Bio-based poly(lactic acid) foams with enhanced mechanical and heat-resistant properties obtained by facilitating stereocomplex crystallization with addition of D-sorbitol.

The preparation of bio-based poly(lactic acid) (PLA) foams with high mechanical properties and heat resistance is of great significance for environmental protection and green sustainable development. In this paper, D-sorbitol (DS) containing six hydroxyl groups was introduced into poly(l-lactide) (PLLA)/poly(d-lactide) (PDLA) blends for first time to promote the formation of stereocomplex (SC) crystals, which could improve the foaming behavior and enhance mechanical properties and heat resistance of PLA foams. The results showed that DS could improve the formation efficiency and crystallinity of SC crystals by enhancing the hydrogen bonding between the enantiomeric molecular chains. Furthermore, the compression modulus and interactions Vicat softening temperature of the PLLA/PDLA/DS blend foam increased about 854% and 16% compared to the pure PLLA foam, respectively. Besides, when the annealing process was introduced, the compression and heat resistance of the PLA foams increased further. This study provided a feasible strategy for the preparation of bio-based and biodegradable PLA foams with outstanding compressive and heat resistance properties.

Cellulose sulfate lithium as a conductive binder for LiFePO4 cathode with long cycle life.

Polysaccharides can be potential binders for lithium-ion batteries due to their strong adhesion through numerous hydroxyl groups. As a novel waterborne lithiated polysaccharide derivative, cellulose sulfate lithium (CSL) is successfully synthesized and used as the binder for LiFePO4 (LFP) cathode. The chemical structure of CSL is verified by FTIR-ATR, XRD, C13-NMR, GPC, EA, ICP and TGA. Compared to LFP cathode using polyvinylidene difluoride binder, electrochemical measurements show that the LFP cathode using CSL (LFP-CSL) has lower polarization and better rate performance owing to higher lithium-ion conductivity of CSL. The result of morphological analysis indicates that CSL binder can maintain an integrated LFP cathode structure during hundreds of cycles. As a result, the LFP-CSL cathode exhibits a discharge capacity of 133.4 mAh g-1 and maintains remarkable cycle stability with retention of 93.1 % after 300 cycles at 1C. These findings provide novel insights into the rational design of the binders for the LFP cathode.

Green and effective fabrication of porous surfaces with adjustable cell structure by foaming at incomplete healed polymer-polymer interface.

Porous surfaces of materials have shown huge potentialities for endowing materials with multifarious functions. Despite introducing gas-confined-barriers in supercritical CO2 foaming technology is effective to weaken the gas escape effect and facilitate the preparation of porous surfaces, the differences in intrinsic properties between barriers and polymers result in bottlenecks like cell structure adjustment limitation and incompletely eliminated solid skin layers. This study undertakes a preparation approach for porous surfaces by foaming at incompletely healed polystyrene/polystyrene interfaces. In contrast with employing gas-confined-barriers reported before, the porous surfaces foamed at incompletely healed polymer/polymer interfaces show a monolayer, full-open cell morphology, and wide adjustable range in cell structures including cell size (120 nm∼15.68 µm), cell density (3.40 × 105 cells/cm2∼3.47 × 109 cells/cm2), and surface roughness (0.50 µm∼7.22 µm). Furthermore, the wettability of obtained porous surfaces depending on the cell structures is systematically discussed. Finally, a super-hydrophobic surface with hierarchical micro-nanoscale roughness, low water adhesion, and high water-impact resistance is built by depositing nanoparticles on a porous surface. Consequently, this study offers a clean and simple method to prepare porous surfaces with adjustable cell structures, which is expected to open a door to developing a new fabrication technique for micro/nano-porous surfaces.

High-expansion-ratio PLLA/PDLA/HNT composite foams with good thermally insulating property and enhanced compression performance via supercritical CO2.

It has been a great challenge to prepare high-expansion-ratio polylactide (PLA) foam with eminent thermal insulation and compression performance in packaging field. Herein, a naturally formed nanofiller halloysite nanotube (HNT) and stereocomplex (SC) crystallites were introduced into PLA with a supercritical CO2 foaming method to improve foaming behavior and physical properties. The compressive performance and thermal insulation properties of the obtained poly(L-lactic acid) (PLLA)/poly(D-lactic acid) (PDLA)/HNT composite foams were successfully investigated. At a HNT content of 1 wt%, the PLLA/PDLA/HNT blend foam with an expansion ratio of 36.7 folds showed a thermal conductivity as low as 30.60 mW/(m·K). Meanwhile, the compressive modulus of PLLA/PDLA/HNT foam was 115% higher than that of PLLA/PDLA foam without HNT. Moreover, the crystallinity of PLLA/PDLA/HNT foam was dramatically improved after annealing, thus the results showed that compressive modulus of the annealed foam increased by as high as 72%, while it still maintained good heat insulation with the thermal conductivity of 32.63 mW/(m·K). This work provides a green method for the preparation of biodegradable PLA foams with admirable heat resistance and mechanical performance.

Serum adropin level is associated with endothelial dysfunction in patients with obstructive sleep apnea and hypopnea syndrome.

