tbuckley/cabot-search huggingface dataset:
Interference Between Lymphocytic Choriomeningitis and Rauscher Leukemia in Mice2
Authors: Jung Koo Youn, Georges Barski
Journal: JNCI Journal of the National Cancer Institute (1966)

In a series of 10 independent experiments, performed on 314 adult and 105 newborn BALB/c mice, preinoculation with lymphocytic choriomeningitis (LCM) virus induced a significant protection against the leukemic disease due to infection with Rauscher virus. This protection was evidenced by lower incidence of leukemia, marked prolongation of incubation period, and delayed mortality. A significant proportion of LCM-pretreated animals remained free of leukemia symptoms for their lifespan. The protection was effective in adult mice when LCM virus was inoculated 1 to 5 days before Rauscher virus, being most effective when done 1 or 2 days in advance. In newborn mice the shielding effect of LCM infection persisted longer. It is concluded that concomitant infection with LCM and Rauscher viruses represents a working model demonstrating an efficient and sparing interference by a nonlethal and even asymptomatic viral infection with the development of usually fatal malignancy induced by an oncogenic virus.
Sedentary Behavior and Colorectal Adenoma – Is it a Risk Factor Independent of Physical Activity?
Authors: Vikneswaran Namasivayam, Assam Nkouibert Pryseley, John Connolly, Wan Wei Keat, Lim Kiat Hon, Rafay Azhar, Wong Wai Yin
Journal: Clinical Gastroenterology and Hepatology (2015)

Colorectal cancer is associated with a sedentary lifestyle. Emerging evidence indicate that sedentary behavior is distinct from physical inactivity (ie. too much sitting vs too little exercise) and may have physiologically distinct effects. Prolonged sedentary time is associated with increased all-cause mortality and colorectal carcinoma independent of physical activity levels. The relationship with colorectal adenoma, however, is less well defined. The objective is to determine whether colorectal adenoma are associated with sedentary behavior (defined by sitting hours) independent of physical activity levels. A cross-sectional study was performed as per STROBE guidelines. Eligible subjects (Table 1, Eligibility criteria), aged 45-70 years, scheduled for ambulatory colonoscopy, were prospectively recruited from December 2013 to January 2015. Interviews and anthropometric assessment was conducted by research coordinators. Physical activity data was collected using the validated IPAQ Long questionnaire. Physical activity was characterized both as continuous and categorical variables. Sedentary time was separately measured using the total time reported sitting per week. Baseline assessment was performed prior to colonoscopy to avoid bias. All colonoscopies were performed by gastroenterologists from a tertiary hospital. All polyps were removed or biopsied if removal was not feasible. Histology was reported by a pathologist blinded to the anthropometric and physical activity data. Continuous and categorical data were summarized by median (interquartile range) and frequency (proportion) respectively. Logistic regression was used to identify risk factors of adenoma. 124 patients undergoing colonoscopies were analyzed. 26 patients (21%; 95% CI: 14.7% to 29.0%) had adenoma. Baseline characteristics are reported in Table 2. There was no difference in sitting hours between patients with and without adenoma (2520 vs 2250 minutes, P = .711) after correction for potential confounders (ie, age, gender, obesity, physical activity, smoking).
Calcified pulmonary tumour with dyspnoea
Authors: B el Nakadi, P de Francquen
Journal: European Respiratory Journal (1990)

A B Fig. lA and B. -Posteroanterior and lateral chest X-Ray film demonstrating a large left lower lobe calcified mass associated with pleural calcification.A 67 yr old woman was admitted with chronic dyspnoea increasing over the last six months.The patient's history revealed a left thoracic trauma 49 yrs previously.Physical examination revealed cyanosis and clubbing.Haematocrit was 58% and haemoglobin 188 g•/• 1 • Arterial oxygen tension was 7 kPa.The chest roemgenogram Correspondence: B .El Nakadi, 85
18S ribosomal RNA gene phylogeny for some Rhabditidae related to Caenorhabditis.
Authors: D H Fitch, B Bugaj-Gaweda, S W Emmons
Journal: Molecular Biology and Evolution (1995)

