tbuckley/cabot-search huggingface dataset:
Role of human selenium-binding protein 56 (hSP56) in selenium’s growth inhibitory action on human prostate cancer cells
Authors: Chong Gao, Yuxun Wang, Changmin Chen, Laurie Feldman, Arthur J. Sytkowski
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

1394 

Low levels of dietary selenium are associated with increased cancer risk, and selenium compounds have been shown to exhibit a chemopreventive effect for malignancies of several organs, including the prostate. Recently, it was reported that treatment with selenomethionine caused G1 arrest and 80% reduction in the S phase of LNCaP human prostate cancer cells, while no such effect was detected on another human prostate cancer cell line, PC-3 (Venkateswaran, V., L.H. Klotz, and N.E. Fleshner Cancer Research, 2002. 62:540). Interestedly, we had shown previously that the human selenium-binding protein gene hSP56, the human homologue of a rodent gene implicated in chemoresistance, is highly expressed in androgen-responsive LNCaP cells but not in androgen-nonresponsive PC-3 cells. This expression in LNCaP cells is reversibly down-regulated by androgen in vitro (Yang, M. and A. J. Sytkowski, Cancer Research, 1998. 58:3150,). Taken together, these data suggest that selenium modulation of prostate cancer cell growth may be mediated, at least in part, by hSP56. To test this hypothesis, we down-regulated the expression of hSP56 in LNCaP cells with siRNA and stably over-expressed it in PC-3 cells using a mammalian expression vector. The cells were then incubated in the absence or presence of selenium (seleno-DL-methionine, 50 μM) for 24, 48, or 72 h. Cell counts were performed in triplicates using a hemacytometer, with trypan blue exclusion to identify viable cells, and growth curves were generated for each cell line. Proliferation of LNCaP cells with down-regulated hSP56 after 48 h of selenium treatment was increased significantly over that of control LNCaP cells, indicating that selenium’s anti-proliferative effect was diminished as hSP56 expression was reduced. Conversely, the growth of PC-3 cells with up-regulated hSP56 was decreased substantially or inhibited virtually completely relative to control PC-3 cells after selenium treatment, indicating the selenium’s anti-proliferative effect was increased by up-regulating hSP56 expression. These data strongly suggest that hSP56 may mediate part or all selenium’s anti-proliferative action on these prostate cancer cells. Increasing hSP56 expression at the clinical level may prove effective in reducing the growth of prostate and other forms of cancer.
Abstract 1372: High Levels of Glucose Induce Apoptosis in Cardiomyocyte via Epigenetic Regulation of the Insulin-Like Growth Factor Receptor
Authors: Xi-Yong Yu, Yao-hua Song, Yong-jian Geng, Jia-liang Liang, Qiu-Xiong Lin, Shu-Guang Lin, Yangxin Li
Journal: Circulation (2009)
Abstract 2789: Evaluation of Risk of Cerebral Infarction by Tissue Characterization of Carotid Artery Plaques using Integrated Backscatter Ultrasound
Authors: Kiyofumi Yamada, Shin-ichi Yoshimura, Masanori Kawasaki, Yukiko Enomoto, Shinya Minatoguchi, Toru Iwama
Journal: Circulation (2007)

