Multiple Stimuli-Responsive Color-Changing Polymer Materials for Reversible Writing and Anti-Counterfeiting.

Polymer materials with multiple stimuli-responsive properties have demonstrated many potential and practical applications. By covalently introducing spiropyran (SP1) and spirothiopyran (STP) into the polyurethane backbone, photochromic, mechanochromic, and thermally discolored polymer materials have been prepared. In this work, we report for the first time that white light (violet, blue, and green light) above a certain intensity can activate STP to green color. Based on the above discovery, the polyurethane with SP1 and STP can exhibit reversible three-color changes (brown, green, and purple) in response to four stimuli: ultraviolet irradiation, white light irradiation, mechanical stress, and heat. The color-changing polymer materials have high color contrast and excellent reversibility, and can be used for reversible writing, anticounterfeiting and information encryption, etc.

Theabrownins in dark tea form complexes with tea polysaccharide conjugates.

BACKGROUND: Theabrownins (TBs) are one of most important quality components in dark tea, but have not been produced industrially. In this study, the aqueous extract was obtained from Pu-erh ripe tea, one kind of dark tea. Caffeine, theaflavin, catechin and saponin were removed by trichloromethane, ethyl acetate and n-butanol in turn to obtain a TB isolate. The TB isolate was subjected to column chromatography using a macroporous resin HPD-750 and eluted with a gradient of 0-700 g kg-1 ethanol aqueous solution. Four fractions were obtained, and named as TBs-FC1, TBs-FC2, TBs-FC3 and TBs-FC4. RESULTS: These four fractions contained polysaccharides and no small molecules such as catechins, caffeine and theaflavins as well as average molecular weights of 123.000 kDa, 23.380 kDa, 89.870 kDa and 106.600 kDa. It was revealed that they were complexes of TBs and tea polysaccharide conjugates (TPCs). Ultraviolet-visible (UV-visible) and infrared (IR) spectra showed the properties of TBs and TPCs. Their zeta potentials ranged from -13.40 mV to -38.80 mV in aqueous solutions at pH 3.0-9.0. CONCLUSION: This study reveals that TBs do not exist in free state but in combined state in dark tea, which provide the theoretical basis for the industrialization of TBs. © 2024 Society of Chemical Industry.

Protective mechanism of fruit vinegar polyphenols against AGEs-induced Caco-2 cell damage.

Accumulation of advanced glycation end products (AGEs) is linked with development or aggravation of many degenerative processes or disorders. Fruit vinegars are rich in polyphenols that can be a good dietary source of AGEs inhibitors. In this study, eight kinds of vinegars were prepared. Among them, the highest polyphenol and flavonoid content were orange vinegar and kiwi fruit vinegar, respectively. Ferulic acid, vanillic acid, chlorogenic acid, p-coumaric acid, caffeic acid, catechin, and epicatechin were main polyphenols in eight fruit vinegars. Then, we measured the inhibitory effect of eight fruit vinegars on fluorescent AGEs, and found that orange vinegar had the highest inhibitory rate. Data here suggested that orange vinegar and its main components catechin, epicatechin, and p-coumaric acid could effectively reduce the level of ROS, RAGE, NADPH and inflammatory factors in Caco-2 cells. Our research provided theoretical basis for the application of orange vinegar as AGEs inhibitor.

2-mercaptobenzothiazole generates γ-H2AX via CYP2E1-dependent production of reactive oxygen species in urothelial cells.

Ortho (o)-toluidine is a widely known carcinogenic substance associated with cancers of the human bladder. A study on British chemical factory workers exposed to 2-mercaptobenzothiazole, phenyl-ß-naphthylamine, aniline, and o-toluidine demonstrated the crucial roles of o-toluidine, 2-mercaptobenzothiazole, and phenyl-ß-naphthylamine in the development of bladder cancer. As genotoxic events are crucial steps in the initiation of cancer, in the present study, we aimed to examine the genotoxic potential of the four chemicals using phosphorylated histone H2AX (γ-H2AX), which is a sensitive and reliable marker of DNA damage, in cultured human urothelial cells. Of the four chemicals, 2-mercaptobenzothiazole was a particularly potent DNA-damaging agent. Moreover, mechanistic studies revealed that γ-H2AX generation by 2-mercaptobenzothiazole was mainly associated with the generation of reactive oxygen species via cytochrome P450 2E1-mediated metabolism. The findings of this study may provide information that is important for the assessment of risks associated with chemicals as well as the interpretation of epidemiological studies investigating occupational bladder cancer.

Toward Fine-Grained Sketch-Based 3D Shape Retrieval.

