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Within the leaf-beetle subfamily Cassidinae (Coleoptera: Chrysomelidae), Aproida Pascoe, 1863 (Aproidini) from Australia has been considered a transitional genus between mining cassidines (“hispines”) and exophagous cassidines (“tortoise beetles”). To illuminate this transition, a detailed study was conducted over one year of the biology of Aproida balyi Pascoe, 1863 on the host plant, Eustrephus latifolius R. Br. ex Ker-Gawl (Asparagaceae). Distribution maps of the host plant and three Aproida species are provided. The life cycle of A. balyi comprises single eggs in a foamy ootheca, three larval instars that feed openly, a pupa suspended from the larva III exuvia, and sexually dimorphic adults. The larva’s green color resembling the host and the narrow body fitted to the narrowed leaf blade allow them to camouflage. They possess a single long caudal process, unlike the paired processes of most other tortoise beetles. Fecal pellets are observed sometimes on this process, but accumulation is rare and lacks the permanent structure of exuvio-fecal shields that distinguishes the ten tribes of tortoise beetles. The larvae exhibit adhesive lobes on the abdominal sternites that appear to help their locomotion, a novel feature in Cassidinae. The pupa is suspended from the larva III exuviae and together they resemble the host’s pendant flower buds, suggesting mimicry. Males have the profemora and protibiae toothed. Both sexes can fly, unlike flightless Aproida cribrata Lea, 1929. These many morphological and behavioral findings contribute potential novel characters that underscore the aberrant nature of Aproidini within Cassidinae and point to another Australian evolutionary oddity.
ZooBank registration. urn:lsid:zoobank.org:pub:025EBD5A-4914-47FE-A33C-1A668B2F440C
Two new species of Agrilus Curtis (Coleoptera: Buprestidae), A. botzi Woodley, new species and A. vachellia Woodley new species, both from southeastern Arizona, are described. Agrilus barri Hespenheide and Westcott and Taphrocerus leoni Dugès are recorded from Arizona and represent new U.S. records. Sixteen new state distributional records are presented, along with a few other significant records.
ZooBank registration. urn:lsid:zoobank.org:pub:A187E9C8-5BB0-4F70-BA66-27233387504C
The Encyclopedia of Scale Insect Pests was published in 2022 by CABI Publishing. Some errors and omissions in Chapter 2, Table 2 have been brought to the attention of the Encyclopedia editors; since some of them have plant quarantine implications, they are corrected in this article.
ZooBank registration. urn:lsid:zoobank.org:pub:0D4F6D41-B8F8-4FB8-B002-609FA838C817
The invasive armored scale, Lepidosaphes laterochitinosa Green 1925 (Hemiptera: Coccomorpha: Diaspididae), was found in the Florida landscape for the first time in November 2022 and is now known from two south Florida counties: Broward and Miami-Dade. In Florida thus far, this polyphagous species has been found on Epipremnum pinnatum (L.) Engl. (Araceae), Dracaena Vand. ex. L. (Asparagaceae), and Breynia disticha J.R.Forst. and G.Forst. (Phyllanthaceae), all common landscape ornamentals. New parasitoid host records are provided for Encarsia lounsburyi (Berlese and Paoli), Encarsia citrina (Craw), and Aphytis lingnanensis Compere (Hymenoptera: Aphelinidae) that emerged from L. laterochitinosa in Broward County, Florida, USA. A key to slide-mounted adult females of the 12 species of Lepidosaphes Shimer present or commonly intercepted in Florida is provided, together with an illustration of each species, and plant host records for these species from the Florida State Collection of Arthropods.
