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SCIT Wasp

✓ Approved

HAL Allergy Group · 治疗药物

什么是 SCIT Wasp?

SCIT Wasp 是一种治疗药物,由HAL Allergy Group研发。该药已获批,用于治疗相关适应症,给药途径:Injectable (Others)、Subcutaneous Injection。

药物档案

公司HAL Allergy Group
给药途径Injectable (Others), Subcutaneous Injection
状态Approved

治疗适应症

SCIT Wasp 针对 1 个适应症,涉及 1 个治疗领域。

治疗领域疾病/病症分期
Immune system disordersAllergy to animal✓ Approved

相关研究文献

PubMedBiomimetics (Basel, Switzerland)2026-10-26

Biomimetic Coverage Optimization in WSNs via an Enhanced Spider-Wasp Optimizer with Adaptive Learning and Dual-Median-Point Guidance.

Nguyen Trong-The TT, Wang Longcun L, Dao Thi-Kien TK

Coverage optimization in wireless sensor networks (WSNs) is a non-convex deployment problem on which population-based optimizers often converge prematurely and lose diversity. This paper proposes the Enhanced Spider-Wasp Optimizer (ESWO), an extension of the Spider-Wasp Optimizer (SWO) conceptually inspired by the foraging and nesting behavior of Pompilidae wasps. ESWO integrates (i) an Adaptive Learning Strategy (ALS) that uses four types of positional gaps among individuals to sustain diversity, (ii) a dual-median-point guidance (DMPG) mechanism that steers exploitation towards the midpoint of two elite solutions, and (iii) a position-update rule with nest-overlap avoidance. Coverage is evaluated on a discretized target grid with a Euclidean binary-disk sensing model and an energy-penalized fitness. In four scenarios (25-65 nodes; 50 × 50 to 165 × 165 m2), ESWO was compared with seven algorithms, including SWO. It achieved coverage rates of 81%, 88%, 92% and 85%, the highest in every scenario (tied with MGWO at 81% in the smallest). In the 100 × 100 m2 scenario it reached 85% coverage after 523 iterations, against 601-698 for the competitors, although final convergence iteration counts were not uniformly the lowest. Over 15 runs, ESWO obtained a mean coverage of 90.2% (SD 1.2), a 95% success rate and the lowest estimated energy consumption (175.3 J).

PMID 42930312
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PubMedFrontiers in oncology2026-10-25

N-WASP deficiency enhances oncogenic KRAS-mediated lung adenocarcinoma progression in mice.

Verma Apoorva A, Li Nanyang N, Kalailingam Pazhanichamy P, Kim Chaiyoung C et al.

Oncogenic KRAS mutations drive 25-30% of western lung adenocarcinoma (LUAD) cases, however the mechanisms that restrain tumor progression remain poorly defined. N-Wiskott-Aldrich syndrome protein (N-WASP) regulates actin cytoskeleton dynamics and epithelial architecture, but its role in KRAS-driven lung tumorigenesis is unclear. We generated a conditional N-WASP knockout in KRASG12D-driven lung adenocarcinoma mice (N-WASPLKO/KRASG12D) using Sftpc-CreERT2, and assessed N-WASP knockdown A549 cells (A549KD) in 3D culture for tumor burden, ERK signaling, transcriptomic changes, and E-cadherin expression. Conditional deletion of N-WASP in type II alveolar cells (N-WASPLKO) markedly increased tumor number and size in KRASG12D mice. The tumors isolated from these mice retained strong pro-surfactant protein C expression, confirming alveolar epithelial origin and predominantly adopted a solid growth pattern, indicative of disrupted epithelial organization. Mechanistically, N-WASP loss enhanced KRAS-driven ERK1/2 activation in lung tissue, consistent with increased mitogenic signaling. In A549 cells, N-WASP deficiency disrupted cytoskeletal architecture, promoted proliferation, and impaired cell-cell adhesion, recapitulating in vivo tumor phenotypes. A kinase inhibitor screen identified Rho-associated protein kinase (ROCK) activity as a driver of this hyperproliferative phenotype, with ROCK inhibition normalizing proliferation in N-WASP-deficient cells, linking elevated Rho/ROCK signaling to the increased ERK1/2 activation observed upon N-WASP loss. Transcriptomic profiling of N-WASP-deficient lungs revealed coordinated upregulation of genes regulating proliferation, cytoskeletal remodeling, and tumor-promoting pathways, alongside downregulation of epithelial differentiation and adhesion programs. These results establish N-WASP as a critical suppressor of KRAS-driven lung adenocarcinoma, linking cytoskeletal integrity to oncogenic signaling and transcriptional regulation. Our findings highlight the interplay between actin dynamics, epithelial architecture, and KRAS signaling, suggesting that targeting N-WASP dependent pathways could modulate lung cancer aggressiveness and offer novel therapeutic opportunities.

PMID 42923069
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PubMedACS omega2026-10-25

Mycobacterial Lipids Orchestrate Infection Stage-Specific Remodeling of the Host Actin Cytoskeleton.

Mishra Manjari M, Roy Saitali Laha SL, Dasgupta Aishi A, Menon Anjana P AP et al.

