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Allogeneic platelet-rich plasma (al-PRP) is gaining attention in clinical practice for treating chronic refractory wounds, though research results remain controversial. To assess the clinical efficacy of al-PRP for chronic refractory wounds. Databases including PubMed, Cochrane Library, Embase, CNKI, SinoMed, VIP, and WFPD were searched for randomized controlled trials comparing al-PRP with conventional treatments up to October 2023. Two researchers independently screened studies, extracted data, and assessed quality. Statistical analysis was conducted using RevMan 5.4, and potential publication bias was assessed and corrected using funnel plots and Egger's test. Twelve studies with 717 cases were included. Meta-analysis showed al-PRP significantly improved outcomes compared to non-al-PRP treatments: increased healing rate (RR 2.72, 95% CI 1.77–4.19, p < 0.00001), shortened healing time (SMD − 1.03, 95% CI -1.31 to -0.75, p < 0.00001), improved efficacy rate (RR 1.19, 95% CI 1.10–1.28, p < 0.00001), increased wound shrinkage (MD 35.65%, 95% CI 21.65–49.64, p < 0.00001), and reduced hospital stays (MD -2.62, 95% CI -4.35 to -0.90, p = 0.003). Al-PRP is a feasible, effective, and safe biological therapy for chronic refractory wounds. Trial registration: PROSPERO Identifier CRD42022374920. [ABSTRACT FROM AUTHOR]

"The Routledge Handbook of Second Language Acquisition and Speaking" is a comprehensive and timely contribution to the field of second language acquisition (SLA) research. The book covers a wide range of topics related to speaking skills in SLA, including theoretical foundations, research methodologies, core topics, pedagogical issues, and emerging topics. It features contributions from outstanding scholars and provides a thorough exploration of the multifaceted landscape of L2 speech acquisition. While the book offers valuable insights and guidance for researchers and advanced students in the field, it could benefit from more practical examples and detailed methodological guidance for new researchers. [Extracted from the article]

Key Clinical Message: Transfusion‐related acute lung injury (TRALI) is characterized by non‐cardiogenic pulmonary edema and acute hypoxemia. There are few reports of HLA‐II antibodies causing TRALI in China. [ABSTRACT FROM AUTHOR]

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Sepsis is one of the most severe complications and causes of mortality in the clinic. It remains a great challenge with no effective treatment for clinicians worldwide. Inhibiting the release of proinflammatory cytokines during sepsis is considered as an important strategy for treating sepsis and improving survival. In the present study, we have observed the effect of dimethyl fumarate (DMF) on lipopolysaccharide- (LPS-) induced sepsis and investigated the possible mechanism. By screening a subset of the Johns Hopkins Drug Library, we identified DMF as a novel inhibitor of nitric oxide synthesis in LPS-stimulated RAW264.7 cells, suggesting that DMF could be a potential drug to treat sepsis. To further characterize the effect of DMF on LPS signaling, TNF-α, MCP-1, G-CMF, and IL-6 expression levels were determined by using cytokine array panels. In addition, an endotoxemia model with C57BL/6 mice was used to assess the in vivo efficacy of DMF on sepsis. The survival rate was assessed, and HE staining was performed to investigate histopathological damage to the organs. DMF was found to increase the survival of septic mice by 50% and attenuate organ damage, consistent with the reduction in IL-10, IL-6, and TNF-α (inflammatory cytokines) in serum. In vitro experiments revealed DMF's inhibitory effect on the phosphorylation of p65, IκB, and IKK, suggesting that the primary inhibitory effects of DMF can be attributed, at least in part, to the inhibition of phosphorylation of IκBα, IKK as well as nuclear factor-κB (NF-κB) upon LPS stimulation. The findings demonstrate that DMF dramatically inhibits NO and proinflammatory cytokine production in response to LPS and improves survival in septic mice, raising the possibility that DMF has the potential to be repurposed as a new treatment of sepsis. [ABSTRACT FROM AUTHOR]

