Optimizing the management of electrophysiology labs in Chinese hospitals using a discrete event simulation tool.

BACKGROUND: The growing demand for electrophysiology (EP) treatment in China presents a challenge for current EP care delivery systems. This study constructed a discrete event simulation (DES) model of an inpatient EP care delivery process, simulating a generalized inpatient journey of EP patients from admission to discharge in the cardiology department of a tertiary hospital in China. The model shows how many more patients the system can serve under different resource constraints by optimizing various phases of the care delivery process. METHODS: Model inputs were based on and validated using real-world data, simulating the scheduling of limited resources among competing demands from different patient types. The patient stay consists of three stages, namely: the pre-operative stay, the EP procedure, and the post-operative stay. The model outcome was the total number of discharges during the simulation period. The scenario analysis presented in this paper covers two capacity-limiting scenarios (CLS): (1) fully occupied ward beds and (2) fully occupied electrophysiology laboratories (EP labs). Within each CLS, we investigated potential throughput when the length of stay or operative time was reduced by 10%, 20%, and 30%. The reductions were applied to patients with atrial fibrillation, the most common indication accounting for almost 30% of patients. RESULTS: Model validation showed simulation results approximated actual data (137.2 discharges calculated vs. 137 observed). With fully occupied wards, reducing pre- and/or post-operative stay time resulted in a 1-7% increased throughput. With fully occupied EP labs, reduced operative time increased throughput by 3-12%. CONCLUSIONS: Model validation and scenario analyses demonstrated that the DES model reliably reflects the EP care delivery process. Simulations identified which phases of the process should be optimized under different resource constraints, and the expected increases in patients served.

Amyloid Protein Cross-Seeding Provides a New Perspective on Multiple Diseases In Vivo.

Amyloid protein cross-seeding is a peculiar phenomenon of cross-spreading among different diseases. Unlike traditional infectious ones, diseases caused by amyloid protein cross-seeding are spread by misfolded proteins instead of pathogens. As a consequence of the interactions among misfolded heterologous proteins or polypeptides, amyloid protein cross-seeding is considered to be the crucial cause of overlapping pathological transmission between various protein misfolding disorders (PMDs) in multiple tissues and cells. Here, we briefly review the phenomenon of cross-seeding among amyloid proteins. As an interesting example worth mentioning, the potential links between the novel coronavirus pneumonia (COVID-19) and some neurodegenerative diseases might be related to the amyloid protein cross-seeding, thus may cause an undesirable trend in the incidence of PMDs around the world. We then summarize the theoretical models as well as the experimental techniques for studying amyloid protein cross-seeding. Finally, we conclude with an outlook on the challenges and opportunities for basic research in this field. Cross-seeding of amyloid opens up a new perspective in our understanding of the process of amyloidogenesis, which is crucial for the development of new treatments for diseases. It is therefore valuable but still challenging to explore the cross-seeding system of amyloid protein as well as to reveal the structural basis and the intricate processes.

Association of smoking with brain gray and white matter volume: a Mendelian randomization study.

BACKGROUND: Observational studies have found a significant association between smoking and smaller gray matter volume, but this finding was limited by the reverse causality bias and possible confounding factors. Therefore, we conducted a Mendelian randomization (MR) study to explore the causal association of smoking with brain gray and white matter volume from a genetic perspective, and to investigate the possible mediators influencing the association. METHODS: Smoking initiation (ever being a regular smoker) was used as the primary exposure from the GWAS & Sequencing Consortium of Alcohol and Nicotine use in up to 1,232,091 individuals of European descent. Their associations with brain volume were acquired from a recent genome-wide association study of brain imaging phenotypes conducted among 34,298 individuals of the UK Biobank. The random-effects inverse-variance weighted method was applied as the main analysis. Multivariable MR analysis was performed to assess the potential interference of confounding factors on causal effect. RESULTS: Genetic liability to smoking initiation was significantly associated with lower gray matter volume (beta, -0.100; 95% CI, -0.156 to -0.043; P=5.23×10-4) but not with white matter volume. Multivariable MR results suggested that the association with lower gray matter volume might be mediated by alcohol drinking. Regarding localized gray matter volume, genetic liability to smoking initiation was associated with lower gray matter volume in left superior temporal gyrus, anterior division and right superior temporal gyrus, posterior division. CONCLUSIONS: This MR study supports the association between smoking and lower gray matter volume, and highlights the importance of never smoking.