Background: Although carotid plaques with large lipid pools may be more likely to cause cerebral infarction (CI), there is little clinical evidence supporting this hypothesis. The purpose of this study was to elucidate whether three dimensional (3D) IB color-coded mapping methods could stratify the risk of CI. Methods: IB values of plaques were measured in 63 carotid plaques (&gt;50% stenosis) in 63 patients [acute CI (&lt;2 days after onset): n=14, old CI (&gt;60 days after onset): n=15, asymptomatic: n=34]. IB images were acquired using an ultrasonic system (Philips Medical, Sonos7500). We set regions of interest (0.6 x 0.6mm) on the echo tomography. Our definition of IB values for each tissue type was determined by comparing the histology reported in our previous study (7&lt;lipid pool ≤ 13; 13&lt;fibrosis ≤ 18; 18&lt;dense fibrosis ≤ 27; 27&lt;calcification ≤ 33dB). The % lipid volume (%LV: lipid volume/plaque volume) was automatically calculated in each plaque. We also characterized lipid-rich plaques using a magnetic resonance imaging (MRI) at the same sites. Results: % lipid volume of acute CI, old CI and asymptomatic were 80±14, 22±15 and 37±24%, respectively. Receiver-operating-characteristic curve analysis showed that a cutoff point of 51% was the most reliable predictor of the CI risk [sensitivity: 93%, specificity: 93%, positive predictive value (PPV): 93%, negative predictive value (NPV): 93%]. These diagnostic accuracies were higher than those of MRI (sensitivity: 85%, specificity: 71%, PPV: 75%, NPV: 83%). Conclusion: Carotid plaques with greater volume of lipid pool are more likely to cause CI. The 3D IB method is more useful to predict CI rather than depending on MRI.
Electron Microscopy of Milk Secretion in the Mammary Gland of the C3H/Crgl Mouse. II. Identification of Fat and Protein Particles in Milk and in Tissue&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: S. R. Wellings, B. W. Grunbaum, K. B. Deome
Journal: JNCI Journal of the National Cancer Institute (1960)

Air-dried mouse-milk films, frozen-dried mouse milk, frozen-dried mouse lactating mammary tissues, and osmium tetroxide-fixed lactating mammary tissues of the mouse were examined by electron microscopy. Air-dried and frozen-dried preparations treated with a solution of absolute methanol and ethyl ether (1:1) solubilized the fat droplets but failed to remove the protein particles. Tryptic digestion of formalin-fixed, methanol ether-treated grids of the same material removed the protein particles. The results established the proteinaceous and fatty characters of these 2 classes of milk particulates observed in the osmium tetroxide-fixed lactating mammary-gland tissue by electron microscopy.
Abstract 3251: Acute Changes in Bio-reactance Based Non Invasive Cardiac Output Measurements Following Biventricular Pacing Predict Left Ventricular Reverse Remodeling at 3 months: A Novel Tool to Guide CRT?
Authors: Fakhar Z Khan, Munmohan S Virdee, Philip A Read, Simon P Fynn, David P Dutka
Journal: Circulation (2009)
PTTG Induces Genomic Instability in Thyroid Cells
Authors: D Kim, A Stratford, K Boelaert, H Pemberton, C Gockce, M Eggo, L Tannahill, J Watkinson, J Franklyn, C McCabe
Journal: Cancer Research (2005)

