tbuckley/cabot-search huggingface dataset:
Effectiveness of a respiratory physiotherapy program on pleural effusion: A randomized controlled trial
Authors: Marie Carmen Valenza, Gerald Valenza-Demet, Irene Torres-Sanchez, Irene Cabrera-Martos
Journal: European Respiratory Journal (2013)

Pleural effusions are due to a variety of diseases. They are usually treated conservatively, sometimes combined with surgery and medical treatment. The aim of the present study is to demonstrate the effectiveness of a respiratory physiotherapy protocol (PT) in patients with Pleural Effusion.  Physical treatment of patients with pleural effusion was accomplished at the San Cecilio University Hospital and it consisted of directed breathing exercises, mobilizations and incentive spirometry. Its effects were examined in a group of 103 patients, who received both conservative and physical treatment and results were compared with the control group patients, treated only conservatively.  Comparative analysis confirmed a significant improvement of lung function parameters (VC, FEV1, PEF) as well as of radiographic repercussions on the affected side of the thorax in favour of the physiotherapy group. The length of hospital stay was also reduced in physiotherapy treatment group when compared by medical treatment only(p  The applied physical therapy resulted in: 1) significant improvement of all examined lung function parameters in the PT group, which was not registered in the control group; 2) significant improvement of the radiology in general; and 3)reduced length of stay. It is finally concluded that PT should necessarily be included in the treatment of pleural effusion.
Interleukin-12 and -23 Control Plasticity of CD127+ Group 1 and Group 3 Innate Lymphoid Cells in the Intestinal Lamina Propria
Authors: Jochem H. Bernink, Lisette Krabbendam, Kristine Germar, Esther de Jong, Konrad Gronke, Michael Kofoed-Nielsen, J. Marius Munneke, Mette D. Hazenberg, Julien Villaudy, Christianne J. Buskens, Willem A. Bemelman, Andreas Diefenbach, Bianca Blom, Hergen Spits
Journal: Immunity (2015)
Perspectives on Biologically Active Camptothecin Derivatives
Authors: Ying-Qian Liu, Wen-Qun Li, Susan L. Morris-Natschke, Keduo Qian, Liu Yang, Gao-Xiang Zhu, Xiao-Bing Wu, An-Liang Chen, Shao-Yong Zhang, Xiang Nan, Kuo-Hsiung Lee
Journal: Medicinal Research Reviews (2015)

Camptothecins (CPTs) are cytotoxic natural alkaloids that specifically target DNA topoisomerase I. Research on CPTs has undergone a significant evolution from the initial discovery of CPT in the late 1960s through the study of synthetic small-molecule derivatives to investigation of macromolecular constructs and formulations. Over the past years, intensive medicinal chemistry efforts have generated numerous CPT derivatives. Three derivatives, topotecan, irinotecan, and belotecan, are currently prescribed as anticancer drugs, and several related compounds are now in clinical trials. Interest in other biological effects, besides anticancer activity, of CPTs is also growing exponentially, as indicated by the large number of publications on the subject during the last decades. Therefore, the main focus of the present review is to provide an ample but condensed overview on various biological activities of CPT derivatives, in addition to continued up-to-date coverage of anticancer effects.
Abstract 813: A combination of cisplatin, irinotecan, and paclitaxel (CIP) as frontline treatment of patients with metastatic esophageal cancer (mEC)
Authors: Thomas A. Giever, Paul S. Ritch, James P. Thomas, Lauren A. Wiebe, George B. Haasler, Mario G. Gasparri, David Johnstone, Candice A. Johnstone, Elizabeth M. Gore, Ben George
Journal: Cancer Research (2014)

