tbuckley/cabot-search huggingface dataset:
Risk of TB infection and smoking: IFN-γ concentration increases with the cigarettes' number in smokers
Authors: Maria N. Altet-Gomez, Jose Dominguez, Maria Louisa de Souza, Maria Angeles Jimenez, Celia Milá, Jordi Solsona, Irene Latorre, Angels Orcau, Joan Cayla
Journal: European Respiratory Journal (2013)

Aims : Active and passive exposure to tobacco smoke are risk factors for TB infection, evidenced previously using Tuberculin Skin Test. We aim to determine the smoking influence on the TB infection in contacts of TB cases by means of IGRAs testing.

Methods: 806 adults from contact tracing studies were included in the study. In all cases QFN-G-IT and TST were performed. The in vitro tests were performed following the manufacturer’s recommendations. We evaluate personal data and factors related with the TB contact.

Results : Smoking was a TB infection predictive factor (Relative Risk (R.R): 1.92; 95% C.I: 1.65 – 2.23; p< 0.0000001). There was a significant tendency of the R.R with the number of cigarettes smoked daily and also with the concentration of IFN-γ released. Other predictive factors also were analyzed. Comparing smoking/ non smoking the association was significant in all the analyzed variables.

View this table:

Impact of Smoking on the TB infection Relative Risk (R.R). QFN-GIT concentration related with the cigarettes number smoked daily





Conclusion . Using QFN-G-IT in contact tracing studies, smoking has been shown to be a risk factor for TB infection, avoiding the BCG interference on the TST. The IFN- γ concentration is on increase when the cigarettes’ number raises.
Overexpression of HMGA2 Promotes Metastasis and Impacts Survival of Colorectal Cancers
Authors: Xiaochen Wang, Xiyong Liu, Angela Ying-Jian Li, Lirong Chen, Lily Lai, Her Helen Lin, Shuya Hu, Lifang Yao, Jiaping Peng, Sofia Loera, Lijun Xue, Bingsen Zhou, Lun Zhou, Shu Zheng, Peiguo Chu, Suzhan Zhang, David Kong Ann, Yun Yen
Journal: Clinical Cancer Research (2011)

This study aims to address the hypothesis that the high-mobility group A2 (HMGA2), an oncofetal protein, relates to survivability and serves as a prognostic biomarker for colorectal cancer (CRC).This is a retroprospective multiple center study. The HMGA2 expression level was determined by performing immunohistochemistry on surgical tissue samples of 89 CRCs from a training set and 191 CRCs from a validation set. The Kaplan-Meier analysis and COX proportional hazard model were employed to analyze the survivability.Multivariate logistic analysis indicated that the expression of HMGA2 significantly correlates with distant metastasis in training set (odds ratio, OR = 3.53, 95% CI: 1.37-9.70) and validation set (OR = 6.38, 95% CI: 1.47-43.95). Survival analysis revealed that the overexpression of HMGA2 is significantly associated with poor survival of CRC patients (P < 0.05). The adjusted HRs for overall survival were 2.38 (95% CI: 1.30-4.34) and 2.14 (95% CI: 1.21-3.79) in training and validation sets, respectively. Further investigation revealed that HMGA2 delays the clearance of γ-H2AX in HCT-116 and SW480 cells post γ-irradiation, which supports our finding that CRC patients with HMAG2-positive staining in primary tumors had augmented the efficacy of adjuvant radiotherapy (HR = 0.18, 95% CI: 0.04-0.63).Overexpression of HMGA2 is associated with metastasis and unequivocally occurred in parallel with reduced survival rates of patients with CRC. Therefore, HMGA2 may potentially serve as a biomarker for predicting aggressive CRC with poor survivability and as an indicator for better response of radiotherapy.
Triggering Myocardial Infarction by Sexual Activity
Authors: James E. Muller
Journal: JAMA (1996)

