102 research outputs found

    Thoracoscopy for Spontaneous Pneumothorax

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    Video-assisted thoracic surgery (VATS) is the treatment of choice for recurrence prevention in patients with spontaneous pneumothorax (SP). Although the optimal surgical technique is uncertain, bullous resection using staplers in combination with mechanical pleurodesis, chemical pleurodesis and/or staple line coverage is usually undertaken. Currently, patient satisfaction, postoperative pain and other perioperative parameters have significantly improved with advancements in thoracoscopic technology, which include uniportal, needlescopic and nonintubated VATS variants. Ipsilateral recurrences after VATS occur in less than 5% of patients, in which case a redo-VATS is a feasible therapeutical option. Randomized controlled trials are urgently needed to shed light on the best definitive management of S

    PD1-2-4: FDG-PET Imaging for Staging Early Intraluminal Squamous Cell Cancers

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    Lung cancer screening

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    Randomised controlled trials, including the National Lung Screening Trial (NLST) and the NELSON trial, have shown reduced mortality with lung cancer screening with low-dose CT compared with chest radiography or no screening. Although research has provided clarity on key issues of lung cancer screening, uncertainty remains about aspects that might be critical to optimise clinical effectiveness and cost-effectiveness. This Review brings together current evidence on lung cancer screening, including an overview of clinical trials, considerations regarding the identification of individuals who benefit from lung cancer screening, management of screen-detected findings, smoking cessation interventions, cost-effectiveness, the role of artificial intelligence and biomarkers, and current challenges, solutions, and opportunities surrounding the implementation of lung cancer screening programmes from an international perspective. Further research into risk models for patient selection, personalised screening intervals, novel biomarkers, integrated cardiovascular disease and chronic obstructive pulmonary disease assessments, smoking cessation interventions, and artificial intelligence for lung nodule detection and risk stratification are key opportunities to increase the efficiency of lung cancer screening and ensure equity of access.</p

    Exploring the use of Facebook in the classroom: A Malaysia case study

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    With the evolution of social media, including major social networking sites that came into existence in the 21st century, social media has burgeoned into one of the most used channels of communication in the society. As it becomes well recognised for its potential as a social communication channel, recent years have witnessed an increased interest of using social media in higher education. The Social Media Survey 2013 by Pearson shows that 41% of higher education faculty in the U.S. population has use social media in teaching in 2013 compared to 34% of them using it in 2012. The survey results also show the increase use of social media for teaching by educators and faculty professionals because they see the potential in applying and integrating social media technology to their teaching. Many higher education institutions and educators are now finding themselves expected to catch up with the world of social media applications and social media users. This creates a growing phenomenon for the educational use of social media to create, engage, and share existing or newly produced information between lecturers and students and among students. However, the use of social media technologies in higher education is not an easy and straightforward process. Some educators perceived social media tool as an effective educational platform, some perceived that it was not useful at all. Some claimed that it allows them to make the classes more interactive, and some stated that the use of social media can help or hinder the achievement of student learning outcomes. Although there is a growing body of empirical research on the use of social media in higher education in the developed countries, there is not abundance in literature in Malaysia context. This study aims to examine the educational use of Facebook by lecturers and students in a private university in the Klang Valley, Malaysia, and to gauge their attitude towards adopting Facebook in the classroom. The research objectives include 1) investigating the use of Facebook for teaching and learning as well as a communication tool between lecturers and students, and 2) exploring the perception of lecturers and students on the usefulness and ease of use of Facebook in the classroom. Using both qualitative and quantitative research methods, this study will achieve two objectives set and the outcome will provides useful insights for academics interested in using social networking sites for teaching and learning and for researchers interested in pursuing social media in higher education research

    Regulation of Embryonic and Induced Pluripotency by Aurora Kinase-p53 Signaling

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    SummaryMany signals must be integrated to maintain self-renewal and pluripotency in embryonic stem cells (ESCs) and to enable induced pluripotent stem cell (iPSC) reprogramming. However, the exact molecular regulatory mechanisms remain elusive. To unravel the essential internal and external signals required for sustaining the ESC state, we conducted a short hairpin (sh) RNA screen of 104 ESC-associated phosphoregulators. Depletion of one such molecule, aurora kinase A (Aurka), resulted in compromised self-renewal and consequent differentiation. By integrating global gene expression and computational analyses, we discovered that loss of Aurka leads to upregulated p53 activity that triggers ESC differentiation. Specifically, Aurka regulates pluripotency through phosphorylation-mediated inhibition of p53-directed ectodermal and mesodermal gene expression. Phosphorylation of p53 not only impairs p53-induced ESC differentiation but also p53-mediated suppression of iPSC reprogramming. Our studies demonstrate an essential role for Aurka-p53 signaling in the regulation of self-renewal, differentiation, and somatic cell reprogramming