Pressure injury often seriously affects the life quality of aged patients, especially the long‐term bedridden casualties. Widely adopted by different disciplines, negative pressure suction has its role in pressure injury. Microskin implantation has been demonstrated powerful in increasing the expansion ratio of donor area‐derived skin and accelerating wound healing by forming "skin islands". The study was designed to evaluate the efficacy and safety of additional use of bedside microskin implantation in the palliative care of pressure injury of aged patients who cannot tolerate surgical treatment as a supplement for standard negative pressure suction. An open‐label within‐patient RCT was conducted in aged patients with pressure injury. Sixteen patients were enrolled. After granulation tissues formed, half of a pressure injury was randomised to receive the negative pressure suction as the control group, and the other half exposed to additional bedside microskin implantation as the experimental group. Efficacy was evaluated within 1 month after treatment, and the primary endpoints included the wound healing rate and pressure ulcer scale for healing (PUSH) scores. The secondary outcomes included survival rate of implanted microskin, pain intensity assessment, satisfaction surveys from patients or their family, and pressure ulcer healing complications. Sixteen patients completed the study. After 14 days of operation, 5.63 ± 1.78 out of 10 pieces of implanted microskin survived and formed neonatal epithelium. The wound healing rates of the control group and the experimental group at 1 month were (26.17 ± 9.03%) and (35.95 ± 16.02%), respectively (P <.01). The mean PUSH score before the surgery was 12.38 ± 2.23. At 1 month after surgery, the mean difference of PUSH score from baseline was 2.13 ± 0.96 in the control group and 2.81 ± 0.83 in the experimental group (P <.01). The treatment of microskin implantation did not cause additional pain or complications to the patients. Accompanied by a better ulcer status, the majority of patients or their guardians have a high degree of acceptance towards the microskin implantation. Bedside microskin implantation could accelerate wound healing with lower PUSH scores. As a complementary palliative treatment, supplementary microskin implantation is effective and well tolerated. [ABSTRACT FROM AUTHOR]

Background: Excess body weight has been found to associate with an increased risk of lymphomas and some metabolic pathways are currently recognized in lymphomagenesis. Bioactive lipid metabolites such as sphingosine-1-phosphate (S1P) have been proposed to play an important role linking obesity and lymphomas. However, the underlying mechanism(s) of S1P signaling in obesity-lymphomagenesis have not been well addressed. Methods: The gene expression of sphingosine kinase (SPHK), lymphoma prognosis, and S1P production were analyzed using Gene Expression Omnibus (GEO) and human lymphoma tissue array. Obesity-lymphoma mouse models and lymphoma cell lines were used to investigate the S1P/SPHK-YAP axis contributing to obesity-lymphomagenesis. By using the mouse models and a monocyte cell line, S1P-mediated polarization of macrophages in the tumor microenvironment were investigated. Results: In human study, up-regulated S1P/SPHK1 was found in human lymphomas, while obesity negatively impacted progression-free survival and overall survival in lymphoma patients. In animal study, obesity-lymphoma mice showed an aggressive tumor growth pattern. Both in vivo and in vitro data suggested the existence of S1P-YAP axis in lymphoma cells, while the S1P-ALOX15 signaling mediated macrophage polarization towards TAMs exacerbated the lymphomagenesis. In addition, treatment with resveratrol in obesity-lymphoma mice showed profound effects of anti-lymphomagenesis, via down-regulating S1P-YAP axis and modulating polarization of macrophages. Conclusion: S1P/S1PR initiated the feedback loops, whereby S1P-S1PR1/S1PR3-YAP signaling mediated lymphomagenesis contributing to tumor aggressive growth, while S1P-ALOX15 signaling mediated TAMs contributing to immunosuppressive microenvironment in obesity-lymphoma. S1P-targeted therapy could be potentially effective and immune-enhancive against obesity-lymphomagenesis. Highlights: • Obesity negatively impacted progression-free survival and overall survival in lymphoma patients while an aggressive tumor growth pattern was found in obesity-lymphoma mice. • S1P-S1PR1/S1PR3-YAP signaling mediated lymphomagenesis contributing to tumor aggressive growth in obesity-lymphoma. • S1P-ALOX15 signaling mediated TAMs contributing to immunosuppressive microenvironment in obesity-lymphoma. • S1P-targeted therapy could be potentially effective and immune-enhancive against obesity-lymphomagenesis. [ABSTRACT FROM AUTHOR]

