tbuckley/cabot-search huggingface dataset:
Lung Cancer Screening
Authors: James L. Mulshine, Daniel C. Sullivan
Journal: New England Journal of Medicine (2005)

A 60-year-old woman who quit smoking 20 years earlier comes for a routine visit. She previously smoked one pack of cigarettes a day for 10 years. Her medical history is otherwise unremarkable. Her husband smoked one pack of cigarettes per day for at least 30 years but stopped smoking a decade ago. She asks whether she and her husband should undergo computed tomographic scanning to screen for lung cancer. What do you advise?
An unusual pancreatic lesion causing biliary obstruction and duodenal invasion
Authors: Jatinder Goyal, Frederick Weber, Shajan Peter
Journal: Endoscopy (2015)

An 84-year-old woman was admitted with melena. She had had an enlarging pancreatic mass 2 years earlier requiring endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy and biliary metal stent placement. Her current presentation included melena for 1 week. She did not have any pain, nausea, vomiting, abdominal fullness or weight loss. Vital signs were within normal limits. On physical examination, mild epigastric tenderness was present. Laboratory studies revealed hemoglobin of 6.6 g/dL, a normal comprehensive metabolic profile, and normal serum lipase. Computed tomography (CT) imaging revealed a 10.9 × 8.2 cm complex heterogeneously enhancing cystic pancreatic head mass with multiple internal septations ([Fig. 1 a]). CT angiography reconstruction imaging showed a hypervascular pancreatic mass ([Fig. 1 b]). Endoscopy revealed friable duodenal mucosa from duodenal infiltration ([Fig. 2]). Cytologic examination through endoscopic ultrasound (EUS)-guided fine-needle aspiration showed scant cellularity. The patient was diagnosed with serous cystadenoma of the pancreas, although evolution to cystadenocarcinoma could not be excluded. Prophylactic embolization of the gastroduodenal and inferior pancreaticoduodenal arteries was performed. The patient was doing well at the time of last follow-up.
Access to stroke prevention surgery varies widely in UK
Authors: J. Wise
Journal: BMJ (2011)

Some patients who need carotid endarterectomy undergo it within two days of symptoms, while others wait almost two months, an audit by the Royal College of Physicians and the Vascular Society has found.

Surgeons say that government stroke targets will not be met unless transient ischaemic attack (TIA) is routinely recognised as an emergency needing a rapid response, and the National Institute for Health and Clinical Excellence has set a target of two weeks from symptoms to treatment. The audit found that only 40% of NHS patients are operated on within that timeframe, up from 33% the previous year.

The government’s national stroke strategy has set a target of 48 hours from symptoms to surgery to be achieved by 2017, and …
Three new variants of glucose‐6‐phosphate dehydrogenase associated with chronic nonspherocytic hemolytic anemia: G‐6‐PD Lincoln Park, G‐6‐PD arlington heights, and G‐6‐PD West Town
Authors: George R. Honig, Evelina Habacon, Loyda N. Vida, Florinda Matsumoto, Ernest Beutler
Journal: American Journal of Hematology (1979)

Abstract Glucose 6‐phosphate dehydrogenase (G‐6‐PD) deficiency was identified in three children who were evaluated because of chronic nonspherocytic hemolytic anemia. One child is of German extraction, another Puerto Rican, and the third Mexican. In each of the patients the hemolytic process was well compensated, but each had one or more episodes of anemia following exposure to an oxidant drug or with infections. The electrophoretic, functional, and kinetic properties of the mutant enzymes, derived both from the patients' erythrocytes and from cultured fibroblasts, allowed each to be distinguished from G‐6‐PD variants previously described.
The inverse association of salmonellosis in infancy with allergic rhinoconjunctivitis and asthma at school‐age: a longitudinal study
Authors: U. Pelosi, G. Porcedda, F. Tiddia, S. Tripodi, A. E. Tozzi, V. Panetta, C. Pintor, P. M. Matricardi
Journal: Allergy (2005)

