Effects of private health insurance on waiting time in public hospitals.

The Australian government pays $6.7 billion per year in rebates to encourage Australians to purchase private health insurance (PHI) and an additional $6.1 billion to cover services provided in private hospitals. What is the justification for large government subsidies to a private industry when all Australians already have free coverage under Medicare? The government argues that more people buying PHI will relieve the burden on the public system and may reduce waiting times. However, the evidence supporting this is sparse. We use an instrumental variable approach to study the causal effects of higher PHI coverage in the area on waiting times in public hospitals in the same area. The instrument used is area-level average house prices, which correlate with average income and wealth, thus influencing the purchase of PHI due to tax incentives, but not directly affecting waiting times in public hospitals. We use 2014-2018 hospital admission and elective surgery waiting list data linked at the patient level from the Victorian Center for Data Linkage. These data cover all inpatient admissions in all hospitals in Victoria (both public and private hospitals) and those registered on the waiting list for elective surgeries in public hospitals in Victoria. We find that one percentage point increase in PHI coverage leads to about 0.34 days (or 0.5%) reduction in waiting times in public hospitals on average. The effects vary by surgical specialities and age groups. However, the practical significance of this effect is limited, if not negligible, despite its statistical significance. The small effect suggests that raising PHI coverage with the aim to taking the pressure off the public system is not an effective strategy in reducing waiting times in public hospitals. Alternative policies aiming at improving the efficiency of public hospitals and advancing equitable access to care should be a priority for policymakers.

Impact of Post-Mastectomy Radiation Therapy for Sentinel Lymph Node Micrometastases in Early-Stage Breast Cancer Patients.

BACKGROUND The association of radiotherapy with breast cancer survival in patients who underwent a mastectomy and had micrometastases in the sentinel lymph node is unclear. MATERIAL AND METHODS The survival benefit of radiotherapy was examined in patients with T0/1-T2N1mi breast cancer undergoing mastectomy plus sentinel lymph node biopsy (SLNB). Kaplan-Meier curves were employed for survival analysis and competing risk analysis, and a propensity score matching (PSM) cohort was enrolled to investigate whether such patients benefit from radiotherapy. RESULTS We identified 2864 patients in the SEER database from 2004 to 2015. All eligible patients were divided into the radiotherapy and the no-radiotherapy cohorts. With the median follow-up of 53 months, 5-year breast cancer-specific survival (BCSS) was 94.4% vs 95.2% (P=0.135), and 5-year overall survival (OS) was 91.2% vs 90.1% (P=0.466) in the radiotherapy cohorts and no-radiotherapy cohorts, respectively. The results of the competing risk analysis showed a comparable 5-year cumulative incidence of breast cancer-specific death (BCSD) in the radiotherapy and no-radiotherapy groups (5.5% vs 4.7%, P=0.107) but a higher 5-year cumulative incidence of other causes of death (OCD) in the no-radiotherapy cohort (3.3% vs 5.3%, P=0.011). No significant difference was observed for BCSS or OS in the PSM cohort. CONCLUSIONS Radiotherapy has no benefit for patients with T0/1-T2 breast cancer undergoing mastectomy with N1mi disease on SLNB. This analysis provides evidence that radiotherapy may safely be omitted in this group of patients.

Genetic deficiency of Phactr1 promotes atherosclerosis development via facilitating M1 macrophage polarization and foam cell formation.

