Nanoscale engineering of solid-state materials for boosting hydrogen storage.

The development of novel materials capable of securely storing hydrogen at high volumetric and gravimetric densities is a requirement for the wide-scale usage of hydrogen as an energy carrier. In recent years, great efforts via nanoscale tuning and designing strategies on both physisorbents and chemisorbents have been devoted to improvements in their thermodynamic and kinetic aspects. Increasing the hydrogen storage capacity/density for physisorbents and chemisorbents and improving the dehydrogenation kinetics of hydrides are still considered a challenge. The extensive and fast development of advanced nanotechnologies has fueled a surge in research that presents huge potential in designing solid-state materials to meet the ultimate U.S. Department of Energy capacity targets for onboard light-duty vehicles, material-handling equipments, and portable power applications. Different from the existing literature, in this review, particular attention is paid to the recent advances in nanoscale engineering of solid-state materials for boosting hydrogen storage, especially the nanoscale tuning and designing strategies. We first present a short overview of hydrogen storage mechanisms of nanoscale engineering for boosted hydrogen storage performance on solid-state materials, for example, hydrogen spillover, nanopump effect, nanosize effect, nanocatalysis, and other non-classical hydrogen storage mechanisms. Then, the focus is on recent advancements in nanoscale engineering strategies aimed at enhancing the gravimetric hydrogen storage capacity of porous materials, reducing dehydrogenation temperature and improving reaction kinetics and reversibility of hydrogen desorption/absorption for metal hydrides. Effective nanoscale tuning strategies for enhancing the hydrogen storage performance of porous materials include optimizing surface area and pore volume, fine-tuning nanopore sizes, introducing nanostructure doping, and crafting nanoarchitecture and nanohybrid materials. For metal hydrides, successful strategies involve nanoconfinement, nanosizing, and the incorporation of nanocatalysts. This review further addresses the points to future research directions in the hope of ushering in the practical applications of hydrogen storage materials.

Patient experiences of receiving a diagnosis of hypermobile Ehlers-Danlos syndrome.

Hypermobile Ehlers-Danlos syndrome (hEDS) presents with a wide range of clinical symptoms and comorbidities that impact quality of life. The diagnosis is challenging and often delayed due to the heterogeneity of the disease and lack of diagnostic biomarkers, which adds to the disease burden by affecting patients' psychosocial adaptation and overall well-being. Previous studies have revealed that healthcare professionals and the public have a limited understanding and familiarity with the condition, which leads to disapproval and skepticism that greatly impact patients' social spheres and welfare. While physical manifestations have been widely discussed, the psychosocial impact and the importance of receiving a diagnosis have not been fully studied in the current literature. This survey study investigated the impact of diagnosis in hEDS patients, selected from the University of Miami's hEDS registry. Survey questions were formulated based on clinical expertise and literature review. Descriptive statistics, Mann-Whitney test, and Spearman's correlation were used for data analysis. The median age at symptom presentation was 10 years, with a median gap of 4 years before the initial medical evaluation. On average, it took 10 years to receive a diagnosis of hEDS. Nearly all participants (95.2%) expressed receiving a diagnosis as "important" or "highly important," with 81.9% agreeing that it helped them cope with their condition better, 76.8% could better manage their symptoms, and felt more in control of their long-term care. Participants mostly had a positive emotional reaction and experienced an improvement in the support they were receiving from their caregivers and healthcare providers after receiving a diagnosis of hEDS. This study demonstrates that receiving a diagnosis could positively impact the patient's support, quality of care, and overall well-being.

Predicting Osteoporotic Fracture in Patients With Early-Stage Diabetic Kidney Disease Using a Radiomic Model: A Longitudinal Cohort Study.

