783 research outputs found

    Strategic Flexibility: Navigator Industri Dalam Mencapai Competitive Advantages

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    Article to describe how to develop a strategic flexibility as company responses and strategy in facing the government regulation of Standard Euro 2. Article also discussed the new product development concept based on market perspective. Research analysis was a descriptive statistic with a simple random sampling from a number of populations. The result describes that the government regulation of Standard Euro2 is supported and positively responses by industry and market. In spite of this, strategic flexibility is an approach to reach industry competitive advantage in term of product development strategy

    The Chandra Multi-Wavelength Project: Optical Spectroscopy and the Broadband Spectral Energy Distributions of X-ray Selected AGN

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    From optical spectroscopy of X-ray sources observed as part of ChaMP, we present redshifts and classifications for a total of 1569 Chandra sources from our targeted spectroscopic follow up using the FLWO, SAAO, WIYN, CTIO, KPNO, Magellan, MMT and Gemini telescopes, and from archival SDSS spectroscopy. We classify the optical counterparts as 50% BLAGN, 16% NELG, 14% ALG, and 20% stars. We detect QSOs out to z~5.5 and galaxies out to z~3. We have compiled extensive photometry from X-ray to radio bands. Together with our spectroscopic information, this enables us to derive detailed SEDs for our extragalactic sources. We fit a variety of templates to determine bolometric luminosities, and to constrain AGN and starburst components where both are present. While ~58% of X-ray Seyferts require a starburst event to fit observed photometry only 26% of the X-ray QSO population appear to have some kind of star formation contribution. This is significantly lower than for the Seyferts, especially if we take into account torus contamination at z>1 where the majority of our X-ray QSOs lie. In addition, we observe a rapid drop of the percentage of starburst contribution as X-ray luminosity increases. This is consistent with the quenching of star formation by powerful QSOs, as predicted by the merger model, or with a time lag between the peak of star formation and QSO activity. We have tested the hypothesis that there should be a strong connection between X-ray obscuration and star-formation but we do not find any association between X-ray column density and star formation rate both in the general population or the star-forming X-ray Seyferts. Our large compilation also allows us to report here the identification of 81 XBONG, 78 z>3 X-ray sources and 8 Type-2 QSO candidates. Also we have identified the highest redshift (z=5.4135) X-ray selected QSO with optical spectroscopy.Comment: 17 pages, 16 figures, accepted for publication in ApJS. Full data table and README file can be found online at http://hea-www.harvard.edu/~pgreen/Papers.htm

    BCAA catabolism in brown fat controls energy homeostasis through SLC25A44.

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    Branched-chain amino acid (BCAA; valine, leucine and isoleucine) supplementation is often beneficial to energy expenditure; however, increased circulating levels of BCAA are linked to obesity and diabetes. The mechanisms of this paradox remain unclear. Here we report that, on cold exposure, brown adipose tissue (BAT) actively utilizes BCAA in the mitochondria for thermogenesis and promotes systemic BCAA clearance in mice and humans. In turn, a BAT-specific defect in BCAA catabolism attenuates systemic BCAA clearance, BAT fuel oxidation and thermogenesis, leading to diet-induced obesity and glucose intolerance. Mechanistically, active BCAA catabolism in BAT is mediated by SLC25A44, which transports BCAAs into mitochondria. Our results suggest that BAT serves as a key metabolic filter that controls BCAA clearance via SLC25A44, thereby contributing to the improvement of metabolic health

    Communications Biophysics

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    Contains research objectives, summary of research and reports on four research projects.National Institutes of Health (Grant 5 P01 GM14940-05)National Institutes of Health (Grant 5 TOl GM01555-05)National Aeronautics and Space Administration (Grant NGL 22-009-304)B-D ElectrodyneBoston City Hospital Purchase Order 1065

    Resectable pancreatic small cell carcinoma

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    Primary pancreatic small cell carcinoma (SCC) is rare, with just over 30 cases reported in the literature. Only 7 of these patients underwent surgical resection with a median survival of 6 months. Prognosis of SCC is therefore considered to be poor, and the role of adjuvant therapy is uncertain. Here we report two institutions' experience with resectable pancreatic SCC. Six patients with pancreatic SCC treated at the Johns Hopkins Hospital (4 patients) and the Mayo Clinic (2 patients) were identified from prospectively collected pancreatic cancer databases and re-reviewed by pathology. All six patients underwent a pancreaticoduodenectomy. Clinicopathologic data were analyzed, and the literature on pancreatic SCC was reviewed. Median age at diagnosis was 50 years (range 27–60). All six tumors arose in the head of the pancreas. Median tumor size was 3 cm, and all cases had positive lymph nodes except for one patient who only had five nodes sampled. There were no perioperative deaths and three patients had at least one postoperative complication. All six patients received adjuvant therapy, five of whom were given combined modality treatment with radiation, cisplatin, and etoposide. Median survival was 20 months with a range of 9–173 months. The patient who lived for 9 months received chemotherapy only, while the patient who lived for 173 months was given chemoradiation with cisplatin and etoposide and represents the longest reported survival time from pancreatic SCC to date. Pancreatic SCC is an extremely rare form of cancer with a poor prognosis. Patients in this surgical series showed favorable survival rates when compared to prior reports of both resected and unresectable SCC. Cisplatin and etoposide appears to be the preferred chemotherapy regimen, although its efficacy remains uncertain, as does the role of combined modality treatment with radiation

