tbuckley/cabot-search huggingface dataset:
The evaluation of the effect of non invazive mechanical ventilation on diaphragmatic function in COPD exacerbation inpatients by using M-mod ultrasonography
Authors: Ülkü Aka Aktürk, Sevda Sener Cömert, Benan Niku Çaglayan, Ali Fidan
Journal: European Respiratory Journal (2013)

To evaluate the effect of non invazive mechanical ventilation(NIMV) on diaphragmatic function in COPD exacerbation inpatients by using M-mod ultrasonography.  In 2009 COPD exacerbation inpatients who meet inclusion criterias and whom have NIMV endication were implicated in our study.Bronchodilator, antibiotherapy and systemic steroid treatment were performed to all patients.In addition to medical therapy,NIMV was applied.Before NIMV application,diaphragmatic excursion during tidal ventilation(TV), deep breathing(DB) and diaphragmatic thickness were measured by using GE Logic 7 US and 3.5MHz konveks probe.After 2 hours NIMV treatment, the same diaphragmatic parameters were measured again by the same radiology physician and by the same US.The measured values of diaphragmatic motion and thickness before and after NIMV treatment were compared by using Wilcoxon sign test.  The mean age of 37 included COPD patients was 64.56±11 years old and 34 of them were male.In our study the mean FVC and FEV1 was 2567 ml and 1342 ml respectively.Before starting NIMV the mean diaphragmatic motion during TV was 1.71±0.53 cm,during DB was 4.25±1.02 cm.After adding short time NIMV treatment,the mean diaphragmatic motion during TV increases to 2.33± 0.74 cm, during DB it was 5.25±1.26 cm.The difference between the diaphragmatic motion during TV and DB before and after the NIMV was statistically significant(p  M-mode ultrasonography is a non invasive and inexpensive method in evaluation of diaphragmatic motion. In our study the positive effect of short duration NIMV treatment on diaphragmatic motion in COPD exacerbation was determined.
The Need for United States–Based Guidelines for Myeloproliferative Neoplasms
Authors: Brady L. Stein, Susan O’Brien, Peter Greenberg, Ruben A. Mesa
Journal: Journal of the National Comprehensive Cancer Network (2015)

][4][5][6][7][8] We believe that because of changing diagnostic algorithms and, importantly, new therapies, US physicians would benefit from comprehensive United States-based guidelines for the management of MPN.Physicians already have such guidelines to aid the evaluation and management of other chronic myeloid neoplasms, including myelodysplastic syndromes (MDS) and chronic myelogenous leukemia (CML). 9,10We believe several areas of interest within MPNs would align nicely with the goals of NCCN Guidelines, and we are happy to note that NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for MPNs are currently in the planning stages.We expect these formal guidelines for hematologists and hematologistoncologists will serve a variety of functions regarding diagnosis.First, such guidelines can increase awareness of the currently recognized MPN molecular markers (JAK2 V617F , CALR, and MPL) and suggest appropriate clinical settings for molecular testing and monitoring.Second, these guidelines can enable navigation through the diagnostic challenges presented by phenotypic mimicry between MPN subtypes and, occasionally, nonmalignant conditions.As an example, these guidelines could display a differential diagnosis for secondary thrombocytosis, erythrocytosis, and fibrosis, along with diagnostic algorithms that aid in distinction of essential thrombocythemia (ET) from prefibrotic myelofibrosis (MF), polycythemia vera (PV) from JAK2 V617Fpositive ET, and recognition of post-ET/post-PV MF.As we noted in the previously published article, modifying thrombosis risk is paramount in the management of ET and PV. 1 Formal guidelines for hematologists and hematologist-oncologists could provide a consensus-based vascular risk assessment and suggest appropriate clinical indications for and goals of cytoreductive therapies.Hydroxyurea is commonly used, but the evidence base in PV is scarce.We believe that NCCN Guidelines will also help providers weigh efficacy and safety of hydroxyurea, interferon-alpha, and anagrelide and busulfan, given the short-and long-term adverse effects that can occur with each agent.Duration and choice of anticoagulant therapy is not well established, but consensus is required, along with indications for plateletpheresis.Finally, hematologists and hematologist-oncologists need guidance on how to best prepare patients with MPNs for elective surgery and pregnancy.Although MPN treatment is in part guided by vascular risk assessment in ET/PV and predicted survival in MF, awareness of the MPN symptom burden is increasing, and accordingly, focus on symptom-directed therapy, which served as a basis for approval of JAK inhibitors, is also increasing.An MPN guideline can emphasize the need for
Characterization of an<i>in vivo</i>model for the study of eyelash biology and trichomegaly: mouse eyelash morphology, development, growth cycle, and anagen prolongation by bimatoprost
Authors: M. Tauchi, T.A. Fuchs, A.J. Kellenberger, D.F. Woodward, R. Paus, E. Lütjen-Drecoll
Journal: British Journal of Dermatology (2010)

