Cathode Electrolyte Interphase (CEI) Endows Mo6 S8 with Fast Interfacial Magnesium-Ion Transfer Kinetics.

Magnesium (Mg) metal secondary batteries have attracted much attention for their high safety and high energy density characteristics. However, the significant issues of the cathode/electrolyte interphase (CEI) in Mg batteries are still being ignored. In this work, a significant CEI layer on the typical Mo6 S8 cathode surface has been unprecedentedly constructed through the oxidation of the chloride-free magnesium tetrakis(hexafluoroisopropyloxy)borate (Mg[B(hfip)4 ]2 ) salt under a proper charge cut-off voltage condition. The CEI has been identified to contain Bx Oy effective species originating from the oxidation of [B(hfip)4 ]- anion. It is confirmed that the Bx Oy species is beneficial to the desolvation of solvated Mg2+ , speeding up the interfacial Mg2+ transfer kinetics, thereby improving the Mg2+ -storage capability of Mo6 S8 host. The firstly reported CEI in Mg batteries will give deeper insights into the interface issues in multivalent electrochemical systems.

Ameliorative effects of the traditional Chinese medicine formula Qing-Mai-Yin on arteriosclerosis obliterans in a rabbit model.

CONTEXT: Qing-Mai-Yin (QMY) is a clinically used herbal formula for treating arteriosclerosis obliterans (ASO). OBJECTIVE: To evaluate the chemical constituents and effects of QMY on ASO rabbit model. MATERIALS AND METHODS: Forty-eight New Zealand rabbits were divided into six groups (n = 8): normal (normal rabbits treated with 0.5% CMC-Na), vehicle (ASO rabbits treated with 0.5% CMC-Na), positive (simvastatin, 1.53 mg/kg), and QMY treatment (300, 600, and 1200 mg/kg). ASO rabbit model was prepared by high fatty feeding, roundly shortening artery, and bovine serum albumin immune injury. QMY (300, 600 and 1200 mg/kg) was orally administered for 8 weeks. The effects and possible mechanisms of QMY on ASO rabbits were evaluated by pathological examination, biochemical assays, and immunohistochemical assays. The compositions of QMY were analysed using HPLC-Q-TOF-MS/MS analysis. RESULTS: Compared to the vehicle rabbit, QMY treatment suppressed plaque formation and intima thickness in aorta, and decreased intima thickness, whereas increased lumen area of femoral artery. Additionally, QMY treatment decreased TC, TG and LDL, decreased CRP and ET, and increased NO and 6-K-PGF1α in serum. Furthermore, the potential mechanisms studied revealed that QMY treatment could suppress expression of TNF-α, IL-6, ICAM-1 and NF-κB in endothelial tissues, and increase IκB. In addition, HPLC analysis showed QMY had abundant anthraquinones, stilbenes, and flavonoids. CONCLUSION: QMY has ameliorative effects on ASO rabbit, and the potential mechanisms are correlated to reducing inflammation and down-regulating NF-κB. Our study provides a scientific basis for the future application and investigation of QMY.

Alleviation of Diabetic Tendon Injury via Activation of Tendon Fibroblasts Autophagy under Berberine Treatment.

Berberine (BBR) is an isoquinoline alkaloid isolated from Coptis chinensis and possesses valuable pharmacological activities, including anti-inflammatory, anti-tumor, and alleviating several complications of type 2 diabetes mellitus (T2DM). However, the role of BBR in regulating diabetic tendon injury remains poorly understood. In this study, a rat model of T2DM was constructed, and cell apoptosis and autophagy were assessed in tendon tissues after BBR treatment through TdT-Mediated dUTP nick-end labeling (TUNEL) assay and immunohistochemical analysis. Tendon fibroblasts were obtained from the rat Achilles tendon, and the role of BBR in regulating cell apoptosis, the production of inflammatory cytokines, and autophagy activation were assessed using flow cytometry, quantitative real-time PCR (qRT-PCR), and western blot analysis. We demonstrated that BBR treatment significantly increased autophagy activation and decreased cell apoptosis in tendon tissues of T2DM rats. In tendon fibroblasts, BBR repressed High glucose (HG)-induced cell apoptosis and production of proinflammatory cytokines. HG treatment resulted in a decrease of autophagy activation in tendon fibroblasts, whereas BBR restored autophagy activation. More important, pharmacological inhibition of autophagy by 3-MA weakened the protective effects of BBR against HG-induced tendon fibroblasts injury. Taken together, the current results demonstrate that BBR helps relieve diabetic tendon injury by activating autophagy of tendon fibroblasts.

High glucose represses the proliferation of tendon fibroblasts by inhibiting autophagy activation in tendon injury.

Diabetic foot ulcer (DFU) is a kind of common and disabling complication of Diabetes Mellitus (DM). Emerging studies have demonstrated that tendon fibroblasts play a crucial role in remodeling phase of wound healing. However, little is known about the mechanism underlying high glucose (HG)-induced decrease in tendon fibroblasts viability. In the present study, the rat models of DFU were established, and collagen deposition, autophagy activation and cell apoptosis in tendon tissues were assessed using Hematoxylin-Eosin (HE) staining, immunohistochemistry (IHC), and TdT-mediated dUTP Nick-End Labeling (TUNEL) assay, respectively. Tendon fibroblasts were isolated from Achilles tendon of the both limbs, and the effect of HG on autophagy activation in tendon fibroblasts was assessed using Western blot analysis, Cell Counting Kit-8 (CCK-8) assay, and flow cytometry. We found that cell apoptosis was increased significantly and autophagy activation was decreased in foot tendon tissues of DFU rats compared with normal tissues. The role of HG in regulating tendon fibroblasts viability was then investigated in vitro, and data showed that HG repressed cell viability and increased cell apoptosis. Furthermore, HG treatment reduced LC3-II expression and increased p62 expression, indicating that HG repressed autophagy activation of tendon fibroblasts. The autophagy activator rapamycin reversed the effect. More importantly, rapamycin alleviated the suppressive role of HG in tendon fibroblasts viability. Taken together, our data demonstrate that HG represses tendon fibroblasts proliferation by inhibiting autophagy activation in tendon injury.