Dorsolateral medullary infarction registry: a study protocol for a prospective, multicentric registry.

BACKGROUND: Dorsolateral medullary infarction is a typical cerebral infarction which is characterized by Wallenberg's syndrome. Neurotrophic keratopathy is an uncommon consequence of dorsolateral medullary infarction. At present, the protocol is aimed to study the dynamic changes in corneal innervation and the ocular surface environment after dorsolateral medullary infarction. METHODS: This study will involve consecutive data from all medical records of patients within 7 days of acute dorsolateral medullary infarction onset at the Departments of Neurology from 10 collaborating stroke centers. Eligible patients will mainly be characterized based on detailed physical examinations, multimodal imaging, and corneal related examinations and patients will be followed-up for 2 years. Neurotrophic keratopathy after dorsolateral medullary infarction is the primary endpoint. The dynamic histological corneal innervation and ocular surface environment after dorsolateral medullary infarction will be observed during the follow-up period. DISCUSSION: This multicentric, prospective registry is the first to identify and characterize the dynamic changes of corneal innervation and the ocular surface environment after acute dorsolateral medullary infarction. The significance of the study is to emphasize that the curative effect is based on the doctors' identification of the disease in the earliest stage before irreversible damage occurs to the cornea. TRIAL REGISTRATION: The registry was registered ( ChiCTR-OPC-17,011,625 ) on June 11, 2017.

Searching for conditions of protein self-assembly by protein crystallization screening method.

The self-assembly of biomacromolecules is an extremely important process. It is potentially useful in the fields of life science and materials science. To carry out the study on the self-assembly of proteins, it is necessary to find out the suitable self-assembly conditions, which have always been a challenging task in practice. Inspired by the screening technique in the field of protein crystallization, we proposed using the same screening technique for seeking suitable protein self-assembly conditions. Based on this consideration, we selected 5 proteins (ß-lactoglobulin, hemoglobin, pepsin, lysozyme, α-chymotrypsinogen (II) A) together with 5 screening kits (IndexTM, BML, Morpheus, JCSG, PEG/Ion ScreenTM) to investigate the performance of these crystallization screening techniques in order to discover new optimized conditions of protein self-assembly. The screens were all kept at 293 K for certain days, and were analyzed using optical microscope, scanning electron microscope, transmission electron microscope, atomic force microscope, fluorescence microscope, and atomic absorption spectroscope. The results demonstrated that the method of protein crystallization screening can be successfully applied in the screening of self-assembly conditions. This method is fast, high throughput, and easily implemented in an automated system, with a low protein consumption feature. These results suggested that such strategy can be applied to finding new conditions or forms in routine research of protein self-assembly. KEY POINTS: • Protein crystallization screening method is successfully applied in the screening of self-assembly conditions. • This screening method can be applied on various kinds of proteins and possess a feature of low protein consumption. • This screening method is fast, high throughput, and easily implemented in an automated system.

Metabolomics and correlation network analyses of core biomarkers in type 2 diabetes.

