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KIF18B is a key member of the kinesin-8 family, involved in regulating various physiological processes such as microtubule length, spindle assembly, and chromosome alignment. This article briefly introduces the structure and physiological functions of KIF18B, examines its role in malignant tumors, and the associated carcinogenic signaling pathways such as PI3K/AKT, Wnt/β-catenin, and mTOR pathways. Research indicates that the upregulation of KIF18B enhances tumor malignancy and resistance to radiotherapy and chemotherapy. KIF18B could become a new target for anticancer drugs, offering significant potential for the treatment of malignant tumors and reducing chemotherapy resistance. [ABSTRACT FROM AUTHOR]

Pheromone receptors (PRs) are key proteins in the molecular mechanism of pheromone recognition, and exploring the functional differentiation of PRs between closely related species helps to understand the evolution of moth mating systems. Pheromone components of the agricultural pest Mythimna loreyi have turned into (Z)‐9‐tetradecen‐1‐yl acetate (Z9‐14:OAc), (Z)‐7‐dodecen‐1‐yl acetate (Z7‐12:OAc), and (Z)‐11‐hexadecen‐1‐yl acetate, while the composition differs from that of M. separata in the genus Mythimna. To understand the molecular mechanism of pheromone recognition, we sequenced and analyzed antennal transcriptomes to identify 62 odorant receptor (OR) genes. The expression levels of all putative ORs were analyzed using differentially expressed gene analysis. Six candidate PRs were quantified and functionally characterized in the Xenopus oocytes system. MlorPR6 and MlorPR3 were determined to be the receptors of major and minor components Z9‐14:OAc and Z7‐12:OAc. MlorPR1 and female antennae (FA)‐biased MlorPR5 both possessed the ability to detect pheromones of sympatric species, including (Z,E)‐9,12‐tetradecadien‐1‐ol, (Z)‐9‐tetradecen‐1‐ol, and (Z)‐9‐tetradecenal. Based on the comparison of PR functions between M. loreyi and M. separata, we analyzed the differentiation of pheromone recognition mechanisms during the evolution of the mating systems of 2 Mythimna species. [ABSTRACT FROM AUTHOR]

Sex pheromones serve a critical role in Lepidopterans finding mates. Male moths perceive and react to sex pheromones emitted by conspecific females through a delicate pheromone communication system. Pheromone receptors (PRs) are the key sensory elements at the beginning of that process. The codling moth (Cydia pomnonella) is an important pome fruit pest globally and a serious invasive species in China. Pheromone‐based techniques have been used successfully in monitoring and controlling this species. We conducted ribonucleic acid sequencing analysis of the codling moth antennal transcriptome and identified 66 odorant receptors (ORs) in a population from Xinjiang province, China, of which 14 were PRs, including two novel PRs (CpomOR2e and CpomOR73). Four PRs that contain full‐length open reading frames (CpomOR1, OR2a, OR5, OR7) and four PRs with ligands that have not been reported previously (CpomOR1, OR2a, OR5, OR7) were selected to deorphanize in the heterologous Xenopus oocyte expression system. Specifically, we found that CpomOR2a and CpomOR5 responded to (E,E)‐8, 10‐dodecadien‐1‐yl acetate (codlemone acetate). Furthermore, CpomOR5 (EC50 = 1.379 × 10−8 mol/L) was much more sensitive to codlemone acetate than CpomOR2a (EC50 = 1.663 × 10−6 mol/L). Since codlemone acetate is an important component of C. pomonella sex pheromone, our results improve the current understanding of pheromone communication in codling moths and will be helpful for the development of pest management strategies. [ABSTRACT FROM AUTHOR]

A method of motion data processing based on sampling-lsomap is proposed. By computing the distance matrix of sample frames, the sample embeddings eigenvectors can be obtained to approximate the eigenvectors of the original embeddings, and then the non-sample frames can be projected in this embeddings to approach the manifold embeddings of non-sampleframes. Experiments proved that approximate embeddings of motion data computed by sampling-Isomap were average 10 times faster than by Isomap, while 10% frame samples were selected. Motion analysis can be performed efficiently even with high-dimensionality of motion capture data. [ABSTRACT FROM AUTHOR]

