tbuckley/cabot-search huggingface dataset:
Abstract 1576: Characterization of a mouse line lacking the PDZ-binding domain of PTEN
Authors: Andrew M. Chan, Hong Guan, Alex M. Many
Journal: Cancer Research (2014)

Abstract PTEN encodes a phosphatase for phosphatidylinositides and serves as a key negative regulator of the phosphatidylinositol 3-kinase signaling pathway. PTEN possesses a carboxyl-terminal Postsynaptic density-95/Dlg-1/ZO-1-binding domain (PDZ-BD) implicated in membrane targeting. Since the physiological function of this domain was unclear, a mouse strain lacking this domain was generated. PtenΔPDZ/ΔPDZ mice developed normally although the haploinsufficient mice (PtenΔPDZ/-) were under represented by 50% based on Mendelian ratio of inheritance. PtenΔPDZ/- mice that survived to adulthood harbored a ∼8 % increase in brain masses when compared to PTEN heterozygous (Pten+/-) animals. However, PtenΔPDZ/- mice do not have a greater propensity in neoplastic progression of the prostate, lymph nodes, and endometrium. Independently, the Primary astrocytes from PtenΔPDZ/ΔPDZ mice displayed marginally greater Akt activation following stimulation by epidermal growth factor although both proliferative and migratory capacities were not altered. Crossing PtenΔPDZ/ΔPDZ mice with a breast cancer model, MMTV-PyMT; and a glioblastoma model, GFAP-Ha-Ras, resulted in enhanced metastasis and reduced survival, respectively. Overall, these data provide the first demonstration of a physiological relevance of PTEN PDZ-BD in embryonic development, brain size regulation and tumor progression. Citation Format: Andrew M. Chan, Hong Guan, Alex M. Many. Characterization of a mouse line lacking the PDZ-binding domain of PTEN. [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 1576. doi:10.1158/1538-7445.AM2014-1576
Albendazole inhibits paclitaxel-resistant 1A9PTX22 ovarian cancer cells.
Authors: Mohammad H. Pourgholami, Ying Lu, David Lawson Morris
Journal: Cancer Research (2006)

5414  Introduction: Paclitaxel is one of the most unique, and successful, chemotherapeutic agents currently used in the clinic for cancer treatment. The drug has anti-mitotic properties derived from binding to tubulin and excessive polymerization of microtubules. Unfortunately, as with other chemotherapeutic drugs, resistance is commonly seen and remains a significant problem when using paclitaxel to treat malignancies. Albendazole (ABZ) is a broad-spectrum safe antihelmintic drug used clinically for the treatment of a number of parasitic infections. ABZ has been the subject of immense research in our laboratories where, potent antitumor effects for the drug have been observed. Strong evidence suggests that the primary action of ABZ is to inhibit microtubule polymerization by binding to β tubulin. This study was therefore designed with the aim to see if paclitaxel resistant cells are sensitive to ABZ. Experimental procedures: 1A9 cells and its resistant sub line 1A9PTX22 were obtained from National Cancer Institute (USA). 1A9 is a clone of the human ovarian carcinoma cell line, A2780. Cells harvested from exponential phase cultures were seeded in 96 well plates and treated with various concentrations of paclitaxel (1-10,000 nM), ABZ (10-1000 nM) or their combination for 5 days. At the end of treatment period, sulforhodamine B (SRB) colorimetric assay was used to study the effect of drugs on cell proliferation. Results: Both paclitaxel and ABZ dose-dependently inhibited 1A9 cell proliferation. Co-treatment of the cells with both drugs led to additive growth inhibitory effect. 1A9 cells proved to be quite sensitive to both paclitaxel and ABZ, where treatment of cells with either 0.1 nM paclitaxel or with a low ABZ concentration of 0.1 μM alone led to 11.8% and 21.8% inhibition respectively, co-incubation of 1A9 cells with the two drugs at the specified concentrations led to 87.7% inhibition of proliferation (p
New HIV Test May Improve Point-of-Care Medicine in Remote Regions
Authors: Julie Jacob
Journal: JAMA (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 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 20129: Polyunsaturated Fat Intake Estimated by Circulating Biomarkers is Inversely Associated with Cardiovascular Disease and All-Cause Mortality in a Large Population-Based Cohort of Swedish Women and Men
Authors: Matti Marklund, Federica Laguzzi, Max Vikström, Zayed Alsharari, Per Sjögren, Bruna Gigante, Tommy Cederholm, Karin Leander, Mai-Lis Hellenius, Ulf De Faire, Ulf Risérus
Journal: Circulation (2014)

