tbuckley/cabot-search huggingface dataset:
P245 A dedicated pneumonia follow up clinic–is it worthwhile?: Abstract P245 Table 1.
Authors: D Komrower, S Iyer, S Kazmi, V Shanker, P Stockton, S Twite, P Malhotra
Journal: Thorax (2013)

<h3>Background</h3> It is routine clinical practice<b>,</b> based on British Thoracic Society recommendations<b>,</b> to arrange a clinical review and chest x-ray approximately 6 weeks following an episode of pneumonia in most patients. However there is a paucity of published evidence to support or refute this practice. <h3>Objective</h3> To determine the clinical and radiological outcomes of patients admitted with an episode of pneumonia. <h3>Methods</h3> This was a retrospective analysis of the post-pneumonia clinic database at a large district general hospital over a one year period from May 2011 to April 2012. Data on demographic characteristics, radiological and clinical follow up, and final diagnosis were collected. Follow up data including a new diagnosis of cancer as well as new benign lung disease was available for most (97%) patients for 12 months after the index episode of pneumonia. Resolution was defined as complete resolution on chest X-ray at 6–8 weeks or &gt;90% resolution on chest X-ray, absence of ongoing physical symptoms and signs, and decision to discharge from clinic after discussion at a multi-disciplinary radiology meeting. <h3>Results</h3> 179 patients were included in the analysis (32 who did not attend for follow up were excluded). One hundred and thirty nine (78%) showed resolution and were discharged. Of the 40 (22%) patients that did not show resolution, 16 (9%) had a new diagnosis made; including 3 (1.7%) lung cancer. One of the identified lung cancers was stage I disease, while the other two were stage IV. New benign diagnoses made on follow up were recurrent aspiration (3), interstitial lung disease (2), pleural effusion (2), allergic bronchopulmonary aspergillosis (1), cryptogenic organising pneumonia (1), functional antibody deficiency (1), lung nodule (1), pleural plaques (1), and pulmonary embolism (1). Males, ever smokers, older patients, and those with a history of pre-existing lung disease (including COPD) had higher rates of non-resolution but the differences were not statistically significant. <h3>Conclusion</h3> Following up patients in a dedicated post pneumonia clinic with a repeat chest radiograph and clinical review had a low but significant pick up rate of new respiratory diagnoses. A larger study will be performed to improve risk stratification and enable more selective follow up.
Preventing Suicides in US Service Members and Veterans
Authors: Charles W Hoge, Carl A Castro
Journal: JAMA (2012)

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Bridging basic science and liver disease: Symposium
Authors: Irwin Rosenberg, Elihu Schimmel
Journal: Hepatology (2015)

Potential conflict of interest: Nothing to report. To the Editor: In the May issue of Hepatology, James Boyer posted a comment on the origins of hepatobiliary and gastrointestinal physiology, noting the need for better grounding in the pathophysiology of liver disease and the in‐depth understanding of basic mechanisms.1 We share the concern that liver fellows—as future investigators—find it difficult to understand how their research findings relate to clinical issues. In Boston, we have a unique day‐long symposium sponsored by the American Liver Foundation aimed at fellows and doctoral candidates whose research is focused on hepatology. For over two decades, the New England division has offered a symposium specifically aimed at bridging basic science and liver disease. Perhaps you can publicize—without official endorsement—the 25th meeting of this symposium on November 10, 2015 at a local venue. In the past, this symposium has often piggybacked to the American Association for the Study of Liver Diseases (AASLD) meeting locally, but this year, the AASLD meeting will be in San Francisco with attendant scheduling and travel issues for those who seek to attend both meetings. Over the years, we have encouraged our trainees to spend a very productive day in attendance, carrying away an excellent exposure to translational research, and the opportunity to spend time with the investigators. Dr. Arias, who continues to direct the symposium, serves as an inspiration and helps identify and recruit the scientists presenting their research. Your journal could help young scientists beyond our local catchment area of a half dozen training programs. It would be most consistent with Dr. Boyer's elegant editorial presentation and offering the pathophysiology program. The Boston program is another opportunity to bridge the rapid, dramatic increase in basic scientific knowledge to more effective clinical care and more research.
Gene Expression Changes during the Development of Acute Lung Injury Role of Transforming Growth Factor β
Authors: Scott C. Wesselkamper, Lisa M. Case, Lisa N. Henning, Michael T. Borchers, Jay W. Tichelaar, John M. Mason, Nadine Dragin, Mario Medvedovic, Maureen A. Sartor, Craig R. Tomlinson, George D. Leikauf
Journal: American Journal of Respiratory and Critical Care Medicine (2005)