ZooBank registration. urn:lsid:zoobank.org:pub:1F9EE396-B0B9-4FF6-BC12-D8477154546B
The impact of 2-desaza-annomontine on processes of inflammation and its resolution in leukocytes
(2024)
This present study investigated the effects of the b-carboline derivative C81, also called 2-desaza-annomontine, on the inflammatory response and resolution processes in vivo and in vitro. The study focused on leukocytes and on the elucidation of the underlying pharmacological mode of action. C81 potently reduced the inflammatory response in an imiquimod-induced psoriasis mouse model and additionally resolved the inflammation more quickly. In a CNV model, C81 significantly decreased the microglial infiltration in the inflamed laser lesion in vivo. In vitro experiments revealed that C81 inhibits the migration of macrophages and leukocyte-endothelial cell interaction by reducing the activation of integrins on leukocytes, in particular LFA-1, without affecting the total protein level on the cell surface.
Further experiments revealed that C81 inhibited the expression of EPAC-1, required for Rap1 activation. Consequently, C81 reduced the LPS/PMA-induced Rap1 activity, which is responsible for integrin activation. Moreover, C81 potently reduced the LPS-induced formation of pro-inflammatory mediators, including cytokines and eicosanoids, in macrophages. The C81-derived inhibition of eicosanoid release was surprisingly potent, probably due to the C81-evoked inhibition of cPLA2 expression, resulting in less liberated arachidonic acid, the precursor for eicosanoids. At the same time, C81 only delayed COX-2 expression, but completely diminished LPS-induced mPGES-1 expression. In addition to the potent anti-inflammatory effects in vitro, C81-derived impact was complemented with promising pro-resolving effects. Hence, C81 significantly induced neutrophil apoptosis without affecting the cell viability of other leukocytes, such as macrophages. Accordingly, the caspase 3 activity in neutrophils increased upon C81 treatment. The underlying mechanism altered by C81 was the expression of the anti-apoptotic mediator Mcl-1, which is required for the survival of neutrophils, but not macrophages. Furthermore, neutrophils treated with C81 were significantly better efferocytosed by macrophages. Analyzes of the pharmacological mode of action of C81 revealed DYRK1B as the key target kinase in inflammatory processes in leukocytes. Of note, experiments with pharmacological inhibition of DYRK1B by C81 or the ‘selective’ DYRK1B inhibitor AZ-DYRK1B-33, could not completely exclude the involvement of the CLKs and other DYRKs. Therefore, DYRK1B knockdown and overexpression experiments were conducted to elucidate the impact of DYRK1B alone. Pharmacological inhibition of DYRK1B and DYRK1B knockdown phenocopied the inhibitory effect of C81 on leukocyte adhesion. In parallel, DYRK1B overexpression mitigated the C81-evoked effect, supporting the hypothesis that C81 inhibits DYRK1B to mediate its effects on leukocytes. Furthermore, DYRK1B inhibition and DYRK1B knockdown resulted in depletion of STAT3 phosphorylation. In addition, C81-evoked STAT3 inhibition was again mitigated by DYRK1B overexpression, suggesting a link or even an interaction between DYRK1B and STAT3. Indeed, direct interaction between DYRK1B and STAT3 was confirmed by a NanoBRET assay. Importantly, in vitro experiments demonstrated, that C81 did not affect LPS recognition mechanisms, investigated by TLR-4 and CD14 expression, and other important inflammatory signaling pathways. Although C81 inhibited the regeneration of IkBa, this had no effect on the translocation of the NFkB subunit p65. Furthermore, C81 did not alter the activation of MAPK pathways, including p38, JNK and ERK. As a result, the focus was on the potent inhibition of LPS-nduced STAT3 activation mediated by DYRK1B, which was shown to be IL-6 independent. Indeed, direct STAT3 inhibition by Stattic phenocopied all tested C81-derived effects on leukocytes, including migration, adhesion, pro-inflammatory cytokine expression, eicosanoid formation and cell type specific induction of neutrophil apoptosis. The underlying mechanisms altered by Stattic in terms of migration/adhesion and lipid mediator formation were the same as for C81. STAT3 inhibition led to decreased EPAC1 expression and accordingly to reduced Rap1 activation. In addition, inhibited STAT3 phosphorylation resulted in reduced cPLA2 expression and also in attenuated mPGES-1 expression.
