tbuckley/cabot-search huggingface dataset:
Acne Conglobata and Arthritis
Authors: MORRIS ZIFF
Journal: Annals of Internal Medicine (1983)

Letters and Corrections1 March 1983Acne Conglobata and ArthritisMORRIS ZIFF, PH.D., M.D., JOHN MALIAKKAL, M.D.MORRIS ZIFF, PH.D., M.D., JOHN MALIAKKAL, M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-98-3-417_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In the article of Rosner and associates (1), 10 patients with spondyloarthropathy associated with acne conglobata or hydradenitis suppurativa were reported. Previous cases of acne conglobata with arthritis reported in the literature were described as being cases of acne fulminans instead. We wish to point out that the first patient reported with acne conglobata and arthritis (2) was correctly diagnosed. The acne lesions, as described in the original paper, were characterized by the presence of multiple, double and single comedones, cystic papules and abscesses, many of which were interconnected by dissecting fistulae. Ulcerative skin lesions were absent....References1. ROSNER I, RICHTER D, HUETTNER T, KUFFNER G, WISNIESKI J, and BURG C. Spondyloarthropathy associated with hidradenitis suppurativa and acne conglobata. Ann Intern Med. 1982;97:520-5. LinkGoogle Scholar2. WINDOM R, SANFORD J, and ZIFF M. Acne conglobata and arthritis. Arthritis Rheum. 1961;4:632-5. CrossrefMedlineGoogle Scholar3. KRAUSER R and SCHUMACHER H. The arthritis of Sweet's syndrome. Arthritis Rheum. 1975;18:35-41. CrossrefMedlineGoogle Scholar4. LAZARUS G, GOLDSMITH L, and ROCKLIN R. Pyoderma gangrenosum, altered delayed hypersensitivity and polyarthritis. Arch Dermatol 1972;105:46-51. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: MORRIS ZIFF, PH.D., M.D.; JOHN MALIAKKAL, M.D.Affiliations: The University of Texas Health Science Center Dallas, TX 75235 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAcne ConglobataMUSCULOSKELETAL FEATURES OF ACNE, HIDRADENITIS SUPPURATIVA, AND DISSECTING CELLULITIS OF THE SCALP 1 March 1983Volume 98, Issue 3 Page: 417-417 Keywords Abscesses Acne Arthritis Lesions ePublished: 1 December 2008 Issue Published: 1 March 1983 PDF downloadLoading ...
Abstract LB-279: Cancer cDNA resequencing with an exon-capture system
Authors: Toshihide Ueno, Yoshihiro Yamashita, Manabu Soda, Hiroyuki Mano
Journal: Cancer Research (2011)

Abstract While cancer is a genetic- and/or epigenetic-disorder, “driver” mutations in the cancer genome/epigenome are yet to be revealed for many cancer subtypes. A whole-genome resequencing should provide us with important information on this issue, but resequencing of multiple samples is still a demanding task. A recent introduction of the exon-capture systems has significantly facilitated the comprehensive resequencing of exonic regions that only occupy ∼1.5% of the human genome. However, such exon resequencing of cancer genome likely fails to identify fusion genes, since gene fusion usually takes place at introns. To efficiently discover gene fusions in addition to point mutations and indels, we here tried to resequence cDNAs of a given gene set by using a custom SureSelect system (Agilent Technologies). First we confirmed, by using the SureSelect X chromosome-purification kit, that capturing efficiency of cDNA is no worse than that of genomic DNA. Then we constructed a custom SureSelect system to capture cDNAs of cancer-related genes (n = 913 corresponding to ∼3.77 Mbp). Such cDNA capture system was then applied to a total of five cell lines of chronic myeloid leukemia. Deep sequencing of the purified cDNA fragments with Illumina Genome Analyzer IIx yielded the nucleotide information for an average of 54 million reads (= ∼4.1 Gbp) per sample. While BCR is not included in our custom SureSelect system, we could successfully isolate 38∼50 reads in each cell line encompassing the fusion points of the BCR-ABL1 cDNA, confirming the ability to detect gene fusions by our cDNA-capture system. A comparison of the read numbers in our data to the expression level defined by DNA microarray analyses has revealed a high concordance between the two data sets (Pearson's correlation coefficient = 0.73, P &amp;lt;2.2 × 10–16). Computational analyses of the read data that passed our quality filtering revealed a total of 199 non-synonymous point mutations on 155 independent genes. Further, we discovered a total of 15 (3 in-frame) independent insertions and 19 (6 in-frame) deletions. Among such mutation profiles, we could readily confirm the G-to-C substitution corresponding to the G266R amino acid change of TP53, one C insertion at nt position 604 of TP53, and one three-base deletion (nt = 894∼896) of TP53. These data confirm that a coupling of a sequence-based cDNA capture system to a next generation sequencer is a feasible approach to discover point mutations and fusions of target genes in the cancer genome. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-279. doi:10.1158/1538-7445.AM2011-LB-279
Genetics Is Coming to Oncology
Authors: David M. Livingston
Journal: JAMA (1997)