To simulate realistically the scene including large-scale motional roles in real-time, proposes a visualization method based on dynamic texture. The role's motional procedure is rendered to Dynamic-Texture using Render-to-Texture technology. Dynamic-Texture is a kind of texture whose content can be updated in runtime. The role's motion is defined via motion-transferring based on the rotate angles of joint-points. The curve-skeleton model is adopted to deform the motional characters. Each character is exhibited using Billboard in 3D scene. GPGPU (General Purpose on GPU) technique accelerates the image deformation and the scene-rendering. The method can render the scene containing ten thousands of motional characters in 30FPS. It has been proved feasible and valid to improve the rendering efficiency for large-scale motional scene. [ABSTRACT FROM AUTHOR]

• Freund's complete adjuvant-induced arthritis (AA) models were obtained with Sprague-Dawley rats. • Fibroblast-like synoviocytes (FLSs) were obtained from the knee joints of AA rats and cultured in vitro. • Sorafenib induced apoptosis in AA FLSs detected by TUNEL method and flow cytometry analysis. • Sorafenib increased the expression levels of Fas , Caspase-3 and Mcl-1 in AA FLSs and decreased NF-κB and C-jun expression. • Sorafenib exerts an inhibitory effect on AA rats in vivo via AA FLS apoptotic induction. • Sorafenib has potential therapeutic use for RA. Rheumatoid arthritis (RA) is a chronic autoimmune disease that is characterized by synovial inflammation and hyperplasia resulting from an imbalance between the proliferation and apoptosis of fibroblast-like synoviocytes (FLSs). Our previous study found that sorafenib had inhibitory effects in rats with adjuvant arthritis (AA). The present study investigated the role of sorafenib in the induction of AA FLS apoptosis in vitro. FLSs obtained from AA rats were cultured in vitro and identified. Cell apoptosis was detected using terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and annexin V-fluorescein isothiocyanate (FITC) and propidium iodide (PI) labeling methods. Real-time PCR and Western blotting assays were used to quantify the expression levels of Fas , Caspase-3 , Mcl-1 , NF-κB and C-jun gene products in AA FLSs. Our data revealed that sorafenib (4 μmol/L) induced apoptosis in AA FLSs, and flow cytometry analysis showed that AA FLSs treated with sorafenib (4 μmol/L) in vitro accumulated in early and late apoptosis. There were significant increases in the expression levels of Fas , Caspase-3 and Mcl-1 , and significant decreases in NF-κB and C-jun expression in AA FLSs treated with sorafenib. In summary, these results demonstrate that sorafenib promotes AA FLS apoptosis, which may be related to the upregulation of Fas and Caspase-3 and downregulation of NF-κB and C-jun. All of these findings suggest that sorafenib exerts an inhibitory effect on AA rats in vivo via AA FLS apoptotic induction, which has potential therapeutic implications for RA. [ABSTRACT FROM AUTHOR]

Hypertrophic scar (HS) is a dermal fibroproliferative disorder characterized by the excessive proliferation of fibroblasts and is thought to result from a cellular imbalance caused by the increased growth and reduced apoptosis of hypertrophic scar fibroblasts (HSFs). Our recent study demonstrated that recombinant human endostatin (rhEndostatin) plays a key role in the inhibition of HSF proliferation in vitro , with a resulting decrease in dermal thickness and scar hypertrophy. However, the effect of this protein on HSF apoptosis is unknown. The present study was undertaken to directly examine the effect of rhEndostatin on HSF apoptosis in the rabbit ear model. Transmission electron microscopy and flow cytometry were used to investigate HSF apoptosis in scar tissues and cultured HSFs in vitro , respectively. The expression levels of the c-jun , c-fos , NF-κB , fas , caspase-3 , and bcl-2 gene products in HSFs were quantified using real-time PCR and Western blotting assays. Our data reveal that rhEndostatin (2.5 or 5 mg/ml) induces HSF apoptotic cell death in scar tissue. Additionally, HSFs treated with rhEndostatin (100 mg/L) in vitro accumulated in early and late apoptosis and displayed significantly decreased expression of c-jun, c-fos, NF-κB, fas, caspase-3 and bcl-2. In sum, these results demonstrate that rhEndostatin induces HSF apoptosis, and this phenotypeis partially due to downregulation of NF-κB and bcl-2. These findings suggest that rhEndostatin may have an inhibitory effect on scar hypertrophy in vivo via HSF apoptotic induction and therefore has potential therapeutic use for the treatment of HS. [ABSTRACT FROM AUTHOR]