Genetic variants in phosphatase and actin regulator-1 (Phactr1) are reported to be associated with arteriosclerotic cardiovascular disease (ASCVD). However, the function of Phactr1 in atherosclerosis remains unclear. Patients with acute coronary syndrome (ACS) who underwent coronary angiography and optical coherence tomography (OCT) were enrolled and divided into non-ST segment elevation (NST-ACS) group and ST-ACS group. The expression of Phactr1 on monocytes was higher in NST-ACS and ST-ACS groups as compared with control group. Furthermore, NST-ACS patients who have more vulnerable features including thin-cap fibroatheroma (TCFA) and large lipid area showed higher levels of Phactr1 on monocytes than those with stable plaques. Through mouse models of atherosclerosis, Phactr1-/-Apoe-/- mice (double knockout mice, DKO) developed more severe atherosclerotic plaques, recruiting more macrophages into subendothelium and having elevated levels of proinflammatory cytokines in plaques. Similarly, Apoe knockout mice (Apoe-/-) receiving DKO bone marrow (BM) exhibited elevated plaque burden compared with Apoe-/- mice receiving Apoe-/- BM, indicating the protective effect of Phactr1 in hematopoietic cells. We found that depletion of Phactr1 in BM-derived macrophages (BMDMs) tended to differentiate into M1 phenotype, produced more proatherogenic cytokines and eventually converted into foam cells driven by oxidized low-density lipoprotein (ox-LDL). Mechanistically, Phactr1 activated CREB signaling via directly binding to CREB, up-regulating CREB phosphorylation and inducing KLF4 expression. Finally, overexpression of KLF4 partly rescued the excessive inflammation response and foam cell formation induced by deficiency of Phactr1. In conclusion, our study demonstrates that elevated Phactr1 in monocytes is a promising biomarker for vulnerable plaques, while increased Phactr1 attenuates atherosclerotic development via activation of CREB and M2 macrophage differentiation.

Bone Marrow Mesenchymal Stem Cell-Derived Exosomal miRNA-29c Decreases Cardiac Ischemia/Reperfusion Injury Through Inhibition of Excessive Autophagy via the PTEN/Akt/mTOR Signaling Pathway.

BACKGROUND: Cardiac ischemia/reperfusion (I/R) injury will cause a large amount of cardiomyocyte loss and cascade reactions such as apoptosis, mitochondrial dysfunction, and excessive autophagy. Mesenchymal stem cells (MSCs) are promising therapeutic tools to replace damaged cardiomyocytes, but the underlying mechanism is still unknown.Methods and Results:Exosomes contain many microRNAs and protein, which are believed to have multiple biological functions. This study explored the role of bone marrow MSCs (BMMSCs)-derived exosomes under different oxidation levels in heart protection and miRNA-related mechanisms. Exosomes extracted from BMMSCs contained a high level of miR-29c, and its expression level changed after cells were treated under hypoxia/reoxygenation (H/R) conditions. In vivo I/R experiments also confirmed an expression change of miR-29c, and PTEN-Akt-mTOR is one of the predominant pathways that regulate autophagic change during this process. CONCLUSIONS: This study highlighted the role of miR-29c in regulating autophagy under cardiac I/R injury, which also extended existing mechanisms of a stem cell and its derivative to explore potential therapeutic interventions in ischemic heart diseases.

The effect of antioxidants on Helicobacter pylori eradication: A systematic review with meta-analysis.

BACKGROUND: The efficacy and safety of the addition of antioxidants to triple or quadruple therapy were unclear. MATERIALS AND METHODS: This systematic review was performed in accordance with the PRISMA 2009 guidelines. A systematic search of PubMed, EMBASE, and the Cochrane Library databases was conducted to identify potentially relevant publications using the following keywords: ([Helicobacter pylori] or [H. pylori] or [Hp]) and ([antioxidant] or [vitamin] or [N-acetylcysteine] or [curcumin] or [cranberry]). The primary end-point of this study was to evaluate the efficacy of the addition of antioxidants to triple or quadruple therapy according to ITT and PP analysis. The second end-points were side effects and the comparative efficacy in terms of H. pylori eradication according to different antioxidant and antibiotic combinations. RESULTS: We included 9 studies with 1260 participants. The total eradication rate of H. pylori in the group combining eradication therapy with antioxidants was not superior to that without antioxidants according to the ITT (pooled RR [95% CI] = 1.17 [0.99-1.38]; P = 0.07) and PP analysis (pooled RR [95% CI] = 1.15 [0.99-1.34; P = 0.07]. There were no differences regarding side effects between the two groups (pooled RR [95% CI], 1.36 [0.81-2.28]; P = 0.24). However, the eradication regimen with vitamin supplementation (1400 mg/day) showed a significant, superior efficacy in eradication relative to those without supplementation (pooled RR [95% CI] = 1.57 [1.35, 1.84]; P < 0.01). In particular, in the amoxicillin-clarithromycin-based subgroup, the crude H. pylori eradication rate determined by ITT analysis was 81.3% and 68.6% for eradication therapy with and without antioxidant supplementation, respectively, which was a statistically significant difference (pooled RR [95% CI] = 1.23 [1.02-1.49]; P = 0.03). CONCLUSIONS: The addition of antioxidants (vitamin, N-acetylcysteine, curcumin, cranberry) to amoxicillin-clarithromycin-based therapy could improve the eradication rate, and vitamin supplementation might be effective at a high dosage. However, antioxidant supplements have no impact on improving side effects.

