tbuckley/cabot-search huggingface dataset:
SELECTIVE ADRENAL NECROSIS AND APOPLEXY INDUCED BY 7,12-DIMETHYLBENZ(a)ANTHRACENE
Authors: Charles Huggins, Sotokichi Morii
Journal: The Journal of Experimental Medicine (1961)

Invariably in every normal rat a single dose of 7, 12-dimethylbenz(a)anthracene, by mouth or injected in a vein, was found to cause apoplexy and massive necrosis in the inner zones of the adrenal cortex; the zona glomerulosa, the adrenal medulla, and a small region of cortex adjacent to the great adrenal vessels were spared from damage. DMBA caused these selective lesions in females and in males of 2 strains of rats. Hemorrhage and necrosis were observed in no organ other than the adrenal gland. Whereas adrenal glands were heavily damaged by DMBA, pituitary and ovary escaped injury by the compound. A single huge but sublethal feeding of o, p'-DDD caused degenerative changes of minor magnitude in the adrenals and only in a small percentage of rats; the property of inducing adrenal damage was not shared by other polynuclear aromatic hydrocarbons which were investigated, including strong carcinogens. Presence of adrenal medulla is not a prerequisite to damage of the adrenal cortex by DMBA. The adrenal damage occurred in rats, given DMBA, from which the pituitary had been removed but the lesions were smaller in extent and less in incidence as post-hypophysectomy atrophy of the adrenal cortex progressed. The entire DMBA molecule was necessary to induce adrenal damage; fragments of this molecule did not induce adrenal lesions. Two components which are of cardinal importance in this specific damaging effect are: (a) electronic factor; (b) steric factor. The level of isocitric dehydrogenase in adrenal is modified considerably by presence or absence of estradiol-17beta.
Book Review The Early Diagnosis of the Acute Abdomen. By Sir Zachary Cope, B.A., M.D., M.S. (Lond.), F.R.C.S. (Eng.). Twelfth edition. 8°, cloth, 10 + 196 pp., with 36 figures, 8 plates and a colored frontispiece. London: Oxford University Press, 1963. $5.50.
Authors: Henry R. Viets
Journal: New England Journal of Medicine (1963)
The Multichain Interleukin 2 Receptor
Authors: Thomas A. Waldmann
Journal: JAMA (1990)

<h3>SELECTED CASE</h3> A 24-YEAR-OLD black man developed nodules on the face and the anterior part of the chest. The nodules were non-tender and a biopsy showed epidermal infiltration with lymphoid cells that possessed convoluted nuclei. The patient also had repeated infections and sepsis and was referred to the National Institutes of Health. A second lymph node biopsy revealed malignant lymphoma recognized to represent human T-cell lymphotropic virus type I (HTLV-I)-related adult T-cell leukemia/lymphoma (ATL). This diagnosis was supported by the finding of high titers of antibodies to HTLV-I in the peripheral blood and the identification of HTLV-I provirus in the genome of the patient's malignant peripheral blood lymphocytes. The patient developed overt leukemia, with a total peripheral white blood cell count of 27 × 10<sup>9</sup>/L, 75% of which were malignant lymphocytes. He also had hypercalcemia and elevated serum levels of alkaline phosphatase and lactic dehydrogenase, typical features of
Redox manipulation using the thiol-oxidizing agent diethyl maleate prevents hepatocellular necrosis and apoptosis in a rodent endotoxemia model
Authors: Julia J. Jones, Jie Fan, Avery B. Nathens, Andras Kapus, Mark Shekhman, John C. Marshall, Jean Parodo, Ori D. Rotstein
Journal: Hepatology (1999)