Increased intake of certain polyunsaturated fatty acids (PUFA) in place of saturated fatty acids has shown beneficial effects on cardiovascular disease (CVD) risk, although results are inconsistent. This may partly be explained by sex differences and shortcomings with self-reported intake data. The objective was to evaluate associations between markers of PUFA intake, from vegetable oils and fish, with CVD incidence and mortality (all-cause). In a representative population-based prospective cohort study including 2193 women and 2039 men (all aged 60 y) in Stockholm County, Sweden, PUFA were measured in serum cholesteryl esters by gas chromatography at baseline (1997-1998). Using national registers, 484 first CVD events (male, n=294; female, n=190) and 456 deaths (n=265; n=191) were identified during follow-up (median 14.5y), in individuals without prior CVD events at baseline. Associations between PUFA intake (assessed by circulating PUFA [linoleic acid, LA; α-linolenic acid, ALA; eicosapentaenoic acid, EPA; docosahexaenoic acid, DHA]) and risk of CVD and mortality were evaluated in men and women separately and together, by Cox proportional hazard models. Hazard ratios (HR) with 95% confidence interval (95%CI) were estimated in crude models and after adjusting for BMI, sex, education, smoking, physical activity, alcohol intake, diabetes, hypertension, and hypercholesterolemia. In the whole population, EPA and DHA were inversely associated with mortality risk in adjusted model; 1 SD increment in EPA and DHA decreased the risk of mortality by 21% (HR 0.79 [95%CI 0.65-0.96]) and 22% (0.78 [0.66, 0.93]), respectively. Among women, EPA and DHA were associated with reduced CVD risk (HR 0.79 [95% CI 0.64-0.97] and 0.74 [0.61-0.89], respectively), whereas women with high ALA levels had moderately increased risk of CVD (1.16 [1.02-1.32]). High LA levels were associated with reduced mortality in men (0.73 [0.64-0.83]). In line with some previous studies, circulating PUFA reflecting dietary n-3 and n-6 PUFA intake were in general inversely linked with CVD and/or mortality. Sex specific relations between PUFA and CVD/mortality motivate further investigations and may partly explain previous inconsistencies regarding dietary PUFA in CVD prevention.
Some aspects of metabolic diseases in man and animals.
Authors: William D. Malherbe
Journal: JAMA (1963)

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
Hermansky-Pudlak syndrome is caused by mutations in HPS4, the human homolog of the mouse light-ear gene
Authors: Tamio Suzuki, Wei Li, Qing Zhang, Amna Karim, Edward K. Novak, Elena V. Sviderskaya, Simon P. Hill, Dorothy C. Bennett, Alex V. Levin, H. Karel Nieuwenhuis, Chin-To Fong, Claudio Castellan, Bianca Miterski, Richard T. Swank, Richard A. Spritz
Journal: Nature Genetics (2002)
Abstract 11947: Unraveling the Mechanism for the Stimulatory Role of Platelet GPIb-IX-V in Thrombin-Induced Platelet Activation
Authors: Brian Estevez, Michael K Delaney, Aleksandra Stojanovic-Terpo, Xiaoping Du
Journal: Circulation (2014)