<h3>Objective.</h3> —To determine the relative risks of nonfatal myocardial infarction (MI) triggered by sexual activity among the general population and in patients with prior coronary heart disease. <h3>Design.</h3> —Relative risks and effect modification were calculated by the case-crossover method, a new epidemiologic technique designed to quantify the transient change in risk following exposure to a potential disease trigger. <h3>Setting/Participants.</h3> —A total of 1774 patients with MI were interviewed in 45 hospitals throughout the United States. Data were gathered on potential triggers of MI occurring immediately prior to the event and during the previous year. Results are presented for the 858 patients who were sexually active in the year prior to the Ml, with attention to the 273 patients who had coronary artery disease prior to their index Ml, and the effect of regular exertion on risk. <h3>Main Outcome Measure.</h3> —The relative risk of nonfatal MI following sexual activity. <h3>Results.</h3> —Of the 858 patients, 79 (9%) reported sexual activity in the 24 hours preceding Ml, and 27 (3%) reported sexual activity in the 2 hours preceding onset of symptoms of MI. The relative risk of MI occurring in the 2 hours after sexual activity was 2.5 (95% confidence interval [CI], 1.7-3.7). The relative risk of triggering onset of Ml among patients with a history of prior angina (2.1 [95% CI, 0.8-5.8]) or prior Ml (2.9 [95% CI, 1.3-6.5) was not greater than that observed in those without prior cardiac disease. Sexual activity was a likely contributor to the onset of Ml in only 0.9% of cases and regular exertion was associated with decreasing risk. <h3>Conclusions.</h3> —Sexual activity can trigger the onset of MI. However, the relative risk is low, and since the absolute hourly risk of MI is extremely low, the absolute risk increase caused by sexual activity also is extremely low (1 chance in a million for a healthy individual). Moreover, the relative risk is not increased in patients with a prior history of cardiac disease and regular exercise appears to prevent triggering. These findings should be useful for counseling patients and decreasing the fear of sexual activity that often prevents complete rehabilitation from cardiovascular disease. (<i>JAMA</i>. 1996;275:1405-1409)
SODIUM FUSIDATE IN THE TREATMENT OF EEYTHRASMA
Authors: DOROTHY A. SOMERVILLE, W. C. NOBLE, PAMELA M. WHITE, R. H. SEVILLE, J. A. SAVIN
Journal: British Journal of Dermatology (1971)

Journal Article SODIUM FUSIDATE IN THE TREATMENT OF EEYTHRASMA Get access DOROTHY A. SOMERVILLE, DOROTHY A. SOMERVILLE Department of Bacteriology, St John's Hospital for Diseases of the Skin, Homerton Grove, London, E.9 (Drs Somerville, Noble and White), Department of Dermatology, Beaumont Hospital, Lancaster (Dr Seville) and Department of Dermatology, St Thomas's Hospital, London (Dr Savin) Search for other works by this author on: Oxford Academic Google Scholar W. C. NOBLE, W. C. NOBLE Department of Bacteriology, St John's Hospital for Diseases of the Skin, Homerton Grove, London, E.9 (Drs Somerville, Noble and White), Department of Dermatology, Beaumont Hospital, Lancaster (Dr Seville) and Department of Dermatology, St Thomas's Hospital, London (Dr Savin) Search for other works by this author on: Oxford Academic Google Scholar PAMELA M. WHITE, PAMELA M. WHITE Department of Bacteriology, St John's Hospital for Diseases of the Skin, Homerton Grove, London, E.9 (Drs Somerville, Noble and White), Department of Dermatology, Beaumont Hospital, Lancaster (Dr Seville) and Department of Dermatology, St Thomas's Hospital, London (Dr Savin) Search for other works by this author on: Oxford Academic Google Scholar R. H. SEVILLE, R. H. SEVILLE Department of Bacteriology, St John's Hospital for Diseases of the Skin, Homerton Grove, London, E.9 (Drs Somerville, Noble and White), Department of Dermatology, Beaumont Hospital, Lancaster (Dr Seville) and Department of Dermatology, St Thomas's Hospital, London (Dr Savin) Search for other works by this author on: Oxford Academic Google Scholar J. A. SAVIN J. A. SAVIN Department of Bacteriology, St John's Hospital for Diseases of the Skin, Homerton Grove, London, E.9 (Drs Somerville, Noble and White), Department of Dermatology, Beaumont Hospital, Lancaster (Dr Seville) and Department of Dermatology, St Thomas's Hospital, London (Dr Savin) Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 85, Issue 5, 1 November 1971, Pages 450–453, https://doi.org/10.1111/j.1365-2133.1971.tb14051.x Published: 01 November 1971 Article history Accepted: 04 April 1971 Published: 01 November 1971
A multivalent lacto-N-fucopentaose III-lysyllysine conjugate decompacts preimplantation mouse embryos, while the free oligosaccharide is ineffective.
Authors: B A Fenderson, U Zehavi, S Hakomori
Journal: The Journal of Experimental Medicine (1984)