In this paper we study, for the first time, the problem of fine-grained sketch-based 3D shape retrieval. We advocate the use of sketches as a fine-grained input modality to retrieve 3D shapes at instance-level - e.g., given a sketch of a chair, we set out to retrieve a specific chair from a gallery of all chairs. Fine-grained sketch-based 3D shape retrieval (FG-SBSR) has not been possible till now due to a lack of datasets that exhibit one-to-one sketch-3D correspondences. The first key contribution of this paper is two new datasets, consisting a total of 4,680 sketch-3D pairings from two object categories. Even with the datasets, FG-SBSR is still highly challenging because (i) the inherent domain gap between 2D sketch and 3D shape is large, and (ii) retrieval needs to be conducted at the instance level instead of the coarse category level matching as in traditional SBSR. Thus, the second contribution of the paper is the first cross-modal deep embedding model for FG-SBSR, which specifically tackles the unique challenges presented by this new problem. Core to the deep embedding model is a novel cross-modal view attention module which automatically computes the optimal combination of 2D projections of a 3D shape given a query sketch.

MicroRNA-185 inhibits the proliferation and migration of HaCaT keratinocytes by targeting peroxisome proliferator-activated receptor ß.

Proliferation and migration of keratinocytes are major processes of skin wound repair after injury. It has been indicated that microRNAs (miRNAs/miRs) are associated with the proliferation and migration of keratinocytes. However, the mechanism by which miR-185 affects these processes in keratinocytes remains unclear. In the present study, the expression level of miR-185 and peroxisome proliferator-activated receptor ß (PPARß) was examined by reverse transcription-quantitative PCR in HaCaT keratinocytes. Cell proliferation was evaluated using Cell Counting Kit-8 and colony formation assays. Western blot analysis was used to detect the levels of cell proliferation, migration and PI3K/AKT signaling pathway-associated proteins. In addition, the migratory capacity of the cells was determined using Transwell assay. The target gene of miR-185 was verified using dual-luciferase reporter assay. The results indicated that overexpression of miR-185 inhibited proliferation, migration and activation of the PI3K/AKT signaling pathway in HaCaT keratinocytes. PPARß was indicated to be a target of miR-185 and its overexpression promoted the proliferation and migration of HaCaT keratinocytes, while its knockdown exhibited the adverse effects. Furthermore, PI3K inhibitor LY294002 inhibited activation of the PI3K/AKT signaling pathway and decreased the proliferation and migration of HaCaT keratinocytes. In addition, overexpressed PPARß reversed the suppressive effects of miR-185 overexpression on proliferation, migration and activation of the PI3K/AKT signaling pathway. In conclusion, the results of the present study demonstrated that miR-185 suppressed activation of the PI3K/AKT signaling pathway via targeting PPARß, thereby regulating proliferation and migration in HaCaT keratinocytes. The present study provided a novel theoretical basis for the use of miR-185 as a target in wound repair.

NEAT1 Knockdown Inhibits Keloid Fibroblast Progression by miR-196b-5p/FGF2 Axis.

BACKGROUND: Keloid is a benign fibroproliferative tumor of the skin caused by abnormal wound healing process after skin injury. Long noncoding RNAs have been reported to be involved in the development of keloid. However, the role and mechanism of nuclear enriched abundant transcript 1 (NEAT1) in keloid are still unknown. METHODS: Quantitative real-time polymerase chain reaction was performed to detect the expression of NEAT1, miR-196b-5p, and fibroblast growth factor 2 (FGF2). Western blot was conducted to measure the levels of collagen I, α-smooth muscle actin, fibronectin, and FGF2. Cell Counting Kit-8 assay and transwell assay were used to evaluate cell viability and migration, respectively. Dual-luciferase reporter assay was conducted to verify the targeting relationship between miR-196b-5p and NEAT1 or FGF2. RESULTS: NEAT1 was increased and miR-196b-5p was decreased in keloid tissues and fibroblasts. NEAT1 knockdown or miR-196b-5p overexpression suppressed cell viability, migration, and extracellular matrix (ECM) component production in keloid fibroblasts. MiR-196 b-5p was a target of NEAT1, and NEAT1 overexpression reversed the effect of miR-196b-5p on keloid fibroblast progression. Moreover, we found that miR-196b-5p directly targeted FGF2. FGF2 knockdown suppressed keloid fibroblast viability, migration, and ECM protein production. FGF2 overexpression abolished the effect of miR-196b-5p overexpression on keloid fibroblast development. CONCLUSIONS: NEAT1 silencing suppressed cell viability, migration, and ECM expression in keloid fibroblasts by regulating miR-196b-5p/FGF2 axis, indicating a promising strategy for keloid treatment.

