A giant gastric stromal tumor with dizziness as the main complaint: A case report and literature review.

INTRODUCTION: Small gastrointestinal stromal tumors (GISTs) are often asymptomatic. However, large tumors can cause symptoms like abdominal pain and GI bleeding. We experienced a unique case where a giant GIST was incidentally found by CT scanning during emergency treatment for dizziness. PRESENTATION OF CASE: A 61-year-old man presented temporary dizziness after exercising three days ago before his admission. Enhanced CT scan of the abdomen and pelvis revealed a large circular mass in the right upper abdominal cavity, with a maximum cross-sectional size of approximately 132 mm × 155 mm. Biopsy and genetic testing confirmed the diagnosis of GIST. The patient underwent successful radical surgery and was discharged at 12th post-operative day without any complications. The patient now is taking imatinib as an adjuvant targeted therapy. DISCUSSION: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the digestive tract with diverse clinical presentations according to their sites and sizes. As in this case, the patient's primary complaint was dizziness, which is uncommon for GISTs. Initial workup, including three-dimensional rebuilding of the enhanced CT scanning and biopsy, was given before surgery. Finally, despite the tumor's large size and attachment to adjacent structures, R0 resection was accomplished without intraoperative rupture. CONCLUSION: This case highlights the importance of healthcare providers vigilant in identifying GISTs with unusual symptoms in emergency situations. A systematic and comprehensive examination can be and should be performed to confirm diagnosis and determine the feasibility of R0 resection. By sharing this unique case, we aim to enhance the understanding of GIST and increase awareness among clinicians about their varied presentations.

Effects of Stigmasterol on 3-Chloropropane-1,2-diol Fatty Acid Esters and Aldehydes Formation in Heated Soybean Oil.

In this study, we investigated the inhibitory effects of three soybean isoflavones and two soybean phytosterols on the formation of 3-chloropropane-1,2-diol fatty acid esters (3-MCPDE) and aldehydes in heated soybean oil model. 0.4 mM of genistin, genistein, daidzein, stigmasterol, and ß-sitosterol significantly reduced 3-MCPDE formation by 25.7, 51.4, 21.4, 61.6, and 55.7%, and total aldehydes formation by 42.03, 43.94, 28.36, 54.74, and 39.23%, respectively. Further study showed that stigmasterol reduced the content of glycidyl esters (GEs) and glycidol, two key intermediates of 3-MCPDE, and prevented fatty acids degradation in the oils. Moreover, the effects of continuous frying time on the content of stigmasterol and the migration of stigmasterol were evaluated in the fried dough sticks model system. The content of stigmasterol in soybean oil was found to be significantly decreased with prolonged heating time. The concentrations of stigmasterol in fried dough sticks and the migration rates of stigmasterol from soybean oil to fried dough sticks decreased with repeated frying sessions. In addition, stigmasterol undergoes oxidative changes during heat treatment, and the oxidation products including 5,6α-epoxystigmasterol, 5,6ß-epoxystigmasterol, 7α-hydroxystigmasterol, 7ß-hydroxystigmasterol, stigmasterlol-3ß,5α,6ß-triol, and 7-ketostigmasterol were identified in the frying oils but not in the fried dough sticks. Overall, stigmasterol could be added to soybean oil to reduce 3-MCPDE and aldehydes formation, and reacting with GEs/glycidol and protection of lipid acids from oxidation may be the mechanism of action of stigmasterol.

Purification, characterization and inactivation kinetics of polyphenol oxidase extracted from Cistanche deserticola.

MAIN CONCLUSION: PPO was purified from Cistanche deserticola, and its enzymatic characteristics were clarified. It was found that microwave treatment was an efficient way to inactivate PPO. Polyphenol oxidase (PPO) from Cistanche deserticola was obtained and purified through an acetone precipitation and anion exchange column, the enzymatic characteristics and inactivation kinetics of PPO were studied. The specific activity of PPO was 73135.15 ± 6625.7 U/mg after purification, the purification multiple was 48.91 ± 4.43 times, and the recovery was 30.96 ± 0.27%. The molecular weight of the PPO component is about 66 kDa by SDS-PAGE analysis. The optimum substrate of PPO was catechol (Vmax = 0.048 U/mL, Km = 21.70 mM) and the optimum temperature and pH were 30 °C and 7, respectively. When the temperature is above 50 °C, pH < 3 or pH > 10, the enzyme activity can be significantly inhibited. The first-order kinetic fitting shows that microwave inactivation has lesser k values, larger D values and shorter t1/2. It was found that microwave treatment is considered as an efficient and feasible way to inactive PPO by comparing the Z values and Ea values of the two thermal treatments.

Chemical composition and anti-inflammatory activities of Castanopsis honey.