A multivalent lacto-N-fucopentaose (LNFP) III-lysyllysine conjugate was observed to decompact preimplantation mouse embryos. Decompaction was not obtained with free oligosaccharides (LNFP II and III), nor with multivalent LNFP II-lysyllysine or chitotriose-lysyllysine conjugates. These results suggest a role for X hapten recognition during compaction and suggest further that X hapten valency may play a key role in modulating this developmental process.
Type 1 Diabetes Caused by Interferon α-2α in Polycythemia Vera Therapy
Authors: Xian-Ling Wang, Yi-Ming Mu, Zhao-Hui Lu, Ju-Ming Lu, Jing-Tao Dou, Chang-Yu Pan
Journal: Diabetes Care (2010)

One of the main problems with long-term interferon α-2α (IFNα-2α) therapy for chronic viral hepatitis and malignant tumors is the development of autoimmune abnormalities. Up until now, there have been few reports about type 1 diabetes caused by IFNα-2α therapy in patients with polycythemia vera (PV) (1).

A 59-year-old male patient without history of diabetes, whose fasting blood glucose (FBG) and A1C were 70.6 mg/dl and 4.8%, respectively, was diagnosed with PV in October 1999. He had been initially treated with Hydrea for 6 months, but the response had been unfavorable. Therefore, he switched to IFNα-2α (recombinant interferon α-2α; Shanghai Roche Pharmaceuticals, Shanghai, China) therapy, …
Macrophage and Cancer Cell Cross-talk via CCR2 and CX3CR1 Is a Fundamental Mechanism Driving Lung Cancer
Authors: Anja Schmall, Hamza M. Al-tamari, Susanne Herold, Marian Kampschulte, Andreas Weigert, Astrid Wietelmann, Natasha Vipotnik, Friedrich Grimminger, Werner Seeger, Soni Savai Pullamsetti, Rajkumar Savai
Journal: American Journal of Respiratory and Critical Care Medicine (2014)

Recent studies indicate that tumor-associated macrophages (MΦ) with an M2 phenotype can influence cancer progression and metastasis, but the regulatory pathways remain poorly characterized.This study investigated the role of tumor-associated MΦ in lung cancer.Coculturing of MΦ with mouse Lewis lung carcinoma (LLC1) and 10 different human lung cancer cell lines (adenocarcinoma, squamous cell carcinoma, and large cell carcinoma) caused up-regulation of CCR2/CCL2 and CX3CR1/CX3CL1 in both the cancer cells and the MΦ.In the MΦ-tumor cell system, IL-10 drove CCR2 and CX3CR1 up-regulation, whereas CCL1, granulocyte colony-stimulating factor, and MIP1α were required for the up-regulation of CCL2 and CX3CL1. Downstream phenotypic effects included enhanced LLC1 proliferation and migration and MΦ M2 polarization. In vivo, MΦ depletion (clodronate, MΦ Fas-induced apoptosis mice) and genetic ablation of CCR2 and CX3CR1 all inhibited LLC1 tumor growth and metastasis, shifted tumor-associated MΦ toward M1 polarization, suppressed tumor vessel growth, and enhanced survival (metastasis model). Furthermore, mice treated with CCR2 antagonist mimicked genetic ablation of CCR2, showing reduced tumor growth and metastasis. In human lung cancer samples, tumor MΦ infiltration and CCR2 expression correlated with tumor stage and metastasis.Tumor-associated MΦ play a central role in lung cancer growth and metastasis, with bidirectional cross-talk between MΦ and cancer cells via CCR2 and CX3CR1 signaling as a central underlying mechanism. These findings suggest that the therapeutic strategy of blocking CCR2 and CX3CR1 may prove beneficial for halting lung cancer progression.
High-Throughput Detection of Clinically Relevant Mutations in Archived Tumor Samples by Multiplexed PCR and Next-Generation Sequencing
Authors: Richard Bourgon, Shan Lu, Yibing Yan, Mark R. Lackner, Weiru Wang, Victor Weigman, David Wang, Yinghui Guan, Lisa Ryner, Hartmut Koeppen, Rajesh Patel, Garret M. Hampton, Lukas C. Amler, Yulei Wang
Journal: Clinical Cancer Research (2014)

