Associations of Intrapancreatic Fat Deposition With Incident Diseases of the Exocrine and Endocrine Pancreas: A UK Biobank Prospective Cohort Study.

INTRODUCTION: To investigate whether increased intrapancreatic fat deposition (IPFD) heightens the risk of diseases of the exocrine and endocrine pancreas. METHODS: A prospective cohort study was conducted using data from the UK Biobank. IPFD was quantified using MRI and a deep learning-based framework called nnUNet. The prevalence of fatty change of the pancreas (FP) was determined using sex- and age-specific thresholds. Associations between IPFD and pancreatic diseases were assessed with multivariate Cox-proportional hazard model adjusted for age, sex, ethnicity, body mass index, smoking and drinking status, central obesity, hypertension, dyslipidemia, liver fat content, and spleen fat content. RESULTS: Of the 42,599 participants included in the analysis, the prevalence of FP was 17.86%. Elevated IPFD levels were associated with an increased risk of acute pancreatitis (hazard ratio [HR] per 1 quintile change 1.513, 95% confidence interval [CI] 1.179-1.941), pancreatic cancer (HR per 1 quintile change 1.365, 95% CI 1.058-1.762) and diabetes mellitus (HR per 1 quintile change 1.221, 95% CI 1.132-1.318). FP was also associated with a higher risk of acute pancreatitis (HR 3.982, 95% CI 2.192-7.234), pancreatic cancer (HR 1.976, 95% CI 1.054-3.704), and diabetes mellitus (HR 1.337, 95% CI 1.122-1.593, P = 0.001). DISCUSSION: FP is a common pancreatic disorder. Fat in the pancreas is an independent risk factor for diseases of both the exocrine pancreas and endocrine pancreas.

Analysis of Factors and T-Lymphocyte Subset Changes in Pediatric Recurrent Respiratory Infections Post-Pidotimod Treatment.

Objective: This study aims to analyze factors contributing to recurrent respiratory tract infections (RRTIs) in pediatric patients and evaluate the efficacy of pidotimod (PI) treatment. Methods: This study utilized a retrospective cohort design, enrolling a total of 85 children diagnosed with RRTIs between September 2020 and September 2022, alongside 54 healthy children. Logistic regression analysis was employed to identify factors contributing to RRTI occurrence. Among the participants, 40 children underwent conventional treatment (control group), while 45 received PI treatment (research group). Comparative analyses were conducted to assess clinical efficacy and adverse effects between the two treatment groups. Results: The history of family members' smoking and parental allergy emerged as independent risk factors for RRTIs (P < .05, OR>1), whereas parental education level, outdoor activity, and micronutrient intake were identified as independent protective factors for RRTIs (P < .05, OR<1). Symptoms such as cough, fever, rhonchi, moist rales, and tonsillar enlargement resolved significantly faster in the research group compared to the control group (P < .05). Additionally, the research group exhibited reduced infection duration and fewer recurrent infections (P < .05). Following treatment, the overall treatment efficacy was superior in the research group compared to the control group (P < .05), with no significant difference in the incidence of adverse effects (P > .05). Post-treatment, levels of CD3+, CD4+, and CD4+/CD8+ were elevated in the research group compared to the control group, while CD8+ levels were lower (P < .05). Conclusions: Daily outdoor activity among children, family members' history of smoking, parental allergy history, education level, and micronutrient intake emerged as independent factors influencing pediatric RRTIs. Furthermore, PI was identified as a significant treatment option for RRTIs.

Research on Foot Contact State Detection Technology of Wheel-Legged Robot.

The accurate perception of external environment information through the robot foot is crucial for the mobile robot to evaluate its ability to traverse terrain. Adequate foot-end contact signals can provide robust support for robot motion control and decision-making processes. The shape and uncertain rotation of the wheel-legged robot foot end represent a significant challenge to sensing the robot foot-end contact state, which current foot-end sensing schemes cannot solve. This paper presents a sensing method for the tire stress field of wheel-legged robots. A finite element analysis was conducted to study the deformation characteristics of the foot-end tire under force. Based on this analysis, a heuristic contact position estimator was designed that utilizes symmetrical deformation characteristics. Strain sensors, arranged in an array, extract the deformation information on the inner surface of the tire at a frequency of 200 Hz. The contact position estimator reduces the dimensionality of the data and fits the eigenvalues to the estimated contact position. Using support vector regression, the force estimator utilizes the estimated contact position and sensor signal to estimate the normal reaction force, designated as FZ. The sensing system is capable of detecting the contact position on the wheel circumference (with a root mean square error of 1.150°), as well as the normal force of 160 N on the Z axis (with a root mean square error of 6.04%). To validate the efficacy of the sensor detection method, a series of randomized and repeated experiments were conducted on a self-constructed test platform. This novel approach offers a promising avenue for perceiving contact states in wheel-legged robots.

