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Contains fulltext : 240741.pdf (Publisher’s version ) (Open Access)

Contains fulltext : 288884.pdf (Publisher’s version ) (Open Access)

Based on a recent Dutch national guideline, we propose a structured stepwise diagnostic approach for children with growth failure (short stature and/or growth faltering), aiming at high sensitivity for pathologic causes at acceptable specificity. The first step is a detailed clinical assessment, aiming at obtaining relevant clinical clues from the medical history (including family history), physical examination (emphasising head circumference, body proportions and dysmorphic features) and assessment of the growth curve. The second step consists of screening: a radiograph of the hand and wrist (for bone age and assessment of anatomical abnormalities suggestive for a skeletal dysplasia) and laboratory tests aiming at detecting disorders that can present as isolated short stature (anaemia, growth hormone deficiency, hypothyroidism, coeliac disease, renal failure, metabolic bone diseases, renal tubular acidosis, inflammatory bowel disease, Turner syndrome [TS]). We advise molecular array analysis rather than conventional karyotyping for short girls because this detects not only TS but also copy number variants and uniparental isodisomy, increasing diagnostic yield at a lower cost. Third, in case of diagnostic clues for primary growth disorders, further specific testing for candidate genes or a hypothesis-free approach is indicated; suspicion of a secondary growth disorder warrants adequate further targeted testing.

Tall stature and/or accelerated growth (TS/AG) in a child can be the result of a primary or secondary growth disorder, but more frequently no cause can be found (idiopathic TS). The conditions with the most important therapeutic implications are Klinefelter syndrome, Marfan syndrome and secondary growth disorders such as precocious puberty, hyperthyroidism and growth hormone excess. We propose a diagnostic flow chart offering a systematic approach to evaluate children referred for TS/AG to the general paediatrician. Based on the incidence, prevalence and clinical features of medical conditions associated with TS/AG, we identified relevant clues for primary and secondary growth disorders that may be obtained from the medical history, physical evaluation, growth analysis and additional laboratory and genetic testing. In addition to obtaining a diagnosis, a further goal is to predict adult height based on growth pattern, pubertal development and skeletal maturation. We speculate that an improved diagnostic approach in addition to expanding use of genetic testing may increase the diagnostic yield and lower the age at diagnosis of children with a pathologic cause of TS/AG.

The spectrum of the $s\bar s$ mesons is studied performing a phenomenological analysis of the Regge trajectories defined for the excitation energies. For the $\phi(3 ^3S_1)$ state the mass $M(\phi(3S))=2100(20)$ MeV and the leptonic width $\Gamma_{ee}(\phi(3S))=0.27(2)$ keV are obtained, while the mass of the $2 ^3D_1$ state, $M(\phi(2 ^3D_3))=2180(5)$ MeV, appears to be in agreement with the mass of the $\phi(2170)$ resonance, and its leptonic width, $\Gamma_{ee}(2 ^3D_1)=0.20\pm 0.10$ keV, has a large theoretical uncertainty, depending on the parameters of the flattened confining potential., Comment: 7 pages, no figures

Contains fulltext : 138859.pdf (Publisher’s version ) (Open Access) PURPOSE: Despite the different etiology of primary open angle glaucoma (POAG), primary angle closure glaucoma (PACG), and pseudoexfoliative glaucoma (PEXG), several studies have suggested that these forms of glaucoma have overlapping genetic risk factors. Therefore, the aim of this study was to evaluate the role of genetic variants recently associated with POAG in different types of glaucoma in Pakistani POAG, PACG, and PEXG patient cohorts. METHODS: Six variants in CDKN2B-AS1 (rs4977756), CDKN2B (rs1063192), ATOH7 (rs1900004), CAV1 (rs4236601), TMCO1 (rs4656461), and SIX1 (rs10483727) were genotyped using TaqMan assays. A total of 513 unrelated patients with glaucoma (268 with POAG, 125 with PACG, and 120 with PEXG) and 233 healthy controls were included in the study. Genotypic and allelic associations were analyzed with a chi-square test. RESULTS: The frequency of the G allele of TMCO1 rs4656461 was significantly lower in the patients with POAG (p=0.003; OR [odds ratio]=0.57), PACG (p=0.009; OR=0.52), and PEXG (p=0.01; OR=0.54) compared to the control individuals. The T allele of ATOH7 rs1900004 was observed less frequently in the patients with PACG (p=0.03; OR=0.69) compared to the control individuals. The A allele of CAV1 rs4236601 was found more frequently in the patients with POAG (p=0.008; OR=1.49) compared to the control individuals. This study demonstrates that the TMCO1 rs4656461 variant is associated with POAG, PACG and PEXG in the Pakistani population. Our study was unable to confirm previous associations reported for variants in CDKN2B-AS1, CDKN2B, and SIX1 with any type of glaucoma. CONCLUSIONS: In conclusion, we found consistent evidence of the significant association of three common variants in TMCO1, ATOH7, and CAV1.