3532  Cancer reflects the progressive accumulation of genetic alterations and subsequent genetic instability of cells. Cytogenetic studies have demonstrated the importance of aneuploidy in differentiated thyroid cancer development. Pituitary tumor transforming gene (PTTG), also known as securin, is a mitotic checkpoint protein which inhibits sister chromatid separation during mitosis. PTTG is highly expressed in many cancers and over-expression of PTTG induces aneuploidy in vitro. Using fluorescent inter-simple sequence repeat PCR and ABI377 sequencer we investigated the relationship between the degree of genetic instability and PTTG expression in normal and tumorous thyroid samples. The genomic instability index (GI-index) was 6.7-72.7% higher in cancers than normal, and in metastatic nodes from 2 patients were 104 & 225% greater than in the corresponding primary cancer. We also found that follicular thyroid tumors exhibited greater genetic instability than papillary tumors (27.6% (n = 9) versus 14.5% (n = 10), p = 0.03). By measuring PTTG mRNA using quantitative-PCR we demonstrated a relationship between PTTG expression and the degree of genetic instability in thyroid cancers (R2 = 0.80, p = 0.007). To further investigate PTTG’s role in genetic instability we transfected FTC133 thyroid follicular cells and observed increased genetic instability in cells over-expressing PTTG compared with vector-only controls (n = 3, GI-Index VO = 29.7 +/–5.2 vs. PTTG = 63.7 +/–6.4, p = 0.013). Consistent with the strong positive correlation in vivo, we also observed a dose response in genetic instability and PTTG expression (GI-Index low dose (0.5μg DNA/ 6-well plate) PTTG = 15.3% +/–1.7 vs. high dose (2 μg DNA) PTTG = 50.8% +/–3.3, p = 0.006). Confirming other reports, our Affymetrix array study of cellular response to irradiation showed significant downregulation of PTTG (2.3 fold) and a significant upregulation of Rad21 expression (1.9 fold). The potential relationship between the DNA repair gene rad21 and PTTG was further investigated in vivo and in vitro. In a cohort of matched normal and thyroid cancer specimens, PTTG mRNA expression negatively correlated with rad21 expression (R2 = 0.5, n = 7, p = 0.048). Transfection of FTC133 cells with PTTG elicited significant downregulation of rad21 mRNA expression (1.54 fold, n = 3, p = 0.009). Consistent findings were seen with HCT116 and H1299 cells. Overall, we describe the first use of FISSR-PCR in human cancers, and demonstrate that the degree of instability strongly correlated with PTTG-expression in differentiated thyroid cancer. Furthermore, in vitro studies demonstrated up-regulation of PTTG in thyroid cells may drive genetic instability through suppression of a rad21-dependent DNA repair mechanism. We conclude that PTTG may be an important gene in the mutator phenotype development in thyroid cancer.
Acute and nine-month clinical outcomes after “suboptimal” coronary stenting
Authors: Donald E Cutlip, Martin B Leon, Kalon K.L Ho, Paul C Gordon, Alessandro Giambartolomei, Daniel J Diver, David M Lasorda, David O Williams, Michelle M Fitzpatrick, April Desjardin, Jeffrey J Popma, Richard E Kuntz, Donald S Baim
Journal: Journal of the American College of Cardiology (1999)
Squamous Carcinomas of the Head and Neck: Some Patterns of Spread
Authors: R L Carter, M R Pittam
Journal: Journal of the Royal Society of Medicine (1980)

Patterns of tumour spread are examined in 160 patients with squamous carcinomas of the head and neck with reference to perineural infiltration, direct invasion of bone and ossified cartilage, and lymph node metastases in the previously irradiated neck. Perineural spread is comparatively common in large (T3, T4) tumours; it may be apparent early in the disease; it is often detectable clinically; and it is an adverse prognostic feature which may modify clinical management. Direct bone invasion is described with particular reference to tumours of the oral cavity. Most bone destruction is mediated by osteoclasts which appear to be stimulated by materials such as prostaglandins released in the vicinity of the tumour. The numbers of involved lymph nodes in surgical dissections from the irradiated neck are usually few and restricted to the submandibular and jugular groups; nodes in the posterior triangle are infrequently involved by metastatic carcinoma. Transcapsular spread and keratin granulomas are common. The scope of modified neck dissections in this group of patients is discussed.
Storm over screening for prostate specific antigen
Authors: M. J Duckworth
Journal: BMJ (2002)

Editor—Yamey and Wilkes argue that questioning cancer screening, specifically prostate specific antigen (PSA) screening can be a risky business in America.1 My prostate cancer, like so many others, was silent and only revealed after a PSA test that my daughter nagged me into adding to my biennial company medical examination—unfortunately too late to guarantee a cure. After surgery and adjuvant radiotherapy I probably have a better prognosis than two colleagues who presented with bone metastases (and PSA values, when tested, in the 100s).

My PSA result alerted me to a potential problem and let me enter an informed debate with the medical profession—no one forced me to have a biopsy, or an operation, or opt for surgery over radiotherapy, or decline hormone therapy, or do nothing. I could talk to my doctors, read books, and use the internet. I could assess the risks and benefits of a radical prostatectomy and, what is more, carry out this assessment against the background of a medical profession uncertain as to the best course of treatment for someone presenting with my results.