Abstract Introduction: Median survival associated with mEC is 9-12 months. While systemic therapy is the mainstay of treatment for mEC, there is no consensus regarding the best frontline chemotherapy combination. We evaluated the efficacy of CIP (Cisplatin 30 mg/m2, Irinotecan 50 mg/m2 and Paclitaxel 50 mg/m2 on days 1 and 8 of a 21 day cycle) in patients with mEC. Methods: We performed a retrospective review to identify mEC patients at the Medical College of Wisconsin (MCW) who were treated with frontline CIP between January 1, 2005 and December 31, 2010. Relevant clinical information was collected through a review of the electronic medical record. This study was approved by the Institutional Review Board at MCW. Results: We identified 13 patients who were treated with CIP as frontline therapy for mEC. The median age at diagnosis was 59 years (range 48-71 years), 12 (92%) patients were male, and 9 patients (69%) had adenocarcinoma with the remaining being squamous cell carcinoma. Eleven patients (85%) presented with metastatic disease, while 2 patients (15%) were diagnosed with metastatic disease after having undergone initial surgical resection with disease free intervals of 39 and 14 months respectively. The most common sites of metastases were lymph nodes (11 patients), liver (6 patients), lung (4 patients), bone (3 patients), and peritoneum (2 patients); 77% of patients had at least 2 sites of metastases. The median number of chemotherapy cycles administered was 7 (range 1-14). Four patients (31%) developed grade 3/4 toxicities including neutropenia in 3 patients, nausea in 1 patient, and anemia in 1 patient. One patient (8%) had a complete response (CR), 7 patients (54%) had a partial response (PR), 2 patients (15%) had stable disease (SD), and 3 patients (23%) developed progressive disease (PD). The median progression free survival (PFS) was 5 months (range 0-29 months) and the median overall survival (OS) was 10 months (range 3-36 months). Conclusion: CIP is an active and well tolerated regimen in patients with mEC that merits prospective evaluation. Citation Format: Thomas A. Giever, Paul S. Ritch, James P. Thomas, Lauren A. Wiebe, George B. Haasler, Mario G. Gasparri, David Johnstone, Candice A. Johnstone, Elizabeth M. Gore, Ben George. A combination of cisplatin, irinotecan, and paclitaxel (CIP) as frontline treatment of patients with metastatic esophageal cancer (mEC). [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 813. doi:10.1158/1538-7445.AM2014-813
Website of the week: The ageing population
Authors: D. Carnall
Journal: BMJ (1999)

Diagnose and be damned Doctors who have exposed child abuse are being hounded.Harvey Marcovitch, editor of Archives of Disease in Childhood, believes that the media are making matters worse A few years ago, I found a neat roll of documents tucked behind a radiator outside my office.It contained letters, minutes of meetings, and suggestions on how to run a campaign to combat doctors' diagnoses of child abuse.Most were reasoned, but some were written in crude language and bristled with anger.The package had been planted where I would find it.I think it was meant to frighten me.Last year, sitting in the editorial office of Archives of Disease in Childhood, I was handed some letters, headed with a private address, asking whether we had ever received for publication, but subsequently rejected, papers from the North Staffordshire Hospital on continuous negative pressure ventilation.My explanation that we did not keep records of rejected submissions beyond one year met with incredulity.The correspondent wrote again complaining that she knew I was covering up the existence of unethical experiments on newborn babies.
384. Stem Cells Expressing SMAD 8: A Platform for Tendon Regeneration
Authors: Gadi Pelled, Andrea Hoffman, Gadi Turgeman, Peter Eberle, Yoram Zilberman, Hadassah Shinar, Keren Keinan-Adamsky, Andreas Winkel, Gil Navon, Gerhard Gross, Dan Gazit
Journal: Molecular Therapy (2004)

Current reconstructive techniques to repair torn tendons consist of autografts, allografts or synthetic prosthesis. Unfortunately, none of these surgical alternatives provide a long-term adequate solution. In this study, we defined a novel mechanism that mediates the differentiation of MSCs into tendon based on the SMAD8 signaling molecule, which could be used as a regenerative platform. A variant of SMAD8, deficient of the MH1 domain, was transfected to MSCs that express bone morphogenetic protein 2 (BMP2). The in vitro phenotype of the engineered MSCs was evaluated using RT-PCR, Histochemistry and morphology. In addition, the cells were injected into subcutaneous tissue and into the kidney capsule of female C3H/HeN mice in order to assess the tissue formation in vivo. Engineered MSCs, also expressing Lacz or Luciferase marker genes, were implanted on a Collagen sponge into a 3 mm partial defect of nude rats Achilles tendon. 5 weeks post implantation, the area of the injection or implantation was isolated and analyzed by light and electron microscopy, histochemical staining, RT-PCR and double quantum filtered (DQF) MRI. Cell survival in the implantation site was non-invasively and quantitatively demonstrated in vivo by the detection of Luciferase bioluminescence, using a CCCD system. Our results indicated a tenocytic phenotype of the engineered MSCs, based on microscopy and the expression of the tendon characteristic genes, Six 1and Scleraxis. Formation of tendon tissue in vivo was confirmed by the analysis of injected implants, which revealed the dense connective tissue with parallel-organized fibers and spindle shaped cells (A). Electron microscopic analysis showed tightly packed collagen fibers adjacent to fibroblast-shaped cells with active Endoplasmic Reticulum (B). Moreover, we were also able to repair Achilles tendon defects with the engineered MSCs. CCCD imaging quantitatively monitored cells survival in the operated tendon, and imunohistochmical staining detected the labeled implanted cells in site (C &F). DQF MRI analysis proved that highly ordered Collagen fibers were formed in the site of implantation as opposed to the control group (D, E). Since the expression of BMP2 is known to drive MSCs to osteogenic differentiation, we propose that the expression of SMAD8 in MSCs induces an inhibition of the BMP2 signaling pathway, resulting in the differentiation of MSCs into tendon cells. This is the first study showing that a particular SMAD signaling cascade is involved in tendon formation. Moreover, this is the first time a regenerative effect is shown to be exerted by the combination of a secreted factor and a signaling molecule. These findings may have considerable importance for therapeutic avenue in tendon in which SMAD 8 signaling plays a pivotal role Figure 1.
Genetic Concepts and Neoplasia
Authors: Anthony C. Allison
Journal: JNCI Journal of the National Cancer Institute (1968)

