UBE2C as an Immune-Related Biomarker for Breast Cancer: A Study Based on Multiple Databases.

Objective To screen the target gene UBE2C and explore its prognostic value and immune correlation in breast cancer (BRCA) using multiple databases. Methods The microarray expression datasets of BRCA were downloaded from the Gene Expresssion Omnibus database (GEO) and analyzed to obtain differentially expressed genes (DEGs). Hub genes were obtained by constructing and visualizing the protein-protein interaction network of DEGs. Then the key gene UBE2C was determined using R language, STRING, and Cytoscape, and the differential expression of UBE2C was verified using the external datasets, The Cancer Genome Atlas (TCGA) , and quantitative real-time PCR (qRT-PCR). The prognostic value and immunological correlation of UBE2C in BRCA were explored using R language, TIMER, and Gene Set Enrichment Analysis (GSEA).Results The expression of UBE2C was differentially upregulated in BRCA, as verified by TCGA and qRT-PCR. Prognostic analysis revealed that UBE2C served as an independent prognostic factor. High expression of UBE2C was associated with decreased immune infiltration levels of B cells, CD4+ T cells, CD8+ T cells, macrophages, and myeloid dendritic cells in BRCA tissue. The expression of UBE2C in BRCA showed a significant correlation with PDCD1, CD274, and CTLA4 expressions. There was a positive correlation between the expression of UBE2C and the tumor mutational burden and microsatellite instability. GSEA demonstrated that UBE2C expression significantly enriched 786 immune-related gene sets.Conclusions UBE2C expression in BRCA tissues can predict the survivals and prognosis of BRCA patients. Also, it is closely related to the BRCA immune microenvironment and can predict the effecacy of immunotherapy in BRCA patients. Therefore, UBE2C may be an potential immune-related prognostic biomarker for BRCA.

Ultrasound Guidance Combined with C-Arm Fluoroscopy in Selective Semilunar Ganglion Radiofrequency Thermocoagulation Through the Foramen Ovale for Trigeminal Neuralgia: A Randomized Controlled Trial.

OBJECTIVE: To explore the clinical value of ultrasound guidance combined with C-arm guidance during selective semilunar ganglion radiofrequency thermocoagulation via the foramen ovale for trigeminal neuralgia. METHODS: This study enrolled 48 patients diagnosed with trigeminal neuralgia between January 2021 and December 2021 in the Department of Pain Management at Xuanwu Hospital. Patients were randomly and equally divided into a C-arm-only group and an ultrasound-combined-with-C-arm (ultrasound+C-arm) group, according to a random number table. After exclusions, 42 patients were analyzed. Of these, 21 patients underwent selective semilunar ganglion radiofrequency thermocoagulation via the foramen ovale guided by the C-arm alone, whereas 21 patients underwent the same procedure guided by ultrasound combined with C-arm. The number of punctures, the amount of time elapsed until the target area of the semilunar ganglion was punctured, the cumulative dose of radiation exposure, and puncture-related complications were recorded during the operation. Numerical rating scale scores and radiofrequency thermocoagulation-related complications were evaluated preoperatively and at 1 day, 3 days, 7 days, 1 month, and 3 months after surgery. RESULTS: The number of punctures, the amount of time elapsed until the target area of the semilunar ganglion was punctured, and the cumulative dose of radiation exposure were all lower in the ultrasound+C-arm group than in the C-arm-only group (all P < 0.05). No significant differences were found in numerical rating scale scores and radiofrequency thermocoagulation-related complications between the two groups (P > 0.05). No puncture-related complications occurred in either of the groups. CONCLUSION: Ultrasound guidance combined with C-arm guidance could be safely used for puncturing the semilunar ganglion via the foramen ovale, with more efficiency and less radiation exposure than C-arm guidance alone.

LncRNA Miat knockdown alleviates endothelial cell injury through regulation of miR-214-3p/Caspase-1 signalling during atherogenesis.