Manipulation of the intracellular redox state has been shown to alter cell activation pathways with resultant changes in cellular function. Previous studies have suggested that thiol oxidation, using the glutathione-depleting agent diethyl maleate (DEM), was able to inhibit endothelial cell activation. We hypothesized that this agent might exert beneficial effects following endotoxemia in the rat, a model in which transendothelial migration of neutrophils is central to the development of hepatocellular injury. Sprague-Dawley rats treated intraperitoneally with lipopolysaccharide (LPS) (200 μg/kg) plus d -galactosamine (GalN) (600 mg/kg) developed hepatocellular necrosis, as evidenced by liver enzyme release and morphological changes. Pretreatment with DEM abrogated this injury in a dose-dependent fashion. Histology revealed reduced neutrophil accumulation in both the parenchyma and sinusoids, consistent with reduced neutrophil sequestration and transendothelial migration. This effect appeared to be related to the ability of DEM to prevent LPS-induced up-regulation of both vascular cell adhesion molecule-1 (VCAM-1) mRNA and intercellular adhesion molecule-1 (ICAM-1) mRNA in the liver, as well as reducing tumor necrosis factor (TNF) mRNA expression. In addition, DEM prevented hepatocyte apoptosis following LPS treatment. The effect was reproduced when TNF was used as an inflammatory stimulus, suggesting a direct protective effect on the hepatocyte. Taken together, these studies show that redox manipulation through thiol oxidation may represent a novel approach to preventing liver necrosis and apoptosis in inflammatory conditions.
Endoscopic ultrasound-guided application of a new hybrid cryotherm probe in porcine pancreas: a preliminary study
Authors: S. Carrara, P. Arcidiacono, L. Albarello, A. Addis, M. Enderle, C. Boemo, M. Campagnol, A. Ambrosi, C. Doglioni, P. Testoni
Journal: Endoscopy (2008)

See also: Commentaire de travail de S. Carrara et al., pp. 321Endoscopy 2008; 40(04): 453-453DOI: 10.1055/s-0032-1306829
CONTACT GLASS OR CROSSED CYLINDERS FOR HIGH ASTIGMATISM
Authors: J. H. Beaumont
Journal: BMJ (1931)

_~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ nni(l vessels in the great, ancd also in the gastro-splenic, ometntum.Stomach, suprarenals, pancreas, kidulcys, and upper inltestinie appear fairly normal on macroscopic examinia- tion.Lower intestine: Acute congestion of the ileum.No ulcers.No s velling of Peyer's patches.Acute congestion of ileum opening inito the caecum.Some little congestion of the ascentdinig coloii.Transverse, descen(dinig, and pelvic colon normal.Lungs: Left-broncho-pneumoniia of both lol)es, the low,er more marked.Right-lower lobe consolidated, marked broncho-pneumonia; upper lobe partly consoli(lated and in samne condition.Culture from gall-bladder contents grewr a pure growth of Bacillus ptAratyphtosus B WVidal serum agglutinates B. paratyplhosus B in dilution of 1 in 2,5(00 B. typhosus, nil.Microscopical Sections.-
PRESENT STATUS OF THE BIOPSY
Authors: A. B. McGRAW
Journal: JAMA (1933)

Notwithstanding the advances which are steadily taking place in knowledge of the chemistry, serologic nature and biology of tumors, gross morphology and, more especially, microscopic morphology remain our best means of determining their histogenesis, classification, activity and prognosis. The diagnostic application of this morphologic knowledge lies in the procedure known as biopsy. Though this word strictly includes the removal of any tissue from a living subject for diagnostic examination, usage has tended to confine it to the examination of tumor tissue suspected of having malignant qualities.  About the middle of the nineteenth century the idea of biopsy began to be voiced in independent reports or suggestions by various authors here and abroad, among them Sedillot, 1 Marmy 2 and Lebert 3 in France, Hannover 4 in Denmark and Donaldson 5 in this country. It was Virchow, 6 however, who first laid the rational foundation of the procedure as a diagnostic
Abstract 2866: Functional impairment of microRNAs induced by chronic inflammation is the cause of inflammation-associated colon tumorigenesis.
Authors: Takeshi Yoshikawa
Journal: Cancer Research (2013)

Abstract Background: A widespread downregulation of microRNAs is commonly observed in human cancers and is involved in cellular transformation and tumorigenesis. Because we previously reported that microRNA functions are inhibited under various kinds of cellular stresses including inflammatory cytokines in vitro, we hypothesized that chronic inflammation in vivo may also cause chronic functional impairment of microRNAs, which mimics a global reduction of microRNA abundance, resulting in a causal role in inflammation-associated tumorigenesis. Methods &amp; Results: 1) To examine this hypothesis, we first confirmed the functional impairment of microRNAs under inflammatory stimuli in vitro using artificial reporter constructs. The derepression of microRNA-targeting reporter activities by inflammatory stimuli could also be observed using reporter constructs containing natural 3’UTR sequences of c-myc and Lin28B genes, which are targeted by endogenous let-7. 2) Next, we constructed reporter transgenic mice bearing CMV-promoter driven GFP construct carrying target sequences of microRNAs in its 3’UTR, and monitored the changes of microRNA functions in vivo during the course of a Dextran Sulfate Sodium (DSS) induced colitis-associated colon tumor model. The expression levels of GFP were significantly increased during colitis, suggesting that microRNA functions were impaired during the chronic inflammation in vivo. The expression levels of microRNA-target oncogenes such as c-myc and Lin28B in the colonic mucosa were indeed upregulated. 3) Lastly, to determine the consequences of the global functional impairment of microRNAs during the colitis, we examined Dicer-deficient mice, which have globally low levels of microRNA expression and may mimic the functional impairment of global microRNAs induced by chronic inflammation described above. As expected, Dicer deficient mice were more liable to have the colitis-associated tumors. This indicates that the global decrease of microRNAs leads to oncogenesis, suggesting that the functional impairment of global miRNAs during chronic inflammation can also be a cause of the inflammation-associated carcinogenesis. Conclusion: In conclusion, we propose a novel concept that the attenuation of global microRNA functions by chronic inflammation is the cause of inflammation-associated tumorigenesis. Citation Format: Takeshi Yoshikawa. Functional impairment of microRNAs induced by chronic inflammation is the cause of inflammation-associated colon tumorigenesis. [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 2866. doi:10.1158/1538-7445.AM2013-2866
Treatment of Erythema Migrans
Authors: Benjamin J. Luft
Journal: Annals of Internal Medicine (1997)