The identification of metabolic pathways and the core metabolites provide novel molecular targets for the prevention and treatment of diseases. Diabetes is often accompanied with multiple metabolic disorders including hyperglycemia and dyslipidemia. Analysis of the variances of plasma metabolites is critical for identifying potential therapeutic targets for diabetes. In the current study, non-diabetic subjects with normal glucose tolerance and diabetics (age 40-60 years; n = 42 per group) were selected and plasma samples were analyzed by GC-MS for various metabolites profiling followed by network analysis. Our study identified 24 differential metabolites that were mainly enriched in protein synthesis, lipid and amino acid metabolism. Furthermore, we applied the correlation network analysis on these differential metabolites in fatty acid and amino acid metabolism and identified glycerol, alanine and serine as the hub metabolites in diabetic group. In addition, we measured the activities of enzymes in gluconeogenesis and amino acid metabolism and found significant higher activities of fructose 1,6-bisphosphatase, pyruvate carboxylase, lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase in diabetic patients. In contrast, the enzyme activities of glycolysis pathway (e.g., hexokinase, phosphofructokinase and pyruvate kinase) and TCA cycle (e.g., isocitrate dehydrogenase, succinate dehydrogenase, fumarate hydratase and malate dehydrogenase) were reduced in diabetes. Together, our studies showed that the linoleic acid and amino acid metabolism were the most affected metabolic pathways and glycerol, alanine and serine could play critical role in diabetes. The integration of network analysis and metabolic data could provide novel molecular targets or biomarkers for diabetes.

Risk factors affecting the 1-year outcomes of minor ischemic stroke: results from Xi'an stroke registry study of China.

BACKGROUND: The prevalence of stroke recurrence, disability, and all-cause mortality of patients with minor ischemic stroke (MIS) remains problematic. The aim of the present study was to identify risk factors associated with adverse outcomes at 1 year after MIS in the Xi'an region of China. METHODS: This prospective cohort study included MIS patients above 18 years old with National Institutes of Health Stroke Scale (NIHSS) score ≤ 3 who were treated in any of four hospitals in Xi'an region of China between January and December 2015. The 1-year prevalence of stroke recurrence, disability, and all-cause mortality were evaluated, respectively. Multivariate logistic regression analysis was performed to assess the association between the identified risk factors and clinical outcomes. RESULTS: In this study, 131(10.5%, 131/1252) patients were lost to follow-up at 1 year. A total of 1121 patients were included for analysis, the prevalence of stroke recurrence, disability, and all-cause mortality at 1 year after MIS were 3.4% (38/1121), 9.3% (104/1121), and 3.3% (37/1121), respectively. Multivariate logistic regression analysis identified age, current smoking, and pneumonia as independent risk factors for stroke recurrence. Age, pneumonia, and alkaline phosphatase were independent risk factors for all-cause mortality. Independent risk factors for disability were age, pneumonia, NIHSS score on admission, and leukocyte count. CONCLUSIONS: The 1-year outcomes of MIS in Xi'an region of China were not optimistic, especially with a high prevalence of disability. The present study indicated that age and pneumonia were the common independent risk factors affecting the 1-year outcomes of MIS in Xi'an region of China.

High-salt diet affects amino acid metabolism in plasma and muscle of Dahl salt-sensitive rats.

Genetic background and high-salt diet are considered key factors contributing to the development of hypertension and its associated metabolic disorders. Metabolomics is an emerging powerful tool to analyze the low-molecular weight metabolites in plasma and tissue. This study integrated metabolomics and correlation network analysis to investigate the metabolic profiles of plasma and muscle of Dahl salt-sensitive (SS) rats and SS.13BN rats (control) under normal and high-salt diet. The hub metabolites, which could play important roles in the metabolic changes, were identified by correlation network analysis. The results of the network analysis were further confirmed by pathway analysis and enzyme activity analysis. The results indicated a higher amino acid levels in both plasma and muscle of SS rats fed with high-salt diet. Alanine was found as a hub metabolite with the highest score of three centrality indices and also as the significant differential metabolite in plasma of SS rats after high-salt diet. Valine and lysine were found as hub metabolites and differential metabolites in muscle of SS rats after high-salt diet. Amino acid levels increased in both plasma and muscle of SS rats fed with a high salt diet. Moreover, alanine in plasma and valine and lysine in muscle as hub metabolites could play important roles in the response to high-salt diet.

Exogenous FGF2 reverses depressive-like behaviors and restores the suppressed FGF2-ERK1/2 signaling and the impaired hippocampal neurogenesis induced by neuroinflammation.