Genome wide association studies (GWAS) have mapped multiple independent cancer susceptibility loci to chr5p15.33. Here, we show that fine-mapping of pancreatic and testicular cancer GWAS within one of these loci (Region 2 in CLPTM1L) focuses the signal to nine highly correlated SNPs. Of these, rs36115365-C associated with increased pancreatic and testicular but decreased lung cancer and melanoma risk, and exhibited preferred protein-binding and enhanced regulatory activity. Transcriptional gene silencing of this regulatory element repressed TERT expression in an allele-specific manner. Proteomic analysis identifies allele-preferred binding of Zinc finger protein 148 (ZNF148) to rs36115365-C, further supported by binding of purified recombinant ZNF148. Knockdown of ZNF148 results in reduced TERT expression, telomerase activity and telomere length. Our results indicate that the association with chr5p15.33-Region 2 may be explained by rs36115365, a variant influencing TERT expression via ZNF148 in a manner consistent with elevated TERT in carriers of the C allele., Genetic variants at multiple loci of chr5p15.33 have been associated with susceptibility to numerous cancers. Here the authors show that the association of one of these loci may be explained by a variant, rs36115365, influencing telomerase reverse transcriptase (TERT) expression via ZNF148.

The leptonic widths of high $��$-resonances are calculated in a coupled-channel model with unitary inelasticity, where analytical expressions for mixing angles between $(n+1)\,^3S_1$ and $n\,^3D_1$ states and probabilities $Z_i$ of the $c\bar c$ component are derived. Since these factors depend on energy (mass), different values of mixing angles $��(��(4040))=27.7^\circ$ and $��(��(4160))=29.5^\circ$, $Z_1\,(��(4040))=0.76$, and $Z_2\,(��(4160))=0.62$ are obtained. It gives the leptonic widths $��_{ee}(��(4040))=Z_1\, 1.17=0.89$~keV, $��_{ee}(��(4160))=Z_2\, 0.76=0.47$~keV in good agreement with experiment. For $��(4415)$ the leptonic width $��_{ee}(��(4415))=~0.55$~keV is calculated, while for the missing resonance $��(4510)$ we predict $M(��(4500))=(4515\pm 5)$~MeV and $��_{ee}(��(4510)) \cong 0.50$~keV., 10 pages, 6 references corrected, some new material added

We performed a multistage genome-wide association study of melanoma. In a discovery cohort of 1804 melanoma cases and 1026 controls, we identified loci at chromosomes 15q13.1 (HERC2/OCA2 region) and 16q24.3 (MC1R) regions that reached genome-wide significance within this study and also found strong evidence for genetic effects on susceptibility to melanoma from markers on chromosome 9p21.3 in the p16/ARF region and on chromosome 1q21.3 (ARNT/LASS2/ANXA9 region). The most significant single-nucleotide polymorphisms (SNPs) in the 15q13.1 locus (rs1129038 and rs12913832) lie within a genomic region that has profound effects on eye and skin color; notably, 50% of variability in eye color is associated with variation in the SNP rs12913832. Because eye and skin colors vary across European populations, we further evaluated the associations of the significant SNPs after carefully adjusting for European substructure. We also evaluated the top 10 most significant SNPs by using data from three other genome-wide scans. Additional in silico data provided replication of the findings from the most significant region on chromosome 1q21.3 rs7412746 (P = 6 × 10(-10)). Together, these data identified several candidate genes for additional studies to identify causal variants predisposing to increased risk for developing melanoma.

