Thermal Decomposition of Two Gaseous Perfluorocarboxylic Acids: Products and Mechanisms.

The thermal decomposition products and mechanisms of per- and polyfluoroalkyl substances (PFASs) are poorly understood despite the use of thermal treatment to remediate PFAS-contaminated media. To identify the thermal decomposition products and mechanisms of perfluorocarboxylic acids (PFCAs), gaseous perfluoropropionic acid (PFPrA) and perfluorobutyric acid (PFBA) were decomposed in nitrogen and oxygen at temperatures from 200 to 780 °C. In nitrogen (i.e., pyrolysis), the primary products of PFPrA were CF2═CF2, CF3CF2H, and CF3COF. CF3CF═CF2 was the dominant product of PFBA. These products are produced by HF elimination (detected as low as 200 °C). CF4 and C2F6 were observed from both PFCAs, suggesting formation of perfluorocarbon radical intermediates. Pyrolysis products were highly thermally stable, resulting in poor defluorination. In oxygen (i.e., combustion), the primary product of both PFPrA and PFBA below 400 °C was COF2, but the primary product was SiF4 above 600 °C due to reactions with the quartz reactor. Oxygen facilitated thermal defluorination by reacting with PFCAs and with pyrolysis products (i.e., fluoroolefins and fluorocarbon radicals). Platinum improved combustion of PFCAs to COF2 at temperatures as low as 200 °C, while quartz promoted the combustion of PFCAs into SiF4 at higher temperatures (>600 °C), highlighting the importance of surface reactions that are not typically incorporated into computational approaches.

Critical Review of Thermal Decomposition of Per- and Polyfluoroalkyl Substances: Mechanisms and Implications for Thermal Treatment Processes.

Per- and polyfluoroalkyl substances (PFASs) are fluorinated organic chemicals that are concerning due to their environmental persistence and adverse human and ecological effects. Remediation of environmental PFAS contamination and their presence in consumer products have led to the production of solid and liquid waste streams containing high concentrations of PFASs, which require efficient and cost-effective treatment solutions. PFASs are challenging to defluorinate by conventional and advanced destructive treatment processes, and physical separation processes produce waste streams (e.g., membrane concentrate, spent activated carbon) requiring further post-treatment. Incineration and other thermal treatment processes are widely available, but their use in managing PFAS-containing wastes remains poorly understood. Under specific operating conditions, thermal treatment is expected to mineralize PFASs, but the degradation mechanisms and pathways are unknown. In this review, we critically evaluate the thermal decomposition mechanisms, pathways, and byproducts of PFASs that are crucial to the design and operation of thermal treatment processes. We highlight the analytical capabilities and challenges and identify research gaps which limit the current understanding of safely applying thermal treatment to destroy PFASs as a viable end-of-life treatment process.

Optimal control of the reaction-diffusion process on directed networks.

Reaction-diffusion processes organized in networks have attracted much interest in recent years due to their applications across a wide range of disciplines. As one type of most studied solutions of reaction-diffusion systems, patterns broadly exist and are observed from nature to human society. So far, the theory of pattern formation has made significant advances, among which a novel class of instability, presented as wave patterns, has been found in directed networks. Such wave patterns have been proved fruitful but significantly affected by the underlying network topology, and even small topological perturbations can destroy the patterns. Therefore, methods that can eliminate the influence of network topology changes on wave patterns are needed but remain uncharted. Here, we propose an optimal control framework to steer the system generating target wave patterns regardless of the topological disturbances. Taking the Brusselator model, a widely investigated reaction-diffusion model, as an example, numerical experiments demonstrate our framework's effectiveness and robustness. Moreover, our framework is generally applicable, with minor adjustments, to other systems that differential equations can depict.

A Facile, Nonreactive Hydrogen Peroxide (H2O2) Detection Method Enabled by Ion Chromatography with UV Detector.

