgitation. In contrast, in the patients with mitral regurgitation, the temporal relation was Tmax (266 +/- 49 msec), zero systolic flow (310 +/- 37 msec, p less than 0.01 vs. Tmax), and then, minV (355 +/- 37 msec, p less than 0.001 vs. Tmax and p less than 0.01 vs. Aodi). Additionally, the average Tmax occurred earlier in the patients with mitral regurgitation than in the control patients and patients with aortic regurgitation (p less than 0.01, for both), whereas the average time to minimum ventricular volume was similar in all three patient groups. Moreover, the average time to zero systolic flow also occurred earlier in the patients with mitral regurgitation than in the control patients (p less than 0.01) and patients with aortic regurgitation (p less than 0.05). Because of the dissociation of end systole from minimum ventricular volume in the patients with mitral regurgitation, the end-ejection pressure-volume relations calculated at minimum ventricular volume did not correlate (r = -0.09), whereas those calculated at zero systolic flow did correlate (r = 0.88) with the Emax slope values. We conclude that end ejection, defined as minimum ventricular volume, dissociates from end systole in patients with mitral regurgitation because of the shortened time to LV end systole in association with preservation of the time to LV end ejection due to the low impedance to ejection presented by the left atrium. Therefore, pressure-volume relations calculated at minimum ventricular volume might not be useful for assessing LV chamber performance in some patients with mitral regurgitation.
Abstract 425: Targeting embryonic signaling pathways in melanoma
Authors: Kathryn E. OReilly, Laura Poliseno, Eleazar Vega-Saenz de Miera, Erica Friedman, Eva Hernando, Iman Osman
Journal: Cancer Research (2012)

Abstract Melanoma incidence is quickly rising and the average survival for a patient with metastatic disease is less than one year. Novel targeted therapies, such as B-Raf mutant kinase inhibitors, have shown dramatic initial responses, but resistance to single agent therapy inevitably ensues. We hypothesize that melanoma stem-like cells may be important in melanoma progression and may play a role in chemoresistance to targeted therapy. We have profiled melanoma cell lines as well as metastatic melanoma tissue for activation of embryonic stem cell pathways via microarray and quantitative RT-PCR. We observed upregulation of the Hedgehog pathway in a subset of cell lines and in human melanoma tissue and found that Smoothened (SMO) expression was associated with significantly shorter recurrence-free survival in metastatic melanoma patients. We also found that small molecule inhibition or genetic silencing of Smoothened (SMO) decreased melanoma cell proliferation and migration in vitro and identified overexpression of GLI2 as a marker of resistance to SMO inhibition. These findings suggest that inhibitors of hedgehog pathway signaling, already in clinical trials in other tumor types, may be a novel strategy for advanced melanoma. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 425. doi:1538-7445.AM2012-425
Abstract LB-202: STAT3 induces pituitary tumor transforming gene (PTTG) expression
Authors: Cuiqi Zhou, Song-Guang Ren, Yunguang Tong, Kolja Wawrowsky, Serguei Bannykh, Shlomo Melmed
Journal: Cancer Research (2010)

