Molecular mechanism of the anti-inflammatory and skin protective effects of Syzygium formosum in human skin keratinocytes.

Irradiation injury, especially caused by UVB, of the skin is one of the critical reasons for skin inflammation and damage. The present study aimed to explore the protective effect of Syzygium formosum leafy extract (SFLE) and its mechanism of action against UVB-induced damages of human keratinocytes. In this study, SFLE was prepared from 100 kg dried leaves using industrial-scale processes. We found that SFLE markedly reduced markers of the skin inflammation in UVB-induced pro-inflammatory cytokines. Only 2 µg/mL of SFLE exhibited significantly stronger anti-inflammatory effects than the fivefold concentration of positive control. Intriguingly, an anti-inflammatory enzyme, heme oxygenase-1 expression was significantly induced by SFLE treatment. MMP-3 and -9 were, but not MMP-1, significantly reduced. SFLE inhibited the expression of the MAPK pathway, resulting in a decrease on UVB-induced reactive oxygen species. In conclusion, SFLE can potentially be used to treat skin inflammatory diseases. Supplementary Information: The online version contains supplementary material available at 10.1007/s10068-023-01380-4.

Precise Filtration of Chronic Myeloid Leukemia Cells by an Ultrathin Microporous Membrane with Backflushing to Minimize Fouling.

A cell filtration platform that affords accurate size separation and minimizes fouling was developed. The platform features an ultra-thin porous membrane (UTM) filter, a pumping head filtration with backflush (PHF), and cell size measurement (CSM) software. The UTM chip is an ultrathin free-standing membrane with a large window area of 0.68 mm2, a pore diameter of 5 to 9 µm, and a thickness of less than 0.9 µm. The PHF prevents filter fouling. The CSM software analyzes the size distributions of the supernatants and subnatants of isolated cells and presents the data visually. The D99 particle size of cells of the chronic myeloid leukemia (CML) line K562 decreased from 22.2 to 17.5 µm after passage through a 5-µm filter. K562 cells could be separated by careful selection of the pore size; the recovery rate attained 91.3%. The method was compared to conventional blocking models by evaluating the mean square errors (MSEs) between the measured and calculated filtering volumes. The filtering rate was fitted by a linear regression model with a significance that exceeded 0.99 based on the R2 value. The platform can be used to separate various soft biomaterials and afford excellent stability during filtration.

Depth Cube-Based Six Degree-of-Freedom Haptic Rendering for Rigid Bodies.

This paper presents a depth image-based six degree-of-freedom (6-DOF) haptic rendering method for rigid bodies. In order to increase the collision detection speed, a depth cube structure is developed, consisting of six-sided orthogonal depth images extracted from six virtual depth cameras located around and fixed with respect to the virtual object. With the depth cube and a set of sample points for the tool object, a quick point-in-object test can be performed. A new local occupancy map instance (LOMI) is also proposed to efficiently search for the ideal proxy location. The proposed approach works with any rigid static or dynamic virtual object, regardless of object data representation type and complexity, and achieves multi-region contacts in real-time. Several experiments subsequently confirm the effectiveness of the proposed algorithm.

NPS-1034, a novel MET inhibitor, inhibits the activated MET receptor and its constitutively active mutants.

The MET proto-oncogene product, which is the receptor for hepatocyte growth factor (HGF), has been implicated in tumorigenesis and metastatic progression. Point mutations in MET lead to the aberrant activation of the receptor in many types of human malignancies, and the deregulated activity of MET has been correlated with tumor growth, invasion, and metastasis. MET has therefore attracted considerable attention as a potential target in anticancer therapy. Here, we report that a novel MET kinase inhibitor, NPS-1034, inhibits various constitutively active mutant forms of MET as well as HGF-activated wild-type MET. NPS-1034 inhibited the proliferation of cells expressing activated MET and promoted the regression of tumors formed from such cells in a mouse xenograft model through anti-angiogenic and pro-apoptotic actions. NPS-1034 also inhibited HGF-stimulated activation of MET signaling in the presence or absence of serum. Furthermore, when tested on 27 different MET variants, NPS-1034 inhibited 15 of the 17 MET variants that exhibited autophosphorylation with nanomolar potency; only the F1218I and M1149T variants were not inhibited by NPS-1034. Notably, NPS-1034 inhibited three MET variants that are resistant to the MET inhibitors SU11274, NVP-BVU972, and PHA665752. Together, these results suggest that NPS-1034 can be used as a potent therapeutic agent for human malignancies bearing MET point mutations or expressing activated MET.