Numerous reports indicate that the platelet glycoprotein (GP) Ib-IX complex (GPIb-IX) binds directly to the potent platelet agonist thrombin and is important for promoting thrombin-induced platelet activation. However, how GPIb-IX contributes to thrombin-induced platelet activation is unclear. It has been suggested that thrombin binding to GPIb facilitates the cleavage, and thus activation, of the protease-activated receptors (PAR). Our data indicate that GPIb-IX promotes thrombin signaling through a GPIb-IX signaling mechanism. Pretreatment of human platelets with MPalphaC, an inhibitory peptide based on a critical 14-3-3 signaling protein binding site on the cytoplasmic domain of the GPIb alpha chain, inhibited thrombin-induced platelet activation. MPalphaC-treatment inhibited thrombin-induced activation of Rac1 and LIMK1, both of which are known to play essential roles in GPIb signaling. To more specifically determine the role of GPIb-IX, we reconstituted GPIb-IX-facilitated thrombin signaling in Chinese Hamster Ovary cells expressing PAR1. Thrombin induced signaling was significantly enhanced by GPIb-expression, and deletion of the cytoplasmic 14-3-3-binding domain of GPIb alpha abolished the stimulatory effect of GPIb on thrombin signaling. Furthermore, the role of GPIb-IX in promoting thrombin signaling requires Rac1, and GPIb-IX-dependent Rac1 activation and LIMK phosphorylation are abolished in delta 605 cells expressing a 14-3-3-binding defective mutant GPIb alpha. Taken together, these data suggest that the stimulatory role of GPIb in thrombin signaling requires a C-terminal 14-3-3-binding region which mediates activation of a Rac1/LIMK1 pathway that promotes thrombin signaling leading to platelet activation.
Media: "Don't smoke," buy Marlboro
Authors: W. D Novelli
Journal: BMJ (1999)

The annals of literature are full of instances of misanthropes, knaves, and other antisocial characters who come to see the error of their ways and spend their declining years doing good works and helping their fellows. We were therefore intrigued by an announcement late last year by tobacco giant Philip Morris that it was prepared to spend $100m a year in a US campaign to reduce young people's smoking. Was this, at last, an honest attempt by Philip Morris to end its seductive marketing practices that have led to the tobacco addiction of millions of children and teenagers around the world?

Philip Morris has produced a series of television advertisements entitled “Think. Don't Smoke” and has made them the centrepiece of its antismoking campaign for teenagers. The advertisements tell children that they have a choice whether to smoke. Do they work?

The answer is probably not, according to a study released earlier this month ( Wall Street Journal 7 April). Focus groups of 12-16 year olds …
Ireland plans huge boost in consultant numbers
Authors: Doug Payne
Journal: BMJ (2001)

The Irish government has sanctioned talks that could bring the appointment of several hundred more hospital consultants and the opening of outpatient clinics from early morning to late evenings. A blueprint designed to improve patients' access to services, drawn up by a government review panel, the Medical Manpower Forum, will form the basis of the talks, which have been welcomed by the Irish Hospital Consultants' Association.

The …
Coxsackie A9 Infections with Exanthems with Particular Reference to Urticaria
Authors: J D CHERRY, A M LERNER, J O KLEIN, M FINLAND
Journal: JAMA (1963)

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
Hepatic Uptake Transporters and Docetaxel Disposition in Mice—Letter
Authors: Alex Sparreboom, Ron H. J. Mathijssen
Journal: Clinical Cancer Research (2014)

We previously reported in Clinical Cancer Research the results of a study evaluating the influence of hepatocellular OATP1B-type uptake transporters on the systemic clearance of docetaxel in mice and patients with inherited, reduced-function variants in the genes encoding these transporters (1). Figure 3A of this article shows plasma levels of docetaxel in adult male DBA/1LacJ mice (wild-type), which served as control data for those obtained in Oatp1b2 knockout animals. At the time of our report, there were no reference values available for docetaxel pharmacokinetic parameters in this mouse strain, and therefore we had no reason to a priori distrust the result. Upon further experimentation using what seem to be identical conditions, we recently found the plasma levels of docetaxel in wild-type DBA/1LacJ mice to be substantially higher than what we originally reported (2, 3).Although kinetic phenotypes of drugs often show considerable variability between different laboratories and/or within the same laboratory when experiments are performed over time, even in a genetically uniform mouse strain, the extent to which our original data differ from more recent findings (>10-fold) seems to be greater than what could have been expected from related literature on this topic. We have not been able to attribute these discrepancies to any particular reason (either biologic, environmental, and/or analytic), and have not identified any calculation errors. Although the pharmacokinetic differences in question are of a quantitative nature and do not affect the posited conclusions of our original article in a qualitative manner, based on the collective evidence now available, the original report likely overestimated the individual contribution of Oatp1b2 to the clearance of docetaxel in mice. This conclusion is consistent with recently reported by two other groups (4,5), and is in better agreement with published studies on the related drug paclitaxel (6, 7).No potential conflicts of interest were disclosed.
METABOLIC STIMULANTS WITH PARTICULAR REFERENCE TO SODIUM DINITROPHENOL
Authors: Edward L. Bortz
Journal: Annals of Internal Medicine (1934)