Analysis of key genes and signaling pathways involved in Helicobacter pylori-associated gastric cancer based on The Cancer Genome Atlas database and RNA sequencing data.

BACKGROUND: Helicobacter pylori (H. pylori) infection is associated with the development of gastric cancer, although the mechanism is unclear. Herein, this study aimed to clarify the key genes and signaling pathways involved in H. pylori pathogenesis based on The Cancer Genome Atlas (TCGA) database and RNA sequencing analysis. MATERIALS AND METHODS: Forty-nine gastric cancer samples (16 with H. pylori and 33 without H. pylori) and 35 cancer-adjacent normal samples from TCGA database were analyzed by bioinformatics. The differentially expressed genes between H. pylori-positive and H. pylori-negative patients were verified in 18 gastric cancer (GC) samples (9 with H. pylori and 9 without H. pylori), which were analyzed using RNA sequencing. Survival analysis was carried out to explore associations between the differentially expressed genes and prognosis. Bioinformatics analysis was performed to determine the signaling pathways associated with H. pylori. RESULTS: The baseline level of clinical features from TCGA database and RNA sequencing showed no differences between the H. pylori-positive and H. pylori-negative GC groups (P > 0.05). TP53 was shown to be upregulated in the H. pylori-positive group in both TCGA database and RNA sequencing data, which also showed higher expression in the GC tissues than in adjacent normal tissues (P < 0.05). CCDC151, CHRNB2, GMPR2, HDGFRP2, and VSTM2L were shown to be downregulated in the H. pylori-positive group by both TCGA database and RNA sequencing, which also showed lower expression in the GC tissues than in adjacent normal tissues (P < 0.05). GC patients with low expression levels of HDGFRP2 had a poor prognosis (P < 0.05). Thirty-three signaling pathways and 10 biological processes were found to be positively associated with H. pylori infection (P < 0.05, FDR < 0.05). CONCLUSIONS: These results indicate that some genes (TP53, CCDC151, CHRNB2, GMPR2, HDGFRP2, VSTM2L) and previously unidentified signaling pathways (eg, the Hippo signaling pathway) might play an important role in H. pylori-associated GC.

The expression of glucocorticoid receptor is negatively regulated by active androgen receptor signaling in prostate tumors.

The glucocorticoid and androgen receptors (GR and AR) can commonly regulate up to 50% of their target genes in prostate cancer (PCa) cells. GR expression is stimulated by castration therapy, which has been proposed to be one mechanism that compensates for AR signaling blockade and promotes castration-resistant PCa (CRPC) progression. However, whether GR functions as a driver for CRPC or a marker reflecting AR activity remains unclear. Here, we applied PCa tissue microarrays to show that GR protein levels were elevated by castration therapy, but reduced to pre-castration levels when tumors were at the CRPC stage. Using subrenal capsule xenograft models, we showed that GR expression was inversely correlated with AR and PSA expressions. GR expression levels are not associated with tumor invasion and metastasis phenotypes. In castration-resistant C4-2 xenografts expressing AR shRNA, regressing tumors induced by AR knockdown expressed higher levels of GR and lower levels of PSA than non-regressing tumors. Immunoblotting and real-time PCR assays further showed that AR knockdown or AR antagonists increased GR expression at both mRNA and protein levels. ChIP combined with DNA sequencing techniques identified a negative androgen responsive element (nARE) 160K base pairs upstream of the GR gene. Gel shift assays confirmed that AR directly interacted with the nARE and luciferase assays demonstrated that the nARE could mediate transcription repression by ligand-activated AR. In conclusion, GR expression is negatively regulated by AR signaling and may serve as a marker for AR signaling in prostate tumors.

Progesterone receptor expression during prostate cancer progression suggests a role of this receptor in stromal cell differentiation.