Background: In 2021, a once-in-a-century heavy rainstorm suddenly attacked Zhengzhou, an important inland city in northern China. However, there have been no studies on the psychological health of disaster-stricken residents. This study is the first to comprehensively report on the mental health status and related factors of local ordinary residents after the heavy rainstorm. Objective: The purpose of this study is to investigate the mental health status and related influencing factors of local ordinary residents after the flood disaster, and to provide reference for government departments to formulate disaster psychological intervention countermeasures based on evidence-driven strategies. Methods: The snowball sampling technique was used in this study, and measurement tools of Rainstorm Exposure Questionnaire, Subjective Perception of Rainstorm, Post-Traumatic Stress Disorder Checklist-Civilian version (PCL-C), Depression, Anxiety and Stress Scale-21 (DAS-21) and Chinese version of Social Support Rating Scale (SSRS) were used to evaluate the rainstorm exposure, subjective perception of the rainstorm, psychological symptoms and social support of the disaster-stricken residents within a week after the rainstorm. Logistic regression analysis was used to examine the psychological status and related factors of local residents after the rainstorm disaster. Results: A total of 469 valid samples were obtained in this study. All the subjects were in the disaster area and experienced the rainstorm personally, with normal intelligence. The statistical results showed that 25.37% people had experienced at least three rainstorm-related stresses, nearly 20.26% people had post-traumatic stress disorder (PTSD) symptoms, and 39.3%, 53.92% and 65.83% people had depression, anxiety and stress symptoms, respectively. Multivariable logistic regression analyses indicated that female (all p < 0.05), the divorced, agricultural workers/farmers (all p < 0.05), students (all p < 0.05), people experiencing at least three rainstorm-related stresses (p < 0.05 or p < 0.01), people with lower satisfaction at the social flood fighting measures (p < 0.05 or p < 0.01) and people with low social support (p < 0.05 or p < 0.01) were all independent risk factors for poor psychological health, and college education or above (p < 0.05 or p < 0.01), the lower degree of worrying about themselves (all p < 0.01), family members (all p < 0.01) and family property (all p < 0.01) were all related to higher psychological health among flood survivors after the disaster. Conclusions: Rainstorm could cause local residents to have various degrees of psychological symptoms. This study identified factors associated with the psychological health of disaster-stricken residents, which could be used to develop psychological interventions in improving psychological health of local residents. [ABSTRACT FROM AUTHOR]

Objectives: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with a poor prognosis. PDAC has poor response to immunotherapy because of its unique tumour microenvironment (TME). In an attempt to stimulate immunologically silent pancreatic cancer, we investigated the role of epigenetic therapy in modulating the TME to improve immunogenicity. Methods: In vitro human PDAC cell lines MiaPaca2 and S2‐013 were treated with 5μm3‐Deazaneplanocin A (DZNep, an EZH2 inhibitor) and 5 μm5‐Azacytidine (5‐AZA, a DNMT1 inhibitor). In vivo orthotopic murine tumour models using both murine PAN02 cells and KPC cells inoculated in immunocompetent C56/BL7 mice were treated with anti‐PD‐L1 combined with DZNep and 5‐AZA. Short hairpin knockdown (KD) of EZH2 and DNMT1 in PAN02 cells for the orthotopic murine tumour model was established to validate the drug treatment (DZNep and 5‐AZA). qRT‐PCR and microarray assays were performed for the evaluation of Th1‐attracting chemokines and cancer‐associated antigen induction. Results: Drug treatments induced significant upregulation of gene expressions of Th1‐attracting chemokines, CXCL9 and CXCL10, and the cancer–testis antigens, NY‐ESO‐1, LAGE and SSX‐4 (P < 0.05). In orthotopic tumour models, inoculation of PAN02 cells or KPC cells demonstrated significant tumour regression with corresponding increased apoptosis and infiltration of cytotoxic T lymphocytes in the combination treatment group. In the orthotopic Pan02‐KD model, the anti‐PD‐L1 treatment also caused significant tumour regression. Conclusion: We demonstrate that immunotherapy for PDAC can be potentiated with epigenetic therapy by increasing cancer‐associated antigen expression and increased T‐cell trafficking across the immunosuppressive tumour microenvironment via upregulation of the repressed chemokines and increased apoptosis with subsequent tumour regression. [ABSTRACT FROM AUTHOR]