Hydrogen peroxide (H2O2) is ubiquitous in the natural environment, and it is now widely used for pollutant control in water and wastewater treatment processes. However, current analytical methods for H2O2 inevitably require reactions between H2O2 and other reactants to yield signals and are thus likely subjective to the interferences of coexisting colored, oxidative, and reductive compounds. In order to overcome these barriers, we herein for the first time propose to analyze H2O2 by ion chromatography (IC) using an ultraviolet (UV) detector. The proposal is based on two principles: first, that H2O2 can deprotonate to hydroperoxyl ion (HO2-) when eluent pH is higher than the acid-dissociation coefficient of H2O2 (pKa = 11.6); and second, that after separation from other compounds via IC column, H2O2 can be quantified by a UV detector. Under favorable operating conditions, this method has successfully achieved acceptable recoveries (>91%) of H2O2 dosed to ultrapure and natural waters, a calibration curve with R2 > 0.99 for a wide range of H2O2 concentrations from 0.1 to 50 mg/L and a method detection limit of 0.027 mg/L. In addition, this approach was shown to be capable of distinguishing H2O2 from anions (e.g., fluoride and chloride) and organics (e.g., glycolate) and monochloramine, suggesting that it is insensitive to many neighboring compounds as long as they do not react quickly with H2O2. Hence, this study proves the combination of IC and UV detector a facile and reliable method for H2O2 measurement.

Fluoxetine induces vascular endothelial growth factor/Netrin over-expression via the mediation of hypoxia-inducible factor 1-alpha in SH-SY5Y cells.

Fluoxetine has become one of the most promising drugs for improving clinical outcome in patients with cerebral infarction. Although the clinical efficacy of fluoxetine has been preliminarily demonstrated, its mechanism remains unclear. Hypoxia-inducible factor 1-alpha (HIF-1α) is upstream to Netrin and vascular endothelial growth factor (VEGF), and under hypoxia conditions it may induce expression of Netrin-1 and VEGF in vascular endothelial cells. We sought to explore whether it can regulate their expression in hypoxia and mediate the effect of fluoxetine in hypoxia. In this study, the effect of hypoxia on the expression of VEGF and Netrin was observed in vitro by real-time PCR and western blotting in SH-SY5Y cells; the binding sites of HIF-1α in VEGF and Netrin gene promoters were identified by luciferase reporter; the effect of fluoxetine on binding of HIF-1α with Netrin and VEGF promoters in hypoxia was observed by Chromatin Immunoprecipitation (ChIP) Assay. We prove that HIF-1α regulates transcription of both VEGF and Netrin, and that in hypoxia fluoxetine up-regulates VEGF and Netrin expression via mediation of HIF-1α that binds to hypoxia-response element sites of VEGF and Netrin promoters. Our study indicates that HIF-1α may play an important role in the treatment of cerebral infarction through mediating the recovery of neurological function induced by fluoxetine, which provides theoretical basis for the development of gene therapeutic drugs targeting HIF-1α. We show that hypoxia-inducible factor 1-alpha (HIF-1α) regulates transcription of both vascular endothelial growth factor (VEGF) and Netrin. Furthermore, we also show that in hypoxia fluoxetine up-regulates VEGF and Netrin expression via mediation of HIF-1α that binds to hypoxia-response element (HRE) sites of VEGF and Netrin promoters. Our study indicates that HIF-1α may play an important role in the treatment of cerebral infarction through mediating the recovery of neurological function induced by fluoxetine. These findings provide a theoretical basis for development of gene therapeutic drugs targeting HIF-1α.

Susceptibility Vessel Sign in Isolated Brainstem Infarction with Large Artery Occlusion.

BACKGROUND/AIMS: It is crucial to detect the composition of the thrombus in isolated brainstem infarction with large artery occlusion. The aim of this study was to explore the susceptibility vessel sign (SVS) whose composition is mainly deoxidized red cells in patients with isolated brainstem infarction and posterior circulation large artery occlusion. METHODS: This was a single-center retrospective study. All patients with posterior circulation large artery occlusion from January 2003 to September 2013 were included. We identified 213 patients who had posterior circulation large artery occlusion, and 81 patients met the imaging eligibility criteria. Among the 81 patients, 21 had isolated brainstem infarction. RESULTS: Among the 21 patients, 7 (33%) had SVS and 2 (10%) had pseudo-SVS (calcified vessels without thrombosis). In the 7 patients with SVS, we found atrial fibrillation in 2 patients, dissection in 3 patients and large artery atherosclerotic disease (LAAD) in 2 patients. There were SVS in 100% (2/2) of patients with atrial fibrillation, 50% (3/6) of patients with dissection, and 20% (2/10) of patients with LAAD. CONCLUSIONS: SVS reflects pathology of deoxidized red cells composition in patients with isolated brainstem infarction. This finding may be useful to explore the different stroke mechanisms and therapy strategies.