Item does not contain fulltext BACKGROUND: CYP1B1 is the most commonly mutated gene in primary congenital glaucoma (PCG), and mutations have also been identified in primary open-angle glaucoma (POAG). This study was undertaken to describe mutations in CYP1B1 in patients and families with PCG and POAG from Pakistan. DESIGN: Case-control series. PARTICIPANTS: Forty families, 190 sporadic POAG cases and 140 controls from Pakistan. METHODS: Patients and healthy individuals of one consanguineous Pakistani family were genotyped with high-resolution single nucleotide polymorphism microarrays. Homozygosity mapping was performed using HomozygosityMapper. Direct sequencing of CYP1B1 gene was performed in probands of the families, sporadic POAG cases and control individuals. MAIN OUTCOME MEASURES: Mutations in the CYP1B1 gene in PCG and POAG patients. RESULTS: Homozygosity mapping in a consanguineous Pakistani family revealed one 11-Mb homozygous region encompassing the CYP1B1 gene. A homozygous CYP1B1 missense mutation (p.Arg390His) was identified in this family. Sequence analysis of CYP1B1 in 39 additional families revealed one known and three novel homozygous mutations in PCG (p.Ala288Pro, p.Asp242Ala, p.Arg355* and p.Arg290Profs*37). In POAG, one novel heterozygous missense mutation (p.Asp316Val) was identified in one family and a previously reported mutation (p.Glu229Lys) was identified in three families. Analysis of CYP1B1 in a panel of 190 sporadic POAG patients revealed three novel heterozygous variants (p.Thr234Lys, p.Ala287Pro and p.Gln362*) and three previously reported heterozygous variants (p.Gly61Glu, p.Glu229Lys and p.Arg368His). The p.Glu229Lys variant was significantly associated with POAG (P = 0.03; odds ratio 2.49). CONCLUSIONS: This study confirms that CYP1B1 mutations are associated with POAG and PCG in the Pakistani population.

Radiative decays of $X(3872)$ are studied in single-channel approximation (SCA) and in the coupled-channel (CC) approach, where the decay channels $D\bar D^*$ are described with the string breaking mechanism. In SCA the transition rate $\tilde��_2=��(2\,{}^3P_1 \rightarrow ����)=71.8$~keV and large $\tilde��_1=��(2\,{}^3P_1\rightarrow J/����)=85.4$~keV are obtained, giving for their ratio the value $\tilde{R_{����}}=\frac{\tilde��_2}{\tilde��_1}=0.84$. In the CC approach three factors are shown to be equally important. First, the admixture of the $1\,{}^3P_1$ component in the normalized wave function of $X(3872)$ due to the CC effects. Its weight $c_{\rm X}(E_{\rm R})=0.200\pm 0.015$ is calculated. Secondly, the use of the multipole function $g(r)$ instead of $r$ in the overlap integrals, determining the partial widths. Thirdly, the choice of the gluon-exchange interaction for $X(3872)$, as well as for other states above threshold. If for $X(3872)$ the gluon-exchange potential is taken the same as for low-lying charmonium states, then in the CC approach $��_1= ��(X(3872)\rightarrow J/����) \sim 3$~keV is very small, giving the large ratio $R_{����}=\frac{\mathcal{B}(X(3872)\rightarrow ��(2S)��)}{\mathcal{B}(X(3872)\rightarrow J/����)}\gg 1.0$. Arguments are presented why the gluon-exchange interaction may be suppressed for $X(3872)$ and in this case $��_1=42.7$~keV, $��_2= 70.5$~keV, and $R_{����}=1.65$ are predicted for the minimal value $c_{\rm X}({\rm min})=0.185$, while for the maximal value $c_{\rm X}=0.215$ we obtained $��_1=30.8$~keV, $��_2=73.2$~keV, and $R_{����}=2.38$, which agrees with the LHCb data., 12 pages, no figures

The assumption underlying the symposium is that teacher education institutions have a dual challenge. At the one hand they need to prepare pre-service students for teaching and facilitating learning in the digital age, including the use of technology in teaching and learning. At the other hand teacher education institutions themselves need to change in order to cope with the challenges of the knowledge society. How Dutch teacher education institutions cope with these challenges is presented and discussed in the symposium.