Small object detection is one of the most challenging and non-negligible fields in computer vision. Inspired by the location–focus–identification process of the avian visual system, we present our location-focused small-object-detection algorithm for video or image sequence, OTNet. The model contains three modules corresponding to the forms of saliency, which drive the strongest response of OT to calculate the saliency map. The three modules are responsible for temporal–spatial feature extraction, spatial feature extraction and memory matching, respectively. We tested our model on the AU-AIR dataset and achieved up to 97.95% recall rate, 85.73% precision rate and 89.94 F1 score with a lower computational complexity. Our model is also able to work as a plugin module for other object detection models to improve their performance in bird-view images, especially for detecting smaller objects. We managed to improve the detection performance by up to 40.01%. The results show that our model performs well on the common metrics on detection, while simulating visual information processing for object localization of the avian brain. [ABSTRACT FROM AUTHOR]

Objective: To assess the potential benefit of chidamide maintenance therapy after induction treatment in peripheral T-cell lymphoma (PTCL). Materials and Methods: The clinical data of 48 transplantation-ineligible patients with different PTCL subtypes who received continuous chidamide treatment after first-line therapy were collected. Progression-free survival (PFS), overall survival (OS), and safety were analyzed. Results: In total, 68.8% of patients were male (33/48), the median age was 59.5 years (22~80). The pathological subtypes were angioimmunoblastic T-cell lymphoma (AITL, 43.8%), anaplastic large cell lymphoma (ALCL, 16.6%), PTCL-not otherwise specified (NOS, 25%), NK/T-cell lymphoma (NKT, 14.6%). 35.4% (7/48) patients had intermediate or high risk (IPI=3~5). 20 patients (41.7%) received chidamide as a maintenance treatment after achieving a complete response (CR). 57.1% (16/28) exhibited a better response after chidamide (9 cases partial response [PR] to CR, 7 from stable disease [SD] to PR). The CR and overall response rate (ORR) were 60.4% and 93.8%, respectively. In addition, 21/21 AITL, 10/12 PTCL-NOS, and 8/8 ALCL, 6/7 NK/T exhibited CR/PR as the best response during the follow-up period. Meanwhile, the CR and ORR did not differ by age (<60 vs ≥60: 50.0% vs 70.8%, P = 0.091; and 91.7% vs 95.8%, P = 0.551). The median follow-up period was 12.8 months (3.0–66.6), 14 patients developed PD (29.2%), 10 of them died of lymphoma (20.8%). Totally, the 40 cases achieved CR/PR from 1st line regimen got better PFS as well as OS than the rest 8 cases (the 1-year PFS was 80.8% vs 46.9% and the 2-year PFS was 71.9% vs 46.9%, P=0.012. the 1-year OS was 89.9% vs 72.6% and the 2-year OS was 85.9% vs 48.6%, P=0.032). No patients discontinued treatment because of adverse events. The most common toxicities were neutropenia (75.0%), anemia (79.2%), thrombocytopenia (58.3%), and anorexia (45.8%), and fatigue (43.8%). Conclusion: Chidamide maintenance therapy led to improvements of PFS and OS with a manageable safety profile in patients with PTCL. Further randomized studies are required to examine the role of chidamide maintenance therapy in PTCL. [ABSTRACT FROM AUTHOR]

With inconsistent findings, evidence has been obtained in recent years that metabolic disorders are closely associated with the development of lymphomas. Studies and multiple analyses have been published also indicating that some solid tumor survivors develop a secondary lymphoma, whereas some lymphoma survivors subsequently develop a second malignant neoplasm (SMN), particularly solid tumors. An interaction between the multiple etiologic factors such as genetic factors and late effects of cancer therapy may play an important role contributing to the carcinogenesis in patients with metabolic diseases or with a primary cancer. In this review, we summarize the current knowledge of the multiple etiologic factors for lymphomagenesis, focusing on the SMN in lymphoma, secondary lymphomas in primary cancers, and the lymphomas associated to metabolic disorders/diseases, which have been received less attention previously. Further, we also review the data of coexistence of lymphomas and hepatocellular carcinoma (HCC) in patients with infection of hepatitis C virus and hepatitis B virus. [ABSTRACT FROM AUTHOR]