BACKGROUND: The progesterone receptor, like the androgen receptor, belongs to the steroid receptor superfamily. Our previous studies have reported that the PR is expressed specifically in prostate stroma. PR inhibits proliferation of, and regulates cytokine secretion by stromal cells. However, PR protein expression in cancer-associated stroma during prostate cancer progression has not been profiled. Since the phenotypes of prostate stromal cells change dynamically as tumors progress, whether the PR plays a role in regulating stromal cell differentiation needs to be investigated. METHODS: Immunohistochemistry assays measured PR protein levels on human prostate tissue microarrays containing 367 tissue cores from benign prostate, prostate tumors with different Gleason scores, tumors under various durations of castration therapy, and tumors at the castration-resistant stage. Immunoblotting assays determined whether PR regulated the expression of alpha smooth muscle actin (α-SMA), vimentin, and fibroblast specific protein (FSP) in human prostate stromal cells. RESULTS: PR protein levels decreased in cancer-associated stroma when compared with that in benign prostate stroma. This reduction in PR expression was not correlated with Gleason scores. PR protein levels were elevated by castration therapy, but reduced to pre-castration levels when tumors progressed to the castration-resistant stage. Enhanced PR expression in human prostate stromal cells increased α-SMA, but decreased vimentin and FSP protein levels ligand-independently. CONCLUSION: These results suggest that PR plays an active role in regulating stromal cell phenotypes during prostate cancer progression.

[The Analgesia of Oxymatrine Affecting Calcium Channel and GABA Release].

OBJECTIVE: To explore the analgesia of oxymatrine (OMT) affecting high voltage-dependent calcium channels (HVDCCs) and GABA release under neuropathic pain condition. METHODS: Totally 66 C57BL/6 mice were randomly divided into the sham-operation group, the model group, and the OMT group, 22 in each group. Neuropathic pain models were established by partial sciatic nerve ligation (PSNL). Hind paw plantar mechanical response threshold (MWT) was measured by up-and-down method with Von-Frey filament. mRNA expression of HVDCCs in brains and spinal cords was detected with Real-time PCR and concentration of GABA was determined using ELISA kit. RESULTS: Compared with day 0, the left hind paw MWTwas decreased on day 7, 10, and 14 in the model group (P < 0.05). Compared with the sham-operation group, the left hind paw MWT was significantly reduced in the model group on day 7 (P < 0.05). The MWT of PSNL ipsilateral hind paw was decreased on day 7 before OMT administration, when compared with day 0 (P < 0.05), and increased after OMT administration (P < 0.05). Compared with the sham-operation group, mRNA levels of Cav1.2, Cav1.3, Cav2.1, and Cav2.3 in brain tissues were increased and those of Cav2.2 were decreased significantly in the model group (P < 0.05). In spinal cord tissues, mRNA levels of Cav1.2 and Cav1.3 were increased, but those of Cav2.1, Cav2.2, and Cav2. 3 were decreased significantly in the model group, when compared with those of the sham-operation group (P < 0.05). Compared with the model group, mRNA levels of Cavl.2, Cavl.3, Cav2.1, and Cav2. 3 in brain tissues were decreased, and those of Cav2.2 were increased significantly in the OMT group (P < 0.05). In spinal cord tissues of the OMT group, mRNA levels of Cav1.3 decreased and those of Cav2.1, Cav2.2, and Cav2.3 increased significantly with statistical difference, when compared with those of the model group (P < 0.05). Compared with the sham-operation group, GABA levels in brain tissues decreased in the model group (P < 0.05). Compared with the model group, GABA levels in brain tissues increased in the OMT group (P < 0.05). There was no statistical difference in GABA levels of spinal cord tissues among these groups (P > 0.05). CONCLUSIONS: OMT had analgesic effect on neuropathic pain, which might be probably related to HVDDCs. Cav2.2 might directly affect GABA release.

The endothelial protective effects of pioglitazone on insulin resistance in endothelial cells.