CONTEXT: Serum IGF-I levels are often low in patients with short stature (SS) without defined etiology. Hence, genetic investigations have focused on the GH-IGF-I axis.OBJECTIVE: Our objectives were to characterize IGF-I axis status and search for a broader range of genetic associations in children with SS and normal GH.DESIGN AND SETTING: We conducted a prospective, cross-sectional, epidemiogenetic case-control study in 9 European countries (2008-2010).PARTICIPANTS: Children (n = 275) aged ≥2 years with SS without defined etiology (≤-2.5 height SD score [SDS]) and ≥1 peak GH ≥7 μg/L) were recruited.METHODS: Serum IGF-I, IGF-binding protein-3 (IGFBP-3), and acid-labile subunit (ALS) levels were measured in a central laboratory. Candidate gene exome sequencing was performed in this cohort and ethnicity-matched controls.RESULTS: Serum IGF-I, IGFBP-3, and ALS levels were highly correlated, but there was a discrepancy between prevalence of IGF-I, IGFBP-3, and ALS deficiencies (53%, 30%, and 0.8%, respectively). An insertion-deletion (Indel) on the IGF1 gene (P = 1.2 × 10(-5), Bonferroni-corrected; case vs control frequency: 0.04 vs 0.112), an Indel on NFKB1 (P = 1.36 × 10(-10); case vs control frequency: 0.464 vs 0.272), and 2 single-nucleotide polymorphisms on ZBTB38 (P < 2.3 × 10(-6)) were associated with SS. At P < 10(-4), single-nucleotide polymorphisms on genes related to protein kinase regulation, MAPK, and Fanconi pathways were also associated with SS.CONCLUSIONS: IGF-I deficiency is a common feature in SS without defined etiology; an Indel in the IGF1 gene was associated with SS. However, genes involved in transcriptional regulation (NFKB1 and ZBTB38) and growth factor signaling were also associated, providing further candidates for genetic investigations on individual patients.

We study the universal static potential $V_{\rm st}(r)$ and the force, which are fully determined by two fundamental parameters: the string tension $��=0.18\pm 0.02$ GeV$^2$ and the QCD constants $��_{\bar{\rm MS}}(n_f)$, taken from pQCD, while the infrared (IR) regulator $M_{\rm B}$ is taken from the background perturbation theory and expressed via the string tension. The vector couplings $��_{\rm V}(r)$ in the static potential and $��_{\rm F}(r)$ in the static force, as well as the characteristic scales, $r_1(n_f=3)$ and $r_0(n_f=3)$, are calculated and compared to lattice data. The result $r_0��_{\bar{\rm MS}}(n_f=3)=0.77\pm 0.03$, which agrees with the lattice data, is obtained for $M_{\rm B}=(1.15\pm 0.02)$ GeV. However, better agreement with the bottomonium spectrum is reached for a smaller $��_{\bar{\rm MS}}(n_f=3)=(325\pm 15)$ MeV and the frozen value of $��_V=0.57\pm 0.02$. The mass splittings $\bar M(1D)-\bar M(1P)$ and $\bar M(2P)-\bar M(1P)$ are shown to be sensitive to the IR regulator used. The masses $M(1\,^3D_3)=10169(2)$ MeV and $M(1\,^3D_1)=10155(3)$ MeV are predicted., 21 pages, 5 figures, revtex4