Journal Article Genetic Concepts and Neoplasia Get access JNCI: Journal of the National Cancer Institute, Volume 41, Issue 6, December 1968, Page 1495, https://doi.org/10.1093/jnci/41.6.1495-a Published: 01 December 1968
Abstract 3601: Stromal fibroblasts mediate extracellular matrix remodeling and invasion of scirrhous gastric carcinoma cells
Authors: Hideki Yamaguchi, Kazuyoshi Yanagihara, Masakazu Yashiro, Ryuichi Sakai
Journal: Cancer Research (2014)

Abstract Scirrhous gastric carcinoma (SGC; also called diffusely infiltrative carcinoma, Borrmann's type-IV carcinoma, or the linitis plastica-type carcinoma) has the worst prognosis of all gastric cancers, owing to its rapid expansion by invasion and frequent peritoneal dissemination. Due to the increased proliferation of stromal fibroblasts (SFs) that occurs within SGC lesions and the peritoneal metastatic sites, SFs have been proposed to support the progression of this disease. However, the biological and molecular basis and the pathological role of the intercellular interaction between SGC cells and SFs remain largely unknown. In this study, we investigated the role of SFs in the invasion of the extracellular matrix (ECM) by SGC cells. When SGC cells were cocultured with SFs derived from SGC tissue on three-dimensional (3D) Matrigel, they were attracted together to form large cellular aggregates that invaded within the Matrigel. Time-lapse imaging revealed that this process was associated with extensive contraction and remodeling of the ECM. Immunofluorescence and biochemical analysis showed that SGC cells stimulate phosphorylation of myosin light chain and actomyosin-mediated mechanical remodeling of the ECM by SFs. By utilizing this assay system for inhibitor library screening, we have identified several inhibitors that potently suppress the cooperation between SGC cells and SFs to form the invasive structures. Among them, a Src inhibitor dasatinib impaired the interaction between SGC cells and SFs both in vitro and in vivo and effectively blocked peritoneal dissemination of SGC cells. These results indicate that SFs mediate mechanical remodeling of the ECM by SGC cells, thereby promoting invasion and peritoneal dissemination of SGC. Citation Format: Hideki Yamaguchi, Kazuyoshi Yanagihara, Masakazu Yashiro, Ryuichi Sakai. Stromal fibroblasts mediate extracellular matrix remodeling and invasion of scirrhous gastric carcinoma cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3601. doi:10.1158/1538-7445.AM2014-3601
Chromosome 7 polysomy and biomarker combinations as potential predictors of gefitinib efficacy in non-small cell lung cancer (NSCLC).
Authors: John S. Coon, Larry Morrison, Kris Jacobson, Susan Jewell, Meryl Gale, Victoria Villaflor, Ann Mauer, Tariq Muzzafar, Lela Buckingham, Philip Bonomi
Journal: Clinical Cancer Research (2006)

