Evidence of a New Excited Charmed Baryon Decaying to Σ_{c}(2455)

We present the study of B[over ¯]^{0}→Σ_{c}(2455)^{0,++}π^{±}p[over ¯] decays based on 772×10^{6} BB[over ¯] events collected with the Belle detector at the KEKB asymmetric-energy e^{+}e^{-} collider. The Σ_{c}(2455)^{0,++} candidates are reconstructed via their decay to Λ_{c}^{+}π^{∓} and Λ_{c}^{+} decays to pK^{-}π^{+}, pK_{S}^{0}, and Λπ^{+} final states. The corresponding branching fractions are measured to be B(B[over ¯]^{0}→Σ_{c}(2455)^{0}π^{+}p[over ¯])=(1.09±0.06±0.07)×10^{-4} and B(B[over ¯]^{0}→Σ_{c}(2455)^{++}π^{-}p[over ¯])=(1.84±0.11±0.12)×10^{-4}, which are consistent with the world average values with improved precision. A new structure is found in the M_{Σ_{c}(2455)^{0,++}π^{±}} spectrum with a significance of 4.2σ including systematic uncertainty. The structure is possibly an excited Λ_{c}^{+} and is tentatively named Λ_{c}(2910)^{+}. Its mass and width are measured to be (2913.8±5.6±3.8) MeV/c^{2} and (51.8±20.0±18.8) MeV, respectively. The products of branching fractions for the Λ_{c}(2910)^{+} are measured to be B(B[over ¯]^{0}→Λ_{c}(2910)^{+}p[over ¯])×B(Λ_{c}(2910)^{+}→Σ_{c}(2455)^{0}π^{+})=(9.5±3.6±1.6)×10^{-6} and B(B[over ¯]^{0}→Λ_{c}(2910)^{+}p[over ¯])×B(Λ_{c}(2910)^{+}→Σ_{c}(2455)^{++}π^{-})=(1.24±0.35±0.10)×10^{-5}. Here, the first and second uncertainties are statistical and systematic, respectively.

[Analysis of clinical characteristics and treatment status of atopic dermatitis in a children's hospital in Beijing from 2015 to 2019].

To analyze the clinical characteristics and treatment status of atopic dermatitis (AD) in children in the outpatient department of a children's hospital in Beijing from 2015 to 2019. This study used a cross-sectional study method to retrospectively analyze the data of AD patients who visited the Dermatology outpatient department of Beijing Children's Hospital, Capital Medical University, from April 2015 to April 2019. A total of 1 926 AD patients aged 0-17.5 years old living in Beijing and its surrounding areas were included, and the general situation, severity and distribution of AD disease, clinical characteristics and severity of AD, relevant influencing factors of AD onset, AD disease prognosis and treatment status were recorded. SAS 9.4, SPSS19.0, and R software were used for data processing, and descriptive statistical analysis, Chi-square test, Analysis of Variance, and correspondence analysis were used for statistical analysis. The results showed that the male to female ratio of AD patients in children included in this study was 1.4∶1; 79.0% (1 522/1 926), 86.1%(1 658/1 926), 91.3%(1 758/1 926), and 97.3%(1 907/1 926) of AD onset at the age of 6 months, 1 year, 2 years, and 5 years, respectively; mild of AD patients accounted for 13.2% (255/1 926)(SCORAD score 0-24), moderate of AD patients accounted for 50.1%(965/1 926) (SCORAD score 25-50), and severe of AD patients accounted for 36.7% (706/1 926)(SCORAD score>50).The age of severe AD patients were younger than mild and moderate AD patients. The face, head, trunk, and lower limbs were common areas of onset for moderate to severe AD, while the hands, feet, and ears were common areas of onset for severe AD patients. Temperature changes, hot water factors, mental and emotional states, and spring and winter were the main aggravation factors of AD;35.2% (678/1 926) aggravated and 61.8% (1 191/1 926) persistent. The more frequent bathing, the less severity of AD disease (χ2=29.791,P<0.001); 28.0% (520/1 856) of AD patients have no moisturizing habits, which were correlated with the severity of AD disease (χ2=15.908, P<0.05); the proportion of combined treatment medications in children with moderate to severe AD was significantly higher than mild AD patients. In conclusion, the patients with AD who went to specialist clinics were mainly moderate to severe patients and developed disease before the age of 5 years from 2015 to 2019.The severity of AD were mainly moderate to severe, and most of these patients had poor disease control. Traditional treatment plans had limitations. Identifying the clinical characteristics and treatment status of childhood AD would help us to carry out more targeted prevention and management work.