Article1 November 1934METABOLIC STIMULANTS WITH PARTICULAR REFERENCE TO SODIUM DINITROPHENOLEDWARD L. BORTZ, F.A.C.P.EDWARD L. BORTZ, F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-8-5-599 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIndividuals coming to the medical service of The Lankenau Hospital with cardiac, nephritic, gastrointestinal, blood and other disorders, as well as diabetes and obesity, have been studied more and more in the nutritional section of the Metabolic Clinic. It is remarkable to note how many functional disturbances clear up when patients are placed on a sensible, restricted but adequate diet with the avoidance of coffee, tea, tobacco and alcohol. The writer has been interested for several years in the relationship of body weight to the optimum functioning of patients and has tried numerous methods to cause a reduction in adiposity....References1. BORY L: Le soufre et la nutrition, Presse méd., 1934, xlii, 348. Google Scholar2. DODDSPOPE ECWJ: Dinitro-o-cresol as stimulator of metabolism, Lancet, 1933, ii, 352-353. CrossrefGoogle Scholar3. DODDSROBERTSON ECJD: Clinical applications of dinitro-o-cresol, Lancet, 1933, ii, 1137-1139, 1197-1198. CrossrefGoogle Scholar4. PERKINS RG: A study of the munitions intoxications in France, Pub. Health Rep., 1919, xxxiv, 2335. CrossrefGoogle Scholar5. POOLEHAINING FERB: Sudden death from dinitrophenol poisoning, Jr. Am. Med. Assoc., 1934, cii, 1141. CrossrefGoogle Scholar6. TAINTERWOOD MLDA: A case of fatal dinitrophenol poisoning, Jr. Am. Med. Assoc., 1934, cii, 1147. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Philadelphia, Pennsylvania*Read at the Chicago meeting of the American College of Physicians, April 17, 1934. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 November 1934Volume 8, Issue 5Page: 599-606KeywordsBody weightCoffeeDietHeart diseasesHospitalsMedical servicesNutritional deficienciesObesitySodiumTea ePublished: 1 December 2008 Issue Published: 1 November 1934 PDF downloadLoading ...
United Kingom lung cancer screening (UKLS) trial [Conference abstract]
Authors: John K. Field, Stephen Duffy, D. Baldwin, Katherine Emma Brain, T. Eisen, Christopher J. D. Hands, K. M. Kerr, R. Page, Mahesh Parmar, N. Wald, D. Weller, D. Whynes, P. Williamson, D. Hansell
Journal: Journal of Thoracic Oncology (2011)
Cytotoxic Action &lt;italic&gt;In Vitro&lt;/italic&gt; of Human Serum on the Metabolism of Mouse Ascites Tumor Cells and Counteraction by Endotoxic and Other Polysaccharides
Authors: Berigoj Stambuk, Dean Burk
Journal: JNCI Journal of the National Cancer Institute (1961)

The cytotoxic action of human serum on mouse tumor cells in vitro involves an extensive inhibition of respiration and of aerobic and anaerobic glycolysis. This action can be counteracted by preincubating the serum with certain polysaccharides or salts and can be enhanced by preincubating the serum with small amounts of distilled water. The cytotoxic action is highly dependent on temperature and involves optimal concentrations of Ca++ and/or Mg++ above and below which cytotoxicity is submaximal. The metabolic effects are closely correlated quantitatively and kinetically with morphologic cellular changes.
Mercury Rule Challenged
Authors: Bridget M. Kuehn
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