Finally, the C81-derived depleted Mcl-1 expression was linked to reduced STAT3 inhibition. As C81 abolished STAT3 phosphorylation, less STAT3 was translocated into the nucleus upon LPS stimulation and less STAT3 enrichment at the MCL1 promoter was observed, leading to reduced gene expression and consequently protein levels.
In summary, using the natural product-derived compound C81, the DYRK1B/STAT3 axis was identified as a novel key regulator of inflammatory processes in human leukocytes. This present study revealed that interfering with the DYRK1B-STAT3 signaling can address essential cell functions including leukocyte extravasation, pro-inflammatory mediator release, neutrophil apoptosis and efferocytosis (Figure 1). Furthermore, two different mouse models demonstrated the in vivo relevance of this signaling axis and highlight DYRK1B as an important kinase modulating inflammation and resolution.
K + is the most abundant cytosolic cation in bacteria, and its homeostasis is vital for bacterial survival, playing roles in many essential processes like pH homeostasis, protein synthesis and osmoregulation. When surrounding K + concentrations become very low, bacteria require an active high-affinity uptake system to ensure sufficient cellular K + levels. In many prokaryotes, this system is the K + pump KdpFABC. Peculiarly, KdpFABC forms a functional chimera between a channel-like subunit (KdpA) and a P-type ATPase (KdpB), and for a long time, the mechanism of how transport and ATP hydrolysis between these subunits are coordinated remained unclear. By applying a combination of cryo-EM, biochemical assays, and MD simulations, we have been able to shed light on a unique transport mechanism that combines both the channel and P-type ATPase subunits.
At high K + levels, KdpFABC needs to be inhibited to prevent excessive K + accumulation. This is achieved by a phosphorylation of the serine residue in the TGES 162 motif in the A domain of the pump subunit KdpB, which was shown to stall the complex in the E1P intermediate. Using cryo-EM studies under turnover conditions, we illuminated how stalling in this high-energy intermediate is possible.
Furthermore, we identify a previously uncharacterized atypical serine kinase domain in the sensor histidine kinase KdpD as the responsible kinase for KdpB phosphorylation, giving it a dual role in transcriptional and post-translational regulation of the Kdp system.
Using an e+e− annihilation data sample corresponding to an integrated luminosity of 2.93fb−1 collected at the center-of-mass energy of 3.773\,GeV with the BESIII detector, we measure the absolute branching fractions of D+→ηηπ+, D+→ηπ+π0, and D0→ηπ+π− to be (2.96±0.24±0.13)×10−3, (2.23±0.15±0.11)×10−3, and (1.20±0.07±0.04)×10−3, respectively, where the first uncertainties are statistical and the second ones systematic. The D+→ηηπ+ decay is observed for the first time and the branching fractions of D+(0)→ηπ+π0(−) are measured with much improved precision. In addition we test for CP asymmetries in the separated charge-conjugate branching fractions; no evidence of CP violation is found.
Based on 4.5 fb−1 of e+e− collision data accumulated at center-of-mass energies between 4.600GeV and 4.699GeV with the BESIII detector, we measure the absolute branching fraction of the Cabibbo-favored decay Λ+c→nK0Sπ+ with the precision improved by a factor of 2.8 and report the first evidence for the singly-Cabibbo-suppressed decay Λ+c→nK0SK+. The branching fractions for Λ+c→nK0Sπ+ and Λ+c→nK0SK+ are determined to be (1.86±0.08±0.04)×10−2 and (4.3+1.9−1.5±0.3)×10−4, respectively, where the first uncertainties are statistical and the second ones are systematic.
By analyzing 7.33\,fb−1 of e+e− collision data collected at center-of-mass energies between 4.128 and 4.226 GeV with the BESIII detector, we search for the semileptonic decays D+s→K1(1270)0e+νe and D+s→b1(1235)0e+νe for the first time. No significant signals are observed for either decay mode. The upper limits on the (product) branching fractions are determined to be B[D+s→K1(1270)0e+νe]<4.1×10−4 and B[D+s→b1(1235)0e+νe]⋅B[b1(1235)0→ωπ0]<6.4×10−4 at 90\% confidence level.