Search for a Light Higgs Boson in Single-Photon Decays of ϒ(1S) Using ϒ(2S)→π

We search for a light Higgs boson (A^{0}) decaying into a τ^{+}τ^{-} or µ^{+}µ^{-} pair in the radiative decays of ϒ(1S). The production of ϒ(1S) mesons is tagged by ϒ(2S)→π^{+}π^{-}ϒ(1S) transitions, using 158×10^{6} ϒ(2S) events accumulated with the Belle detector at the KEKB asymmetric energy electron-positron collider. No significant A^{0} signals in the mass range from the τ^{+}τ^{-} or µ^{+}µ^{-} threshold to 9.2 GeV/c^{2} are observed. We set the upper limits at 90% credibility level (C.L.) on the product branching fractions for ϒ(1S)→γA^{0} and A^{0}→τ^{+}τ^{-} varying from 3.8×10^{-6} to 1.5×10^{-4}. Our results represent an approximately twofold improvement on the current world best upper limits for the ϒ(1S)→γA^{0}(→τ^{+}τ^{-}) production. For A^{0}→µ^{+}µ^{-}, the upper limits on the product branching fractions for ϒ(1S)→γA^{0} and A^{0}→µ^{+}µ^{-} are at the same level as the world average limits, and vary from 3.1×10^{-7} to 1.6×10^{-5}. The upper limits at 90% credibility level on the Yukawa coupling f_{ϒ(1S)} and mixing angle sinθ_{A^{0}} are also given.

Measurements of the Branching Fractions of the Semileptonic Decays Ξ_{c}

Using data samples of 89.5 and 711 fb^{-1} recorded at energies of sqrt[s]=10.52 and 10.58 GeV, respectively, with the Belle detector at the KEKB e^{+}e^{-} collider, we report measurements of branching fractions of semileptonic decays Ξ_{c}^{0}→Ξ^{-}ℓ^{+}ν_{ℓ} (ℓ=e or µ) and the CP-asymmetry parameter of Ξ_{c}^{0}→Ξ^{-}π^{+} decay. The branching fractions are measured to be B(Ξ_{c}^{0}→Ξ^{-}e^{+}ν_{e})=(1.31±0.04±0.07±0.38)% and B(Ξ_{c}^{0}→Ξ^{-}µ^{+}ν_{µ})=(1.27±0.06±0.10±0.37)%, and the decay parameter α_{Ξπ} is measured to be 0.63±0.03±0.01 with much improved precision compared with the current world average. The corresponding ratio B(Ξ_{c}^{0}→Ξ^{-}e^{+}ν_{e})/B(Ξ_{c}^{0}→Ξ^{-}µ^{+}ν_{µ}) is 1.03±0.05±0.07, which is consistent with the expectation of lepton flavor universality. The first measured asymmetry parameter A_{CP}=(α_{Ξ^{-}π^{+}}+α_{Ξ[over ¯]^{+}π^{-}})/(α_{Ξ^{-}π^{+}}-α_{Ξ[over ¯]^{+}π^{-}})=0.024±0.052±0.014 is found to be consistent with zero. The first and the second uncertainties above are statistical and systematic, respectively, while the third ones arise due to the uncertainty of the Ξ_{c}^{0}→Ξ^{-}π^{+} branching fraction.

