tbuckley/cabot-search huggingface dataset:
Abstract B35: The role of tumor associated macrophages (TAMs) in triple-negative breast cancer (TNBC) invasion revealed by species-specific RNA sequencing
Authors: Daniel C. Rabe, Casey A. Frankenberger, Russell Bainer, Devipriya Sankarasharma, Kiran Chada, Thomas Krausz, Yoav Gilad, Marsha Rich Rosner
Journal: Cancer Research (2015)

Abstract Triple-negative breast cancer (TNBC) is the most aggressive form of breast cancer. While five-year survival rates have reached 98% in patients treated with anti-ER or anti-HER2 therapies, patients with TNBC have a five-year survival rate of only 24%. Currently, the only form of therapy for these patients is surgery and platinum based chemotherapy. However, patient outcome is generally poor. Additionally, this disease disproportionately affects African-American women and lower income women, with rates seen approximately three times higher in African-American women compared to the rest of the population. An alternative strategy for treating TNBC patients involves targeting the tumor stroma. To better understand interaction between the tumor and stroma necessary for metastasis and invasion, we employed a triple-negative breast cancer (TNBC) model in which the metastasis suppressor Raf Kinase Inhibitory Protein (RKIP) controls primary tumor invasiveness. RKIP expression, which converts invasive tumors to non-invasive tumors, dramatically inhibits macrophage infiltration. The mechanism, which is dependent on Let-7 suppression of HMGA2, involves decreased expression of the chemokine CCL5. Furthermore, overexpression of CCL5 partially rescued the infiltration of macrophages into the tumor and intravasation of tumor cells into the blood stream. The relationships of the genes in the RKIP, HMGA2, CCL5, and macrophage pathways were observed in multiple sets of expression array data from breast cancer patients. Regulation of macrophage infiltration was observed in tumors from an HMGA2 knockout mouse model. These results show that RKIP regulates macrophage recruitment by tumors and demonstrate for the first time that metastasis suppressor genes can regulate the tumor microenvironment. Citation Format: Daniel C. Rabe, Casey A. Frankenberger, Russell Bainer, Devipriya Sankarasharma, Kiran Chada, Thomas Krausz, Yoav Gilad, Marsha Rich Rosner. The role of tumor associated macrophages (TAMs) in triple-negative breast cancer (TNBC) invasion revealed by species-specific RNA sequencing. [abstract]. In: Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; 2014 Feb 26-Mar 1; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(1 Suppl):Abstract nr B35. doi:10.1158/1538-7445.CHTME14-B35
THE USE OF OXALATED AND CITRATED BLOOD FOR ROUTINE CLASS STUDY
Authors: Frederick Howard Falls
Journal: JAMA (1918)

The problem of presenting to students various pathologic blood specimens in connection with clinical laboratory work is often one of considerable difficulty. This is especially true of colleges which have a small teaching hospital or none at all, or which are far removed from the large medical centers. Ideally, of course, each student should come in contact with the various diseases studied and observe the blood picture in connection with the other symptoms of the disease. Even in the more fortunately located institutions with attached teaching hospitals, it is sometimes impossible to bring the students in contact with the patients having blood diseases, because of the size of the classes and because of the inconvenience afforded to patients who may be severely sick at the time of the examination. These objections have been met in the past by obtaining blood smears in the usual way and passing them out stained
Abstract LB-51: p53 transcriptionally represses the SALL2 transcription factor under genotoxic stress.
Authors: Carlos Farkas, Carla Martins, David Escobar, Ariel Castro, David Donner, Roxana Pincheira
Journal: Cancer Research (2013)