LncRNA AGAP2 antisense RNA 1 stabilized by insulin-like growth factor 2 mRNA binding protein 3 promotes macrophage M2 polarization in clear cell renal cell carcinoma through regulation of the microRNA-9-5p/THBS2/PI3K-Akt pathway.

BACKGROUND: Increasing evidence highlights the potential role of long non-coding RNAs (lncRNAs) in the biological behaviors of renal cell carcinoma (RCC). Here, we explored the mechanism of AGAP2-AS1 in the occurrence and development of clear cell RCC (ccRCC) involving IGF2BP3/miR-9-5p/THBS2. METHODS: The expressions of AGAP2-AS1, IGF2BP3, miR-9-5p, and THBS2 and their relationship were analyzed by bioinformatics. The targeting relationship between AGAP2-AS1 and miR-9-5p and between miR-9-5p and THBS2 was evaluated with their effect on cell biological behaviors and macrophage polarization assayed. Finally, we tested the effect of AGAP2-AS1 on ccRCC tumor formation in xenograft tumors. RESULTS: IGF2BP3 could stabilize AGAP2-AS1 through m6A modification. AGAP2-AS1 was highly expressed in ccRCC tissues and cells. The lentivirus-mediated intervention of AGAP2-AS1 induced malignant behaviors of ccRCC cells and led to M2 polarization of macrophages. In addition, THBS2 promoted M2 polarization of macrophages by activating the PI3K/AKT signaling pathway. AGAP2-AS1 could directly bind with miR-9-5p and promote the expression of THBS2 downstream of miR-9-5p. These results were further verified by in vivo experiments. CONCLUSION: AGAP2-AS1 stabilized by IGF2BP3 competitively binds to miR-9-5p to up-regulate THBS2, activating the PI3K/AKT signaling pathway and inducing macrophage M2 polarization, thus facilitating the development of RCC.

Classification of left-side hepatolithiasis for laparoscopic middle hepatic vein-guided anatomical hemihepatectomy combined with transhepatic duct lithotomy.

BACKGROUND: Laparoscopic middle hepatic vein-guided anatomical hemihepatectomy combined with transhepatic duct lithotomy (MATL) is an approach that can substantially improve stone clearance rates while reducing the rate of postoperative biliary fistula formation, residual stone rates, and rates of recurrence. In this study, we classified left-side hepatolithiasis cases into four subtypes based upon the diseased stone-containing bile duct, the middle hepatic vein, and the right hepatic duct. We then investigated the risk associated with different subtypes and evaluated the safety and efficacy of the MATL procedure. METHODS: In total, 372 patients who underwent left hemihepatectomy for left intrahepatic bile duct stones were enrolled. Based on the distribution of the stones, the cases could be divided into four types. The risk of surgical treatment was compared for the four types and the safety, short-term efficacy, and long-term efficacy of the MATL procedure in the four types of left intrahepatic bile duct stones were studied. RESULTS: Type II was found to be the most likely to cause intraoperative bleeding while type III was likely to cause biliary tract damage and type IV was associated with the highest stone recurrence rate. The MATL procedure did not increase the risk of surgery and was found to reduce the rate of bile leakage, residual stones, and stone recurrence. CONCLUSION: Left-side hepatolithiasis-associated risk classification is feasible and may represent a viable means of improving the safety and feasibility of the MATL procedure.

miR-24-3p Regulates Epithelial-Mesenchymal Transition and the Malignant Phenotype of Pancreatic Adenocarcinoma by Regulating ASF1B Expression.