First Measurements of Absolute Branching Fractions of the Ξ_{c}

We present the first measurements of absolute branching fractions of Ξ_{c}^{0} decays into Ξ^{-}π^{+}, ΛK^{-}π^{+}, and pK^{-}K^{-}π^{+} final states. The measurements are made using a dataset comprising (772±11)×10^{6} BB[over ¯] pairs collected at the ϒ(4S) resonance with the Belle detector at the KEKB e^{+}e^{-} collider. We first measure the absolute branching fraction for B^{-}→Λ[over ¯]_{c}^{-}Ξ_{c}^{0} using a missing-mass technique; the result is B(B^{-}→Λ[over ¯]_{c}^{-}Ξ_{c}^{0})=(9.51±2.10±0.88)×10^{-4}. We subsequently measure the product branching fractions B(B^{-}→Λ[over ¯]_{c}^{-}Ξ_{c}^{0})B(Ξ_{c}^{0}→Ξ^{-}π^{+}), B(B^{-}→Λ[over ¯]_{c}^{-}Ξ_{c}^{0})B(Ξ_{c}^{0}→ΛK^{-}π^{+}), and B(B^{-}→Λ[over ¯]_{c}^{-}Ξ_{c}^{0})B(Ξ_{c}^{0}→pK^{-}K^{-}π^{+}) with improved precision. Dividing these product branching fractions by the result for B^{-}→Λ[over ¯]_{c}^{-}Ξ_{c}^{0} yields the following branching fractions: B(Ξ_{c}^{0}→Ξ^{-}π^{+})=(1.80±0.50±0.14)%, B(Ξ_{c}^{0}→ΛK^{-}π^{+})=(1.17±0.37±0.09)%, and B(Ξ_{c}^{0}→pK^{-}K^{-}π^{+})=(0.58±0.23±0.05)%. For the above branching fractions, the first uncertainties are statistical and the second are systematic. Our result for B(Ξ_{c}^{0}→Ξ^{-}π^{+}) can be combined with Ξ_{c}^{0} branching fractions measured relative to Ξ_{c}^{0}→Ξ^{-}π^{+} to yield other absolute Ξ_{c}^{0} branching fractions.

Observation of e+e- → π+π-π(0)(χbJ) and Search for X(b) → ωϒ(1S) at sqrt[s] = 10.867 GeV.

The e(+)e(-) → π(+)π(-)π(0)χ(bJ) (J = 0,1,2) processes are studied using a 118 fb(-1) data sample acquired with the Belle detector at a center-of-mass energy of 10.867 GeV. Unambiguous π(+)π(-)π(0)χ(bJ) (J = 1,2), ωχ(b1) signals are observed, and indication for ωχ(b2) is seen, both for the first time, and the corresponding cross section measurements are presented. No significant π(+)π(-)π(0)χ(b0) or ωχ(b0) signals are observed, and 90% confidence level upper limits on the cross sections for these two processes are obtained. In the π(+)π(-)π(0) invariant mass spectrum, significant non-ω signals are also observed. We search for the X(3872)-like state (named X(b)) decaying into ωϒ(1S); no significant signal is observed with a mass between 10.55 and 10.65 GeV/c(2).

Study of e+ e- → π+ π- J/ψ and observation of a charged charmoniumlike state at Belle.

The cross section for ee+ e- → π+ π- J/ψ between 3.8 and 5.5 GeV is measured with a 967 fb(-1) data sample collected by the Belle detector at or near the Υ(nS) (n = 1,2,…,5) resonances. The Y(4260) state is observed, and its resonance parameters are determined. In addition, an excess of π+ π- J/ψ production around 4 GeV is observed. This feature can be described by a Breit-Wigner parametrization with properties that are consistent with the Y(4008) state that was previously reported by Belle. In a study of Y(4260) → π+ π- J/ψ decays, a structure is observed in the M(π(±)J/ψ) mass spectrum with 5.2σ significance, with mass M = (3894.5 ± 6.6 ± 4.5) MeV/c2 and width Γ = (63 ± 24 ± 26) MeV/c2, where the errors are statistical and systematic, respectively. This structure can be interpreted as a new charged charmoniumlike state.

