Method and system for providing beam polarization

A radiation polarizer, controller, and a method of radiation polarization and beam control, are disclosed. The radiation polarizer includes a substrate, at least one anti-reflection coating layer communicatively coupled to the substrate, at least two nanostructures communicatively coupled to the at least one anti-reflection coating layer, and at least two groove layers, wherein each one of the at least two groove layers is interstitial to a respective one of the at least two nanostructures. The method may include the steps of communicatively coupling at least one anti-reflection coating layer to a substrate, communicatively coupling at least two nanostructures to at least one of the at least one anti-reflection coating layer, providing interstitially to a respective one of the at least two nanostructures at least two groove layers, coupling the at least two groove layers and the at least two nanostructures to provide a pass wavelength in the range of about 250 nm to less than about a microwave wavelength, and allowing for examining of radiation having a wavelength in a range of about 250 nm to less than about a microwave wavelength, and having an electric field orthogonal to the at least two groove layers, by allowing for a passing of the radiation through said coupling of the at least two groove layers and the at least two nanostructures.Published versio

Comparison of the efficacy of lamivudine and telbivudine in the treatment of chronic hepatitis B: a systematic review

<p>Abstract</p> <p>Background</p> <p>Chronic viral hepatitis B remains a global public health concern. Currently, several drugs, such as lamivudine and telbivudine, are recommended for treatment of patients with chronic hepatitis B. However, there are no conclusive results on the comparison of the efficacy of lamivudine (LAM) and telbivudine (LdT) in the treatment of chronic hepatitis B.</p> <p>Results</p> <p>To evaluate the comparison of the efficacy of LAM and LdT in the treatment of chronic hepatitis B by a systematic review and meta-analysis of clinical trials, we searched PUBMED (from 1990 to April 2010), Web of Science (from 1990 to April 2010), EMBASE (from 1990 to April 2010), CNKI (National Knowledge Infrastructure) (from 1990 to April 2010), VIP database (from 1990 to April 2010), WANFANG database (from 1990 to April 2010), the Cochrane Central Register of Controlled Trials and the Cochrane Database of Systematic Review. At the end of one-year treatment, LdT was better than LAM at the biochemical response, virological response, HBeAg loss, therapeutic response, while less than at the viral breakthrough and viral resistance, but there was no significant difference in the HBeAg seroconversion and HBsAg response. LdT was better than LAM at the HBeAg seroconversion with prolonged treatment to two years.</p> <p>Conclusions</p> <p>In summary, LdT was superior in inhibiting HBV replication and preventing drug resistance as compared to LAM for CHB patients. But LdT may cause more nonspecific adverse events and can lead to more CK elevation than LAM. It is thus recommended that the LdT could be used as an option for patients but adverse events, for example CK elevation, must be monitored.</p

Detection of hepatitis B surface antigen, hepatitis B core antigen, and hepatitis B virus DNA in parotid tissues

SummaryObjectiveTo examine the presence of hepatitis B surface antigen (HBsAg), hepatitis B core antigen (HBcAg), and hepatitis B virus (HBV) DNA in parotid tissues from patients with positive serum HBV markers.MethodsHBsAg and HBcAg were examined in parotid biopsy tissues from patients with suspected parotid tumor and positive serum HBV markers by immunocytochemistry, and HBV DNA was detected in parotid tissues by PCR.ResultsAmong the 22 patients with a parotid tumor, only one was pathologically confirmed as a neoplasm; all others were benign. HBsAg and HBcAg were present in parotid cells with positive rates of 45.5% (10/22) and 40.9% (9/22), respectively, with an overall positive rate of 54.5% (12/22). Of the 22 cases with serum markers of HBV infection, seven (31.8%) had both HBsAg and HBcAg in the parotid cells. HBV DNA was present in seven of the 12 samples in which hepatitis B antigen was detected (58.3%).ConclusionsHBV in saliva might originate from the infected salivary glands and the infectious saliva could transmit HBV

Proteomic analysis of differentially expressed proteins in hepatitis B virus-related hepatocellular carcinoma tissues