Anti-silencing function protein 1 homolog B (ASF1B) has been implicated in the occurrence and development of cancers. The present work explored the functional role and the expression regulation of ASF1B in pancreatic ductal adenocarcinoma (PDAC). Based on the real-time quantitative PCR (qRT-PCR) and immunohistochemistry (IHC), ASF1B was significantly upregulated in PDAC tissues. High expression of ASF1B was associated with a poor overall survival (OS) and recurrence-free survival (DFS) in the PDAC patients. ASF1B also showed a relatively higher expression in PDAC cells (AsPC-1, PANC-1) when compared with human pancreatic ductal epithelial cells (HPDFe-6). CCK8 and clone formation assay demonstrated that silencing ASF1B impaired the proliferation in PANC-1 and AsPC-1 cells, and Annexin V-PI staining showed an increased level of apoptosis upon ASF1B silencing. ASF1B silencing also suppressed the migration and invasion in PDAC cells, as revealed by Transwell assays. We further showed that miR-24-3p was downregulated in PDAC tissues and cells, which functionally interacted with ASF1B by dual-luciferase reporter assay. miR-24-3p negatively regulated ASF1B expression to modulate the malignant phenotype of PDAC cells. ASF1B shows high expression in PDAC, which promotes the malignancy and EMT process of PDAC cells. miR-24-3p is a negative regulator of ASF1B and is downregulated in PDAC cells. Our data suggest that targeting ASF1B/miR-24-3p axis may serve as an intervention strategy for the management of PDAC.

KMT2B promotes the growth of renal cell carcinoma via upregulation of SNHG12 expression and promotion of CEP55 transcription.

BACKGROUND: This study aims to clarify the mechanistic action of long non-coding RNA (lncRNA) SNHG12 in the development of renal cell carcinoma (RCC), which may be associated with promoter methylation modification by KMT2B and the regulation of the E2F1/CEP55 axis. METHODS: TCGA and GEO databases were used to predict the involvement of SNHG12 in RCC. Knockdown of SNHG12/E2F1/CEP55 was performed. Next, SNHG12 expression and other mRNAs were quantified by RT-qPCR. Subsequently, CCK-8 was used to detect cell proliferation. Wound healing assay and Transwell assay were used to detect cell migration and invasion, respectively. The in vitro angiogenesis of human umbilical vein endothelial cells (HUVECs) was explored by matrigel-based capillary-like tube formation assay. ChIP assay was used to detect H3K4me3 in SNHG12 promoter region. The binding of E2F1 to CEP55 promoter region was analyzed with ChIP and dual luciferase reporter assays. RIP assay was used to detect the binding of SNHG12 to E2F1. Finally, the effect of SNHG12 on the tumor formation and angiogenesis of RCC was assessed in nude mouse xenograft model. RESULTS: SNHG12 was highly expressed in RCC tissues and cells, and it was related to the poor prognosis of RCC patients. SNHG12 knockdown significantly inhibited RCC cell proliferation, migration, and invasion and HUVEC angiogenesis. KMT2B up-regulated SNHG12 expression through modifying H3K4me3 in its promoter region. In addition, SNHG12 promoted CEP55 expression by recruiting the transcription factor E2F1. Knockdown of SNHG12 blocked E2F1 recruitment and down-regulated the expression of CEP55, thereby inhibiting tumor formation and angiogenesis in nude mice. CONCLUSION: The evidence provided by our study highlighted the involvement of KMT2B in up-regulation of lncRNA as well as the transcription of CEP55, resulting in the promotion of angiogenesis and growth of RCC.

Optimization of a laparoscopic procedure for advanced intrahepatic cholangiocarcinoma based on the concept of "waiting time": a preliminary report.