Atherosclerosis is a common problem in healthy people around the world. Long noncoding RNAs (lncRNAs) play important roles in atherosclerosis. Myocardial infarction-associated transcript (Miat) is a cardiovascular disease-associated lncRNA. Its role and mechanism in atherosclerosis is still not fully clarified. Our study aims to explore the role and mechanism of lncRNA Miat in atherosclerosis. The atherosclerosis models were established both in vitro and in vivo. Real-time PCR was used to measure the expression of lncRNA Miat, miR-214, Caspase-1 and IL-1ß. Western blot was performed to detect the protein expression of Caspase-1. CCK-8 assay, Tunel staining, and flow cytometry analysis were conducted to detect proliferation and apoptosis of human aortic endothelial cells (HAECs), respectively. Oil red O staining and HE staining were used to evaluated the histological changes of the aorta. The results found that lncRNA Miat was upregulated in ox-LDL-induced atherosclerosis model in vitro. The inhibition of lncRNA Miat protects against ox-LDL-induced HAEC injury, presented as increased cell viability and decreased apoptosis. LncRNA Miat and miR-214 has binding site, and CASP1, which encodes Caspase-1, is a target of miR-214. The downregulation of lncRNA Miat increased the expression of miR-214-3p and decreased the expression of Caspase-1, as well as its downstream molecule IL-1ß in HAECs. However, the inhibition of miR-214-3p attenuated the effect of lncRNA Miat downregulation on HAECs. Furthermore, the downregulation of lncRNA Miat alleviated atherosclerosis in ApoE-deficient mice. Correspondingly, the expression of miR-214-3p was upregulated and Caspase-1 was downregulated after knockdown of lncRNA Miat. In conclusion, downregulation of lncRNA Miat exerts a protective effect against atherosclerosis through the regulation miR-214-3p/Caspase-1 signalling pathway. Therefore, the inhibition of lncRNA Miat expression may be an effective strategy in the treatment of atherosclerosis.

Cathepsin B links oxidative stress to the activation of NLRP3 inflammasome.

Oxidative stress-mediated activation of NLRP3 inflammasome in microglia is critical in the development of neurodegerative diseases such as Alzheimer's disease (AD), Parkinson disease (PD). However, the mechanism underlying oxidative stress activates NLRP3 inflammasome remains exclusive. Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2·H2O2 induced IL-1ß secretion in NLRP3 inflammasome-dependent manner·H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 ß secretion. Genetic inhibition or pharmacological inhibition of CTSB blocked the cleavage of pro-caspase-1 into caspase-1 and subsequent IL-1 ß secretion induced by H2O2. Importantly, CTSB activity, IL-1ß levels and malondialdehyde (MDA) were remarkably elevated in plasma of AD patients compared to healthy controls, while glutathione was significantly lower than healthy controls. Correlation analyses showed that CTSB activity was positively correlated with IL-1ß and MDA levels, but negatively correlated with GSH levels in plasma of AD patients. Taken together, our results indicate that oxidative stress activates NLRP3 through upregulating CTSB activity. Our results identify an important biological function of CTSB in neuroinflammation, suggesting that CTSB is a potential target in AD therapy.

Resveratrol Protects Against Pulmonary Arterial Hypertension in Rats via Activation of Silent Information Regulator 1.

BACKGROUND/OBJECTIVES: The polyphenol resveratrol (Rev) has been found to exhibit various beneficial effects including prevention of pulmonary arterial hypertension (PAH). The present study was designed to investigate the action and potential mechanism of Rev on PAH, focusing on the role of SIRT1 (Silent Information Regulator 1) in apoptosis of pulmonary artery smooth muscle cells (PASMCs). METHODS: PAH rats were established by exposure to hypoxia for 21 days. Rev and SRT1720 (a selective SIRT1 activator) were used to reverse PAH by gavaging rats. PASMCs were confronted with hypoxia for 24 h or 48 h and were then treated with Rev or SRT1720 in vitro. Western blot was performed to detect the protein expression of SIRT1. CCK-8 and scratch wound experiments were carried out to verify cell proliferation. In addition, the TUNEL positive assay and flow cytometry assay were used to measure PASMC apoptosis. Mitochondrial permeability transition (mPT) was identified by confocal microscopy. Right ventricular systolic pressure (RVSP) was determined with a Gould pressure transducer, and right ventricular hypertrophy (RVH) was determined by weighing the cardiac muscle. RESULTS: We demonstrated that Rev could reverse the remodelling of the pulmonary vasculature, thus contributing to alleviating the severity of PAH. Down-regulation of SIRT1 was observed in PAH, but administration of Rev had no obvious effect on the protein expression of SIRT1. In addition, Rev could induce mitochondrial swelling and nuclear pyknosis, leading to small, dense, and dysmorphic mitochondria in rats exposed to hypoxia alone. Rev treatment inhibited PASMC proliferation in a dose-dependent manner in vitro. Incubation with SRT1720, a specific activator of SIRT1, significantly retarded PASMC proliferation and promoted PASMC apoptosis in vitro. The mechanism could be associated with inducing mPT damage in PASMCs. Rev and SRT1720 treatment mitigated RVSP and reduced RVH. CONCLUSION: Rev produced a beneficial effect partially by enhancing the activation of SIRT1, thus improving RVSP and reducing RVH. SIRT1 activation increased PASMC apoptosis by inducing mPT dysfunction, which might be a novel future strategy for the treatment of PAH.

