Synergistic effect and mechanism of Cd(II) and As(III) adsorption by biochar supported sulfide nanoscale zero-valent iron.

Biochar derived from bamboo was used to support sulfide nanoscale zero-valent iron (S-nZVI@BC) for simultaneous removal of Cd(II) and As (III) from aqueous media. Scanning electron microscopy (SEM) and X-ray diffraction spectroscopy (XRD) characterization confirmed the successful synthesis of the S-nZVI@BC. Adsorption kinetics and isotherms indicated that co-adsorption of Cd(II) and As(III) onto S-nZVI@BC was well represented by pseudo-second-order model (R2Cd(II) = 0.990, R2As(III) = 0.995) and Langmuir model (R2Cd(II) = 0.954, R2As(III) = 0.936). The maximum adsorption was 162.365 and 276.133 mg/g for Cd(II) and As(III), respectively, in a co-adsorption system, which was significantly higher than that in a single adsorption system (103.195 and 223.736 mg/g, respectively). Batch experiments showed that the Cd(II)-to-As(III) concentration ratio significantly affected the co-adsorption with the optimal ratio of 1:2. Ca2+ and Mg2+ significantly inhibited Cd(II) removal. In contrast, phosphate and humic acid significantly inhibited As(III) removal. Electrochemical analysis indicated S-nZVI@BC had a lower corrosion potential and resistance than nZVI@BC, making it more conducive to electron transfer and chemical reaction. Electrostatic adsorption, complexation, co-precipitation, and redox were the primary mechanisms for Cd(II) and As(III) removal. Overall, the present study provides new insights into the synergistic removal of Cd(II) and As(III) by S-nZVI@BC, which is a very promising adsorbent for the effective removal of Cd(II) and As(III) from contaminated wastewater.

Porcine reproductive and respiratory syndrome virus regulates lipid droplet accumulation in lipid metabolic pathways to promote viral replication.

Porcine reproductive and respiratory syndrome (PRRS) is a severe respiratory disease caused by porcine reproductive and respiratory syndrome virus (PRRSV) that can lead to the abortion of pregnant sows and decreased boar semen quality. However, the mechanisms of PRRSV replication in the host have not yet been fully elucidated. As lipid metabolism and lipid droplets (LDs) have been reported to play important roles in the replication of various viruses, we aimed to explore the mechanisms through which LDs affect PRRSV replication. Laser confocal and transmission electron microscopy revealed that PRRSV infection promoted intracellular LD accumulation, which was significantly reduced by treatment with the NF-κB signaling pathway inhibitors BAY11-7082 and metformin hydrochloride (MH). In addition, treatment with a DGAT1 inhibitor significantly reduced the protein expression of Phosphorylated NF-ΚB P65and PIκB and the transcription of IL-1ß and IL-8 in the NF-κB signaling pathway. Furthermore, we showed that the reduction of the NF-κB signaling pathway and LDs significantly reduced PRRSV replication. Together, the findings of this study suggest a novel mechanism through which PRRSV regulates the NF-κB signaling pathway to increase LD accumulation and promote viral replication. Moreover, we demonstrated that both BAY11-7082 and MH can reduce PRRSV replication by reducing the NF-κB signaling pathway and LD accumulation. This study lays a theoretical foundation for research on the mechanism of PRRS prevention and control, as well as the research and development of antiviral drugs.

Association of mortality with fludrocortisone addition to hydrocortisone treatment among septic shock patients: a propensity score matching analysis.