We show that there are two reasons why the partial width for the transition $��_1(��(3S)\rightarrow ����_{b1}(1P))$ is suppressed. Firstly, the spin-averaged matrix element (m.e.) $\bar{I(3S|r|1P_J)}$ is small, being equal to 0.023 GeV$^{-1}$ in our relativistic calculations. Secondly, the spin-orbit splittings produce relatively large contributions, giving $I(3S|r|1P_2)=0.066$ GeV$^{-1}$, while due to large cancellation the m.e. $I(3S|r|1P_1)=-0.020$ GeV$^{-1}$ is small and negative; at the same time the magnitude of $I(3S|r|1P_0)=-0.063$ GeV$^{-1}$ is relatively large. These m.e. give rise to the partial widths: $��_2(��(3S)\rightarrow ����_{b2}(1P))=212$ eV, $��_0(��(3S)\rightarrow ����_{b0}(1P))=54$ eV, which are in good agreement with the CLEO and BaBar data, and also to $��_1(��(3S)\rightarrow ����_{b1}(1P))=13$ eV, which satisfies the BaBar limit, $��_1(exp.) < 22$ eV., 8 pages

Radiative decays of X(3872) with $J^{PC}=1^{++}$ are studied in the coupled-channel approach, where the $c\bar c$ states are described by relativistic string Hamiltonian, while for the decay channels $DD^*$ a string breaking mechanism is used. Within this method a sharp peak and correct mass shift of the $2 {}^3P_1$ charmonium state just to the $D^0D^{*0}$ threshold was already obtained for a prescribed channel coupling to the $DD^*$ decay channels. For the same value of coupling the normalized wave function (w.f.) of X(3872) acquires admixture of the $1 {}^3P_1$ component with the w.f. fraction $c_1=0.153 (��=8.8^\circ$), which increases the transition rate $��(X(3872)\rightarrow J/����)$ up to 50-70 keV, making the ratio $R=\frac{\mathcal{B}(X(3872)\rightarrow ��^{\prime}��)}{\mathcal{B}(X(3872)\rightarrow J/����)}=0.8\pm 0.20 (th)$ significantly smaller, as compared to $R\simeq 5$ for X(3872) as a purely $2 {}^3P_1$ state., 14 pages,2 Tables

The masses of higher $D(nL)$ and $D_s(nL)$ excitations are shown to decrease due to the string contribution, originating from the rotation of the QCD string itself: it lowers the masses by 45 MeV for $L=2 (n=1)$ and by 65 MeV for $L=3 (n=1)$. An additional decrease $\sim 100$ MeV takes place if the current mass of the light (strange) quark is used in a relativistic model. For $D_s(1\,{}^3D_3)$ and $D_s(2P_1^H)$ the calculated masses agree with the experimental values for $D_s(2860)$ and $D_s(3040)$, and the masses of $D(2\,{}^1S_0)$, $D(2\,{}^3S_1)$, $D(1\,{}^3D_3)$, and $D(1D_2)$ are in agreement with the new BaBar data. For the yet undiscovered resonances we predict the masses $M(D(2\,{}^3P_2))=2965$ MeV, $M(D(2\,{}^3P_0))=2880$ MeV, $M(D(1\,{}^3F_4))=3030$ MeV, and $M(D_s(1\,{}^3F_2))=3090$ MeV. We show that for $L=2,3$ the states with $j_q=l+1/2$ and $j_q=l-1/2$ ($J=l$) are almost completely unmixed ($\phi\simeq -1^\circ$), which implies that the mixing angles $\theta$ between the states with S=1 and S=0 ($J=L$) are $\theta\approx 40^\circ$ for L=2 and $\approx 42^\circ$ for L=3., Comment: 22 pages, no figures, 4 tables Two references and corresponding discussion added