Preparation of self-reinforced starch films for use as hard capsule material.

A strategy for preparation of self-reinforced starch films for use as hard capsule material is introduced. In this study, the hydroxypropylated-crosslinked potato starch (HCPS) was prepared and used to reinforce the hydroxypropylated-hydrolyzed potato starch (HHPS) films. The paste properties of starch samples and the morphology of starch films were investigated by a rapid visco analyzer (RVA) and scanning electron microscope (SEM), respectively. It was found that the matrix/particle interface was greatly improved after the hydroxypropylation of crosslinked starch. The strain and toughness of the starch composite films were increased by about 30% and 50% after addition of 10 wt% HCPS particles, respectively. In addition, the self-reinforced starch film also had good oxygen barrier property, with its oxygen permeating coefficient (OPC) at 5.09 × 10-12 cm3·cm/cm2·s·cmHg (50% RH). The fragmentation rate of starch capsules has also decreased, indicating it is an alternative material for the preparation of hard capsules.

[Relationship between ultrasound imaging and traditional Chinese medicine syndrome in limb lymphedema].

OBJECTIVE: To study the correlation between traditional Chinese medicine (TCM) syndrome type and the ultrasound imaging changes in patients with limb lymphedema, and to provide evidence for TCM syndrome differentiation. METHODS: Syndrome typing was done and ultrasonography was performed in 107 patients with limb lymphedema. The thickenings of derma, hypodermis and deep-fascia were measured. The ultrasound echo intensity and the morphology of the hypodermis were classified into five degrees according to the ultrasonogram. The ultrasound indexes in the limb lymphedema patients with different syndromes were compared, and the relationship between TCM syndromes and the ultrasound indexes was analyzed. RESULTS: There were specific ultrasound image features in different TCM syndromes of limb lymphedema. The thickenings of derma, hypodermis and deep-fascia in the limb lymphedema patients with downward migration of damp-heat or phlegm stagnation and blood stasis were more significant than those in the patients with collateral obstruction due to cold-dampness (P<0.05, P<0.01). The thickenings of derma and hypodermis in the patients with phlegm stagnation and blood stasis were obviously more severe than those in the patients with downward migration of damp-heat (P<0.01). The maximum and minimum ultrasound echo intensities of hypodermis were in phlegm stagnation and blood stasis and downward migration of damp-heat respectively (P<0.05), and there was a significant difference in the hypodermal morphology among the three syndrome types (P<0.05). The most obvious structure disturbance was observed in the patients with phlegm stagnation and blood stasis syndrome. CONCLUSION: TCM syndrome type of limb lymphedema is related to ultrasound image changes. The imaging data can be regarded as new objective indexes for TCM syndrome differentiation, and it has an important value for diagnosis and treatment of limb lymphedema.

Cilostazol on the expression of ICAM-1, VCAM-1 and inflammatory factors in plasma in patients with thromboangiitis obliterans.

The effects of cilostazol on the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and inflammatory factors in plasma in patients with thromboangiitis obliterans (TAO) were studied. Plasma viscosity, fibrinogen, total cholesterol (TC) and triglyceride (TG) were detected for the healthy control, TAO and cilostazol groups, respectively. Results showed that compared with those in the control group, the plasma viscosity, fibrinogen, TC and TG levels in TAO group were significantly increased. By contrast, compared with those in TAO group, the plasma viscosity, fibrinogen, TC and TG levels in the cilostazol group were significantly decreased. ELISA results revealed that ICAM-1 and VCAM-1 expression levels in TAO group were obviously increased compared with those in control group. ICAM-1 and VCAM-1 expression levels in cilostazol group were obviously decreased compared with those in TAO group. According to RT-PCR, the mRNA expression levels of IL-1ß, IL-6 and TNF-α in TAO group were significantly higher than those in control group, while the levels in cilostazol group were significantly decreased compared with those in TAO group. In addition, RT-PCR and western blotting proved that expression of both mRNA and protein of ICAM-1 and VCAM-1 in TAO group was significantly increased and obviously decreased after administration of cilostazol. The results of analysis of variance showed that the differences of ICAM-1 and VCAM-1 expression was statistically significant among the control, TAO and cilostazol groups (p<0.01). Cilostazol can significantly reduce the TAO-induced abnormal increase in ICAM-1, VCAM-1 and inflammatory factor expression in plasma in patients. It was proven that cilostazol has a good anti-TAO effect.

MicroRNA-141 inhibits vascular smooth muscle cell proliferation through targeting PAPP-A.

It is well known that ox-LDL plays key roles in the development of atherosclerosis, partly by inducing vascular smooth muscle cells (VSMCs) proliferation. Recent findings have revealed that microRNAs, a class of small noncoding RNAs, could regulate cell proliferation in many physiological and pathological conditions. However, the role and function of miRNAs on ox-LDL induced VSMC proliferation are not fully elucidated. In this study, we showed that ox-LDL could suppress miR-141 expression and inhibition of miR-141 could promote VSMCs proliferation. Moreover, we found that PAPPA was the direct target gene of miR-141. Overexpression of PAPPA impaired the miR-141-induced inhibition of proliferation in the VSMCs. Taken together; miR-141 may play important roles in ox-LDL-induced abnormal proliferation of the VSMC.