Journal Article Characterization of an in vivo model for the study of eyelash biology and trichomegaly: mouse eyelash morphology, development, growth cycle, and anagen prolongation by bimatoprost Get access M. Tauchi, M. Tauchi Institute of Anatomy II, University of Erlangen‐Nuremberg, Erlangen, Germany Miyuki Tauchi. E‐mail: miyuki.tauchi@uk‐erlangen.de Search for other works by this author on: Oxford Academic Google Scholar T.A. Fuchs, T.A. Fuchs Institute of Anatomy II, University of Erlangen‐Nuremberg, Erlangen, Germany Search for other works by this author on: Oxford Academic Google Scholar A.J. Kellenberger, A.J. Kellenberger Institute of Anatomy II, University of Erlangen‐Nuremberg, Erlangen, Germany Search for other works by this author on: Oxford Academic Google Scholar D.F. Woodward, D.F. Woodward Department of Biological Sciences, Allergan, Inc., Irvine, CA, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar R. Paus, R. Paus Department of Dermatology, University Hospital Schleswig‐Holstein, University of Lübeck, Lübeck, GermanySchool of Translational Medicine, University of Manchester, Manchester, U.K. Search for other works by this author on: Oxford Academic Google Scholar E. Lütjen‐Drecoll E. Lütjen‐Drecoll Institute of Anatomy II, University of Erlangen‐Nuremberg, Erlangen, Germany Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 162, Issue 6, 1 June 2010, Pages 1186–1197, https://doi.org/10.1111/j.1365-2133.2010.09685.x Published: 01 June 2010
Absence of H(+)-ATPase in cortical collecting tubules of a patient with Sjogren's syndrome and distal renal tubular acidosis.
Authors: E P Cohen, B Bastani, M R Cohen, S Kolner, P Hemken, S L Gluck
Journal: Journal of the American Society of Nephrology (1992)

Distal urinary acidification abnormalities may arise from transepithelial voltage defects, permeability defects, or proton-secretory defects, but tests to determine the cellular mechanisms underlying secretory abnormalities have not previously been reported. A patient with Sjogren's syndrome and distal renal tubular acidosis due to a secretory defect is described, whose kidney biopsy was examined by fluorescent immunocytochemistry with an antibody to the M(r) 31,000 subunit of the mammalian kidney vacuolar H(+)-ATPase and was compared with normal human kidney. Staining with the anti-H(+)-ATPase antibody in normal human kidney was detected in the brush border microvilli and subvillar invaginations of the proximal tubule and in intercalated cells in the collecting duct. A biopsy sample from the patient was devoid of any anti-H+-ATPase staining in the intercalated cells. Staining was also absent from the proximal tubule brush border microvilli but was present in the subvillar invaginations. Although autoantibodies to normal human kidney membrane proteins were detected in the serum by immunoblot analysis, no immunocytochemical evidence for anti-intercalated cell autoantibodies was observed in the patient's serum. This report demonstrates that the basis for the proton secretory defect in some patients with distal renal tubular acidosis is likely the absence of H(+)-ATPase in the intercalated cells. It also illustrates the potential diagnostic utility of anti-H(+)-ATPase antibodies in the classification of distal renal tubular acidoses.
KAT6B Is a Tumor Suppressor Histone H3 Lysine 23 Acetyltransferase Undergoing Genomic Loss in Small Cell Lung Cancer
Authors: Laia Simó-Riudalbas, Montserrat Pérez-Salvia, Fernando Setien, Alberto Villanueva, Catia Moutinho, Anna Martínez-Cardús, Sebastian Moran, Maria Berdasco, Antonio Gomez, Enrique Vidal, Marta Soler, Holger Heyn, Alejandro Vaquero, Carolina de la Torre, Silvia Barceló-Batllori, August Vidal, Luca Roz, Ugo Pastorino, Katalin Szakszon, Guntram Borck, Conceição S. Moura, Fátima Carneiro, Ilse Zondervan, Suvi Savola, Reika Iwakawa, Takashi Kohno, Jun Yokota, Manel Esteller
Journal: Cancer Research (2015)