Natural vs. anthropogenic sources of N-Nitrosodimethylamine precursors in surface water.

N-nitrosodimethylamine (NDMA) is a carcinogenic disinfection byproduct formed from reactions between dichloramine and organic nitrogen-containing precursors. It is unclear if NDMA precursors in surface water intakes originate in anthropogenic (i.e., wastewater) or natural sources. The Truckee River has a single point source release of treated wastewater effluent, making it an ideal system to study the relative importance of precursor sources. Three Lagrangian sampling events were conducted. NDMA formation potential (FP, a measurement of precursors) above the wastewater outfall indicated that the natural background of NDMA precursors was 2-28 ng/L. NDMA FP increased to 18-31 ng/L immediately downstream of the wastewater outfall, but decreased rapidly in a first order manner, and were not statistically different from the upstream samples in only ∼6 km. This suggests that the dominant source of NDMA precursors may be wastewater derived only near wastewater outfalls and deviates from the previous belief that wastewater-derived precursors are responsible for NDMA formation in drinking water sources located further downstream. Additionally, given the rapid loss of the wastewater precursors in this study, precursors which are slow to biodegrade/photolyze/adsorb to sediment are likely to be poor surrogates for the overall wastewater NDMA precursor pool. To understand temporal changes in the wastewater impact on environmental NDMA precursor loading, two 24-hour sampling events were conducted near (<3 km) the wastewater outfall and demonstrated that temporal changes in the NDMA precursors directly downstream of the wastewater outfall are directly linked to the wastewater flow contribution.

Bacterial dealkylation of benzalkonium chlorides in wastewater produces benzyldimethylamine, a potent N-nitrosodimethylamine precursor.

N-nitrosodimethylamine (NDMA) is a carcinogenic disinfection byproduct that forms during chloramine disinfection of municipal wastewater effluents which are increasingly used to augment drinking water supplies due to growing water scarcity. Knowledge of wastewater NDMA precursors is limited and the known pool of NDMA precursors has not closed the mass balance between precursor loading, precursor NDMA yield, and formed NDMA. Benzalkonium chlorides (BACs) are the most prevalent quaternary ammonium surfactants and have antimicrobial properties. The extensive utilization of BACs in household, commercial and industrial products has resulted in their detection in wastewater at elevated concentrations. We report the formation of a potent NDMA precursor, benzyldimethylamine (BDMA) from the biodegradation of BACs during activated sludge treatment. BDMA formation and NDMA formation potential (FP) were functions of BAC and mixed liquor suspended solids concentration at circumneutral pH, and the microbial community source. Sustained exposure to microorganisms reduced NDMA FP through successive dealkylation of BDMA to less potent precursors. BAC alkyl chain length (C8 - C16) had little impact on NDMA FP and BDMA formation because chain cleavage occurred at the C-N bond. Wastewater effluents collected from three facilities contained BDMA from 15 to 106 ng/L, accounting for an estimated 4 to 38 % of the NDMA precursor pool.

Granulocyte colony-stimulating factor mediates bone loss via the activation of IL-1ß/JNK signaling pathway in murine Staphylococcus aureus-induced osteomyelitis.

Staphylococcus aureus (S. aureus)-induced bone loss is a significant challenge in the treatment of osteomyelitis. Our previous study was the first to confirm that granulocyte colony-stimulating factor (G-CSF) mediates S. aureus-induced bone loss. However, the underlying mechanism remains unknown. The objective of this study was to elucidate this. We found G-CSF mediated BMSC senescence and increased IL-1ß concentration of serum and bone marrow in mice after S. aureus infection. Furthermore, we demonstrated that G-CSF promoted the expression of IL1b in murine bone marrow-derived neutrophils. Notably, we identified that IL-1ß mediated BMSC (bone marrow mesenchymal stromal cell) senescence in mice after S. aureus infection. Importantly, IL-1ß neutralizing antibody effectively alleviated BMSC senescence and bone loss caused by S. aureus infection in mice. In terms of molecular mechanism, we found IL-1ß induced BMSC senescence by JNK/P53 and JNK/BCL2 pathways. Collectively, G-CSF promotes IL-1ß production which induces BMSC senescence via JNK/P53 and JNK/BCL2 pathways, leading to S. aureus-induced bone loss. This study identified novel targets for preventing and treating S. aureus-induced bone loss in osteomyelitis.