The key issue is that I could participate in making a life threatening personal decision, rather than have participation (and, by extension, timely treatment) denied to me because PSA screening had been ruled out for the entire male population on the basis of historical statistics. I am enough of a cynic to believe that some of the uncertainty surrounding PSA testing policy in the United Kingdom relates to resources.

During my decision making process, I came across a paper on dilemmas in treating early prostate cancer.2 It was easy to work out that there just aren't enough experienced urologists (who are dextrous enough to carry out this tricky operation successfully and have the courage to attempt it) to carry out the number of radical prostatectomies that early detection by PSA testing would indicate. This sample of 244 urologists had a mean of 14.1 years' experience (range 2-30 years), and 130 of them managed 100 patients or more with prostate cancer. Expertise in performing radical prostatectomy was restricted to comparatively few—98 reported having ever performed the procedure and only 12 (14%) that they performed 20 or more operations yearly.

I also suspect that the United Kingdom is far short of the number of three dimensional conformal radiotherapy machines needed to offer that treatment option.
Anaesthesia in the United States
Authors: E. M Cornish
Journal: BMJ (1996)

cancer units in district general hospitals.'It refers to the number of patients with common cancers whom surgeons need to treat to ensure adequate skill and suggests that figures regarded as adequate now will be revised upwards in the future.At present no firm recommendations exist about the critical number of patients who are required to ensure adequate clinical skill, though 50-80 per specialist has been suggested by the British Association of Surgical Oncology and the British Breast Group.The only evidence currently available suggests that outcome is bet- ter when the annual caseload per consultant
Abstract 163: Does Primary Coronary Angioplasty Improve Outcome in Patients Who Are Victims of Out-of-Hospital Cardiac Arrest?
Authors: Ali Farhat, Matthieu Godin, Caroline Abriou, Bogdan Borz, Christophe Tron, Brahim Baala, Fabienne Tamion, Helene Eltchaninoff
Journal: Circulation (2011)

Introduction: Patients presenting with out of hospital cardiac arrest (OHCA) and no evidence of extra-cardiac cause have a catastrophic short term outcome. Identifying predictors of improved surviv...
DISABILITY FOLLOWING GASTRIC SURGERY FOR BENIGN DISEASE, AS OBSERVED BY THE INTERNIST
Authors: Eddy D. Palmer
Journal: Annals of Internal Medicine (1959)

Article1 April 1959DISABILITY FOLLOWING GASTRIC SURGERY FOR BENIGN DISEASE, AS OBSERVED BY THE INTERNISTEDDY D. PALMEREDDY D. PALMERSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-50-4-928 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIt is only natural that the internist should obtain a somewhat different impression of the nature and incidence of illness which follows gastric surgery than does the surgeon. In addition to the difference in the class of patient that is likely to be referred to each specialist, there is a certain amount of disagreement over diagnostic semantics. The internist sometimes finds himself confused by the neatness with which the surgeon is accustomed to categorize postoperative diseases and syndromes, and by his willingness to translate all postoperative problems into terms of specific lesions or of mechanical complications about the anastomosis. The...Bibliography1. Ellison EH: Malabsorption syndromes in the postgastrectomy patient, Am. J. Digest. Dis. 2 (n.s.): 669-676, 1957. CrossrefMedlineGoogle Scholar2. Palmer ED: On the management of duodenal ulcer in the Armed Forces, Military Med. 118: 195-204, 1956. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: MC New York, N. Y.*Received for publication January 3, 1958.From the Out Patient Service, 2nd General Hospital, APO 180, New York, N. Y.Requests for reprints should be addressed to Eddy D. Palmer, Lt. Colonel (MC)—0-43224, Second General Hospital, APO 180, New York, N. Y. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1959Volume 50, Issue 4Page: 928-935KeywordsApolipoproteinsDisabilitiesDuodenal ulcersEmotionsLesionsOutpatientsSurgeonsSurgeryUlcers ePublished: 1 December 2008 Issue Published: 1 April 1959 PDF downloadLoading ...
Brain Fluids and Metabolism
Authors: Gary A. Rosenberg
Journal: Annals of Internal Medicine (1991)