Background: Several clinical trials of corticosteroids have been carried out in the treatment of septic shock, however, the therapeutic effect of the most widely used hydrocortisone is still controversial, and no studies have directly compared hydrocortisone versus hydrocortisone plus fludrocortisone for patients with septic shock. Methods: Baseline characteristics and treatment regimens of patients with septic shock treated with hydrocortisone from the Medical Information Mart for Intensive Care-IV database were collected. Patients were divided into hydrocortisone treatment groups and hydrocortisone plus fludrocortisone treatment groups. The primary outcome was 90-day mortality, and secondary outcomes included 28-day mortality, in-hospital mortality, length of hospital stay, and length of intensive care unit (ICU) stay. Binomial Logistic regression analysis was performed to identify independent risk factors for mortality. Survival analysis was performed and Kaplan-Meier curves were drawn for patients in different treatment groups. Propensity score matching (PSM) analysis was performed to reduce bias. Results: Six hundred and fifty three patients were enrolled, of which 583 were treated with hydrocortisone alone, and 70 with hydrocortisone plus fludrocortisone. After PSM, 70 patients were included in each group. The proportion of patients with acute kidney injury (AKI) and the proportion of renal replacement therapy (RRT) treatment in the hydrocortisone plus fludrocortisone group were higher than those in the hydrocortisone alone group, and there was no significant difference in other baseline characteristics. Compared with hydrocortisone alone, hydrocortisone plus fludrocortisone did not reduce the 90-day mortality (after PSM, relative risk/RR = 1.07, 95%CI 0.75-1.51), 28-day mortality (after PSM, RR = 0.82, 95%CI 0.59-1.14) and in-hospital mortality (after PSM, RR = 0.79, 95%CI 0.57-1.11) of the enrolled patients, nor did it affect the length of hospital stay (after PSM, 13.9 days vs. 10.9 days, p = 0.34) and ICU stay (after PSM, 6.0 days vs. 3.7 days, p = 0.14), and the survival analysis showed no statistically significant difference in the corresponding survival time. After PSM, binomial Logistic regression analysis showed that SAPS II score was an independent risk factor for 28-day morality (OR = 1.04, 95%CI 1.02-1.06, p < 0.01) and in-hospital morality (OR = 1.04, 95%CI 1.01-1.06, p < 0.01), while hydrocortisone plus fludrocortisone was not an independent risk factor for 90-day mortality (OR = 0.88, 95%CI 0.43-1.79, p = 0.72), 28-day morality (OR = 1.50, 95%CI 0.77-2.91, p = 0.24), or in-hospital morality (OR = 1.58, 95%CI 0.81-3.09, p = 0.18). Conclusion: In the treatment of patients with septic shock, hydrocortisone plus fludrocortisone did not reduce 90-day mortality, 28-day mortality, and in-hospital mortality compared with hydrocortisone alone, and had no effect on the length of hospital stay and ICU stay.

3D Printing and processing of miniaturized transducers with near-pristine piezoelectric ceramics for localized cavitation.

The performance of ultrasonic transducers is largely determined by the piezoelectric properties and geometries of their active elements. Due to the brittle nature of piezoceramics, existing processing tools for piezoelectric elements only achieve simple geometries, including flat disks, cylinders, cubes and rings. While advances in additive manufacturing give rise to free-form fabrication of piezoceramics, the resultant transducers suffer from high porosity, weak piezoelectric responses, and limited geometrical flexibility. We introduce optimized piezoceramic printing and processing strategies to produce highly responsive piezoelectric microtransducers that operate at ultrasonic frequencies. The 3D printed dense piezoelectric elements achieve high piezoelectric coefficients and complex architectures. The resulting piezoelectric charge constant, d33, and coupling factor, kt, of the 3D printed piezoceramic reach 583 pC/N and 0.57, approaching the properties of pristine ceramics. The integrated printing of transducer packaging materials and 3D printed piezoceramics with microarchitectures create opportunities for miniaturized piezoelectric ultrasound transducers capable of acoustic focusing and localized cavitation within millimeter-sized channels, leading to miniaturized ultrasonic devices that enable a wide range of biomedical applications.

Sleep problems mediate the influence of childhood emotional maltreatment on adolescent non-suicidal self-injury: The moderating effect of rumination.

BACKGROUND: Non-suicidal self-injury (NSSI) is a highly serious public health problem among adolescents in China, and childhood emotional maltreatment has been found to be a risk factor for NSSI. OBJECTIVE: Little is known about the longitudinal association between childhood emotional maltreatment and NSSI as well as its underlying mediating and moderating mechanisms. Thus, we hypothesized whether sleep problems mediated the association between childhood emotional maltreatment and NSSI, and whether this indirect effect was moderated by rumination. PARTICIPANTS AND SETTING: A total of 1987 Chinese adolescents (56.1 % males; ages 10 to 14, M = 12.32, SD = 0.53) completed self-report questionnaires regarding childhood emotional maltreatment, sleep problems, rumination non-suicidal self-injury (NSSI) in three waves. METHODS: Structural equation model was used to test a moderated mediation model, with gender, age and socioeconomic status and baseline measures as covariates. RESULTS: Childhood emotional maltreatment was significantly associated with NSSI, and this association was mediated by sleep problems. Moderated mediation analyses revealed that rumination intensified the relation between childhood emotional maltreatment and sleep problems as well as the relation between sleep problems and NSSI. CONCLUSIONS: Findings of this study demonstrate a relationship among childhood emotional maltreatment, sleep problems, rumination and NSSI. Interventions that target sleep problems and rumination may be beneficial for reducing NSSI for at-risk adolescents.