Nicotine promotes Staphylococcus aureus-induced osteomyelitis by activating the Nrf2/Slc7a11 signaling axis.

Although smoking is a significant risk factor for osteomyelitis, there is limited experimental evidence that nicotine, a key tobacco constituent, is associated with this condition, leaving its mechanistic implications uncharacterized. This study revealed that nicotine promotes Staphylococcus aureus-induced osteomyelitis by increasing Nrf2 and Slc7a11 expression in vivo and in vitro. Inhibition of Slc7a11 using Erastin augmented bacterial phagocytosis/killing capabilities and fortified antimicrobial responses in an osteomyelitis model. Moreover, untargeted metabolomic analysis demonstrated that Erastin mitigated the effects of nicotine on S. aureus-induced osteomyelitis by altering glutamate/glutathione metabolism. These findings suggest that nicotine aggravates S. aureus-induced osteomyelitis by activating the Nrf2/Slc7a11 signaling pathway and that Slc7a11 inhibition can counteract the detrimental health effects of nicotine.

Clinical characteristics, treatment and efficacy of calcaneal osteomyelitis: A systematic review with synthesis analysis 1118 reported cases.

BACKGROUND: Calcaneal osteomyelitis (CO) still poses great challenges to orthopaedic surgeons due to unique anatomic and functional features of the calcaneus. This study summarized the current data regarding clinical characteristics, treatment and efficacy of CO, based on an analysis of literature-reported cases. MATERIALS AND METHODS: We searched the PubMed, Embase, and Cochrane Library databases to find English and Chinese studies reporting on CO patients between 2000 and 2021, with available data for synthesis analysis. The quality of the included studies was evaluated by the National Institutes of Health (NIH) assessment scale. Effective data were extracted and pooled for analysis. RESULTS: Altogether 198 studies involving 1118 patients were included, with a male-to-female ratio of 2.3 (724 males and 310 females). The median age at CO diagnosis was 46 years, with a median symptom duration of 3 months. Injury-related infections (524 cases) and diabetic foot infections (336 cases) were the two most common causes, with ulcer (468 cases) and wound sinus or exudation (209 cases) being the predominant symptoms. The overall positive culture rate was 80.2%, with polymicrobial infections accounting for 18.1%. Staphylococcus aureus was the most frequently detected pathogen (42.7%), with fungal-related infections isolated in 17 cases. Although most patients received surgical interventions (96.9%), the recurrence rate was 20.1%. The incidence of infection relapse following partial calcanectomy, total calcanectomy, debridement with implantation of local antibiotics, and debridement with or without flap or skin coverage were 31.7%, 45.0%, 16.8%, and 15.1%, respectively. The overall incidence of limb amputation was 12.4%, with all-cause and CO-related mortalities of 2.8% and 0.2%, separately. CONCLUSIONS: CO shared similar characteristics with extremity chronic osteomyelitis, primarily affecting young males, with trauma and diabetic foot as the leading causes and Staphylococcus aureus as the most frequently detected pathogen. Despite surgery being the primary treatment modality, clinical outcomes remained unsatisfactory, marked by high rates of infection recurrence and limb amputation.

Per- and polyfluoroalkyl substances and organofluorine in lakes and waterways of the northwestern Great Basin and Sierra Nevada.

Per- and polyfluoroalkyl substances (PFAS) are anthropogenic chemicals that occur ubiquitously in the environment and have been linked to numerous adverse health effects in humans and aquatic organisms. Although numerous environmental monitoring studies have been conducted, only one has evaluated PFAS in surface waters of the northwestern Great Basin, which features unique topography that results in dozens of endorheic basins and terminal lakes with no natural outlet, where PFAS may accumulate. To close this knowledge gap, we evaluated the occurrence of PFAS in grab samples from 15 lakes (headwater and terminal lakes) and 10 rivers in the Great Basin located in Nevada and California of the United States. PFAS and organofluorine were quantified by liquid chromatography tandem mass spectroscopy (LC-MS/MS) and combustion ion chromatography, respectively. The highest concentrations of PFAS occurred in samples taken near sites with known or suspected prior aqueous film forming foam (AFFF) application (~20 to 4754 ng/L). Samples near wastewater treatment plants and in urban areas also tended to have PFAS concentrations greater than those measured in remote, less anthropogenically influenced areas (~2 to 15 ng/L, <3 ng/L respectively). In limited snapshot sampling events PFAS appeared to accumulate in terminal lakes to some extent; in-lake concentrations were two to five times greater than those of their inflows. Fluorotelomer sulfonates were present downstream of a known AFFF application area likely to have had fluorotelomer-based foams applied to it, and the concentrations decayed in a predictable manner, suggesting they may be used as an indicator of PFAS transport away from an AFFF source. In all but two samples, organofluorine concentrations were greater than the sum of targeted PFAS (on a F basis) (median of 0.6 % of organofluorine identified via LC-MS/MS), although there was considerable variability in organofluorine measured in replicate samples.