Rationale: Acute lung injury can occur from multiple causes, resulting in high mortality. The pathophysiology of nickel-induced acute lung injury in mice is remarkably complex, and the molecular mechanisms are uncertain.Objectives: To integrate molecular pathways and investigate the role of transforming growth factor β (TGF-β) in acute lung injury in mice.Methods: cDNA microarray analyses were used to identify lung gene expression changes after nickel exposure. MAPPFinder analysis of the microarray data was used to determine significantly altered molecular pathways. TGF-β1 protein in bronchoalveolar lavage fluid, as well as the effect of inhibition of TGF-β, was assessed in nickel-exposed mice. The effect of TGF-β on surfactant-associated protein B (Sftpb) promoter activity was measured in mouse lung epithelial cells.Measurements and Main Results: Genes that decreased the most after nickel exposure play important roles in lung fluid absorption or surfactant and phospholipid synthesis, and genes that increased the most were involved in TGF-β signaling. MAPPFinder analysis further established TGF-β signaling to be significantly altered. TGF-β–inducible genes involved in the regulation of extracellular matrix function and fibrinolysis were significantly increased after nickel exposure, and TGF-β1 protein was also increased in the lavage fluid. Pharmacologic inhibition of TGF-β attenuated nickel-induced protein in bronchoalveolar lavage. In addition, treatment with TGF-β1 dose-dependently repressed Sftpb promoter activity in vitro, and a novel TGF-β–responsive region in the Sftpb promoter was identified.Conclusions: These data suggest that TGF-β acts as a central mediator of acute lung injury through the alteration of several different molecular pathways.
Relationships between radiological pattern and cell-mediated immune response in Mycoplasma pneumoniae pneumonia
Authors: H Tanaka, H Koba, S Honma, F Sugaya, S Abe
Journal: European Respiratory Journal (1996)

The aim of this study was to determine the relationship between the radiological pattern of Mycoplasma pneumoniae and the level of cell-mediated immunity of the host. Computed tomographic (CT) scans of the chest and the results of the purified protein derivative (PPD) test were studied during the acute stage of infection in 54 patients with M. pneumoniae pneumonia. The CT findings were used to divide the patients into two groups: one group had a predominance of nodular opacities with a centrilobular distribution (Group N; n = 29); and the other showed a predominance of an airspace consolidation (Group C; n = 25). Forty out of 54 subjects had negative tuberculin skin tests ( &lt; 10 mm induration). The positive rate of PPD reaction was higher in Group N (13 out of 29) compared to Group C (1 out of 25) (p = 0.0005); whilst pleural effusion appeared more frequently in Group C (10 out of 25) than in Group N (3 out of 29) (p = 0.023). There was no significant difference between Groups N and C in white blood cell and lymphocyte counts, level of antibodies to M. pneumoniae in sera, and severity of the disease. These findings suggest that the characteristics of the host cell-mediated immunity might influence the pattern of pulmonary lesions in M. pneumoniae infection.
Effects of the Vascular Disrupting Agent ZD6126 on Interstitial Fluid Pressure and Cell Survival in Tumors
Authors: Julia V. Skliarenko, Sarah Jane Lunt, Maggie L. Gordon, Alex Vitkin, Michael Milosevic, Richard P. Hill
Journal: Cancer Research (2006)