Abstract Purpose: Tailoring cancer treatment to tumor molecular characteristics promises to make personalized medicine a reality. However, reliable genetic profiling of archived clinical specimens has been hindered by limited sensitivity and high false-positive rates. Here, we describe a novel methodology, MMP-seq, which enables sensitive and specific high-throughput, high-content genetic profiling in archived clinical samples. Experimental Design: We first validated the technical performance of MMP-seq in 66 cancer cell lines and a Latin square cross-dilution of known somatic mutations. We next characterized the performance of MMP-seq in 17 formalin-fixed paraffin-embedded (FFPE) clinical samples using matched fresh-frozen tissue from the same tumors as benchmarks. To demonstrate the potential clinical utility of our methodology, we profiled FFPE tumor samples from 73 patients with endometrial cancer. Results: We demonstrated that MMP-seq enabled rapid and simultaneous profiling of a panel of 88 cancer genes in 48 samples, and detected variants at frequencies as low as 0.4%. We identified DNA degradation and deamination as the main error sources and developed practical and robust strategies for mitigating these issues, and dramatically reduced the false-positive rate. Applying MMP-seq to a cohort of endometrial tumor samples identified extensive, potentially actionable alterations in the PI3K (phosphoinositide 3-kinase) and RAS pathways, including novel PIK3R1 hotspot mutations that may disrupt negative regulation of PIK3CA. Conclusions: MMP-seq provides a robust solution for comprehensive, reliable, and high-throughput genetic profiling of clinical tumor samples, paving the way for the incorporation of genomic-based testing into clinical investigation and practice. Clin Cancer Res; 20(8); 2080–91. ©2014 AACR.
Efficient gene transfer into rhesus repopulating hematopoietic stem cells using a simian immunodeficiency virus–based lentiviral vector system
Authors: Hideki Hanawa, Peiman Hematti, Keyvan Keyvanfar, Mark E. Metzger, Allen Krouse, Robert E. Donahue, Steve Kepes, John Gray, Cynthia E. Dunbar, Derek A. Persons, Arthur W. Nienhuis
Journal: Blood (2004)
Beneficial effects of a 3-week course of intramuscular glucocorticoid injections in patients with very early inflammatory polyarthritis: results of the STIVEA trial
Authors: S M M Verstappen, M J McCoy, C Roberts, N E Dale, A B Hassell, D P M Symmons
Journal: Annals of the Rheumatic Diseases (2009)

Objective To evaluate whether treating patients with very early inflammatory polyarthritis (IP) with a 3-week course of intramuscular (IM) methylprednisolone acetate may postpone the need for disease-modifying antirheumatic drugs (DMARDs) and prevent IP from evolving into rheumatoid arthritis (RA). Methods Patients with very early IP (4–10 weeks’ duration) were randomised to receive three injections of either 80 mg IM methylprednisolone acetate or placebo, given at weekly intervals. Assessments were monthly until 6 months after the first injection, and then concluded at 12 months. The primary outcome was the need to start DMARDs by the 6-month assessment. Secondary outcomes included disease activity and final clinical diagnosis by the rheumatologist at 12 months. Results Patients in the placebo group (76%) were more likely to need DMARDs during the first 6 months of the trial than patients in the glucocorticoid group (61%) (adjusted OR = 2.11, 95% CI 1.16 to 3.85, p = 0.015). Disease activity did not differ between the two groups at 12 months, probably because many patients in the placebo group started DMARDs early in the study. After 12 months, the arthritis had resolved without the need for DMARDs in 9.9% (11/111) of the patients in the placebo group and in 19.8% (22/111) in the glucocorticoid-treated group (adjusted OR = 0.42, 95% CI 0.18 to 0.99, p = 0.048). Conclusion Treatment of patients with very early IP with IM methylprednisolone acetate appears to postpone the prescription of DMARDs and prevent one in 10 patients from progressing into RA.
Accumulation of interleukin-1 and interleukin-6 in amniotic fluid: a sequela of labour at term and preterm
Authors: S. Cox
Journal: Human Reproduction Update (1997)