INTRODUCTION: Clinicians increasingly perform laparoscopic surgery for intrahepatic cholangiocarcinoma (ICC). However, this surgery can be difficult in patients with advanced-stage ICC because of the complicated procedures and difficulty in achieving high-quality results. We compared the effects of a three-step optimized procedure with a traditional procedure for patients with advanced-stage ICC. METHODS: Forty-two patients with advanced-stage ICC who received optimized laparoscopic hemihepatectomy with lymph node dissection (LND, optimized group) and 84 propensity score-matched patients who received traditional laparoscopic hemihepatectomy plus LND (traditional group) were analyzed. Surgical quality, disease-free survival (DFS), and overall survival (OS) were compared. RESULTS: The optimized group had a lower surgical bleeding score (P = 0.038) and a higher surgeon satisfaction score (P = 0.001). Blood loss during hepatectomy was less in the optimized group (190 vs. 295 mL, P < 0.001). The optimized group had more harvested LNs (12.0 vs. 8.0, P < 0.001) and more positive LNs (8.0 vs. 5.0, P < 0.001), and a similar rate of adequate LND (88.1% vs. 77.4%, P = 0.149). The optimized group had longer median DFS (9.0 vs. 7.0 months, P = 0.018) and median OS (15.0 vs. 13.0 months, P = 0.046). In addition, the optimized group also had a shorter total operation time (P = 0.001), shorter liver resection time (P = 0.001), shorter LND time (P < 0.001), shorter hospital stay (P < 0.001), and lower incidence of total morbidities (14.3% vs. 36.9%, P = 0.009). CONCLUSIONS: Our optimization of a three-step laparoscopic procedure for advanced ICC was feasible, improved the quality of liver resection and LND, prolonged survival, and led to better intraoperative and postoperative outcomes.

Laparoscopic segment 4b+5 liver resection for stage T3 gallbladder cancer.

BACKGROUND: There is still controversy over whether to perform laparoscopic surgery for T3 stage gallbladder cancer. In addition, the necessity of segment 4b+5 liver resection for stage T3 gallbladder has not been reported. This article aims to explore the safety, effectiveness, and short-term prognosis of laparoscopic segment 4b+5 liver resection for T3 stage gallbladder cancer. METHODS: This is a retrospective multicenter propensity score-matched study. Disease-free survival, perioperative complications, and intraoperative safety were analyzed to evaluate safety and effectiveness. RESULTS: There was no significant difference in the incidence of intraoperative bleeding, number of lymph nodes obtained, postoperative complications, or disease-free survival (DFS) between the open group (OG) and laparoscopic group (LG) (P > 0.05). The DFS time of the S4b+5 resection group (S4b5) was longer than that of the wedge group (P = 0.016). Cox regression showed that positive margins (HR, 5.32; 95% CI 1.03-27.63; P = 0.047), lymph node metastasis (HR, 2.70; 95% CI 1.31-5.53; P = 0.007), and liver S4b+5 resection (HR, 0.30; 95% CI 0.14-0.66; P = 0.003) were independent risk factors for DFS. The operative time of indocyanine green (ICG) fluorescence-guided liver S4b5 segment resection was shorter than that of traditional laparoscopic S4b+5 resection guided by hepatic veins (P ≤ 0.001). CONCLUSION: Laparoscopic liver S4b+5 resection for T3 stage gallbladder cancer is safe and feasible and can prolong DFS. ICG fluorescence-guided negative staining may reduce the difficulty of the operation.

SHCBP1 interacting with EOGT enhances O-GlcNAcylation of NOTCH1 and promotes the development of pancreatic cancer.

O-GlcNAcylation is important in the development and progression of pancreatic ductal adenocarcinoma (PDAC). The glycosyltransferase EGF domain-specific O-linked GlcNAc transferase (EOGT) acts as a key participant in glycosylating NOTCH1. High-throughput sequencing of specimens from 30 advanced PDAC patients identified SHCBP1 and EOGT as factors of poor prognosis. We hypothesized that they could mediate PDAC progression by influencing NOTCH1 O-GlcNAcylation. Thus, 186 PDAC tissue specimens were immunostained for EOGT and SHCBP1. Pancreatic cancer cell lines and nude mouse models were used for in vitro and in vivo experiments. Respectively, The protein expression of EOGT and SHCBP1 was significantly elevated and correlated with worse prognosis in PDAC patients. In vitro, SHCBP1 overexpression promoted pancreatic cancer cell proliferation, migration and invasion, while knocking down SHCBP1 and EOGT inhibited these malignant processes. In vivo data showed that SHCBP1 overexpression promoted xenograft growth and lung metastasis and shortened survival in mice, whereas knocking down either EOGT or SHCBP1 expression suppressed xenograft growth and metastasis and prolonged survival. We further clarified the molecular mechanisms by which EOGT and SHCBP1 enhance the O-GlcNAcylation of NOTCH1, Subsequently promoting the nuclear localization of the Notch intracellular domain (NICD) and inhibiting the transcription of E-cadherin and P21 in pancreatic cancer cells.