Abstract Interstitial fluid pressure (IFP) is elevated in tumors due to abnormal vasculature, lack of lymphatic drainage, and alterations in the tumor interstitium. ZD6126 is a tubulin-binding agent that selectively disrupts tumor vasculature resulting in tumor necrosis. This study examined the effect of ZD6126 on tumor IFP and the response of tumors with different IFP levels to ZD6126. Pretreatment IFP was measured using the wick-in-needle method in tumors (murine KHT-C and human CaSki) growing i.m. in the hind legs of mice. Mice were treated i.p. with a single dose of ZD6126 (100 or 200 mg/kg) and posttreatment IFP measurements were made. Blood flow imaging was conducted using Doppler optical coherence tomography, whereas oxygen partial pressure was measured using a fiber optic probe. Clonogenic assays were done to determine tumor cell survival. In KHT-C tumors, IFP dropped significantly at 1 hour posttreatment, returned to pretreatment values at 3 hours, and then declined to ∼25% of the pretreatment values by 72 hours. In CaSki tumors, the IFP decreased progressively, beginning at 1 hour, to ∼30% of pretreatment values by 72 hours. Clonogenic cell survival data indicated that ZD6126 was less effective in tumors with high IFP values (&amp;gt;25 mm Hg). Vascular disrupting agents, such as ZD6126, can affect IFP levels and initial IFP levels may predict tumor response to these agents. The higher cell survival in high IFP tumors may reflect greater microregional blood flow limitations in these tumors and reduced access of the drug to the target endothelial cells. (Cancer Res 2006; 66(4): 2074-80)
The role of ovarian volume in reproductive medicine
Authors: A Lass, P Brinsden
Journal: Human Reproduction Update (1999)

The human ovary is a dynamic organ which continually changes in size and activity through life, as an integral part of the changes that the female is going through before during and after her reproductive life. Following the rapid increase in the use of transvaginal scan in recent years, the measurement of ovarian volume has become quick, accurate and cost-effective. Ovarian volume is an important tool in the screening, diagnosis and monitoring the treatment of conditions such as polycystic ovarian syndrome, ovarian cancer and adolescent abnormalities. In reproductive medicine, measurement of ovarian volume has a role in the assessment of ovarian reserve and prediction of response to superovulation.
Birth-and-Death Evolution in Primate MHC Class I Genes: Divergence Time Estimates
Authors: Helen Piontkivska, Masatoshi Nei
Journal: Molecular Biology and Evolution (2003)

The major histocompatibility complex (MHC) is a multigene family that mediates the host immune response by helping T lymphocytes to recognize and respond to foreign antigens. The high degree of polymorphism and a quick turnover of the genetic loci make the evolution of MHC genes an intriguing subject of study. To understand the evolutionary pattern of this multigene family, we studied the phylogeny and divergence times of six functional MHC class I loci from primate species. On the phylogenetic trees, locus F occupies the most basal position among these loci. Our results suggest that the F locus diverged from the other MHC class I loci about 46–66 MYA. The major diversification of the other class I loci was estimated to have occurred at about 35–49 MYA, which is before the time of separation of Old World–New World monkeys. The gene duplication leading to the classical C locus in great apes appears to have occurred about 21–28 MYA. At approximately the same time the duplication of the B locus occurred in macaques. The oldest allelic lineages of A, B, and C loci in humans seem to have appeared at least 14–19, 10–15, and 13–17 MYA, respectively. Our phylogenetic analysis supports the hypothesis that the nonclassical locus F has diverged from the rest of class I loci very early in primate evolution. The overall phylogenetic pattern observed among class I genes is consistent with the model of birth-and-death evolution.
Treatment strategies for Cheyne-Stokes respiration
Authors: T. Köhnlein, T. Welte
Journal: European Respiratory Journal (2005)

In a recent issue of the European Respiratory Journal, GABOR et al.[1] reported the effects of standard cardiac resynchronisation therapy (CRT) on nocturnal central sleep apnoea (Cheyne-Stokes respiration).CRT was shown to reduce Cheyne-Stokes respiration significantly in six out of 10 patients.
Enhanced Targeting and Killing of Tumor Cells Expressing the CXC Chemokine Receptor 4 by Transducible Anticancer Peptides
Authors: Eric L. Snyder, Cheryl C. Saenz, Catherine Denicourt, Bryan R. Meade, Xian-Shu Cui, Ian M. Kaplan, Steven F. Dowdy
Journal: Cancer Research (2005)