BACKGROUND: Insulin resistance plays an important role in vascular endothelial damage and atherosclerosis. Pioglitazone is an insulin-sensitizing agent and can reduce insulin resistance. METHODS: In this study, the cellular model of insulin resistance was used to investigate the mechanisms involved in the endothelial protective effects of pioglitazone in a vascular endothelial cell damage model. RESULTS: The results showed that pioglitazone could effectively increase the survival rate of human umbilical vein endothelial cells (ECV), reduce apoptosis, and relieve insulin resistance damage. To understand the endothelial protective effect mechanisms of pioglitazone, we showed that 50 ng/mL and 100 ng/mL of pioglitazone could upregulate the levels of inducible nitric oxide synthase (NOS) and pioglitazone could induce NO levels. CONCLUSIONS: These results suggested that pioglitazone could have endothelial protective effects in a vascular endothelial cell damage model of insulin resistance and used to prevent beforehand and treat a vascular endothelial cell damage of insulin resistance.

[Diagnostic value of automated breast volume scanner in high-risk and small breast lesions].

OBJECTIVE: To assess the accuracy of detection by automated breast volume scanner (ABVS) in diagnosis of high-risk and small breast lesions. METHODS: One hundred and twelve patients with solid high-risk and small breast lesions were identified by ABVS. The patients were divided into benign lesion group and cancer group after pathological examination. The clinicopathological findings and ultrasonographic features of the lesions were compared. RESULTS: Among the 112 lesions there were 49 benign and 63 malignant lesions. The mean size on ABVS and pathology were (1.59 ± 0.52) cm and (1.52 ± 0.58) cm. There was no significant difference in tumor sizes determined by ABVS and pathology (P = 0.194). The mean age of patients with benign lesions was (38.5 ± 7.4) years and that of malignant lesions was (52.4 ± 13.6) years, showing a significant difference between the two groups (P < 0.001) . The mass shape, orientation, margin, lesion boundary, echo pattern, calcification, BI-RADS category and retraction phenomenon were significantly different of the malignant and benign masses (P < 0.05). But there was no significant difference in the location of lesions and posterior acoustic features (P > 0.05) . Retraction phenomenon was significantly associated with pathological type and histologic grade of the breast cancer (P < 0.01). The specificity, sensitivity and accuracy of retraction phenomenon were 100% (46/46), 73.0% (46/63), and 84.8% (95/112), respectively. CONCLUSIONS: ABVS provides advantages of better size prediction of high-risk and small breast lesions. Furthermore, the retraction phenomenon in coronal plane shows high specificity and sensitivity in detecting breast cancer.

Nursing Home Competition, Prices, and Quality: A Scoping Review and Policy Lessons.

BACKGROUND AND OBJECTIVES: In recent years, countries have increasingly relied on markets to improve efficiency, contain costs, and maintain quality in aged care. Under the right conditions, competition can spur providers to compete by offering better prices and higher quality of services. However, in aged care, market failures can be extensive. Information about prices and quality may not be readily available and search costs can be high. This study undertakes a scoping review on competition in the nursing home sector, with an emphasis on empirical evidence in relation to how competition affects prices and quality of care. RESEARCH DESIGN AND METHODS: Online databases were used to identify studies published in the English language between 1988 and 2020. A total of 50 studies covering 9 countries are reviewed. RESULTS: The review finds conflicting evidence on the relationship between competition and quality. Some studies find greater competition leading to higher quality, others find the opposite. Institutional features such as the presence of binding supply restrictions on nursing homes and public reporting of quality information are important considerations. Most studies find greater competition tends to result in lower prices, although the effect is small. DISCUSSION AND IMPLICATIONS: The literature offers several key policy lessons, including the relationship between supply restrictions and quality, which has implications on whether increasing subsidies can result in higher quality and the importance of price transparency and public reporting of quality.

Energy policy and financial performance in China: mediation effect of financial inclusion.

The issues of cleaner production and socioeconomic advancements have taken a central stage due to the dynamism of the correlation between energy use and ecology. Given this background, the research delves into how to construct a framework to unravel diverse understandings of energy policy vis-a-vis green economy by examining the mediating role of financial inclusion. The analysis applied a non-radial DEA and longitudinal dataset model for the scenarios of thirty regions in China, relying on their longitudinal dataset from 2010-2017. The findings indicate that the Chinese regions' total green economic performance indicator (EPI) has advanced by 9.88% between 2010 and 2017. In addition, the econometric analyses prove that regional renewable energy policies and pollution abatement programs explicitly influence the improvement of the environmental performance index. Again, the results show that the probability figures of the individual specific limit equation and the dual limit values crossed the 1% significance analysis level simultaneously, indicating a dual limit impact. 0.74 to 1 is the range that marks the green EPI for Jiangsu, Shandong, Guangdong, Hainan, Zhejiang, Shanghai and Fujian. Ultimately, the analysis serves as a policy inference tool for policy formulators and regulators on encouraging green economic performance in China.