OBJECTIVE: Adropin is a recently discovered peptide hormone that plays a vital role in metabolism and cardiovascular-cerebrovascular function. The purpose of this study is to investigate the role of circulating adropin levels in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and further determine the relationship between serum adropin concentration and endothelial dysfunction in patients with OSAHS. METHODS: Forty polysomnography-diagnosed patients with OSAHS and 21 age and sex-matched healthy controls were enrolled in the current study. Serum adropin level, endothelial function parameters including flow-mediated dilatation (FMD) of brachial artery, endothelin-1 (ET-1), and nitric oxide (NO) were measured in all participants. RESULTS: Serum adropin levels were significantly lower in patients with OSAHS compared to the control subjects. FMD was lower and serum ET-1 levels were higher in patients with OSAHS compared to control subjects. No significant difference was seen in serum NO levels between the two groups. Multivariate linear regression analysis revealed that serum adropin level was positively associated with FMD and negatively correlated with AHI. Additionally, serum adropin levels were lower in patients with OSAHS who had endothelial dysfunction compared with those patients without endothelial dysfunction. The receiver operating characteristic (ROC) analysis showed that area under the curve (AUC) for serum adropin in predicting endothelial dysfunction status in patients with OSAHS was 0.815 (95% CI 0.680-0.951, p = 0.001). The cutoff value of serum adropin level was less than 235.0 pg/mL, which provided the sensitivity and specificity of 81% and 75%, respectively, for the detection of endothelial dysfunction in patients with OSAHS. CONCLUSION: Lower circulating adropin levels are closely associated with endothelial dysfunction in patients with OSAHS. Circulating adropin level may serve as an early biomarker to predict the development of endothelial dysfunction before the emergence of clinical symptoms in patients with OSAHS.

Toll-Like Receptor-4-Mediated Inflammation is Involved in Intermittent Hypoxia-Induced Lung Injury.

PURPOSE: Intermittent hypoxia (IH) is a recognized risk factor for multiple organs damage, resulting in lung injury. Its pathophysiology is still poorly understood. Toll-like receptor 4 (TLR4) signaling plays a critical role in host immune response to invading pathogen and non-infectious tissue injury. The role of TLR4-mediated inflammation in IH-induced lung injury was investigated in this study. METHODS: Lean adult male TLR4-deficient (TLR4-/-) mice and their controls (C57BL/6 mice) were exposed to either IH (FiO2 6-8% for 25 s, 150 s/cycle, 8 h/day) or air (normoxic mice) for 6 weeks. Animals were sacrificed after 6-week exposure, and the lung tissues were harvested for morphological and inflammatory analyses. The expression of TLR4 and nuclear factor kappa-B (NF-κB) P65 were examined by real-time quantitative polymerase chain reaction and immunohistochemical method. Serum cytokine levels of interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α) were analyzed by enzyme-linked immunosorbent assay. RESULTS: IH induced morphological and inflammation changes in the lung. IH for 6 weeks induced higher expression of TLR4 (C57BL/6-N vs C57BL/6-IH, P < 0.05) and resulted in higher release of TNF-α, IL-6 (P < 0.05), and NF-κB P65 (P < 0.05). These alterations were remitted by TLR4 deletion. CONCLUSIONS: TLR4-mediated inflammation plays an important role in the development of IH-induced lung injury in mice, possibly through mechanisms involving nuclear factor-κB. Targeting TLR4/NF-κB pathway could represent a further therapeutic option for sleep apnea patients.

A porous collagen-carboxymethyl cellulose/hydroxyapatite composite for bone tissue engineering by bi-molecular template method.

Inspired by the mechanism of bone formation, a porous collagen-carboxymethyl cellulose/hydroxyapatite (Col-CMC/HA) composite was designed and fabricated using a biomimetic template of Col and CMC protein-polysaccharide bi-molecules. The morphology, composition and physical properties of Col-CMC/HA composites were characterized systematically. It was found that the nano-HA homogenously distributed on the surface of Col-CMC bi-templates while the composite presented 3D porous structure with pore size from 100 µm to 300 µm. The porosities of composites were located at the range of 71%-85%. Besides, the compressive strength of composites was highly depended on the ratio of Col to CMC in the organic template. The optimized composite in respect to physical properties showed a compressive strength as high as 7.06 MPa, quite close to that of natural bone. The high relative growth rate of wild-type mouse embryonic fibroblasts cells was found for the composite, indicating a good biocompatibility. The organic-inorganic composite also behaved good in collagenase resistance and could be biodegraded in 8 weeks, with about 50% of initial weight left at the ratio of Col to CMC of 1:9. The results demonstrated that the Col-CMC/HA composite by bi-molecular template method was a rational and safe method to prepare biomaterials with tunable properties.

Toll-like receptor-4 deficiency alleviates chronic intermittent hypoxia-induced renal injury, inflammation, and fibrosis.