OBJECTIVE: There is an urgent need for effective predictive strategies to accurately evaluate the risk of fragility fractures in elderly patients in the early stages of diabetic kidney disease (DKD). METHODS: This longitudinal cohort study included 715 older patients in the early stages of DKD diagnosed between January 2015 and August 2019. Patients were randomly allocated to a training cohort (n = 499) and a validation cohort (n = 216). The least absolute shrinkage and selection operator method was used to select key features for dual-energy x-ray absorptiometry-based radiomic analysis. A radiomic model was constructed using Cox proportional hazards regression. The performance of the radiomic model was compared with that of traditional fracture assessment tools through a receiver operating characteristic curve, calibration curve, and decision curve analysis. RESULTS: Over a mean follow-up period of 4.72 ± 1.60 years, 65 participants (9.09%) experienced incident fragility fractures. Seventeen features were ultimately selected to create the radiomic model. The calibration plots of this model demonstrated satisfactory agreement between the observed and predicted outcomes. Moreover, the radiomic model outperformed traditional fracture assessment tools in both the training and validation cohorts according to the area under the receiver operating characteristic curve and decision curve analysis. CONCLUSIONS: The novel radiomic model has demonstrated a more effective prediction of fragility fracture in elderly patients in the early stages of DKDcompared to traditional fracture assessment tools.

3,6'-Disinapoylsucrose alleviates the amyloid precursor protein and lipopolysaccharide induced cognitive dysfunction through upregulation of the TrkB/BDNF pathway.

The aim of this study is to explore the effect and mechanism of 3,6'-disinapoylsucrose (DISS) on an Alzheimer's disease (AD) mice model induced by APPswe695 lentivirus (LV) and intraperitoneal injection of lipopolysaccharide (LPS). The results show that DISS improves cognitive ability, decreases the levels of IL-2, IL-6, IL-1ß, and TNF-α, reduces the expression of NF-κB p65, and alleviates Aß deposition and nerve cell damage. DISS can regulate tyrosine kinase B (TrkB)/brain-derived neurotrophic factor (BDNF) signaling in the hippocampus. In summary, DISS can significantly alleviate neuroinflammation, spatial learning and memory disorders in AD model mice.

The future trajectory of carbon emissions in the process of carbon neutrality in South Korea.

The excessive use of fossil energy in industrialization has caused the frequent occurrence of global warming and environmental pollution issues, which seriously threaten the sustainable social and economic development of South Korea and other countries. In response to the international community's call to effectively address climate change, South Korea has announced achieving carbon neutrality by 2050. In this context, this paper takes the carbon emission of South Korea from 2016 to 2021 as a sample and focuses on using the GM(1,1) model to predict the carbon emission change trajectory of South Korea in the process of achieving carbon neutrality. The results show: first, in the process of carbon neutrality, South Korea's carbon emissions show a downward trend, with an average annual rate of 2.34%. Second, by 2030, carbon emissions will decline to 502.34 Mt CO2e, down about 26.79% from the 2018 peak. By 2050, South Korea's carbon emissions will decline to 312.65 Mt CO2e, down about 54.44% from the 2018 peak. Third, it is difficult for South Korea to achieve its carbon neutrality target by 2050 based solely on its forest carbon sink storage capacity. Therefore, this study is expected to provide a reference for improving the carbon neutrality promotion strategy in South Korea and strengthening the construction of relevant systems of carbon neutrality, and so can provide some reference for other countries, including China, to improve policy design to promote the green and low-carbon transformation of the global economy.

Chemical Energy-Driven Lithiation Preparation of Defect-Rich Transition Metal Nanostructures for Electrocatalytic Hydrogen Evolution.

Transition metal nanostructures are widely regarded as important catalysts to replace the precious metal Pt for hydrogen evolution reaction (HER) in water splitting. However, it is difficult to obtain uniform-sized and ultrafine metal nanograins through general high-temperature reduction and sintering processes. Herein, a novel method of chemical energy-driven lithiation is introduced to synthesize transition metal nanostructures. By taking advantage of the slow crystallization kinetics at room temperature, more surface and boundary defects can be generated and remained, which reduce the atomic coordination number and tune the electronic structure and adsorption free energy of the metals. The obtained Ni nanostructures therein exhibit excellent HER performance. In addition, the bimetal of Co and Ni shows better electrocatalytic kinetics than individual Ni and Co nanostructures, reaching 100 mA cm-2 at a low overpotential of 127 mV. The high HER performance originates from well-formed synergistic effect between Ni and Co by tuning the electronic structures. Density functional theory simulations confirm that the bimetallic NiCo possesses a low Gibbs free energy of hydrogen adsorption, which are conducive to enhance its intrinsic activity. This work provides a general strategy that enables simultaneous defect engineering and electronic modulation of transition metal catalysts to achieve an enhancement in HER performance.