<p>Abstract</p> <p>Background</p> <p>Hepatocellular carcinoma (HCC), a major cause of cancer death in China, is preceded by chronic hepatitis and liver cirrhosis (LC). Although hepatitis B virus (HBV) has been regarded as a clear etiology of human hepatocarcinogenesis, the mechanism is still needs to be further clarified. In this study, we used a proteomic approach to identify the differential expression protein profiles between HCC and the adjacent non-tumorous liver tissues.</p> <p>Methods</p> <p>Eighteen cases of HBV-related HCC including 12 cases of LC-developed HCC and 6 cases of chronic hepatitis B (CHB)-developed HCC were analyzed by two-dimensional electrophoresis (2-DE) combined with matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS), and the results were compared to those of paired adjacent non-tumorous liver tissues.</p> <p>Results</p> <p>A total of 17 differentially expressed proteins with diverse biological functions were identified. Among these, 10 proteins were up-regulated, whereas the other 7 proteins were down-regulated in cancerous tissues. Two proteins, c-Jun N-terminal kinase 2 and ADP/ATP carrier protein were found to be up-regulated only in CHB-developed HCC tissues. Insulin-like growth factor binding protein 2 and Rho-GTPase-activating protein 4 were down-regulated in LC-developed and CHB-developed HCC tissues, respectively. Although 11 out of these 17 proteins have been already described by previous studies, or are already known to be involved in hepatocarcinogenesis, this study revealed 6 new proteins differentially expressed in HBV-related HCC.</p> <p>Conclusion</p> <p>These findings elucidate that there are common features between CHB-developed HCC and LC-developed HCC. The identified proteins are valuable for studying the hepatocarcinogenesis, and may be potential diagnostic markers or therapeutic targets for HBV-related HCC.</p

Infrared spectroscopy of small-molecule endofullerenes

Hydrogen is one of the few molecules which has been incarcerated in the molecular cage of C$_{60}$ and forms endohedral supramolecular complex H$_2$@C$_{60}$. In this confinement hydrogen acquires new properties. Its translational motion becomes quantized and is correlated with its rotations. We applied infrared spectroscopy to study the dynamics of hydrogen isotopologs H$_2$, D$_2$ and HD incarcerated in C$_{60}$. The translational and rotational modes appear as side bands to the hydrogen vibrational mode in the mid infrared part of the absorption spectrum. Because of the large mass difference of hydrogen and C$_{60}$ and the high symmetry of C$_{60}$ the problem is identical to a problem of a vibrating rotor moving in a three-dimensional spherical potential. The translational motion within the C$_{60}$ cavity breaks the inversion symmetry and induces optical activity of H$_2$. We derive potential, rotational, vibrational and dipole moment parameters from the analysis of the infrared absorption spectra. Our results were used to derive the parameters of a pairwise additive five-dimensional potential energy surface for H$_2$@C$_{60}$. The same parameters were used to predict H$_2$ energies inside C$_{70}$[Xu et al., J. Chem. Phys., {\bf 130}, 224306 (2009)]. We compare the predicted energies and the low temperature infrared absorption spectra of H$_2$@C$_{70}$.Comment: Updated author lis

Identifying potential cancer driver genes by genomic data integration.

Cancer is a genomic disease associated with a plethora of gene mutations resulting in a loss of control over vital cellular functions. Among these mutated genes, driver genes are defined as being causally linked to oncogenesis, while passenger genes are thought to be irrelevant for cancer development. With increasing numbers of large-scale genomic datasets available, integrating these genomic data to identify driver genes from aberration regions of cancer genomes becomes an important goal of cancer genome analysis and investigations into mechanisms responsible for cancer development. A computational method, MAXDRIVER, is proposed here to identify potential driver genes on the basis of copy number aberration (CNA) regions of cancer genomes, by integrating publicly available human genomic data. MAXDRIVER employs several optimization strategies to construct a heterogeneous network, by means of combining a fused gene functional similarity network, gene-disease associations and a disease phenotypic similarity network. MAXDRIVER was validated to effectively recall known associations among genes and cancers. Previously identified as well as novel driver genes were detected by scanning CNAs of breast cancer, melanoma and liver carcinoma. Three predicted driver genes (CDKN2A, AKT1, RNF139) were found common in these three cancers by comparative analysis

Nuclear magnetic resonance of hydrogen molecules trapped inside C70 fullerene cages