Similarities and Differences Between Diabetes-Related and Trauma-Related Calcaneal Osteomyelitis: Comparisons Based on 681 Reported Cases.

Background: Current information were still limited regarding clinical characteristics, diagnosis, and treatment efficacy of calcaneal osteomyelitis (CO). The present study summarized similarities and differences between diabetes-related CO (DRCO) and trauma-related CO (TRCO) based on synthesis analysis of literature-reported cases. Methods: We searched the PubMed, Embase, and Cochrane Library databases to find English studies reporting DRCO and TRCO published between January 2000 and December 2021. Effective data were extracted and synthesized for comparisons. Results: Altogether 108 studies with 278 DRCO and 403 TRCO patients were analyzed. The ratio of females among the DRCO patients was significantly higher than that of the TRCO patients (37.4% vs 24.3%, P < 0.001). The median age at diagnosis of the DRCO patients was statistically older than the TRCO patients (56 vs 44 years, P < 0.001). The median symptom duration of the DRCO patients was longer than the TRCO patients (4 vs 2 months, P = 0.136), with ulcer and sinus as the top symptoms for the DRCO and TRCO patients, respectively. The positive rate of pathogen culture for the DRCO patients was significantly higher than that for the TRCO patients (94.8% vs 69.5%, P < 0.001). The DRCO patients had higher risks of infection relapse (32.3% vs 16.3%, P < 0.001) and amputation (24.8% vs 1.4%, P < 0.001), and a higher all-cause mortality (4.9% vs 1.3%, P = 0.03) than the TRCO patients. Conclusion: DRCO and TRCO shared similar and different clinical features and diagnostic issues. However, compared with TRCO, the clinical efficacy and prognosis of DRCO were worse.

TWIST1 rescue calcium overload and apoptosis induced by inflammatory microenvironment in S. aureus-induced osteomyelitis.

Currently, there is no effective therapy for Staphylococcus aureus-induced osteomyelitis. It is widely recognized that the inflammatory microenvironment around abscess plays an essential role in protracting the course of S. aureus-induced osteomyelitis. In this study, we found TWIST1 was highly expressed in macrophages around abscesses but less related to local S. aureus in the later stages of Staphylococcus aureus-infected osteomyelitis. Mouse bone marrow macrophages show apoptosis and elevated TWIST1 expression when treated with the inflammatory medium. Knockdown of TWIST1 induced macrophage apoptosis, impaired the bacteria phagocytosis/killing abilities, and promoted cell apoptosis markers expression in inflammatory microenvironment stimulation. Furthermore, inflammatory microenvironments were responsible for inducing calcium overload in macrophage mitochondrial while calcium overload inhibition significantly rescued macrophage apoptosis, bacteria phagocytosis/killing abilities and improved the mice's antimicrobial ability. Our findings indicated that TWIST1 is a crucial molecule that protects macrophages from calcium overload induced by inflammatory microenvironments.

Dysfunction of GluN3A subunit is involved in depression-like behaviors through synaptic deficits.