Rational Surface and Interfacial Engineering of IrO2 /TiO2 Nanosheet Arrays toward High-Performance Chlorine Evolution Electrocatalysis and Practical Environmental Remediation.

The chlorine evolution reaction (CER) is a critical and commercially valuable electrochemical reaction in industrial-scale utilization, including the Chlor-alkali industry, seawater electrolysis, and saline wastewater treatment. Aiming at boosting CER electrocatalysis, hybrid IrO2 /TiO2 nanosheet arrays (NSAs) with rational surface and interfacial tuning strategies are proposed in this study. The IrO2 /TiO2 NSAs exhibit superb CER electrocatalytic activity with a low overpotential (44 mV) at 10 mA cm-2 , low Tafel slope of 40 mV dec-1 , high CER selectivity (95.8%), and long-term durability, outperforming most of the existing counterparts. The boosting mechanism is proposed that the aerophobic/hydrophilic surface engineering and interfacial electronic structure tuning of IrO2 /TiO2 are beneficial for the Cl- mass-transfer, Cl2 release, and Volmer-Heyvrosky kinetics during the CER. Practical saline wastewater treatment by using the IrO2 /TiO2 NSAs electrode is further conducted, demonstrating it has a higher p-nitrophenol degradation ratio (95.10% in 60 min) than that of other electrodes. The rational surface and interfacial engineering of IrO2 /TiO2 NSAs can open up a new way to design highly efficient electrocatalysts for industrial application and environmental remediation.

Unique three-site compound heterozygous mutation in the WFS1 gene in Wolfram syndrome.

BACKGROUND: Wolfram syndrome (WFS) is a rare autosomal recessive genetic disease whose main cause is mutations in the WFS1 and CISD2 genes. Its characteristic clinical manifestations are diabetes insipidus, diabetes mellitus, optic atrophy and deafness. METHODS: In this study, two patients from this particular family underwent complete routine biochemical and ophthalmic tests. Blood, urine, routine stool test, visual acuity (VA) examination, visual field assessment, funduscope, optical coherence tomography and periorbital magnetic resonance imaging (MRI) scans were performed for each patient to evaluate whether the nerve fiber layer around the optic nerve head was atrophied and next-generation sequencing of target genes was performed in two patients. RESULTS: When the patients were diagnosed with Wolfram syndrome, their genetic analyses suggested unique three-site compound heterozygous mutations (c.2314C > T + c.2194C > T + c.2171C > T) in exon 8 of both patients' chromosome 4. One mutation (c.2314C > T) was a novel mutation in the known reports of Wolfram syndrome. As a degenerative genetic disease, the types of gene mutations in the Chinese population are generally homozygous mutations at the unit point or compound heterozygous mutations at two nucleotide change sites. However, the two patients reported in this study are the first known cases of compound heterozygous mutations with three mutation sites coexisting on the WFS1 gene in China or even globally. CONCLUSIONS: This study expands the phenotypic spectrum of Wolfram syndrome and may reveal a novel mutation pattern of pathogenesis of Wolfram syndrome. The implications of this discovery are valuable in the clinical diagnosis, prognosis, and treatment of patients with WFS1.

Retrospective study on the potential of albumin/globulin ratio as a prognostic biomarker for oral cavity cancer patients.