Comparative γ-H2AX analysis for assessment of the genotoxicity of six aromatic amines implicated in bladder cancer in human urothelial cell line.

Recently, it was reported that ten cases of bladder cancer occurred among employees, who handled several kinds of aromatic amines, at a Japanese chemical plant. The common aromatic amines were identified as ortho-toluidine, para-toluidine, aniline, ortho-chloroaniline, ortho-anisidine, and 2,4-dimethylaniline. All of these aromatic amines, except ortho-chloroaniline, have been found to be carcinogenic in animals and/or humans. Genotoxic events are known to be crucial steps in the initiation of cancer; information on the genotoxicity of these aromatic amines is insufficient and consistent results have not been obtained. In this study, we examined the genotoxicity of the six different aromatic amines associated with bladder cancer by assessing phosphorylated histone H2AX (γ-H2AX) in a cultured human urothelial cell line, 1T1. We showed that all six aromatic amines generated γ-H2AX. In addition, the γ-H2AX-inducing potential of these six aromatic amines was distinctly different; ortho-chloroaniline and 2,4-dimethylaniline showed particularly high potential, followed by ortho-toluidine, ortho-anisidine, para-toluidine ≒ aniline. The findings of this study may provide important information for the risk assessment of chemicals and for interpreting epidemiological studies on occupational bladder cancer.

Role of metallothionein-like cadmium-binding protein (MTLCdBP) in the protective mechanism against cadmium toxicity in the testis.

The role of metallothionein (MT)-like cadmium (Cd) binding protein (MTLCdBP) in protecting the testes against Cd toxicity was examined. In the acute Cd exposure treatment, cadmium chloride was intraperitoneally injected at 2 mg Cd/kg to Wistar male rats. In the chronic Cd toxicity treatments, 20 mg Cd/kg/d was orally administered for 5 d a week for 5, 10, and 15 wk. MT (-I,-II) and MTLCdBP were measured using ELISA and Cd-Hem methods, respectively. Testicular tissues were immunostained with antibodies of MT-I,-II, MT-III, and MTLCdBP. Expression of HO1, OGG, iNOS, COX2, and p53 was measured by RT-PCR. Cd concentration in the testis increased dose-dependently in response to Cd exposure. MTLCdBP concentration increased markedly with increasing Cd accumulation. Significant increases in expression of iNOS, HO1, COX2, and OGG1 were observed in the acute exposure treatment. In the chronic oral administration group, expression of MT-I, MT-II, MT-III, iNOS, HO1, and COX2 did not change. Positive immunostaining of MTLCdBP was observed in testicular interstitial tissue. In the testis protected from Cd toxicity, MTLCdBP induction increased significantly with increasing Cd accumulation. Our results suggest that MTLCdBP plays an important role in protecting the testis against Cd toxicity.

2,4-Dimethylaniline generates phosphorylated histone H2AX in human urothelial and hepatic cells through reactive oxygen species produced by cytochrome P450 2E1.

The Japanese Ministry of Health, Labour, and Welfare recently reported an outbreak of bladder cancer among workers who handled aromatic amines in Japan. 2,4-dimethylaniline (2,4-DMA) is one of the chemicals that workers are considered to have the most opportunities to be exposed. Genotoxic events are known to be crucial steps in the initiation of cancer. However, studies on the genotoxicity of 2,4-DMA are limited, particularly studies investigating the mechanism behind the genotoxicity by 2,4-DMA are completely lacking. We examined genotoxic properties of 2,4-DMA using phosphorylated histone H2AX (γ-H2AX), a sensitive and reliable marker of DNA damage, in cultured human urothelial and hepatic cells. Our results clearly showed that 2,4-DMA at a concentration range of 1-10 mM generates γ-H2AX in both cell lines, indicating that 2,4-DMA is genotoxic. During mechanistic investigation, we found that 2,4-DMA boosts intracellular reactive oxygen species, an effect clearly attenuated by disulfiram, a strong inhibitor of cytochrome P450 2E1 (CYP2E1). In addition, CYP2E1 inhibitors and the antioxidant, N-acetylcysteine, also attenuated γ-H2AX generation following exposure to 2,4-DMA. Collectively, these results suggest that γ-H2AX is formed following exposure to 2,4-DMA via reactive oxygen species produced by CYP2E1-mediated metabolism. Continuous exposure to genotoxic aromatic amines such as 2,4-DMA over a long period of time may have contributed to the development of bladder cancer. Our results provide important insights into the carcinogenicity risk of 2,4-DMA in occupational bladder cancer outbreaks at chemical plants in Japan.