tbuckley/cabot-search huggingface dataset:
Pulmonary artery sling.
Authors: R J McCormack
Journal: Thorax (1969)

Proceedings of the Thoracic Society occluded pulmonary artery, the saturation fell only in those instances when a pressor response was obtained.On bilateral air injection the degree of unsaturation was quantitatively related to the rise in PA pressure.The saturation fell 6-21 % (average 14-3 %).In six experiments, arterial CO2 pressure changed less than ± 2 mm. Hg.During oxygen breathing, embolization lowered the arterial Po2 from 490 to 399 mm.Hg, corresponding to a shunt of 18 % of the cardiac output.This explains only part of the desaturation during air breathing.
ESAM supports neutrophil extravasation, activation of Rho, and VEGF-induced vascular permeability
Authors: Frank Wegmann, Björn Petri, Alexander Georg Khandoga, Christian Moser, Andrej Khandoga, Stefan Volkery, Hang Li, Ines Nasdala, Oliver Brandau, Reinhard Fässler, Stefan Butz, Fritz Krombach, Dietmar Vestweber
Journal: The Journal of Experimental Medicine (2006)

Endothelial cell–selective adhesion molecule (ESAM) is specifically expressed at endothelial tight junctions and on platelets. To test whether ESAM is involved in leukocyte extravasation, we have generated mice carrying a disrupted ESAM gene and analyzed them in three different inflammation models. We found that recruitment of lymphocytes into inflamed skin was unaffected by the gene disruption. However, the migration of neutrophils into chemically inflamed peritoneum was inhibited by 70% at 2 h after stimulation, recovering at later time points. Analyzing neutrophil extravasation directly by intravital microscopy in the cremaster muscle revealed that leukocyte extravasation was reduced (50%) in ESAM−/− mice without affecting leukocyte rolling and adhesion. Depletion of &amp;gt;98% of circulating platelets did not abolish the ESAM deficiency–related inhibitory effect on neutrophil extravasation, indicating that it is only ESAM at endothelial tight junctions that is relevant for the extravasation process. Knocking down ESAM expression in endothelial cells resulted in reduced levels of activated Rho, a GTPase implicated in the destabilization of tight junctions. Indeed, vascular permeability stimulated by vascular endothelial growth factor was reduced in ESAM−/− mice. Collectively, ESAM at endothelial tight junctions participates in the migration of neutrophils through the vessel wall, possibly by influencing endothelial cell contacts.
Spice allergy in celery‐sensitive patients
Authors: J. STÄGER, B. WÜTHRICH, S.G.O. JOHANSSON
Journal: Allergy (1991)

Scratch tests (SCT) with powdered commercial spices were performed in 70 patients with positive skin tests to birch and/or mugwort pollens and celery. Positive SCT to aniseed, fennel, coriander and cumin ‐ all from the same botanical family (Apiaceae) as celery ‐ were observed in more than 24 patients. Spices from unrelated families (red pepper, white pepper, ginger, nutmeg, cinnamon) elicited positive immediate skin test reactions only in three of 11 patients. Specific serum IgE to spices (determined in 41 patients with positive RAST to celery) up to class 3 were seen especially in patients with celerymugwort or celery‐birch‐mugwort association, and concerned various botanical families. Celery‐birch association pattern was linked to positive reactions (RAST classes 1–2) to spices from the Apiaceae family only.
Serum Procollagen Peptides and Collagen Type Vi for the Assessment of Activity and Degree of Hepatic Fibrosis in Schistosomiasis and Alcoholic Liver Disease
Authors: Manal Shahin, Detlef Schuppan, Rüdiger Waldherr, Juha Risteli, Leila Risteli, Eeva-Riitta Savolainen, Christine Oesterling, Hosna M. Abdel Rahman, Abdul M. El Sahly, Samia M. Abdel Razek, Omar El Ruby, Armin Koch, Helmut K. Seitz
Journal: Hepatology (1992)