Abstract Protein transduction domains (PTDs), such as the TAT PTD, have been shown to deliver a wide variety of cargo in cell culture and to treat preclinical models of cancer and cerebral ischemia. The TAT PTD enters cells by a lipid raft–dependent macropinocytosis mechanism that all cells perform. Consequently, PTDs resemble small-molecule therapeutics in their lack of pharmacologic tissue specificity in vivo. However, several human malignancies overexpress specific receptors, including HER2 in breast cancer, GnRH in ovarian carcinomas, and CXC chemokine receptor 4 (CXCR4) in multiple malignancies. To target tumor cells that overexpress the CXCR4 receptor, we linked the CXCR4 DV3 ligand to two transducible anticancer peptides: a p53-activating peptide (DV3-TATp53C′) and a cyclin-dependent kinase 2 antagonist peptide (DV3-TAT-RxL). Treatment of tumor cells expressing the CXCR4 receptor with either the DV3-TATp53C′ or DV3-TAT-RxL targeted peptides resulted in an enhancement of tumor cell killing compared with treatment with nontargeted parental peptides. In contrast, there was no difference between DV3 targeted peptide and nontargeted, parental peptide treatment of non-CXCR4-expressing tumor cells. These observations show that a multidomain approach can be used to further refine and enhance the tumor selectivity of biologically active, transducible macromolecules for treating cancer.
Oral Contraceptives and Risk of Ovarian Cancer and Breast Cancer Among High-Risk Women: A Systematic Review and Meta-Analysis
Authors: Patricia G. Moorman, Laura J. Havrilesky, Jennifer M. Gierisch, Remy R. Coeytaux, William J. Lowery, Rachel Peragallo Urrutia, Michaela Dinan, Amanda J. McBroom, Vic Hasselblad, Gillian D. Sanders, Evan R. Myers
Journal: Journal of Clinical Oncology (2013)

To estimate the risks of ovarian cancer and breast cancer associated with oral contraceptive (OC) use among women at elevated risk owing to mutations in BRCA1/2 or a strong family history.We searched PubMed, Embase, the Cochrane Database of Systematic Reviews, and ClinicalTrials.gov for studies published 2000 to 2012 that evaluated associations between OC use and breast or ovarian cancer among women who are carriers of a BRCA1/2 mutation or have a family history of breast or ovarian cancer.From 6,476 unique citations, we identified six studies examining ovarian cancer risk in BRCA1/2 mutation carriers and eight studies examining breast cancer risk in BRCA1/2 mutation carriers. For BRCA1/2 mutation carriers combined, meta-analysis showed an inverse association between OC use and ovarian cancer (odds ratio [OR], 0.58; 95% CI, 0.46 to 0.73) and a nonstatistically significant association with breast cancer (OR, 1.21; 95% CI, 0.93 to 1.58). Findings were similar when examining BRCA1 and BRCA2 mutation carriers separately. Data were inadequate to perform meta-analyses examining duration or timing of use. For women with a family history of ovarian or breast cancer, we identified four studies examining risk for ovarian cancer and three for breast cancer, but differences between studies precluded combining the data for meta-analyses, and no overall pattern could be discerned.Our analyses suggest that associations between ever use of OCs and ovarian and breast cancer among women who are BRCA1 or BRCA2 mutation carriers are similar to those reported for the general population.
Contrasuppression in autoimmunity. Abnormal contrasuppression facilitates expression of nephritogenic effector T cells and interstitial nephritis in kdkd mice.
Authors: C J Kelly, E G Neilson
Journal: The Journal of Experimental Medicine (1987)

We have used the murine model of spontaneous autoimmune interstitial nephritis in kdkd mice to examine the importance of abnormal immunoregulation in the expression of disease. T cells from naive congenic CBA/Ca mice suppress both histologic renal injury in the kdkd strain as well as the DTH reactivity to CBA/Ca renal tubular antigens mediated by lymphocytes from nephritic kdkd mice. These antigen-specific suppressor T cells are Lyt-2+, L3T4+, I-Jk+, genetically dominant and I-Jk restricted. Unfractionated spleen cells from young, prenephritic kdkd mice also demonstrate such suppressor function. Shortly preceding disease onset, however, net suppression is functionally bypassed by emergent contrasuppressor T cells. These regulatory cells are also Lyt-2+ and I-Jk+, and adhere both to the Vicia Villosa lectin and CBA/Ca TBM. By admixing these contrasuppressor cells with spleen cells from non-disease-prone CBA/Ca mice we were able to demonstrate the presence of DTH-reactive and nephritogenic effector cells in the latter population. Such nephritogenic effector cells could also be simply demonstrated after depletion of the suppressor cells with anti-I-Jk mAbs and complement. These findings support a role for contrasuppressor cells in the abrogation of tolerance to parenchymal self-antigens.
Physiological Action of Progesterone in Target Tissues*
Authors: J. Dinny Graham, Christine L. Clarke
Journal: Endocrine Reviews (1997)

