CD105
- Known as:
- CD105
- Catalog number:
- 11-298-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD105
Related genes to: CD105
- Gene:
- ENG NIH gene
- Name:
- endoglin
- Previous symbol:
- ORW1, ORW
- Synonyms:
- END, HHT1, CD105
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-03
- Date modifiied:
- 2019-04-23
Related products to: CD105
Related articles to: CD105
- - Source: PubMed
Publication date: 2026/09/07
Cui ChongWang ShengyiWang DaqiZhao JingjingHuang BoweiZhu BiyunChen YuxinTang HonghaiHan YuYe ChengMu DanZhang ChengdongYang YuanBao YihanLv JunHan ShuangLi Geng-LinLi HuaweiShu Yilai - The papaya mealybug, , has emerged as a formidable threat to global tropical agriculture, capable of inducing devastating yield losses through its invasive sap-sucking behavior. While conventional models often overlook environmental complexities, in this study, we introduced a sophisticated multi-seasonal mathematical framework designed to unravel the intricate interplay between mealybug population dynamics, fluctuating climatic conditions, and the persistence of off-season natural reservoirs. Sensitivity analysis highlighted how parameter influences shift across seasons, while our qualitative analysis revealed a dual-threshold mechanism, governed by the local offspring number $ \mathcal{N}_0 $ and the global stability threshold $ \mathcal{N}_g $, as the definitive driver of the system's long-term evolution. While $ \mathcal{N}_0 < 1 $ analytically ensures local asymptotic stability, our theoretical discussion suggested the existence of a conjectured regime of bistability within the threshold range $ \mathcal{N}_g < \mathcal{N}_0 < 1 $. This finding highlighted a critical regime where the success of eradication efforts is strictly contingent upon the initial infestation levels. Furthermore, by employing uniform persistence theory, we proved that the pest inevitably establishes a permanent foothold whenever $ \mathcal{N}_0 > 1 $. To mitigate these agricultural losses, we evaluated the efficacy of two distinct intervention frameworks: (ⅰ) Pulsed biological control via impulsive parasitoid releases and (ⅱ) a synergistic integrated pest management (IPM) strategy combining biopesticides with natural enemies. Our simulations demonstrated that while impulsive parasitoid releases alone achieved substantial suppression, reducing immature and mature female populations by 89.35% and 93.04%, respectively, and recovering 75.92% of papaya production, the integrated approach proved transformative. By synchronizing biopesticide applications with parasitoid pulses, mealybug populations were nearly decimated, with reduction rates reaching 99.70% for immatures and an exhaustive 99.90% for adults. Although this intensive suppression yielded a 44.92% increase in net productivity, its primary value lies in providing a robust, non-linear pathway toward total pest eradication, effectively breaking the cycle of reinfestation. - Source: PubMed
Dountio MartinOnana MaximilienBowong Samuel - Oncolytic virotherapy uses viruses that selectively infect and lyse tumor cells while promoting antitumor immunity. Because viral spread, tumor growth, and immune-cell migration are spatially heterogeneous, purely temporal models may miss important treatment dynamics. We develop a reaction-diffusion delay model for spatial tumor virotherapy with a virus-induced cytotoxic T-lymphocyte (CTL) response, thereby incorporating tumor growth, infection, lysis, immune-mediated killing, diffusion, and delayed immune activation. We prove positivity, local well-posedness, and global boundedness under explicit sufficient conditions, and analyze spatially homogeneous equilibria and modal stability. Then, we extend the model with a numerical optimal-control formulation for viral administration and immune stimulation, thus minimizing tumor burden, treatment cost, and excessive CTL proliferation. Simulations indicate that tumor-virus-immune dynamics can remain spatially heterogeneous and that the computed optimal control schedules improve tumor suppression for the chosen parameter set. - Source: PubMed
Rihan Fathalla A - - Source: PubMed
Fujiwara SeikoNishiura Hiroshi - Portal hypertension is clinically defined by invasive hepatic venous pressure gradient (HVPG) thresholds, whereas routine assessment relies on non-invasive markers that are biologically heterogeneous and only indirectly related to portal pressure. We have developed a computational framework designed as a threshold-translation and scenario-exploration tool rather than a predictive or mechanistic model with three explicitly separated components: a data-driven empirical core, a literature-informed delayed dynamic layer, and a synthetic scenario module. Using HVPG-linked datasets, the empirical core has constructed a constrained latent burden score from liver stiffness, inverse platelet count, spleen diameter, inverse albumin, and bilirubin and has compared it with an equal-weight score. The constrained score has improved threshold discrimination more than continuous prediction at clinically relevant HVPG levels. A monotone burden-to-HVPG mapping has translated the latent burden axis into the clinically interpretable HVPG scale and has yielded cohort-specific burden thresholds. Leave-one-source-out (LOSO) technique shows that pooled burden learning is informative but not source-invariant, indicating limited transportability across cohorts. To examine delayed separation between latent burden evolution and visible pressure manifestation, we have introduced a delay differential equation model with literature-informed parameters. The resulting temporal gaps are illustrative scenario outputs and not patient-specific predictions. Overall, the framework provides a transparent, threshold-oriented computational approach for translating heterogeneous biomarkers into interpretable HVPG thresholds while linking data-based burden learning with scenario-based dynamic simulation. - Source: PubMed
Fakharany MAlharthi Thoraya NElfouly M A