tbuckley/cabot-search huggingface dataset:
Abstract 2006: Mathematical and computational models for cellular space in cancer growth
Authors: Megan Olsen, Ramesh Sitaraman, Nava Siegelmann-Danieli, Hava Siegelmann
Journal: Cancer Research (2010)

Abstract This study investigates the dependency of tumor cell growth on specific spatial regulations for both normal and tumor cells. In general it is known that cellular growth is affected by contact inhibition, but many models fail to include this aspect explicitly. Our work studies the extent to which spatial constraints and interactions between normal and tumor cells affect tumor growth. We model spatial constraints via a set of differential equations, modified from the classic logistic equation. These equations represent the hallmarks of cancer, with the addition of spatial rules based on the ratio of living tumor to normal cells in the tissue. Four different sets of equations are analyzed and compared, each representing a different potential scenario of how tumor and normal cells differ in their views of space. Most computational models of cancer do not investigate the interactions between normal cells and tumor cells, and our approach demonstrates that these interactions are crucial for modeling and understanding cancer growth. Our results provide a delineation of when tumor growth will take over an area versus when it will be slowed or stopped for each type of spatial constraint. Our results indicate that different combinations of spatial regulations cause different outcomes in tumor growth. They also demonstrate that cells following the same set of rules for proliferation, death, and mutation meet different outcomes given a change in spatial constraints. Thus, an accurate modeling of spatial interactions between two cellular populations is crucial to adequately examine tumor cells. Our results suggest that a treatment assuming one set of rules will fail if another set of rules is in place. Further, if we learn to modify these spatial rules in a tissue then tumor growth could be decreased. Our work also implies that to be able to use computational models for evaluating options for treatment proper spatial rules must be taken into account in the model. In conclusion, we recognize that the influence of contact inhibition on different populations of cells can drive one cancer to take over the system, while it can significantly slow the growth of another. Such spatial constraints are extremely crucial to modeling and understanding cancer growth and in evaluating options for treatment. 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 2006.
Opioid Overdose Fatality Prevention
Authors: Pamela Leece, Aaron Orkin
Journal: JAMA (2013)

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
Antibiotic Growth Stimulation
Authors: T. D. Luckey
Journal: BMJ (1963)

that venous thrombosis is initiated by an injury of the vessel wall which causes a localized liberation of tissue thromboplastin to produce a clot attached to the area of injury."4There is more evidence against than in favour of this theory.Tissue thromboplastin is an intracellular particulate substance, and cellular destruc- tion, therefore, is necessary to release it.Further, the difference between thrombosis and intravascular coagu- lation has by now been well established.If Dr. Quick's theory was correct one would not expect venous thrombosis in factor VII deficiency cases.We have, however, observed post-operative thrombo-embolism in two patients with total factor VII deficiency.5Platelets play a major role in the first stages of thrombus formation.Since the discovery of adenosine diphosphate6 as a key-factor at this stage and the significance of the platelet surface clotting systems for the progression and consolidation of the platelet thrombus it seems more profitable to pursue this line of investigation along with studies on plasma coagulation.-I am, etc.,
Bone deficit in ovariectomized rats. Functional contribution of the marrow stromal cell population and the effect of oral dihydrotachysterol treatment.
Authors: C Tabuchi, D J Simmons, A Fausto, J E Russell, I Binderman, L V Avioli
Journal: Journal of Clinical Investigation (1986)

This study investigates the proliferative and osteogenic role of marrow stromal/osteoprogenitor cells in the development of the cortical bone deficit in ovariectomized (OVX) female rats. In vitro, clonal growth of marrow stromal cells from OVX rats was significantly impaired (vs. sham-operated controls). Yet in vivo, cells from sham-operated and OVX rats had equal osteogenic potential in several in vivo experimental situations, such as in intraperitoneally implanted millipore diffusion chambers and in intramuscular implants of marrow plus osteoinductive bone matrix (composite grafts). Long-term (6 mo) dihydrotachysterol (DHT) treatment of OVX rats enhanced their in vitro proliferative potential and clonal growth, as well as their osteogenic expression in composite grafts. The observation that the in vivo osteogenic performance of OVX rat marrow stromal cells was normal at extraosseous sites suggests that the mechanisms leading to osteopenia may involve an abnormality in cell-matrix interactions.
Intestinal Infections with Aeromonas
Authors: WILLIAM A. AGGER
Journal: Annals of Internal Medicine (1987)

