Effects of the Taste Substances and Metal Cations in Green Tea Infusion on the Turbidity of EGCG-Mucin Mixtures.

Astringency has an important impact on the taste quality of tea infusion, a process which occurs when polyphenols complex with salivary proteins to form an impermeable membrane. (-)-Epigallocatechin gallate (EGCG) is the main astringent compound found in green tea and mucin is the main protein present in saliva. Determining the turbidity of EGCG-mucin mixtures is an effective method to quantify the astringency intensity of EGCG solutions. In this study, the effects of taste-related, substances present during green tea infusion, on the turbidity of EGCG-mucin mixtures was investigated under the reacting conditions of a pH value of 5.0, at 37 °C, and for 30 min. The results showed that epicatechins, caffeic acid, chlorogenic acid, and gallic acid reduced the turbidity of EGCG-mucin mixtures, while rutin increased turbidity. Metal ions increased the turbidity of EGCG-mucin mixtures. These can be arranged by effectiveness as Al3+ > K+ > Mg2+ > Ca2+. Caffeine, theanine, and sodium glutamate all decreased the turbidity values of EGCG-mucin mixtures, but sucrose had a weak effect. Further experiments confirmed that the turbidity of green tea infusion-mucin mixture indicated the astringent intensity of green tea infusion, and that the turbidity was significantly correlated with the contents of tea polyphenols and EGCG.

Ghrelin Induces the Production of Hypothalamic NPY Through the AMPK-mTOR Pathway to Alleviate Cancer-induced Bone Pain.

BACKGROUND/AIM: Cancer-induced bone pain (CIBP) is one of the most common symptoms of bone metastasis of tumor cells. The hypothalamus may play a pivotal role in the regulation of CIBP. However, little is known about the exact mechanisms. MATERIALS AND METHODS: First, we established a CIBP model to explore the relationship among hypothalamic ghrelin, NPY and CIBP. Then, we exogenously administered NPY and NPY receptor antagonists to investigate whether hypothalamic NPY exerted an antinociceptive effect through binding to NPY receptors. Finally, we exogenously administered ghrelin to investigate whether ghrelin alleviated CIBP by inducing the production of hypothalamic NPY through the AMPK-mTOR pathway. Body weight, food intake and behavioral indicators of CIBP were measured every 3 days. Hypothalamic ghrelin, NPY and the AMPK-mTOR pathway were also measured. RESULTS: The expression of hypothalamic ghrelin and NPY was simultaneously decreased in cancer-bearing rats, which was accompanied by CIBP. Intracerebroventricular (i.c.v.) administration of NPY significantly alleviated CIBP in the short term. The antinociceptive effect of NPY was reversed with the i.c.v. administration of the Y1R and Y2R antagonists. The administration of ghrelin activated the AMPK-mTOR pathway and induced hypothalamic NPY production to alleviate CIBP. This effect of ghrelin on NPY and antinociception was reversed with the administration of a GHS-R1α antagonist. CONCLUSION: Ghrelin could induce the production of hypothalamic NPY through the AMPK-mTOR pathway to alleviate CIBP, which can provide a novel therapeutic mechanism for CIBP.

Radiation-Hardened and Flexible Pb(Zr0.53Ti0.47)O3 Piezoelectric Sensor for Structural Health Monitoring.

Piezoelectric sensors are excellent damage detectors that can be applied to structural health monitoring (SHM). SHM for complex structures of aerospace vehicles working in harsh conditions is frequently required, posing challenging requirements for a sensor's flexibility, radiation hardness, and high-temperature tolerance. Here, we fabricate a flexible and lightweight Pb(Zr0.53Ti0.47)O3 piezoelectric film on flexible KMg3(AlSi3O10)F2 substrate via van der Waals (vdW) heteroepitaxy, endowing it with robust ferroelectric and piezoelectric properties under low energy-high flux protons (LE-HFPs) radiation (1015 p/cm2). More importantly, the Pb(Zr0.53Ti0.47)O3 film sensor maintains highly stable damage monitoring sensitivity on an aluminum plate under harsh conditions of LE-HFPs radiation (1015 p/cm2, flat structure), high temperature (175 °C, flat structure), and mechanical fatigue (bending 105 cycles under a radius of 5 mm, curved structure). All these superior qualities are suggested to result from the outstanding film crystal quality due to vdW epitaxy. The flexible and lightweight Pb(Zr0.53Ti0.47)O3 film sensor demonstrated in this work provides an ideal candidate for real-time SHM of aerospace vehicles with flat and complex curve-like structures working in harsh aerospace environments.

Erratum: MiR-143 targets CTGF and exerts tumor-suppressing functions in epithelial ovarian cancer.

[This corrects the article on p. 2716 in vol. 8, PMID: 27398154.].

MiR-143 targets CTGF and exerts tumor-suppressing functions in epithelial ovarian cancer.

A series of recent studies suggested that miR-143 might involve in the tumorigenesis and metastasis of various cancer types. However, the biological function and underlying mechanisms of miR-143 in human epithelial ovarian carcinoma (EOC) remain unknown. Therefore, this study aimed to investigate the miR-143 expression and its clinical diagnosis significance in patients suffering EOC and to analyze its role and underlying molecular mechanism in EOC. Our result showed that the expression levels of miR-143 were downregulated in EOC tissues and cell lines, was associated with International Federation of Gynaecology and Obstetrics (FIGO) stage, pathological grade and lymph node metastasis (all P < 0.01) . Overexpression of miR-143 significantly inhibited EOC cell proliferation, migration, and invasion. Furthermore, computational algorithm combined with luciferase reporter assays identified connective tissue growth factor (CTGF) as the direct target of miR-143 in EOC cells. The expression level of CTGF was significantly increased in EOC tissues, was inversely correlated with miR-143 expression in clinical EOC tissues. Knockdown of CTGF mimicked the suppression effect induced by miR-143 overexpression. Restoration of CTGF expression partially reversed the suppression effect induced by miR-143 overexpression. These results suggested that miR-143 inhibited EOC cell proliferation, migration, and invasion, at least in part, via suppressing CTGF expression.