I. Introduction II. Synthesis and Secretion of Progesterone III. The Progesterone Receptor A. PR expression and regulation IV. Progesterone Regulation of Gene Expression in the Uterus, Ovary, and Chick Oviduct A. Progesterone effects on proliferation and decidualization in the uterus during the menstrual cycle B. Progesterone regulation of insulin-like growth factor (IGF) pathways in the endometrium C. Control of ovulation D. Implantation, uterine proliferation, and early pregnancy E. Myometrial contractility F. Chick oviduct V. Progesterone Action in the Breast A. Effect of progesterone on proliferation of the normal breast B. Progesterone regulation of genes associated with cell cycle progression C. Progesterone regulation of growth factors and growth factor receptors in the breast D. Markers of progestin action in the breast E. Progesterone effects on lactation VI. Progesterone Effects in the Brain VII. Progesterone Effects on Bone VIII. Antiestrogen Action of Progesterone A. Inhibition of ER expressio...
coordinating perceptually grounded categories through language: a case study for colour
Authors: luc steels, tony belpaeme
Journal: Behavioral and Brain Sciences (2005)

this article proposes a number of models to examine through which mechanisms a population of autonomous agents could arrive at a repertoire of perceptually grounded categories that is sufficiently shared to allow successful communication. the models are inspired by the main approaches to human categorisation being discussed in the literature: nativism, empiricism, and culturalism. colour is taken as a case study. although we take no stance on which position is to be accepted as final truth with respect to human categorisation and naming, we do point to theoretical constraints that make each position more or less likely and we make clear suggestions on what the best engineering solution would be. specifically, we argue that the collective choice of a shared repertoire must integrate multiple constraints, including constraints coming from communication.
Functional Characterization of an Isoform-Selective Inhibitor of PI3K-p110β as a Potential Anticancer Agent
Authors: Jing Ni, Qingsong Liu, Shaozhen Xie, Coby Carlson, Thanh Von, Kurt Vogel, Steve Riddle, Cyril Benes, Michael Eck, Thomas Roberts, Nathanael Gray, Jean Zhao
Journal: Cancer Discovery (2012)

Genetic approaches have shown that the p110β isoform of class Ia phosphatidylinositol-3-kinase (PI3K) is essential for the growth of PTEN-null tumors. Thus, it is desirable to develop p110β-specific inhibitors for cancer therapy. Using a panel of PI3K isoform-specific cellular assays, we screened a collection of compounds possessing activities against kinases in the PI3K superfamily and identified a potent and selective p110β inhibitor: KIN-193. We show that KIN-193 is efficacious specifically in blocking AKT signaling and tumor growth that are dependent on p110β activation or PTEN loss. Broad profiling across a panel of 422 human tumor cell lines shows that the PTEN mutation status of cancer cells strongly correlates with their response to KIN-193. Together, our data provide the first pharmacologic evidence that PTEN-deficient tumors are dependent on p110β in animals and suggest that KIN-193 can be pursued as a drug to treat tumors that are dependent on p110β while sparing other PI3K isoforms.We report the first functional characterization of a p110β-selective inhibitor, KIN-193, that is efficacious as an antitumor agent in mice. We show that this class of inhibitor holds great promise as a pharmacologic agent that could be used to address the potential therapeutic benefit of treating p110β-dependent PTEN-deficient human tumors.
Ink4a/Arf and Oncogene-Induced Senescence Prevent Tumor Progression during Alternative Colorectal Tumorigenesis
Authors: Moritz Bennecke, Lydia Kriegl, Monther Bajbouj, Kristin Retzlaff, Sylvie Robine, Andreas Jung, Melek C. Arkan, Thomas Kirchner, Florian R. Greten
Journal: Cancer Cell (2010)
Sequence Therapy in Patients with Metastatic Renal Cell Carcinoma: Comparison of Common Targeted Treatment Options Following Failure of Receptor Tyrosine Kinase Inhibitors
Authors: Jonas Busch, Christoph Seidel, Carsten Kempkensteffen, Manfred Johannsen, Ingmar Wolff, Stefan Hinz, Ahmed Magheli, Kurt Miller, Viktor Grünwald, Steffen Weikert
Journal: European Urology (2011)