Picture the mechanisms that govern the behavior of a cell as an enormous puzzle. Each piece represents a critical function responsible for some aspect(s) of cellular behavior. In normal cells, all of the pieces fit perfectly. Those that touch one another represent communicating functions that carry vital chemical signals from one point to another in the cell. This function-to-function communication or signaling contributes to the normal control of growth and differentiation and the failure of a cell to develop neoplastic characteristics. In a cancer cell, some of the pieces do not fit, because of distortions of shape, size, or both. Others are lost altogether. Yet others are abnormally replicated, sometimes many times over. By comparison with that of a normal cell, the picture that emerges from a cancer cell puzzle is disorderly. However, it is still a picture of limited size and shape, and discoveries of the last 20 years
Zinc Treatment of Wilson's Disease
Authors: GEORGE J. BREWER
Journal: Annals of Internal Medicine (1984)

Letters and Corrections1 July 1984Zinc Treatment of Wilson's DiseaseGEORGE J. BREWER, M.D., GRETCHEN M. HILL, PH.D., ANANDA S. PRASAD, M.D., PARVIZ RABBANI, PH.D.GEORGE J. BREWER, M.D.Search for more papers by this author, GRETCHEN M. HILL, PH.D.Search for more papers by this author, ANANDA S. PRASAD, M.D.Search for more papers by this author, PARVIZ RABBANI, PH.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-101-1-144_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We are disturbed by some statements in the editorial by Dr. Deiss (1) in the issue in which our paper on zinc treatment of Wilson's disease (2) appeared.First, Dr. Deiss mistakenly states that we have confirmed that zinc therapy produces a negative copper balance in patients with Wilson's disease. There have not been previous reports on copper balance in patients during zinc treatment of Wilson's disease, so this is an original aspect of our work. One of our concerns has been that various physicians around the country are using zinc as an alternative to penicillamine for...References1. DEISS A. Treatment of Wilson's disease [Editorial]. Ann Intern Med. 1983;99:398-400. LinkGoogle Scholar2. BREWERHILLPRASADCOSSACKRABBANI GGAZP. Oral zinc therapy for Wilson's disease. Ann Intern Med. 1983;99:314-20. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: GEORGE J. BREWER, M.D.; GRETCHEN M. HILL, PH.D.; ANANDA S. PRASAD, M.D.; PARVIZ RABBANI, PH.D.Affiliations: The University of Michigan Medical School Ann Arbor, MI 48109 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byElevated copper impairs hepatic nuclear receptor function in Wilson’s diseaseExcretion of copper complexed with thiomolybdate into the bile and blood in LEC rats 1 July 1984Volume 101, Issue 1Page: 144-145KeywordsPatientsZinc ePublished: 1 December 2008 Issue Published: 1 July 1984 PDF downloadLoading ...
Misoprostol and Pregnancy
Authors: Alisa B. Goldberg, Mara B. Greenberg, Philip D. Darney
Journal: New England Journal of Medicine (2001)

Misoprostol is a prostaglandin E1 analogue that has been approved by the Food and Drug Administration (FDA) to be taken orally for the prevention and treatment of gastric ulcers associated with the use of nonsteroidal antiinflammatory drugs. It has also become an important drug in obstetrical and gynecologic practice because of its uterotonic and cervical-ripening actions. Misoprostol is useful for elective medical abortion, cervical ripening before surgical abortion, evacuation of the uterus in cases of embryonic or fetal death, and induction of labor. The drug may also be used to treat and even prevent postpartum hemorrhage. However, misoprostol is . . .
Interaction of signal transducer and activator of transcription 3 polymorphisms with hepatitis B virus mutations in hepatocellular carcinoma
Authors: Jiaxin Xie, Yuwei Zhang, Qi Zhang, Yifang Han, Jianhua Yin, Rui Pu, Qiuxia Shen, Wei Lu, Yan Du, Jun Zhao, Xue Han, Hongwei Zhang, Guangwen Cao
Journal: Hepatology (2013)

