Self Interference of Single Electrodynamic Particle in Double Slit

It is by the long established fact in experiment and theory that electromagnetic waves, here as one component of an IED particle, passing a double slit will undergo self inference each, producing at a detector plane fringed intensities. The wave generating point charge of a zero rest mass, as the other component of the particle, is maintained a constant energy and speed by a repeated radiation reabsorption/reemission scheme, and in turn steered in direction in its linear motion by the reflected radiation field, and will thereby travel to the detector along (one of) the optical path(s) of the waves leading to a bright interference fringe. We elucidate the process formally based on first principles solutions for the IED particle and known principles for wave-matter interaction.Comment: Presentation at The 6th Int. Symp. Quantum Theory and Symmetries, Univ. Kent, 2009

Safety and Immunogenicity of H5N1 Influenza Vaccine Based on Baculovirus Surface Display System of Bombyx mori

Avian influenza virus (H5N1) has caused serious infections in human beings. This virus has the potential to emerge as a pandemic threat in humans. Effective vaccines against H5N1 virus are needed. A recombinant Bombyx mori baculovirus, Bmg64HA, was constructed for the expression of HA protein of H5N1 influenza virus displaying on the viral envelope surface. The HA protein accounted for approximately 3% of the total viral proteins in silkworm pupae infected with the recombinant virus. Using a series of separation and purification methods, pure Bmgp64HA virus was isolated from these silkworm pupae bioreactors. Aluminum hydroxide adjuvant was used for an H5N1 influenza vaccine. Immunization with this vaccine at doses of 2 mg/kg and 0.67 mg/kg was carried out to induce the production of neutralizing antibodies, which protected monkeys against influenza virus infection. At these doses, the vaccine induced 1:40 antibody titers in 50% and 67% of the monkeys, respectively. The results of safety evaluation indicated that the vaccine did not cause any toxicity at the dosage as large as 3.2 mg/kg in cynomolgus monkeys and 1.6 mg/kg in mice. The results of dose safety evaluation of vaccine indicated that the safe dose of the vaccine were higher than 0.375 mg/kg in rats and 3.2 mg/kg in cynomolgus monkeys. Our work showed the vaccine may be a candidate for a highly effective, cheap, and safe influenza vaccine for use in humans

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases: A Mendelian Randomization Study.

Importance: The causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation. Objective: To conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases. Data Sources: Genomewide association studies (GWAS) published up to January 15, 2015. Study Selection: GWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available. Data Extraction and Synthesis: Summary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population. Main Outcomes and Measures: Odds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation. Results: Summary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer cancers and at tissue sites with lower rates of stem cell division. There was generally little evidence of association between genetically increased telomere length and risk of psychiatric, autoimmune, inflammatory, diabetic, and other non-neoplastic diseases, except for coronary heart disease (OR, 0.78 [95% CI, 0.67-0.90]), abdominal aortic aneurysm (OR, 0.63 [95% CI, 0.49-0.81]), celiac disease (OR, 0.42 [95% CI, 0.28-0.61]) and interstitial lung disease (OR, 0.09 [95% CI, 0.05-0.15]). Conclusions and Relevance: It is likely that longer telomeres increase risk for several cancers but reduce risk for some non-neoplastic diseases, including cardiovascular diseases

Observation of chi(cJ) -> Lambda(Lambda)over-bar(eta)

By analyzing (448.1 +/- 2.9) x 10(6) psi(3686) events collected with the BESIII detector operating at the BEPCII collider, the decays of chi(cJ) -> Lambda(Lambda) over bar (eta) (J = 0, 1, and 2) are observed for the first time with statistical significances of 13.9 sigma, 6.7 sigma, and 8.2 sigma, respectively. The product branching fractions of psi(3686) -> gamma chi(cJ) and chi(cJ) -> Lambda(Lambda) over bar (eta) are measured. Dividing by the world averages of the branching fractions of psi(3686) -> gamma chi(cJ), the branching fractions of chi(cJ) -> Lambda(Lambda) over bar (eta) decays are determined to be (2.31 +/- 0.30 +/- 0.21) x 10(-4), (5.86 +/- 1.38 +/- 0.68) x 10(-5), and (1.05 +/- 0.21 +/- 0.15) x 10(-4) for J = 0, 1 and 2, respectively, where the first uncertainties are statistical and the second systematic

Study of the resonance structures in the process e(+) e(-) -> pi(+) pi(-) J/psi

Using about 23 fb(-1) of data collected with the BESIII detector operating at the BEPCII storage ring, a precise measurement of the e(+) e(-) -> pi(+) pi(-) J/psi Born cross section is performed at center-of-mass energies from 3.7730 to 4.7008 GeV. Two structures, identified as the Y(4220) and the Y(4320) states, are observed in the energy-dependent cross section with a significance larger than 10 sigma. The masses and widths of the two structures are determined to be (M,(sic)) = (4221.4 +/- 1.5 +/- 2.0 MeV=c(2); 41.8 +/- 2.9 +/- 2.7 MeV) and (M,(sic)) = (4298 +/- 12 +/- 26 MeV=c(2); 127 +/- 17 +/- 10 MeV)respectively. A small enhancement around 4.5 GeV with a significance about 3s, compatible with the psi(4415), might also indicate the presence of an additional resonance in the spectrum. The inclusion of this additional contribution in the fit to the cross section affects the resonance parameters of the Y(4320) state