(NH4)2Mo3S13/MnFe2O4 hybrid with multiple active sites boosted activation of peroxymonosulfate for removal of tetracycline.

Advanced oxidation processes (AOPs) based on peroxymonosulfate (PMS) activation have attracted much attention in wastewater treatment. Here, a series of (NH4)2Mo3S13/MnFe2O4 (MSMF) composites were prepared and used as PMS activators to remove tetracycline (TC) for the first time. When the mass ratio of (NH4)2Mo3S13 to MnFe2O4 was 4.0 (MSMF4.0), the composite showed remarkable catalytic efficiency for activating PMS to remove TC. Over 93% of TC was removed in MSMF4.0/PMS system in 20 min. The aqueous •OH as well as the surface SO4•- and •OH were the primary reactive species for TC degradation in MSMF4.0/PMS system, and the comprehensive experimental results excluded the contributions of aqueous SO4•-, O2•-, and 1O2, high-valent metal-oxo species, and surface-bound PMS. The Mn(II)/Mn(III), Fe(II)/Fe(III), Mo(IV)/Mo(VI), and S2-/SOx2- all contributed to the catalytic process. MSMF4.0 also showed excellent activity and stability after five cycles and significant degradation efficiency for a variety of pollutants. This work will provide theoretical basis for applying MnFe2O4-based composites in PMS-based AOPs.

African Swine Fever Virus Envelope Glycoprotein CD2v Interacts with Host CSF2RA to Regulate the JAK2-STAT3 Pathway and Inhibit Apoptosis to Facilitate Virus Replication.

African swine fever (ASF) is a highly infectious disease caused by the African swine fever virus (ASFV) in swine. It is characterized by the death of cells in infected tissues. However, the molecular mechanism of ASFV-induced cell death in porcine alveolar macrophages (PAMs) remains largely unknown. In this study, transcriptome sequencing of ASFV-infected PAMs found that ASFV activated the JAK2-STAT3 pathway in the early stages and apoptosis in the late stages of infection. Meanwhile, the JAK2-STAT3 pathway was confirmed to be essential for ASFV replication. AG490 and andrographolide (AND) inhibited the JAK2-STAT3 pathway, promoted ASFV-induced apoptosis, and exerted antiviral effects. Additionally, CD2v promoted STAT3 transcription and phosphorylation as well as translocation into the nucleus. CD2v is the main envelope glycoprotein of the ASFV, and further investigations showed that CD2v deletion downregulates the JAK2-STAT3 pathway and promotes apoptosis to inhibit ASFV replication. Furthermore, we discovered that CD2v interacts with CSF2RA, which is a hematopoietic receptor superfamily member in myeloid cells and a key receptor protein that activates receptor-associated JAK and STAT proteins. In this study, CSF2RA small interfering RNA (siRNA) downregulated the JAK2-STAT3 pathway and promoted apoptosis to inhibit ASFV replication. Taken together, ASFV replication requires the JAK2-STAT3 pathway, while CD2v interacts with CSF2RA to regulate the JAK2-STAT3 pathway and inhibit apoptosis to facilitate virus replication. These results provide a theoretical basis for the escape mechanism and pathogenesis of ASFV. IMPORTANCE African swine fever is a hemorrhagic disease caused by the African swine fever virus (ASFV), which infects pigs of different breeds and ages, with a fatality rate of up to 100%. It is one of the key diseases affecting the global livestock industry. Currently, no commercial vaccines or antiviral drugs are available. Here, we show that ASFV replicates via the JAK2-STAT3 pathway. More specifically, ASFV CD2v interacts with CSF2RA to activate the JAK2-STAT3 pathway and inhibit apoptosis, thereby maintaining the survival of infected cells and promoting viral replication. This study revealed an important implication of the JAK2-STAT3 pathway in ASFV infection and identified a novel mechanism by which CD2v has evolved to interact with CSF2RA and maintain JAK2-STAT3 pathway activation to inhibit apoptosis, thus elucidating new information regarding the signal reprogramming of host cells by ASFV.

Rapid Vital Sign Extraction for Real-time Opto-physiological Monitoring at Varying Physical Activity Intensity Levels.