B65   Studies of epidermal growth factor receptor (EGFR) protein expression,  EGFR  gene copy number on 7p12, and mutational status have yielded conflicting results with regard to efficacy of tyrosine kinase inhibitors (TKIs). The discrepant results may be due to methodology differences between laboratories and variation in patient populations affording different sensitivities to TKIs. To address these inconsistencies, several biomarkers were analyzed in assessable tumor tissue from 82 NSCLC patients treated with gefitinib using the endpoints of progression-free survival (PFS) and overall survival (OS). Chromosome 7 (C7) and  EGFR  copy numbers were tested by FISH (C7 represented by centromeric probe).  EGFR  activating gene mutations were detected by single strand conformation polymorphism, sequence specific primer-PCR, and sequencing. EGFR, pAKT, and PTEN protein expression were measured by immunohistochemistry.  EGFR  activating gene mutations [p = 0.047, 23.8 vs. 7.6 months (mo)] and polysomy 7, >3.6 C7/cell (p = 0.015; 16.2 vs. 6.0 mo) were significantly associated with longer OS. In contrast, relative  EGFR  copy gain ( EGFR /C7 >1) was associated with longer PFS (p =0.022; 4.1 vs. 2.0 mo), but not OS (p = 0.15). EGFR protein expression was marginally associated with PFS (p = 0.0765), but not OS (p=0.75). Although protein expression of the downstream markers, pAKT and PTEN alone, were not significantly associated with PFS (p = 0.758 and p = 0.127, respectively), or OS (p=0.094 and 0.091, respectively), the combination of polysomy 7 with pAKT or PTEN expression were associated with longer OS [24.5 mo for either biomarker vs. 5.9 mo (p = 0.002) or 7.1 months (p = 0.040), respectively]. Other combinations significantly associated with longer OS included EGFR and pAKT protein expression (p = 0.030),  EGFR  mutation status and pAKT protein expression (p = 0.040),  EGFR  mutation status and PTEN protein expression (p = 0.023), and relative  EGFR  copy gain (specimens with ≥34 % cells with  EGFR >C7) and PTEN protein expression (p = 0.004). Polysomy 7 was the single significant biomarker with the lowest p-value for longer OS in this patient group. Furthermore, the state of downstream factors may contribute to associations between OS and  EGFR  protein expression, mutation status or copy number.
Neutrophil function in chronic bronchitis
Authors: P Venge, S Rak, L Steinholtz, L Håkansson, G Lindblad
Journal: European Respiratory Journal (1991)

This study was initiated with the question: Do defects in neutrophil functions predispose patients with chronic bronchitis to their recurrent bacterial infections? Forty five patients with chronic bronchitis and recurrent bacterial infections were studied. A number of aspects of neutrophil functions reflecting migratory and phagocytic functions and oxidative metabolism were measured in vitro, once in all 45 patients and 3 times in 22 patients over a period of 6 months. A great number of abnormalities was found on the first occasion with a complete normalization for all variables except one at the end of the observation period. The number of infectious exacerbations was significantly higher (p less than 0.05) at the start of the observation period i.e. October-November, as compared to the end, i.e. April-May. The oxidative metabolism, as reflected by lucigenin-enhanced chemiluminescence, was significantly reduced (p less than 0.001) also at the period of few infections, suggesting a primary defect of the neutrophil. Smoking was shown to adversely affect luminol-enhanced chemiluminescence and the chemokinetic activity of the patients' cells. We conclude that most variables were altered in a way which was anticipated from the study of individuals with acute bacterial infections. The probable primary defect in oxidative metabolism of the neutrophils in addition to the acquired defects as a consequence of smoking may add to the predisposition of some individuals to their recurrent bacterial infections.
Physiology of Muscular Activity
Authors: Peter V. Karpovich
Journal: JAMA (1953)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
青霉素治疗儿童急性咽喉痛：随机、双盲临床试验
Authors: SjoerdZwart, MaroeskaMRovers, RuutAdeMelker, ArnoWHoes
Journal: BMJ (2004)

甲状腺功能亢进症(甲亢)是指甲状腺合成和分泌甲状腺激素增多,导致机体多个系统兴奋性增加和代谢亢进引发的一系列临床病症.引起甲亢的病因有十余种,最常见的是Graves病(毒性弥漫性甲状腺肿),其次为毒性结节性甲状腺肿和毒性甲状腺腺瘤。
Bilastine in allergic rhinoconjunctivitis and urticaria
Authors: C. Bachert, P. Kuna, T. Zuberbier
Journal: Allergy (2010)