BACKGROUND: N-methyl-d-aspartate receptor (NMDAR) has been implicated in the pathophysiology of depression. However, as the unique inhibitory subunit of NMDARs, the role of GluN3A in depression is largely unclear. METHODS: Firstly, expression of GluN3A was examined in a mouse model of depression induced by chronic restraint stress (CRS). Then, rescue experiment with rAAV-Grin3a injection into hippocampus of CRS mice was carried out. Lastly, GluN3A knockout (KO) mouse was generated via CRISPR/Cas9 technique, and the molecular mechanism underlying involvement of GluN3A in depression was initially explored using RNA-seq technique, RT-PCR and western blotting. RESULTS: GluN3A expression in hippocampus was significantly decreased in CRS mice. Depression-like behaviors induced by CRS were ameliorated when the decrease of GluN3A expression in mice exposed to CRS was restored. GluN3A KO mice exhibited symptoms of anhedonia reported as reduced sucrose preference, and symptoms of despair assayed by a longer immobility time in FST. Transcriptome analysis revealed genetic ablation of GluN3A was associated with downregulation of genes implicated in synapse and axon development. Postsynaptic protein PSD95 was decreased in GluN3A KO mice. More importantly, reduction of PSD95 in CRS mice can be rescued by viral mediated Grin3a re-expression. LIMITATIONS: The mechanism underlying GluN3A involvement in depression is not fully determined. CONCLUSIONS: Our data suggested that GluN3A dysfunction is involved in depression, which might be mediated by synaptic deficits. These findings will facilitate the understanding of the role of GluN3A in depression, and they might provide a new strategy for the development of subunit-selective NMDAR antagonists as antidepressant drugs.

The Role of Senescence-Associated Secretory Phenotype in Bone Loss.

As the population of most nations have a large proportion of older individuals, there is an increase in the prevalence of osteoporosis. Consequently, scientists have focused their attention on the pathogenic mechanisms of osteoporosis. Owing to an increase in studies on cellular senescence in recent years, research has begun to focus on the function of the senescent microenvironment in osteoporosis. With chronic inflammation, senescent cells in the bone marrow secrete a series of factors known as senescence-associated secretory phenotype (SASP) factors, acting on their own or surrounding healthy cells and consequently exacerbating ageing.The components of the SASP may differ depending on the cause of osteoporosis. This review aimed to summarize the relationship between SASP factors and osteoporosis and suggest new insights into the mechanistic investigation of osteoporosis.

High-Fat Diet Increases Bone Loss by Inducing Ferroptosis in Osteoblasts.

Current research suggests that chronic high-fat dietary intake can lead to bone loss in adults; however, the mechanism by which high-fat diets affect the development of osteoporosis in individuals is unclear. As high-fat diets are strongly associated with ferroptosis, whether ferroptosis mediates high-fat diet-induced bone loss was the focus of our current study. By dividing the mice into a high-fat diet group, a high-fat diet + ferroptosis inhibitor group and a normal chow group, mice in the high-fat group were given a high-fat diet for 12 weeks. The mice in the high-fat diet + ferroptosis inhibitor group were given 1 mg/kg Fer-1 per day intraperitoneally at the start of the high-fat diet. Microscopic CT scans, histological tests, and biochemical indicators of ferroptosis were performed on bone tissue from all three groups at the end of the modelling period. Mc3t3-E1 cells were also used in vitro and divided into three groups: high-fat medium group, high-fat medium+ferroptosis inhibitor group, and control group. After 24 hours of incubation in high-fat medium, Mc3t3-E1 cells were assayed for ferroptosis marker proteins and biochemical parameters, and osteogenesis induction was performed simultaneously. Cellular alkaline phosphatase content and expression of osteogenesis-related proteins were measured at day 7 of osteogenesis induction. The results showed that a high-fat diet led to the development of femoral bone loss in mice and that this process could be inhibited by ferroptosis inhibitors. The high-fat diet mainly affected the number of osteoblasts produced in the bone marrow cavity. The high-fat environment in vitro inhibited osteoblast proliferation and osteogenic differentiation, and significant changes in ferroptosis-related biochemical parameters were observed. These findings have implications for the future clinical treatment of bone loss caused by high-fat diets.

Antimicrobial potency, prevention ability, and killing efficacy of daptomycin-loaded versus vancomycin-loaded ß-tricalcium phosphate/calcium sulfate for methicillin-resistant Staphylococcus aureus biofilms.

