The existence of Helicobacter pylori in the biliary tract was investigated. Seven bile samples were included in this study. Among them, six bile samples were collected by percutaneous transhepatic cholangiodrainage and the other by needle aspiration during cholecystectomy. Using nested PCR with two sets of primers homologous to the urease A gene, Helicobacter pylori DNA was detected. Three samples, one from a patient with advanced gastric cancer involving the pancreatic head and two from patients with pancreatic head tumor, were found to be positive for Helicobacter pylori DNA. On the other hand, three samples from patients with cholangiocarcinoma and one from a patient with chronic cholecystitis were all negative. To further verify the specificity of our PCR analysis, partial sequences of the PCR products from the three positive samples were analyzed by direct sequencing. Several silent mutations and a missense mutation (AAA to AGA; Lys-164 to Arg-164) were identified in the urease A gene. We conclude that Helicobacter pylori DNA can be easily detected in the bile samples. The possibility of asymptomatic cholangitis caused by this organism requires further investigation.

A series of four Pt(II) metal complexes with trans-arranged isoquinolinyl azolates have been prepared, [Pt(Lx)2], x = 1-4, (1-4). The associated chelates possess various substituents; namely: one t-butyl (Bu(t)) at the 6-position (L1), two Bu(t) groups at the 5,7-positions (L2), one dip (2,6-di-isopropylphenyl) group at the 6-position (L3), and a single dip group at the 4-position of the 1-isoquinolinyl fragment (L4), respectively. Crystal structures of 1 and 4 were determined to shed light on the relationship of photophysics and packing arrangements. Their photophysical properties were measured and compared, for which the solid-state emission spectra of 2 and 4 are nearly identical to the solution spectra of all the Pt(II) complexes, showing the formation of isolated molecular entities. In contrast, the Pt(II) complexes 1 and 3 are found to be sensitive to their morphological states and external stimulus. This is confirmed by the gradual red-shifting of the emission with increasing concentration in the PMMA matrix, and the eventual formation of the broadened, metal-metal-to-ligand charge transfer (MMLCT) emission, by (i) wetting with acetone and drying in air, or (ii) grinding with a mortar and pestle, respectively. Organic light-emitting diodes (OLEDs) were also fabricated using multiple layered architecture and lowered doping concentration (e.g. 8 wt%), the latter is for avoiding dopant aggregation in the emitting layer. The associated OLED performances (i.e. η(max) = 11.5%, 8.5%, and 11.2% for 1, 2 and 3) confirmed their suitability and potential as dopants for phosphorescent OLEDs.

FinFET integration challenges and solutions are discussed for the 22 nm node and beyond. Fin dimension scaling is presented and the importance of the sidewall image transfer (SIT) technique is addressed. Diamond-shaped epi growth for the raised source-drain (RSD) is proposed to improve parasitic resistance (R para ) degraded by 3-D structure with thin Si-body. The issue of V t -mismatch is discussed for continuous FinFET SRAM cell-size scaling.IEDM09-290 12.1.2

Emissive Ir(iii) complexes bearing two tridentate chelates were synthesized. The multiple coordination mode of the chelate warrants a new class of metal-based phosphors for OLED applications.

Heat shock protein 60 (HSP60) and survivin reside in both the cytosolic and mitochondrial compartments under physiological conditions. They can form HSP60-survivin complexes through protein-protein interactions. Their expression levels in cancer tissues are positively correlated and higher expression of either protein is associated with poor clinical prognosis. The subcellular location of HSP60-survivin complex in either the cytosol or mitochondria is cell type-dependent, while the biological significance of HSP60-survivin interaction remains elusive. Current knowledge indicates that the function of HSP60 partly rests on where HSP60-survivin interaction takes place. HSP60 has a pro-survival function when binding to survivin in the mitochondria through interacting with other factors such as CCAR2 and p53. In response to cell death signals, mitochondrial survivin functions through preventing procaspase activation. Degradation of cytosolic survivin leads to the loss of mitochondrial membrane potential and aberrant mitosis processes. On the other hand, HSP60 release from mitochondria to cytosol upon death stimuli might exert a pro-death function, either through stabilizing Bax, enhancing procaspase-3 activation, or increasing protein ubiquitination. Combining the knowledge of mitochondrial HSP60-survivin complex function, cytosolic survivin degradation effect, and pro-death function upon mitochondria release of HSP60, a hypothetical scenario for HSP60-survivin shuttling upon death stimuli is proposed.

Os(ii) complexes bearing chromophoric 1,10-phenanthroline, diphosphine and bipyrazolate ancillaries display efficient NIR emission ranging from 717 nm to 779 nm in the solid state at RT.

An ordinal tree is an arbitrary rooted tree where the children of each node are ordered. Succinct representations for ordinal trees with efficient query support have been extensively studied. The best previously known result is due to Geary, Raman, and Raman [SODA 2004, pages 1-10]. The number of bits required by their representation for an n-node ordinal tree T is 2n + o(n), whose first-order term is information-theoretically optimal. Their representation supports a large set of O(1)-time queries on T . Based upon a balanced string of 2n parentheses, we give an improved 2n + o(n)-bit representation for T . Our improvement is two fold: Firstly, the set of O(1)-time queries supported by our representation is a proper superset of that supported by the representation of Geary, Raman, and Raman. Secondly, it is also much easier for our representation to support new queries by simply adding new auxiliary strings.

The tumor microenvironment is an important concept that defines cancer development not only through tumor cells themselves but also the surrounding cellular and non-cellular components, including stromal cells, blood vessels, infiltrating inflammatory cells, cancer stem cells (CSC), cytokines, and growth factors, which act in concert to promote tumor cell survival and metastasis. Hepatocellular carcinoma (HCC) is one of the most common and aggressive human malignancies worldwide. Poor prognosis is largely attributable to the high rate of tumor metastasis, highlighting the importance of identifying patients at risk in advance and developing novel therapeutic targets to facilitate effective intervention. Long non-coding RNAs (lncRNA) are a class of non-protein coding transcripts longer than 200 nucleotides frequently dysregulated in various cancer types, which have multiple functions in widespread biological processes, including proliferation, apoptosis, metastasis, and metabolism. lncRNAs are involved in regulation of the tumor microenvironment and reciprocal signaling between cancer cells. Targeting of components of the tumor microenvironment or cancer cells has become a considerable focus of therapeutic research and establishing the effects of different lncRNAs on this network should aid in the development of effective treatment strategies. The current review provides a summary of the essential properties and functional roles of known lncRNAs associated with the tumor microenvironment in HCC.