Castanopsis is diffusely spread in tropical and subtropical regions and is an important nectar source plant in China. The Castanopsis honey (CH) is characterized by its bitter taste. However, its composition and functions remain unclear. In this study, the physicochemical parameters, chemical composition, and antioxidant capacity of CH were comprehensively investigated, with the anti-inflammatory effects of the Castanopsis honey extract (CHE) evaluated based on the RAW 264.7 cell inflammatory model. The results revealed a high level of quality in CH based on the quality standards. Among a total of 84 compounds identified in CH, 5 high response compounds and 29 phenols were further quantified by UPLC-Q/TOF-MS. The high content of phenylethylamine (117.58 ± 64.81 mg kg-1) was identified as a potential marker of CH. Furthermore, the CH showed evident antioxidant activities, and the anti-inflammatory activities of CHE were observed to inhibit the release of nitric oxide (NO) and reduce the content of tumor necrosis factor alpha (TNF-α) and improve the content of interleukin-10 (IL-10) by regulating the NF-κB pathway. Our study indicates that CH has sound physicochemical properties and biological activities with a high level of quality, providing strong experimental evidence to support the further economic and agricultural development and application of CH.

Detection of ochratoxin A using a "turn-on" fluorescence assay based on guanine quenching of the aptamer.

Ochratoxin A (OTA) is a common mycotoxin with high carcinogenicity; therefore, it is crucial to establish a simple, rapid, and sensitive method for its detection. In this study, we developed a "turn-on" fluorescence assay for detecting OTA based on guanine quenching of the aptamer. The method uses fluorescein (FAM) fluorophore to label the complementary strand of the OTA aptamer, Fc-DNA. In the absence of OTA, the Fc-DNA hybridizes with the aptamer to form a double strand. Due to the occurrence of photo-induced electron transfer (PET), the FAM fluorescence signal is quenched as the FAM on the Fc-DNA approaches the guanine of the aptamer at the 5' end. When OTA is present, the aptamer binds to it and thus, is unable to hybridize with Fc-DNA to form a double strand; the FAM fluorescence signal is restored as FAM moves away from the guanine of the aptamer. The assay achieved OTA detection at a detection limit of 28.4 nM. The application of the original guanine of the aptamer as the quenching agent helps avoid the complex designing and labeling of the aptamer, which ensures the high affinity of the aptamer for OTA. Meanwhile, this "turn-on" detection mode helps avoid potential false-positive results as in the "turn-off" mode and improves the assay's sensitivity. Additionally, the method has good selectivity and can be used to detect OTA in traditional Chinese medicine. This method provides a simple, low-cost, and rapid method for OTA detection.

Lithium Antievaporation-Loss Engineering via Sodium/Potassium Doping Enables Superior Electrochemical Performance of High-Nickel Li-Rich Layered Oxide Cathodes.

Low-cost Mn- and Li-rich layered oxides suffer from rapid voltage decay, which can be improved by increasing the nickel content to derive high nickel Li-rich layered oxides (HNLO) but is normally accompanied by reduced capacity and inferior cycling stability. Herein, Na or K ions are successfully doped into the lattice of high nickel Li-rich Li1.2-xMxNi0.32Mn0.48O2 (M = Na, K) layered oxides via a facile expanded graphite template-sacrificed approach. Both Na- and K-doped samples exhibit excellent rate capability and cycling stability compared with the un-doped one. The Na-doped sample shows a capacity retention of 93% after 200 cycles at 1C, which is quite outstanding for HNLO. The greatly improved electrochemical performances are attributed to the increased effective Li content in the lattice via Li antievaporation-loss engineering, the expanded Li slab, the pillaring effect, the increased C2/m component, and the improved electronic conductivity. Different performances by the introduction of sodium and potassium ions may be ascribed to their different ionic radii, which give rise to their different doping behaviors and threshold doping amounts. This work provides a new idea of enhancing electrochemical performance of HNLO by doping proper alien elements to increase the lattice lithium content effectively.

An Efficient Deacidification Process for Safflower Seed Oil with High Nutritional Property through Optimized Ultrasonic-Assisted Technology.

Safflower seed oil (SSO) is considered to be an excellent edible oil since it contains abundant essential unsaturated fatty acids and lipid concomitants. However, the traditional alkali-refined deacidification process of SSO results in a serious loss of bioactive components of the oil and also yields massive amounts of wastewater. In this study, SSO was first extracted by ultrasonic-assisted ethanol extraction (UAEE), and the extraction process was optimized using random centroid optimization. By exploring the effects of ethanol concentration, solid−liquid ratio, ultrasonic time, and the number of deacidification times, the optimum conditions for the deacidification of safflower seed oil were obtained as follows: ethanol concentration 100%, solid−liquid ratio 1:4, ultrasonic time 29 min, and number of deacidification cycles (×2). The deacidification rate was 97.13% ± 0.70%, better than alkali-refining (72.16% ± 0.13%). The values of acid, peroxide, anisidine and total oxidation of UAEE-deacidified SSO were significantly lower than those of alkali-deacidified SSO (p < 0.05). The contents of the main lipid concomitants such as tocopherols, polyphenols, and phytosterols in UAEE-decidified SSO were significantly higher than those of the latter (p < 0.05). For instance, the DPPH radical scavenging capacity of UAEE-processed SSO was significantly higher than that of alkali refining (p < 0.05). The Pearson bivariate correlation analysis before and after the deacidification process demonstrated that the three main lipid concomitants in SSO were negatively correlated with the index of peroxide, anisidine, and total oxidation values. The purpose of this study was to provide an alternative method for the deacidification of SSO that can effectively remove free fatty acids while maintaining the nutritional characteristics, physicochemical properties, and antioxidant capacity of SSO.