Porphyromonas gingivalis , a keystone periodontal pathogen, has emerged as a risk factor for systemic chronic diseases, including non-alcoholic fatty liver disease (NAFLD). To clarify the mechanism by which this pathogen induces such diseases, we simultaneously analyzed the transcriptome of intracellular P. gingivalis and infected host cells via dual RNA sequencing. Pathway analysis was also performed to determine the differentially expressed genes in the infected cells. Further, the infection-induced notable expression of P. gingivalis livk and livh genes, which participate in branched-chain amino acid (BCAA) transfer, was also analyzed. Furthermore, given that the results of recent studies have associated NAFLD progression with elevated serum BCAA levels, which reportedly, are upregulated by P. gingivalis , we hypothesized that this pathogen may induce increases in serum BCAA levels and exacerbate liver injury via livh/livk. To verify this hypothesis, we constructed P. gingivalis livh/livk -deficient strains (Δlivk , Δlivh) and established a high-fat diet (HFD)-fed murine model infected with P. gingivalis. Thereafter, the kinetic growth and exopolysaccharide (EPS) production rates as well as the invasion efficiency and in vivo colonization of the mutant strains were compared with those of the parental strain. The serum BCAA and fasting glucose levels of the mice infected with either the wild-type or mutant strains, as well as their liver function were also further investigated. It was observed that P. gingivalis infection enhanced serum BCAA levels and aggravated liver injury in the HFD-fed mice. Additionally, livh deletion had no effect on bacterial growth, EPS production, invasion efficiency, and in vivo colonization, whereas the Δlivk strain showed a slight decrease in invasion efficiency and in vivo colonization. More importantly, however, both the Δlivk and Δliv h strains showed impaired ability to upregulate serum BCAA levels or exacerbate liver injury in HFD-fed mice. Overall, these results suggested that P. gingivalis possibly aggravates NAFLD progression in HFD-fed mice by increasing serum BCAA levels, and this effect showed dependency on the bacterial BCAA transport system. [ABSTRACT FROM AUTHOR]

Background: Myocardial Ischemia with No Obstructive Coronary Artery Disease (MINOCA) is a common cause of type 2 acute myocardial infarction (AMI) which requires careful differential diagnosis. Coronary artery spasm (CAS) syndrome is one etiology that can lead to MINOCA. Nilotinib, a targeted treatment for chronic myeloid leukemia (CML), has been reported to be related with increased risk of adverse vascular events.Case Presentation: A 67-year-old male patient was admitted to hospital with acute chest pain. He had a past medical history of CML and a history of treatment with nilotinib for 12 months. Coronary angiography (CAG) showed no significant stenosis. Since the onset of angina was generally in the early morning, and ECG and echocardiography suggested right coronary artery (RCA) disease, an ergonovine provocation test was performed to confirm the diagnosis of CAS. After intracoronary administration of ergonovine, middle and distal RCA showed over 90% vasoconstriction. Nilotinib related MINOCA, CAS and CML were diagnosed. Lifestyle changes (cessation of smoking), anti-spasmodics, statin treatment and adjustment of the nilotinib dose (from 200 mg bid, to 150 mg bid) were recommended for this patient. Six-month's follow-up showed good recovery with no onsets of angina.Conclusions: Physicians should be vigilant to adverse vascular events when treating patients who have been prescribed nilotinib. It is suggested that in patients with MINOCA who have a history of treatment with nilotinib, CAS-induced MINOCA should be included in the differential diagnosis. Further studies are needed to clarify the mechanism and to find better management. [ABSTRACT FROM AUTHOR]