Hepatitis B virus (HBV) mutations and signal transducer and activator of transcription 3 (STAT3) activation are closely associated with hepatocellular carcinoma (HCC). However, single nucleotide polymorphisms (SNPs) of STAT3 have not been implicated in HCC susceptibility. This study was designed to evaluate the effect of STAT3 SNPs and their interactions with HBV mutations on HCC risk. A total of 2,011 HBV-infected subjects (including 1,021 HCC patients) and 1,012 healthy controls were involved in this study. SNPs rs4796793 (−1697, C>G), rs2293152 (intron 11, C>G), and rs1053004 (3′ untranslated region, T>C) were genotyped using quantitative polymerase chain reaction. HBV mutations were determined via direct sequencing. It was found that rs2293152 (GG versus CC) was significantly associated with HCC risk compared with the subjects without HCC, adjusting for age and sex (adjusted odds ratio [AOR], 1.30; 95% confidence interval [CI], 1.04-1.62). The impact of rs2293152 was greater in women compared with men. Compared with HCC-free HBV-infected subjects, rs2293152 GG was solely associated with HCC in women (AOR, 2.04; 95% CI, 1.15-3.61). rs2293152 GG was significantly associated with high viral load (≥1 × 104 copies/mL) (AOR, 1.37; 95%, CI 1.01-1.88) and increased frequencies of T1674C/G (AOR, 1.61; 95% CI, 1.06-2.46) and A1762T/G1764A (AOR, 1.64; 95% CI, 1.14-2.35). In multivariate regression analyses, multiplicative interaction of rs1053004 with T1674C/G significantly increased HCC risk, whereas rs2293152 and A1726C interaction reduced it, adjusting for covariates including HBV mutations in the enhancer II/basal core promoter/precore region; the interaction of rs4796793 with preS2 start codon mutation significantly increased HCC risk, adjusting for covariates including HBV mutations in the preS region. Conclusion: STAT3 SNPs appear to predispose the host with HBV mutations to hepatocarcinogenesis, and this effect may differ in men versus women. STAT3 SNPs may have applicability in future HCC surveillance algorithms. (Hepatology 2013;57:2369–2377)
S-phenylcysteine in albumin as a benzene biomarker.
Authors: W E Bechtold, M R Strunk
Journal: Environmental Health Perspectives (1996)

Biological markers of internal dose are useful for improving the extrapolation of health effects from exposures to high levels of toxic air pollutants in animals to low, ambient exposures in humans. Previous results from our laboratory have shown that benzene is metabolized by humans to form the adduct S-phenylcysteine (SPC). Levels of SPC measured in humans occupationally exposed to benzene were increased linearly relative to exposure concentrations ranging from 0 to 23.1 ppm for 8 hr/day, 5 days/week. However, the method of measurement used was laborious, prone to imprecision and interferences, and insufficiently sensitive for the low-dose exposures anticipated in the United States (100 ppb >). An improved chemical method was necessary before SPC adducts in albumin could be used as a benzene biomarker. A simple, sensitive method to measure SPC adducts is being developed and is based on the cleavage of the cysteine sulfhydryl from blood proteins treated with Raney nickel (RN) in deuterium oxide. The product of the reaction with SPC is monodeuterobenzene. SPC treated with RN released monodeuterobenzene in a concentration-dependent fashion. SPC was measured by RN treatment of globin from rats repeatedly exposed by inhalation to 600 ppm benzene. SPC levels measured using the RN approach were 690 +/- 390 pmol SPC/mg Hb (mean +/- % difference, n = 2), as opposed to 290 +/- 45 pmol SPC/mg Hb (mean +/- SEM, n = 3) as measured by our previous method. This method may facilitate the cost-effective, routine analysis of SPC in large populations of people exposed to ambient levels of benzene.
Contempo '81. Obstetrics-gynecology
Authors: E. C. Hill
Journal: JAMA (1981)