Our previous work demonstrated that neuroinflammation evoked by triple repeated central LPS challenges inhibited adult hippocampal neurogenesis that were correlated with the depressive-like behavioral symptoms induced by neuroinflammation. These findings suggest that hippocampal neurogenesis might be one of biological mechanisms underlying depression induced by neuroinflammation and targeting neurogenesis might lead to new therapeutic strategies for the treatment of depression. In this study, we manipulated adult hippocampal neurogenesis using fibroblast growth factor 2 (FGF2), one crucial molecule modulating cell proliferation and survival in central nervous system, and investigate the involvement and the potential therapeutic effects of FGF2 on neuroinflammation-induced depression. Central lipopolysaccharides (LPS) challenges were used as previously to evoke the neuroinflammatory state in the brain of rat. Exogenous FGF2 was infused into lateral ventricle during the neuroinflammatory state. It was found that the protein expression of FGF2 in hippocampus was inhibited by neuroinflammation. The activation of extracellular signal-regulated kinase (ERK), the downstream molecule of FGF2, was also inhibited by neuroinflammation. Exogenous FGF2 infusions prevented the decrease in phosphorylation of ERK1/2 under neuroinflammation state. Exogenous FGF2 reversed depressive-like behaviors and the impaired hippocampal neurogenesis induced by neuroinflammation. These findings provide evidence that the FGF2-ERK1/2 pathway is involved in the pathophysiology of depressive-like behaviors, and manipulating the neurogenesis pathway is a viable therapeutic approach to inflammation-associated depression.

Specificity may count: not every aspect of coping self-efficacy is beneficial to quality of life among Chinese cancer survivors in China.

BACKGROUND: General self-efficacy has been shown to be a protective factor of cancer survivors' quality of life (QoL). Coping self-efficacy includes multiple aspects, such as maintaining positive attitudes, regulating emotion, seeking social support, and seeking medical information. How these various aspects are related to multiple domains of QoL is unclear. PURPOSE: This study examined the associations between different aspects of coping self-efficacy and QoL among Chinese cancer survivors. METHODS: A sample of 238 Chinese cancer survivors (mean age = 55.7, 74.4 % female) in Beijing, China participated in the survey. Coping self-efficacy and QoL were measured by the Cancer Behavior Inventory and Quality of Life-Cancer Survivor Instrument. RESULTS: After controlling for demographic and disease-related variables, hierarchical regression analyses showed that coping self-efficacy in accepting cancer/maintaining a positive attitude was positively associated with physical, psychological, and spiritual QoL. Self-efficacy in affective regulation was positively associated with psychological and social QoL, but negatively associated with spiritual well-being. Self-efficacy in seeking support was positively associated with spiritual well-being, but negatively associated with physical QoL. Self-efficacy in seeking and understanding medical information was negatively associated with psychological and social QoL. CONCLUSIONS: Our findings imply the specificity of coping self-efficacy in predicting QOL. Our findings could be helpful for designing future interventions. Increasing cancer survivors' self-efficacies in accepting cancer/maintaining a positive attitude, affective regulation, and seeking support may improve cancer survivors' QoL depending on the specific domains.

Asynchronous adaptive event-triggered fault detection for delayed Markov jump neural networks: A delay-variation-dependent approach.

This paper presents a delay-variation-dependent approach to fault detection of a discrete-time Markov jump neural network (MJNN) with a time-varying delay and mismatched modes. The goal is to detect the potential fault of delayed MJNNs by constructing an appropriate adaptive event-triggered and asynchronous H∞ filter. By choosing a delay-product-type Lyapunov-Krasovskii (L-K) functional with a delay-dependent matrix and exploiting some matrix polynomial inequalities, bounded real lemmas (BRLs) are obtained on the existence of suitable adaptive event generator and filters. These BRLs are dependent not only on the delay bounds but also on the delay variation rate. Simulation results are given to show the validity of the proposed theoretical method.

High-efficiency antibacterial calcium alginate/lysozyme/AgNPs composite sponge for wound healing.

