tbuckley/cabot-search huggingface dataset:
The air crescent sign of invasive pulmonary aspergillosis in acute leukaemia.
Authors: M L Slevin, G K Knowles, M J Phillips, A G Stansfeld, T A Lister
Journal: Thorax (1982)

<h3>Introduction</h3> Women may seek abortion at gestations when there is no visible intrauterine pregnancy on ultrasound scanning. Clinical protocols for pregnancy of unknown location (PUL) require measurement of serum human chorionic gonadotrophin (hCG), with the National Institute for Health and Care Excellence recommending that values above 1500 IU/L be further investigated to exclude ectopic pregnancy. Our aim was to determine whether a point-of-care test (POCT) could be used instead of laboratory serum hCG measurement. <h3>Methods</h3> Over 12 months, women who presented to an abortion service with a PUL had a POCT for blood or urine hCG and laboratory serum hCG measurement. The POCT machine used provides a discrete hCG value below 1000 IU/L and above this gives results as a range. The sensitivity and specificity of the POCT in identifying cases where laboratory serum hCG results were above 1500 IU/L were calculated. <h3>Results</h3> A total of 118 women presented with a PUL, of whom 70 had a POCT on blood (n=49) or urine (n=21) and a corresponding laboratory serum hCG. The sensitivity of the blood POCT was 0.67 (95% CI 0.38 to 0.87) and the specificity was 0.97 (95% CI 0.83 to 0.99). The sensitivity of the urine POCT was 0.25 (CI 0.01 to 0.78) and the specificity was 0.94 (CI 0.69 to 0.99). <h3>Conclusion</h3> Although both the blood and urine POCTs had a high level of specificity, neither test was acceptably sensitive. While promising, this POCT for hCG is not sufficiently reliable to replace laboratory serum hCG testing in the management of women with PUL in an abortion service.
PCPH/ENTPD5 Expression Confers to Prostate Cancer Cells Resistance against Cisplatin-Induced Apoptosis through Protein Kinase Cα–Mediated Bcl-2 Stabilization
Authors: Joaquín Villar, Humair S. Quadri, Insun Song, York Tomita, Oscar M. Tirado, Vicente Notario
Journal: Cancer Research (2008)

Abstract Prostate cancer (PCa) frequently develops antiapoptotic mechanisms and acquires resistance to anticancer drugs. Therefore, identifying PCa drug resistance determinants should facilitate designing more effective chemotherapeutic regimens. Recently, we described that the PCPH protein becomes highly expressed in human prostatic intraepithelial neoplasia and in PCa, and that the functional interaction between PCPH and protein kinase Cδ (PKCδ) increases the invasiveness of human PCa. Here, we report that the functional interaction between PCPH and a different PKC isoform, PKCα, confers resistance against cisplatin-induced apoptosis to PCa cells. This interaction elicits a mechanism ultimately resulting in the posttranslational stabilization and subsequent elevated expression of Bcl-2. Stable knockdown of either PCPH, mt-PCPH, or PKCα in PCa cells decreased Ser70-phosphorylated Bcl-2 and total Bcl-2 protein, thereby increasing their cisplatin sensitivity. Conversely, forced expression of the PCPH protein or, in particular, of the mt-PCPH oncoprotein increased the levels of phosphorylated PKCα concurrently with those of Ser70-phosphorylated and total Bcl-2 protein, thus promoting cisplatin resistance. Consistently, Bcl-2 knockdown sensitized PCa cells to cisplatin treatment and, more importantly, reversed the cisplatin resistance of PCa cells expressing the mt-PCPH oncoprotein. Moreover, reexpression of Bcl-2 in PCPH/mt-PCPH knockdown PCa cells reversed the cisplatin sensitization caused by PCPH or mt-PCPH down-regulation. These findings identify PCPH and mt-PCPH as important participants in the chemotherapy response of PCa cells, establish a role for PCPH-PKCα-Bcl-2 functional interactions in the drug response process, and imply that targeting PCPH expression before, or simultaneously with, chemotherapy may improve the treatment outcome for PCa patients. [Cancer Res 2009;69(1):102–10]
Annual Report to the Nation on the Status of Cancer, 1975–2002, Featuring Population-Based Trends in Cancer Treatment
Authors: Brenda K. Edwards, Martin L. Brown, Phyllis A. Wingo, Holly L. Howe, Elizabeth Ward, Lynn A. G. Ries, Deborah Schrag, Patricia M. Jamison, Ahmedin Jemal, Xiao Cheng Wu, Carol Friedman, Linda Harlan, Joan Warren, Robert N. Anderson, Linda W. Pickle
Journal: JNCI Journal of the National Cancer Institute (2005)