BACKGROUND: Obstructive sleep apnea (OSA)-associated chronic kidney disease is mainly caused by chronic intermittent hypoxia (CIH) triggered renal damage. This study aims to investigate the role of toll-like receptor-4 (TLR4) in underlying mechanism involved chronic intermittent hypoxia (CIH)-induced renal damage. METHODS: C57BL/6J mice with normal TLR4 (TLR4 WT) or deficient TLR4 (TLR4 KO) were divided into four groups and exposed to normal air (NA) and CIH: TLR4 WT + NA, TLR4 KO + NA, TLR4 WT + CIH, and TLR4 KO + CIH. CIH lasted for 8 h/day and 7 days/week for 6 weeks. Renal injury and inflammation were evaluated by histology and ELISA. Renal tubular apoptosis, macrophages, and fibroblasts recruitment were determined by TUNEL assay, immunofluorescence, and western blot. RESULTS: In response to CIH, TLR4 deficiency alleviated renal histological injury, renal dysfunction, and fibrosis. TLR4 deficiency ameliorated renal dysfunction (serum BUN and creatinine) and tubular endothelial apoptosis determined by immunofluorescence staining of CD31 and TUNEL, and western blot of apoptotic protein (caspase-3, c-caspase-3, and Bax/Bcl-2 ratio). Furthermore, we also found TLR4 deficiency abrogated CIH-induced macrophages (CD68) and fibroblasts (α-SMA) recruitment, further reducing expression of extra-cellular matrix protein (collagen I and collagen IV) and inflammatory cytokines release (IL-6, TNF-α, and MCP-1). Finally, we used immunohistochemistry to demonstrate that TLR4 deficiency attenuated increased expression of MyD88 and NF-kB p65 after CIH treatment. CONCLUSIONS: Our data suggest that TLR4 plays a vital role in CIH-induced renal injury, inflammation and fibrosis, and inhibition of TLR4 probably provides a therapeutic potential for CIH-induced kidney damage.

Cyclooxygenase-2-derived prostaglandin E2 promotes injury-induced vascular neointimal hyperplasia through the E-prostanoid 3 receptor.

RATIONALE: Vascular smooth muscle cell (VSMC) migration and proliferation are the hallmarks of restenosis pathogenesis after angioplasty. Cyclooxygenase (COX)-derived prostaglandin (PG) E2 is implicated in the vascular remodeling response to injury. However, its precise molecular role remains unknown. OBJECTIVE: This study investigates the impact of COX-2-derived PGE2 on neointima formation after injury. METHODS AND RESULTS: Vascular remodeling was induced by wire injury in femoral arteries of mice. Both neointima formation and the restenosis ratio were diminished in COX-2 knockout mice as compared with controls, whereas these parameters were enhanced in COX-1>COX-2 mice, in which COX-1 is governed by COX-2 regulatory elements. PG profile analysis revealed that the reduced PGE2 by COX-2 deficiency, but not PGI2, could be rescued by COX-1 replacement, indicating COX-2-derived PGE2 enhanced neointima formation. Through multiple approaches, the EP3 receptor was identified to mediate the VSMC migration response to various stimuli. Disruption of EP3 impaired VSMC polarity for directional migration by decreasing small GTPase activity and restricted vascular neointimal hyperplasia, whereas overexpression of EP3α and EP3ß aggravated neointima formation. Inhibition or deletion of EP3α/ß, a Gαi protein-coupled receptor, activated the cAMP/protein kinase A pathway and decreased activation of RhoA in VSMCs. PGE2 could stimulate phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase3ß signaling in VSMCs through Gßγ subunits on EP3α/ß activation. Ablation of EP3 suppressed phosphatidylinositol 3-kinase signaling and reduced GTPase activity in VSMCs and altered cell polarity and directional migration. CONCLUSIONS: COX-2-derived PGE2 facilitated the neointimal hyperplasia response to injury through EP3α/ß-mediated cAMP/protein kinase A and phosphatidylinositol 3-kinase pathways, indicating EP3 inhibition may be a promising therapeutic strategy for percutaneous transluminal coronary angioplasty.

Activating transcription factor 3 regulates survivability and migration of vascular smooth muscle cells.

Activating transcription factor 3 (ATF3) is a member of the ATF/CREB (CAMP responsive element binding protein) family of transcription factors. The expression and the function of ATF3 in vascular smooth muscle cells (VSMCs) remain unknown. The aim of this work is to determine the expression and possible function of ATF3 in VSMCs. We found that VSMCs expressed ATF3, and expression of ATF3 in VSMCs was induced by a variety of stimuli including serum, angiotensin II, and H(2)O(2). Knockdown of ATF3 induced apoptosis of VSMCs, caspase-3 cleavage, and cytochrome c release. The results suggest that ATF3 regulates survivability of VSMCs. Moreover, we found that overexpression of ATF3 promoted migration of VSMCs and induced expression of matrix metalloproteinase 1, 3, and 13. These results suggest that ATF3 plays a role in regulating migration of VSMCs. In addition, we found that the expression of ATF3 was upregulated in smooth muscle cells in the injured mouse femoral arteries compared with the uninjured control group. These results suggest that ATF3 is relevant to disease physiology.