Minimal-access video-assisted retroperitoneal and/or transperitoneal debridement (VARTD) in the management of infected walled-off pancreatic necrosis with deep extension: initial experience from a prospective single-arm study.

BACKGROUND: The currently preferred minimally invasive approaches have substantially improved outcomes of infected walled-off pancreatic necrosis (iWON). However, iWON with deep extension (iWONde) still poses a tricky challenge for sufficient necrosis evacuation by one stand-alone approach, often requiring repeated interventions. The aim of this study was to assess the effectiveness and safety of a minimal-access video-assisted retroperitoneal and/or transperitoneal debridement (hereafter called VARTD) in the management of iWONde. METHODS: Patients who had developed an iWONde were recruited to receive the VARTD in this prospective single-arm study. The primary efficacy endpoint was clinical improvement up to day 28 after the VARTD, defined as a ≥ 75% reduction in size of necrotic collection (in any axis) on CT and clinical resolution of sepsis or organ dysfunction. The primary safety endpoint was a composite of major complications or death during follow-up. Six-month postdischarge follow-up was available. RESULTS: Between July 18, 2018, and November 12, 2020, we screened 95 patients with necrotizing pancreatitis; of these, 21 iWONde patients (mean [SD] age, 42.9 [11.7] years; 10 [48%] women) were finally enrolled. The primary efficacy endpoint was achieved by most participants (14/21, 67%). No participants required repeated interventions. The primary safety endpoint occurred in six patients (29%). Except one in-hospital death attributable to repeated intra-abdominal hemorrhage, others were discharged without any major complication. CONCLUSIONS: The VARTD approach appears to have a reasonable efficacy with acceptable complication rates and thus might be an option for improving clinical management of iWONde. TRIAL REGISTRATION: This study is registered with Chinese Clinical Trial Registry (chictr.org.cn number, ChiCTR1800016950).

Iron-Modified Biochar Strengthens Simazine Adsorption and Decreases Simazine Decomposition in the Soil.

Currently, modified biochar has been successfully used in the remediation of soil polluted with heavy metals. However, the effects of the modified biochar on pesticides (such as simazine) are still unclear. Herein, the environmental fate of simazine, such as decomposition, leaching, and adsorption in unamended soil, in the soil amended with unmodified and modified biochar (biochar + FeCl3, biochar + FeOS, biochar + Fe) were evaluated. In addition, an incubation experiment was also performed to observe the influence of modified biochar on the microbial community and diversity in the soil. The results showed that modified biochar significantly decreased the decomposition of simazine in the soil compared to its counterpart. Modified biochar also reduced the concentration of simazine in the leachate. Compared with the control, soil microbial biomass in the soil amended with unmodified biochar, biochar + FeCl3, biochar + Fe, and biochar + FeOS was decreased by 5.3%, 18.8%, 8.7%, and 18.1%, respectively. Furthermore, modified biochar changed the structure of the microbial community. This shows that modified biochar could increase the soil adsorption capacity for simazine and change the amount and microbial community that regulates the fate of simazine in the soil. This study concludes that iron-modified biochar has positive and negative effects on the soil. Therefore, its advantages and side effects should be considered before applying it to the soil.

Acupoint for angina pectoris: A protocol for systematic review and meta-analysis.

INTRODUCTION: Patients with angina pectoris (AP) often experience heavy psychological distress, especially anxiety and depression, which results in poorer quality of life, shorter survival time. Acupoint therapies, including massage, acupuncture, acupoints injection, acupressure, and moxibustion, showed clinical and long-lasting benefits for AP, but the efficiency of acupoint therapies was poorly evaluated. The current review is attempted to evaluate the efficacy and safety of the different acupoint-based therapies for AP. METHODS AND ANALYSIS: A literature search will be conducted in MEDLINE, EMBASE, Web of Science, Cochrane Library, Web of Science, PubMed, Science Direct, Wan Fang Data Knowledge Service Platform, Chinese Biomedical Literature Database (CBM), Chinese Scientific Journal Database (VIP database), and China National Knowledge Infrastructure (CNKI). Observational studies regarding the association between liver cancer and depression and anxiety written in English or Chinese will be included. Study inclusion, data extraction, and quality assessment will be performed independently by 2 reviewers. We will use RevMan V.5.0 and STATA V.12.0 software for statistical analysis. The I2 test will be used to identify the extent of heterogeneity. Publication bias will be assessed by generating a funnel plot and performing the Begg and Egger test. The quality of the systematic review will be evaluated using the Measurement Tool to Assess Systematic Reviews (AMSTAR) and Grading of Recommendations Assessment Development and Evaluation (GRADE) criteria. With the permitted numeric data, we will carry out a meta-analysis. RESULTS: This study will provide a high-quality synthesis of pain VAS and functional disability or the quality of life, the success treatment rate, the recurrent rate and the complications rate to assess the effectiveness and safety of acupoint for AP patients. This systematic review will provide evidence to judge whether acupoint is an effective intervention for patients with AP. CONCLUSION: This systematic review and meta-analysis will provide evidence to judge whether acupoint is an effective intervention for patients with AP and provide evidence for designing early targeted interventions for high-risk survivors that can attenuate negative reactions. PROSPERO REGISTRATION NUMBER: 10.17605/OSF.IO/VNXWE.

Protection from lipopolysaccharide-induced pulmonary microvascular endothelial cell injury by activation of hedgehog signaling pathway.