Fluids, circulation, and metabolism: an overview Anatomy of the brain interface Physiology of cerebrospinal and interstitial fluids Mathematics of transport Radioisotopes in metabolic studies Nuclear magnetic resonance spectroscopy Glucose, amino acids, and lipids Hypoxia-Ischemia Brain edema.
Abstract 11683: Class IIb Histone Deacetylase 6 Regulates Endothelial Cell Migration and Angiogenesis by Deacetylation of Cortactin
Authors: David Kaluza, Jens Kroll, Sabine Gesierich, Tso-Pang Yao, Reinier A Boon, Eduard Hergenreider, Marc Tjwa, Lothar Rossig, Edward Seto, Hellmut G Augustin, Andreas M Zeiher, Stefanie Dimmeler, Carmen Urbich
Journal: Circulation (2011)

Histone deacetylases (HDACs) deacetylate histones and non-histone proteins, thereby affecting protein activity and gene expression. Previous studies identified HDAC5 and HDAC7 as regulators of angi...
Abstract 15084: Safety and Efficacy of Anti-von Willebrand Factor Nanobody® ALX-0081 in Stable Angina Patients Undergoing Percutaneous Coronary Intervention
Authors: Jozef Bartunek, Emanuele Barbato, Kristof Vercruysse, Christian Duby, William Wijns, Guy Heyndrickx, Josefin-Beate Holz
Journal: Circulation (2010)

Introduction: The Nanobody ALX-0081 specifically targets the A1 domain of von Willebrand factor (vWF) and blocks the interaction between vWF and the GPIb receptor on the surface of platelets. ALX-0081 selectively prevents thrombus formation under high shear stress conditions. Hypothesis: We evaluated the safety, pharmacokinetics and efficacy of ALX-0081 in patients with stable angina undergoing an elective percutaneous coronary intervention. The effect of ALX-0081 on platelet reactivity after clopidogrel treatment was also examined. Methods: In total, 46 patients receiving a standard antithrombotic regimen (aspirin, heparin and clopidogrel) were included in this randomised, placebo-controlled Phase Ib study. Single and multiple doses of ALX-0081 were administered as 1 hour i.v. infusions. In addition, 22 patients were included in an open-label extension of the study and received i.v. bolus injections (Table 1). Results: (Table 1) ALX-0081 was safe and well tolerated at all doses, both after i.v. infusion ...
Difficulties Associated with Breast-feeding
Authors: F. E. Hytten, J. C. Yorston, A. M. Thomson
Journal: BMJ (1958)

VAGINAL SMEARS MEDICALJOHUNALThe technique of taking vaginal smears and a method of staining them for examination are described.A short account of the cells found in vaginal smears is given.We would like to thank Dr. P. M. F. Bishop for his help and permission to study his patients.We
Durable complete response (CR) and suppression of the human T-cell leukemia virus (HTLV-1) viral load (VL) with alemtuzumab in refractory adult T-cell leukemia (ATL)
Authors: P. Porcu, A. Mone, S. Puhalla, S. Whitman, R. Baiocchi, M. Caligiuri, J. Byrd
Journal: Journal of Clinical Oncology (2005)