In considering advances of the past year in obstetrics and gynecology, three areas of clinical significance have been selected. They are (1) the use of ritodrine hydrochloride in preterm labor, (2) the increasing recognition of<i>Chlamydia trachomatis</i>as a significant pathogen in the female reproductive organs, and (3) the use of fine-needle aspiration biopsy in lieu of the more traditional methods of tissue sampling. Of course, these events did not occur during just the past year, but they gained considerable attention during 1980. <h3>Ritodrine</h3> Prematurity is the leading cause of perinatal morbidity and mortality. It has been estimated that about 8% of liveborn infants in the United States weigh less than 2,500 g. Many cases are the result of "accidents" of pregnancy such as abruptio placentae, premature rupture of the membranes, and placenta previa. A large number, however, are caused by labor that begins prematurely without known cause. It is
Ex-vivo perfusion of donor hearts for human heart transplantation (PROCEED II): a prospective, open-label, multicentre, randomised non-inferiority trial
Authors: Abbas Ardehali, Fardad Esmailian, Mario Deng, Edward Soltesz, Eileen Hsich, Yoshifumi Naka, Donna Mancini, Margarita Camacho, Mark Zucker, Pascal Leprince, Robert Padera, Jon Kobashigawa
Journal: The Lancet (2015)
10-minute consultation: Chronic low back pain
Authors: Jo Samanta, Julia Kendall, Ash Samanta
Journal: BMJ (2003)

A 40 year old man presents with a two year history of chronic low back pain. For the past week he has had an exacerbation of his symptoms and intermittent pain radiating down his right leg. Symptoms —Discuss the likely causes. Show him a diagram or model of the lumbar spine indicating the vertebrae, discs, and nerve roots. Explain that his leg pain is due to irritation of the nerve roots and that effective treatment should alleviate both his back pain and his leg pain. #### "Red flag" and "yellow flag" signs Red flags are possible indicators of serious spinal pathology:
Inhibitory effect of human fibroblast interferon (HuIFN-β) on the growth and invasive potential of cultured human melanoma cells in vitro
Authors: K. FUKUZAWA, T. HORIKOSHI
Journal: British Journal of Dermatology (1992)

The effect of HuIFN-beta on the invasive potential of melanoma cells was studied using an in-vitro model system with Transwell chambers equipped with matrigel-coated polycarbonate filters. When (10(2), 10(3) and 10(4) IU/ml) for 3 days and then grown in medium without HuIFN-beta for another 7 days. On day 7, the proliferation of melanoma cells was inhibited by 77 and 87%, respectively, when cells were treated with 10(2) and 10(4) IU/ml of HuIFN-beta. This antiproliferative effect was dose-dependent and more pronounced on day 11. The effect of HuIFN-beta on the invasive potential of melanoma cells was studied using an in-vitro model system with Transwell chambers equipped with Matrigel-coated polycarbonate filters. When cells were treated with HuIFN-beta (10(2), 10(3) and 10(4) IU/ml) for 24 h, the amount of tritiated thymidine incorporated into cells was increased, indicating that cell growth was not inhibited. However, the number of cells that invaded to the filter decreased significantly by 15-40%. HuIFN-beta did not have an inhibitory effect on the haptotactic migration of melanoma cells. These data indicate that the antiproliferative effect of HuIFN-beta occurs after 24 h and that the direct anti-invasive effect is independent of any effect on proliferation.
Cardiac causes of shock early after open heart surgery: etiologic classification by radionuclide ventriculography.
Authors: T M Bateman, L S Czer, R M Kass, M J Raymond, A Chaux, J M Matloff, D S Berman, R J Gray
Journal: Circulation (1985)

Early after open heart surgery, cardiac shock due to tamponade is easily misdiagnosed as ventricular dysfunction. The distinction is critical to successful therapy. We assessed the utility of 99mTc-red blood cell, gated equilibrium radionuclide ventriculography in 50 patients with early postoperative cardiac shock after historical, clinical, and invasive hemodynamic evaluation failed to identify either tamponade or ventricular dysfunction as the specific cause of their shock. The cause was established by radionuclide ventriculography in 45 of 50 patients and led to a change in therapy in 21 patients. A single cause was found in 35 patients: 13 had severe global dysfunction of the left ventricle (three patients), right ventricle (seven patients), or both ventricles (three patients); three had severe segmental left ventricular dysfunction; and 19 had an exaggerated region of photon deficiency (nine patients) or an abnormal and accumulating blood pool (10 patients) surrounding small hyperdynamic ventricles. Sixteen of these 19 patients with scintigraphic evidence of tamponade underwent aspiration with a pericardial needle or reoperation early after radionuclide ventriculography, resulting in confirmation of scintigraphic findings and improved hemodynamics. Ten additional patients had combined ventricular dysfunction and a pericardial abnormality, and five of these underwent reoperation resulting in improved hemodynamics. Radionuclide ventriculography provided no explanation for the cause of cardiac shock in five patients. Thus, the various causes of cardiac shock early after open heart surgery can be distinguished by 99mTc-red blood cell, gated equilibrium radionuclide ventriculography, eliminating diagnostic uncertainty that can occur with traditional evaluation.
Vascular Smooth Muscle Cell Heme Oxygenases Generate Guanylyl Cyclase–Stimulatory Carbon Monoxide
Authors: Nick Christodoulides, William Durante, Michael H. Kroll, Andrew I. Schafer
Journal: Circulation (1995)