The American Cancer Society (ACS), the Centers for Disease Control and Prevention (CDC), the National Cancer Institute (NCI), and the North American Association of Central Cancer Registries (NAACCR) collaborate annually to provide information on cancer rates and trends in the United States. This year's report updates statistics on the 15 most common cancers in the five major racial/ethnic populations in the United States for 1992-2002 and features population-based trends in cancer treatment.The NCI, the CDC, and the NAACCR provided information on cancer cases, and the CDC provided information on cancer deaths. Reported incidence and death rates were age-adjusted to the 2000 U.S. standard population, annual percent change in rates for fixed intervals was estimated by linear regression, and annual percent change in trends was estimated with joinpoint regression analysis. Population-based treatment data were derived from the Surveillance, Epidemiology, and End Results (SEER) Program registries, SEER-Medicare linked databases, and NCI Patterns of Care/Quality of Care studies.Among men, the incidence rates for all cancer sites combined were stable from 1995 through 2002. Among women, the incidence rates increased by 0.3% annually from 1987 through 2002. Death rates in men and women combined decreased by 1.1% annually from 1993 through 2002 for all cancer sites combined and also for many of the 15 most common cancers. Among women, lung cancer death rates increased from 1995 through 2002, but lung cancer incidence rates stabilized from 1998 through 2002. Although results of cancer treatment studies suggest that much of contemporary cancer treatment for selected cancers is consistent with evidence-based guidelines, they also point to geographic, racial, economic, and age-related disparities in cancer treatment.Cancer death rates for all cancer sites combined and for many common cancers have declined at the same time as the dissemination of guideline-based treatment into the community has increased, although this progress is not shared equally across all racial and ethnic populations. Data from population-based cancer registries, supplemented by linkage with administrative databases, are an important resource for monitoring the quality of cancer treatment. Use of this cancer surveillance system, along with new developments in medical informatics and electronic medical records, may facilitate monitoring of the translation of basic science and clinical advances to cancer prevention, detection, and uniformly high quality of care in all areas and populations of the United States.
High Serum Concentration of YKL-40 Is Associated with Short Survival in Patients with Acute Myeloid Leukemia
Authors: Olav J. Bergmann, Julia S. Johansen, Tobias W. Klausen, Anne K. Mylin, Jørgen S. Kristensen, Eigil Kjeldsen, Hans E. Johnsen
Journal: Clinical Cancer Research (2005)