Infection poses a significant barrier to effective wound repair, leading to increased inflammatory responses that ultimately result in incomplete and prolonged wound healing. To address this challenge, numerous antibacterial ingredients have been incorporated into dressings to inhibit wound infection. Our previous work demonstrated that lysozyme/silver nanoparticles (LYZ/AgNPs) complexes, prepared using an eco-friendly one-step aqueous method, exhibited excellent antibacterial efficacy with favorable biosafety. To further explore its potential application in advancing wound healing, calcium alginate (CA) with good porosity, water absorption, and water retention capacities was formulated with LYZ/AgNPs to prepare composite sponge (CA/LYZ/AgNPs). As expected, in vivo experiments involving full-thickness skin wound and scald wound healing experiments demonstrated that CA-LYZ-AgNPs composite sponges with excellent biocompatibility exhibited remarkable antibacterial activity against gram-positive bacteria, gram-negative bacteria and fungi, and outperformed the wound healing process efficacy of other commercially available AgNPs-loaded wound dressings. In summary, this work introduces a CA/LYZ/AgNPs sponge featuring exceptional antibacterial efficacy and biocompatibility, thus holding promising potential in wound care applications.

Kounis syndrome caused by bee sting: a case report and literature review.

Kounis syndrome is defined as an acute coronary syndrome (ACS) secondary to allergic or hypersensitivity reactions. It can be further categorised into subtypes such as coronary vasospasms, acute myocardial infarction or stent thrombosis based on the pathogenesis. Kounis syndrome is most likely an underdiagnosed condition in China, given the many triggers reported in the literature. Herein, we report a case of Kounis syndrome, possibly triggered by a bee sting. The patient had late onset of angina symptoms with delayed diagnosis due to unfamiliarity with this condition. In patients with clinical signs of ACS that are superimposed on a hypersensitivity reaction, especially those with pre-existing cardiovascular risk factors, Kounis syndrome should be considered, so that appropriate assessment and treatment can be initiated. Prompt management of both the allergic reaction and the ACS is vital for Kounis syndrome.

Magnetic Fields Reduce Apoptosis by Suppressing Phase Separation of Tau-441.

The biological effects of magnetic fields (MFs) have been a controversial issue. Fortunately, in recent years, there has been increasing evidence that MFs do affect biological systems. However, the physical mechanism remains unclear. Here, we show that MFs (16 T) reduce apoptosis in cell lines by inhibiting liquid-liquid phase separation (LLPS) of Tau-441, suggesting that the MF effect on LLPS may be one of the mechanisms for understanding the "mysterious" magnetobiological effects. The LLPS of Tau-441 occurred in the cytoplasm after induction with arsenite. The phase-separated droplets of Tau-441 recruited hexokinase (HK), resulting in a decrease in the amount of free HK in the cytoplasm. In cells, HK and Bax compete to bind to the voltage-dependent anion channel (VDAC I) on the mitochondrial membrane. A decrease in the number of free HK molecules increased the chance of Bax binding to VDAC I, leading to increased Bax-mediated apoptosis. In the presence of a static MF, LLPS was marked inhibited and HK recruitment was reduced, resulting in an increased probability of HK binding to VDAC I and a decreased probability of Bax binding to VDAC I, thus reducing Bax-mediated apoptosis. Our findings revealed a new physical mechanism for understanding magnetobiological effects from the perspective of LLPS. In addition, these results show the potential applications of physical environments, such as MFs in this study, in the treatment of LLPS-related diseases.

Curcumin inhibits liquid-liquid phase separation of fused in sarcoma and attenuates the sequestration of pyruvate kinase to restore cellular metabolism.

The abnormal accumulation of fused in sarcoma (FUS) is a pathological hallmark in a proportion of patients with frontotemporal dementia and amyotrophic lateral sclerosis. Therefore, the clearance of FUS aggregates is a possible therapeutic strategy for FUS-associated neurodegenerative diseases. This study reports that curcumin can strongly suppress FUS droplet formation and stress granule aggregation of FUS. Fluorescence spectra and isothermal titration calorimetry showed that curcumin can bind FUS through hydrophobic interactions, thereby reducing the ß-sheet content of FUS. Aggregated FUS sequesters pyruvate kinase, leading to reduced ATP levels. However, results from a metabolomics study revealed that curcumin changed the metabolism pattern and differentially expressed metabolites were enriched in glycolysis. Curcumin attenuated FUS aggregation-mediated sequestration of pyruvate kinase and restored cellular metabolism, consequently increasing ATP levels. These results indicate that curcumin is a potent inhibitor of FUS liquid-liquid phase separation and provide novel insights into the effect of curcumin in ameliorating abnormal metabolism.