Introduction: Several maintenance therapies are available for treatment of patients with relapsed/refractory (R/R) diffuse large B cell lymphoma (DLBCL). The objective of this review was to assess the efficacy and safety of lenalidomide monotherapy in these patients. Methods: MEDLINE, EMBASE, and the Cochrane Library databases were searched for publications up to April 7, 2021. Original studies that had information on lenalidomide monotherapy for DLBCL patients with R/R status were included. Meta-analyses of response rates, adverse events (AEs), overall survival (OS), and progression-free survival (PFS) were performed. The pooled event rates were calculated using a double arcsine transformation to stabilize the variances of the original proportions. Subgroup analysis was used to compare patients with different germinal center B-cell-like (GCB) phenotypes. Results: We included 11 publications that examined DLBCL patients with R/R status. These studies were published from 2008 to 2020. The cumulative objective response rate (ORR) for lenalidomide monotherapy was 0.33 (95% CI: 0.26, 0.40), and the ORR was better in patients with the non-GCB phenotype (0.50; 95% CI: 0.26, 0.74) than the GCB phenotype (0.06; 95% CI: 0.03, 0.11). The major serious treatment-related AEs were neutropenia, thrombocytopenia, respiratory disorders, anemia, and diarrhea. The median PFS ranged from 2.6 to 34 months and the median OS ranged from 7.8 to 37 months. Conclusion: This study provides evidence that lenalidomide monotherapy was active and tolerable in DLBCL patients with R/R status. Patients in the non-GCB subgroup had better responsiveness. [ABSTRACT FROM AUTHOR]

Glutamate has been implicated in exercise‐induced fatigue, but the underlying mechanism is unknown. This study aimed to determine whether glutamate transporter‐1 (GLT‐1) has a key role in the regulation of exercise‐induced fatigue. The expressions of GLT‐1 and glial fibrillary acidic protein (GFAP) in the supplementary motor area of rats exposed to exhaustion were analyzed by immunohistochemistry. The expression of GLT‐1 was further confirmed by Western blotting. The effects of GLT‐1 on extracellular levels of glutamate and lactate and on exercise endurance were studied by microdialysis. GLT‐1 expression was decreased in rats subjected to exercise‐induced fatigue. Functional inhibition of GLT‐1 using dihydrokainate and transcriptional inhibition of GLT‐1 using antisense oligodeoxynucleotides led to a decrease in exercise endurance with a subsequent increase in extracellular glutamate concentration and decrease in extracellular lactate concentration. The expression of GLT‐1 in the supplementary motor area is reduced after strenuous exercise, resulting in an increased extracellular glutamate concentration and decreased extracellular lactate level that may be responsible for the development of fatigue. GLT‐1‐mediated uptake of glutamate ameliorates exercise‐induced fatigue in rat models. [ABSTRACT FROM AUTHOR]

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematopoietic malignancy mainly affecting elderly patients. Most patients present with asymptomatic skin lesions as the first symptom and has a high frequency of bone marrow involvement. BPDCN is typically characterized by CD4+ and CD 56+ co-expression without common lymphoid or myeloid lineage markers. There is no consensus on the optimal therapeutic strategy for BPDCN. It is highly responsive to chemotherapy but the median event-free survival is very short. Allogeneic stem cell transplantation may improve the prognosis of BPDCN but the rate of relapse is still high. There are no specific targeted agents approved for patients with BPDCN, but advances in the understanding of the pathobiology of BPDCN and the results of early clinical studies have revealed novel targets and potentially effective agents. Novel targeted therapies may improve outcomes for patients with BPDCN in the future. [ABSTRACT FROM AUTHOR]