Background: Respiratory allergies are inversely related to early acquisition of food‐borne and fecal‐oral infections, consumption of unpasteurized milk, early exposure to stables and high endotoxin concentrations in a farming environment. We tested therefore if infection by Salmonella in early life can protect from development of respiratory allergies later in life. Methods: During 2003, we studied two groups of Sardinian children (age 6–18 years) who had been hospitalized before 4 years of age (during 1989–2001) with non‐typhoid salmonellosis ( n = 148) or acute enteritis of nonbacterial etiology (NB‐enteritis) ( n = 167). Allergic rhinoconjunctivitis (AR) and asthma were evaluated by telephonic interview with a ISAAC questionnaire; participants reporting AR and/or asthma were further examined through a complete diagnostic work‐up to objectively confirm or exclude current disease. Kaplan–Meier curves and Cox proportional hazard models were used to analyze the role of different types of enteritis on the risk of developing allergic rhinoconjunctivitis or asthma over time. Results: Children who had been hospitalized with salmonellosis had a lower prevalence of allergic rhinoconjunctivitis (eight of 148, 5.4% vs 23 of 167, 13.8%; P = 0.019) or asthma (five of 148, 3.4% vs 21 of 167, 12.6%; P = 0.006) than those who had been hospitalized with NB‐enteritis. The proportional hazard of salmonellosis for asthma was 0.23 (95% CI: 0.08–0.67; P &lt; 0.01) and for allergic rhinoconjunctivitis was 0.40 (95% CI: 0.17–0.95; P = 0.04), after adjusting for confounders. Discussion: The strength of the observed associations suggests that Salmonella may contribute to shape the natural history of respiratory allergies. However, further studies are needed to test in other settings the association observed in Sardinian children. We speculate that clinical or subclinical infection by Salmonella may contribute to the atopy protective influence of a traditional farming environment or of areas endemic for food‐borne and fecal‐oral infections. Food hygiene and prevention of salmonellosis must remain however a public health priority.
Glucocorticoid-mediated inhibition of endotoxin-induced intratumor tumor necrosis factor production and tumor hemorrhagic necrosis and regression.
Authors: R J North, E A Havell
Journal: The Journal of Experimental Medicine (1989)

Intravenous injection of 25 micrograms of bacterial endotoxin on day 9 of growth of the SA1 sarcoma results in extensive necrosis of the core of this tumor and in its subsequent complete regression. Tumor hemorrhagic necrosis and regression failed to occur in mice that were given a subcutaneous injection of cortisone acetate or dexamethasone 12 h before being giving endotoxin. Inhibition of tumor hemorrhagic necrosis and regression by glucocorticoids was associated with inhibition of endotoxin-induced intratumor TNF production that normally takes place several h after endotoxin is given. In contrast, glucocorticoids had no effect on the ability of intravenously injected rTNF to cause tumor hemorrhagic necrosis and regression. The results lend further support to the belief that TNF is the predominant mediator of endotoxin-induced hemorrhagic necrosis of established murine tumors, and that hemorrhagic necrosis is a prerequisite for the immunologically mediated regression that follows.
Gold-Induced Thrombocytopenia
Authors: JONATHAN S. COBLYN
Journal: Annals of Internal Medicine (1981)

Thrombocytopenia developed in 23 patients with rheumatoid arthritis treated with gold salts over 25 years. All patients recovered, and there were no episodes of life-threatening hemorrhage; four patients eventually needed splenectomy. The clinical presentation of gold-induced thrombocytopenia and its treatment and outcome are reviewed. Because gold-induced thrombocytopenia is believed to have an immunologic basis, we sought an association between this complication and antigens of the human leukocyte antigen (HLA) region. The most significant finding was the association of the HLA-DR3 alloantigen in 12 of 15 of these patients compared with 26 of 84 in a control population (x2 12.9,p <This study provides further evidence that gold-induced thrombocytopenia is immunologically mediated and that genes of the major histocompatibility complex are involved.
Sirolimus-Induced Interstitial Pneumonitis in an Islet Transplant Recipient
Authors: Benigno J. Digon, Kristina I. Rother, Boaz Hirshberg, David M. Harlan
Journal: Diabetes Care (2003)

