tbuckley/cabot-search huggingface dataset:
Abstract 3262: Windows of susceptibility to endocrine disruptors and gene expression in mammary tissue
Authors: Kalpana Gopalakrishnan, Qian Li, Yula Ma, Luca Lambertini, Jia Chen, Susan L. Teitelbaum, Fabiana Manservisi, Fiorella Belpoggi, Luciano Bua, Laura Falcioni
Journal: Cancer Research (2014)

Abstract Breast cancer is hormonally driven. Endocrine disruptors (EDs) are exogenous substances that mimic or antagonize endogenous hormone action and disrupt endocrine system function. While EDs have been shown to modulate the risk for mammary tumors in animal models, their effects at biologically relevant doses and during critical developmental windows remain poorly understood. We sought to examine the individual and combinatorial effects of three common EDs, diethyl phthalate, methyl paraben and triclosan in rats exposed at five distinct developmental windows of susceptibility - prenatal, neonatal, prepubertal, pubertal and parous/nulliparous. Pathological features and whole genome expression of normal rat mammary tissues were profiled to provide both qualitative and quantitative biological effects of EDs. ED exposure at levels comparable to human exposure resulted in profound changes in both gross phenotypes (e.g. reproductive mortality and mammary gland morphology) as well as in molecular genome profiles. Specifically, ED exposure appeared to hamper normal breast development and resulted in increased mortality in the offspring, possibly due to reduced milk production. Whole genome expression profiling of mammary tissues revealed that in the course of development, the number of differentially expressed genes was lower in ED-exposed rats compared to controls, suggesting developmental delay or suppression by EDs. Pathway enrichment analysis indicated that several processes including inflammation, metabolism and development were disrupted by ED exposure. Taken together, our findings reveal novel mechanisms of ED action in mammary development and strongly suggest the importance of taking into account the timing of exposure when studying the relationship between environment and disease. Citation Format: Kalpana Gopalakrishnan, Qian Li, Yula Ma, Luca Lambertini, Jia Chen, Susan L. Teitelbaum, Fabiana Manservisi, Fiorella Belpoggi, Luciano Bua, Laura Falcioni. Windows of susceptibility to endocrine disruptors and gene expression in mammary tissue. [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 3262. doi:10.1158/1538-7445.AM2014-3262
Irritation of Urinary Tract by "Doped" Beer
Authors: G. A. Ballance
Journal: BMJ (1943)

This last, in view of lknown facts as to sensitization and allergy, appears to be rational, and was therefore adopted in this investigation.That negative skin tests do not exclude intolerance to liver extract is shown by Case 2, in which these were negative 18 months after the onset of symptoms and became positive only during the attempt at desensitization.Two methods may be adopted for the parenteral administration of liver extract to intolerant patients: lasting desensitization can be achieved by a course of liver injections in increasing doses over several weeks; alternatively, the required dose may be given in small injections, preferably over two days.The latter method does not increase the tolerance of the patient to future doses.Summary Three cases of pernicious anaemia are described in which the patient had become " sensitive " to the parenteral injection, of liver extract.Skin tests cannot be relied upon to indicate intolerance.By the use of divided doses of liver extract over a period of several weeks it proved possible to desensitize two patients to the extent that they became able to tolerate their full require- ment, of liver extract in one injection at monthly intervals.In a third case the required dose is being given in small injections over two days without attempt at permanent desensitization.My thanks are due to Dr. S. C. Dyke for access to records and advice, and to Sister Dora Martin for care and supervision
Endothelial Cell–Specific Deletion of Transcription Factor FoxM1 Increases Urethane-Induced Lung Carcinogenesis
Authors: David Balli, Yufang Zhang, Jonathan Snyder, Vladimir V. Kalinichenko, Tanya V. Kalin
Journal: Cancer Research (2011)