Robustness of physiological parameters obtained from photoplethysmographic (PPG) signals is highly dependent on a signal quality that is often affected by the motion artefacts (MAs) generated during physical activity. This study aims to suppress MAs and obtain reliable physiological readings using the part of the pulsatile signal, captured by a multi-wavelength illumination optoelectronic patch sensor (mOEPS), that minimizes the residual between the measured signal and the motion estimates obtained from an accelerometer. The minimum residual (MR) method requires the simultaneous collection of (1) multiple wavelength data from the mOEPS, and (2) motion reference signals from a triaxial accelerometer attached to the mOEPS. The MR method suppress those frequencies associated with motion in a manner that is easily embedded on a microprocessor. The performance of the method in reducing both in-band and out-of-band frequencies of MAs is evaluated through two protocols with 34 subjects engaged in the study. The MA-suppressed PPG signal, obtained through MR, enables the calculation of the heart rate (HR) with an average absolute error of 1.47 beats/min for the IEEE-SPC datasets, and the calculation of HR and respiration rate (RR) to 1.44 beats/min and 2.85 breaths/min respectively for our in-house datasets. Oxygen saturation (SpO 2) levels calculated from the minimum residual waveform are consistent with the expected values of ≥ 95%. The comparison with the reference HR and RR show errors with an absolute accuracy of and the Pearson correlation ( R) for HR and RR are 0.9976 and 0.9118 respectively. These outcomes demonstrate that MR is capable of effective suppression of MAs for a range of physical activity intensities and to achieve real-time signal processing for wearable health monitoring.

Molybdenum disulfide co-catalysis boosting nanoscale zero-valent iron based Fenton-like process: Performance and mechanism.

The conventional Fenton process has the drawbacks of low efficiency of Fe3+/Fe2+ conversion, low utilization of H2O2, and narrow range of pH. In this paper, molybdenum sulfide (MoS2) was used as a co-catalyst to boost the nanoscale zero-valent iron (nZVI) based heterogeneous Fenton-like process for the degradation of Rhodamine B (RhB). The catalytic performance, influences of parameters, degradation mechanism, and toxicity of intermediates were explored. Compared with the conventional like-Fenton process, the existence of MoS2 accelerated the decomposition of H2O2 and the RhB degradation rate constant of MoS2/nZVI/H2O2 reached more than six times that of nZVI/H2O2. In addition, the effective pH range of MoS2/nZVI/H2O2 was broadened to 9.0 with 84.9% of RhB being removed within 15 min. The co-catalytic system of MoS2 and nZVI was stable and had high reusability according to the results of four consecutive runs. Quenching tests and electron paramagnetic resonance (EPR) demonstrated that hydroxyl radical (·OH), superoxide anions (·O2-), and singlet oxygen (1O2) were all involved in MoS2/nZVI/H2O2. Compared with nZVI/H2O2 system, MoS2 not only increased the corrosion of nZVI but also accelerated the conversion of Fe3+/Fe2+. ECOSAR analysis suggested that the overall acute and chronic toxicity of the degradation products decreased after treatment. Hence, this MoS2 co-catalytic nZVI based Fenton-like process can be used as a promising alternative for the treatment of organic wastewater.

Modulation of SREBP Expression and Fatty Acid Levels by Bacteria-Induced ER Stress Is Mediated by Hemocyanin in Penaeid Shrimp.

Many environmental and pathogenic insults induce endoplasmic reticulum (ER) stress in animals, especially in aquatic ecosystems, where these factors are crucial for life. In penaeid shrimp, pathogens and environmental stressors induce hemocyanin expression, but the involvement of hemocyanin in ER stress response is unknown. We demonstrate that in response to pathogenic bacteria (Vibrio parahaemolyticus and Streptococcus iniae), hemocyanin, ER stress proteins (Bip, Xbp1s, and Chop), and sterol regulatory element binding protein (SREBP) are induced to alter fatty acid levels in Penaeus vannamei. Interestingly, hemocyanin interacts with ER stress proteins to modulate SREBP expression, while ER stress inhibition with 4-Phenylbutyric acid or hemocyanin knockdown attenuates the expression of ER stress proteins, SREBP, and fatty acid levels. Contrarily, hemocyanin knockdown followed by tunicamycin treatment (ER stress activator) increased their expression. Thus, hemocyanin mediates ER stress during pathogen challenge, which consequently modulates SREBP to regulate the expression of downstream lipogenic genes and fatty acid levels. Our findings reveal a novel mechanism employed by penaeid shrimp to counteract pathogen-induced ER stress.

PTN inhibited chondrogenic differentiation potential of dental pulp stem cells.