Recent efforts to sequence human cancer genomes have highlighted that point mutations in genes involved in the epigenetic setting occur in tumor cells. Small cell lung cancer (SCLC) is an aggressive tumor with poor prognosis, where little is known about the genetic events related to its development. Herein, we have identified the presence of homozygous deletions of the candidate histone acetyltransferase KAT6B, and the loss of the corresponding transcript, in SCLC cell lines and primary tumors. Furthermore, we show, in vitro and in vivo, that the depletion of KAT6B expression enhances cancer growth, while its restoration induces tumor suppressor-like features. Most importantly, we demonstrate that KAT6B exerts its tumor-inhibitory role through a newly defined type of histone H3 Lys23 acetyltransferase activity.
Plasma surfactant protein D (SP-D) and smoking status in healthy persons
Authors: Tetyana Pertseva, Kateryna Gashynova
Journal: European Respiratory Journal (2014)

SPD is a lung derived protein that suggests being specific marker for the lung injury.  The   aim   of study was to evaluate SP-D level in healthy persons with different smoking status.    Study population and methods  . 26 healthy individuals were surveyed. Plasma SP-D, spirometry and smoking status evaluation were performed for all persons.    Results  . In accordance with smoking status all study population was divided on three groups: Group I – persons who have never smoked; Group II – current smokers and Group III – ex-smokers.  All groups were similar regarding to sex, age and spirometry data.  SP-D level in persons with different smoking status presents in table 1.    Conclusion.    Both current and ex-smokers with COPD have higher SP-D level than persons, who have never smoked, however only for current smokers this difference is statistically significant.
In Vitro Migration of Walker 256 Carcinosarcoma Cells: Dependence on Microtubule and Microfilament Function&lt;xref ref-type="fn" rid="fn2"&gt;2&lt;/xref&gt;
Authors: Timothy P. Spiro, Gregory R. Mundy
Journal: JNCI Journal of the National Cancer Institute (1980)

Walker 256 carcinosarcoma cells have been shown to respond in vitro to two chemotactic factors: one derived from the trypsinized fifth component of complement, and the other derived from resorbing bone. The effects of inhibited microtubule and microfilament function on the ability of tumor cells to uindergo both random and directed migration in response to these factors were examined. Directed tumor cell migration was inhibited by colchicine and vinblastine, agents that interfere with microtubule assembly., Lumicolchicine, a structural analog of colchicine that does not bind to microtubules, did not inhibit tumor cell migration. Cytochalasin B, which interferes with microfilament function, also inhibited tumor cell migration in vitro. Colchicine inhibited random or spontaneous cell movement as well as directed migration. These experiments indicated that random and directed tumor cell migrations were dependent on microtubules and microfilaments, and interference with the function of these subcellular organelles inhibited tumor cell movement.
Cell‐based therapies for cardiac repair: a meeting report on scientific observations and European regulatory viewpoints
Authors: Martina Schüssler‐Lenz, Claire Beuneu, Margarida Menezes‐Ferreira, Veronika Jekerle, Jozef Bartunek, Steven Chamuleau, Patrick Celis, Pieter Doevendans, Maura O'Donovan, Jonathan Hill, Marit Hystad, Stefan Jovinge, Ján Kyselovič, Metoda Lipnik‐Stangelj, Romaldas Maciulaitis, Krishna Prasad, Anthony Samuel, Olli Tenhunen, Torsten Tonn, Giuseppe Rosano, Andreas Zeiher, Paula Salmikangas
Journal: European Journal of Heart Failure (2015)
Evaluation of pre- and postoperative chemotherapy for resectable adenocarcinoma of the esophagus or gastroesophageal junction.
Authors: J A Ajani, J A Roth, B Ryan, M McMurtrey, T A Rich, D E Jackson, J L Abbruzzese, B Levin, L DeCaro, C Mountain
Journal: Journal of Clinical Oncology (1990)