PURPOSE: Although the serum albumin/globulin ratio (AGR) is recognized as a valuable prognostic biomarker in various cancers, its clinical value in oral cavity squamous cell carcinoma (OSCC) is still unclear. We aimed to probe the prognostic value of AGR in patients with OSCC undergoing curative surgery. METHODS: This retrospective study analyzed 306 patients who were newly diagnosed as having OSCC and receiving curative surgery between 2008 and 2017. The correlation of AGR with survival outcomes was estimated using Cox proportional hazards models and Kaplan-Meier analysis. A nomogram based on AGR was established, and its accuracy was assessed according to the concordance index. RESULTS: The log rank test and Kaplan-Meier analysis indicated that patients who had low AGR had significantly shorter disease-free survival (DFS) as well as 5-year overall survival (OS) than those with high AGR. The multivariate Cox analysis revealed that low AGR was an independent predictor of poor OS and DFS (adjusted hazard ratio [aHR] = 2.812; 95% CI 1.729-4.573; p < 0.001, and aHR = 1.743; 95% CI 1.201-2.530; p = 0.003, respectively). The concordance index of the nomogram model based on TNM staging alone was 0.656 and could increase to 0.783 with the inclusion of AGR and other prognostic variables in the calculation. CONCLUSION: Preoperative AGR may represent an accessible, valuable prognostic biomarker in patients with OSCC. The nomogram model incorporating AGR and clinicopathological prognostic variables may improve the accuracy of prognostic predictions in these patients.

Rapid Identification of 3,6'-Disinapoyl Sucrose Metabolites in Alzheimer's Disease Model Mice Using UHPLC-Orbitrap Mass Spectrometry.

Alzheimer's disease (AD) is a degenerative disease of the central nervous system characterized by the progressive impairment of neural activity. Studies have shown that 3,6'-disinapoyl sucrose (DISS) can alleviate the pathological symptoms of AD through the activation of the cAMP/CREB/BDNF signaling pathway. However, the exact biochemical mechanisms of action of DISS are not clear. This study explores metabolism of DISS in an AD mouse model, induced by the microinjection of a lentiviral expression plasmid of the APPswe695 gene into CA1 of the hippocampus. After gavage administration of DISS (200 mg/kg), the kidneys, livers, brains, plasma, urine, and feces were collected for UHPLC-Orbitrap mass spectrometry analysis. Twenty metabolites, including the prototype drug of DISS, were positively or tentatively identified based on accurate mass measurements, characteristic fragmentation behaviors, and retention times. Thus, the metabolic pathways of DISS in AD mice were preliminarily elucidated through the identification of metabolites, such as ester bond cleavage, demethoxylation, demethylation, and sinapic acid-related products. Furthermore, differences in the in vivo distribution of several metabolites were observed between the model and sham control groups. These findings can provide a valuable reference for the pharmacological mechanisms and biosafety of DISS.

Electrochemical and Photoelectrochemical Water Oxidation for Hydrogen Peroxide Production.

Hydrogen peroxide (H2 O2 ), as a green fuel and oxidant, has drawn increasing attention in the energy and environmental research. Compared with the traditional anthraquinone process, the electrochemical (EC) and photoelectrochemical (PEC) syntheses of H2 O2 are cost-effective and environmentally friendly. In order to construct membraneless EC/PEC devices for the full H2 O2 synthesis, anodic H2 O2 production by water oxidation, which is less developed than cathodic H2 O2 generation, is highly desirable. Here, we review recent developments for the EC/PEC H2 O2 production by water oxidation, including fundamental aspects, benchmarking activity evaluation, material/catalyst selection, and strategies for increasing selectivity, efficiency, and accumulation. Furthermore, we discuss the challenges and outlook of water oxidation for H2 O2 production, especially device-level development, accumulation and stability, and industrial applications. Our review is intended to stimulate studies further improving EC/PEC H2 O2 production.

Thrombomodulin facilitates peripheral nerve regeneration through regulating M1/M2 switching.