Hybrid Space Vector PWM Strategy for Three-Phase VIENNA Rectifiers.

Vienna rectifiers are widely used, but they have problems of zero-crossing current distortion and midpoint potential imbalance. In this paper, an improved hybrid modulation strategy is proposed. According to the phase difference between the reference voltage vector and the input current vector, the dynamic current crossing distortion sector is divided at each phase current crossing, and the discontinuous pulse width modulation strategy is adopted in the sector to suppress the redundant small vector mutation and improve the current crossing distortion. To solve the problem of midpoint potential balance, a space vector modulation strategy is adopted outside the sector to control the midpoint potential balance by allocating the time of small vector action by voltage balance factor. Finally, the effectiveness of the proposed method is verified by simulation and experiment.

Long-Term Outcomes of Anatomic Versus Nonanatomic Resection in Hepatocellular Carcinoma Patients with Bile Duct Tumor Thrombus: A Propensity Score Matching Analysis.

BACKGROUND: Anatomic resection (AR) of the liver is generally recommended in hepatocellular carcinoma (HCC) patients. However, the benefits of AR and nonanatomic resection (NAR) in HCC patients with bile duct tumor thrombus (BDTT) are unknown. This study aimed to compare long-term outcomes of AR and NAR in HCC patients with BDTT after curative resection. PATIENTS AND METHODS: A total of 175 consecutive HCC patients with BDTT after curative resection between April 2009 and December 2017 were included. One-to-one propensity score matching (PSM) was performed to minimize the influence of potential confounders. Recurrence-free survival (RFS) and overall survival (OS) were compared between the cohorts. RESULTS: After PSM, 120 patients were analyzed. The AR group had better RFS than the NAR group (P = 0.010). Even though there was no statistically significant difference in OS (P = 0.140, power = 0.33), the 3- and 5-year OS rates in the AR group (52.4% and 44.2%, respectively) were obviously higher than those in the NAR group (35.4% and 30.4%, respectively). When patients were further stratified according to tumor size, better RFS and OS were observed in patients with small (≤ 5 cm) tumors after AR (P < 0.001 and P = 0.004, respectively). Multivariate analysis identified AR (P = 0.024) as an independent favorable prognostic factor for RFS in HCC patients with BDTT. CONCLUSIONS: AR is recommended for HCC patients with BDTT, especially in patients with small (≤ 5 cm) tumors.

Circular RNA circ_001842 plays an oncogenic role in renal cell carcinoma by disrupting microRNA-502-5p-mediated inhibition of SLC39A14.

Renal cell carcinoma (RCC) is a common urologic malignancy, and up to 30% of RCC patients present with locally advanced or metastatic disease at the time of initial diagnosis. Increasing evidence suggests that circular RNAs (circRNAs) serve as genomic regulatory molecules in various human cancers. Our initial in silico microarray-based analysis identified that circRNA circ_001842 was highly expressed in RCC. Such up-regulation of circ_001842 in RCC was experimentally validated in tissues and cell lines using RT-qPCR. Thereafter, we attempted to identify the role of circ_001842 in the pathogenesis of RCC. Through a series of gain- and loss-of function assays, cell biological functions were examined using colony formation assay, Transwell assay, annexin V-FITC/PI-labelled flow cytometry and scratch test. A high expression of circ_001842 in tissues was observed as associated with poor prognosis of RCC patients. circ_001842 was found to elevate SLC39A14 expression by binding to miR-502-5p, consequently resulting in augmented RCC cell proliferation, migration and invasion, as well as EMT in vitro and tumour growth in vivo. These observations imply the involvement of circ_001842 in RCC pathogenesis through a miR-502-5p-dependent SLC39A14 mechanism, suggesting circ_001842 is a potential target for RCC treatment.

Specific tumor-derived CCL2 mediated by pyruvate kinase M2 in colorectal cancer cells contributes to macrophage recruitment in tumor microenvironment.