We have investigated the molecular evolution of the nucleotide sequences of 18S ribosomal RNA genes (18S rDNA) from a set of nematodes in the family Rhabditidae (Nematoda: Secernentea). Our aim was to evaluate the usefulness of this gene for molecular systematics of this family, as well as to establish phylogenetic relationships within a group that has potential for comparative studies of the relationship between development and evolution. We determined the 18S rDNA sequences of nine species of nematodes representing six genera within this family (Caenorhabditis briggsae, C. vulgaris, C. remanei, Rhabditis blumi, Rhabditis sp. br, Rhabditella axei, Pellioditis typica. Teratorhabditis palmarum, and Pelodera strongyloides dermatitica). Using hypothetical models for secondary structure as well as nucleotide similarity, these sequences were aligned with the 18S rDNA sequence published by Ellis et al. for C. elegans and with the partial sequences published by Nadler for eight ascaridoid species. We find that 18S rDNA is likely to be a useful tool to resolve relationships at the intrafamilial level. However, 18S rDNA sequences cannot be used to resolve relationships between taxa as closely related as the Caenorhabditis species. Parsimony, minimum-evolution, and maximum-likelihood methods strongly reject Andrássy's proposed phylogenetic classification based on adult morphological characters but support that of Sudhaus as one alternative of a few possible phylogenies. Distances between genera in this family are about eight times as great as distances between tetrapod classes, suggesting rapid rates of substitution, ancient divergence, or both.
Isolation and Identification of a Helper Virus Found in the Moloney Sarcoma-Leukemia Virus Complex
Authors: Peter J. Fischinger, Carolyn O. Moore, Timothy E. O'Connor
Journal: JNCI Journal of the National Cancer Institute (1969)

A leukemia helper virus indigenous to the Moloney isolate of sarcoma virus was isolated in pure form from an infected clone of 3T3 cells. The helper virus has been propagated in chronically infected 3T3 cell subline (IC line) for over 70 weekly transfers. Morphologically the IC cell line does not show overt signs of viral transformation. The IC cells contained no detectable sarcoma virus but they produced high titers of a helper virus (IC) for defective sarcoma. This helper virus could be propagated indefinitely in other susceptible murine cells. Attempts at superinfection of IC cells by either Rauscher or Moloney pseudotypes of sarcoma virus showed that IC cells were completely resistant to either sarcoma variant. Both the helper virus and the defective sarcoma virus could be specifically neutralized by anti-Moloney leukemia virus antisera. Inoculation of newborn Swiss mice with the IC virus resulted in a lymphoma essentially identical to the Moloney leukemia syndrome. Cell-free extracts of lymphomatous organs contained high titers of leukemogenic virus. It is concluded that the helper virus found in the Moloney isolate of murine sarcoma is true Moloney leukemia virus.
L-arginine does not prevent the renal effects of endothelin in humans.
Authors: J A Bijlsma, A J Rabelink, K A Kaasjager, H A Koomans
Journal: Journal of the American Society of Nephrology (1995)

The infusion of endothelin to obtain plasma levels as present in sodium-retaining conditions such as heart failure and hepatorenal syndrome has been shown to cause sodium retention and renal vasoconstriction. Whether these renal effects of endothelin could be modulated by the stimulation of nitric oxide production by the infusion of L-arginine was examined. Therefore, the renal and endocrine effects of the systemic administration of endothelin (2.5 ng/kg per minute for 90 min), L-arginine (5 mg/kg per minute for 90 min), or the combination of endothelin and L-arginine were studied in healthy subjects under clearance conditions. During endothelin infusion, plasma endothelin levels rose from 3.0 +/- 0.2 to 14.1 +/- 2.4 pmol/L (P < 0.01). Mean arterial pressure increased by 7 mm Hg (P < 0.01). The effects on renal function were disproportionately large: renal vascular resistance increased from 77.5 +/- 3.2 to 124.1 +/- 6.7 mm Hg/min per liter (P < 0.01), and sodium excretion fell from 178 +/- 30 to 83 +/- 11 mumol/min (P < 0.01). Endothelin had no effect on urinary nitrite excretion. L-Arginine caused a fall in blood pressure of 5 mm Hg (P < 0.01) and decreased renal vascular resistance by 12% (P < 0.05). Sodium excretion increased twofold. This was associated with an increase in urinary nitrite excretion from 112 +/- 36 to 465 +/- 190 nmol/min (P < 0.01), suggesting stimulation of renal nitric oxide production. During the combination of endothelin and L-arginine, urinary nitrite excretion increased similarly.(ABSTRACT TRUNCATED AT 250 WORDS)
Microfluidic Generation of Monodisperse, Structurally Homogeneous Alginate Microgels for Cell Encapsulation and 3D Cell Culture
Authors: Stefanie Utech, Radivoje Prodanovic, Angelo S. Mao, Raluca Ostafe, David J. Mooney, David A. Weitz
Journal: Advanced Healthcare Materials (2015)