BACKGROUND: Inflammatory microenvironment can influence the efficiency of cartilage regeneration of MSCs. Some studies have shown that pleiotrophin could be re-detected in synovial fluid and cartilage of osteoarthritis. Therefore, the purpose of this study is to investigate the effect of pleiotrophin on DPSCs chondrogenesis in inflammatory microenvironment and its possible mechanism. MATERIALS AND METHODS: Lentivirus was used to deplete or over-express the PTN expression of DPSCs. The inflammatory environment was simulated in vitro by adding IL-1ß. The chondrogenic differentiation potential was assessed by Alcian Blue staining and main chondrogenic markers. Dual-luciferase reporter assay was used to explore the relationship of miR-137 and PTN. RESULTS: The results showed that 0.1ng/ml IL-1ß treatment during chondrogenic induction greatly impaired the chondrogenic differentiation of DPSCs. 500pg/ml PTN supplementation and PTN overexpression inhibited chondrogenic differentiation of DPSCs, while PTN depletion could promote chondrogenic differentiation. MiR-137 negatively regulated the expression of PTN by binding to its 3'UTR. Moreover, miR-137 could promote chondrogenic differentiation of DPSCs in normal and inflammatory microenvironment. CONCLUSION: Our results suggested that PTN may play an inhibitory role in chondrogenic differentiation of DPSCs in normal and inflammatory microenvironment, which is regulated by miR-137.

Spike Gene Target Amplification in a Diagnostic Assay as a Marker for Public Health Monitoring of Emerging SARS-CoV-2 Variants - United States, November 2021-January 2023.

Monitoring emerging SARS-CoV-2 lineages and their epidemiologic characteristics helps to inform public health decisions regarding vaccine policy, the use of therapeutics, and health care capacity. When the SARS-CoV-2 Alpha variant emerged in late 2020, a spike gene (S-gene) deletion (Δ69-70) in the N-terminal region, which might compensate for immune escape mutations that impair infectivity (1), resulted in reduced or failed S-gene target amplification in certain multitarget reverse transcription-polymerase chain reaction (RT-PCR) assays, a pattern referred to as S-gene target failure (SGTF) (2). The predominant U.S. SARS-CoV-2 lineages have generally alternated between SGTF and S-gene target presence (SGTP), which alongside genomic sequencing, has facilitated early monitoring of emerging variants. During a period when Omicron BA.5-related sublineages (which exhibit SGTF) predominated, an XBB.1.5 sublineage with SGTP has rapidly expanded in the northeastern United States and other regions.

Monocyte-derived immature dendritic cells negatively regulate hepatic stellate cells in vitro by secreting IL-10.

The development of liver fibrosis is associated with inflammatory responses resulting from chronic liver disease. Immature dendritic cells (imDCs) play an important role in modulating the inflammatory environment of the liver. This study investigated the effects of imDCs on the regulation of hepatic stellate cells (HSCs) during liver fibrosis. We isolated and induced imDCs from monocytes of healthy volunteers, activated LX-2 cells with TGF-ß to establish in vivo liver fibrosis HSCs model, and then set up a cell co-culture system with transwell membranes. imDC surface markers and apoptosis rates of LX-2 cells were detected by flow cytometry. The concentration of IL-10 secreted by imDC was measured through ELISA. The expression of α-SMA in LX-2 after co-culture was examined by qRT­PCR. Proliferation of LX-2 cells were detected by CCK-8. The western blot was used to illustrate the LX-2 activation-related proteins such as Smad3/7 and TGF-ß1. The imDCs co-culture group and the interleukin-10 (IL-10) treatment group had similar results, as they were both able to increase apoptosis, inhibit proliferation, downregulate α-SMA mRNA, and reduce TGF-ß1 and Smad3 protein expression in LX-2 cells. Additionally, the Smad7 protein level was increased after treatment with imDC and IL-10. However, the results in the IL-10 antagonist group showed the opposite trend to that of imDCs and IL-10 groups. Thus, these results suggest that imDC secretion of IL-10 negatively regulates activated LX-2 cells, probably via inhibition of the TGF-ß1/Smad3 pathway and increased expression of Smad7 protein. This may be a potential therapeutic target for liver fibrosis.

Ultrafast Synthesis of Metal-Layered Hydroxides in a Dozen Seconds for High-Performance Aqueous Zn (Micro-) Battery.