BACKGROUND: Excessive inflammation within damaged tissue usually leads to delayed or insufficient regeneration, and nerves in the peripheral nervous system (PNS) generally do not recover fully following damage. Consequently, there is growing interest in whether modulation of the inflammatory response could help to promote nerve regeneration in the PNS. However, to date, there are no practical therapeutic strategies for manipulating inflammation after nerve injury. Thrombomodulin (TM) is a transmembrane glycoprotein containing five domains. The lectin-like domain of TM has the ability to suppress the inflammatory response. However, whether TM can modulate inflammation in the PNS during nerve regeneration has yet to be elucidated. METHODS: We investigated the role of TM in switching proinflammatory type 1 macrophages (M1) to anti-inflammatory type 2 macrophages (M2) in a human monocytic cell line (THP-1) and evaluated the therapeutic application of TM in transected sciatic nerve injury in rats. RESULTS: The administration of TM during M1 induction significantly reduced the expression levels of inflammatory cytokines, including TNF-a (p < 0.05), IL-6 (p < 0.05), and CD86 (p < 0.05), in THP-1 cells. Simultaneously, the expression levels of M2 markers, including IL-10 (p < 0.05) and CD206 (p < 0.05), were significantly increased in TM-treated THP-1 cells. Inhibition of IL-4R-c-Myc-pSTAT6-PPARγ signaling abolished the expression levels of IL-10 (p < 0.05) and CD206 (p < 0.05). The conditioned medium (CM) collected from M1 cells triggered an inflammatory response in primary Schwann cells, while CM collected from M1 cells treated with TM resulted in a dose-dependent reduction in inflammation. TM treatment led to better nerve regeneration when tested 6 weeks after injury and preserved effector muscle function. In addition, TM treatment reduced macrophage infiltration at the site of injury and led to potent M1 to M2 transition, thus indicating the anti-inflammatory capacity of TM. CONCLUSIONS: Collectively, our findings demonstrate the anti-inflammatory role of TM during nerve regeneration. Therefore, TM represents a potential drug for the promotion and modulation of functional recovery in peripheral nerves that acts by regulating the M1/M2 ratio.

Contribution of transcription factor EB to adipoRon-induced inhibition of arterial smooth muscle cell proliferation and migration.

Abnormal vascular smooth muscle cell (SMC) dedifferentiation with increased proliferation and migration during pathological vascular remodeling is associated with vascular disorders, such as atherosclerosis and in-stent restenosis. AdipoRon, a selective agonist of adiponectin receptor, has been shown to protect against vascular remodeling by preventing SMC dedifferentiation. However, the molecular mechanisms that mediate adipoRon-induced SMC differentiation are not well understood. The present study aimed to elucidate the role of transcription factor EB (TFEB), a master regulator of autophagy, in mediating adipoRon's effect on SMCs. In cultured arterial SMCs, adipoRon dose-dependently increased TFEB activation, which is accompanied by upregulated transcription of genes involved in autophagy pathway and enhanced autophagic flux. In parallel, adipoRon suppressed serum-induced cell proliferation and caused cell cycle arrest. Moreover, adipoRon inhibited SMC migration as characterized by wound-healing retardation, F-actin reorganization, and matrix metalloproteinase-9 downregulation. These inhibitory effects of adipoRon on proliferation and migration were attenuated by TFEB gene silencing. Mechanistically, activation of TFEB by adipoRon is dependent on intracellular calcium, but it is not associated with changes in AMPK, ERK1/2, Akt, or molecular target of rapamycin complex 1 activation. Using ex vivo aortic explants, we demonstrated that adipoRon inhibited sprouts that had outgrown from aortic rings, whereas lentiviral TFEB shRNA transduction significantly reversed this effect of adipoRon on aortic rings. Taken together, our results indicate that adipoRon activates TFEB signaling that helps maintain the quiescent and differentiated status of arterial SMCs, preventing abnormal SMC dedifferentiation. This study provides novel mechanistic insights into understanding the therapeutic effects of adipoRon on TFEB signaling and pathological vascular remodeling.

Prevalence of low lean mass in patients with adult growth hormone deficiency with or without low-dose growth hormone therapy.