Monodisperse alginate microgels (10–50 μm) are created via droplet-based microfluidics by a novel crosslinking procedure. Ionic crosslinking of alginate is induced by release of chelated calcium ions. The process separates droplet formation and gelation reaction enabling excellent control over size and homogeneity under mild reaction conditions. Living mesenchymal stem cells are encapsulated and cultured in the generated 3D microenvironments. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Evaluation of Minimal Residual Disease Using Reverse-Transcription Polymerase Chain Reaction in t(8;21) Acute Myeloid Leukemia: A Multicenter Study of 51 Patients
Authors: F. Morschhauser, J.M. Cayuela, S. Martini, A. Baruchel, P. Rousselot, G. Socié, P. Berthou, J.P. Jouet, N. Straetmans, F. Sigaux, P. Fenaux, C. Preudhomme
Journal: Journal of Clinical Oncology (2000)

PURPOSE: Most studies using various reverse-transcription polymerase chain reaction (RT-PCR) techniques reported that the detection of the AML1-ETO fusion transcript was a common finding in long-term complete remission (CR) in acute myeloid leukemia (AML) with t(8;21) translocation. However, larger prospective studies with interlaboratory quality control may be important to investigate more precisely the clinical usefulness of studying minimal residual disease with RT-PCR in t(8;21) AML. PATIENTS AND METHODS: We collected 223 marrow samples from 51 patients with t(8;21) AML diagnosed in five centers and tested all samples by two different RT-PCR techniques (a nested technique and a one-step technique, with a sensitivity of 10 −6 and 10 −5 , respectively) in two different laboratories. RESULTS: Samples from 14 patients in long persistent CR (median follow-up duration, 112 months) were taken at least twice, and all were PCR-negative by both techniques. Samples were prospectively taken from 37 patients after achievement of first CR and/or second CR, before intensive consolidation treatment, and every 3 to 6 months after completion of therapy. Patients who converted to PCR negativity with the one-step technique (60%) or both techniques (48%) after CR achievement had a longer CR duration than those with persistently positive PCR results (two-sided log-rank test, P = .0001). Patients who became PCR-negative with the one-step technique before intensive consolidation (23%) had a lower relapse rate (11% v 72%) and a longer CR duration than those who remained persistently PCR-positive at that point (two-sided log-rank test, P = .0015). CONCLUSION: Patients with AML with t(8;21) in long-term remission were all PCR-negative. In prospectively studied patients, a good correlation was found between negative PCR results and absence of relapse. Early negative results with the one-step RT-PCR technique, before consolidation treatment, seemed to carry an especially good prognosis, suggesting that RT-PCR analysis could help in choosing the type of consolidation therapy in patients with t(8;21) AML.
A short-term model of COPD identifies a role for mast cell tryptase
Authors: Philip Hansbro, Emma Beckett, Richard Stevens, Andrew Jarnicki, Peter Wark, Paul Foster
Journal: European Respiratory Journal (2013)

Chronic obstructive pulmonary disease (COPD) represents a group of diseases that are difficult to treat effectively, with cigarette smoke (CS) being the main causative agent. COPD is currently irreversible, and often continues to develop even after smoking cessation. Lack of suitable models that represent the key features of the disease in a reasonable amount of time have been lacking, which would aid in the development of appropriate therapies. We have developed a mouse model of CS-induced COPD that manifests key components of the human disease. These mice develop inflammation, mucus hypersecretion, airway remodeling as well as emphysema, accompanied by reduced lung function after 8 weeks of exposure. These characteristic features of COPD were glucocorticoid-resistant and did not spontaneously resolve. In addition, smoke induced systemic effects including changes in skeletal muscle and the heart, and increased susceptibility to respiratory infections also were observed. As tryptases can play an important role in tissue destruction and lung homeostasis, we determined whether mast cell (MC)-derived protease-6 affected disease, and whether it effected activation of key immune cells. We demonstrate here that key disease aspects are significantly reduced in MC-derived protease-6 deficient mice. In addition, macrophages are also required for disease development. MC-derived protease-6 mediated its effects partly through the induction of pro-inflammatory cytokines from macrophages, including TNFα, CXCL1 and IL-1b. This model can be used to further our knowledge of mechanisms involved in and effect of therapies on COPD development.
Treg-Mediated Immune Tolerance and the Risk of Solid Cancers: Findings From EPIC-Heidelberg
Authors: Sebastian Dietmar Barth, Janika Josephine Schulze, Tilman Kühn, Eva Raschke, Anika Hüsing, Theron Johnson, Rudolf Kaaks, Sven Olek
Journal: JNCI Journal of the National Cancer Institute (2015)