Background Carbon monoxide (CO), like nitric oxide (NO), stimulates soluble guanylyl cyclase and thereby raises intracellular levels of cGMP. We examined the endogenous capacity of vascular smooth muscle cells (SMCs) to produce CO from heme through the activity of heme oxygenases. Methods and Results Cultured SMCs from rat aorta (RASMCs) expressed immunoreactive inducible heme oxygenase-1 (HO-1) and constitutive HO-2. Treatment of RASMCs with hemin and sodium arsenite, which are inducers of HO-1, stimulated RASMC cGMP without stimulating nitrite release or inducible NO synthase expression, and the induced elevations of cGMP were not inhibited by the NO synthase inhibitor N G -methyl- l -arginine. Induced CO from RASMCs likewise caused elevation of cGMP levels in platelets coincubated with the vascular cells. Zinc protoporphyrin IX, an inhibitor of HO, reversed the inducible increases in platelet cGMP. Conclusions These results indicate that vascular SMCs have both constitutive and inducible HO activity, and they respond to specific stimuli to generate guanylyl cyclase–stimulatory CO in the same SMCs and in coincubated platelets.
Portable Cholesterol Analyzers
Authors: Gregory A. Tetrault
Journal: JAMA (1990)

<h3>To the Editor.—</h3> Naughton et al<sup>1</sup>concluded that portable cholesterol analyzers at three of four sites had insufficient accuracy, resulting in a high percentage of misclassified patients (mostly false negatives). However, the study has a number of flaws and omissions that may invalidate their results. A significant problem is the effect of posture on blood cholesterol measurements. Blood cholesterol concentrations fall significantly when an ambulatory patient sits or lies supine.<sup>2,3</sup>The National Cholesterol Education Program Expert Panel recommends that patients be seated for at least 5 minutes before blood is drawn.<sup>4</sup>The authors do not describe any attempt at minimizing the effects of postural changes. In their study, venous samples were obtained after finger-stick samples. If the patients were seated prior to their finger-stick cholesterol determination and were ambulatory prior to venipuncture, then the venipuncture cholesterol levels would be higher than those obtained by finger stick because
BM-11 * LEPTOMENINGEAL METASTASES IN HIGH-GRADE ADULT GLIOMA: DEVELOPMENT, DIAGNOSIS, MANAGEMENT AND OUTCOMES IN A SERIES OF 34 PATIENTS
Authors: C. Dardis, K. Milton, L. Ashby, W. Shapiro
Journal: Neuro-Oncology (2014)

Leptomeningeal metastases (LM) in the setting of glioma have often been thought to carry a particularly poor prognosis. We sought to better characterize this phenomenon through a review of patients with glioma seen in our institution over the preceding 10 years. This series of 34 in grade III or IV glioma is the largest of which we are aware. Leptomeningeal spread was present at the time of initial diagnosis in 4 patients. In the others, LM occurred at the time of first progression of disease in 17. The median time to development of LM (excluding those where it was present at initial diagnosis) was 16.4 months (95% confidence interval (CI) 8.2-43.9). The median time to further progression of disease following LM was 4.9 months (95% CI 3.1-6.9). 25 patients were known to have died at the time of writing. Thus median overall survival (OS) was 10.2 months (95% CI 8.8-14.7) following LM. At the time of diagnosis of LM, some form of treatment (chemotherapy and/or radiation vs. no treatment) increased OS (median 11.7 vs. 3.3 months, p < 0.001 by log-rank test). Use of radiation therapy (vs. no radiation) also increased OS, although the effect was more modest (7.8 vs. 16.8 months, p = 0.07). Higher Karnofsky Performance Status (KPS) at the time of diagnosis of LM was associated with OS (p = 0.007, median OS for KPS <= 90 19 months vs. 7.8 for KPS <90). In a two-variable model incorporating the use any treatment (vs. none) and KPS, KPS tended to be a more significant predictor of survival (p = 0.22 vs. p = 0.06 by likelihood-ratio test). This was also true for radiation (vs. none) and KPS (p = 0.27 vs. p = 0.02). No significant benefit could be demonstrated for the use of chemotherapy considered alone, either systemic or intrathecal. However 4/9 receiving intrathecal chemotherapy had a ventriculoperitoneal shunt in place.