Abstract SALL2- a member of the Spalt gene family- is a poorly characterized transcription factor found deregulated in various cancers, which suggest it plays a role in the disease. We previously identified SALL2 as a novel interacting protein of neurotrophin receptors and showed that it plays a role in neuronal function, which does not necessarily explain why or how SALL2 is deregulated in cancer. Previous evidences indicate that SALL2 gene is regulated by the WT1 and AP4 transcription factors. Here, we identified SALL2 as a novel downstream target of the P53 tumor suppressor protein. Bioinformatic analysis of the SALL2 gene revealed several putative P53 half sites along the promoter region. Either overexpression of wild-type P53 or induction of the endogenous P53 by the genotoxic agent doxorubicin repressed SALL2 promoter activity in various cell lines. However, Q143A, R175H and R248W P53 mutants, which are frequently found in the tumors of cancer patients, were unable to repress SALL2 promoter activity. Chromatin immunoprecipitation analysis using a specific P53 antibody further supported the binding to, and regulation of the SALL2 promoter by P53. Importantly, by using a p53ERTAM knockin model expressing a variant of P53 that is completely dependent on 4-hydroxy-tamoxifen for its activity, we show that P53 activation diminished SALL2 RNA and protein levels during genotoxic cellular stress in primary mouse embryo fibroblasts (MEFs) and radiosentive tissues in vivo. Thus, our finding indicates that P53 represses SALL2 expression in a context-specific manner, adding knowledge to understanding SALL2 gene regulation, and a potential mechanism for its deregulation in cancer Citation Format: Carlos Farkas, Carla Martins, David Escobar, Ariel Castro, David Donner, Roxana Pincheira. p53 transcriptionally represses the SALL2 transcription factor under genotoxic stress. [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 LB-51. doi:10.1158/1538-7445.AM2013-LB-51
EFFECTS OF 1,25-DIHYDROXYCHOLECALCIFEROL ON CALCIUM ABSORPTION, MUSCLE WEAKNESS, AND BONE DISEASE IN CHRONIC RENAL FAILURE
Authors: R.G Henderson, J.G.G Ledingham, D.O Oliver, D.G Small, R.G.G Russell, R Smith, R.J Walton, C Preston, G.T Warner, A.W Norman
Journal: The Lancet (1974)
Plastic Surgery: Tissue and Organ Homotransplantation
Authors: Bradford Cannon, Joseph E. Murray
Journal: New England Journal of Medicine (1956)

THE important observation of Medawar1 that a second homograft of skin from the same donor rabbit to the same recipient rabbit was rejected more rapidly than the first stimulated hope that perhaps a recognized biologic reaction could explain the mysterious "individual tissue specificity" originally theorized by Loeb.2 This evidence of a specific sensitization of the recipient by the donor tissue and the antigen–antibodylike reaction in the rejection of the transplant has been the impetus for a series of further investigative projects on both sides of the Atlantic.Among the earliest technics of study was parabiosis (1860),3 the physical union between . . .
Differences between Inhaled and Oral Glucocorticoid Therapy
Authors: Robert D. Utiger
Journal: New England Journal of Medicine (1993)

Administration of a glucocorticoid by inhalation has assumed a prominent role in the treatment of asthma in both children and adults. The reasons are that asthma is now viewed as a disease with an important inflammatory component and that there are inhaled glucocorticoid preparations that are highly active topically yet weakly active systemically, which minimizes the risks of suppressing endogenous pituitary-adrenal function and causing iatrogenic Cushing's syndrome.The glucocorticoids used most widely for inhalation therapy -- beclomethasone dipropionate and budesonide (the latter not available in the United States) -- have very high affinity for intracellular glucocorticoid receptors but are rapidly . . .
Axial heterogeneity of intracellular pH in rat proximal convoluted tubule.
Authors: E Pastoriza-Munoz, R M Harrington, M L Graber
Journal: Journal of Clinical Investigation (1987)

In the proximal convoluted tubule (PT), the HCO3- reabsorptive rate is higher in early (EPS) compared with late proximal segments (LPS). To examine the mechanism of this HCO3- reabsorption profile, intracellular pH (pHi) was measured along the superficial PT of the rat under free-flow and stationary microperfusion using the pH-sensitive fluorescence of 4-methylumbelliferone (4MU). With 4MU superfusion, pHi was found to decline along the PT. Observation with 365-nm excitation revealed that EPS were brightly fluorescent and always emerged away from their star vessel. Midproximal segments were darker and closer to the star vessel which was surrounded by the darkest LPS. Decreasing luminal HCO3- from 15 to 0 mM lowered pHi in both EPS and LPS, but pHi remained more alkaline in EPS with both perfusates. Thus the axial decline in pHi along the PT is due to both luminal factors and intrinsic differences in luminal H+ extrusion in PT cells.
Genetic Susceptibility to Distinct Bladder Cancer Subphenotypes
Authors: Lin T. Guey, Montserrat García-Closas, Cristiane Murta-Nascimento, Josep Lloreta, Laia Palencia, Manolis Kogevinas, Nathaniel Rothman, Gemma Vellalta, M. Luz Calle, Gaëlle Marenne, Adonina Tardón, Alfredo Carrato, Reina García-Closas, Consol Serra, Debra T. Silverman, Stephen Chanock, Francisco X. Real, Núria Malats
Journal: European Urology (2009)
New Contract for Junior Hospital Staff
Authors: B. F. Boyce, J. C. Campbell, K. A. Fleming, A. L. C. McLay, A. M. McNicol, R. P. O'Hare, K. O'Reilly, N. M. Pettigrew, W. A. Reid, J. Rodger, W. Stockwell, W. D. Thompson
Journal: BMJ (1975)
α-Linolenic Acid and Risk of Nonfatal Acute Myocardial Infarction
Authors: Hannia Campos, Ana Baylin, Walter C. Willett
Journal: Circulation (2008)