Growing evidence has shown that the efficacy of systemic administration of daptomycin for the treatment of methicillin-resistant Staphylococcus aureus (MRSA)-related infections is satisfactory. However, the clinical efficacy of the local administration of daptomycin for the management of osteoarticular infections remains unclear. This in vitro study compared the efficacy of daptomycin and vancomycin against MRSA biofilms. The elution kinetics of daptomycin and vancomycin, combined with gentamicin and loaded with either ß-tricalcium phosphate/calcium sulfate or calcium sulfate, in the presence of MRSA infection, was assessed. Their efficacy in preventing biofilm formation and killing pre-formed biofilms was assessed using colony-forming unit count and confocal laser scanning microscopy. In addition, the efficacy of daptomycin, vancomycin, and gentamicin in prophylaxis and eradication of MRSA biofilms was also evaluated. Daptomycin + gentamicin and vancomycin + gentamicin displayed similar antimicrobial potency against MRSA, by either ß-tricalcium phosphate/calcium sulfate or calcium sulfate. In the prevention assays, both daptomycin + gentamicin and vancomycin + gentamicin showed similar efficacy in preventing bacterial colony formation, with approximately 6 logs lower colony-forming units than those in the control group at both 1 and 3 days. The killing effect on pre-formed biofilms showed significant decreases of approximately 4 logs at 1 and 3 days following treatment with daptomycin + gentamicin and vancomycin + gentamicin. In addition, the confocal laser scanning microscopy results support the colony-forming unit data. Moreover, single use of vancomycin and gentamicin showed similar efficacies in preventing and killing MRSA biofilms, both of which were better than that of gentamicin. Our study demonstrated that vancomycin + gentamicin and daptomycin + gentamicin loaded with ß-tricalcium phosphate/calcium sulfate or calcium sulfate showed similar prophylactic and killing effects on MRSA biofilms, implying a potential indication of local administration daptomycin for the treatment of MRSA-associated osteoarticular infections, especially if vancomycin administration presents limitations.

Higher serum apolipoprotein B level will reduce the bone mineral density and increase the risk of osteopenia or osteoporosis in adults.

Objective: There is very limited evidence in the NHANES database linking serum apolipoprotein B and lumbar bone mineral density (BMD) in adults aged 20-59 years. There are few studies associating apolipoprotein B concentrations with BMD, and there is some debate about the association between obesity and BMD. Therefore, the purpose of this study was to determine the association between serum apolipoprotein B concentrations and lumbar spine BMD in adults aged 20-59 years and to predict its association with risk of osteopenia or osteoporosis. Methods: A cross-sectional study of the entire US ambulatory population was conducted using data from the National Health and Nutrition Examination Survey (NHANES) database. Weighted multiple regression equation models were used to assess the association between serum apolipoprotein B and lumbar BMD. A logistic weighted regression model was used to assess the association between serum apolipoprotein B concentrations and risk of osteopenia or osteoporosis. Subsequent stratified analyses were performed to refine the primary population of association. Results: Our study showed a significant negative association between serum apolipoprotein B concentration and lumbar BMD and a significant positive association with the risk of osteoporosis or osteopenia in the total population. After stratifying by sex, age and race, we concluded differently. The association of serum apolipoprotein B concentration with lumbar spine BMD and risk of osteopenia or osteoporosis was significant in male, but not in female. After stratification by age, the negative association between serum apolipoprotein B concentrations and lumbar BMD and the positive association with risk of osteopenia or osteoporosis was more significant in the 30-39 and 50-59 years age groups. When stratified by race, serum apolipoprotein B concentrations were significantly negatively associated with lumbar BMD and positively associated with risk of osteopenia or osteoporosis in Mexican American and non-Hispanic black populations. Thus, these findings suggest that these associations are influenced by sex, age, and race, respectively. Conclusion: Our results suggest that the association between serum apolipoprotein B levels and the risk of lumbar BMD and osteopenia or osteoporosis varies by sex, age, and race. In men, elevated serum apolipoprotein B levels were negative for bone quality. Elevated serum apolipoprotein B levels in the age groups 30-39 and 50-59 years also had a negative effect on bone quality. In the Mexican American and Non-Hispanic Black populations, elevated serum apolipoprotein B levels also had a significant negative effect on bone quality.

The Influence Exerted by Time Frames on Consumers' Willingness to Buy Nearly Expired Food.

With the development of Internet e-commerce channels, online shopping platforms have become the main channel for consumers to buy nearly expired food. Date labels, as one of the main external clues, play a decisive role in nearly expired food purchasing. Therefore, based on attention-related theory, this study attempts to explore the influence exerted by different time frames on consumers' willingness to buy and its mechanism. The results show that compared with the date, consumers have a higher willingness to buy nearly expired food when the expiration time is framed by delay. More specifically, compared to the date, the delay causes the individual to have a longer time perception, thus more preference for nearly expired food. Meanwhile, the mediating effect of time perception is moderated by food type. The conclusion of this research is helpful to expand the theoretical framework of time frames and related fields on nearly expired food, as well as provide practical guidance for marketers to effectively promote nearly expired food.