[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.

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.

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.

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.

Observation of two resonant structures in e+ e- -->pi+ pi- psi(2S) via initial-state radiation at Belle.

The cross section for e+ e- --> pi+ pi- psi(2S) between threshold and sqrt[s]=5.5 GeV is measured using 673 fb(-1) of data on and off the Upsilon(4S) resonance collected with the Belle detector at KEKB. Two resonant structures are observed in the pi+ pi- psi(2S) invariant-mass distribution, one at 4361 +/- 9 +/- 9 MeV/c2 with a width of 74 +/- 15 +/- 10 MeV/c2, and another at 4664 +/- 11 +/- 5 MeV/c2 with a width of 48 +/- 15 +/- 3 MeV/c2, if the mass spectrum is parametrized with the coherent sum of two Breit-Wigner functions. These values do not match those of any of the known charmonium states.

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.

Miranda as a multidomain adapter linking apically localized Inscuteable and basally localized Staufen and Prospero during asymmetric cell division in Drosophila.

Neuroblasts in the developing Drosophila CNS asymmetrically localize the cell fate determinants Numb and Prospero as well as prospero RNA to the basal cortex during mitosis. The localization of Prospero requires the function of inscuteable and miranda, whereas prospero RNA localization requires inscuteable and staufen function. We demonstrate that Miranda contains multiple functional domains: an amino-terminal asymmetric localization domain, which interacts with Inscuteable, a central Numb interaction domain, and a more carboxy-terminal Prospero interaction domain. We also show that Miranda and Staufen have similar subcellular localization patterns and interact in vitro. Furthermore, miranda function is required for the asymmetric localization of Staufen. Miranda localization is disrupted by the microfilament disrupting agent latrunculin A. Our results suggest that Miranda directs the basal cortical localization of multiple molecules, including Staufen and prospero RNA, in mitotic neuroblasts in an actin-dependent manner.

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.

Synovial fibroblasts and the sphingomyelinase pathway: sphingomyelin turnover and ceramide generation are not signaling mechanisms for the actions of tumor necrosis factor-alpha.

The activation of sphingomyelinase and the generation of ceramide has been proposed to mediate tumor necrosis factor-alpha (TNF-alpha)-induced nuclear factor (NF)-kappaB activation through its second messenger ceramide. Ceramide may also be an important regulator of cell growth, senescence, and apoptosis. Aberrant cell proliferation and apoptosis have been implicated in the rampant fibroblast proliferation and pannus formation characteristic of rheumatoid arthritis. However, the role of TNF-alpha and the sphingomyelinase pathway in the process have not been determined. The objective of this study was to determine whether TNF-alpha activates the sphingomyelin pathway in human synovial fibroblasts (HSF) and the potential role of ceramide in HSF proliferation and apoptosis. Cultured human synovial fibroblasts were stimulated with exogenous TNF-alpha, sphingomyelinase, and ceramide. Apoptosis was assessed by cell morphology and annexin V labeling. NF-kappaB and stress kinase pathway activation were determined by immunoblotting techniques. Sphingomyelinase activation was determined by quantitation of sphingomyelin and ceramide radioactivity in [14C]serine-prelabeled HSF cells. The addition of TNF-alpha (50 ng/ml) to HSF did not elicit detectable sphingomyelinase activation. TNF-alpha was shown to activate NF-kappaB (p65 translocation and degradation of IkappaBalpha) and the stress kinase pathway (phosphorylation of ATF-2, p38, and c-jun). In contrast, exogenous ceramide had no effect on these signaling pathways nor did ceramide stimulate the generation of interleukin-6 or interleukin-8. High concentrations of ceramide (> or =25 micromol/L) were cytotoxic, whereas lower concentrations of ceramide inhibited cell cycle progression. Thus, although TNF-alpha stimulates the NF-kappaB and stress kinase pathways in HSF, these effects of TNF-alpha are not associated with sphingomyelinase turnover or induction of apoptosis.

Miranda is required for the asymmetric localization of Prospero during mitosis in Drosophila.

Asymmetric division of Drosophila neuroblasts, sensory organ precursor cells, and cells in the procephalic neurogenic region involves the segregation of Numb and Prospero proteins into one of the two daughter cells. We have isolated a novel gene, miranda, based on the ability of its gene product to interact with the Prospero asymmetric localization domain. miranda expression coincides spatially and temporally with asymmetric cell divisions and asymmetric localization of Prospero. Miranda protein is localized asymmetrically, along with Prospero, to the basal cell membrane during mitosis. Loss of miranda gene function abolishes asymmetric Prospero localization during mitosis. The asymmetric localization of Miranda protein requires inscuteable. Our results suggest that miranda functions downstream of inscuteable and works as an adapter that connects Prospero to the basal cell membrane during asymmetric cell division.

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.