Analysis of mental health status before and after psychological intervention in response to public health emergencies by medical students: a prospective single-arm clinical trial.

Background: Many human mobility restrictions have been adopted during the novel 2019 coronavirus disease (COVID-19) pandemic. Here we explored the effects of psychological interventions on the mental health status of medical students under the regular prevention and control of the pandemic. Methods: By voluntarily participating in interest groups, 121 third-year medical undergraduate students in a university in Jiangsu Province underwent psychological interventions for 1 year. Their mental status was assessed by using Zung's Self-rating Anxiety Scale (SAS), Self-rating Depression Scale (SDS), and Somatic Self-rating Scale (SSS) before and after the interventions. Psychological coping styles were compared by using the trait coping style questionnaire (TCSQ). Each assessment scale is evaluated every 3 months, with the first survey results as the baseline data and compared with the last results. The resulting data was passed by SPSS 23 0 for normal testing and Analysis of Variance (ANOVA). Results: During the regular response to the COVID-19 pandemic, the prevalence of anxiety, depression, and somatization symptoms was 25.62% vs. 7.44%, 28.93% vs. 18.18%, and 21.49% vs. 9.92%, respectively, before and after psychological interventions (all P<0.05). The positive (31.73±4.26 vs. 38.26±3.72) and negative (27.69±3.19 vs. 20.73±2.8) coping styles significantly differed before and after intervention (both P<0.05). Conclusions: Varying degrees of anxiety, depression, and somatization symptoms can occur in medical students during the regular response to COVID-19 pandemic, highlighting the impact of public health emergencies on college students. Interest group-based psychological intervention, along with individual mental health counseling, can positively promote the mental health of college students and effectively improve their anxiety.

Treatment of Elderly Patients with Acute Symptomatic OVCF: A Study of Comparison of Conservative Treatment and Percutaneous Kyphoplasty.

Objective: The present study was designed for the contrastive analysis of conservative and percutaneous kyphoplasty (PKP) on pain severity and recovery of injured vertebrae in elderly patients with acute symptomatic osteoporotic vertebral compression fracture (OVCF). Methods: A total of 60 elderly patients with acute symptomatic OVCF were divided into two groups according to different treatment protocols, with 30 patients in each group. Patients in the Con group received conservative treatment, while patients in the PKP group received percutaneous kyphoplasty treatment. Clinical evaluation included the visual analogue scale (VAS), the Dallas pain questionnaire, the vertebral body leading edge height, the Cobb angle of injured vertebrae, the MOS item short-form health survey (SF-36), the Barthel index, and the mini-mental state examination (MMSE). Results: At 3 days, 3 months, and 6 months post-treatment, the score of VAS and the Cobb angle of injured vertebrae in patients of the PKP group were all significantly lower than those in the Con group (P < 0.05), while the height of vertebral body leading edge in patients of the PKP group was significantly longer than that in the Con group (P < 0.05). At 6 months post-treatment, the scores of the four dimensions of the Dallas pain questionnaire scale in the PKP group were all significantly lower than those in the Con group (P < 0.05), while the score of SF-36 (PCS), SF-36 (MCS), and Barthel index in patients of the PKP group were all significantly lower than those in the Con group (P < 0.05), and there was no significant difference in the scores of MMSE between these two groups (P > 0.05). Conclusion: Compared with conservative treatment, PKP treatment of elderly patients with acute symptomatic OVCF provides rapid pain relief, restoration of damaged vertebral body height, correction of Cobb's angle, and improved quality of life.

TRPV3 promotes the angiogenesis through HIF-1α-VEGF signaling pathway in A549 cells.