Thyroid DiseaseT ype 1 diabetes is associated with other autoimmune diseases.Many diabetes centers routinely screen patients with type 1 diabetes for autoimmune thyroid disease (ATD).The presence of two autoimmune diseases raises the possibility of polyendocrine autoimmune disease.The association of autoimmune adrenal insufficiency, or Addison's disease, with type 1 diabetes is described in case reports dating back more than a century (1,2).Studies have i l l u s t r a t e d s h a r e d H L A a l l e l e s (DQA1*0501, for example) among patients with type 1 diabetes, ATD, and Addison's disease (3,4).Pancreatic islet cell antibodies have been detected in 6.2% of patients with Addison's disease ( 5).Yet, it is unclear whether patients with type 1 diabetes should be routinely screened for Addison's disease.Our study's objective was to determine whether routine screening for Addison's disease is warranted in children with both type 1 diabetes and ATD.Children were diagnosed with thyroid disease if they had thyroid peroxidase antibodies (TPOs Ͼ50 Ku/l) and/or were receiving thyroid hormone replacement for primary hypothyroidism.A population of children with type 1 diabetes but without thyroid disease was also screened.The study population consisted of 114 children with type 1 diabetes, 35 (25 girls and 10 boys) with thyroid disease (28 on L- thyroxine) and 79 (42 girls and 37 boys) without thyroid disease (normal thyroidstimulating hormone and TPO Ͻ50 Ku/ l).Adrenal antibodies were measured by standard immunofluorescent technique (Nova Century Scientific-Immco antiadrenal slides), and TPOs were measured by an automated electrochemiluminescence immunoassay (Roche Elecsys 2010).
Emphasizing Chest Pain as a Symptom of Heart Attack
Authors: Raymond D. Bahr
Journal: JAMA (1993)

<h3>To the Editor.</h3> —Drs Kerber, Paraskos, and Montgomery miss the point of Dr Baird's letter<sup>1</sup>when they state that it would be unrealistic to think that emphasis on risk-factor identification and modification will entirely prevent myocardial infarctions (MIs) and cardiac arrests. Hence, they quickly skip on to guidelines for managing the cardiac emergencies that will inevitably occur. They get off the hook by saying that the American Heart Association (AHA) is ready to review new scientific data and change its recommendations. Lost in this rhetoric is the fact that awareness of chest pain and chest discomfort is not emphasized to the same degree as are the traditional risk factors.<sup>2</sup>It is true that chest pain is mentioned in the guidelines for cardiopulmonary resuscitation and emergency cardiac care—the emphasis is just not there. This is a major blunder. Identifying chest pain and chest discomfort as acute risk factors for
Abstract 3062: Isolation and characterization of circulating tumor cells (CTCs) from peripheral blood specimens of patients with advanced solid tumor malignancies (using ApoStream™ instrumentation)
Authors: Priya Balasubramanian, Lihua Wang, Scott M. Lawrence, Tony Navas, Shivaani Kummar, Melinda Hollingshead, Francis Owusu, Ralph E. Parchment, Joseph E. Tomaszewski, James H. Doroshow, Robert J. Kinders
Journal: Cancer Research (2014)

Abstract Circulating tumor cells (CTCs) isolated from the peripheral blood of cancer patients provide prognostic information and may inform treatment decisions. Current strategies for CTC isolation and characterization commonly employ epithelial marker-specific antibody capture of fixed cells from blood and detection based on cytokeratin (CK) expression. Our laboratory is currently evaluating an antibody-independent CTC enrichment technology, ApoStream™, which isolates live CTCs from blood, enabled by critical dissimilarities in morphology and dielectric properties of CTCs and blood cells rather than surface marker expression. CTCs isolated with the ApoStream™ instrument are amenable to further high resolution phenotypic characterization, enabling unambiguous identification of enriched cells as malignant cells. We previously reported on the utility of ApoStream™ technology for the isolation of CTCs from patients with advanced alveolar soft part sarcoma (ASPS) with unambiguous confirmation of CTCs by break-apart fluorescent in situ hybridization (FISH) for ASPL-TFE3 gene translocation. Here, we show the isolation of viable CTCs from patients with advanced solid tumors from ongoing clinical studies at the NCI. Since during progression, cancer cells undergo epithelial to mesenchymal transitions (EMT) and mesenchymal to epithelial transitions (MET), we sought to characterize ApoStream™-isolated CTCs using a multiplex phenotyping assay for CD45 (hematopoietic marker), EMT markers (CK, EpCAM, β-catenin and Vimentin), and tumor specific markers (MUC1 and CEA). A user-defined processing algorithm and CTC scoring criteria developed using Definiens® software was used for rare cell detection and enumeration. Our current efforts are focused on evaluating the utility of ApoStream™-isolated CTCs for assessing pharmacodynamic effects of anticancer agents on DNA damage response in patients with refractory solid tumors. Funded by NCI Contract No. HHSN261200800001E. Citation Format: Priya Balasubramanian, Lihua Wang, Scott M. Lawrence, Tony Navas, Shivaani Kummar, Melinda Hollingshead, Francis Owusu, Ralph E. Parchment, Joseph E. Tomaszewski, James H. Doroshow, Robert J. Kinders. Isolation and characterization of circulating tumor cells (CTCs) from peripheral blood specimens of patients with advanced solid tumor malignancies (using ApoStream™ instrumentation). [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 3062. doi:10.1158/1538-7445.AM2014-3062
Frequency of Germline Genomic Homozygosity Associated With Cancer Cases
Authors: Guillaume Assié, Thomas LaFramboise, Petra Platzer, Charis Eng
Journal: JAMA (2008)