Thirty-five consecutive patients with resectable adenocarcinoma of the esophagus or gastroesophageal junction were treated with two preoperative and three or four postoperative chemotherapy courses consisting of etoposide, fluorouracil, and cisplatin (EFP) to evaluate the rate of curative resection, clinical and pathologic response, toxic effects, and survival. One hundred thirty-seven courses with a median number of five courses (range, one to six) were administered. Preoperative EFP resulted in 17 (49%) major responses, including six patients who did not have carcinoma cells in the repeat endoscopic biopsy specimens and cytologic brushings. Among 32 patients who had surgery, 25 (78%) had curative resection, one patient had a complete pathologic response, and one had microscopic carcinoma in the resected specimen. Six patients had microscopic carcinoma at the resection margins and received postoperative radiotherapy. At a median follow-up of 20 months, the projected survival of 35 patients is 23 months (range, 6 to 33+). Fifteen patients died of their carcinomas, and 15 patients were alive (median follow-up, 20+ months; range, 15+ to 33+ months) with no evidence of relapse. There were no deaths related to chemotherapy, surgery, or radiotherapy. EFP-induced toxic reactions were moderate. Our data suggest that multiple courses of EFP are feasible. Future strategies for this disease should consider prolonged chemotherapy with regimens that result frequently in pathologic complete responses.
Evolution of treatment with CPAP over 21 months of follow-up in patients with sleep apnea hypopnea syndrome
Authors: Juan Fernández-Lahera, Francisco García Río, Carlos Carpio, Darwin Feliz, David Romero, Eli Martínez, Concepciόn Prados, Rodolfo Alvarez-Sala
Journal: European Respiratory Journal (2011)

Objectives:  1) Analyse the evolution of the hours/days ratio of the use of CPAP in patients with sleep apnea hypopnea syndrome over a period of 21 months.  2) Study the factors related to poor treatment compliance (   Material and method:  A total of 83 patients with sleep apnea hypopnea syndrome (AHI 49±22 h-1) treated with CPAP were included. The utilisation ratio of CPAP was recorded at 3, 6, 9, 12, 15, 18, and 21 months.  Anthropometric and socio-work variables were also recorded, as well as sleep and CPAP parameters, Epworth scale, comorbidity and evolution.   Results:  The ratio (hours/day) of real use of CPAP at 3, 6, 9, 12, 15, 18, and 21 months was: 4.9±2.3; 5.1±2.2; 5.3±2.5; 5.2±2.4; 5.3±2.5; 5.2±2.6 y 5.2±2.5. A univariate analysis and another adjusted by variables showed that the time of use did not differ significantly over the 21 months.  Patients who did not comply with treatment (31.6%; use    Conclusions:  1) The CPAP use pattern 3 months after starting treatment is stably maintained over a 21-month period.  2) Those who did not comply with treatment presented less serious sleep parameters, lower cervical perimeters, and lower prescribed CPAP pressure than those who complied.
Abstract 5483: Deficiency Of The Stimulatory G Protein alpha-subunit Gs (alpha) Leads To Reduced ApoA-I Mediated Cellular Lipid Efflux and Impaired ABCA1-dependent Nascent HDL Biogenesis Pathway
Authors: Dana Bailey, Safia Chatur, Anouar Hafiane, Bassam Haidar, Harald Juppner, Murat Bastepe, Larbi Krimbou, Jacques Genest
Journal: Circulation (2008)

It has been suggested that initial apoA-I binding to ABCA1 is coupled to the activation of signal transduction pathways, allowing excess cholesterol removal from tissues. However, the role of the h...
Hypercapnic hypoventilation in tracheobroncomalacia: The success of dynamic CT scan for diagnosis and of non-invasive continuous positive pressure ventilation (CPAP) for treatment
Authors: Valeria Caldarelli, Teresa Salerno, Elisabetta Verrillo, Martino Pavone, Marina Macchiaiolo, Serena Soldini, Andrea Bartuli, Renato Cutrera
Journal: European Respiratory Journal (2013)

