Cold Sintering Mediated Engineering of Polycrystalline SnSe with High Thermoelectric Efficiency.

Despite the attractive thermoelectric properties in single crystals, the fabrication of high-performance polycrystalline SnSe by a cost-effective strategy remains challenging. In this study, we prepare the undoped SnSe ceramic with remarkable thermoelectric efficiency by the combination of a cold sintering process (CSP) and thermal annealing. The high sintering pressure during CSP induces not only highly oriented grains but also a high concentration of lattice dislocations and stacking faults, which leads to large lattice strain that can shorten the phonon relaxation time. Meanwhile, the thermal annealing breaks the highly resistive SnOx layers at grain boundaries, which improves the electrical conductivity and power factor. In addition, the grain growth during annealing further turns the broken SnOx layers into nanoparticles, which further lowers the thermal conductivity by enhanced scattering. As a result, a peak ZT of 1.3 at 890 K and a high average ZT of 0.69 are achieved in the polycrystalline SnSe, suggesting great potential in mid-temperature power generation. This work may pave the way for the mass production of SnSe-based ceramics for thermoelectric devices.

Panax notoginseng saponins improves healing of high glucose-induced wound through the GSK-3ß/ß-catenin pathway.

Chronic non-healing wounds are one of the most common complications of diabetes mellitus and results in a huge physical and mental burden for patients. Panax notoginseng saponins (PNS) have a wide range of applications in anti-apoptosis, anti-oxidation, and promoting blood circulation. Our study aimed to explore whether PNS could improve diabetic wound healing. High-glucose (HG, 30 Mm) were used to incubated human umbilical vein endothelial cells (HUVECs) to simulate the hyperglycemia environment in vivo, and 200 µg/ml (optimum harmless concentration screened) PNS was added into HG-incubated HUVECs to investigate the protective effect of PNS on the cells. Compared with control, high glucose treatment significantly suppressed HUVEC proliferation, invasion, migration, angiogenesis, malondialdehyde (MDA) production and nitric oxide (NO) release, promoted cell apoptosis, and deactivated the GSK-3ß/ß-catenin/VEGF pathway. PNS treatment could largely rescue the effects of HG on cell dysfunction and improve the deactivation of GSK-3ß/ß-catenin/VEGF pathway. ICG-001, a small molecular ß-catenin inhibitor that can selectively antagonize ß-catenin mediated transcriptional activity, could eliminate the protective effects of PNS on cell dysfunction and activation of GSK-3ß/ß-catenin/VEGF pathway. Moreover, Furthermore, a diabetic model (50 mg/kg streptozotocin induced) with back skin wound was established in rats, and the wounds were administrated with petrolatum, gelatin/Bletilla striata gelatin (GT/BSGT), or GT/BSGT plus PNS. We found that PNS signally facilitated wound healing and matrix remodeling in vivo. In conclusion, our study verified that PNS improved wound healing in hyperglycemic rats via promoting endothelial cell proliferation, invasion, migration, angiogenesis, suppressing cell apoptosis and oxidative damage, and activating the GSK-3ß/ß-catenin pathway.

Inhibition of zinc finger protein 367 exerts a tumor suppressive role in colorectal cancer by affecting the activation of oncogenic YAP1 signaling.

Zinc finger protein 367 (ZNF367) has been documented as a new cancer-related protein that exerts a pivotal role in the carcinogenesis of multiple cancers. However, whether ZNF367 plays a role in colorectal cancer has not been fully understood. Our data showed that ZNF367 expression was higher in colorectal cancer. Depletion of ZNF367 weakened the proliferative and invasive capabilities of colorectal cancer cells. Up-regulation of ZNF367 enhanced the in vitro malignant features of colorectal cancer cells. Knockdown of ZNF367 impeded the activation of Yes-associated protein (YAP1). Reactivation of YAP1 reversed the ZNF367-knockdown-mediated anticancer effects. Suppression of YAP1 significantly abolished ZNF367-overexpression-induced tumor-promotion effects. Depletion of ZNF367 repressed the tumorigenicity of colorectal cancer cells in vivo. These findings demonstrate that ZNF367 is overexpressed in colorectal cancer and acts as a potential tumor-promoter that contributes to the proliferation and invasion of colorectal cancer by enhancing the activation of YAP1 signaling.

CircTP53 promotes colorectal cancer by acting as a miR-876-3p sponge to increase cyclin-dependent kinase-like 3 expression.

According to ceRNA theory, circular RNAs could regulate certain protein expression through targeting corresponding microRNAs to affect the progression of multiple diseases, including colorectal cancer. CircTP53 (hsa_circ_0107702), highly expressed in thyroid cancer tissues, could promote the proliferation of thyroid cancer. However, the function of circTP53 in colorectal cancer is still unclear. In our study, we found circTP53 was significantly up-regulated in colorectal cancer tissues from patients and in colorectal cell lines. Next, using colorectal cell lines, we confirmed that circTP53 promoted the proliferation, migration and invasion, and reduced the apoptotic rate. Furthermore, through bioinformatics analysis and experimental confirmation, we found circTP53 functioned as the sponge of miR-876-3p, and miR-876-3p reversed the phenotype of circTP53 on the facilitation of colorectal cancer. Additionally, we found circTP53 promoted the progression of colorectal cancer by elevating the expression of CDKL3. At last, we suggested that circTP53 knockdown could inhibit colorectal cancer progression in vivo. In conclusion, circTP53 was highly expressed in colorectal cancer tissues, and promoted colorectal cancer progression via modulating miR-876-3p/CDKL3 axis.

Celecoxib prevents pressure overload-induced cardiac hypertrophy and dysfunction by inhibiting inflammation, apoptosis and oxidative stress.

To explore the effects of celecoxib on pressure overload-induced cardiac hypertrophy (CH), cardiac dysfunction and explore the possible protective mechanisms. We surgically created abdominal aortic constrictions (AAC) in rats to induce CH. Rats with CH symptoms at 4 weeks after surgery were treated with celecoxib [2 mg/100 g body-weight(BW)] daily for either 2 or 4 weeks. Survival rate, blood pressure and cardiac function were evaluated after celecoxib treatment. Animals were killed, and cardiac tissue was examined for morphological changes, cardiomyocyte apoptosis, fibrosis, inflammation and oxidative stress. Four weeks after AAC, rats had significantly higher systolic, diastolic and mean blood pressure, greater heart weight and enlarged cardiomyocytes, which were associated with cardiac dysfunction. Thus, the CH model was successfully established. Two weeks later, animals had impaired cardiac function and histopathological abnormalities including enlarged cardiomyocytes and cardiac fibrosis, which were exacerbated 2 weeks later. However, these pathological changes were remarkably prevented by the treatment of celecoxib, independent of preventing hypertension. Mechanistic studies revealed that celecoxib-induced cardiac protection against CH and cardiac dysfunction was due to inhibition of apoptosis via the murine double mimute 2/P53 pathway, inhibition of inflammation via the AKT/mTOR/NF-κB pathway and inhibition of oxidative stress via increases in nuclear factor E2-related factor-2-mediated gene expression of multiple antioxidants. Celecoxib suppresses pressure overload-induced CH by reducing apoptosis, inflammation and oxidative stress.