Letters and Corrections1 March 1987Intestinal Infections with AeromonasWILLIAM A. AGGER, M.D., STEVEN M. CALLISTER, M.S.WILLIAM A. AGGER, M.D.Search for more papers by this author, STEVEN M. CALLISTER, M.S.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-106-3-479_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The clinical aspects of intestinal infections with Aeromonas species reported by Holmberg and colleagues (1) are similar to those we have seen in western Wisconsin (2), including the more prolonged course in adults. However, we disagree that selective media, such as sheep blood agar with ampicillin, should be avoided when screening for Aeromonas species in stools.When using this agar, stools negative forAeromonasspecies are often indicated by a negative (no growth) culture plate.Aeromonasspecies as the causative agents of that patient's gastroenteritis are therefore effectively eliminated from consideration. The testing of predominant colonies on...References1. HOLMBERGSCHELLFANNING SWG. Aeromonas intestinal infections in the United States. Ann Intern Med. 1986;105:683-9. LinkGoogle Scholar2. AGGERMCCORMICKGURWITH WJM. Clinical and microbiological features of Aeromonas hydrophila-associated diarrhea. J Clin Microbiol. 1985;21:909-13. CrossrefMedlineGoogle Scholar3. KELLYBRENNERFARMER MDJ. Enterobacteriaceae. In: LENNETTE EW, BALOWS A, HANSTER WJ, SHADOMY HJ, eds. Manual of Clinical Microbiology. Washington, D.C: American Society for Microbiology; 1985:263-77. Google Scholar4. PALUMBOMAXINOWILLIAMSBUCHANANTHAYER SFARD. Starch-ampicillin agar for the quantitative detection of Aeromonas hydrophila. Appl Environ Microbiol. 1985;50:1027-30. CrossrefMedlineGoogle Scholar5. CALLISTERAGGER SW. Enumeration and characterization of Aeromonas hydrophila and Aeromonas caviae isolated from grocery store produce. Appl Environ Microbiol. 1987. (In press). CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: WILLIAM A. AGGER, M.D.; STEVEN M. CALLISTER, M.S.Affiliations: Gundersen Clinic, Ltd. La Crosse, WI 54601 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1987Volume 106, Issue 3Page: 479-479KeywordsBloodGastroenteritis ePublished: 1 December 2008 Issue Published: 1 March 1987 PDF downloadLoading ...
Alcohol and Drug Testing of Health Professionals Following Preventable Adverse Events: A Bad Idea
Authors: John Banja
Journal: The American Journal of Bioethics (2014)

Various kinds of alcohol and drug testing, such as preemployment, routine, and for-cause testing, are commonly performed by employers. While healthcare organizations usually require preemployment drug testing, they vary on whether personnel will be subjected to further testing. Recently, a call has gone out for postincident testing among physicians who are involved in serious, preventable events, especially ones leading to a patient's death. This article will offer a number of counterarguments to that proposal and discuss an alternate approach: that health institutions can better improve patient safety and employees' well-being by implementing an organizational policy of "speaking up" when system operators notice work behaviors or environmental factors that threaten harm or peril. The article will conclude with a description of various strategies that facilitate speaking up, and why the practice constitutes a superior alternative to mandatory alcohol and drug testing in the wake of serious, harm-causing medical error.
GMC hears parents' complaints about Southall
Authors: Owen Dyer
Journal: BMJ (2006)

The paediatrician David Southall faced fresh charges before the General Medical Council this week over his investigations of parents whom he suspected of harming their children. 

Professor Southall adopted the role of “detective or crown prosecutor” when interviewing the mother of a 10 year old boy who had been found hanging in his bedroom, alleged the GMC's counsel Richard Tyson QC. The GMC's charges allege that Professor Southall accused the woman of drugging and hanging her son, adding to the distress of a bereaved parent. 