Laboratory-based, mechanistic, and prognosis studies suggest that a shift from antitumor immunity towards tumor-immune tolerance plays a major role in carcinogenesis. However, prospective epidemiological studies on the consequences of differing immune tolerance levels prior to clinical manifestation are missing. A case-cohort study embedded in EPIC-Heidelberg was conducted comprising incident cases of breast (n = 399), colorectal (n = 185), lung (n = 149), and prostate (n = 378) cancer, which occurred during 6.6 years of follow-up, and a subcohort (n = 807). Foxp3+ regulatory T-lymphocytes and CD3+ T-lymphocytes were measured by quantitative polymerase chain reaction–based DNA methylation analysis in prediagnostic leukocyte samples. Hazard ratios (HRs) for associations of cancer risk with the ratio of both parameters, the "cellular ratio of immune tolerance" (ImmunoCRIT), were estimated using Cox regression models. All statistical tests were two-sided. ImmunoCRIT values were positively associated with the risk of lung (highest vs lowest tertile, HR = 1.98, 95% confidence interval = 1.06 to 3.69, Ptrend = .0263) and colorectal cancer (HR = 1.59, 95% CI = 0.99 to 2.54, Ptrend = .0069) after multivariable adjustment, but not with prostate cancer risk. Regarding breast cancer significant heterogeneity by estrogen receptor (ER) status was observed (Pheterogeneity = .02), and the ImmunoCRIT was associated with the risk of ER-negative breast cancer (HR = 3.34, 95% CI = 1.52 to 7.35, Ptrend ≤ .001), but not ER-positive breast cancer. The present study indicates that increased peripheral immune tolerance may be an independent risk factor for lung, colorectal, and ER-negative breast cancer, whereas its role on the development of prostate and ER-positive breast tumors remains uncertain.
Eosinophilic pleural effusions - Is everything clear?
Authors: Jan Plutinsky, FrantiÅ¡ek Dvorak, Zuzana Taligova, Renata Sabova, Stanislava Sabova
Journal: European Respiratory Journal (2012)

Introduction: Eosinophilic pleural effusion (EPE) for long time was considered a result of benign concomitant diseases with a good prognosis. Blood or air in the pleural fluid (PF) could cause EPE in most cases. In some EPE the aetiology is unknown. Epidemiology is varied from 5-12%. We analysed our patients (pts) with PF and we focused on the group with EPE.  Aim: To share our own experience with diagnosis, differential diagnosis and prognosis of EPE.  Methods: We analysed 390 pts with a definitely confirmed diagnosis of pleural effusion. The diagnosis was confirmed biochemically, cytological analyses of PF, histologically by blind pleural biopsy or by medical thoracoscopy. Cell count was made routinely. Light9s rule was used for the diagnosis of transudates and exudates. EPE was defined when 10% or more eosinophilic leucocytes appeared on a differential cell count.  Results: 3 M and 10 F, median age 71 years (51-85 yrs) had EPE (3.33%). From them 3 had lung carcinoma, 1 breast carcinoma, 2 had pneumonia, 2 heart failure, 1 pneumothorax, 1 traumatic PE, 1 pancreatitis as diseases causing EPE and only 1/13 had idiopathic EPE (7.6%), or 0.25% from 390 pts. Median of eosinophils in PE was 25% (from 10% to 88%). Ten of the EPE were exudates and 3 transudates.  Conclusions: In our cohort of pts with EPE 30.8% had carcinoma and only 1 was idiopathic. Median age is high. Prognosis is better in 2/3 pts and it was interesting that 3 pts had transudates. Also of interest was the lower incidence of EPE in our cohort in comparison to literature sources. EPEs present the inhomogeneous group of pleural diseases with unclear prognosis.
Deficiency of <scp>FHL</scp>2 attenuates airway inflammation in mice and genetic variation associates with human bronchial hyper‐responsiveness
Authors: K. Kurakula, M. Vos, A. Logiantara, J. J. T. H. Roelofs, M. A. Nieuwenhuis, G. H. Koppelman, D. S. Postma, C. A. Brandsma, D. D. Sin, Y. Bossé, D. C. Nickle, L. S. van Rijt, C. J. M. de Vries
Journal: Allergy (2015)