The actin cytoskeleton is a central target of host-pathogen interactions, yet how distinct microbial factors engage specific actin regulatory pathways remains poorly understood. Here, we show that mycobacterial envelope lipids directly modulate host actin dynamics through distinct molecular mechanisms. Using quantitative imaging and lipidomic analysis, we demonstrate that sulfoglycolipids (SL-1) and phenolic glycolipid-1 (PGL-1) promote actin depolymerization via cofilin-mediated severing, whereas phthiocerol dimycocerosate (PDIM) and trehalose dimycolate (TDM) induce actin polymerization through activation of the WASP-Arp2/3 pathway. These lipid-specific effects correspond to changes in lipid abundance across infection stages, linking cytoskeletal remodeling to temporal regulation of infection. Functionally, actin depolymerization enhances bacterial uptake or release depending on lipid context, while polymerization differentially impacts host cell entry and intracellular persistence. Together, our findings establish that mycobacterial lipids act as molecular determinants of cytoskeletal organization, engaging distinct actin regulatory pathways to shape infection dynamics.

PMID 42923443
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PubMedJournal of agricultural and food chemistry2026-10-23

Host Volatiles Drive Host Preference and Consequently Shape the Fitness of a Generalist Parasitoid Wasp, Meteorus pulchricornis (Hymenoptera: Braconidae).

Li Zhen-Xiao ZX, Hu Ruo-Lan RL, Yuan Rui-Zhong RZ, Wang Peng-Zhan PZ et al.

Host preference is critical to the efficacy of parasitoids in biological control, while the underlying mechanisms remain unclear. Here, we found that the host preference of the generalist parasitoid Meteorus pulchricornis revealed an innate preference for Spodoptera frugiperda, followed by Plodia interpunctella. GC-MS analysis showed distinct volatile organic compound profiles between the two hosts, with 2-hexanol as a shared component. Electroantennogram (EAG) recordings showed that wasp antennae responded more strongly to S. frugiperda than to P. interpunctella odors, suggesting olfaction mediates host preference. Knockdown of the odorant receptor co-receptor, MpulORco, impaired both EAG responses and host preference behavior. Furthermore, wasps reared on S. frugiperda had larger body size and higher fecundity, providing a plausible fitness-based explanation for the observed preference. Collectively, our study reveals olfaction is involved in host preference behavior in a generalist parasitoid and establishes a functional connection between olfactory cues and individual fitness.

PMID 42916024
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PubMedJournal of invertebrate pathology2026-10-23

The honey bee mite Tropilaelaps mercedesae can feed on paper wasp brood: Preliminary laboratory evidence.

Gill Maggie C MC, Medwell Jane J, Janashia Irakli I

Tropilaelaps mercedesae is an emerging parasite of honey bees, but how do Tropilaelaps mites survive on native hosts when these bees swarm and abscond? Although occasional associations with non-Apis hymenopterans have been reported, they have never been tested experimentally. We exposed larvae of the bumble bee Bombus terrestris and the paper wasp Polistes dominula (n = 10 per species) to five adult female T. mercedesae each and monitored mite survival for up to 120 h. Live mites were recorded for up to 108 h on P. dominula and 36 h on B. terrestris, and mite survival was longer on P. dominula (larva-level hazard ratio = 0.44, 95% CI: 0.25-0.79). No feeding-associated lesions were detected on B. terrestris larvae or the unexposed controls, whereas feeding-associated lesions were found on all ten exposed P. dominula larvae (2-39 per larva) and on the pupal cuticle of one individual after larval-pupal metamorphosis. These findings provide the first experimental evidence that T. mercedesae can feed on P. dominula brood under laboratory conditions. These results suggest that transient interactions with non-Apis hymenopterans deserve further investigation, particularly in relation to the persistence and reinfestation dynamics of Tropilaelaps populations associated with migratory Apis dorsata.

PMID 42914072
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PubMedZooKeys2026-10-23

Revised relationships of the endemic New Zealand subfamily Pronkiinae stat. nov. (Hymenoptera, Braconidae).

Quicke Donald L J DLJ, Ward Darren F DF, Sharkey Michael J MJ, Butcher Buntika A BA

The endemic New Zealand braconid wasp tribe Pronkiini (type and only genus Pronkia van Achterberg, 1990) has, until now, been placed in the subfamily Meteorideinae. We obtained the first molecular data for Pronkia comprising sequences for five heritage gene fragments (the barcoding region of COI, the nuclear protein-coding elongation factor-1 alpha gene, and three ribosomal genes, 28S, 18S, and 16S) and analysed them together with data from a wide range of other non-cyclostome braconid subfamilies. None of our analyses support the inclusion of Pronkia within Meteorideinae; instead, Pronkia was placed in the strongly supported sigalphoid clade when each of the genes was analysed separately, as well as in the analysis of the combined dataset. In the latter, it was recovered as a sister group to Sigalphinae, but with very low support, essentially in a trichotomy with each of the three sigalphoid subfamilies monophyletic with both 100% UFB and SH-aLTR support. We therefore elevate Pronkiini to subfamily status, Pronkiinaestat. nov., and provide a diagnosis of the new subfamily, along with a photographic portfolio of representative species. Morphological characters relevant to Pronkiinaestat. nov. relationships are discussed.

PMID 42909407
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