Abstract PTTG is overexpressed in multiple human tumors, but mechanisms regulating tumor PTTG abundance remain elusive. As EGF induces pituitary cell PTTG expression, and as STAT3 is required for pituitary cytokine responses, we investigated STAT3 regulation of PTTG. STAT3 and PTTG were both concordantly overexpressed in 79 human pituitary tumor specimens (62% and 56% respectively; p&amp;lt;0.01) as assessed by confocal immunofluorescence. We therefore treated ACTH-secreting AtT20 corticotroph tumor cells with IL-6 which dose-dependently increased STAT3 phosphorylation, PTTG and POMC expression. STAT3 also specifically bound to the human PTTG promoter (−2000 to −3000 bp) and induced PTTG transcriptional activity (2.2-fold) as assessed by chromatin immunoprecipitation and luciferase reporter assay, implying that PTTG acts as an intracellular STAT3 target. To elucidate the function of this pathway, we constructed WT STAT3, constitutively activated STAT3 (STAT3-C) and dominant negative STAT3 (STAT3-DN) plasmids, and selected respective stable transfectants. STAT3 transfection doubled PTTG mRNA and protein abundance, while PTTG induction was enhanced 3-fold in STAT3-C, and totally abrogated in STAT3-DN transfectants (0.7-fold). Stable STAT3 overexpression also enabled in vitro colony formation which was strongly attenuated by PTTG RNAi (∼50%, p&amp;lt;0.01). Elevated STAT3 expression, or STAT3 activation, both increased HCT116 cell migration and invasion 5-fold as measured by in vitro cell assays, whereas cell mobility was abolished by STAT3-DN (&amp;gt;90%). Knockdown of PTTG expression by RNAi strongly suppressed STAT3-induced cell migration and invasion by up to 80%. Attenuating PTTG expression by RNAi in STAT3-C stable cells constrained downstream myc, cyclin D3, K-Ras and MMP expression. Moreover, STAT3 inhibitor VI dose-dependently (10-150 M) suppressed STAT3 phosphorylation and subsequently inhibited PTTG, cyclin D3, POMC expression and ACTH secretion as treated for 24 hours. We also generated PTTG RNAi stable transfectants on STAT3-C stable cells and injected these compound transfectants s. c. to nude mice. PTTG RNAi decreased STAT3-C-induced in vivo tumor volume (32%, p&amp;lt;0.01), compared to injected scrambled control transfectants which readily formed tumors. These results elucidate a mechanism for tumor PTTG abundance, whereby STAT3 activation induces PTTG expression to facilitate tumor formation. These findings further elucidate PTTG actions in tumor progression and support the rationale for targeting PTTG to abrogate endocrine tumor growth. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-202.
Visualization of Bullet Track and Bullet by Radionuclide Brain Scintigraphy
Authors: Partha Sinha, Gary R. Conrad, Brad L. Williams
Journal: Clinical Nuclear Medicine (2005)

Radionuclide brain scintigraphy is a commonly performed examination for the confirmation of brain death. Although the absence of scintigraphically detectable flow of lipophilic tracers to the brain combined with the lack of uptake in the brain is considered consistent with brain death in the appropriate clinical scenario, the cause of death itself is usually not apparent on the scan. A case of bullet track and bullet visualization during a radionuclide brain death study with Tc-99m hexamethylpropyleneamine oxime (HMPAO) is described.
Cilostazol, a potent phosphodiesterase type III inhibitor, selectively increases antiatherogenic high-density lipoprotein subclass LpA-I and improves postprandial lipemia in patients with type 2 diabetes mellitus
Authors: Katsunori Ikewaki, Keiko Mochizuki, Masafumi Iwasaki, Ryoichi Nishide, Seibu Mochizuki, Norio Tada
Journal: Metabolism (2002)
Fallout and the Water Supply
Authors: Charles C. Dennie
Journal: JAMA (1962)

<h3>To the Editor:—</h3> In regard to the article, When Do You Leave a Fallout Shelter? (<i>JAMA</i><b>180</b>:144 [April 14] 1962), I wish to say this: In the articles written about fallout shelters and methods of survival during an explosion, no one has mentioned what would be used for water when the survivors came out of a fallout shelter. If there is enough danger to warrant the building of these shelters, then plans for the survival of those who remain alive must be forthcoming. If an H bomb explosion is powerful enough to produce the destruction that we think it will, all water mains, sewage systems, and reservoirs will be destroyed, so that only surface water will remain for drinking. This water need not be contaminated by fallout. It will be contaminated by many bacterial growths. For this reason underground reservoirs of water, which can not be contaminated by either
Analogy and conceptual change in childhood
Authors: John E. Opfer, Leonidas A. A. Doumas
Journal: Behavioral and Brain Sciences (2008)

Abstract Analogical inferences are an important consequence of the way semantic knowledge is represented, that is, with relations as explicit structures that can take arguments. We review evidence that this feature of semantic cognition successfully predicts how quickly and broadly children's concepts change with experience and show that Rogers &amp; McClelland's (R&amp;M's) parallel distributed processing (PDP) model fails to simulate these cognitive changes due to its handling of relational information.
On the nature of clear cell acanthomas
Authors: D.W.K. COTTON, P.M. MILLS, T.J. STEPHENSON, J.C.E. UNDERWOOD
Journal: British Journal of Dermatology (1987)