BACKGROUND: Angiogenesis is an essential physiological process in the growth and metastasis of primary tumors. Ca2+ signaling is crucial for tumor angiogenesis. The purpose of this study was to detect the potential role of Ca2+ permeable transient receptor potential vanilloid-3 (TRPV3) in the angiogenesis of non-small cell lung cancer (NSCLC). METHODS: Small interfering RNA was used to down-regulate TRPV3 expression in A549 cells. A laser scanning confocal microscope was used to examine intracellular calcium concentration ([Ca2+]i). Human umbilical vein endothelial cells (HUVECs) tube formation and migration assay, Western blot, MTT and ELISA were performed to detect the potential mechanisms of TRPV3 in tumor angiogenesis. A mouse tumor xenograft model was performed to expound the effects of TRPV3 on tumor cell growth. RESULTS: Inhibition of TRPV3 reduced [Ca2+]i and protein expressions of VEGF and HIF-1α in A549 cells. Moreover, HIF-1α depletion decreased the secretion and expression of VEGF. Depletion of TRPV3 inhibited HUVECs proliferation, tube formation and migration induced by conditioned medium. And TRPV3 inhibition could decrease the volume of xenograft tumors and MVD of CD34+ cells. The expression levels of HIF-1α, VEGF and p-CaMKП in the xenograft tumors in RuR and siTRPV3 groups was reduced. CONCLUSIONS: TRPV3 calcium channel protein may play a key role in NSCLC angiogenesis. TRPV3 could promote the angiogenesis through HIF-1α-VEGF signaling pathway. Targeting TRPV3 channel protein by novel approaches would be useful for reversing NSCLC angiogenesis.

Serum Metabonomics Reveals Key Metabolites in Different Types of Childhood Short Stature.

Nowadays, short stature (SS) in childhood is a common condition encountered by pediatricians, with an increase in not just a few families. Various studies related to the variations in key metabolites and their biological mechanisms that lead to SS have increased our understanding of the pathophysiology of the disease. However, little is known about the role of metabolite variation in different types of childhood SS that influence these biological processes and whether the understanding of the key metabolites from different types of childhood SS would predict the disease progression better. We performed a systematic investigation using the metabonomics method and studied the correlation between the three groups, namely, the control, idiopathic short stature (ISS), and short stature due to growth hormone deficiency (GHD). We observed that three pathways (viz., purine metabolism, sphingolipid signaling pathway, and sphingolipid metabolism) were significantly enriched in childhood SS. Moreover, we reported that two short peptides (Thr Val Leu Thr Ser and Trp Ile Lys) might play a significant role in childhood SS. Various metabolites in different pathways including 9,10-DiHOME, 12-HETE, 12(13)-EpOME, arachidonic acid methyl ester, glycerophospho-N-arachidonoyl ethanolamine, curvulinic acid (2-acetyl-3,5-dihydroxyphenyl acetic acid), nonanoic acid, and N'-(2,4-dimethylphenyl)-N-methylformamidine in human serum were compared between 60 children diagnosed with SS and 30 normal-height children. More investigations in this area may provide insights and enhance the personalized treatment approaches in clinical practice for SS by elucidating pathophysiology mechanisms of experimental verification.

Serum metabolomic analysis reveals key metabolites in drug treatment of central precocious puberty in female children.

Precocious puberty (PP) is a common condition among children. According to the pathogenesis and clinical manifestations, PP can be divided into central precocious puberty (CPP, gonadotropin dependent), peripheral precocious puberty (PPP, gonadotropin independent), and incomplete precocious puberty (IPP). Identification of the variations in key metabolites involved in CPP and their underlying biological mechanisms has increased the understanding of the pathological processes of this condition. However, little is known about the role of metabolite variations in the drug treatment of CPP. Moreover, it remains unclear whether the understanding of the crucial metabolites and pathways can help predict disease progression after pharmacological therapy of CPP. In this study, systematic metabolomic analysis was used to examine three groups, namely, healthy control (group N, 30 healthy female children), CPP (group S, 31 female children with CPP), and treatment (group R, 29 female children) groups. A total of 14 pathways (the top two pathways were aminoacyl-tRNA biosynthesis and phenylalanine, tyrosine, and tryptophan biosynthesis) were significantly enriched in children with CPP. In addition, two short peptides (His-Arg-Lys-Glu and Lys-Met-His) were found to play a significant role in CPP. Various metabolites associated with different pathways including amino acids, PE [19:1(9Z)0:0], tumonoic acid I, palmitic amide, and linoleic acid-biotin were investigated in the serum of children in all groups. A total of 45 metabolites were found to interact with a chemical drug [a gonadotropin-releasing hormone (GnRH) analog] and a traditional Chinese medicinal formula (DBYW). This study helps to understand metabolic variations in CPP after drug therapy, and further investigation may help develop individualized treatment approaches for CPP in clinical practice.