Development of colorectal cancer has been considered as a result of imbalance of pro- and anti-inflammatory intestinal microenvironment accompanied by macrophage recruitment. Despite macrophages are implicated in remodeling tumor microenvironment, the mechanism of macrophage recruitment is not fully elucidated yet. In this study, we reported clinical association of highly expressed pyruvate kinase M2 in colorectal cancer with macrophage attraction. The conditioned medium from Caco-2 and HT-29 cells with depleted pyruvate kinase M2 dramatically reduced macrophage recruitment, which is reversed by addition of, a critical chemotaxis factor to macrophage migration, rCCL2. Silencing of endogenous pyruvate kinase M2 markedly decreased CCL2 expression and secretion by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Endogenous pyruvate kinase M2 interacted with p65 and mediated nuclear factor-κB signaling pathway and mainly regulated phosphorylation of Ser276 on p65 nuclear factor-κB. In addition, inhibition of macrophage recruitment caused by pyruvate kinase M2 silencing was rescued by ectopic expression of p65. Interestingly, pyruvate kinase M2 highly expressed in colorectal cancer tissue, which is correction with macrophage distribution. Taken together, we revealed a novel mechanism of pyruvate kinase M2 in promoting colorectal cancer progression by recruitment of macrophages through p65 nuclear factor-κB-mediated expression of CCL2.

Chronic subdural haematoma evolving from traumatic subdural hydroma.

OBJECTIVE: This study aimed to investigate the incidence and clinical characteristics of chronic subdural haematoma (CSDH) evolving from traumatic subdual hydroma (TSH). METHODS: The clinical characteristics of 44 patients with CSDH evolving from TSH were analysed retrospectively and the relevant literature was reviewed. RESULTS: In 22.6% of patients, TSH evolved into CSDH. The time required for this evolution was 14-100 days after injury. All patients were cured with haematoma drainage. CONCLUSIONS: TSH is one possible origin of CSDH. The clinical characteristics of TSH evolving into CSDH include polarization of patient age and chronic small effusion. The injuries usually occur during deceleration and are accompanied by mild cerebral damage.

Accumulation and distribution characteristics of zinc and cadmium in the hyperaccumulator plant Sedum plumbizincicola.

Accumulation and distribution of Zn and Cd in the hyperaccumulator plant Sedum plumbizincicola were investigated in a hydroponic experiment. Mean Cd and Zn concentrations in shoots (7,010 and 18,400 mg kg(-1)) were about sevenfold and fivefold higher than those in roots (840 and 3,000 mg kg(-1)) after exposure to 100 µM CdSO4 and 600 µM ZnSO4, respectively. Cd and Zn concentrations in young leaves (4,330 and 9,820 mg kg(-1)) were about sixfold and twofold higher than those in mature leaves (636 and 2,620 mg kg(-1)), respectively. MicroPIXE analysis showed that Zn was predominantly localized in epidermal cells in both young and mature leaves, but large amounts of Zn occurred in mesophyll cells in young leaves. Leaf tissue fractionation showed that soluble and cell wall fractions were different at the two stages of leaf growth. Young and mature leaves of S. plumbizincicola also showed different accumulation and distribution characteristics for Zn and Cd.

Quercetin Regulates Lipid Metabolism and Fat Accumulation by Regulating Inflammatory Responses and Glycometabolism Pathways: A Review.

Fat synthesis and lipolysis are natural processes in growth and have a close association with health. Fat provides energy, maintains physiological function, and so on, and thus plays a significant role in the body. However, excessive/abnormal fat accumulation leads to obesity and lipid metabolism disorder, which can have a detrimental impact on growth and even harm one's health. Aside from genetic effects, there are a range of factors related to obesity, such as excessive nutrient intake, inflammation, glycometabolism disease, and so on. These factors could serve as potential targets for anti-obesity therapy. Quercetin is a flavonol that has received a lot of attention recently because of its role in anti-obesity. It was thought to have the ability to regulate lipid metabolism and have a positive effect on anti-obesity, but the processes are still unknown. Recent studies have shown the role of quercetin in lipid metabolism might be related to its effects on inflammatory responses and glycometabolism. The references were chosen for this review with no date restrictions applied based on the topics they addressed, and the databases PubMed and Web of Sicence was used to conduct the references research, using the following search terms: "quercetin", "obesity", "inflammation", "glycometabolism", "insulin sensitivity", etc. This review summarizes the potential mechanisms of quercetin in alleviating lipid metabolism through anti-inflammatory and hypoglycemic signaling pathways, and describes the possible signaling pathways in the interaction of inflammation and glycometabolism, with the goal of providing references for future research and application of quercetin in the regulation of lipid metabolism.