YKL-40 is secreted by cancer cells, macrophages, and neutrophils. It may be a growth or differentiation factor, play a role in angiogenesis, or protect against apoptosis. High serum YKL-40 is associated with poor prognosis in solid carcinomas. The aim was to examine serum YKL-40 in patients with acute myeloid leukemia (AML).YKL-40 was measured by ELISA in serum from 77 patients recently diagnosed with AML before and during the first month of chemotherapy.Forty (52%) of the AML patients had elevated serum YKL-40 (compared with age-matched healthy subjects) and their survival was shorter than in patients with normal serum YKL-40 (median, 128 days; interquartile range, 18-629 days versus 386 days; interquartile range, 180-901; P=0.018 Mann-Whitney test). Univariate analysis of serum YKL-40 (logarithmically transformed and treated as a continuous covariate) showed significant association with survival within the first month after start of chemotherapy [hazard ratio (HR), 1.7; 95% confidence interval (CI), 1.2-2.4; P=0.002], first 12 months (HR, 1.6; 95% CI, 1.2-2.0; P=0.0002), and overall survival (HR, 1.3; 95% CI, 1.1-1.6; P=0.003). Multivariate Cox analysis showed that serum YKL-40 was an independent prognostic variable for survival (first month: HR, 1.7; P=0.011; 12 months: HR, 1.6; P=0.0002; overall survival: HR, 1.4; P=0.002). High serum YKL-40 at start of chemotherapy was a risk factor for pneumonia within the first month, and serum YKL-40 increased (P=0.002) at time of pneumonia and was unchanged in patients without infections.Serum YKL-40 is a prognostic biomarker of survival in AML patients. Its role in AML and infections needs to be determined.
A STUDY OF THE EFFECT OF SERUM ON THE IMMUNOLOGICAL REACTION OF A BACTERIAL ENDOTOXIN
Authors: Leighton E. Cluff
Journal: The Journal of Experimental Medicine (1956)

Contact of a purified endotoxin from Shigella fiexneri Type Z with normal rabbit or human serum results in an alteration of its immunological reaction with antiserum, as determined by precipitation in gel. Analysis of fractions of normal serum obtained by zone electrophoresis in starch indicates that the component responsible for altering the immunological reaction of endotoxin is associated with beta globulin. Normal serum has no similar effect on the immunological reaction of a variety of other protein and polysaccharide antigens. Serum from rabbits made tolerant to the pyrogenic action of an endotoxin from Serratia marcescens (P-35) possesses the ability to alter the reaction of Shigella endotoxin with its specific antiserum, although the serum from tolerant rabbits does not significantly enhance the pyrogenicity of Shigella toxm. The component of normal rabbit serum responsible for the effect on the immunological reaction of Shigella endotoxin is not destroyed by heating at 56 degrees C. The possible relationship of the effect of normal serum on the immunological reaction of endotoxin and the augmentation of fever induced by endotoxins is discussed.
Intestinal lamina propria dendritic cells maintain T cell homeostasis but do not affect commensalism
Authors: Nathan E. Welty, Christopher Staley, Nico Ghilardi, Michael J. Sadowsky, Botond Z. Igyártó, Daniel H. Kaplan
Journal: The Journal of Experimental Medicine (2013)

Dendritic cells (DCs) in the intestinal lamina propria (LP) are composed of two CD103(+) subsets that differ in CD11b expression. We report here that Langerin is expressed by human LP DCs and that transgenic human langerin drives expression in CD103(+)CD11b(+) LP DCs in mice. This subset was ablated in huLangerin-DTA mice, resulting in reduced LP Th17 cells without affecting Th1 or T reg cells. Notably, cognate DC-T cell interactions were not required for Th17 development, as this response was intact in huLangerin-Cre I-Aβ(fl/fl) mice. In contrast, responses to intestinal infection or flagellin administration were unaffected by the absence of CD103(+)CD11b(+) DCs. huLangerin-DTA x BatF3(-/-) mice lacked both CD103(+) LP DC subsets, resulting in defective gut homing and fewer LP T reg cells. Despite these defects in LP DCs and resident T cells, we did not observe alterations of intestinal microbial communities. Thus, CD103(+) LP DC subsets control T cell homeostasis through both nonredundant and overlapping mechanisms.
Genetics of Vascular Calcification
Authors: Elizabeth M. McNally
Journal: Circulation Research (2011)