Analysis on the Effect of Different Surgical Methods on the Treatment of Senile Osteoporotic Spinal Compression Fractures and the Influencing Factors of Complications.

Osteoporotic fractures are a common type of fractures in the elderly, among which spinal compression fractures are more common. After the occurrence of fractures, due to the compression and burst of the vertebral body, this will lead to local kyphosis deformity and even affect the balance of the sagittal spine. In the past, conservative treatments were used for osteoporotic spinal compression fractures. Although it can relieve pain symptoms, it can easily lead to complications such as aggravation of osteoporosis and deep vein thrombosis of the lower extremities. At present, percutaneous vertebroplasty (PVP) and percutaneous kyphoplasty (PKP) are the main clinical surgical treatments, both of which are minimally invasive surgery, short operation time, effective pain relief, and rapid postoperative recovery. Although both of them are effective, there is still controversy over the efficacy of both in the treatment of osteoporotic spinal compression fractures. The purpose of this study was to investigate the efficacy of PVP and PKP in the treatment of elderly osteoporotic spinal compression fractures and to analyze the related factors that affect the occurrence of postoperative complications. The results show that both PVP and PKP can effectively improve the pain and dysfunction of elderly patients with osteoporotic spinal compression fracture, restoration of vertebral height, and correct kyphosis, but PKP has better effect and higher safety and is worth promoting. Postoperative complications of patients are related to their age, bone mineral density, use of hormones, and antiosteoporosis treatment.

Novel lncRNA PSMG3­AS1 functions as a miR­143­3p sponge to increase the proliferation and migration of breast cancer cells.

Long non­coding RNAs (lncRNAs) are considered to be important regulators in breast cancer. In the present study, the potential mechanisms and functional roles of lncRNA PSMG3­antisense (AS)1 were investigated in vivo and in vitro. The relative expression levels of lncRNA PSMG3­AS1 and microRNA (miR)­143­3p were determined using reverse­transcription quantitative PCR. The protein expression levels of collagen type 1 alpha 1 (COL1A1) and proliferating cell nuclear antigen (PCNA) were obtained using western blot analysis. Bioinformatics analysis was used to identify the relationship between PSMG3­AS1, miR­143­3p and COL1A1. Colony forming and Cell Counting Kit­8 assays were used to detect cell proliferation. Transwell and wound­healing assays were used to determine cell migration. The results of the present study demonstrated that PSMG3­AS1 expression was increased in breast cancer tumor tissues and cell lines, and that of miR­143­3p was decreased. Knockdown of PSMG3­AS1 increased the level of miR­143­3p expression, which led to the mitigation of proliferation and migration capacity in breast carcinoma cells. Additionally, PSMG3­AS1 knockdown was demonstrated to reduce the mRNA and protein expression levels of COL1A1. miR­143­3p mimic transfection reduced proliferation and migration in MDA­MB­231 and MCF­7 cell lines. Furthermore, miR­143­3p inhibition significantly increased the proliferation and migration of breast cancer cells compared with the negative control group. The mRNA and protein expression levels of PCNA were reduced in the MCF­7 cell line when transfected with miR­143­3p mimics and si­PSMG3­AS1. However, PCNA expression was increased in cells transfected with a miR­143­3p inhibitor. In conclusion, the results of the present study identified a novel lncRNA PSMG3­AS1, which serves as a sponge for miR­143­3p in the pathogenesis of breast cancer. PSMG3­AS1 may be used as a potential therapeutic target gene in breast cancer treatment.

The inhibition of microRNA-203 on ischemic reperfusion injury after total knee arthroplasty via suppressing MYD88-mdiated toll-like receptor signaling pathway.