Efficient synthesis of transition metal hydroxides on conductive substrate is essential for enhancing their merits in industrialization of energy storage field. However, most of the synthetic routes at present mainly rely on traditional bottom-up method, which involves tedious steps, time-consuming treatments, or additional alkaline media, and is unfavorable for high-efficiency production. Herein, we present a facile, ultrafast and general avenue to synthesize transition metal hydroxides on carbon substrate within 13 s by Joule-heating method. With high reaction kinetics caused by the instantaneous high temperature, seven kinds of transition metal-layered hydroxides (TM-LDHs) are formed on carbon cloth. Therein, the fastest synthesis rate reaches ~ 0.46 cm2 s-1. Density functional theory calculations further demonstrate the nucleation energy barriers and potential mechanism for the formation of metal-based hydroxides on carbon substrates. This efficient approach avoids the use of extra agents, multiple steps, and long production time and endows the LDHs@carbon cloth with outstanding flexibility and machinability, showing practical advantages in both common and micro-zinc ion-based energy storage devices. To prove its utility, as a cathode in rechargeable aqueous alkaline Zn (micro-) battery, the NiCo LDH@carbon cloth exhibits a high energy density, superior to most transition metal LDH materials reported so far.

[Protection of salidroside on endothelial cell barrier in cerebral ischemia-reperfusion model rats].

This study aims to observe the therapeutic effect of salidroside on cerebral ischemia-reperfusion(I/R) model rats, and to specifically explore the protection of salidroside on endothelial cell barrier after I/R and the mechanism. In the experiment, SD rats were randomized into sham group, model group, and high-, medium-, and low-dose(10, 5, and 2.5 mg·kg~(-1)) salidroside groups. The suture method was used to induce I/R in rats. The infarct area, neurobehavioral evaluation, and brain water content were used to evaluate the efficacy of salidroside. As for the experiment on the mechanism, high-dose and low-dose salidroside groups were designed. The pathological morphology was observed based on hematoxylin and eosin(HE) staining, and ultrastructure of vascular endothelial cells based on transmission electron microscopy. The content of nitric oxide(NO) in serum, four indexes of blood coagulation, and the content of von Willebrand factor(vWF) in plasma were measured. Western blot(WB) and immunofluorescence(IF) were employed to determine the expression of tight junction proteins(ZO-1, occluding, and claudin-1) and matrix metalloproteinase 9(MMP-9) in the cortex. The results showed that the model group had obvious neurological deficit, obvious infarct in the right brain tissue, and significant increase in water content in brain tissue compared with the sham group. Compared with the model group, high-dose and low-dose salidroside groups showed decrease in neurobehavioral score, and the high-, medium-, and low-dose salidroside groups demonstrated obviously small infarct area and significant decrease in water content in brain tissue. The results of HE staining and transmission electron microscopy showed that rats had necrosis of neurons, damage of original physiological structure of endothelial cells, and disintegration of the tight junction between endothelial cells after I/R compared with the sham group. Compared with the model group, the high-dose and low-dose salidroside groups showed alleviation of neuron injury and intact physiological structure of endothelial cells. The model group had significantly lower serum level of NO, significantly higher plasma levels of vWF and fibrinogen(FIB), and significantly shorter thrombin time(TT) and prothrombin time(PT) than the sham group. Compared with model group, the high-dose and low-dose salidroside groups increased the serum content of NO in serum, decreased the plasma levels of FIB and vWF, and significantly prolonged TT and PT. WB and IF results showed that the model group had significantly lower levels of ZO-1, occluding, and claudin-1 among endothelial cells and significantly higher level of MMP-9 than the sham group. Compared with the model group, high-dose and low-dose salidroside significantly increased the levels of ZO-1, occluding, and claudin-1 in the cortex. The above experimental results show that salidroside has clear therapeutic effect on I/R rats and protects the brain. To be specific, it alleviates the damage of endothelial cells by increasing NO synthesis in endothelial cells, inhibiting coagulation reaction and MMP-9 expression, up-regulating the expression of ZO-1, occludin, and claudin-1, thereby protecting the brain.

2D Co3O4 modified by IrO2 nanozyme for convenient detection of aqueous Fe2+ and intercellular H2O2.