Cancer is a multigenic disease resulting from both germline susceptibility and somatic events. While studying loss of heterozygosity (LOH) in cancer tissues, we anecdotally observed a low frequency of heterozygosity in cancer patients compared with controls, raising the question whether homozygosity could play a role in cancer predisposition.To determine the frequency of germline homozygosity in a large series of patients with 3 different types of solid tumors compared with population-based controls.Germline and corresponding tumor DNA isolated from 385 patients with carcinomas (147 breast, 116 prostate, and 122 head and neck carcinomas) were subjected to whole genome (345-microsatellite marker) LOH analysis.Frequency of homozygosity at microsatellite markers in cancer cases vs controls and frequency of somatic LOH in cancers at loci with the highest homozygosity.We identified 16 loci in common among the 3 cancer types, with significantly increased germline homozygosity frequencies in the cancer patients compared with controls (P < .001). In the cases who happened to be germline heterozygous at these 16 loci, we found a mean (SD) LOH frequency of 58% (4.2%) compared with 50% (7.5%) at 197 markers without increased germline homozygosity (P < .001). Across the genome, this relationship holds as well (r = 0.46; 95% confidence interval, 0.37-0.53; P < .001). We validated the association of specific loci with high germline homozygosity frequencies in an independent, single-nucleotide polymorphism-based, public data set of 205 lung carcinomas from white individuals (P < .05 to P < .001) as well as the correlation between genome-wide germline homozygosity and LOH frequencies (r = 0.21; 95% confidence interval, 0.18-0.24; P < .001).In our study of 4 different types of solid tumors (our data for 3 types validated in a fourth type), increased germline homozygosity occurred at specific loci. When the germline was heterozygous at these loci, high frequencies of LOH/allelic imbalance occurred at these loci in the corresponding carcinomas.
Treatment of Chylothorax by Producing Pleurodesis Using Iodized Talc
Authors: J. C. Gingell
Journal: Thorax (1965)

CASE 1 A woman of 68 years was referred on 17 December 1956 with a diagnosis of right-sided chylo- thorax, which was confirmed by pleural aspiration.She gave a history of progressive breathlessness on exertion for eight months, until just before admission she was breathless at rest.She also complained of weakness, anorexia, and a considerable loss of weight.
Genetic and molecular analysis of six tumor suppressor genes in Drosophila melanogaster
Authors: Thomas Löffler, Jasmin Wismar, Heinz Sass, Tomio Miyamoto, Gerhard Becker, Lutz Konrad, Maria Blondeau, Ursula Protin, Sibylle Kaiser, Petra Gräf, Martin Haas, Gerd Schuler, Janet Schmidt, Bounpheng Phannavong, Dietmar Gundacker, Elisabeth Gateff
Journal: Environmental Health Perspectives (1990)

Six Drosophila melanogaster tumor suppressor genes causing malignant or benign tumors in specific cell types are described. The wild-type alleles of these genes are instrumental in the differentiation of particular cell types. In the homozygous state, recessive mutations in the genes interrupt the differentiation of the cells and thus cause their uncontrolled, autonomous, lethal proliferation. The tumors show all major characteristics of malignant and benign neoplastic growth. Genomic sequences of four of the genes have been identified and are currently being characterized.
Health minister is stripped of his right to veto use of abortion pill
Authors: Christopher Zinn
Journal: BMJ (2006)

The abortion pill mifepristone (known as RU486) is to become available for the first time in Australia after a contentious parliamentary debate that saw the federal health minister stripped of his power to veto the use of the drug.

In a rare conscience vote after three days of heated argument, MPs in the House of Representatives voted in favour of a bill giving the drug regulator, the Therapeutic Goods Administration, the power of approval.