Abstract Vascular endothelial cells provide essential support to the tumor microenvironment, but little is known about the transcriptional control of endothelial functions during tumorigenesis. Here we define a critical role for the Forkhead transcription factor FoxM1 in modulating the development of tumor-associated endothelial cells. Pulmonary tumorigenesis induced by urethane administration was compared in mice genetically deleted for FoxM1 in endothelial cells (enFoxm1−/− mice). Notably, lung tumor number and size were increased in enFoxm1−/− mice. Increased tumorigenesis was associated with increased proliferation of tumor cells and increased expression of c-Myc and cyclin D1. Furthermore, perivascular infiltration by inflammatory cells was elevated and inflammatory cells in BAL fluid were increased. Expression of Flk-1 (vascular endothelial growth factor receptor 2) and FoxF1, known regulators of pulmonary inflammation, was decreased in enFoxm1−/− mice. siRNA-mediated knockdown of FoxM1 in endothelial cells reduced Flk-1 and FoxF1 expression, which was driven by direct transcriptional induction by FoxM1 as target genes. Endothelial specific deletion of FoxM1 in vivo or in vitro also decreased expression of Sfrp1 (secreted frizzled-related protein 1), a known inhibitor of canonical Wnt signaling, in a manner that was associated with increased Wnt signaling. Taken together, our results suggest that endothelial-specific expression of FoxM1 limits lung inflammation and canonical Wnt signaling in lung epithelial cells, thereby restricting lung tumorigenesis. Cancer Res; 71(1); 40–50. ©2011 AACR.
Amodiaquine and Hepatitis
Authors: B. HIRSCHEL
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 September 1986Amodiaquine and HepatitisB. HIRSCHEL, M.D.B. HIRSCHEL, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-3-467_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Prophylaxis of malaria by amodiaquine is dangerous (1, 2). At least 20 cases of amodiaquine-associated agranulocytosis have been discovered so far in Switzerland, and 12 of these were associated with hepatitis. Six were fatal (Drs. Neftel and Somaini. Personal communication). The following case reports suggest that the drug is not only toxic but also may not prevent malaria even in areas of low chloroquine resistance.Patient 1:A 32-year-old man visited Cameroon from 24 December 1985 to 10 January 1986. He had taken amodiaquine (Camoquin; Parke-Davis, Morris Plains, New Jersey), 400 mg/wk, until January 17th. On the...References1. HATTONPETOBUNCH CTC. Frequency of severe neutropenia associated with amodiaquine prophylaxis against malaria. Lancet. 1986;1:411-4. CrossrefMedlineGoogle Scholar2. LARREYCASTOTPESSAYRE DAD. Amodiaquine-induced hepatitis: a report of seven cases. Ann Intern Med. 1986;104:801-3. LinkGoogle Scholar3. WATKINSSIXSMITHSPENCER WDH. Effectiveness of amodiaquine as treatment for chloroquine-resistant Plasmodium falciparum malaria infections in Kenya. Lancet. 1984;1:357-9. CrossrefMedlineGoogle Scholar4. COOSMANSHENDRIXBARUTWANAYO MLM. Pharmacorésistance de Plasmodium falciparum au Burundi. Bull OMS. 1985;63:331-8. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: B. HIRSCHEL, M.D.Affiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAmodiaquineAntiprotozoal drugs 1 September 1986Volume 105, Issue 3Page: 467-467KeywordsChloroquineDrugsHepatitisMalariaProphylaxis ePublished: 1 December 2008 Issue Published: 1 September 1986 PDF downloadLoading ...
High affinity binding of 125I-labeled human tumor necrosis factor (LuKII) to specific cell surface receptors.
Authors: B Y Rubin, S L Anderson, S A Sullivan, B D Williamson, E A Carswell, L J Old
Journal: The Journal of Experimental Medicine (1985)

125I-labeled TNF(LuKII) (tumor necrosis factor) binds specifically to human and mouse cell lines sensitive to the cytotoxic effect of TNF, but not to cells made resistant to TNF. TNF-sensitive cells have cell surface receptors with a high affinity for TNF(LuKII). Mouse TNF competes with TNF(LuKII) for receptor binding. Scatchard analysis of the binding data yielded linear plots and suggests that TNF(LuKII) binds to homogeneous receptor sites. The number of TNF(LuKII) receptors on two TNF-sensitive cell lines is 200-300 per cell and the affinity constant of the receptor for TNF(LuKII) is approximately 1 X 10(-10) M.
The World in Medicine
Authors: Rebecca Voelker
Journal: JAMA (1997)