The boy, identified only as M1, died in June 1996, and his inquest ended in an open verdict. His …
Prophylactic effect of cimetidine in duodenal ulcer disease.
Authors: E Gudmand-Hoyer, K B Jensen, E Krag, J Rask-Madsen, I Rahbek, S J Rune, H R Wulff
Journal: BMJ (1978)

Fifty-seven symptom-free patients with duodenal ulcer entered a double-blind trial to assess the prophylactic effect of cimetidine. Patients were randomly allocated to receive cimetidine 400 mg twice daily (29 patients) or placebo (28 patients). The trial was designed to imitate daily clinical practice, so duodenal ulcer disease was diagnosed by means of x-ray examination. Three patients from each group withdrew from the trial. All remaining patients continued to receive treatment for 12 months or until symptoms recurred. Three out of 26 patients suffered relapses during cimetidine treatment, compared with 20 out of 25 receiving placebo. No side effects were attributable to cimetidine. Long-term cimetidine treatment had no curative effect as relapses occurred soon after treatment was stopped. The estimated chance (cumulative remission rate +/- 2 SE) of remaining symptom-free 13 weeks after one year's cimetidine treatment had been completed was 47 +/- 21%. Maintenance treatment with cimetidine is a suitable alternative to elective in surgery in patients with duodenal ulcer subjects frequent relapses. Further study is needed to establish the optimal duration and safety of prolonged cimetidine treatment.
ACCURACY OF 320-DETECTOR ROW COMPUTED TOMOGRAPHY TO IDENTIFY SIGNIFICANT CORONARY STENOSES IN PATIENTS WITH ATRIAL FIBRILLATION
Authors: Seitetsu Lee, Kengo Tanabe, Satoru Kishi, Tatsuhiko Otsuka, Masahiko Asami, Mika Watanabe, Eri Yoshida, Takuya Hashimoto, Hironori Hara, Kazuyuki Yahagi, Makoto Nakashima, Jiro Aoki, Kazuhiro Hara
Journal: Journal of the American College of Cardiology (2012)
507 ROLE OF HELICOBACTER PYLORI IN PATIENTS WITH HCV-RELATED CHRONIC HEPATITIS, CIRRHOSIS WITH OR WITHOUT HEPATOCELLULAR CARCINOMA: POSSIBLE ASSOCIATION WITH DISEASE PROGRESSION
Authors: G. Esmat, M. El-Bendary, S. Zakarya, M. Abou Ela, K. Zalata
Journal: Journal of Hepatology (2010)
ON THE PHOSPHOTUNGSTATES OF CERTAIN AMINOACIDS
Authors: P. A. Levene, W. A. Beatty
Journal: The Journal of Experimental Medicine (1906)

In a communication to the Chemical Society ~ one of us reported on the property of aminoacids to form insoluble phosphotungstates.In a later publication 2 the writers showed the degree of precipitability of aminoacids by means of phosphottmgstic acid, and stated that a separation of aminoacids may be accomplished by means of this reagent.The attempt was made to apply the method to the study of the acids resulting from the hydrolysis of gelatine by means of mineral acids.Unfortunately, through an accident in the laboratory, the greater part of the material for this study was lost, and hence in this place there will be reported a method of the separation of oxyprolin and of an acid having the composition CTH14N202.
Arginine-Induced Insulin Release in Glucokinase-Deficient Subjects
Authors: Maria E Pueyo, Karine Clement, Martine Vaxillaire, Philippe Passa, Philippe Froguel, Jean-Jacques Robert, Gilberto Velho
Journal: Diabetes Care (1994)