Background— Intake of long-chain n-3 fatty acids found in fish is low in many countries worldwide. α-Linolenic acid could be a viable cardioprotective alternative to these fatty acids in these countries. Methods and Results— Cases (n=1819) with a first nonfatal acute myocardial infarction and population-based controls (n=1819) living in Costa Rica matched for age, sex, and area of residence were studied. Fatty acids were assessed by gas chromatography in adipose tissue samples and by a validated food frequency questionnaire specifically designed for this population. Odds ratios and 95% confidence intervals were calculated from multivariate conditional logistic regression models. α-Linolenic acid in adipose tissue ranged from 0.36% in the lowest decile to 1.04% in the highest decile. The corresponding median levels of intake were 0.42% and 0.86% energy. Greater α-linolenic acid (assessed either in adipose or by questionnaire) was associated with lower risk of myocardial infarction. The odds ratios for nonfatal myocardial infarction for the highest compared with the lowest deciles were 0.41 (95% confidence interval, 0.25 to 0.67) for α-linolenic acid in adipose tissue and 0.61 (95% confidence interval, 0.42 to 0.88) for dietary α-linolenic acid. The relationship between α-linolenic acid and myocardial infarction was nonlinear; risk did not decrease with intakes &gt;≈0.65% energy (1.79 g/d). Fish or eicosapentaenoic acid and docosahexaenoic acid intake at the levels found in this population did not modify the observed association. Conclusions— Consumption of vegetable oils rich in α-linolenic acid could confer important cardiovascular protection. The apparent protective effect of α-linolenic acid is most evident among subjects with low intakes.
Infected Knee Prosthesis
Authors: M MINOVES, J R GARCIA, S MA??E, L del RIO, R HERRANZ, J SETOAIN
Journal: Clinical Nuclear Medicine (1992)

Studies have shown the usefulness of labeled leukocyte scintigraphy as a specific tracer to detect inflammatory-infectious conditions in orthopedic surgery. The authors submit the case of a 69-year-old woman who had a total left knee prosthesis implanted 2 months earlier. At the time of exploration, the patient complained of knee pain and local clinical signs of soft tissue infection adjacent to the surgical scar. A fistulous orifice on the front of the leg, immediately below the knee, with abundant suppuration was observed.
Abstract 321: IL-6 in the tissue microenvironment plays a direct role in normal prostatic neoplastic transformation
Authors: Jennifer D. Wu, Gang Liu
Journal: Cancer Research (2012)