Plasma lncRNA LIPCAR Expression Levels Associated with Neurological Impairment and Stroke Subtypes in Patients with Acute Cerebral Infarction: A Prospective Observational Study with a Control Group.

INTRODUCTION: This prospective observational study with a control group aimed to compare the plasma levels of long non-coding RNA (lncRNA) LIPCAR between patients with acute cerebral infarction (ACI) and healthy controls, and to assess the prognostic abilities of LIPCAR for adverse outcomes of patients with ACI at 1-year follow-up. METHODS: Eighty patients with ACI, of whom 40 had large artery atherosclerosis (LAA) and 40 had cardioembolism (CE) and who were hospitalized at Xi'an No. 1 Hospital from July 2019 to June 2020, were selected as the case group. Age- and sex-matched non-stroke patients from the same hospital throughout the same time period were chosen as the control group. Real-time quantitative reverse transcription polymerase chain reaction was used to measure the levels of plasma lncRNA LIPCAR. The correlations of LIPCAR expression among the LAA, CE, and control groups were assessed using Spearman's correlation analysis. Curve fitting and multivariate logistic regression were used to analyze the LIPCAR levels and 1-year adverse outcomes of patients with ACI and its subtypes. RESULTS: The expression of plasma LIPCAR in the case group was noticeably higher than that of the control group (2.42 ± 1.49 vs. 1.00 ± 0.47, p < 0.001). Patients with CE had considerably higher levels of LIPCAR expression than those with LAA. The National Institute of Health Stroke Scale score and modified Rankin scale score on admission were significantly positively correlated with LIPCAR expression in patients with CE and LAA. Furthermore, the correlation was stronger in patients with CE than in those with LAA, with correlation coefficients of 0.69 and 0.64, respectively. Curve fitting revealed a non-linear correlation between LIPCAR expression levels, 1-year recurrent stroke, all-cause mortalities, and poor prognoses, with a cut-off value of 2.2. CONCLUSION: The expression level of lncRNA LIPCAR may play a potential role in the identification of neurological impairment and CE subtype in patients with ACI. Increased 1-year risk of adverse outcomes may be associated with high levels of LIPCAR expression.

Acute cerebral infarction is the second-leading cause of death worldwide. Therefore, available diagnostic and prognostic tools are of the utmost importance. It is easy to acquire hematologic biomarkers and to provide direct information related to the severity of brain injury and the risk of stroke. However, it has been shown that the study of hematologic markers in aspects of both identifying stroke subtypes and predicting neurological impairment are still few and imperfect in clinical application of stroke prognosis. The long non-coding RNA LIPCAR plays an important role in the pathophysiology of cardiovascular disease. Nonetheless, to date, no exploration has been carried out on the correlation between lncRNA LIPCAR, severity on admission, and prognosis of stroke subtypes. Thus, this study aimed to investigate the plasma levels of lncRNA LIPCAR expression and their correlations in patients with acute cerebral infarction and its subtypes. Our results show that the plasma levels of LIPCAR expression of the patients with acute cerebral infarction were noticeably higher than those of the non-stroke control patients. Patients with cardioembolism subtype had considerably higher levels of LIPCAR expression than those with large artery atherosclerosis. The National Institute of Health Stroke Scale score and modified Rankin scale score on admission were significantly correlated with LIPCAR expression in patients with cardioembolism and large artery atherosclerosis; the correlation was stronger in patients with cardioembolism than in patients with large artery atherosclerosis, with correlation coefficients of 0.69 and 0.64, respectively. Furthermore, curve fitting revealed a non-linear correlation between LIPCAR expression levels and 1-year outcome events. The expression level of lncRNA LIPCAR may play a potential role in the identification of neurological impairment and cardioembolism subtype in patients with acute cerebral infarction.