R ecessive mutations in the NTE5 gene were recently described in lower-extremity vascular calcification.ENPP1 mutations were previously described in a severe disorder of vascular calcification in infancy.Together these data support that extracellular adenosine and pyrophosphate are essential components of the pathways in vascular disease.Arterial calcification by impairing blood flow and reducing vessel compliance increases the risk for vascular disease in aging, diabetes, and renal disease.Whether or not arterial calcification is an active participant in vascular disease, it is readily identifiable, providing the rationale for less invasive means of coronary artery screening.The molecular mechanisms governing vascular calcification overlap substantially with the mechanisms of bone formation.The recent work of St Hilaire et al 1 demonstrates that mutations in the gene encoding CD73, an ectonucleotidase, cause peripheral arterial calcification.The NT5E gene encodes the cell surface protein CD73, which catalyzes the conversion of AMP to adenosine and inorganic phosphate (Figure).The genetic defect was identified using a single family with 5 affected individuals, ages 44 to 54 years, each of whom had significant vascular calcification of the lower extremities.Because their parents were third cousins, it was reasonable to assume that a homozygous recessive gene was responsible.Using a genotyping array containing a million single nucleotide polymorphisms, the authors identified a single region of homozygosity shared among the affected siblings.This region spanned 22 MB and contained 92 genes, including the NT5E gene.NT5E encodes the second enzyme in the pathway that converts extracellular ATP to adenosine.The first enzyme in this pathway, ENPP1 (also known as NPP1), was previously implicated in a more severe calcification disorder known as idiopathic infantile arterial calcification. 2 Idiopathic infantile arterial calcification
Regulation of COX-2 protein expression by Akt in endometrial cancer cells is mediated through NF-kappaB/IkappaB pathway.
Authors: Marie-Eve St-Germain, Veronique Gagnon, Sophie Parent, Eric Asselin
Journal: Molecular Cancer (2004)

Cyclooxygenase-2 (COX-2) has been shown to be highly expressed in a broad series of primary endometrial tumors and its expression may be closely associated with parameters of tumor aggressiveness. In human endometrial cancer, tumor suppressor phosphatase tensin homologue (PTEN) is frequently mutated. In the presence of a mutated PTEN protein, Akt phosphorylation levels increase leading to the activation of this survival pathway. The nuclear transcription factor κB (NF-κB) is a well establish regulator of genes encoding cytokines, cytokine receptors, and cell adhesion molecules that drive immune and inflammatory responses. More recently, NF-κB activation has been connected with multiple aspects of oncogenesis, including the control of apoptosis, cell cycle, differentiation, and cell migration. It is known that Akt may act through NF-κB pathway and that COX-2 gene has been shown to be regulated at the promoter level by NF-κB. Recently, we showed that Akt regulates COX-2 gene and protein expressions in phospho-Akt expressing endometrial cancer cells. The present study was undertaken to determine the involvement of NF-κB pathway and IκB (an inhibitor of NF-κB) in the regulation of COX-2 expression and to determine more precisely the downstream targets of Akt involved in this process. Three different human endometrial cancer cell lines known to have wild type PTEN (HEC 1-A) or a mutated inactive PTEN protein (RL 95-2 and Ishikawa) were used for these studies. Expression IκB and Phospho-IκB were evaluated by Western analysis. The presence of IκB phosphorylation was found in all cell lines studied. There was no difference between cell lines in term of NF-κB abundance. Inhibition of PI 3-K with Wortmannin and LY294002 blocked IκB phosphorylation, reduced NF-κB nuclear activity, reduced COX-2 expression and induced apoptosis. Transfection studies with a dominant negative Akt vector blocked IκB phosphorylation and reduced COX-2 expression. On the opposite, constitutively active Akt transfections resulted in the induction of IκB phosphorylation and up-regulation of COX-2. These results demonstrate that Akt signals through NF-κB/IκB pathway to induce COX-2 expression in mutated PTEN endometrial cancer cells.
Major risk factors for stillbirth in high-income countries: a systematic review and meta-analysis
Authors: Vicki Flenady, Laura Koopmans, Philippa Middleton, J Frederik Frøen, Gordon C Smith, Kristen Gibbons, Michael Coory, Adrienne Gordon, David Ellwood, Harold David McIntyre, Ruth Fretts, Majid Ezzati
Journal: The Lancet (2011)
Adenosine A <sub>1</sub> Receptor Induced Delayed Preconditioning in Rabbits
Authors: Ali Dana, Maria Skarli, Jenny Papakrivopoulou, Derek M. Yellon
Journal: Circulation Research (2000)