Traffic light control is one of the main means of controlling road traffic. Improving traffic control is important because it can lead to higher traffic throughput and reduced traffic congestion. This chapter describes multiagent reinforcement learning techniques for automatic optimization of traffic light controllers. Such techniques are attractive because they can automatically discover efficient control strategies for complex tasks, such as traffic control, for which it is hard or impossible to compute optimal solutions directly and hard to develop hand-coded solutions. First, the general multi-agent reinforcement learning framework is described, which is used to control traffic lights in this work. In this framework, multiple local controllers (agents) are each responsible for the optimization of traffic lights around a single traffic junction, making use of locally perceived traffic state information (sensed cars on the road), a learned probabilistic model of car behavior, and a learned value function which indicates how traffic light decisions affect long-term utility, in terms of the average waiting time of cars. Next, three extensions are described which improve upon the basic framework in various ways: agents (traffic junction controllers) taking into account congestion information from neighboring agents; handling partial observability of traffic states; and coordinating the behavior of multiple agents by coordination graphs and the max-plus algorithm.

This paper introduces a sensor management approach that integrates distributed Bayesian inference (DBI) and reinforcement learning (RL). DBI is implemented using distributed perception networks (DPNs), a multiagent approach to performing efficient inference, while RL is used to automatically discover a mapping from the beliefs generated by the DPNs to the actions that enable active sensors to gather the most useful observations. The resulting method is evaluated on a simulation of a chemical leak localization task and the results demonstrate 1) that the integrated approach can learn policies that perform effective sensor management, 2) that inference based on a correct observation model, which the DPNs make feasible, is critical to performance, and 3) that the system scales to larger versions of the task.

The di-electron widths of $\psi(4040)$, $\psi(4160)$, and $\psi(4415)$, and their ratios are shown to be in good agreement with experiment, if in all cases the $S-D$ mixing with a large mixing angle $\theta\approx 34^\circ$ is taken. Arguments are presented why continuum states give small contributions to the wave functions at the origin. We find that the Y(4360) resonance, considered as a pure $3 {}^3D_1$ state, would have very small di-electron width, $\Gamma_{ee}(Y(4360))=0.060$ keV. On the contrary, for large mixing between the $4 {}^3S_1$ and $3 {}^3D_1$ states with the mixing angle $\theta=34.8^\circ$, $\Gamma_{ee}(\psi(4415))=0.57$ keV coincides with the experimental number, while a second physical resonance, probably Y(4360), has also a rather large $\Gamma_{ee} (Y(\sim 4400))=0.61$ keV. For the higher resonance Y(4660), considered as a pure $5 {}^3S_1$ state, we predict the di-electron width $\Gamma_{ee}(Y(4660))=0.70$ keV, but it becomes significantly smaller, namely 0.31 keV, if the mixing angle between the $5 {}^3S_1$ and $4 {}^3D_1$ states $\theta=34^\circ$. The mass and di-electron width of the $6 {}^3S_1$ charmonium state are calculated., Comment: 19 pages, no figures

There exist several types of monopole - like topological defects in Electroweak theory. We investigate properties of these objects using lattice numerical methods. The intimate connection between them and the dynamics of the theory is established. We find that the density of Nambu monopoles cannot be predicted by the choice of the initial parameters of Electroweak theory and should be considered as the new external parameter of the theory. We also investigate the difference between the versions of Electroweak theory with the gauge groups $SU(2)\otimes U(1)$ and $SU(2)\otimes U(1)/Z_2$. We do not detect any difference at $\alpha \sim {1/128}$. However, such a difference appears in the unphysical region of large coupling constant $\alpha > 0.1$., Comment: to appear in Proceedings of SPMTP08

This paper proposes a reinforcement learning architecture con taining multiple "experts", each of which is a specialist in a dif ferent region in the overall state space. The central idea is that the different experts use qualitatively different (but sufficiently Markov) state representations, each of which captures different information regarding the true underlying world state, and which for that reason is suitable for a different part of the state space. The experts themselves learn to switch to another state represen tation (other expert) by having switching actions. Value functions can be learned using standard reinforcement learning algorithms. This architecture has important advantages in RL problems that have large state spaces or where a sensor system must inherently choose between mutually exclusive state representations. Experi ments in a small, proof-of-principle experiment as well as a larger, more realistic experiment illustrate the validity of this approach.