Schistosomiasis, in contrast to alcoholic liver disease, leads to presinusoidal hepatic fibrosis, which determines the prognosis of the disease. Because conventional liver function tests and liver biopsy specimens provide little information about the dynamics of the fibrotic process, we measured the serum concentrations of procollagen type III N-propeptide and procollagen type I C-propeptide, believed to mainly reflect collagen synthesis, and procollagen type IV C-propeptide and collagen type VI, two presumptive markers of collagen degradation. Determinations were performed in 15 healthy control subjects, 69 patients with various stages of infection with Schistosoma mansoni/Schistosoma haematobium (28 with an early active infection and no organ involvement, 27 with hepatosplenic involvement and 14 with complications of portal hypertension) and 16 patients with alcoholic cirrhosis. In addition, liver biopsy specimens were obtained from 30 schistosomal patients (18 with hepatosplenic involvement and 12 with complications of portal hypertension for histopathological grading and collagen histochemistry. Procollagen type III N-propeptide was significantly elevated in the three patient groups with schistosomiasis when compared with controls (p less than 0.01). Also, patients with higher histological grading showed significantly higher procollagen type III N-propeptide values (p less than 0.05). In alcoholic patients, procollagen type III N-propeptide was even higher and increased parallel to the severity of the disease, determined by using a combined clinical and laboratory index. Procollagen type I C-propeptide was only elevated in early infection (p less than 0.05) and steadily decreased with disease progression.(ABSTRACT TRUNCATED AT 250 WORDS)
A New Fork for Clinical Application: Targeting Forkhead Transcription Factors in Cancer
Authors: Jer-Yen Yang, Mien-Chie Hung
Journal: Clinical Cancer Research (2009)

Abstract Forkhead O transcription factors (FOXO) play a pivotal role in the regulation of a myriad of cellular functions including cell cycle arrest, cell death, and protection from stress stimuli. Activation of cell survival pathways such as phosphoinositide-3-kinase/AKT/IKK or RAS/mitogen-activated protein kinase are known to phosphorylate FOXOs at different sites which cause FOXOs nuclear exclusion and degradation, resulting in the suppression of FOXO's transcriptional activity. Perturbation of FOXO's function leads to deregulated cell proliferation and accumulation of DNA damage, resulting in diseases such as cancer. Emerging evidence shows that active FOXO proteins are crucial for keeping cells in check; and inactivation of FOXO proteins is associated with tumorigenesis, including breast cancer, prostate cancer, glioblastoma, rhabdomyosarcoma, and leukemia. Moreover, clinically used drugs like paclitaxel, imatinib, and doxorubicin have been shown to achieve their therapeutic effects through activation of FOXO3a and FOXO3a targets. In this review, we will focus the novel functions of FOXOs revealed in recent studies and further highlight FOXOs as new therapeutic targets in a broad spectrum of cancers.
Use of alveolar carbon monoxide to measure the effect of ribavirin on red blood cell survival†
Authors: Mark A. Virtue, Julie K. Furne, Samuel B. Ho, Michael D. Levitt
Journal: American Journal of Hematology (2004)

Abstract A major side effect of ribavirin (RBV) treatment is anemia. While this anemia is thought to result from increased RBC turnover, RBC survival has not been determined in subjects receiving RBV due to the complexity of the techniques commonly used to quantitate RBC life span. We recently described a simple, rapid, non‐invasive technique that utilizes measurements of alveolar carbon monoxide (CO) concentration to determine RBC survival. In the present report, this method was employed to assess RBC survival in patients receiving RBV for hepatitis C. Each of the 31 measurements of RBC survival in 12 subjects with RBV‐associated anemia was below the lower limit of normal (77 days), and the average survival (46 ± 14 days) in these subjects was only about 38% of that of healthy controls (122 ± 23 days). Five hepatitis C patients not undergoing RBV treatment had normal RBC survivals (112 ± 17 days). While the mean reticulocyte percentage was significantly elevated in subjects treated with RBV, 59% of these measurements fell within the limits of normal. We conclude that RBV‐associated anemia consistently is associated with reduced RBC survival as determined from breath CO measurements and that this reduced survival frequently is not associated with an elevated reticulocyte count. Am. J. Hematol. 76:107–113, 2004. Published 2004 Wiley‐Liss, Inc.
Effect of zinc supplementation started during diarrhoea on morbidity and mortality in Bangladeshi children: community randomised trial
Authors: Abdullah H Baqui, Robert E Black, Shams El Arifeen, Mohammad Yunus, Joysnamoy Chakraborty, Saifuddin Ahmed, J Patrick Vaughan
Journal: BMJ (2002)