Self-Powered Seawater Electrolysis Based on a Triboelectric Nanogenerator for Hydrogen Production.

Water splitting for yielding high-purity hydrogen represents the ultimate choice to reduce carbon dioxide emission owing to the superior energy density and zero-pollution emission after combustion. However, the high electricity consumption and requirement of large quantities of pure water impede its large-scale application. Here, a triboelectric nanogenerator (W-TENG) converting offshore wind energy into electricity is proposed for commercial electric energy saving and cost reduction. By introducing PTFE/POM dielectric pairs with matched HOMO/LUMO band gap energy, a high charge density is achieved to promote the output of W-TENG. With the impedance matching design of transformers with the internal resistance of W-TENG, the output current is further enhanced from 1.42 mA to 54.5 mA with a conversion efficiency of more than 92.0%. Furthermore, benefiting from the high electrocatalytic activity (overpotential = 166 mV and Tafel slope = 181.2 mV dec-1) of a carbon paper supported NiCoP-MOF catalyst, natural seawater can be adopted as a resource for in situ hydrogen production without acid or alkaline additives. Therefore, the self-powered seawater electrolysis system achieves a H2 production rate as high as 1273.9 µL min-1 m-2 with a conversion efficiency of 78.9%, demonstrating a more practical strategy for conversion of wind energy into renewable hydrogen energy.

A Dual-Mode Triboelectric Nanogenerator for Wind Energy Harvesting and Self-Powered Wind Speed Monitoring.

The triboelectric nanogenerator shows a broad application potential in wind energy collection and wind speed sensing. However, it is difficult to realize wind energy collection and real-time wind speed monitoring in one simple device without external power support. Here, a high-performance dual-mode triboelectric nanogenerator is proposed to simultaneously collect wind energy efficiently and monitor wind speed in real time, which is composed by an alternating current triboelectric nanogenerator (AC-TENG) and a direct-current triboelectric nanogenerator (DC-TENG). Based on the material optimization, the charge density of the AC-TENG improves by a factor of 1 compared with previous works. Moreover, benefiting from the elastic structure and material optimization to realize a low friction force, the AC-TENG shows an excellent durability and obtains a retention of 87% electric output after 1 200 000 operation cycles. Meanwhile, thanks to the high charge density and low friction force, the energy-harvesting efficiency of the AC-TENG is doubled. In addition, the DC-TENG not only displays an excellent real-time sensing performance but also can provide gale warning. Our finding exhibits a strategy for efficiently collecting wind energy and achieving fully self-powered and real-time wind speed monitoring.

Highly Stable and Eco-friendly Marine Self-Charging Power Systems Composed of Conductive Polymer Supercapacitors with Seawater as an Electrolyte.

A self-charging power system harvesting random and low-frequency wave energy into electricity provides a promising strategy for the construction of smart oceans. However, the system faces huge challenges of easy corrosion in the marine environment and the utilization of toxic organic electrolytes in energy storage devices. To address the issues above, a seawater supercapacitor (SWSC) for the marine self-charging power system is rationally proposed by using a conductive polymer, polypyrrole with hollow morphology (h-PPy), to enhance the stability and capacitance while using seawater as an eco-friendly electrolyte to reduce the cost and achieve sustainability. The hollow design provides a shortcut for the ion transportation of seawater into the h-PPy electrode, and the SWSC achieves a high power density of 4.32 kW kg-1 under an energy density of 5.12 W h kg-1. Even after 180 days in seawater, h-PPy still endows a mass retention of 99.9%, enabling the SWSC to maintain a stability of 99.3% after 6000 cycles. More importantly, when combined with a TENG module as the marine self-charging power system to harvest wave energy, the system provides a stable output in water wave to drive electronics and sensors, which shows a competitive potential in the smart ocean and marine internet of things.

Seawater-Based Triboelectric Nanogenerators for Marine Anticorrosion.