Five clear cell acanthomas were studied using a panel of immunohistological markers. The results were compared with those from basal cell papillomas, with and without clear cell change, and with lesions of psoriasis and lichen planus. The results do not support the contention that these lesions are variants of basal cell papillomas nor that they are true neoplasms.
TCT-92 Transcatheter Mitral Valve-in-Valve / Valve-in-Ring Implantations for Degenerative Post Surgical Valves: Results from the Global Valve-in-Valve Registry
Authors: Danny Dvir, Ran Kornowski, Dominique Himbert, Francesco Maisano, Ulrich Schaefer, Hendrik Treede, Sabine Bleiziffer, Manuel Wilbring, Enrico Ferrari, Didier Tchetche, Claudia Fiorina, Anna Sonia Petronio, Anson Cheung, Mathew Williams, Webb John
Journal: Journal of the American College of Cardiology (2013)
Abstract 914: CIP2A mediates the effect of tamoxifen-induced apoptosis in estrogen receptor negative breast cancer cells.
Authors: Ling-Min Tseng, Chun-Yu Liu, Kung-Chi Chang, Duen-Shian Wang, Chung-Wai Shiau, Kuen-Feng Chen
Journal: Cancer Research (2013)

Abstract Background: Tamoxifen is an antagonist of the estrogen receptor (ER) in breast tissue and has been a standard anti-estrogen agent in hormone receptor-positive breast cancers. Previous studies have indicated that tamoxifen also induces estrogen receptor-independent cell death in ER-negative breast cancer cells. Our previous study has shown that CIP2A, cancerous inhibitor of PP2A, may be a novel target in breast cancer cells (Breast Cancer Research 2012). Here, we tested efficacy of tamoxifen in a panel of ER-negative breast cancer cells and examined the drug mechanism. Methods: ER-negative breast cancer cell lines (HCC-1937, SK-BR3, MDA-MB-468, MDA-MB-453, MDA-MB-231) were used for in vitro studies. Apoptosis was examined by both flow cytometry and Western blot. Signal transduction pathways in cells were assessed by Western Blot. Gene silencing was done by small interference RNA (siRNA). In vivo efficacy of tamoxifen was tested in nude mice with breast cancer xenografts. Results: Tamoxifen showed differential effects on apoptosis in human ER-negative breast cancer cell lines. Tamoxifen induced significant apoptosis in SK-BR3, MDA-MB-468, MDA-MB-453, MDA-MB-231 cell lines; however, HCC-1937 cells were resistance to tamoxifen-induced apoptosis. Tamoxifen inhibited CIP2A in a dose-dependent manner in all sensitive ER-negative breast cancer cells, but not in resistant cells (HCC-1937). Overexpression of CIP2A protected MDA-MB-231 cells from tamoxifen-induced apoptosis. In addition, silencing CIP2A by siRNA sensitized HCC-1937 cells to tamoxifen-induced apoptosis. Moreover, in vivo xenograft data showed that tamoxifen inhibited the growth of MDA-MB-468 tumors but had no effect on HCC-1937 tumors. Furthermore, tamoxifen downregulated CIP2A in sensitive MDA-MB-468 xenograft tumors, but not in HCC-1937 tumors. Conclusions: Inhibition of CIP2A determines the effects of tamoxifen-induced apoptosis in ER-negative breast cancer cells. (Supported by Yen Tjing Ling Medical Foundation; NSC 101-2325-B-075-006 and NSC 100-2325-B-010-007; and V100-D-005-4) Citation Format: Ling-Min Tseng, Chun-Yu Liu, Kung-Chi Chang, Duen-Shian Wang, Chung-Wai Shiau, Kuen-Feng Chen. CIP2A mediates the effect of tamoxifen-induced apoptosis in estrogen receptor negative breast cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 914. doi:10.1158/1538-7445.AM2013-914
Inherited Susceptibility to Common Cancers
Authors: William D. Foulkes
Journal: New England Journal of Medicine (2008)

This review deals with germ-line genes that increase susceptibility to five major types of cancer: breast, lung, pancreatic, prostate, and colorectal cancer. Often familial, often appearing at a young age, and often with atypical features, these cancers are caused by mutations in a germ-line gene and frequently with a second mutation in a gene in a somatic cell. The review ends with a discussion of clinical implications, especially for genetic counseling.
A sickening system
Authors: K. Patel
Journal: BMJ (2009)

It was a rather crackly telephone line. “I can’t come in tonight,” said the junior doctor to the consultant. After a slightly awkward pause she added, quietly, “I’ve got dysmenorrhoea.” Mishearing her words, flustered by the overly detailed description of the problem, and seeking to end the telephone call as quickly as possible, the consultant muttered. “Fine, fine.” Turning to me he said, “What’s she doing having sex when on night shifts anyway?”

Sick leave is always a thorny issue. How unwell is not well enough to come to work? Is it …