Ischemia reperfusion injury (IRI), a complex phenomenon often encountered in surgery, can lead to local and distant tissue destruction and sometimes even death. microRNA-203 (miR-203) has been reported to negatively regulate ischemia induced microglia activation with a feedback to myeloid differentiation primary-response gene 88 (MYD88). Accordingly, our study is to verify the effect of miR-203 and MYD88 on mice in IRI after total knee arthroplasty (TKA). After establishment of IRI mouse model, heart rate (HR) and mean arterial pressure (MAP) in mice were determined. The functional role of miR-203 in IRI was determined using ectopic expression, knockdown and reporter assay experiments. Levels of interferon γ (IFN-γ), interleukin 10 (IL-10), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), creatine kinase (CK), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) were detected, and expression of miR-203, MYD88, toll-like receptor 4 (TLR4), Faslg, Cleaved-Caspase-3, B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) was evaluated. Initially, HR and MAP were decreased in IRI mice. Forced expression of miR-203 and silencing of MYD88 increased levels of SOD and IL-10 but decreased levels of MDA, CK, LDH, TNF-α, IL-6 and IFN-γ. Additionally, forced expression of miR-203 and silencing of MYD88 increased Bcl-2 expression but decreased MYD88, TLR4, Cleaved-Caspase-3, Falsg and Bax expression. MYD88, a target gene of miR-203, was decreased following miR-203 promotion, while the TLR signaling pathway inactivation occurred following MYD88 silencing. Generally, our study demonstrated the protective effects of miR-203 on mice with IRI after TKA through inhibiting TLR signaling pathway by negatively regulating MYD88.

Fabrication of methyl acrylate and tetraethylenepentamine grafted magnetic chitosan microparticles for capture of Cd(II) from aqueous solutions.

MCS-MA-TEPA microparticles, with 251.22 mg g-1 of adsorption capacity for Cd(II), higher than most of the counterparts, were first fabricated by chemical coprecipitation, spray drying, and Michael addition reaction, without any cross-linker participation. These Fe3O4-nanoparticle-embedded microparticles of 5.95 µm in size, derived from modifications by methyl acrylate (MA) and tetraethylenepentamine (TEPA) on magnetic chitosan (MCS) microparticles, were of plum-pudding-like and wrinkle-like topography portrayed by TEM and SEM. Such features were beneficial to adsorbent recycling and Cd(II) capture. BET examinations illustrated 6.084 m2 g-1 of specific surface area, 0.015 mL g-1 of pore volume, and 6.536 nm of pore diameter. FTIR, VSM, XRD, TEM-SAED, TG, and DTG characterizations were indicative of successful synthesis, satisfactory magnetism, well-defined architecture, and good thermostability. Optimal adsorption parameters for Cd(II) were determined via batch experiments. Thermodynamic parameters and adsorption data fitting implied an exothermic, spontaneous, monolayer, and chemisorption process. XPS analyses confirmed a potential adsorption mechanism that N and O atoms on microparticles chelated with Cd(II) ions in solutions. Additionally, MCS-MA-TEPA-Cd(II) microparticles were magnetically separated easily and had outstanding reusability even after five-time recycling, with a slight adsorption capability loss (< 12%). Altogether, MCS-MA-TEPA microparticles might serve as a promising adsorbent for contaminated water scavenging.

Cr(VI) and Pb(II) capture on pH-responsive polyethyleneimine and chloroacetic acid functionalized chitosan microspheres.

PEI-ECH-CMCS microspheres (MPs) were first constructed via elaborately programmed procedures. Fourier transform infrared spectroscopy, conductometric titration, Brunauer-Emmett-Teller, X-ray diffraction, pH at zero point of charge (pHzpc), scanning electron microscopy, X-ray photoelectron spectroscopy, and swelling results demonstrated that chitosan-based adsorbent had ample -NH2 and -COOH, specific surface area of 29.040 m2/g, porous 3D architectures, pHzpc of 4.2, uniform spherical surfaces, narrow size distribution (19-33 µm), and pH-responsive swelling features, advantageous to Cr(VI) and Pb(II) capture. Adsorption parameters were obtained from batch experiments and pH 3 and 5 were chosen for Cr(VI) and Pb(II) capture. Pseudo-second-order kinetic and Liu isotherm models well interpreted adsorption behavior, and thermodynamic, isotherm, and kinetic studies revealed an exothermic, spontaneous, monolayer, and chemical adsorption process. Maximum adsorption capacity for Cr(VI) or Pb(II) was 331.32 or 302.56 mg/g, exceeding CS-based adsorbents reported. Excellent reusability and feasibility were evidenced by adsorption capacity loss < 12.10% and high removal efficiency for Cr(VI) (95.79%) and Pb(II) (91.40%) in synthetic effluents. Finally, potential adsorption mechanisms were proposed.