Letters1 March 1997Treatment of Erythema MigransBenjamin J. Luft, MDBenjamin J. Luft, MDState University of New York at Stony Brook, Stony Brook, NY 11794Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-126-5-199703010-00015 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Dr. Collins's point is well taken, especially given the nature of Lyme disease, which is complicated by a lack of microbiological markers of infection and cure. It was our intention to underscore the difficulty of comparing these many, often small, Lyme disease trials, which use different designs and analyses as well as variable definitions of clinical end points. These “striking contrasts” may in fact be due more to differences in study design than to antimicrobial activity. However, until a careful, double-blind, randomized trial of the various oral antimicrobial agents is done, it is impossible to determine the optimal ... Author, Article, and Disclosure InformationAuthors: Benjamin J. Luft, MDAffiliations: State University of New York at Stony Brook, Stony Brook, NY 11794 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1997Volume 126, Issue 5Page: 408-409KeywordsAntimicrobialsClinical trialsErythemaInfectious diseasesLyme diseaseRandomized trials ePublished: 15 August 2000 Issue Published: 1 March 1997 Copyright & PermissionsCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Effect of myocardial ischemia on stimulation-evoked noradrenaline release. Modulated neurotransmission in rat, guinea pig, and human cardiac tissue.
Authors: M Seyfarth, Y Feng, S Hagl, F Sebening, G Richardt, A Schömig
Journal: Circulation Research (1993)

The effect of myocardial ischemia and its major metabolic changes, such as anoxia, acidosis, and hyperkalemia, on exocytotic noradrenaline release was investigated in rat, guinea pig, and human cardiac tissue. Noradrenaline release was evoked by electrical field stimulation, and the effect of each experimental intervention on stimulation-evoked noradrenaline release (S2) was intraindividually compared with the release induced by a control stimulation (S1). In perfused hearts, 10 minutes of global ischemia caused a reduction of noradrenaline overflow in rat hearts (mean S2/S1, 0.31), whereas the overflow was increased in guinea pig hearts (S2/S1, 1.89). This species-dependent effect may be caused by quantitatively different responses to facilitating and suppressing factors of noradrenaline release in both species. Anoxia and substrate-free perfusion increased noradrenaline overflow in guinea pig hearts (S2/S1, 2.40) but had no significant effect in rat hearts (S2/S1, 0.75). Acidosis (pH 6.0) resulted in a suppression of noradrenaline release in rat hearts (S2/S1, 0.16), whereas it had only a minor inhibiting effect in guinea pig hearts (S2/S1, 0.67). Hyperkalemia had a comparable effect in both species (S2/S1 at 15 mmol/L K+, 1.17 in rat and 1.14 in guinea pig; and S2/S1 at 20 mmol/L K+, 0.64 in rat and 0.41 in guinea pig). To obtain results regarding the modulation of noradrenaline release in human myocardium, human atrial tissue was incubated, and the effect of anoxia, acidosis, and hyperkalemia on stimulation-evoked noradrenaline release was investigated.(ABSTRACT TRUNCATED AT 250 WORDS)
Genetic Alterations in the Phosphoinositide 3-Kinase/Akt Signaling Pathway Confer Sensitivity of Thyroid Cancer Cells to Therapeutic Targeting of Akt and Mammalian Target of Rapamycin
Authors: Dingxie Liu, Peng Hou, Zhi Liu, Guojun Wu, Mingzhao Xing
Journal: Cancer Research (2009)