Pulmonary microvascular endothelial cells (PMVECs) are critically involved in the pathogenesis of acute lung injury. Hedgehog signaling pathway plays a fundamental role in embryonic development as well as adult morphogenesis and carcinogenesis. As the priming protein of hedgehog signaling pathway, sonic hedgehog (Shh) may recently be advantage for decreasing endothelial injury and promoting the repair of endothelial barrier function. To investigate the expression and role of hedgehog signal pathway in PMVECs injured by lipopolysaccharide (LPS), cells were divided into six groups: control group, LPS group, rhShh group, LPS+rhShh group, rhShh+cyclopamine group, and LPS+rhShh+cyclopamine group. Real time RT-PCR and Western blotting were used to detect the mRNA and protein expression of hedgehog signal molecules including Shh, Patched-1 (Ptc-1) and Gli1 in nucleus. The activity of PMVECs was examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In this study, we found that Shh, Ptch1, and Gli1 were expressed in rat PMVECs and their expression decreased when cells were treated by LPS. In the other hand, LPS inhibited the activity of rat PMVECs and caused the cells injury. Activation of Hedgehog signaling pathway by Shh could elevate the activity of PMVECs with pretreatment by LPS. Therefore, hedgehog signaling pathway should play a protective role on injury PMVECs by LPS.

SIGIRR inhibits toll-like receptor 4, 5, 9-mediated immune responses in human airway epithelial cells.

Human airway epithelial cells (HAEC) may contribute to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) through toll-like receptors (TLRs)-mediated molecular mechanisms. TLRs exist on the surface of HAEC where binding to their cognate ligands initiates airway inflammation. Single immunoglobulin interleukin-1 receptor-related protein (SIGIRR) is a member of the toll-interleukin-1 receptor (TIR) family that can negatively modulate the immune response. We carried out studies to characterize SIGIRR modulation of TLR-mediated immune response in HAEC and to define its mechanisms of action. Following treatment with various concentrations of LPS, flagellin and CpG DNA, the levels of cognate TLRs 4, 5, and 9 were measured in the supernatants of HAEC over-expressing the SIGIRR molecule. Moreover, the interaction of the TLR adaptor myeloid differentiation factor 88 (MyD88) with SIGIRR in response to LPS-, flagellin- and CpG DNA-stimulation was examined by co-immunoprecipitation. The findings from this study revealed that overexpression of SIGIRR in HAEC stimulated by LPS, flagellin or CpG DNA resulted in attenuated production of the inflammatory mediators IL-6 and TNF-α. This attenuation was not the result of decreased expression of TLR4, 5 or 9, but rather a sequestration of MyD88 to the TLRs. In conclusion, SIGIRR can inhibit TLR4, 5, and 9-mediated immune responses in HAEC and may be a valuable therapeutic target for the prevention of ALI/ARDS.

Quantitative analysis of glioma cell invasion by diffusion tensor imaging.

We aimed to quantitatively analyze the invasion of glioma cells by diffusion tensor imaging (DTI). Twenty patients with glioma, who required surgical decompression, were included in this study. Peritumoral edematous regional tissues were harvested for tumor cell counting and cell density analysis to establish standards for degrees of tumor infiltration. Fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values of water molecules in brain in five regions of interest (ROI) were measured by DTI: (i) the glioma region; (ii) peritumoral edematous tissue; (iii) surrounding edematous tissue; (iv) white matter; and (v) contralateral white matter. The correlation between FA and ADC values from different ROI, and degree of tumor infiltration was analysed. FA values tended to increase from the glioma region outwards, and the maximum amplification appeared between peritumoral edematous and surrounding edematous regions. FA values from peritumoral edematous regions were negatively correlated with the degree of glioma infiltration. ADC values increased significantly in the peritumoral edematous region, but changes in other regions were variable. FA values from peritumoral edematous regions should be used as an evaluation index for the invasion of glioma cells.

[The effect of seawater on expression of protease-activated receptor 2 in adenocarcinoma of lung cell line A549 cells].

OBJECTIVE: To investigate the effect of seawater on expression of protease-activated receptor 2 (PAR-2) in adenocarcinoma of lung cell line A549 cells, and the inflammatory injury on A549 cells induced by seawater. METHODS: A549 cells were randomly divided into four groups: control group, 2 hours group, 4 hours group, 8 hours group, in which cells were treated with seawater for 2, 4 and 8 hours respectively. After seawater treatment, cells were collected for real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting analysis to determine the expression of PAR-2 mRNA and its protein. Supernatant were collected for tumor necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8) which were determined by enzyme-linked immunosorbent essay (ELISA). RESULTS: The expression of PAR-2 mRNA and protein of A549 cells increased in a time-dependent manner after seawater treatment, significantly so after 2 hours in all groups (both P<0.05), and peaked at 4 hours after seawater treatment (1.8-fold and 2.2-fold respectively, both P<0.01), followed by a decrease though still higher than those of control group significantly (both P<0.01). TNF-alpha and IL-8 in supernatant increased significantly after seawater treatment, peaking at 2 hours after seawater treatment [(214.35+/-20.85) ng/L, (55.86+/- 5.65) ng/L ] and then followed by a slight decrease though still significantly higher than those of control group [(25.86+/-3.85) ng/L, (6.97+/-1.77) ng/L, all P<0.01]. CONCLUSION: Seawater can induce significant inflammation of A549 cells and up-regulate the expression of PAR-2 on A549 cells.