A portable sensor for visual monitoring of Fe2+ and H2O2, two-dimensional Co3O4 modified by nano-IrO2 (IrO2@2D Co3O4) was prepared in this work, for the first time, with the help of microwave radiation at 140 °C, which was further stabilized onto common test strips. The present IrO2@2D Co3O4 possessed superior dual-function enzyme-like activity with low toxicity and excellent biocompatibility. Especially, trace Fe2+ and H2O2 could exclusively alter their enzyme-like catalytic activity with discriminating hyperchromic or hypochromic effect, i.e., from blue to colorless or to dark blue for both IrO2@2D Co3O4 dispersion and its functionalized test strips. The linear regression equations were A652 = 0.5940 - 0.00041 cFe2+ (10-8 M, R2 = 0.9927) for Fe2+ and ∆A652 = 0.0023 cH2O2 + 0.00025 (10-7 M, R2 = 0.9982) for H2O2, respectively. When applied to visual monitoring of aqueous Fe2+ and intercellular H2O2, the recoveries were 101.2 ~ 102.5% and 95.8 ~ 103.7% with detection limits of 1.25 × 10-8 mol/L and 1.02 × 10-7 mol/L, respectively, far below the permitted values in drinking water set by the World Health Organization. The mechanisms for the enhancing enzyme-mimetic activity of IrO2@2D Co3O4 and its selective responses to Fe2+ and H2O2 were investigated in detail.

Distribution of multiple chalazia in eyelids of pediatrics requiring surgery in southeast China: a hospital-based cross-sectional study.

Background: Multiple chalazia are common in children, and many are treated by surgery. However, the distribution of different types of multiple chalazia has not been studied. This research aimed to investigate the location and number of multiple chalazia in pediatrics who need surgical treatments. Methods: Patients with multiple chalazia treated by incision and curettage surgery (I&C) in a tertiary children's hospital between June and December 2016 were reviewed. Demographic data, locations, and numbers of chalazia were recorded. Data were analyzed using generalized linear models of the counts and the occurrences of chalazia. Hypotheses were tested using likelihood ratio tests appropriate for each type of data. Results: The study included 128 subjects, most of which were 1-3 years old. The majority of patients had bilateral chalazia (95.3%), and the proportions of patients with internal, external, and marginal chalazion differed dramatically (99.2%, 61.7%, and 2.3%, respectively). The number of internal and external chalazia did not vary significantly with gender, age, or residence of the patients. Internal chalazia were located more frequently in the upper lids (p<0.001). External chalazia showed no preference of localization. The average number of internal chalazia in each eyelid did not relate to the presence of external chalazia. Conclusions: Multiple chalazia are common among younger children in southeast China. The anatomical distribution varies depending on the type of chalazion. Multiple chalazia often occur bilaterally and internally. If doctors are more aware of the anatomical distribution of chalazia, this might result in a higher success rate of I&C.

Simplified acute physiology score III is excellent for predicting in-hospital mortality in coronary care unit patients with acute myocardial infarction: A retrospective study.

Background: Coronary care unit (CCU) patients with acute myocardial infarction (AMI) lack effective predictors of in-hospital mortality. This study aimed to investigate the performance of four scoring systems in predicting in-hospital mortality in CCU patients with AMI. Methods: The baseline data, the logistic organ dysfunction system (LODS), the Oxford acute severity of illness score (OASIS), the simplified acute physiology score II (SAPS II), and the simplified acute physiology score III (SAPS III) scores of the patients were extracted from the fourth edition of the Medical Information Mart for Critical Care (MIMIC-IV) database. Independent risk factors for in-hospital mortality were identified by regression analysis. We performed receiver operating characteristic (ROC) curves and compared the area under the curve (AUC) to clarify the predictive value of the four scoring systems. Meanwhile, Kaplan-Meier curves and decision curve analysis (DCA) were performed to determine the optimal scoring system for predicting in-hospital mortality. Results: A total of 1,098 patients were included. The SAPS III was an independent risk factor for predicting in-hospital mortality in CCU patients with AMI before and after the propensity score matching (PSM) analysis. The discrimination of in-hospital mortality by SAPS III was superior to that of LODS, OASIS, and SAPS II. The AUC of the SAPS III scoring system was the highest among the four scoring systems, at 0.901 (before PSM) and 0.736 (after PSM). Survival analysis showed that significantly more in-hospital mortality occurred in the high-score SAPS III group compared to the low-score SAPS III group before PSM (HR 7.636, P < 0.001) and after PSM (HR 2.077, P = 0.005). The DCA curve of SAPS III had the greatest benefit score across the largest threshold range compared to the other three scoring systems. Conclusion: The SAPS III was an independent risk factor for predicting in-hospital mortality in CCU patients with AMI. The predictive value for in-hospital mortality with SAPS III is superior to that of LODS, OASIS, and SAPS II. The results of the DCA analysis suggest that SAPS III may provide a better clinical benefit for patients. We demonstrated that SAPS III is an excellent scoring system for predicting in-hospital mortality for CCU patients with AMI.