The liquid-solid triboelectric nanogenerator is broadly studied for its self-powered sensing and blue energy harvesting, thanks to its low wear and highly efficient contact. However, the corresponding research studies focusing on deionized-water liquid-solid triboelectric nanogenerators (DL-TENGs) and seawater-type liquid-solid TENGs (SL-TENGs) are rarely being carried out at present. Here, a SL-TENG is fabricated by applying a dielectric film as the organic coating and coated and uncoated steel hull as the two electrodes. Based on the reasonable material selection of the dielectric film, the SL-TENG showed excellent performance, which benefits from the good triboelectrification performance and weak ion adsorption effect. In addition, compared with commercial marine anticorrosive coatings, the friction coefficient of the SL-TENG with the seawater can be reduced 43.8%, which is significantly beneficial to reduce the sailing resistance of ships. More importantly, the uncoated steel electrode can obtain a high potential in highly corrosive seawater, which can enable it to perform the function of marine anticorrosive agents. Our finding provides a potential strategy to evade the marine anticorrosion of ships.

lncRNA MALAT1 mediates osteogenic differentiation of bone mesenchymal stem cells by sponging miR-129-5p.

Background: Bone mesenchymal stem cells (BMSCs) have good osteogenic differentiation potential and have become ideal seed cells in bone tissue engineering. However, the osteogenic differentiation ability of BMSCs gradually weakens with age, and the regulatory mechanism is unclear. Method: We conducted a bioinformatics analysis, dual-luciferase reporter (DLR) experiment, and RNA binding protein immunoprecipitation (RIP) to explore the hub genes that may affect BMSC functions. Results: The expression level of long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (Malat1) was significantly higher in the BMSCs from elderly than younger mice, while miR-129-5p showed the opposite trend. The results of alkaline phosphatase staining, quantitative reverse transcription PCR and western blot experiments indicated that inhibiting the expression of Malat1 inhibits the osteogenic differentiation of BMSCs. This effect can be reversed by reducing the expression of miR-129-5p. Additionally, DLR and RIP experiments confirmed that Malat1 acts as a sponge for miR-129-5p. Conclusion: Overall, our study findings indicated that lncRNA Malat1 may play a critical role in maintaining the osteoblast differentiation potential of BMSCs by sponging miR-129-5p.

Does socioeconomic status affect hospital utilization and health outcomes of chronic disease patients?

This study quantifies the extent socioeconomic status (SES) affects hospital utilization and adverse hospital events of chronic disease patients. After identifying the initial first-year spell of the disease, we examine six outcomes that include measures of utilization and incidence of adverse in-hospital events. Three years of hospital administrative data from the state of Victoria, Australia, are used to extract a sample of 237,743 patients with chronic disease spells. SES is measured using the utilization records of specific health and human services. The study finds that, compared to patients with no disadvantage, SES disadvantaged patients tend to incur higher hospital costs and longer utilization by about 20% and greater incidence of in-hospital adverse outcomes by up to 80% than non-disadvantaged patients. Further analysis shows that hospital adverse outcomes indirectly contribute to about a quarter of the observed difference in hospital costs between SES disadvantaged and non-disadvantaged patients.

Ownership, quality and prices of nursing homes in Australia: Why greater private sector participation did not improve performance.

OBJECTIVE: This study examines whether greater private-sector participation in aged care can lead to better outcomes by comparing quality of care and prices of residential aged care facilities across three ownership types: government-owned, private not-for-profit and for- profit facilities. Australia, like many other countries, has been implementing market-oriented reforms aiming to promote greater consumer choice and increase the role of markets and private-sector participation in aged care. METHODS: Using retrospective facility-level data, the study relates several measures of quality of care and a measure of price to ownership types while controlling for facility characteristics. The data covered six financial years (2013/14-2018/19) and contained 2,900 residential aged-care facilities, capturing almost all facilities in Australia. About 55% were private not-for-profit, 30% private for-profit and 15% government-owned. RESULTS: Government-owned facilities provide higher quality of care in most quality measures and charge the lowest average price than private for-profit and not-for-profit facilities. DISCUSSION: Reforms promoting private-sector participation in aged care are unlikely to result in effective competition to drive quality up or prices down unless sources of market failure are addressed. In Australia, the lack of public reporting of quality and the complex pricing structure are key issues that prevent market forces and consumer choice from working as intended.