OBJECTIVE: The importance of muscle mass has been emphasized in various studies, and growth hormone (GH) deficiency is tightly associated with lean mass loss. Therefore, we aimed to investigate the prevalence of low lean mass in patients with adult growth hormone deficiency (AGHD) who received or did not receive GH therapy. METHODS: In this retrospective study, we included patients diagnosed with AGHD by using the insulin tolerance test (ITT) in our hospital. Patients without completed follow-up data were excluded, and data for 56 patients were analysed. Twenty-six patients who had received GH therapy for more than 6 months, based on the medical record, were included in the GH group and received recombinant human growth hormone (rhGH) at a dose of 0.5 IU/d. Thirty patients who had not previously received GH treatment were included in the non-GH group. Many anthropometric and blood biochemical indicators were measured. Body composition was measured on a dual-energy X-ray-absorptiometry (DXA) scanner. Low lean mass was defined as a skeletal muscle index (SMI) <7.0 kg/m2 in males or 5.7 kg/m2 in females. Statistical analyses were performed using GraphPad Prism 5.0. RESULTS: Compared to the non-GH group, the patients who received GH therapy had significantly lower total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c) and fasting plasma glucose (FPG). The percentage of patients with low lean mass in GH and non-GH groups was 30.77% and 60%, respectively. The percentage of total lean was lower in the GH group than in the non-GH group, but the difference in total lean mass was not statistically significant. Conversely, patients with GH treatment had significantly lower fat mass and percentage than non-GH-treated patients (P < 0.05). The GH group had significantly higher serum levels of both IGF-1 and IGFBP3. Moreover, both IGF-1 and IGFBP3 were significantly correlated with SMI (r2  = 0.275, P = 0.003, and r2  = 0.138, P = 0.005, respectively). CONCLUSIONS: Our data showed that AGHD patients who received low-dose GH treatment had a lower prevalence of low lean mass than those who did not receive GH treatment. Patients with GH treatment had significantly lower cardiovascular risk factors, especially the lipid profile.

CORRELATION OF INCREASED SERUM ADIPSIN WITH INCREASED CARDIOVASCULAR RISKS IN ADULT PATIENTS WITH GROWTH HORMONE DEFICIENCY.

Objective: Adult growth hormone deficiency (AGHD) patients have an increased cardiovascular morbidity and mortality. Adipsin is an adipokine that is significantly correlated with metabolic disease, especially in people with obesity. The objective of our study was to compare AGHD patients with healthy subjects to evaluate whether adipsin levels are closely related to glycolipid metabolism and cardiovascular risks in AGHD patients. Methods: Our study included 88 AGHD patients and 88 age-, weight-, and body mass index (BMI)-matched healthy subjects. Anthropometric parameters such as BMI, waist circumference, and blood pressure were measured. Biochemical indicators such as serum adipsin, lipids, and fasting insulin levels were determined. Results: Adipsin levels in AGHD patients were significantly increased compared to levels of the control group (11,567.29 ng/mL, interquartile [9,856.46 to 13,360.60 ng/mL]) versus (9,127.86 ng/mL, interquartile [8,061.82 to 10,647.06 ng/mL], P = .000). Increased serum adipsin levels are correlated with cardiovascular risk factors such as a higher waist-to-hip ratio, serum lipids levels, and insulin resistance. Adipsin levels were inversely related to insulin-like growth factor 1 (IGF-1) (r = -0.6363, P<.0001) and insulin-like growth factor binding protein 3 levels (r = -0.498, P<.0001). The odds ratio (OR) for AGHD in the highest quartile was found to be 4.491 times the ratio in the lowest quartile (OR = 4.491, P = .048). Additionally, adipsin was found to be the most independent factor to influence IGF-1 levels in AGHD subjects. Conclusion: The serum levels of adipsin were significantly correlated with glucolipid metabolism disorder with a growth hormone deficiency status. Furthermore, serum levels of adipsin might be a good marker for the occurrence and development of cardiovascular diseases in AGHD patients. Abbreviations: AGHD = adult growth hormone deficiency; ASCVD = atherosclerotic cardiovascular disease; BMI = body mass index; DBP = diastolic blood pressure; FINS = fasting insulin; FPG = fasting plasma glucose; GH = growth hormone; HOMA-IR = homeostatic model to assess insulin resistance index; hsCRP = high-sensitivity C-reactive protein; IGF-1 = insulin-like growth factor 1; IGFBP-3 = insulin-like growth factor binding protein 3; LAP = lipid accumulation products; LDL = low-density lipoprotein; SBP = systolic blood pressure; TC = total cholesterol; TG = triglycerides; WC = waist circumference; WHR = waist-to-hip ratio; OR = odds ratio.