<h3>Abstract</h3> <b>Objective:</b> To evaluate the effect on morbidity and mortality of providing daily zinc for 14 days to children with diarrhoea. <b>Design:</b> Cluster randomised comparison. <b>Setting:</b> Matlab field site of International Center for Diarrhoeal Disease Research, Bangladesh. <b>Participants:</b> 8070 children aged 3-59 months contributed 11 881 child years of observation during a two year period. <b>Intervention:</b> Children with diarrhoea in the intervention clusters were treated with zinc (20 mg per day for 14 days); all children with diarrhoea were treated with oral rehydration therapy. <b>Main outcome measures:</b> Duration of episode of diarrhoea, incidence of diarrhoea and acute lower respiratory infections, admission to hospital for diarrhoea or acute lower respiratory infections, and child mortality. <b>Results:</b> About 40% (399/1007) of diarrhoeal episodes were treated with zinc in the first four months of the trial; the rate rose to 67% (350/526) in month 5 and to &gt;80% (364/434) in month 7 and was sustained at that level. Children from the intervention cluster received zinc for about seven days on average during each episode of diarrhoea. They had a shorter duration (hazard ratio 0.76, 95% confidence interval 0.65 to 0.90) and lower incidence of diarrhoea (rate ratio 0.85, 0.76 to 0.96) than children in the comparison group. Incidence of acute lower respiratory infection was reduced in the intervention group but not in the comparison group. Admission to hospital of children with diarrhoea was lower in the intervention group than in the comparison group (0.76, 0.59 to 0.98). Admission for acute lower respiratory infection was lower in the intervention group, but this was not statistically significant (0.81, 0.53 to 1.23). The rate of non-injury deaths in the intervention clusters was considerably lower (0.49, 0.25 to 0.94). <b>Conclusions:</b> The lower rates of child morbidity and mortality with zinc treatment represent substantial benefits from a simple and inexpensive intervention that can be incorporated in existing efforts to control diarrhoeal disease. <h3>What is already known on this topic</h3> Zinc deficiency is highly prevalent in children in developing countries Zinc supplements given during diarrhoea reduce the duration and severity of treated episodes If given for 14 days during and after diarrhoea, zinc reduces the incidence of diarrhoea and pneumonia in the subsequent two to three months <h3>What this study adds</h3> Zinc used as a treatment for diarrhoea reduces mortality in children Zinc reduces admissions to hospital for diarrhoea The impact of zinc on mortality and morbidity can be achieved in a realistic large scale public health programme
Disodium cromoglycate in dermatitis herpetiformis
Authors: LIONEL FRY, FRANCES SWAIN, JONATHAN LEONARD, R.M.H. McMINN
Journal: British Journal of Dermatology (1981)

Eleven patients with dermatitis herpetiformis, all requiring dapsone to control their rash and taking a normal diet, were given disodium cromoglycate (DSCG) 1.5-1.6 g daily. Eight out of the eleven patients continued to take DSCG for periods varying from 6-11 months, the other three patients chose to discontinue the DSCG before 6 months. Of the eight patients taking DSCG for at least 6 months, none was able to stop taking dapsone. In three of the eight, the dapsone requirements were unaltered, whilst in two it decreased and in three it increased. The mean daily dose of dapsone was 105 mg/day before DSCG and 141 mg/day after DSCG. In the eight patients who took DSCG for at least 6 months, intestinal biopsies were performed before and after this drug. The macroscopic appearance was unchanged in four, improved in two and worse in two. The mean interepithelial lymphocyte count was 346 before and 342 after DSG.
Percutaneous Transhepatic Cholangiography
Authors: S. G. Elkington, D. C. Bernstein
Journal: BMJ (1964)

Chemical and histological studies are often unable to differen tiate chronic extrahepatic obstructive jaundice (due to calculi, neoplasia, or stricture) from chronic intrahepatic obstructive jaundice (caused by primary biliary cirrhosis or by drugs, . notably anabolic steroids and phenothiazine derivatives). Oral and intravenous cholangiography are also ineffective when the serum bilirubin is greater than 2-3 mg./100 ml. In such circumstances percutaneous transhepatic cholangiography may be useful, since this method can demonstrate the dilated intra hepatic biliary system which develops in chronic extrahepatic obstruction ; while a negative result may remove the need for laparotomy in a patient with hepatocellular disease. Since Atkinson et al. (1960) remarked on the revival of interest in this investigation numerous authors (Santos et al., 1960 ; Kaplan, et al., 1961 ; Shaldon et al., 1962 ; Arner et al., 1962 ; Flemma et al., 1963) have agreed on its value. Only one of these reports has come from this country, and the British Medical Journal (1964) suggests that percutaneous transhepatic cholangiography has still to gain general acceptance in Great Britain. This report of a small series with a case history and a brief survey of recent studies may be of interest.
In Patients Younger Than Age 55 Years With Lymph Node–Negative Breast Cancer, Proliferation by Mitotic Activity Index Is Prognostically Superior to Adjuvant!
Authors: Tone Hoel Lende, Emiel A.M. Janssen, Einar Gudlaugsson, Feja Voorhorst, Rune Smaaland, Paul van Diest, Håvard Søiland, Jan P.A. Baak
Journal: Journal of Clinical Oncology (2010)