Genetic variability in copper-transporting P-type adenosine triphosphatase (ATP7B) is associated with Alzheimer's disease in a Chinese population.

Previous experiments demonstrated that transgenic mice carrying both amyloid precursor protein and mutant ATP7B transgenes reduce amyloid plaques and diminish plasma Abeta levels. These experiments showed that a structural change of ATP7B may affect Alzheimer’s disease (AD) susceptibility. In this study three missense SNPs in ATP7B gene (rs1801243, rs1801244, and rs1801249) were chosen to test whether they were associated with AD. We tested this hypothesis using a case control design. The experimental data showed that there was a significant deviation from Hardy-Weinberg equilibrium (HWE) for SNP rs1801249 (c.3419 T greater than C, Val1140Ala) in the case group (p = 0.014) but not in the control group and that there was an association between SNP rs1801249 and AD under a recessive model (p = 0.003). The data also showed that the genotype frequency distribution of the ATP7B c.1366 G greater than C polymorphism (rs1801244, Val456Leu) differed significantly between the AD patients and the normal subjects (p = 0.012). In addition, the frequency of the TGC haplotype of SNPs rs1801243, rs1801244, and rs1801249 was significantly higher in the AD patients compared with the normal subjects (p = 8.49×10-7). These observations suggested that genetic variations in the copper transporter gene ATP7B might contribute to AD pathogenesis in the Taiwanese population.

Observation of new resonant structures in γγ → ωϕ, ϕϕ, and ωω.

The processes γγ → ωϕ, ϕϕ, and ωω are measured using an 870 fb(-1) data sample collected with the Belle detector at the KEKB asymmetric-energy e+ e- collider. Production of vector meson pairs is clearly observed and their cross sections are measured for masses that range from threshold to 4.0 GeV. In addition to signals from well established spin-zero and spin-two charmonium states, there are resonant structures below charmonium threshold, which have not been previously observed. We report a spin-parity analysis for the new structures and determine the products of the η(c), χ(c0), and χ(c2) two-photon decay widths and branching fractions to ωϕ, ϕϕ, and ωω.

Evidence for a new resonance and search for the Y(4140) in the gammagamma-->phiJ/psi process.

The process gammagamma-->phiJ/psi is measured using a data sample of 825 fb{-1} collected with the Belle detector. A narrow peak of 8.8{-3.2}{+4.2} events, with a significance of 3.2 standard deviations including systematic uncertainty, is observed. The mass and natural width of the structure [named X(4350)] are measured to be [4350.6{-5.1}{+4.6}(stat)+/-0.7(syst)] MeV/c{2} and [13{-9}{+18}(stat)+/-4(syst)] MeV, respectively. The product of its two-photon decay width and branching fraction to phiJ/psi is [6.7{-2.4}{+3.2}(stat)+/-1.1(syst)] eV for J{P}=0{+}, or [1.5{-0.6}{+0.7}(stat)+/-0.3(syst)] eV for J{P}=2{+}. No signal for the Y(4140)-->phiJ/psi structure reported by the CDF Collaboration in B-->K{+}phiJ/psi decays is observed, and limits of Gamma_{gammagamma}(Y(4140))B(Y(4140)-->phiJ/psi)<41 eV for J{P}=0;{+} or <6.0 eV for J{P}=2{+} are determined at the 90% C.L. This disfavors the scenario in which the Y(4140) is a D{s}{*+}D{s}{*-} molecule.

B-cell-specific DNA binding by an E47 homodimer.