The Mechanism of Electroacupuncture at Zusanli Promotes Macrophage Polarization during the Fibrotic Process in Contused Skeletal Muscle.

INTRODUCTION: Currently, many clinical experiments are being conducted to study the effect of acupuncture on skeletal muscle contusions, and its therapeutic effect has been confirmed to some extent. However, the mechanism of recovery by electroacupuncture (EA) in skeletal muscles after blunt trauma remains unknown. OBJECTIVE: To determine whether EA at Zusanli can contribute to the regeneration of contused skeletal muscle and the molecular mechanism involved. METHODS: Masson's trichrome staining and hematoxylin and eosin staining were used to measure the area of fibrotic tissue and determine the number of centrally nucleated muscle fibers respectively. The different immune phenotypes of macrophages were determined by flow cytometry. Then, ELISA was used to analyze the levels of interleukin-4 (IL-4), IL-6, interferon-α (IFN-α) and interferon-γ (IFN-γ) in the injured tissue. Finally, the expression of MyoD in the tissue was detected by quantitative real-time polymerase chain reaction. RESULTS: EA at Zusanli helped regenerate contused skeletal muscle by alleviating fibrosis and increasing the size of the regenerating myofibres in the injured skeletal muscle. EA at Zusanli increased the number of M2 macrophages and decreased the number of M1 macrophages in contused skeletal muscle. EA at Zusanli decreased the level of cytokine IFN-γ and increased the levels of IL-4, interleukin-13 (IL-13), and IFN-α, which promoted macrophage polarization during the fibrosis recovery process in the contused skeletal muscle. EA at Zusanli could increase the expression of MyoD in tissues. CONCLUSIONS: EA at Zusanli promoted macrophage polarization during the fibrotic process in contused skeletal muscle by decreasing cytokine IFN-γ and increasing IL-4, IL-13, and IFN-α, which contributed to the regeneration of the contused skeletal muscle.

MicroRNA-92a Mediates Endothelial Dysfunction in CKD.

CKD is an independent risk factor for cardiovascular disease (CVD). The accumulation of uremic toxins in CKD induces oxidative stress and endothelial dysfunction. MicroRNA-92a (miR-92a) is induced by oxidative stress in endothelial cells (ECs) and involved in angiogenesis and atherosclerosis. We investigated a role for oxidative stress-responsive miR-92a in CKD. Our study of patients at three clinical sites showed increased serum miR-92a level with decreased kidney function. In cultured ECs, human CKD serum or uremic toxins (such as indoxyl sulfate), compared with non-CKD serum, induced the levels of miR-92a and suppressed the expression of miR-92a targets, including key endothelial-protective molecules. The antioxidant N-acetylcysteine inhibited these vasculopathic properties. In rats, adenine-induced CKD associated with increased levels of miR-92a in aortas, serum, and CD144+ endothelial microparticles. Furthermore, CD144+ microparticles from human uremic serum contained more miR-92a than those from control serum. Additional analysis showed a positive correlation between serum levels of miR-92a and indoxyl sulfate in a cohort of patients with ESRD undergoing hemodialysis. Collectively, our findings suggest that the uremic toxins accumulated in CKD can upregulate miR-92a in ECs, which impairs EC function and predisposes patients to CVD.

A Single LiDAR-Based Feature Fusion Indoor Localization Algorithm.