    Aberrant let7a/HMGA2 signaling activity with unique clinical phenotype in JAK2-mutated myeloproliferative neoplasms

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    High mobility group AT-hook 2 (HMGA2) is an architectural transcription factor that is negatively regulated by let-7 microRNA through binding to it’s 3′-untranslated region. Transgenic mice expressing Hmga2 with a truncation of its 3′-untranslated region has been shown to exhibit a myeloproliferative phenotype. To decipher the let-7-HMGA2 axis in myeloproliferative neoplasms, we employed an in vitro model supplemented with clinical correlation. Ba/F3 cells with inducible JAK2V617F expression (Ton.JAK2.V617F cells) showed upregulation of HMGA2 with concurrent let-7a repression. Ton.JAK2.V617F cells treated with a let-7a inhibitor exhibited further escalation of Hmga2 expression, while a let-7a mimic diminished the Hmga2 transcript level. Hmga2 overexpression conferred JAK2-mutated cells with a survival advantage through inhibited apoptosis. A pan-JAK inhibitor, INC424, increased the expression of let-7a, downregulated the level of Hmga2, and led to increased apoptosis in Ton.JAK2.V617F cells in a dose-dependent manner. In samples from 151 patients with myeloproliferative neoplasms, there was a modest inverse correlation between the expression levels of let-7a and HMGA2. Overexpression of HMGA2 was detected in 29 (19.2%) of the cases, and it was more commonly seen in patients with essential thrombocythemia than in those with polycythemia vera (26.9% vs. 12.7%, P=0.044). Patients with upregulated HMGA2 showed an increased propensity for developing major thrombotic events, and they were more likely to harbor one of the 3 driver myeloproliferative neoplasm mutations in JAK2, MPL and CALR. Our findings suggest that, in a subset of myeloproliferative neoplasm patients, the let-7-HMGA2 axis plays a prominent role in the pathogenesis of the disease that leads to unique clinical phenotypes

    Down-Regulation of NDRG1 Promotes Migration of Cancer Cells during Reoxygenation

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    One characteristic of tumor microenvironment is oxygen fluctuation, which results from hyper-proliferation and abnormal metabolism of tumor cells as well as disorganized neo-vasculature. Reoxygenation of tumors can induce oxidative stress, which leads to DNA damage and genomic instability. Although the cellular responses to hypoxia are well known, little is known about the dynamic response upon reoxygenation. In order to investigate the transcriptional responses of tumor adaptation to reoxygenation, breast cancer MCF-7 cells were cultured under 0.5% oxygen for 24 h followed by 24 h of reoxygenation in normoxia. Cells were harvested at 0, 1, 4, 8, 12, and 24 h during reoxygenation. The transcriptional profile of MCF-7 cells upon reoxygenation was examined using Illumina Human-6 v3 BeadChips. We identified 127 differentially expressed genes, of which 53.1% were up-regulated and 46.9% were down-regulated upon reoxygenation. Pathway analysis revealed that the HIF-1-alpha transcription factor network and validated targets of C-MYC transcriptional activation were significantly enriched in these differentially expressed genes. Among these genes, a subset of interest genes was further validated by quantitative reverse-transcription PCR. In particular, human N-MYC down-regulated gene 1 (NDRG1) was highly suppressed upon reoxygenation. NDRG1 is associated with a variety of stress and cell growth-regulatory conditions. To determine whether NDRG1 plays a role in reoxygenation, NDRG1 protein was overexpressed in MCF-7 cells. Upon reoxygenation, overexpression of NDRG1 significantly inhibited cell migration. Our results revealed the dynamic nature of gene expression in MCF-7 cells upon reoxygenation and demonstrated that NDRG1 is involved in tumor adaptation to reoxygenation

    Finishing the euchromatic sequence of the human genome

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    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead
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