B cells express a unique E-box-binding activity that contains basic helix-loop-helix (bHLH) proteins encoded by the E2A gene. E2A proteins play a central role in immunoglobulin gene transcription and are also required for the generation of the B-lymphocyte lineage. In muscle, E2A proteins bind DNA as heterodimers with muscle-specific bHLH partners, such as MyoD and myogenin, and these heterodimers are thought to be both necessary and sufficient for muscle determination in cultured cells. Our results indicate that in B cells, the bHLH partners for E2A proteins are not B-cell-restricted proteins, but are the E2A proteins themselves. UV cross-linking, gel purification, and the analysis of "forced heterodimers" indicate that BCF1 is primarily a homodimer of the E2A protein E47. Since E47 is widely expressed, our results argue for a difference in the inherent DNA-binding properties of the E47 protein in B cells and may help explain the restricted B-lineage defect observed in E2A-deficient mice.

Phosphorylation of E47 as a potential determinant of B-cell-specific activity.

The E2A gene encodes two basic helix-loop-helix proteins designated E12 and E47. Although these proteins are widely expressed, they are required only for the B-lymphocyte lineage where DNA binding is mediated distinctively by E47 homodimers. By studying the properties of deltaE47, an N-terminal truncation of E47, we provide evidence that phosphorylation may contribute to B-cell-specific DNA binding by E47. Two serines N terminal to the deltaE47 basic helix-loop-helix domain were found to be phosphorylated in a variety of cell types but were hypophosphorylated in B cells. Phosphorylating these serines in vitro inhibited DNA binding by deltaE47 homodimers but not by deltaE47-containing heterodimers, such as deltaE47:MyoD. These results argue that hypophosphorylation may be a prerequisite for activity of E47 homodimers in B cells, suggesting the use of an inductive (nonstochastic) step in early B-cell development.

Notch inhibition of E47 supports the existence of a novel signaling pathway.

E47 is a widely expressed transcription factor that activates B-cell-specific immunoglobulin gene transcription and is required for early B-cell development. In an effort to identify processes that regulate E47, and potentially B-cell development, we found that activated Notch1 and Notch2 effectively inhibit E47 activity. Only the intact E47 protein was inhibited by Notch-fusion proteins containing isolated DNA binding and activation domains were unaffected-suggesting that Notch targets an atypical E47 cofactor. Although overexpression of the coactivator p300 partially reversed E47 inhibition, results of several assays indicated that p300/CBP is not a general target of Notch. Notch inhibition of E47 did not correlate with its ability to activate CBF1/RBP-Jkappa, the mammalian homolog of Suppressor of Hairless, a protein that associates physically with Notch and defines the only known Notch signaling pathway in drosophila. Importantly, E47 was inhibited independently of CBF1/RPB-Jkappa by Deltex, a second Notch-interacting protein. We provide evidence that Notch and Deltex may act on E47 by inhibiting signaling through Ras because (i) full E47 activity was found to be dependent on Ras and (ii) both Notch and Deltex inhibited GAL4-Jun, a hybrid transcription factor whose activity is dependent on signaling from Ras to SAPK/JNK.

Repression of immunoglobulin enhancers by the helix-loop-helix protein Id: implications for B-lymphoid-cell development.

It has been proposed that the helix-loop-helix (HLH) protein Id serves as a general antagonist of cell differentiation by inhibiting bHLH (HLH with an adjacent stretch of basic amino acids) proteins specifically required for developmental programs (such as MyoD). We show here that ectopic expression of Id represses in vivo activity of the bHLH protein E2-5 (encoded by the E2A gene) and of both the immunoglobulin heavy-chain (IgH) and kappa-light-chain gene enhancers to which E2-5 binds. Id does not affect the activity of the bHLH-zip protein, TFE3, which also binds these enhancers. We examined a large panel of B-cell lines that represent different stages of lymphoid development and found only two that express Id mRNA. The cell lines Ba/F3 and LyD9 have been categorized previously as early B-lymphoid-cell progenitors. Unlike their more mature B-lymphoid-cell counterparts, Ba/F3 and LyD9 cells do not express I mu sterile transcripts, which are indicative of IgH enhancer activity. Moreover, Ba/F3-derived nuclear extracts lack E2-box-binding activity, indicating the absence of free bHLH proteins, and transfected Ba/F3 cells fail to support the activity of the IgH enhancer. Hence, expression of Id correlates inversely with bHLH protein activity and enhancer function in vivo. These results suggest that Id may play a role early in B-lymphoid-cell development to regulate transcription of the IgH locus.