    Adjuvant gemcitabine versus NEOadjuvant gemcitabine/oxaliplatin plus adjuvant gemcitabine in resectable pancreatic cancer: a randomized multicenter phase III study (NEOPAC study)

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    <p>Abstract</p> <p>Background</p> <p>Despite major improvements in the perioperative outcome of pancreas surgery, the prognosis of pancreatic cancer after curative resection remains poor. Adjuvant chemotherapy increases disease-free and overall survival, but this treatment cannot be offered to a significant proportion of patients due to the surgical morbidity. In contrast, almost all patients can receive (neo)adjuvant chemotherapy before surgery. This treatment is safe and effective, and has resulted in a median survival of 26.5 months in a recent phase II trial. Moreover, neoadjuvant chemotherapy improves the nutritional status of patients with pancreatic cancer. This multicenter phase III trial (NEOPAC) has been designed to explore the efficacy of neoadjuvant chemotherapy.</p> <p>Methods/Design</p> <p>This is a prospective randomized phase III trial. Patients with resectable cytologically proven adenocarcinoma of the pancreatic head are eligible for this study. All patients must be at least 18 years old and must provide written informed consent. An infiltration of the superior mesenteric vein > 180° or major visceral arteries are considered exclusion criteria. Eligible patients will be randomized to surgery followed by adjuvant gemcitabine (1000 mg/m<sup>2</sup>) for 6 months or neoadjuvant chemotherapy (gemcitabine 1000 mg/m<sup>2</sup>, oxaliplatin 100 mg/m<sup>2</sup>) followed by surgery and the same adjuvant treatment. Neoadjuvant chemotherapy is given four times every two weeks. The staging as well as the restaging protocol after neoadjuvant chemotherapy include computed tomography of chest and abdomen and diagnostic laparoscopy. The primary study endpoint is progression-free survival. According to the sample size calculation, 155 patients need to be randomized to each treatment arm. Disease recurrence will be documented by scheduled computed tomography scans 9, 12, 15, 21 and thereafter every 6 months until disease progression. For quality control, circumferential resection margins are marked intraoperatively, and representative histological sections will be centrally reviewed by a dedicated pathologist.</p> <p>Discussion</p> <p>The NEOPAC study will determine the efficacy of neoadjuvant chemotherapy in pancreatic cancer for the first time and offers a unique potential for translational research. Furthermore, this trial will provide the unbiased overall survival of all patients undergoing surgery for resectable cancer of the pancreatic head.</p> <p>Trial registration</p> <p>clinicalTrials.gov <a href="http://www.clinicaltrials.gov/ct2/show/NCT01314027">NCT01314027</a></p

    Association between hMLH1 hypermethylation and JC virus (JCV) infection in human colorectal cancer (CRC)

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    Incorporation of viral DNA may interfere with the normal sequence of human DNA bases on the genetic level or cause secondary epigenetic changes such as gene promoter methylation or histone acetylation. Colorectal cancer (CRC) is the second leading cause of cancer mortality in the USA. Chromosomal instability (CIN) was established as the key mechanism in cancer development. Later, it was found that CRC results not only from the progressive accumulation of genetic alterations but also from epigenetic changes. JC virus (JCV) is a candidate etiologic factor in sporadic CRC. It may act by stabilizing β-catenin, facilitating its entrance to the cell nucleus, initialing proliferation and cancer development. Diploid CRC cell lines transfected with JCV-containing plasmids developed CIN. This result provides direct experimental evidence for the ability of JCV T-Ag to induce CIN in the genome of colonic epithelial cells. The association of CRC hMLH1 methylation and tumor positivity for JCV was recently documented. JC virus T-Ag DNA sequences were found in 77% of CRCs and are associated with promoter methylation of multiple genes. hMLH1 was methylated in 25 out of 80 CRC patients positive for T-Ag (31%) in comparison with only one out of 11 T-Ag negative cases (9%). Thus, JCV can mediate both CIN and aberrant methylation in CRC. Like other viruses, chronic infection with JCV may induce CRC by different mechanisms which should be further investigated. Thus, gene promoter methylation induced by JCV may be an important process in CRC and the polyp-carcinoma sequence
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