Abstract —Transient adenosine A 1 receptor (A 1 R) activation in rabbits induces delayed preconditioning against myocardial infarction 24 to 72 hours later. The cellular mechanisms downstream of A 1 R mediating this delayed cardioprotection have not been elucidated. This study examined the role of protein kinase C (PKC) and tyrosine kinases (TKs) in the signaling cascade mediating A 1 R-induced late preconditioning in rabbits. The small heat shock protein Hsp27 has been shown to confer cytoskeletal protection when in the phosphorylated state. We therefore also evaluated the potential role of the p38 mitogen-activated protein kinase (p38 MAPK) and Hsp27 as distal mediators of A 1 R-induced delayed preconditioning. Pharmacological preconditioning of rabbits with the selective A 1 agonist 2-chloro- N 6 -cyclopentyladenosine (CCPA; 100 μg/kg) significantly reduced myocardial infarct size compared with control animals, after 30-minute regional ischemia/2-hour reperfusion in vivo 24 hours later (23.7±3.1 versus 43.0±4.1%; P &lt;0.05). This delayed protection was abrogated by prior inhibition of either PKC with chelerythrine chloride (5 mg/kg) or of TKs with lavendustin A (1.3 mg/kg), suggesting that both PKC and TK are crucial for the development of delayed preconditioning after A 1 receptor activation in the rabbit. Myocardial tissue extracts obtained 24 hours after CCPA treatment were analyzed for p38 MAPK catalytic activity using an in vitro kinase assay. This showed an almost 7-fold increase in p38 MAPK activity in myocardial samples pretreated with CCPA compared with control hearts. Two-dimensional gel electrophoresis revealed an increase in the phosphorylated isoforms of Hsp27 in hearts pretreated with CCPA compared with control hearts. Prior inhibition of either PKC or TK prevented the CCPA-induced increase in p38 MAPK activity and phosphorylation of Hsp27. This study identifies new components of the signaling mechanism of A 1 R-induced delayed preconditioning. Our results suggest an important role for both PKC and TK as mediators of late preconditioning against infarction after A 1 R activation and, although correlative, point to the p38 MAPK/Hsp27 pathway as a potential distal effector of this protection.
Growth of Murine Sarcoma Virus-Transformed Rat Kidney Cells in Nude Mice: Absence of Induction of Host Endogenous Viruses 2
Authors: John A. Bilello, Victoria H. Freedman, Seung-il Shin
Journal: JNCI Journal of the National Cancer Institute (1977)

Journal Article Growth of Murine Sarcoma Virus-Transformed Rat Kidney Cells in Nude Mice: Absence of Induction of Host Endogenous Viruses Get access John A. Bilello, John A. Bilello Search for other works by this author on: Oxford Academic PubMed Google Scholar Victoria H. Freedman, Victoria H. Freedman Search for other works by this author on: Oxford Academic PubMed Google Scholar Seung-il Shin Seung-il Shin Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 58, Issue 6, June 1977, Pages 1691–1694, https://doi.org/10.1093/jnci/58.6.1691 Published: 01 June 1977 Article history Received: 26 July 1976 Accepted: 09 November 1976 Published: 01 June 1977
AL amyloidosis enhances development of amyloid A amyloidosis
Authors: J.C.H. van der Hilst, J.W.M. van der Meer, J.P.H. Drenth, A. Simon
Journal: British Journal of Dermatology (2007)