Abstract Increased elevated levels of serum IL-6, the major inflammatory mediator, has been shown to be associated with development of progressive diseases in many types of cancers. We have previously shown that chronic exposure of immortalized benign prostate epithelial cells to paracrine IL-6 can induce tumorigenic transformation and further EMT (epithelial-mesochymal-transition)-associated metastasis in xenografts through stimulating autocrine IL-6 signaling and transactivating type I Insulin-like Growth Factor Receptor (IGF-IR). Whether IL-6, as a result of inflammation, in the tissue microenvironment can solely initiate tissue-specific de novo tumorigenesis is unclear. To address this question, we have generated a novel line of prostate-specific IL-6 transgenic mouse, in which human IL-6 (hIL-6) was expressed under the prostate-specific probasin promoter. We found that enforced expression of hIL-6 transgene in normal mouse prostate epithelium is sufficient to induce neoplastic transformation of the prostate gland, demonstrated by disappearance of base cell layer of the prostate gland and loss of E-cadherin and increased proliferation of the epithelium. Expression of the hIL-6 transgene also induced autocrine mouse IL-6 secretion in the prostate gland and sustained activation of STAT3 pathway in the epithelium and the stroma. Strikingly, IL-6 transgenic mice have increased peri-prostatic adipose tissue in which STAT3 was highly phosphorylated in comparison to the wild-type littermate. There is no significant increase in infiltration of T cells or B cells in the prostate of IL-6 transgenic animals. However, significantly increased infiltration (P&amp;lt;0.01) of FoxP3+ lymphocytes was seen in the stroma of the prostate in the IL-6 transgenic animals in comparison to wild-type littermates. These data suggest that IL-6 as a pro-inflammatory cytokine alone can induce tissue-specific tumorigenesis through induction of autocrine IL-6 secretion and remodeling tissue microenvironment. Our finding suggests that inflammation may play a direct role beyond being the “stimuli” or “fuel” in tumorigenesis. 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 321. doi:1538-7445.AM2012-321
Increasing Rates of Depression
Authors: Rafiq Waziri
Journal: JAMA (1989)

<h3>To the Editor. —</h3> It would have been appropriate if Drs Klerman and Weissman<sup>1</sup>had ended the title of their article "Increasing Rates of Depression" with a large question mark. They have presented data from their own work with colleagues or other researchers suggesting that the rates of depression, especially in the younger age groups, are increasing. Some of this work is on populations and some on selected patients and their first-degree relatives. Unlike studies in medical epidemiology, where diagnoses are made with standard laboratory tests or instruments with known sensitivities and specificities, psychiatric studies use self-reports, complaints, and symptoms as the bases for recording psychopathology. The specificity of these techniques is unknown or low. These techniques have introduced so much elasticity in the concept of depression that stuporous or severely melancholic patients as well as those complaining from unhappiness owing to adverse conditions or character defects are all
THE ORAL MANIFESTATIONS OF DIABETES MELLITUS.
Authors: HERMANN PRINZ
Journal: JAMA (1905)

Within the last twenty-five years, a vast amount of literature has been produced concerning the etiology, pathology and therapeutics of pyorrhea alveolaris, and, with it all, to-day we are about as far away from its true etiology as in the days of Celsus, who probably was the first medical writer to call attention to this ailment. To J. M. Riggs of Hartford, Conn., American dentistry is indebted for first calling the attention of the profession to this disease in 1869, although it must have been recognized by him as early as 1844. Rehwinkel is usually quoted as being the first (1877) to use the term pyorrhea alveolaris, a name which he borrowed from Albrecht of Berlin. This term, however, is of French origin and is employed for the first time in an article published by Toirac-Desirabode1 in 1839, in which he speaks of the disease as<i>pyorrhea alveolodentaire.</i>Fauchard, in
Quebec's Medical Mystery
Authors: Yves Morin
Journal: JAMA (1966)

To the Editor:—  With reference to the report Quebec's Medical Mystery ( 196 , June 13, 1966, adv p 25), we were recently shown a documented series of 50 identical cases by Drs. James F. Sullivan, John Egan, and Paul McDermott from Omaha. This series was presented at the last meeting of the American Society for Clinical Nutrition. In addition, similar cases were also kindly presented to us by Dr. Carl S. Alexander in Minneapolis. We have reasons to believe that this new syndrome is occurring in other well-localized centers.  Common etiological factors are at play in these geographically distant areas and to track them down we feel more series of this syndrome should be collected. The diagnosis, once attention has been drawn to its most impressive features, is generally easy to make, especially as these cases tend to occur in a relatively large number in a well-localized area.  The patients are
Abstract 4309: Isolation, expansion and molecular characterization of lung cancer stem cells from NSCLC cell lines
Authors: Sandeep Singh, Srikumar Chellappan
Journal: Cancer Research (2010)