Purpose In breast cancer, different tools are used for prognostication and adjuvant systemic therapy selection. We compared the accuracy of the online program Adjuvant!, the Norwegian Breast Cancer Group (NBCG) guidelines, and the proliferation factor mitotic activity index (MAI) in patients with lymph node (LN) –negative disease (pN0). Patients and Methods Adjuvant! and MAI thresholds were set to 90% to 95% breast cancer–specific survival (BCSS) rates. These thresholds were 95% for Adjuvant!, 3 for MAI, and as follows for NBCG: pT1 grade 1 + pT1a-b grade 2 to 3; all pN0M0 and estrogen receptor/progesterone receptor positive versus all others. In 516 patients younger than age 55 years (T1-3N0M0) without adjuvant systemic therapy, univariable and multivariable 10-year BCSS rates were estimated. Results Median follow-up time was 118 months. The concordance between MAI and Adjuvant! or NBCG was fair (κ = 0.35 and κ = 0.29, respectively). Adjuvant!, NBCG, and MAI were all prognostically significant (P ≤ .001). In the univariable analysis, the 10-year BCSS of MAI less than 3 versus ≥ 3 was 95% v 71%, respectively, with a hazard ratio of 7.0. In multivariable analysis, MAI was superior to Adjuvant! and NBCG. The 10-year survival of Adjuvant! ≥ 95% versus less than 95% was 91% v 74%, respectively, but stratification by MAI identified subgroups with different prognosis. Similar results occurred for NBCG and MAI. Adjuvant! and NBCG were not prognostic to each other. Conclusion MAI is superior to Adjuvant! and NBCG in prognostication of patients with LN-negative breast cancer younger than age 55 years.
The bradykinin B1 receptor contributes to the cardioprotective effects of AT1 blockade after experimental myocardial infarction
Authors: C TSCHOPE
Journal: Cardiovascular Research (2003)

To investigate the role of the bradykinin B1 receptor (B1R) on the angiotensin receptor AT1 blockade-dependent cardioprotective effects, we studied the B1R regulation in wild-type rats treated with the AT1 antagonist, irbesartan (IRB), and also in transgenic rats with cardiac overexpression of the human AT1 (TGR-alphaMHCAT1) after induction of myocardial infarction (MI). In addition, we treated wild-type rats with IRB and/or the B1R antagonist, B9958, and determined the left ventricular (LV) function.Untreated, IRB (50 mg/kg/day/p.o.), B9958 (0.1 mg/kg/48 h/s.c.), and IRB/B9958-treated Sprague-Dawley rats were submitted to a permanent occlusion of the left descending coronary artery. Six days and three weeks after induction of MI, the LV function was characterized by using a Millar-tip catheter. Myocardial AT1- and B1-mRNA expression were analyzed by RNase-protection assays, B1R protein density by immunohistochemistry.At both time points, LV function had improved by almost 50% after treatment with IRB but remained unchanged in TGR-alphaMHCAT1 after induction of MI compared to their untreated controls. The beneficial effect of IRB was reversed by co-treatment with B9958. The B1R antagonist treatment alone had no effect. A cross-talk between AT1 and B1R was also indicated by an up-regulation of B1R after treatment with IRB on protein and RNA level, while AT1 overexpression reduced B1R expression after induction of MI.These results indicate that the mechanisms of B1R regulation are influenced by the AT1 receptor. Thus, we are able to demonstrate for the first time that the B1R contributes to the cardio-beneficial effects of AT1 blockade.
Quality of life, geriatric assessment and survival in elderly patients with non-small-cell lung cancer treated with carboplatin–gemcitabine or carboplatin–paclitaxel: NVALT-3 a phase III study
Authors: B. Biesma, A.N.M. Wymenga, A. Vincent, O. Dalesio, H.J.M. Smit, J.A. Stigt, E.F. Smit, C.L. van Felius, J.W.G. van Putten, J.P.J. Slaets, H.J.M. Groen
Journal: Annals of Oncology (2011)
The Stress Kinase p38α as a Target for Cancer Therapy
Authors: Ana Igea, Angel R. Nebreda
Journal: Cancer Research (2015)