In past years, there has been significant progress in the field of indoor robot localization. To precisely recover the position, the robots usually relies on multiple on-board sensors. Nevertheless, this affects the overall system cost and increases computation. In this research work, we considered a light detection and ranging (LiDAR) device as the only sensor for detecting surroundings and propose an efficient indoor localization algorithm. To attenuate the computation effort and preserve localization robustness, a weighted parallel iterative closed point (WP-ICP) with interpolation is presented. As compared to the traditional ICP, the point cloud is first processed to extract corners and line features before applying point registration. Later, points labeled as corners are only matched with the corner candidates. Similarly, points labeled as lines are only matched with the lines candidates. Moreover, their ICP confidence levels are also fused in the algorithm, which make the pose estimation less sensitive to environment uncertainties. The proposed WP-ICP architecture reduces the probability of mismatch and thereby reduces the ICP iterations. Finally, based on given well-constructed indoor layouts, experiment comparisons are carried out under both clean and perturbed environments. It is shown that the proposed method is effective in significantly reducing computation effort and is simultaneously able to preserve localization precision.

Investigating clinical failure of core decompression with autologous bone marrow mononuclear cells grafting for the treatment of non-traumatic osteonecrosis of the femoral head.

OBJECTIVE: This study aimed to analyze the clinical factors related to the failure of autologous bone marrow mononuclear cells grafting (BMMCG) following core decompression (CD) in early stage osteonecrosis of the femoral head (ONFH). METHODS: In total, 148 patients (192 hips) underwent CD with autologous BMMCG for treatment of non-traumatic ONFH. The patients were classified by their ARCO staging and China-Japan Friendship Hospital (CJFH) typing system. All patients were clinically and radiographically followed up every three months during the first year and every six months in the following years. The clinical evaluation was conducted by pre- and post-operative Harris hip scores (HHS), while serial anteroposterior (AP) and frog lateral radiographs were used for post-operative radiographic evaluation. RESULTS: There were 56 hips as clinical failure cases, and 50 hips (89.29%) of failure cases developed between three and ten months after operation. Based on CJFH classification system, type L2 showed more failure rate with 60.0% (9 of15). The Cox risk model showed that disease type was an independent risk factor for post-operative clinical failure (P = 0.042). Multivariate analysis of the Cox proportional-hazards model showed that type L1 had a hazard ratio (HR) of 0.286 (95% CI 0.100-0.816), type L3 with HR of 0.245 (95% CI 0.079-0.759), respectively. CONCLUSION: Disease type is an important risk factor for autologous BMMCG combined with CD, and the degree of lateral pillar necrosis is a significant reference index for prognosis evaluation in early stage of ONFH.

Retinoic acid morpholine amide (RAMA) inhibits expression of Fas ligand through EP1 receptor in colon cancer cells.

Among the members of tumour necrosis factor family Fas ligand on binding to its receptor strongly induces apoptosis of tumour-infiltrating lymphocytes (TIL). Thus, FasL acts as an inhibitor of anti-tumour immune response. The present study demonstrates that retinoic acid morpholine amide (RAMA) significantly suppresses FasL expression in colon cancer cells in a dose- and time-dependent manner. The suppression of FasL mRNA and proteins was significant at a concentration of 30 µM after 48 h in CLT85 and HT26 colon cancer cells. There was around 2.6- and 3.2-fold decrease in FasL mRNA after incubation with 30 µM of RAMA in CLT85 cells and HT26 cells, respectively. The results from Western blot showed a decrease in FasL mRNA and protein expression in both CLT85 and HT26 cells after suppression of cyclooxygenase (COX)-2 and COX-1 by RNAi. However, when COX-2-specific silencer RNA (siCOX-2)- and siCOX-1-treated CLT85 and HT26 cells were exposed to RAMA, inhibition of FasL expression was further suppressed. The siCOX-2-treated CLT85 and HT26 cells on exposure to RAMA showed ∼87 and ∼54 % reduction in FasL mRNA, respectively. Co-culture of Jurkat T cells with RAMA-treated HT26 and CLT85 cells decreased the viability of Jurkat T cells by only 2 and 4.3 %, respectively, compared to 19.5 and 37.3 % in control HT26 and CLT85 cells. The results from real-time reverse transcription polymerase chain reaction (RT-PCR) and immunoblotting showed that suppression of EP1 prevented RAMA-induced FasL suppression in CLT85 cells at both the mRNA and protein levels. Thus, RAMA can be a potent therapeutic agent for the treatment of colon tumours.