Abstract We investigated the genotype-dependent therapeutic potential of targeting the phosphoinositide 3-kinase (PI3K)/Akt pathway for thyroid cancer. Proliferation of TPC1, Hth7, FTC133, OCUT1, K1, and BCPAP cells that harbored PI3K/Akt-activating genetic alterations was potently inhibited by the Akt inhibitor perifosine, whereas SW1736, Hth74, WRO, KAT18, and TAD2 cells that harbored no genetic alterations had no or only modest responses. Inhibition of Akt phosphorylation by perifosine was seen in these cells. Genetic-dependent apoptosis was induced by perifosine in cells selectively tested. Similarly, potent inhibition of cell proliferation by the mammalian target of rapamycin (mTOR) inhibitor temsirolimus occurred in virtually all the cells harboring genetic alterations, whereas modest inhibition was seen in some of the cells not harboring genetic alterations. Temsirolimus inhibited the phosphorylation of p70S6K, a substrate of mTOR. Knockdown of Akt1/2 or mTOR by shRNA approach inhibited the proliferation and colony formation of FTC133 and OCUT1 cells that harbored genetic alterations in the PI3K/Akt pathway but had no effect on SW1736 and KAT18 cells that did not. Transfection with PIK3CA mutants greatly sensitized SW1736 cells to perifosine and temsirolimus. Growth of xenograft tumors derived from FTC133 cells but not SW1736 cells in nude mice was dramatically inhibited by perifosine. Thus, this work for the first time shows that genetic alterations in the PI3K/Akt pathway confer thyroid cancer cells addiction to this pathway and their sensitivity to inhibition by targeting Akt and mTOR. This genotype-based targeting of the PI3K/Akt pathway using Akt and mTOR inhibitors may offer an effective therapeutic strategy for thyroid cancer and warrants further studies. [Cancer Res 2009;69(18):7311–9]
Atrial Fibrillation — Risk Marker for Stroke
Authors: James H. Chesebro, Valentin Fuster, Jonathan L. Halperin
Journal: New England Journal of Medicine (1990)

Atrial fibrillation not related to valvular heart disease (nonvalvular atrial fibrillation) is associated with nearly half the arterial emboli presumed to be of cardiac origin. It starts at a mean age of 64 years, affects 2 to 5 percent of the general population over the age of 60 (more than 1 million people), and is associated with a fivefold increase in the risk of ischemic stroke and a 5 to 7 percent yearly risk that increases with age. Cerebral infarction eventually occurs in up to 35 percent of patients with nonvalvular atrial fibrillation. The risk is even higher if "silent" . . .
Hint1 Inhibits Growth and Activator Protein-1 Activity in Human Colon Cancer Cells
Authors: Lin Wang, Yujing Zhang, Haiyang Li, Zhiheng Xu, Regina M. Santella, I. Bernard Weinstein
Journal: Cancer Research (2007)

Abstract There is accumulating evidence that histidine triad (HIT) nucleotide-binding protein 1 (HINT1), a member of the evolutionary highly conserved HIT protein super family, is a novel tumor suppressor. However, the mechanism of action of HINT1 with respect to tumor suppression is not known. In the present study, we found that a series of human colon cancer cell lines displayed various levels of expression of HINT1, with a very low level in SW480 cells. This cell line also displayed partial methylation of the promoter region of the Hint1 gene, and treatment of these cells with 5-azadeoxycitidine increased expression of Hint1 mRNA and protein. Therefore, the decreased expression of HINT1 in SW480 cells seems to be due to epigenetic silencing. Increased expression of HINT1 in these cells, using a retrovirus vector (pLNCX2) that encodes either wild-type (WT) Hint1 or a point mutant (His112/Asn112) of Hint1, inhibited the proliferation of SW480 cells. Because of the important role of the activator protein-1 (AP-1) transcription factor in cancer cells, we examined possible effects of HINT1 on AP-1 transcription factor activity in SW480 cells transfected with an AP-1-luciferase reporter. We found that cotransfection with a pHA-Hint1 plasmid DNA significantly inhibited this activity. Studies with inhibitors indicated that AP-1 activity in SW480 cells requires the activity of c-Jun NH2-terminal kinase (JNK) 2 and not JNK1. Cotransfection with the Hint1 plasmid DNA also inhibited AP-1-luciferase reporter activity in WT mouse embryo fibroblast (MEF) studies, and studies with JNK1 deleted or JNK2 deleted MEFs confirmed the essential role for JNK2, but not JNK1, in mediating AP-1 activity. Recent studies indicate that the protein plenty of SH3 (POSH) provides a scaffold that enhances JNK activity. We found that cotransfection of a plasmid DNA encoding POSH stimulated the phosphorylation of c-Jun and also AP-1 reporter activity, and cotransfection with Hint1 inhibited both of these activities. Furthermore, coimmunoprecipitation studies provided evidence that HINT1 forms an in vivo complex with POSH and JNK. These results suggest that HINT1 inhibits AP-1 activity by binding to a POSH-JNK2 complex, thus inhibiting the phosphorylation of c-Jun. This effect could contribute to the tumor suppressor activity of HINT1. [Cancer Res 2007;67(10):4700–8]
Driving-Impaired Patients Leaving the Emergency Department
Authors: David L. Simel
Journal: Annals of Internal Medicine (1990)