The hyperfine splittings in heavy quarkonia are studied in a model-independent way using the experimental data on di-electron widths. Relativistic correlations are taken into account together with the smearing of the spin-spin interaction. The radius of smearing is fixed by the known $J/��-��_c(1S)$ and $��(2S)-��'_c(2S)$ splittings and appears to be small, $r_{ss} \cong 0.06$ fm. Nevertheless, even with such a small radius an essential suppression of the hyperfine splittings ($\sim 50%)$ is observed in bottomonium. For the $nS~ b\bar b$ states $(n=1,2,...,6)$ we predict the values (in MeV) 28, 12, 10, 6, 6, and 3, respectively. For the $3S$ and $4S$ charmonium states the splittings 16(2) MeV and 12(4) MeV are obtained., 23 pages

The hyperfine splittings in heavy quarkonia are studied using new experimental data on the di-electron widths. The smearing of the spin-spin interaction is taken into account, while the radius of smearing is fixed by the known $J/��-��_c(1S)$ and $��(2S)-��'_c(2S)$ splittings and appears to be small, $r_{ss} \approx 0.06$ fm. Nevertheless, even with such a small radius an essential suppression of the hyperfine splittings ($\sim 50%)$ is observed in bottomonium. For the $nS b\bar b$ states $(n=1,2,...6)$ the values we predict (in MeV) are 28, 12, 10, 6, 6, and 3, respectively. In single-channel approximation for the $3S$ and $4S$ charmonium states the splittings 16(2) MeV and 12(4) MeV are obtained., 13 pages, no figures

The precision measurement of the hyperfine splitting $��_{\rm HF} (1P, c\bar c)=M_{\rm cog} (��_{cJ}) - M(h_c) = -0.5 \pm 0.4$ MeV in the Fermilab--E835 experiment allows to determine the gluonic condensate $G_2$ with high accuracy if the gluonic correlation length $T_g$ is fixed. In our calculations the negative value of $��_{\rm HF} = -0.3 \pm 0.4$ MeV is obtained only if the relatively small $T_g = 0.16$ fm and $G_2 = 0.065 (3)$ GeV${}^4$ are taken. These values correspond to the ``physical'' string tension $(��\approx 0.18 $ GeV$^2$). For $T_g \ge 0.2$ fm the hyperfine splitting is positive and grows for increasing $T_g$. In particular for $T_g = 0.2$ fm and $G_2 = 0.041 (2)$ GeV${}^4$ the splitting $��_{\rm HF} = 1.4 (2)$ MeV is obtained, which is in accord with the recent CLEO result., 9 pages revtex 4, no figures

Our purpose is to calculate relativistic bound states in a quantum filed theoretical approach. We work in the Yukawa model and first calculate the bound-state equation in the ladder approximation. We discuss why this is not a complete treatment and what possibilities there are to extend this equation., Comment: Proceedings of the international workshop on: Light Cone Physics: Hadrons and Beyond, Durham (UK), August 5th-9th 2003

The hyperfine splitting for the 2S charmonium state is calculated and the predicted number is $��_{\rm HF}(2S) = 57 \pm 8$ MeV, being by derivation the lower bound of this splitting. It results in $M(��_c(2S))= 3630 \pm 8$ MeV, which is smaller by two standard deviations than found in the Belle experiment \cite{ref.01}, but close to the $��_c(2S)$ mass observed by the same group in the experiment $e^+e^- \to J/����_c$ \cite{ref.06} where $M(��_c(2S)) = 3622 \pm 12$ MeV was found., 8 pages RevTex