From the finding of miro-organisms or inflammatory mediators, or both, in amniotic fluid (AF), it has been proposed that intrauterine infection is one cause of preterm labour (PTL, intact fetal membranes). This theory, however, remains unproved, i.e. the accumulation of micro-organisms and inflammatory mediators in AF after labour is in progress may be the consequence, not the cause, of labour both at term and preterm. This study was conducted to evaluate this possibility by a comparison of the concentrations of interleukin (IL)-1β and IL-6 in AFs collected before and during PTL (<34 weeks gestation) with those in AFs collected at term (before labour and from the forebag and upper compartments of the amniotic sac during labour). The concentrations of IL-1β and IL-6 in AF were also analysed as a function of the duration of labour (term or preterm) before fluid collection. In addition, studies were conducted to define the sources of IL-1β in AF. A total of 666 AFs were evaluated. IL-1β was not detected (<50 pg/ml) in AFs collected before the onset of labour at any stage of gestation (n = 320), including 170 fluids obtained at term. During labour, IL-1β was detected (<50 pg/ml) in 58 out of 106 (54.7%), 17 out of 64 (26.6%) and 60 out of 176 (34%) of AF samples obtained during PTL, term labour (upper compartment) and term labour (forebag) respectively. AF sampling, as well as labour and delivery, were completed in <18 h in all term pregnancies. However, labour (with cervical dilation) was in progress for >18 h before AF was collected in 39 out of 106 (37%) PTL pregnancies. The incidence of IL-1β-positive samples among AFs collected before 18 h of PTL (23 out of 67; 34%) was indistinguishable from that in AFs collected during labour at term. However, in AFs collected after >18 h PTL, the incidence of IL-1β-positive samples was 35 out of 39 (89.7%). The concentrations of IL-1β (pg/ml; mean ± SEM) in AFs collected during PTL (2680 ± 730; n = 106) were greater than those in AFs collected from the upper compartment and forebag during term labour (436 ± 244, n = 64; and 468 ± 119, n = 176) respectively; this difference, however, was attributable to very high concentrations of IL-1β in AFs in which PTL was in progress for >18 h before AF collection (6021 ± 1832; n = 39). The concentrations of IL-6 in AF were correlated with those of IL-1β (P <0.001). We conclude that IL-1β and IL-6 accumulate in AF in a similar proportion of pregnancies during the first 18 h of term and preterm labour. Therefore, the accumulation of these cytokines in AF cannot be taken as evidence for a role for infection in the pathogenesis of PTL.
Screening for hepatocellular carcinoma in chronic carriers of hepatitis B virus: Incidence and prevalence of hepatocellular carcinoma in a North American urban population
Authors: Morris Sherman, Kevork M. Peltekian, Cindy Lee
Journal: Hepatology (1995)

To prospectively determine the prevalence and annual incidence of hepatocellular carcinoma in hepatitis B carriers in a heterogeneous urban North American population and to assess the diagnostic accuracy of tests used for screening for this cancer.Prospective cohort study of 1,069 chronic carriers of hepatitis B virus using screening with alpha-fetoprotein alone or in combination with ultrasonography every 6 months.The mean age of the cohort was 39 +/- 12 years (+/- SD), 65% were men, 71% were Asians. At the first screening visit, serum alpha-fetoprotein was > or = 20 micrograms/L in 4%. In those subjects who were also screened by ultrasonography during the first visit, 9% were found to have focal lesions. Only 3 subjects were found to have hepatocellular carcinoma at the first screening, giving a prevalence of 281/100,000 chronic carriers of hepatitis B virus. The cohort was followed for 2,340 person-years (mean, 26 months follow-up, with a range from 6 to 60 months). During this period, 11 more subjects, 10 men and 1 woman, were diagnosed to have hepatocellular carcinoma (annual incidence, 470/100,000). In men only, the annual incidence was 657/100,000. During the study, 5 subjects died from hepatocellular carcinoma (annual mortality rate, 214/100,000). Sensitivity and specificity of serum alpha-fetoprotein > 20 micrograms/L were 64.3% and 91.4%, respectively. For ultrasonography, sensitivity was 78.8% and specificity 93.8%.These data suggest that the incidence and prevalence of hepatocellular carcinoma in hepatitis B carriers in our area, an urban North American setting, are as high as in countries where hepatitis B is endemic. Current screening tests have significant false-positive and false-negative rates raising questions about the cost-benefit of screening for hepatocellular carcinoma in our study population.
The Supreme Court and Bedside Rationing
Authors: M. Gregg Bloche
Journal: JAMA (2000)

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