Journal Article AL amyloidosis enhances development of amyloid A amyloidosis Get access J.C.H. Van Der Hilst, J.C.H. Van Der Hilst Departments of General Internal Medicine (463) Search for other works by this author on: Oxford Academic Google Scholar J.W.M. Van Der Meer, J.W.M. Van Der Meer Departments of General Internal Medicine (463) Search for other works by this author on: Oxford Academic Google Scholar J.P.H. Drenth, J.P.H. Drenth Gastroenterology and Hepatology, Radboud University Medical Centre St Radboud, Geert Grooteplein 8, PO Box 9101, 6500 HB Nijmegen, the Netherlands Search for other works by this author on: Oxford Academic Google Scholar A. Simon A. Simon Departments of General Internal Medicine (463)National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, U.S.A. E‐mail: j.vanderhilst@aig.umcn.nl Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 156, Issue 4, 1 April 2007, Pages 748–749, https://doi.org/10.1111/j.1365-2133.2006.07709.x Published: 01 April 2007
UK lags behind other countries on cancer survival but outperforms on low antibiotic prescribing, report finds
Authors: Jacqui Wise
Journal: BMJ (2015)

The United Kingdom lags behind most other high income countries in several measures of healthcare, including preventable admissions to hospital, cancer survival, and mortality from heart attacks and strokes, says a new report by the think tanks the Nuffield Trust and the Health Foundation.1

However, the UK’s performance has improved on almost every measure since 2000, and it does better than other countries in achieving high rates of flu vaccination and lower rates of prescribing of antibiotics.

The report …
Randomized Clinical Trials on Surrogate End Points
Authors: Alberto Morganti
Journal: Journal of the American Society of Nephrology (2006)

Hard end point studies represent the best available evidence for demonstrating the cardiovascular and renal protection that is achievable with a given treatment in hypertensive patients, yet properly designed end point studies require large cohorts of patients and long follow-up, are expensive, and do not provide any insight on the mechanisms that lead to the clinical manifestations. Studies that are based on the incidence of preclinical alterations, i.e., the surrogate end points, may circumvent these limitations provided that their relationship with the major cardiovascular events is scientifically proved. In this respect, among the many surrogate end points that are under investigation, left ventricular hypertrophy, microalbuminuria, and treatment-induced diabetes seem most promising for replacing the hard end points in view of their undisputed mechanistic relationship with the clinical events and of the mounting evidence indicating that from their changes it is possible to predict the clinical outcome of patients. In addition, the limited resources that are required to carry out this kind of investigations make them preferable to hard end point studies for anticipating the cardiovascular and renal benefit associated with the use of antihypertensive agents.
Tuberculosis burden in households of patients with multidrug-resistant and extensively drug-resistant tuberculosis: a retrospective cohort study
Authors: Mercedes C Becerra, Sasha C Appleton, Molly F Franke, Katiuska Chalco, Fernando Arteaga, Jaime Bayona, Megan Murray, Sidney S Atwood, Carole D Mitnick
Journal: The Lancet (2010)
LYMPHOCYTIC AND EOSINOPHILIC REACTION TO ELECTRIC SHOCK TREATMENT
Authors: NAOMI RASKIN, GLADYS HOWARD, SYLVIA SINGER
Journal: American Journal of Psychiatry (1951)

1. A study of lymphocytic and eosinophilic reaction to EST in 23 psychotic patients is presented with a proof that this is a nonspecific reaction to stress. 2. An idea is expressed that lymphocytes contribute to the increase of the immunological reaction of the patient to the potential danger of stress.
Radiofrequency Ablation Versus Partial Nephrectomy in Patients with Solitary Clinical T1a Renal Cell Carcinoma: Comparable Oncologic Outcomes at a Minimum of 5 Years of Follow-Up
Authors: Ephrem O. Olweny, Samuel K. Park, Yung K. Tan, Sara L. Best, Clayton Trimmer, Jeffrey A. Cadeddu
Journal: European Urology (2012)