Item does not contain fulltext PURPOSE: In recent studies, we showed that TP53 gene mutation or high levels of cytosolic vascular endothelial growth factor (VEGF) in estrogen receptor (ER)-alpha-positive primary breast tumors predict a poor disease outcome for patients treated with first-line tamoxifen for advanced disease. Mutant TP53 may up-regulate VEGF, whereas, on the other hand, wild-type TP53 may decrease VEGF production. EXPERIMENTAL DESIGN: In the present study, we aimed to assess the combined predictive value of TP53 gene mutation and VEGF status of 160 advanced breast cancer patients with ER-positive tumors who were treated with tamoxifen (median follow-up from start of tamoxifen treatment, 64 months). To assess TP53 gene mutation status, the entire open reading frame was sequenced; for VEGF status, an ELISA was used. RESULTS: In univariate analysis, both TP53 gene mutation (28% of the tumors) and a VEGF level above the median value were significantly associated with a short progression-free survival, post-relapse overall survival, and a poor rate of response to tamoxifen. In Cox multivariate regression analysis including the traditional predictive factors, the addition of TP53 gene mutation and VEGF status, alone or in combination, significantly predicted a poor efficacy of tamoxifen treatment. When the two factors were combined, a significantly decreased odds ratio was seen for the rate of response (odds ratio, 0.27). Similarly, an increased hazard ratio (HR) was seen for progression-free survival (HR, 2.32) and post-relapse overall survival (HR, 1.68) in the group with mutant TP53 and high VEGF compared with the group with both risk factors absent. CONCLUSIONS: Combined TP53 gene mutation status and high VEGF levels of ER-positive primary breast tumors independently predict a poor course of the disease of patients with advanced breast cancer treated with tamoxifen. These patients, having unfavorable tumor characteristics, might benefit more from other types of (individualized) treatment protocols.

We show that large ensembles of (neural network) models, obtained e.g. in bootstrapping or sampling from (Bayesian) probability distributions, can be effectively summarized by a relatively small number of representative models. We present a methodto findrepresen tative models through clustering based on the models' outputs on a data set. We apply the methodon models obtainedthrough bootstrapping (Boston housing) and on a multitask learning example.

Item does not contain fulltext BNAIC'01 : 13th Belgium-Netherlands Artificial Intelligence Conference, Amsterdam, The Netherlands, October 25-26

In this article we show that traditional Cox survival analysis can be improved upon when written in terms of a multi-layered perceptron and analyzed in the context of the Bayesian evidence framework. The obtained posterior distribution of network parameters is approximated both by Hybrid Markov Chain Monte Carlo sampling and by variational methods. We discuss the merits of both approaches. We argue that the neural-Bayesian approach circumvents the shortcomings of the original Cox analysis, and therefore yields better predictive results. As a bonus, we apply the Bayesian posterior (the probability distribution of the network parameters given the data) to estimate p-values on the inputs.

Contains fulltext : 18875_jaarvahek(2).pdf ( ) (Closed access) 166 p.

Contains fulltext : 100972.pdf (Publisher’s version ) (Open Access) European Symposium on Artificial Neural Networks '99, 21 april 1999

We discuss some properties of abelian monopoles in the Maximal Abelian projection of the SU(2) lattice gluodynamics. We show that in the maximal abelian projection abelian monopoles carry fluctuating electric charge and that the monopole currents are correlated with the magnetic and the electric parts of the SU(2) action density., Comment: 4 pages, LaTeX, 2 figures, uses epsf.sty; Talk given by M.I. Polikarpov at 31st International Symposium Ahrenshoop on the Theory of Elementary Particles, Buckow, September 2-6, 1997

Genotypes of wild Solanum species were tested to determine the level of resistance to root-knot nematodes and to detect the presence of virulent populations within Meloidogyne chitwoodi, M. fallax and M. hapla. High resistance to all tested populations of M. chitwoodi and M. fallax was observed in genotypes of Solanum bulbocastanum, S. hougasii, S. cardiophyllum and S. fendleri. Some genotypes of S. chacoense and S. stoloniferum showed moderate resistance to M. fallax, but no or lesser resistance to M. chitwoodi. There was little variation in virulence in populations of M. chitwoodi and M. fallax found on resistant plants. In contrast, large differences in virulence toward resistant genotypes of S. bulbocastanum, S. hougasii, S. chacoense, S. gourlayi, S. sparsipilum and S. spegazzinii were observed between four populations of M. hapla. It was found that resistance to M. chitwoodi, M. fallax and/or M. hapla is not linked to resistance to the nematode species adapted to high temperature, i.e., M. incognita, M. arenaria and M. javanica.

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