History and main research of psychoneuroimmunology in China.

The concept of mind-body integration was born in China with a long history and is naturally compatible with the psychoneuroimmunology (PNI). Since PNI was introduced into China in the 1990s, increasingly Chinese researchers from different fields were attracted to the psychoneuroimmunology research of health and disease. This review includes two parts: in the first part, we summarize a brief history of the development of PNI in China from 1992 to 2012, which mainly happened before the establishment of PNIRSChina in 2013. In the second part, some representative studies in the different fields of PNI conducted in China are reviewed, mainly including conditioned immunity, emotional stress and immunity, and inflammation and depression.

Event-Triggered Fault Detection Filter Design for Discrete-Time Memristive Neural Networks With Time Delays.

In this article, the fault detection (FD) filter design problem is addressed for discrete-time memristive neural networks with time delays. When constructing the system model, an event-triggered communication mechanism is investigated to reduce the communication burden and a fault weighting matrix function is adopted to improve the accuracy of the FD filter. Then, based on the Lyapunov functional theory, an augmented Lyapunov functional is constructed. By utilizing the summation inequality approach and the improved reciprocally convex combination method, an FD filter that guarantees the asymptotic stability and the prescribed H∞ performance level of the residual system is designed. Finally, numerical simulations are provided to illustrate the effectiveness of the presented results.

Antibacterial activity of lysozyme-loaded cream against MRSA and promotion of scalded wound healing.

Staphylococcus aureus (S. aureus) infection, especially its drug-resistant bacterial infection, is a great challenge often faced by clinicians and patients, and it is also one of the most important threats to public health. Finding a safe and effective antibacterial agent is of great significance for the prevention and treatment of S. aureus infection. Lysozyme is known to have antibacterial effects against Gram-positive bacteria including S. aureus. Here, high-quality lysozyme with a purity of more than 99% and an activity of more than 60, 000 U/mg was prepared from egg white, which showed excellent antibacterial activity against three strains of S. aureus, especially against MRSA. Furthermore, an antibacterial cream loaded with lysozyme was prepared and tested in scald wound healing. The lysozyme-loaded cream exhibited the effect of preventing wound infection and promoting wound healing on scalds, and no toxicity was found in animal organs. Overall, lysozyme showed great application potential in the prevention and treatment of infections caused by S. aureus and scalded wound healing. The most remarkable discovery in this work is the unexpectedly powerful inhibitory effect of lysozyme on the drug-resistant bacterial, especially MRSA, which is usually very difficult to deal with using normal antibacterial drugs.

Chronic blockade of glucocorticoid receptors by RU486 enhances lipopolysaccharide-induced depressive-like behaviour and cytokine production in rats.

Although accumulating evidence supports a role for cytokines in the pathophysiology of depression, the cytokine hypothesis of depression is debatable. It has been suggested that neuroendocrine and immune systems acting in concert may have roles in the development and the maintenance of the disease. Glucocorticoid receptor (GR) is the key element which exerts both anti-inflammatory and cytokine-inhibiting effects. Whether functional changes of GR are involved in the pathophysiology of cytokine-induced depression remains elusive. In the present study, the effects of both acute and chronic GR blockade on depressive-like behaviour and cytokine production induced by lipopolysaccharides (LPS), cytokine inducer, were investigated in rats. Acute or chronic blockade of GR was achieved by a single administration or repeated administrations, respectively, of the GR antagonist RU486 (RU). Behavioural measurements, including saccharin preference, locomotor activity, and immobility time, were assessed. The serum levels of proinflammatory cytokines (TNFα, IL-1ß, and IFNγ) were determined by ELISA. The results showed that LPS induced significant but transient depressive-like behaviour. Repeated, but not single, administration of RU significantly enhanced and prolonged LPS-induced depressive-like behaviour and an increase in the serum production of TNFα and IFNγ. These results indicate that the effective blockade of GR enhanced the depressive-like behaviour induced by cytokines. Findings from this study suggest that GR dysfunction may be an important contributing factor to the development of cytokine-related depression. These findings add to the growing evidence of mechanisms by which cytokines influence depression.