6639 Background: Of the 20 million HTLV-1-infected people worldwide, 3–5% develops ATL, an aggressive and highly chemoresistant disease, often associated with impaired p53. Second-line antiretrovirals (ARs) and interferon-alpha (IFNα) produce responses but progression and death are the rule. Novel agents and tools to detect and treat minimal residual disease (MRD) could improve outcomes. ATL cells express CD52, the target of the antibody alemtuzumab (A), which is cytotoxic in p53-deficient cells and active in a preclinical model of ATL. This is the first analysis of response to alemtuzumab in ATL. Methods: A patient with ATL that relapsed after chemotherapy, ARs and progressed on IFNα and thalidomide received (A) (30 mg subcutaneously thrice weekly x 12 weeks). (A)-mediated cytotoxicity was studied in the patient’s ATL cells as well as in an archived sample from a previous ATL patient. Serial HTLV-1 VL were monitored by real-time (RT)-polymerase chain reaction (PCR) on peripheral blood mononuclear cells. Results: After 12 weeks of (A) the patient achieved a hematological complete response that persists for greater than 12-months. All therapy was administered as outpatient. Transient neutropenia, requiring growth factors support occurred. No opportunistic infections occurred except for asymptomatic CMV reactivation, rapidly cleared with oral valganciclovir. Post-(A) neutrophil count is normal off growth factors. Persistent suppression of HTLV-1 VL even at recovery of T-cells post-(A) was observed. Efficient complement-mediated cytotoxicity (CDC) in vitro, but only modest antibody-dependent cytotoxicity (ADCC) and direct induction of apoptosis were observed in both samples analyzed. Conclusion: (A) as a single agent and given in the outpatient setting appears to have remarkable activity in relapsed ATL and lead to a profound, durable reduction in HTLV-1 VL. (A)-mediated cytotoxicity in ATL cells was predominantly complement-mediated. (A) may represent a novel outpatient treatment option for many refractory ATL patients worldwide. MRD monitoring by RT-PCR for HTLV-1 VL should be studied as a biomarker of response and progression in ATL. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Berlex Berlex
TREATMENT OF UNDULANT FEVER WITH SULPHANILAMIDE; CASE REPORT
Authors: Austin B. Chinn
Journal: Annals of Internal Medicine (1940)

Case Reports1 November 1940TREATMENT OF UNDULANT FEVER WITH SULPHANILAMIDE; CASE REPORTAUSTIN B. CHINN, M.D.AUSTIN B. CHINN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-14-5-921 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe use of sulphanilamide in the treatment of undulant fever has been recently advocated.1, 2, 3, 4 In the case herein described, features other than the disappearance of fever seem to make it worthy of recording.CASE REPORTC. R., a white male, aged 32 years, a department store executive, was first seen on May 14, 1938. He complained of chilly sensations, fever, sweats, and malaise. Hisfamily medical history was unimportant. In the past he had been free from major illnesses, with the exception of an attack of polyarthritis during childhood. This was thought to have been rheumatic fever,...Bibliography1. RICHARDSON LA: Infection with Brucella abortus treated with prontosil, Lancet, 1938, i, 495. CrossrefGoogle Scholar2. FRANCIS AE: Sulphanilamide in the treatment of undulant fever, Lancet, 1938, i, 496. CrossrefGoogle Scholar3. STERNBLAKE RLKW: Undulant fever: its treatment with sulphanilamide, Jr. Am. Med. Assoc., 1938, cx, 1550. CrossrefGoogle Scholar4. BLUMGART HL: Sulphanilamide in undulant fever, Jr. Am. Med. Assoc., 1938, cxi, 521. CrossrefGoogle Scholar5. WELCHWENTWORTHMICKLE HJAFL: The use of sulphanilamide in the diagnosis and treatment of brucellosis, Jr. Am. Med. Assoc., 1938, cxi, 226. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Washington, D. C.*Received for publication August 18, 1939. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDie BrucelloseTreatment of Undulant Fever with Sulphapyridine. 1 November 1940Volume 14, Issue 5Page: 921-924KeywordsArthritisFeversRheumatic feverSweat ePublished: 1 December 2008 Issue Published: 1 November 1940 PDF downloadLoading ...