Using a data sample of (448.1±2.9)×106 ψ(3686) decays collected by the BESIII detector at the Beijing Electron Positron Collider (BEPCII), we observe the decays χcJ→ϕϕη (J=0, 1, 2), where the χcJ are produced via the radiative processes ψ(3686)→γχcJ. The branching fractions are measured to be B(χc0→ϕϕη)=(8.41±0.74±0.62)×10−4, B(χc1→ϕϕη)=(2.96±0.43±0.22)×10−4, and B(χc2→ϕϕη)=(5.33±0.52±0.39)×10−4, where the first uncertainties are statistical and the second are systematic. We also search for intermediate states in the ϕϕ or ηϕ combinations, but no significant structure is seen due to the limited statistics.
We present the first search for the leptonic decays D∗+→e+νe and D∗+→μ+νμ by analyzing a data sample of electron-positron collisions recorded with the BESIII detector at center-of-mass energies between 4.178 and 4.226 GeV, corresponding to an integrated luminosity of 6.32~fb−1. No significant signal is observed. The upper limits on the branching fractions for D∗+→e+νe and D∗+→μ+νμ are set to be 1.1×10−5 and 4.3×10−6 at 90\% confidence level, respectively.
We present a study of the process e+e−→ηϕ using data samples collected with the BESIII detector corresponding to an integrated luminosity of 15.03 fb−1 at 23 center-of-mass energies from 3.773 to 4.600 GeV. The Born cross sections are measured at each energy and a coherent fit to cross-section lineshape is performed using a Breit-Wigner parametrization to search for charmonium-like vector states. No significant signals of the Y(4230) and Y(4360) resonances are observed.
Production of the doubly charged Δ baryon in e⁺e⁻ annihilation at energies from 2.3094 to 2.6464 GeV
(2023)
The processes e+e−→Δ++Δ¯−− and e+e−→Δ++p¯π−+c.c. are studied for the first time with 179 pb−1 of e+e− annihilation data collected with the BESIII detector at center-of-mass energies from 2.3094 GeV to 2.6464 GeV. No significant signal for the e+e−→Δ++Δ¯−− process is observed and the upper limit of the Born cross section is estimated at each energy point. For the process e+e−→Δ++p¯π−+c.c., a significant signal is observed at center-of-mass energies near 2.6454 GeV and the corresponding Born cross section is reported.
Based on (10087±44)×106 J/ψ events collected with the BESIII detector, a partial wave analysis of the decay J/ψ→γK0SK0Sη′ is performed. The mass and width of the X(2370) are measured to be 2395±11(stat)+26−94(syst) MeV/c2 and 188+18−17(stat)+124−33(syst) MeV, respectively. The corresponding product branching fraction is B[J/ψ→γX(2370)]×B[X(2370)→f0(980)η′]×B[f0(980)→K0SK0S]=(1.31±0.22(stat)+2.85−0.84(syst))×10−5. The statistical significance of the X(2370) is greater than 11.7σ and the spin-parity is determined to be 0−+ for the first time. The measured mass and spin-parity of the X(2370) are consistent with the predictions of the lightest pseudoscalar glueball.
Observation of ψ(3686) → 3ϕ
(2024)
Using (2.712±0.014)×109 ψ(3686) events collected by the BESIII detector operating at the BEPCII collider, we report the first observation of ψ(3686)→3ϕ decay with a significance larger than 10σ. The branching fraction of this decay is determined to be (1.46±0.05±0.17)×10−5, where the first uncertainty is statistical and the second is systematic. No significant structure is observed in the ϕϕ invariant mass spectra.