We evaluated the frequency with which blood alcohol concentrations were obtained in emergency department patients with presumed alcohol impairment, whether physicians counseled impaired patients not to drive, and whether safe transportation was available.Retrospective chart review and search of the North Carolina Driver History file.Emergency departments of a university and affiliated Veterans Affairs Medical Center (VAMC).Consecutive adult patients at the university (n = 1554) and VAMC (n = 1461) emergency departments. Patients with presumed alcohol-induced impairment (university, 75; VAMC, 88) who did not require hospital admission were identified. Presumed alcohol-induced impairment was defined by any of the following: nurse or physician note specifying the patient was intoxicated; indication in the medical record that the patient had alcohol on their breath; claim by the patient of alcohol use the day of evaluation; or measurement of blood alcohol concentration.Blood alcohol concentrations were measured in 80% of presumed alcohol-impaired university patients (median blood alcohol concentration, 45 mmol/L) and 68% of VAMC patients (median blood alcohol concentration, 58 mmol/L). Driving skills deteriorate with blood alcohol concentrations of 11 mmol/L or greater; however, 63% of university and 88% of VAMC patients with measured blood alcohol concentrations of 11 mmol/L or greater were still impaired when discharged. Only 3.5% of university and 8.7% of VAMC patients impaired at discharge were advised not to drive, whereas 31% of university and 20% of VAMC patients impaired at discharge were supervised by a responsible person. The prevalence of previous driving-while-impaired convictions was high (university, 34%; VAMC, 58%).Presumed alcohol-impaired patients seen in emergency departments frequently have blood alcohol concentrations measured. Despite documented evidence of driving impairment there is little evidence that such patients are counseled not to drive or that safe transportation home is available.
Cellular survival pathways and resistance to cancer therapy
Authors: Phillip A. Dennis, Michael B. Kastan
Journal: Drug Resistance Updates (1998)

Chemotherapy and irradiation induce programmed cell death (apoptosis) in their target cells. Dysregulated apoptosis is a feature that is selected for during tumor formation and contributes to therapeutic resistance. Cell survival in the face of cytotoxic therapy is dictated by both internal properties of the cell, such as status of components of the apoptotic machinery, and its extracellular milieu, such as extracellular matrix (ECM) and growth factor receptor expression and signaling. The importance of extracellular survival signals as key regulators of apoptosis is now being recognized by the ability of growth factors (GFs), GF receptors (GFRs), and GFR signaling to promote cellular survival. GFs can mitigate or abrogate the effectiveness of cancer therapy and protect against other cellular insults. Because survival signals generated by different extracellular sources converge at key molecules, new molecular targets have been identified which could be exploited to maximize the effectiveness of cytotoxic cancer therapy.
ROENTGEN RADIATION NECROSIS OF LARYNX AND OTHER STRUCTURES OF THE NECK
Authors: PETER A. NELSON
Journal: JAMA (1935)

According to Hahn, 1 when irradiation in 1910-1912 replaced surgery in the treatment of tuberculosis of the neck, many patients suffered roentgen injuries of the throat. Even after the radiation had been reduced to three fourths of the toxic skin dose, patients so treated, after several weeks, became hoarse. Because these patients had no skin reaction, their hoarseness was not associated with the radiation therapy. As the number of patients with hoarseness increased and examinations of the larynx demonstrated an obstinate edema which lasted several weeks, radiation was recognized as the etiologic agent. The only reference to irradiation injury of the throat at that time, according to Hahn, was by Muhlmann, who had often noted a stubborn hoarseness in irradiated patients and, in two, a chronic laryngitis. Other reports of severe damage to the larynx and tissues of the neck by radiation were published in 1921 by Wetzel, 2 Holfelder,