Lectin analysis of common glycoproteins detected on the surface of continuous microvascular endothelium in situ and in culture: identification of sialoglycoproteins.

For many years, molecular interactions with vascular endothelium have been studied in vitro on cultured endothelial cells. Yet, it is clear that the different environmental conditions in vivo vs. in vitro may cause phenotypic drift and altered expression of cell surface molecules. In this study, we identify several endothelial surface proteins of similar apparent molecular mass by radioiodination of cultured microvascular cells and by intravascular radioiodination of rat heart endothelium in situ. The radioiodinated surface polypeptides detected by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) (followed by autoradiography) were subjected to lectin affinity chromatography in order to provide an additional screen for identifying common surface glycoproteins and a means for partial characterization of their glycans. With a battery of 18 lectins, seven major (gp140, gp120, gp100, gp85, gp75, gp60, gp47) and 6 minor (gp330, gp300, gp180, gp160, gp150, gp42) glycoproteins were identified on the cultured cells each with a different lectin binding profile. The lectin binding profiles of many endothelial glycoproteins in situ were similar to those of their counterparts in culture. A common set of seven major glycoproteins with the same apparent molecular masses was found in situ as well as in vitro. These common glycoproteins were characterized further using both sialidase digestion and sequential lectin affinity chromatography of cell lysates. Most of the glycoproteins appear to have both complex-type N-linked and O-linked glycans except for gp60 with only O-linked glycans, gp47 with only complex N-linked sugars, and gp42 with only simple N-linked sugars. A subset of sialoglycoproteins (gp140, gp120, gp100, gp60, gp47) was identified. One of them, gp120, is podocalyxin based on immunoprecipitation with specific antiserum and another one, gp60, is a recently identified albumin binding protein on the surface of cultured microvascular endothelial cells. This study shows that gp60 is indeed present on the surface of endothelium in situ and that it is a sialoglycoprotein with typical O-linked glycans. It is apparent that the continuous type of microvascular endothelium can indeed express in culture and in situ a common set of major glycoproteins.

Plasma agouti-related protein level: a possible correlation with fasted and fed states in humans and rats.

We measured plasma concentrations of agouti-related protein (AGRP) in humans and rats and determined whether these were affected by ingestion of a meal after fasting. In 17 healthy human subjects, the mean plasma concentration of AGRP was lower in the fed state than in the fasted state. Two hours after a breakfast meal, AGRP levels dropped by 39%. By contrast, a continued fast for 2 h increased the average AGRP concentration by 73%. In rats with diet-induced obesity, refeeding resulted in a 50% decrease in plasma AGRP concentrations following a fasting-refeeding protocol. Our results support the notion that plasma AGRP may serve as a biomarker for the transition from a fasted to the satiated state.

Measurement of the e+e- -->pi+pi- J/psi cross section via initial-state radiation at Belle.

The cross section for e(+)e(-)-->pi(+)pi(-)J/psi between 3.8 and 5.5 GeV/c(2) is measured using a 548 fb(-1) data sample collected on or near the Upsilon(4S) resonance with the Belle detector at KEKB. A peak near 4.25 GeV/c(2), corresponding to the so called Y(4260), is observed. In addition, there is another cluster of events at around 4.05 GeV/c(2). A fit using two interfering Breit-Wigner shapes describes the data better than one that uses only the Y(4260), especially for the lower-mass side of the 4.25 GeV enhancement.