We present a solid-state NMR study of H2 molecules confined inside the cavity of C70 fullerene cages over a wide range of temperatures (300?K to 4?K). The proton NMR spectra are consistent with a model in which the dipole–dipole coupling between the ortho-H2 protons is averaged over the rotational/translational states of the confined quantum rotor, with an additional chemical shift anisotropy ?HCSA=10.1?ppm induced by the carbon cage. The magnitude of the chemical shift anisotropy is consistent with DFT estimates of the chemical shielding tensor field within the cage. The experimental NMR data indicate that the ground state of endohedral ortho-H2 in C70 is doubly degenerate and polarized transverse to the principal axis of the cage. The NMR spectra indicate significant magnetic alignment of the C70 long axes along the magnetic field, at temperatures below ~10?

Cannabinoid Receptor Subtype 2 (Cb2R) Agonist Gw405833 Reduces Agonist-Induced Ca2+ Oscillations In Mouse Pancreatic Acinar Cells

Emerging evidence demonstrates that the blockade of intracellular Ca 2+ signals may protect pancreatic acinar cells against Ca 2+ overload, intracellular protease activation, and necrosis. The activation of cannabinoid receptor subtype 2 (CB 2 R) prevents acinar cell pathogenesis in animal models of acute pancreatitis. However, whether CB 2 Rs modulate intracellular Ca 2+ signals in pancreatic acinar cells is largely unknown. We evaluated the roles of CB 2 R agonist, GW405833 (GW) in agonist-induced Ca 2+ oscillations in pancreatic acinar cells using multiple experimental approaches with acute dissociated pancreatic acinar cells prepared from wild type, CB 1 R-knockout (KO), and CB 2 R-KO mice. Immunohistochemical labeling revealed that CB 2 R protein was expressed in mouse pancreatic acinar cells. Electrophysiological experiments showed that activation of CB 2 Rs by GW reduced acetylcholine (ACh)-, but not cholecystokinin (CCK)-induced Ca 2+ oscillations in a concentration-dependent manner; this inhibition was prevented by a selective CB 2 R antagonist, AM630, or was absent in CB 2 R-KO but not CB 1 R-KO mice. In addition, GW eliminated L-arginine-induced enhancement of Ca 2+ oscillations, pancreatic amylase, and pulmonary myeloperoxidase. Collectively, we provide novel evidence that activation of CB 2 Rs eliminates ACh-induced Ca 2+ oscillations and L-arginine-induced enhancement of Ca 2+ signaling in mouse pancreatic acinar cells, which suggests a potential cellular mechanism of CB 2 R-mediated protection in acute pancreatitis

A Hepatic Protein, Fetuin-A, Occupies a Protective Role in Lethal Systemic Inflammation

A liver-derived protein, fetuin-A, was first purified from calf fetal serum in 1944, but its potential role in lethal systemic inflammation was previously unknown. This study aims to delineate the molecular mechanisms underlying the regulation of hepatic fetuin-A expression during lethal systemic inflammation (LSI), and investigated whether alterations of fetuin-A levels affect animal survival, and influence systemic accumulation of a late mediator, HMGB1.LSI was induced by endotoxemia or cecal ligation and puncture (CLP) in fetuin-A knock-out or wild-type mice, and animal survival rates were compared. Murine peritoneal macrophages were challenged with exogenous (endotoxin) or endogenous (IFN-γ) stimuli in the absence or presence of fetuin-A, and HMGB1 expression and release was assessed. Circulating fetuin-A levels were decreased in a time-dependent manner, starting between 26 h, reaching a nadir around 24-48 h, and returning towards base-line approximately 72 h post onset of endotoxemia or sepsis. These dynamic changes were mirrored by an early cytokine IFN-γ-mediated inhibition (up to 50-70%) of hepatic fetuin-A expression. Disruption of fetuin-A expression rendered animals more susceptible to LSI, whereas supplementation of fetuin-A (20-100 mg/kg) dose-dependently increased animal survival rates. The protection was associated with a significant reduction in systemic HMGB1 accumulation in vivo, and parallel inhibition of IFN-γ- or LPS-induced HMGB1 release in vitro.These experimental data suggest that fetuin-A is protective against lethal systemic inflammation partly by inhibiting active HMGB1 release