Abstract p38α is a ubiquitous protein kinase strongly activated by stress signals, inflammatory cytokines, and many other stimuli, which has been implicated in the modulation of multiple cellular processes. There is good evidence in the literature that p38α plays an important tumor-suppressor role by interfering with malignant cell transformation. This is mainly based on the ability of the p38α pathway to regulate tissue homeostasis by integrating signals that balance cell proliferation and differentiation or induce apoptosis. However, recent reports have also illustrated protumorigenic functions for p38α. Thus, p38α signaling may facilitate the survival and proliferation of tumor cells contributing to the progression of some tumor types. In addition, p38α activation helps tumor cells to survive chemotherapeutic treatments. In all these cases, the inhibition of p38α has a potential therapeutic interest. Further elucidation of the context-dependent functions of p38α signaling in tumoral processes is of obvious importance for the use of inhibitors of this pathway in cancer therapy. Cancer Res; 75(19); 3997–4002. ©2015 AACR.
UK Lung Screen (UKLS) nodule management protocol: modelling of a single screen randomised controlled trial of low-dose CT screening for lung cancer
Authors: D. R. Baldwin, S. W. Duffy, N. J. Wald, R. Page, D. M. Hansell, J. K. Field
Journal: Thorax (2011)

The UK Lung Screen (UKLS) is a randomised controlled trial of the use of low-dose multidetector CT for lung cancer screening. It completed the Health Technology Appraisal (HTA)-funded feasibility stage in October 2009 and the pilot UKLS will be initiated in early 2011. The pilot will randomise 4000 subjects to either low-dose CT screening or no screening. The full study, due to start in September 2012, if progression criteria are met, will randomise a further 28 000 subjects from seven centres in the UK. Subjects will be selected if they have sufficient risk of developing lung cancer according to the Liverpool Lung Project risk model. The UKLS employs the ‘Wald Single Screen Design’, which was modelled in the UKLS feasibility study. This paper describes the modelling of nodule management in UKLS by using volumetric analysis with a single initial screen design and follow-up period of 10 years. This modelling has resulted in the development and adoption of the UKLS care pathway, which will be implemented in the planned CT screening trial in the UK.
Conditionally Replicative Adenovirus with Tropism Expanded towards Integrins Inhibits Osteosarcoma Tumor Growth <b> <i>in Vitro</i> </b> and <b> <i>in Vivo</i> </b>
Authors: Adhiambo M. Witlox, Victor W. van Beusechem, Bonnie Molenaar, Hans Bras, Gerard R. Schaap, Ramon Alemany, David T. Curiel, Herbert M. Pinedo, Paul I. J. M. Wuisman, Winald R. Gerritsen
Journal: Clinical Cancer Research (2004)

Abstract Purpose: The clinical course of osteosarcoma (OS) demands the development of new therapeutic options. Conditionally replicative adenoviruses (CRAds) represent promising agents for the treatment of solid tumors, because CRAds have an intrinsic replication capacity that allows in situ amplification and extensive tumor infection through lateral spread. The CRAd AdΔ24 has been developed to replicate selectively in cells with a defective retinoblastoma (Rb) pathway. Because genetic alterations in the Rb pathway are frequently observed in OS, AdΔ24 might be useful in the treatment of this cancer. Experimental Design: Because the lack of Coxsackie adenovirus receptor on OS cells limits the efficacy of CRAd treatment, we explored alternative target molecules on OS. Insertion of an Arg-Gly-Asp (RGD-4C) integrin-targeting motif into the adenovirus fiber knob expanded tropism toward the ανβ3 and ανβ5 integrins. The oncolytic capacity of the CRAd Ad5-Δ24RGD was tested on primary OS cells in vitro and in vivo. Results: The ανβ3and ανβ5 integrins are abundantly expressed on OS cells. RGD-mediated infection augmented adenovirus infection of primary OS cells by two orders of magnitude. Ad5-Δ24RGD was shown to be highly active in killing human OS cell lines, as well as primary cell cultures. Furthermore, intratumoral injections with Ad5-Δ24RGD into established human OS xenografts that were derived directly from a patient with OS refractory for chemotherapeutic treatment caused a significant tumor-growth delay. Furthermore, adenoviral particles could be detected in tumor cells 25 days posttumor injection. Conclusions: Targeting adenovirus toward integrins rendered OS cells more sensitive to killing by Ad5-Δ24RGD. These findings suggest that Ad5-Δ24RGD has potential for use in OS treatment.