Asthma is an inflammatory disease that involves airway hyper-responsiveness and mucus hypersecretion. The LIM-only protein FHL2 is a crucial modulator of multiple signal transduction pathways and functions as a scaffold in specific protein-protein interactions.We sought to investigate the role of FHL2 in airway inflammation.Allergic airway inflammation was induced in WT and FHL2-knock out (FHL2-KO) mice with ovalbumin (OVA). Lung tissue, bronchoalveolar lavage fluid (BALF) and draining lymph node cells were analysed for inflammation. FHL2 loss and gain of function studies were performed in lung epithelial cells.FHL2-deficient mice challenged with OVA show significantly reduced airway inflammation as evidenced by reduced infiltration of inflammatory cells including eosinophils, dendritic cells, B cells and T cells. Furthermore, mucus production was decreased in FHL2-KO mice. In BALF, the levels of IL-5, IL-13, eotaxin-1 and eotaxin-2 were significantly lower in FHL2-KO mice. In addition, draining lymph node cells from FHL2-KO mice show reduced levels of IL-5 and IL-13. Consistent with this, OVA-specific serum IgG and IgE levels were reduced in FHL2-KO mice. We also found that phosphorylation of ERK1/2 is markedly attenuated in FHL2-KO lung. Knock-down of FHL2 in human lung epithelial cells resulted in a striking decrease in ERK1/2 phosphorylation and mRNA levels of inflammatory cytokines and MUC5AC, whereas FHL2 overexpression exhibited opposite effects. Finally, the SNP rs4851765 shows an association with the severity of bronchial hyper-responsiveness.These results highlight functional involvement of FHL2 in airway inflammation and identify FHL2 as a novel gene associated with asthma severity in human.
What happens to pneumocystis prophylaxis use when antiretroviral therapy is widely available
Authors: Santino Capocci, Colette Smith, Neal Marshall, Rob Tsintas, Fernandez Thomas, Mervyn Tyrer, Margaret Johnson, Marc Lipman
Journal: European Respiratory Journal (2012)

Background and Aims:  International guidance advocates primary prophylaxis to prevent Pneumocystis pneumonia (PCP) predominantly in HIV infected individuals with a blood CD4 count   Methods:  Observational cohort review using the Royal Free Hospital HIV database of subjects accessing care between 2002 and 2011. Use of PCP prophylaxis medication was recorded cross sectionally at the beginning of each calendar year. Data were related to pharmacy prescriptions and clinical and immune outcomes.  Results:  The number in the total cohort rose from 1553 to 2739 persons; and the overall use of ART increased from 63% to 81%. The proportion of subjects with blood CD4   Discussion:  Changes in the HIV population and their use of ART has led to quantitative and qualitative shifts in PCP prophylaxis. How much this reflects local issues, such as the relative availability of nebulised pentamidine in our Centre, remains to be determined.
Bladder preservation by combined modality therapy for invasive bladder cancer.
Authors: L A Kachnic, D S Kaufman, N M Heney, A F Althausen, P P Griffin, A L Zietman, W U Shipley
Journal: Journal of Clinical Oncology (1997)

To update the efficacy of a selective multimodality bladder-preserving approach by transurethral resection (TURBT), systemic chemotherapy, and radiation therapy.From 1986 through 1993, 106 patients with muscle-invading clinical stage T2 to T4a,Nx,M0 bladder cancer were treated with induction by maximal TURBT and two cycles of chemotherapy (methotrexate, cisplatin, vinblastine [MCV]) followed by 39.6-Gy pelvic irradiation with concomitant cisplatin. Patients with a negative postinduction therapy tumor site biopsy and cytology (a T0 response, 70 patients) plus those with less than a T0 response but medically unfit for cystectomy (six patients), received consolidative chemoradiation to a total of 64.8 Gy. Surgical candidates with less than a T0 response (13 patients) and patients who could not tolerate the chemoradiation (six patients) went to immediate cystectomy. The median follow-up duration is 4.4 years.The 5-year actuarial overall survival and disease-specific survival rates of all patients are 52% and 60%, respectively. For clinical stage T2 patients, the actuarial overall survival rate is 63%, and for T3-4, 45%. Thirty-six patients (34%) underwent cystectomy, all with evidence of tumor activity, including 17 with an invasive recurrence. The 5-year overall survival rate with an intact functioning bladder is 43%. Among 76 patients who completed bladder-preserving therapy, the 5-year rate of freedom from an invasive bladder relapse is 79%. No patient required cystectomy for treatment-related bladder morbidity.Combined modality therapy with TURBT, chemotherapy, radiation, and selection for organ-conservation by response has a 52% overall survival rate. This result is similar to cystectomy-based studies for patients of similar age and clinical stages. The majority of the long-term survivors retain fully functional bladders.