Photo-Reactivity of dissolved black carbon unveiled by combination of optical spectroscopy and FT-ICR MS analysis: Effects of pyrolysis temperature.

Dissolved black carbon (DBC) has high photoactivity, which plays an important role in contaminants photodegradation. However, it is unclear how pyrolysis temperatures would affect the composition and photo-reactivity of DBC at the molecular level. Herein, we combined complementary techniques to study the characteristics of DBC pyrolyzed at 200 - 500 ℃, as well as the photoproduction of reactive species and the photodegradation of tetracycline (TC). Bulk composition characterization found that condensed aromatic carbonyl compounds (ConAC) with narrow molecular weights in DBC experienced an increase from 200 to 500 °C, which enhanced the photoproduction of 3DBC*,1O2, and ·OH. Molecular-level data suggested that 3DBC* and 1O2 were both related to the same DBC compounds. Comparatively, the patterns for ·OH were less pronounced, implying its precursor was not 3DBC* and had more complexity. Plentiful CHOx species of ConAC in DBC400 and DBC500 (DBCT, where T = pyrolysis temperature) accelerated the generation of 3DBC* and 1O2, enhancing the photodegradation of TC, and mainly triplet states of quinones reacted with TC. In contrast, DBC200 and DBC300 exhibited inhibition since massive CHOx species in lignin-like reduced 3TC* to TC. Our data revealed the diverse photochemical behavior mechanisms of DBC pyrolyzed at 200 - 500 ℃ at the molecular level and the implications for aquatic contaminants photochemistry.

Activation of peroxymonosulfate with natural pyrite-biochar composite for sulfamethoxazole degradation in soil: Organic matter effects and free radical conversion.

Peroxymonosulfate (PMS)-based advanced oxidation processes (AOPs) represent an effective method for the remediation of antibiotic-contaminated soils. In this study, a natural pyrite-biochar composite material (FBCx) was developed, demonstrating superior activation performance and achieving a 76% removal rate of SMX from soil within 120 min. There existed different degradation mechanisms for SMX in aqueous and soil solutions, respectively. The production of 1O2 and inherent active species produced by soil slurry played an important role in the degradation process. The combination of electron paramagnetic resonance (EPR) and free radical probe experiments confirmed the presence of free radical transformation processes in soil. Wherein, the·OH and SO4·- generated in soil slurry did not directly involve in the degradation process, but rather preferentially reacted with soil organic matter (SOM) to form alkyl-like radicals (R·), thereby maintaining a high concentration of reactive species in the system. Furthermore, germination and growth promotion of mung bean seeds observed in the toxicity test indicated the environmental compatibility of this remediation method. This study revealed the influence mechanism of SOM in the remediation process of contaminated soil comprehensively, which possessed enormous potential for application in practical environments.

Malat1 regulates PMN-MDSC expansion and immunosuppression through p-STAT3 ubiquitination in sepsis.

Myeloid-derived suppressor cells (MDSCs) expand during sepsis and contribute to the development of persistent inflammation-immunosuppression-catabolism syndrome. However, the underlying mechanism remains unclear. Exploring the mechanisms of MDSCs generation may provide therapeutic targets for improving immune status in sepsis. Here, a sepsis mouse model is established by cecal ligation and perforation. Bone marrow cells at different sepsis time points are harvested to detect the proportion of MDSCs and search for differentially expressed genes by RNA-sequence. In lethal models of sepsis, polymorphonuclear-MDSCs (PMN-MDSCs) decrease in early but increase and become activated in late sepsis, which is contrary to the expression of metastasis-associated lung adenocarcinoma transcript 1 (Malat1). In vivo, Malat1 inhibitor significantly increases the mortality in mice with late sepsis. And in vitro, Malat1 down-regulation increases the proportion of PMN-MDSCs and enhanced its immunosuppressive ability. Mechanistically, Malat1 limits the differentiation of PMN-MDSCs by accelerating the degradation of phosphorylated STAT3. Furthermore, Stattic, an inhibitor of STAT3 phosphorylation, improves the survival of septic mice by inhibiting PMN-MDSCs. Overall, the study identifies a novel insight into the mechanism of sepsis-induced MDSCs and provides more evidence for targeting MDSCs in the treatment of sepsis.