The prime minister, John Howard, opposed the move, saying: “To suggest that this drug RU486 is just another drug is patently absurd, …
SUBTROCHANTERIC AMPUTATION FOR DIFFUSE SKIN CARCINOMA.
Authors: EMANUEL J. SENN
Journal: JAMA (1900)

The following case is of interest on account of the extent of the carcinomatous invasion and the clinical history, which gives another instance of the origin of carcinoma from post-natal embryonic tissue. The clinical examination revealed much evidence in favor of blastomycetes, and it was only after a most painstaking pathologic study by Professor Hektoen that a positive diagnosis of carcinoma was made. Mr. W. P. R., age 23, American, had good health until 9 years of age, when he became the victim of a severe accident. While hanging on a train, he was struck on the inner side of the thigh by the sharp point of a diamond-shaped switch that caused a gaping wound of the thigh, extending below the knee. There was considerable hemorrhage at the time and the wound is said to have been closed by sixty-three stitches. After the injury there was a denuded surface on
Abstract 660: Clinical significance of <i>FGFR2</i> amplification in gastric cancer
Authors: Joon Oh Park, Jeeyun Lee, Hye-Lim Jang, Jiryeon Jang, Se Hoon Park, Young Suk Park, Ho Yeong Lim, Won Ki Kang
Journal: Cancer Research (2010)

Abstract Background: The fibroblast growth factor receptor (FGFR) tyrosine kinase family, which is comprised of four kinases that differentially respond to 18 FGF ligands, has long been implicated in cancer. Among them, activating somatic mutations in FGFR2 have been recently identified in several types of human cancer and are shown to be sensitive to FGFR2 kinase inhibition in the cell lines bearing such FGFR2 mutations, implicating FGFR2 as a novel therapeutic target. Therefore, we undertook this study to understand the clinical impact of FGFR2 amplification on gastric cancer patients. Patients and Methods: FGFR2 amplification was tested by qPCR using TaqMan probe and dual-color FISH in a panel of 37 gastric cancer cell lines and tumor specimens from 482 gastric cancer patients. Results: Of the 482 patients, 119 (24.8%) of the patients had FGFR2 copy number greater than 3.0 copies. FGFR2 amplification was not associated with clinicopathological parameters such as age, sex, histology, Bormann type, Lauren Classification, tumor location and TNM staging. Patients with FGFR2 amplification showed a trend toward shorter DFS (5-year DFS; 49.6% vs. 59.6%; FGFR2 amplification (+) vs. FGFR2 amplification (-); P=.065) and poorer survival (5-year OS; 47.9% vs. 58.41%; P=.084). We are currently performing preclinical study to investigate FGFR2-correlated sensitivity to several types of molecular-targeted agents. Conclusion: These results suggest that the FGFR2 amplification plays an important role in determining prognosis in gastric cancer patients. However, this study did not cover a predictive role of the FGFR2 amplification for the treatment response to FGFR2 kinase inhibitors, which should be further explored as a novel therapeutic target in upcoming clinical trials. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 660.
A nonsense mutation in the carboxyl-terminal domain of type X collagen causes haploinsufficiency in schmid metaphyseal chondrodysplasia.
Authors: D Chan, Y M Weng, H K Graham, D O Sillence, J F Bateman
Journal: Journal of Clinical Investigation (1998)

Type X collagen is a short-chain homotrimeric collagen expressed in the hypertrophic zone of calcifying cartilage. The clustering of mutations in the carboxyl-terminal NC1 domain in Schmid metaphyseal chondrodysplasia (SMCD) suggested a critical role for this type X collagen domain, but since no direct analysis of cartilage has been conducted in SMCD patients, the mechanisms of type X collagen dysfunction remain controversial. To resolve this problem, we obtained SMCD growth plate cartilage, determined the type X collagen mutation, and analyzed the expression of mutant and normal type X collagen mRNA and protein. The mutation was a single nucleotide substitution that changed the Tyr632 codon (TAC) to a stop codon (TAA). However, analysis of the expression of the normal and mutant allele transcripts in growth plate cartilage by reverse transcription PCR, restriction enzyme mapping, and a single nucleotide primer extension assay, demonstrated that only normal mRNA was present. The lack of mutant mRNA is most likely the result of nonsense-mediated mRNA decay, a common fate for transcripts carrying premature termination mutations. Furthermore, no mutant protein was detected by immunoblotting cartilage extracts. Our data indicates that a functionally null allele leading to type X collagen haploinsufficiency is the molecular basis of SMCD in this patient.
Fibrinolytic and fibrin stabilizing activity of synovial membranes.
Authors: R B Andersen, J Gormsen
Journal: Annals of the Rheumatic Diseases (1970)

Lack, 1965). This activity might be demonstrated by applying the tissue itself or a tissue extract on a fibrin plate (Astrup and Permin, 1947; Caughey and Highton, 1967) or by the histiochemical fibrin slide technique (Todd