Using 2.93fb−1 of e+e− collision data collected at a center-of-mass energy of 3.773\,GeV with the BESIII detector, we present a measurement of the branching fraction of the doubly Cabibbo-suppressed (DCS) decay D0→K+π−π0 and a search for the DCS decay D0→K+π−π0π0. The branching fraction of D0→K+π−π0 is determined to be [3.13+0.60−0.56(stat)±0.09(syst)]×10−4. No signal is observed for D0→K+π−π0π0 and an upper limit of 3.6×10−4 is set on the branching fraction at the 90\% C.L. We combine these results with the world-average branching fractions of their counterpart Cabibbo-favored decays to determine the ratios of the doubly Cabibbo-suppressed over the Cabibbo-favored branching fractions, B(D0→K+π−π0)/B(D0→K−π+π0)=(0.22±0.04)%~and B(D0→K+π−π0π0)/B(D0→K−π+π0π0)<0.40% at the 90\% C.L., which correspond to (0.75±0.14)tan4θC~and 1.37×tan4θC, respectively, where θC is the Cabibbo angle.
Measurement of e⁺e⁻ → ΛΛ¯η from 3.5106 to 4.6988 GeV and study of ΛΛ¯ mass threshold enhancement
(2022)
Using data samples with a total integrated luminosity of approximately 18 fb−1 collected by the BESIII detector operating at the BEPCII, the process e+e−→ΛΛ¯η is studied at center-of-mass energies between 3.5106 and 4.6988 GeV. The Born cross section for the process e+e−→ΛΛ¯η is measured. No significant structure is observed in the Born cross section line shape. An enhancement near the ΛΛ¯ mass threshold is observed for the first time in the process. The structure can be described by an S-wave Breit-Wigner function. Neglecting contribution of excited Λ states and potential interferences, the mass and width are determined to be (2356±7±17) MeV/c2 and (304±28±54) MeV, respectively, where the first uncertainties are statistical and the second are systematic.
Measurement of e⁺e⁻ → ΛΛ¯η from 3.5106 to 4.6988 GeV and study of ΛΛ¯ mass threshold enhancement
(2022)
Using data samples with a total integrated luminosity of approximately 18 fb−1 collected by the BESIII detector operating at the BEPCII, the process e+e−→ΛΛ¯η is studied at center-of-mass energies between 3.5106 and 4.6988 GeV. The Born cross section for the process e+e−→ΛΛ¯η is measured. No significant structure is observed in the Born cross section line shape. An enhancement near the ΛΛ¯ mass threshold is observed for the first time in the process. The structure can be described by an S-wave Breit-Wigner function. Neglecting contribution of excited Λ states and potential interferences, the mass and width are determined to be (2356±7±17) MeV/c2 and (304±28±54) MeV, respectively, where the first uncertainties are statistical and the second are systematic.
Measurement of e⁺e⁻ → ΛΛ¯η from 3.5106 to 4.6988 GeV and study of ΛΛ¯ mass threshold enhancement
(2023)
Using data samples with a total integrated luminosity of approximately 18 fb−1 collected by the BESIII detector operating at the BEPCII, the process e+e−→ΛΛ¯η is studied at center-of-mass energies between 3.5106 and 4.6988 GeV. The Born cross section for the process e+e−→ΛΛ¯η is measured. No significant structure is observed in the Born cross section line shape. An enhancement near the ΛΛ¯ mass threshold is observed for the first time in the process. The structure can be described by an S-wave Breit-Wigner function. Neglecting contribution of excited Λ states and potential interferences, the mass and width are determined to be (2356±7±17) MeV/c2 and (304±28±54) MeV, respectively, where the first uncertainties are statistical and the second are systematic.
A search has been performed for the semileptonic decays D0→K0SK−e+νe, D+→K0SK0Se+νe and D+→K+K−e+νe, using 7.9 fb−1 of e+e− annihilation data collected at the center-of-mass energy s√=3.773 GeV by the BESIII detector operating at the BEPCII collider. No significant signals are observed, and upper limits are set at the 90\% confidence level of 2.13×10−5, 1.54×10−5 and 2.10×10−5 for the branching fractions of D0→K0SK−e+νe, D+→K0SK0Se+νe and D+→K+K−e+νe, respectively.