Downregulation of signal transduction and STAT3 expression exacerbates oxidative stress mediated by NLRP3 inflammasome.

Activated nucleotide binding to the oligonucleotide receptor protein 3 (NLRP3) inflammasome is possibly involved in the pathogenesis of Alzheimer's disease through oxidative stress and neurogenic inflammation. Low expression of the signal transducer and activator of transcription 3 (STAT3) gene may promote the occurrence of neurodegenerative diseases to some extent. To clarify the roles of the NLRP3 inflammasome and STAT3 expression in oxidative stress, (1) SHSY5Y cells were incubated with 1 mM H2O2 to induce oxidative stress injury, and the expression of human-cell-specific signal transduction, STAT3-shRNA silencing signal transduction and STAT3 were detected. Cells were pretreated with Ca2+ chelator BAPATA-AM (0.1 mM) for 30 minutes as a control. (2) Western blot assay was used to analyze the expression of caspase-1, NLRP3, signal transduction and STAT3. Enzyme-linked immunosorbent assay was used to analyze interleukin-1ß levels. Flow cytometry was carried out to calculate the number of apoptotic cells. We found that H2O2 treatment activated NLRP3 inflammasomes and decreased phosphorylation of signal transduction and STAT3 serine 727. BAPTA-AM pretreatment abolished the H2O2-induced activation of NLRP3 inflammasomes, caspase-1 expression, interleukin-1ß expression and apoptosis in SHSY5Y cells, and had no effect in cells with downregulated STAT3 expression by RNAi. The findings suggest that downregulation of signal transduction and STAT3 expression may enhance the oxidative stress mediated by NLRP3, which may not depend on the Ca2+ signaling pathway.

Selective Adsorption toward Hg(II) and Inhibitory Effect on Bacterial Growth Occurring on Thiosemicarbazide-Functionalized Chitosan Microsphere Surface.

The work presented here aims to fabricate dual-purpose adsorbent with adsorption selectivity for Hg(II) and antibacterial activity. TSC-PGMA-MACS microspheres were first constructed via esterification of malic acid (MA) with chitosan (CS) and through successively grafting glycidyl methacrylate (GMA) and thiosemicarbazide (TSC) onto MACS microsphere surfaces. Fourier transform infrared spectroscopy, elemental analysis, energy-dispersive X-ray spectrometry, X-ray diffraction, differential scanning calorimetry, thermogravimetry, differential thermogravimetry, scanning electron microscopy, and Brunauer-Emmett-Teller results provided ample evidence that new mesoporous adsorbent, with 35.340 m2 g-1 of specific surface area and abundant -NH2 and C═S, was successfully fabricated and had loose crystalline, thermodynamically stable, and well-defined architectures, beneficial for Hg(II) adsorption and bacterial cell killing. Optimal adsorption parameters were determined via varying pH, time, concentrations, and temperatures, and pH 6.0 was chosen as an optimal pH for Hg(II) adsorption. Adsorption behavior, described well by pseudo-second-order kinetic and Langmuir isotherm models, and thermodynamic parameters implied a chemical, monolayer, endothermic, and spontaneous adsorption process, and the maximum adsorption capacity for Hg(II) was 242.7 mg g-1, higher than most of the available adsorbents. Competitive adsorption exhibited excellent adsorption selectivity for Hg(II) in binary-metal solutions. Besides, TSC-PGMA-MACS microspheres had outstanding reusability even after five times recycling, with adsorption capability loss <14%. Several potential adsorption sites and bonding modes were proposed. Notably, TSC-PGMA-MACS microspheres before and after adsorption were of high antibacterial activity against Escherichia coli and Staphylococcus aureus (MICs, 2 and 0.25 mg mL-1), superior to CS powders, and possible antibacterial mechanisms were also summarized. Altogether, dual-purpose TSC-PGMA-MACS microspheres might be promising adsorbent for contaminated water scavenging.