OBJECTIVE In eight glucokinase (GCK)-deficient subjects, we have investigated insulin secretion rates (ISRs) in response to intravenous arginine. Impairment in the enzymatic activity of mutant GCK leads to a reduced glycolytic flux in β-cells. This defect translates in vivo as a right shift in the glucose/ISR dose-response curve. Insulin secretion in response to other secretagogues has not been reported. RESEARCH DESIGN AND METHODS The arginine test was performed immediately after a 2-h hyperglycémie (10 mM) clamp. ISR was computed by decon-volution of peripheral C-peptide levels. Linear regression analyses were performed to assess correlations between the /3-cell secretory responses to the arginine test, an intravenous glucose tolerance test (IVGTT), and a hyperglycemie clamp (areas under the C-peptide curves), and between these parameters and the glucose tolerance status (area under the glucose curve during an oral glucose tolerance test). RESULTS Two minutes after the injection of arginine, the increment in ISR was 30.17 ± 10.01 pmol insulin · kg−1 · min−1 in patients and 36.25 ± 15.46 pmol insulin · kg−1 · min−1 in control subjects (P = 0.38). Throughout the experiment, increments in ISR were comparable in both groups. The amount of insulin secreted in response to arginine (0-5 min) was similar in patients and control subjects: 81 ± 28 vs. 119 ± 55 pmol/kg (P = 0.16), respectively. The arginine test C-peptide response was not correlated with the IVGTT or hyperglycémie clamp responses. The arginine test and hyperglycemie clamp responses were not correlated to the glucose tolerance status. The best predictor of the glucose tolerance was the C-peptide response to the IVGTT (r2 = 0.78; P = 0.002). CONCLUSIONS β-cell secretory increment in response to arginine was found to be in the normal range in GCK-deficient subjects. The arginine test does not seem to reflect either the /3-cell secretory defect or the glucose tolerance status of these subjects. IVGTT seems to be the best predictor of the latter parameter in this population.
Bacterial Pneumonia in Patients with the Acquired Immunodeficiency Syndrome
Authors: BRUCE POLSKY
Journal: Annals of Internal Medicine (1986)

Eighteen episodes of community-acquired bacterial pneumonia were diagnosed in 13 patients among 336 with the acquired immunodeficiency syndrome (AIDS) cared for at Memorial Sloan-Kettering Cancer Center since 1979. Bacterial pathogens isolated in 16 of 18 episodes were Haemophilus influenzae in 8, Streptococcus pneumoniae in 6, group B streptococcus in 1, and Branhamella catarrhalis in 1. Eight episodes were presumed Pneumocystis carinii pneumonia until cultures obtained at bronchoscopy confirmed a bacterial cause. Specific antibacterial therapy was curative in 16 of 18 episodes; 2 patients died. Given an estimated yearly incidence of pneumococcal pneumonia in the general population of 2.6/1000, 1.09 cases were expected in our patients with AIDS; we saw 6 (p = 0.001), for an attack rate of 17.9/1000. Bacteria associated with B-cell defects should be anticipated when formulating empiric antibiotic therapy, pending a definitive diagnosis, for pulmonary infiltrates in patients with AIDS.
Combination Pill for Cardiovascular Disease
Authors: Tetsuro Tsujimoto, Ritsuko Yamamoto-Honda
Journal: JAMA (2013)

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
Thrombin Suppresses Endothelial Nitric Oxide Synthase and Upregulates Endothelin-Converting Enzyme-1 Expression by Distinct Pathways
Authors: Masato Eto, Christine Barandiér, Lisa Rathgeb, Toshiyuki Kozai, Hana Joch, Zhihong Yang, Thomas F. Lüscher
Journal: Circulation Research (2001)