To cite this article: Bachert C, Kuna P, Zuberbier T. Bilastine in allergic rhinoconjunctivitis and urticaria. Allergy 2010; 65 (Suppl. 93): 1–13. Abstract Allergic rhinoconjunctivitis and urticaria are increasing in prevalence in many developed countries. The role of histamine in such conditions is well documented and clinical guidelines recommend non‐sedating H 1 ‐receptor antagonists as first‐line treatment choices. Bilastine is a novel non‐sedating histamine H 1 ‐receptor antagonist developed for the treatment of allergic rhinoconjunctivitis and urticaria. The aim of this review is to critique the scientific evidence relating to the pharmacological properties of bilastine and the clinical evidence regarding its potential as an antihistamine. In vitro binding studies and investigations in animal tissue have demonstrated the high specificity of bilastine for H 1 ‐receptors, and preclinical animal studies have also yielded promising results in terms of a reduction of histamine‐mediated inflammatory effects, including capillary permeability and bronchospasm. In pharmacodynamic studies bilastine was found to down‐regulate histamine‐induced flare and wheal responses in healthy volunteers. Preclinical and clinical pharmacokinetic studies showed that bilastine has dose‐dependent kinetics following oral administration. Excretion is almost exclusively via urine and faeces as unchanged drug. Early clinical trials have shown that bilastine has similar efficacy to other second‐generation H 1 ‐receptor antagonists such as cetirizine, desloratadine, fexofenadine and levocetirizine, in terms of reducing allergic symptoms. Clinical findings also indicate that bilastine has a rapid onset of action and a 20 mg single dose is effective throughout a 24‐h period. Furthermore, bilastine has been associated with improved quality of life in allergic rhinoconjunctivitis and urticaria patients. Adverse effects have generally been minimal in these studies and doses up to twice those proposed did not exhibit differences in adverse events compared to placebo. Moreover, in vivo investigations have found no evidence of accumulation of bilastine in the central nervous system, and various studies have confirmed minimal effects on psychomotor performance in healthy volunteers administered up to four times the usual dose. Clinical studies have also found no effect of bilastine on the QTc interval and other ECG parameters, even at supratherapeutic dosages, confirming the good cardiac safety profile of this newer antihistamine. Given its pharmacodynamic profile, which appears to be similar to other second‐generation H 1 ‐receptor antagonists, and its favourable safety and tolerability, bilastine has the attributes of a potentially clinically useful non‐sedating antihistamine. Larger clinical studies are now necessary to fully elucidate the clinical potential of this novel antihistamine.
Abstract 1863: Androgen receptor CAG repeat length and TMPRSS2:ETS prostate cancer risk: results from the Prostate Cancer Prevention Trial
Authors: Douglas K. Price, Cindy H. Chau, William D. Figg, Catherine A. Till, Phyllis J. Goodman, Yonggon Cho, Marileila Garcia, Juergen Reichardt, Catherine M. Tangen, Robin J. Leach, Adrie van Bokhoven, Alan R. Kristal, Ian M. Thompson, M Scott Lucia
Journal: Cancer Research (2014)

Abstract Recent evidence suggests that genetic variations within the androgen receptor (AR) may influence the formation of TMPRSS2:ETS gene fusions, which are detected in more than half of all prostate cancers. We investigated the association between the length of the polymorphic trinucleotide CAG microsatellite repeats in exon 1 of the AR gene and risk of prostate cancer containing these fusion genes. This nested case-control study came from subjects enrolled in the Prostate Cancer Prevention Trial and included 195 biopsy-proven prostate cancer cases with known TMPRSS2:ETS status and 1344 matched controls. There was no association between CAG repeat length and risk of TMPRSS2:ETS-positive (OR=0.97, 95% CI, 0.91-1.04) or TMPRSS2:ETS-negative prostate cancer (OR=1.04, 95% CI, 0.97-1.10) and in patients with low- or high-grade disease. Our findings suggested that AR CAG repeats are not associated with TMPRSS2:ETS formation in prostate cancer. Citation Format: Douglas K. Price, Cindy H. Chau, William D. Figg, Catherine A. Till, Phyllis J. Goodman, Yonggon Cho, Marileila Garcia, Juergen Reichardt, Catherine M. Tangen, Robin J. Leach, Adrie van Bokhoven, Alan R. Kristal, Ian M. Thompson, M Scott Lucia. Androgen receptor CAG repeat length and TMPRSS2:ETS prostate cancer risk: results from the Prostate Cancer Prevention Trial. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1863. doi:10.1158/1538-7445.AM2014-1863