Abstract Lung cancer is the leading cause of death from cancer worldwide. NSCLC represents the most common subtype of lung cancer with the average five-year survival rate is only 16%. The majorities of these tumors are refractory to chemotherapeutics or acquire resistance to the therapy. In addition, most of the patients develop distant metastases even tough their primary tumors are surgically removed. Cancer stem cell hypothesis has emerged as a possible explanation for tumor growth, recurrence after treatment and metastasis in a variety of cancer. This hypothesis suggests that tumors are maintained by the subset of cancer stem cells (CSCs) that has the ability to self-renew and generate the diverse cells that comprise the tumor. While evidence supporting the existence of CSCs has been demonstrated in many solid cancers, it is largely underdeveloped in lung cancer. Here we have isolated cancer stem like cells from NSCLC cell lines either through isolating the side population (SP) cells based on their property to exclude Hoechst 33342 dye or enriched them by cultivating cancer cells in defined serum free medium containing N2-supplement, EGF and bFGF. Cells obtained from both these methods demonstrated higher clonogenic as well as sphere forming ability which is the typical characteristics associated with CSCs. We further characterized these cells for their ability to express progenitor/stem cell marker genes like Oct4, Sox2 and Nanog. Total RNA from SP cells showed higher expression of these genes as compared to main population. Similarly, the expression of Oct4, Sox2 and Nanog was found elevated after culturing H1650, H358, H322 and H292 cells in defined serum free medium for 10 days. Interestingly, CSCs enriched in this condition also showed the loss of E-cadherin expression and consequent gain of mesenchymal proteins like fibronectin and vimentin. Additionally, ABCG2, which is closely associated with the drug resistance and responsible for side population phenotype, was also upregulated in cancer stem like cells enriched from culturing in serum free defined media. In conclusion, results revealed that lung cancer stem like cells could be isolated and expanded from the established lung cancer cell lines by two different methodologies described here. These cells possess the characteristics of both stem cells and malignant tumors. Therefore, further studies towards targeting these cells may result in effective therapy against lung cancer. 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 4309.
MicroRNA-146a and AMD3100, two ways to control CXCR4 expression in acute myeloid leukemias
Authors: I Spinello, M T Quaranta, R Riccioni, V Riti, L Pasquini, A Boe, E Pelosi, A Vitale, R Foà, U Testa, C Labbaye
Journal: Blood Cancer Journal (2011)

CXCR4 is a negative prognostic marker in acute myeloid leukemias (AMLs). Therefore, it is necessary to develop novel ways to inhibit CXCR4 expression in leukemia. AMD3100 is an inhibitor of CXCR4 currently used to mobilize cancer cells. CXCR4 is a target of microRNA (miR)-146a that may represent a new tool to inhibit CXCR4 expression. We then investigated CXCR4 regulation by miR-146a in primary AMLs and found an inverse correlation between miR-146a and CXCR4 protein expression levels in all AML subtypes. As the lowest miR-146a expression levels were observed in M5 AML, we analyzed the control of CXCR4 expression by miR-146a in normal and leukemic monocytic cells and showed that the regulatory miR-146a/CXCR4 pathway operates during monocytopoiesis, but is deregulated in AMLs. AMD3100 treatment and miR-146a overexpression were used to inhibit CXCR4 in leukemic cells. AMD3100 treatment induces the decrease of CXCR4 protein expression, associated with miR-146a increase, and increases sensitivity of leukemic blast cells to cytotoxic drugs, this effect being further enhanced by miR-146a overexpression. Altogether our data indicate that miR-146a and AMD3100, acting through different mechanism, downmodulate CXCR4 protein levels, impair leukemic cell proliferation and then may be used in combination with anti-leukemia drugs, for development of new therapeutic strategies.
Time to Operate
Authors: Gunter K. von Noorden
Journal: JAMA (1964)

<h3>To the Editor:—</h3> After reading Taylor's communication on early surgery in strabismus (<i>Arch Ophthal [Chicago]</i><b>70</b>:752, 1963) to which further attention was directed by an editorial inThe Journal(<b>187</b>:298 [Jan 25] 1964), I feel that a word of caution is in order. While I agree that it would be desirable to have the eyes straight as early as possible to permit simultaneous bifoveal stimulation, I would like to warn against general acceptance of the recommendations according to which surgery in congenital strabismus should preferably be performed between the ages of 6 and 12 months. Most surgeons will agree that the diagnosis has to come before the operation. However, an adequate diagnosis in a strabismic child who is less than a year old is not possible in every case. Measurements of the deviation both near and at a distance will have to be delayed until the child has