Of mice and men: a semiquantitative analysis of Kv4.3 expression in mouse and human midbrains
(2024)
Idiopathic Parkinson syndrome is one of the most common neurodegenerative diseases and plays a major role in clinical neurological practice. However, the exact pathogenesis has not yet been fully elucidated. It is assumed that a combination of genetic and environmental factors fuels a neurodegenerative process during aging, which result in a selective loss of dopaminergic neurons in the substantia nigra. In rare instances, Parkinson disease (PD) is caused by single toxic-gain of function mutations for instance a single amino acid exchange (A53T) in the gene coding for a-synuclein (SNCA). A central event in idiopathic and mono-genetic PD is the formation of intracytoplasmic accumulation of α-synuclein in so-called Lewy bodies. On this basis, a mouse model was developed that overexpresses human α-synuclein through an A53T mutation in the SNCA gene. In previous work, this mutation was found to lead to both oxidative dysfunction and enhanced expression of Kv4.3 channels in middle-aged mice. Given the central role of aging in the pathogenesis of neurodegeneration, this study analyzed Kv4.3 protein expression in dopamine midbrain neurons using immunohistochemical methods in aged male transgenic A53T SNCA and wildtype mice.
Using semi-quantitative analysis of confocal images of fluorescent Kv4.3 immunosignals, I found significantly reduced Kv4.3 protein expression in old A53T SNCA animals compared to those in age-matched WT mice.
To improve comparison between mouse models and human brain tissue, I also developed a protocol for identical histological processing of human and murine brain sections and Kv4.3 immunohistochemistry. This protocol will be useful to study Kv4.3 expression in DA neurons of human control brains and in various stages of PD.
With the escalating demand in the realm of natural language processing (NLP), the development of contextualized language models has become a major research focus. These models have demonstrated to be highly effective across a wide range of tasks. Nevertheless, their tokenization methodologies mostly rely on statistical measures, not taking linguistic knowledge into account. This thesis investigates the idea of directly injecting morphological knowledge into contextualized language models without the need for a full pre-training. I introduce MoVE (Morphological Vocabulary Extension), an approach that employs a database of morphological segmentations to enhance the initial tokenization. Additionally, fine-tuning the model's word embeddings to directly incorporate morphological information into the token embeddings. The proposed method is evaluated on a morphologically challenging task-created through the extraction of complex words from Amazon reviews-in both English and German, showing that it is able to outperform the baseline model.
The paper presents an analysis of control switch in German and Norwegian, as exemplified in the German pair "Ich verspreche ihm zu kommen" 'I promise him to come' vs. "Ich verspreche ihm kommen zu dürfen" 'I promise him to be allowed to come'. The phenomenon is induced by deontic modals in the context of suasive verbs of communication. The analysis is cast both in LFG and HPSG framework, in both cases deploying a pronounced feature-based semantic component. Our core assumption is that a normative agent is computed on top of control relations.
Capturing word order asymmetries in English Left-Peripheral Constructions: A Domain-Based Approach
(2003)
Left-Peripheral Constructions: A Domain-Based Approach Even though the word order in English is rather straightforward, the distributional possibilities of left-peripheral elements like topic phrases, wh-phrases, and negative operators (introducing an SAI) are quite intriguing and complex. In particular, there seems to exist no straightforward way of capturing the linear order asymmetries of these elements in the main and embedded clauses. The prevailing analyses have resorted to movement processes with multiple functional projections. The goal of this paper is to explore an alternative analysis to such movement-based analyses. In particular, this paper adopts the notion of topological fields (DOMAIN) proposed by Kathol (2000, 2001) within the framework of HPSG. The paper shows that within this DOMAIN system, the distributional possibilities as well as the asymmetries we find in English left peripheral constructions can easily follow from the two traditional views: (i) a topic precedes a focus element, and (ii) in English a wh-phrase and a complementizer competes with each other for the same position.