Abstract— An imbalance of nitric oxide and endothelin plays an important role in cardiovascular disease. Thrombin exerts profound effects on endothelial function. The present study investigated the molecular mechanisms by which thrombin regulates endothelial nitric oxide synthase (eNOS) and endothelin-converting enzyme (ECE)-1 expression in human endothelial cells. Incubation of human umbilical vein endothelial cells with thrombin (0.01 to 4 U/mL) for 15 to 24 hours markedly downregulated eNOS and increased ECE-1 protein level in a dose-dependent manner. Thrombin also decreased eNOS mRNA and increased ECE-1 mRNA level. In mRNA stability assay, thrombin shortened the half-life of eNOS mRNA but not that of ECE-1 mRNA. Activation of protease-activated receptor 1 by the agonist (SFLLRN, 10 to 100 μmol/L) had no effect on eNOS expression but increased ECE-1 level as thrombin. Thrombin activated Rho A and extracellular signal–regulated kinase (ERK)1 and ERK2. Inhibition of Rho A by C3 exoenzyme (20 μg/mL) and ROCK by Y-27632 (10 μmol/L) prevented the downregulation of eNOS expression by thrombin. Y-27632 also prevented the reduction in NOS activity induced by prolonged incubation with thrombin. On the other hand, inhibition of ERK1 and ERK2 activation by PD98059 (50 μmol/L) prevented the upregulation of ECE-1 expression by thrombin as well as the increase in ECE activity and ET-1 accumulation in the medium. Treatment of rat aorta with thrombin overnight impaired endothelium-dependent relaxations but not endothelium-independent relaxations. Thus, thrombin suppresses eNOS and upregulates ECE-1 expression via Rho/ROCK and ERK pathway, respectively. These effects of thrombin may be important for endothelial dysfunction in cardiovascular disease, particularly during acute coronary episodes.
The Mast Cell in Inflammatory Arthritis
Authors: David E. Woolley
Journal: New England Journal of Medicine (2003)

Rheumatoid arthritis is a chronic destructive disease of joints, characterized by inflammation, synovial hyperplasia, and abnormal cellular and humoral immune responses. Although several types of cells have been proposed to trigger synovial inflammation, the etiologic process and pathogenesis of the disease remain controversial. But, as indicated by a recent study by Lee et al.,1 the mast cell is emerging as a key player in the erosive and inflammatory events leading to joint destruction (Figure 1).The inflammatory processes that result in rheumatoid arthritis are multifactorial, involving complex interactions among the cytokine network, autoantibodies, and the complement cascade. Various mediators are . . .
FMS-Like Tyrosine Kinase 3–Internal Tandem Duplication Tyrosine Kinase Inhibitors Display a Nonoverlapping Profile of Resistance Mutations <i>In vitro</i>
Authors: Nikolas von Bubnoff, Richard A. Engh, Espen Åberg, Jana Sänger, Christian Peschel, Justus Duyster
Journal: Cancer Research (2009)

FMS-like tyrosine kinase 3 (FLT3) inhibitors have shown activity in the treatment of acute myelogenous leukemia (AML). Secondary mutations in target kinases can cause clinical resistance to therapeutic kinase inhibition. We have previously shown that sensitivity toward tyrosine kinase inhibitors varies between different activating FLT3 mutations. We therefore intended to determine whether different FLT3 inhibitors would produce distinct profiles of secondary, FLT3 resistance mutations. Using a cell-based screening approach, we generated FLT3-internal tandem duplication (ITD)-expressing cell lines resistant to the FLT3 inhibitors SU5614, PKC412, and sorafenib. Interestingly, the profile of resistance mutations emerging with SU5614 was limited to exchanges in the second part of the kinase domain (TK2) with exchanges of D835 predominating. In contrast, PKC412 exclusively produced mutations within tyrosine kinase domain 1 (TK1) at position N676. A mutation at N676 recently has been reported in a case of PKC412-resistant AML. TK1 mutations exhibited a differential response to SU5614, sorafenib, and sunitinib but strongly impaired response to PKC412. TK2 exchanges identified with SU5614 were sensitive to PKC412, sunitinib, or sorafenib, with the exception of Y842D, which caused a strong resistance to sorafenib. Of note, sorafenib also produced a highly distinct profile of resistance mutations with no overlap to SU5614 or PKC412, including F691L in TK1 and exchanges at position Y842 of TK2. Thus, different FLT3 kinase inhibitors generate distinct, nonoverlapping resistance profiles. This is in contrast to Bcr-Abl kinase inhibitors such as imatinib, nilotinib, and dasatinib, which display overlapping resistance profiles. Therefore, combinations of FLT3 inhibitors may be useful to prevent FLT3 resistance mutations in the setting of FLT3-ITD-positive AML.