A novel risk model based on white blood cell-related biomarkers for acute kidney injury prediction in patients with ischemic stroke admitted to the intensive care unit.

Background: Conventional systemic inflammatory biomarkers could predict prognosis in patients with ischemic stroke (IS) admitted to the intensive care unit (ICU). Acute kidney injury (AKI) is common in patients with IS admitted to ICU, but few studies have used systemic inflammatory biomarkers to predict AKI in critically ill patients with IS. This study aimed to establish a risk model based on white blood cell (WBC)-related biomarkers to predict AKI in critically ill patients with IS. Methods: Data were extracted from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) for a training cohort, and data were extracted from the Medical Information Mart for eICU Collaborative Research Database (eICU-CRD) for a validation cohort. Logistic regression analysis was used to determine the significant predictors of WBC-related biomarkers on AKI prediction, and a risk model was established based on those significant indicators in multivariate logistic regression. The receiver operating characteristics (ROC) curve was utilized to obtain the best cut-off value of the risk model. The Kaplan-Meier curve was used to evaluate the prognosis-predictive ability of the risk model. Results: The overall incidence of AKI was 28.4% in the training cohort and 33.2% in the validation cohort. WBC to lymphocyte ratio (WLR), WBC to basophils ratio (WBR), WBC to hemoglobin ratio (WHR), and neutrophil to lymphocyte ratio (NLR) could independently predict AKI, and a novel risk model was established based on WLR, WBR, WHR, and NLR. This risk model depicted good prediction performance both in AKI and other clinical outcomes including hemorrhage, persistent AKI, AKI progression, ICU mortality, and in-hospital mortality both in the training set and in the validation set. Conclusion: A risk model based on WBC-related indicators exhibited good AKI prediction performance in critically ill patients with IS which could provide a risk stratification tool for clinicians in the ICU.

Altered Liver Metabolism, Mitochondrial Function, Oxidative Status, and Inflammatory Response in Intrauterine Growth Restriction Piglets with Different Growth Patterns before Weaning.

Frequent occurrence of intrauterine growth restriction (IUGR) causes huge economic losses in the pig industry. Accelerated catch-up growth (CUG) in the early stage of life could restore multiple adverse outcomes of IUGR offspring; however, there is little knowledge about this beneficial phenomenon. We previously found that nutrient absorption related to intestinal function was globally promoted in CUG-IUGR piglets before weaning, which might be the dominant reason for CUG, but what this alteration could lead to in subsequent liver metabolism is still unknown. Firstly, a Normal, CUG, and non-catch-up growth (NCUG) piglet model before weaning was established by dividing eighty litters of newborn piglets into normal birth weight (NBW) and IUGR groups according to birth weight, and those piglets with IUGR but above-average weanling body weight were considered CUG, and the piglets with IUGR still below average body weight were considered NCUG at weaning day (d 26). Liver samples were collected and then systematically compared in glycolipid metabolism, mitochondrial function, antioxidant status, and inflammatory status among these three different growth models. Enhanced hepatic uptake of fatty acids, diminished de novo synthesis of fatty acids, and increased oxidation of fatty acids were observed in CUG livers compared to Normal and NCUG. In contrast, the NCUG liver showed enhanced glucose uptake and gluconeogenesis compared to Normal and CUG. We also observed deteriorating hepatic vacuolation in NCUG piglets, while increasing hepatic lipid deposition in CUG piglets. Besides, the expression of genes related to mitochondrial energy metabolism and biogenesis was reduced in CUG piglets and the phosphorylation level of AMPK was significantly higher compared to Normal (p < 0.05). Moreover, NCUG liver showed decreased T-AOC (p < 0.01) and GSH-PX (p < 0.05), increased MDA concentrations (p < 0.01), upregulated phosphorylation levels of ERK and NF-κB (p < 0.05), and elevated pro-inflammatory factors IL-1ß, IL-6 and TNF-α (p < 0.05) compared to Normal. Furthermore, correlation analysis revealed a significant positive correlation between glucose metabolism and inflammatory factors, while a negative correlation between mitochondrial function-related genes and fatty acid transport. NGUG piglets showed simultaneous enhancement of glucose uptake and gluconeogenesis, as well as reduced antioxidant capacity and increased inflammatory status, whereas CUG comes at the expense of impaired hepatic mitochondrial function and pathological fat accumulation.