<h3>Focus on Disabled Children</h3> The United Nations Committee on the Rights of the Child will begin 1998 by developing an action plan to reform laws that result in maltreatment and isolation for the world's 140 million disabled children. During a planning meeting last month in Geneva, Switzerland, the committee noted that 1 of every 10 children has some type of physical, mental, sensory, intellectual, or psychological disability caused by preventable disease, malnutrition, unintentional injury, armed conflict, or land mines. What's more, the committee observed, only 1% of the 300 million disabled children and adults who live in developing nations ever receive rehabilitation or other services that could help them lead healthier, more independent lives. But the denial of rights and acts of physical and sexual abuse directed toward disabled children are not restricted to poor nations. In many parts of the world, said a representative of the United Nations Children's
Reducing Dietary Intake of Fat and Cholesterol in Children-Reply
Authors: Ronald M. Lauer
Journal: JAMA (1995)

In Reply.  —The correspondents appear to agree that the relationship between diet and heart disease is causal and reducing dietary fat will reduce heart disease risk in adults, but they question whether dietary recommendations are appropriate for children and whether the  magnitude of the dietary effect found in DISC is of importance.  On a population level, it has been estimated that a mean change of -0.09 mmol/L (-3.3 mg/dL), or a net 2.5% reduction in LDL-C, is associated with a 5% to 7.5% reduction in CHD risk. 1 Such small changes translate into large numbers for highly prevalent conditions such as elevated LDL-C and high incident conditions like CHD. Also, the net change of 0.08 mmol/L (3.23 mg/dL) represents an average. Included in this average are the results of intervention children who were not adherent to the DISC diet as well as the results of nonintervention children who changed
Allergen-specific challenge induces intercellular adhesion molecule 1 (ICAM-1 or CD54) on nasal epithelial cells in allergic subjects. Relationships with early and late inflammatory phenomena.
Authors: G Ciprandi, C Pronzato, V Ricca, G Passalacqua, M Bagnasco, G W Canonica
Journal: American Journal of Respiratory and Critical Care Medicine (1994)

Intercellular adhesion molecule 1 (ICAM-1 or CD54) expression on epithelial cells (EC) has been demonstrated to play a role in the local molecular events of inflammation following allergen-specific conjunctival challenge. In the light of these observations, we evaluated the possible expression of ICAM-1 on nasal EC after allergen-specific challenge. Three groups of subjects were studied: (1) 14 symptomless patients sensitized to mites, (2) 15 symptomless patients sensitized to pollen, and (3) 10 healthy volunteers as controls. The study was performed during winter. At baseline we found that both pollinosic and healthy subjects did not express CD54 on epithelial cells, whereas mite-sensitive patients showed a mild expression (possibly caused by a persistent natural allergen exposure). In addition, clinical and cellular responses were induced by lower allergen dosages in mite-sensitive patients compared with pollen-sensitive patients. CD54 was detectable in all the allergic patients but not in the control subjects 30 min after challenge. At 6 h all patients showed a marked inflammatory infiltration and CD54 persistence on EC: such an infiltration was more relevant in patients developing clinical late-phase reaction (LPR). Finally, 24 h after challenge EC CD54 expression persisted, as well as a cellular infiltrate mainly caused by eosinophils (the latter being more pronounced in mite-sensitive individuals). CD54 should be regarded as an early and sensitive marker of inflammation in both LPR-positive and LPR-negative patients. A cellular inflammatory infiltrate was detectable in both LPR-positive and LPR-negative subjects, although relevant differences in eosinophil counts were observed between the two groups. The study emphasizes the importance of the different events of inflammation in allergy.
Inhibition of the SDF-1α–CXCR4 axis by the CXCR4 antagonist AMD3100 suppresses the migration of cultured cells from ATL patients and murine lymphoblastoid cells from HTLV-I Tax transgenic mice
Authors: Akira Kawaguchi, Yasuko Orba, Takashi Kimura, Hidekatsu Iha, Masao Ogata, Takahiro Tsuji, Akira Ainai, Tetsutaro Sata, Takashi Okamoto, William W. Hall, Hirofumi Sawa, Hideki Hasegawa
Journal: Blood (2009)
Brain failure in private and public life.
Authors: W Gooddy
Journal: BMJ (1979)