Stress-induced gastric ulcer is an important life-threatening condition, while the molecular basis of its development is incompletely understood. Toll-like receptor 4 (TLR4), an innate immune pattern recognition receptor, can induce pro-inflammatory transcription, aggravating a stress ulcer. The present study found that TLR4 played a protective role in a mouse model of water immersion (23 °C) restraint stress. Wild-type (WT) and TLR4−/−male mice were respectively divided into five groups (5 per group), and exposed to the stressor for 0, 0.5, 1, 2, or 4 hours. Gastric ulcer index, determined post mortem, increased with time in both types of mice but was greater in TLR4−/−mice. Furthermore, increased serum cortisol and corticosterone concentrations were observed in WT mice only, and such increases were detected only in WT mice 4 h after lipopolysaccharide (LPS) treatment (2 mg/kg, intraperitoneal injection). Moreover, the administration of cortisol alleviated the gastric injury in TLR4−/−mice. Western blotting showed expression in the adrenal of P450scc (CYP11A1), the first rate-limiting enzyme in the synthesis of steroids, was increased 4 h after water immersion restraint stress or LPS treatment in WT mice, but was conversely decreased in TLR4−/−mice after either stressor. Furthermore, in adrenal glands of TLR4−/−mice, structural distortion of mitochondria (which contain CYP11A1) was found with electron microscopy, and lack of lipid-storing droplets was found using light microscopy on adrenal cryosections stained with Oil red O. These data indicate that TLR4 plays a protective role in stress-induced gastric ulcer that is exerted via impacting synthesis of glucocorticoid in the adrenal gland. [ABSTRACT FROM PUBLISHER]

Inflammatory response and oxidative stress are considered to play an important role in the development of acute liver injury induced by carbon tetrachloride (CCl4) and galactosamine (GalN)/lipopolysaccharides (LPS). Esculentoside A (EsA), isolated from the Chinese herb phytolacca esculenta, has the effect of modulating immune response, cell proliferation and apoptosis as well as anti-inflammatory effects. The present study is to evaluate the protective effect of EsA on CCl4 and GalN/LPS-induced acute liver injury. In vitro, CCK-8 assays showed that EsA had no cytotoxicity, while it significantly reduced levels of TNF-α and cell death rate challenged by CCl4. Moreover, EsA treatment up-regulated PPAR-γ expression of LO2 cells and reduced levels of reactive oxygen species (ROS) challenged by CCl4. In vivo, EsA prevented mice from CCl4-induced liver histopathological damage. In addition, levels of AST and ALT were significantly decreased by EsA treatment. Furthermore, the mice treated with EsA had a lower level of TNF-α, Interleukin (IL)-1β and IL-6 in mRNA expression. EsA prevented MDA release and increased GSH-Px activity in liver tissues. Immunohistochemical staining showed that over-expression of F4/80 and CD11b were markedly inhibited by EsA. The western bolt results showed that EsA significantly inhibited CCl4-induced phosphonated IkBalpha (P-IκB) and ERK. Furthermore, EsA treatment also alleviated GalN/LPS-induced acute liver injury on liver enzyme and histopathological damage. Unfortunately, our results exhibited that EsA had no effects on CCl4-induced hepatocyte apoptosis which were showed by TUNEL staining and Bax, Caspase-3 and cleaved Caspase-3 expression. Our results proved that EsA treatment attenuated CCl4 and GalN/LPS-induced acute liver injury in mice and its protective effects might be involved in inhibiting inflammatory response and oxidative stress, but not apoptosis with its underlying mechanism associated with PPAR-γ, NF-κB and ERK signal pathways. [ABSTRACT FROM AUTHOR]

The effects of a diesel oxidation catalytic (DOC) converter on diesel engine emissions were investigated on a diesel bench at various loads for two steady-state speeds using diesel fuel and B20. The DOC was very effective in hydrocarbon (HC) and CO oxidation. Approximately 90%-95% reduction in CO and 36%-70% reduction in HC were realized using the DOC. Special attention was focused on the effects of the DOC on elemental carbon (EC) and organic carbon (OC) fractions in fine particles (PM) emitted from the diesel engine. The carbonaceous compositions of PM were analyzed by the method of thermal/optical reflectance (TOR). The results showed that total carbon (TC), OC and EC emissions for PM from diesel fuel were generally reduced by the DOC. For diesel fuel, TC emissions decreased 22%-32% after the DOC depending on operating modes. The decrease in TC was attributed to 35%-97% decrease in OC and 3%-65% decrease in EC emissions. At low load, a significant increase in the OC/EC ratio of PM was observed after the DOC. The effect of the DOC on the carbonaceous compositions in PM from B20 showed different trends compared to diesel fuel. At low load, a slight increase in EC emissions and a significant decrease in OC/EC ratio of PM after DOC were observed for B20. [ABSTRACT FROM AUTHOR]