Tracheobroncomalacia increases the respiratory load and decreases alveolar ventilation developing an hypoventilation.  We describe a case of a 3 months-old child affected by Costello syndrome who was referred to our Hospital for persistent dyspnoea, stridor and hypercapnic respiratory failure without hypoxia.  Bronchoscopy were normal. Nocturnal sleep study showed an isolated hypercapnia (Mean SaO2 99.6%, SaO2  50mmHg 97.3 % TST).  Dynamic CT scan of the thorax showed an expiratory deformation of the main airways with significant caliber reduction of the main left bronchus, carina, and upper lobar right bronchus consistent with a diagnosis of tracheobronchomalacia. He underwent CPAP (5 cmH2O) with Helmet interface that was well tolerated.  The child was discharged with home CPAP with nasal interface with a normalized hypoventilation after two weeks of treatment (Mean SaO2 99.1 %, Minimal SaO2 93 %, SaO2  50mmHg 11 % time).  This case underlines that thacheobronchomalacia can also be diagnosed by dynamic CT scan and that a diffuse condition cause an hypercapnic hypoventilation. Even in severe cases, a non invasive approach can be tried to resolve the hypoventilation and to avoid surgery. Helmet interface could allow the patient to attaint a good acceptance of the CPAP then to switch to nasal mask for starting a long term nocturnal treatment.
Activation of <i>EZH2</i> and <i>SUZ12</i> Regulated by E2F1 Predicts the Disease Progression and Aggressive Characteristics of Bladder Cancer
Authors: Se-Ra Lee, Yun-Gil Roh, Seon-Kyu Kim, Ju-Seog Lee, So-Young Seol, Hyun-Hee Lee, Won-Tae Kim, Wun-Jae Kim, Jeonghoon Heo, Hee-Jae Cha, Tae-Hong Kang, Jin Woong Chung, In-Sun Chu, Sun-Hee Leem
Journal: Clinical Cancer Research (2015)

Previous study identified E2F1 as a key mediator of non-muscle-invasive bladder cancer (NMIBC) progression. The aim of this study was to identify the E2F1-related genes associated with poor prognosis and aggressive characteristics of bladder cancer.Microarray analysis was performed to find E2F1-related genes associated with tumor progression and aggressiveness in the gene expression data from 165 primary patients with bladder cancer. The biologic activity of E2F1-related genes in tumor progression and aggressiveness was confirmed with experimental assays using bladder cancer cells and tumor xenograft assay.The expression of E2F1 was significantly associated with EZH2 and SUZ12. The overexpression of E2F1, EZH2, and SUZ12 enhanced cancer progression including cell colony formation, migration, and invasiveness. Knockdown of these genes reduced motility, blocked invasion, and decreased tumor size in vivo. E2F1 bound the proximal EZH2 and SUZ12 promoter to activate transcription, suggesting that E2F1 and its downstream effectors, EZH2 and SUZ12, could be important mediators for the cancer progression. In addition, we confirmed an association between these genes and aggressive characteristics. Interestingly, the treatment of anticancer drugs to the cells overexpressing E2F1, EZH2, and SUZ12 induced the expression of CD44, KLF4, OCT4, and ABCG2 known as cancer stem cell (CSC)-related genes.The link between E2F1, EZH2, and/or SUZ12 revealed that E2f1 directly regulates transcription of the EZH2 and SUZ12 genes. The signature of E2F1-EZH2-SUZ12 shows a predictive value for prognosis in bladder tumors and the E2F1-EZH2-SUZ12-driven transcriptional events may regulate the cancer aggressiveness and chemo-resistance, which may provide opportunity for development of new treatment modalities.
Induction of renal arachidonate cytochrome P-450 epoxygenase after uninephrectomy
Authors: K Takahashi, R C Harris, J H Capdevila, A Karara, K Makita, H R Jacobson, K A Munger, K F Badr
Journal: Journal of the American Society of Nephrology (1993)

After unilateral nephrectomy (UNx) in the rat, cytochrome P-450 (cP-450)-linked arachidonate enzymatic activity was markedly and specifically induced in microsomal fractions from the remaining kidney. The enzymatic activity reached 200% at 1 wk and 285% at 2 wk post-UNx as compared with non-UNx controls. Mean baseline values for GFR and RPF rate in the remaining kidney 2 wk after UNx were 1.56 +/- 0.10 and 6.47 +/- 0.35 mL/min, respectively. In these rats, the administration of ketoconazole, a cP-450 inhibitor, led to 75% inhibition of renal cP-450 arachidonate metabolism and was associated with acute augmentations in both GFR and RPF to 1.82 +/- 0.18 (P < 0.05 versus baseline) and 7.54 +/- 0.37 mL/min (P < 0.05 versus baseline), respectively. Because vasoconstrictor arachidonate epoxygenase products are endogenously generated in the rat kidney, these findings suggest that the stimulation of renal cP-450-mediated oxygenation of arachidonic acid may subserve an important counterregulatory function in mitigating the renal hyperperfusion and hyperfiltration that follow reductions in renal mass.
Evidence of transmission of a Panton-Valentine leukocidin-positive community-acquired methicillin-resistant Staphylococcus aureus clone: a family affair
Authors: P. Cocchi, G. Taccetti, C. Montagnani, S. Campana, L. Galli, C. Braggion, M. de Martino
Journal: Clinical Microbiology and Infection (2013)