I suspect that there is one matter on which all human beings would agree, whatever their racial, religious, or political beliefs: that so long as life is desirable we must strive and succeed in keeping our brains at a high level of excellence of performance.In our professional lives as doctors we are often reminded how precarious this achievement is.We see the demented; the mentally defective; the psychotic; the depressed; the addict; the hallucinated; the hemiplegic, perhaps with a language disturb- ance; or organically or psychiatrically ill patients with space- time disorientation.It is difficult to know into which or how many of these diagnostic groups we should classify the politician who regularly shows defective judgment, heart failure, stroke, alcoholism, psychopathy; the religious or political fanatic, who may also be a head of state; the public figure who has furthered his ends by corruption; or the maintainers of outmoded dogmas who have the power to inflict misery on countless millions of life hours.Socially we may be aware of the troublemaker, the neurotically indecisive personality, again the alcoholic, the unscrupulous, or the "drop out."The situation is clearest of all in ourselves, when we are at a loss for an idea, a word, or a name. An unavoidable and increasing problemOf the many reasons for concentrating on the subject of brain failure the first is the most delicate-the personal reason.If we succeed in giving up drinking, smoking, and eating butter; keeping slim; avoiding a sluggish bowel; wearing a seat belt and crash helmet; reacting only homoeostatically to the news of plutonium in the *Based on the 17th Victor Horsley memorial lecture given at Ur*ersitv College Hospital on 23 November 1978.laundry or a locked car in one's parking space; and if we thereby avoid cancer, coronaries, strokes, traffic accidents, and suicide, we are all bound to decline into one of the most terrible of all medical fates- brain failure.
Familial amyloidosis: Great progress for an orphan disease
Authors: Ana Paula Barreiros, Gerd Otto, Bita Kahlen, Andreas Teufel, Peter R Galle
Journal: Journal of Hepatology (2014)

Familial amyloidosis: Great progress for an orphan disease Ana Paula Barreiros1,2,*, Gerd Otto3, Bita Kahlen1, Andreas Teufel1,2, Peter R. Galle1 1Department of Internal Medicine I, Universitatsmedizin of the Johannes Gutenberg-University Mainz, Germany; 2Department of Internal Medicine I, Universitatsklinikum of the University Regensburg, Germany; 3Department of Hepatobiliary and Transplantation Surgery, Universitatmedizin of the Johannes Gutenberg-University Mainz, Germany. *Corresponding author. Address: Universitatsklinikum Regensburg, Department of Internal Medicine I, Franz-Josef-Strauss Allee 11, 93053 Regensburg, Germany. Tel.: +49 941-944-7021. E-mail address: Ana.Barreiros@ukr.de (A. P. Barreiros).
MEMBERSHIP IN THE BRITISH MEDICAL ASSOCIATION
Authors: George F. Lull
Journal: JAMA (1952)

To the Editor:  —The secretary of the British Medical Association has informed me that a number of their members are working for oil companies in the Persian Gulf area and that there is a branch of the British Medical Association in that part of the world; in fact, it is 30 years of age.  The British Medical Association has recently decided to extend the boundaries of this branch so as to include all the territory surrounding the Persian Gulf. This branch, which will be known as the Middle East Branch of the British Medical Association, will arrange regular scientific meetings and social gatherings, mostly in Basra.  As there are a number of American physicians working around the Persian Gulf, the British Medical Association has informed me that if these physicians desire to become associate or complimentary members of the Middle East Branch they will be warmly welcomed. They should address
Observations ON THE ELEMENTS OF THE PSYCHO-NEUROSES: A Paper addressed to the Society of Medical Officers of the Pensions Board, Lancaster Gate, London
Authors: H. Head
Journal: BMJ (1920)

fT would be an impertinence on my part to talk to you of thle treatment of war pensioners, for each of you is more practised tlhan I am in this class of work.But I venture to approacli you to-day because I believe your experience vvill be of inestimable advantage in the more difficult task Df understanding thie psyclho-neuroses of civilian life.
High-Speed Chases to High-Powered Squirters, Moving Traffic Violations Pose Variety of Threats
Authors: Phil Gunby
Journal: JAMA (1992)

HIGH-SPEED PURSUIT of a smuggler last month by Immigration and Naturalization Service border patrol officers led to the death of six Californians hit by the vehicle being chased. <h3>'Hot Pursuit'</h3> Such "hot pursuit," says the Washington, DC—based Automobile Association of America Foundation for Traffic Safety, occurs an estimated 50 000 times and results in more than 300 deaths and some 20000 injuries annually in this country. The foundation bases these estimates on data from a study by Illinois State University (Normal) researchers who, like investigators in South Carolina and Florida, note that comparatively minor suspected offenses often are involved. Besides more clear-cut policies on when officers may undertake pursuit, Illinois researchers Michael T. Charles, PhD, David N. Falcone, PhD, and Edward Wells, PhD, recommend additional training in emergency vehicle handling and careful monitoring of this aspect of police work. They also suggest use of video and still cameras by police
Zonal differences in ethanol-induced impairments in receptor-mediated endocytosis of asialoglycoproteins in isolated rat hepatocytes
Authors: Carol A. Casey, Sandra L. Kragskow, Michael F. Sorrell, Dean J. Tuma
Journal: Hepatology (1991)

We have shown previously that ethanol-induced defects in receptor-mediated endocytosis of asialoorosomucoid occurred as early as 1 wk after ethanol feeding. This study was undertaken as an initial attempt to establish a possible role of defective receptormediated endocytosis in liver injury by investigating whether differences exist in the effects of ethanol on receptor-mediated endocytosis in hepatocytes isolated from different regions of the liver. Perivenule cells, present in the distal half of the liver, are thought to be more susceptible to ethanol-induced liver injury than are the periportal cells located in the proximal half of the liver acini. For these studies, we fed male Sprague-Dawley rats for 7 days with liquid diets containing either ethanol (36% of calories) or isocaloric carbohydrate. Perivenule and periportal hepatocytes were then isolated using a digitonin-collagenase perfusion method. In control animals, cells isolated from the perivenule region bound significantly more ligand than did cells from the periportal region. Amounts of ligand internalized and degraded were also greater in perivenule than in periportal cells in these animals. After ethanol feeding, cells isolated from both the perivenule and periportal regions bound significantly less ligand than their respective controls. This impairment in surface and total binding was more pronounced in perivenule than in periportal cells. Internalization and degradation of the ligand were also more adversely affected in the centrilobular region as shown by decreases of greater than 60% in perivenule cells and by only 20% to 30% in periportal cells of ethanol-fed animals compared with controls. Receptor recycling was impaired in the perivenule region by ethanol administration as shown by receptor cycle times that were significantly prolonged in cells from the perivenule region but were relatively unchanged in periportal cells. These results indicate that ethanolinduced impairments in receptor-mediated endocytosis are more dramatic in the perivenule region of the liver, thus suggesting a potential role of defective receptor-mediated endocytosis in ethanol-induced liver injury. (Hepatology 1991;13:260—266).
Both Intravenous and Inhaled Lidocaine Attenuate Reflex Bronchoconstriction but at Different Plasma Concentrations
Authors: HARALD GROEBEN, MARIE-THERES SILVANUS, MECHTHILD BESTE, JÜRGEN PETERS
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Intravenous lidocaine can attenuate bronchial hyperreactivity. However, lidocaine inhalation might yield the same or better results at higher airway and lower lidocaine plasma concentrations. Therefore, we tested in awake volunteers with bronchial hyperreactivity the effect of lidocaine on histamine-induced bronchoconstriction administered either intravenously or as an aerosol. After approval of the local ethics committee, 15 volunteers were enrolled in this placebo-controlled, double-blinded, randomized study. Volunteers were selected by showing a decrease in FEV1 greater than 20% of baseline (PC20) in response to histamine inhalation. On three different days the challenge was repeated after pretreatment with either intravenous lidocaine, inhaled lidocaine, or placebo. Blood samples for determination of lidocaine plasma concentration were drawn. Comparisons were made using the Friedman and Wilcoxon signed-rank tests. Baseline PC20 was 6.4 ± 1.1 mg · ml− 1. Both inhalation of lidocaine and intravenous administration significantly increased PC20 to 14.8 ± 3.5 mg · ml− 1 and 14.2 ± 2.5 mg · ml− 1, respectively (p = 0.0007). Peak plasma lidocaine concentrations at the end of challenges were 0.7 ± 0.1 μ g · ml− 1 (inhaled) and 2.2 ± 0.1 μ g · ml− 1 (i.v.). However, 7 of 15 subjects showed an initial decrease of FEV1 greater than 5% following lidocaine inhalation. While both intravenous as well as inhaled lidocaine attenuate reflex bronchoconstriction significantly, lidocaine plasma concentrations are significantly lower after inhalation. However, the high incidence of initial bronchoconstriction to lidocaine inhalation may limit its use in patients with asthma and thus offers therapeutic advantages for intravenous lidocaine.