LINC02381, a sponge of miR-21, weakens osteogenic differentiation of hUC-MSCs through KLF12-mediated Wnt4 transcriptional repression.

INTRODUCTION: Human umbilical cord blood-derived MSCs (hUC-MSCs) have the potential to differentiate into osteoblasts. This study investigated the function and potential mechanisms of a novel lncRNA LINC02381 in hUC-MSC osteogenic differentiation. MATERIALS AND METHODS: hUC-MSCs were maintained in osteogenic differentiation medium. RT-qPCR assay was performed to assess LINC02381 expression. Alizarin Red S (ARS) and alkaline phosphatase (ALP) staining were performed to evaluate osteogenic differentiation. The interaction between miR-21 and LINC0238/KLF12 was determined by luciferase reporter and RNA immunoprecipitation (RIP) assays. Chromatin immunoprecipitation (ChIP) assay was used to confirm the transcriptional regulation of KLF12 on Wnt4 promoter. The nuclear translocation of ß-catenin was evaluated using immunofluorescence. hUC-MSCs seeded on Bio-Oss Collagen scaffolds were transplanted into nude mice to assess in vivo osteogenesis. Bone formation was observed by H&E and Masson's trichrome staining. OSX and OPN levels were assessed by immunohistochemistry. RESULTS: LINC02381 was up-regulated in the clinical samples of osteoporotic patients. However, LINC02381 expression was reduced during osteogenic differentiation of hUC-MSCs. Enforced expression of LINC02381 suppressed the osteogenic differentiation of hUC-MSCs. Mechanistically, LINC02381 sponged miR-21 to enhance KLF12 expression, which led to the inactivation of Wnt/ß-catenin signaling pathway. Furthermore, miR-21 mimics or KLF12 silencing counteracted LINC02381-induced inhibition of osteogenic differentiation, whereas IWP-4 (an inhibitor of Wnt pathway) abolished this effect. CONCLUSION: In summary, LINC02381 repressed osteogenic differentiation of hUS-MSCs through sponging miR-21 to enhance KLF12-mediated inactivation of Wnt/ß-catenin pathway, indicating that LINC02381 might be a therapeutic target for osteoporosis.

[Exosomal miR-10b Promotes Invasion and Epithelial-mesenchymal Transformation of Lung Adenocarcinoma A549 Cells by Regulating Macrophage M2 Polarization].

BACKGROUND: Metastasis is the main cause of death in patients with lung cancer. Macrophages are innate immune cells that play important roles in cancer metastasis. Exosomes could play an important role of communication between tumor cells and macrophages. This study investigated the effect of miR-10b on cell growth invasion and epithelial mesenchymal transition (EMT) in lung adenocarcinoma A549 cell exosomes. METHODS: Exosomes were isolated from A549 cells and identified by transmission electron microscopy (TEM) and Western blot. CCK-8 assay and flow cytometry were used to detect cell proliferation and apoptosis. Cell migration and invasion were detected by Transwell assay. The expression of mRNA and protein were assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot, respectively. RESULTS: The expression of miR-10b was up-regulated in non-small cell lung cancer, and miR-10b inhibitor could inhibit the proliferation of A549 cell. Meanwhile, the tumor cell-derived exosome miR-10b promoted the invasion of A549 cell and EMT by promoting the M2 polarization of macrophages. CONCLUSIONS: Tumor cell-derived exosome miR-10b promotes A549 cell invasion and EMT through M2 macrophage polarization.

Predictable Roles of Peripheral IgM Memory B Cells for the Responses to Anti-PD-1 Monotherapy Against Advanced Non-Small Cell Lung Cancer.

Tumor-infiltrating B cells and tertiary lymphoid structures have been identified to predict the responses to immune checkpoint inhibitors (ICIs) in cancer immunotherapy. Considering the feasibility of sample collection, whether peripheral B cell signatures are associated with the responses to ICI therapy remains unclear. Herein, we have defined peripheral B cell signatures in advanced non-small cell lung cancer (NSCLC) patients receiving anti-PD-1 monotherapy and investigated their associations with clinical efficacy. It was found that the percentages of B cells before the treatment (baseline) were significantly higher (P = 0.004) in responder (R, n = 17) than those in non-responder (NonR, n = 33) NSCLC patients in a discovery cohort. Moreover, the percentages of baseline IgM+ memory B cells were higher (P < 0.001) in R group than those in NonR group, and associated with a longer progression free survival (PFS) (P = 0.003). By logistic regression analysis peripheral baseline IgM+ memory B cells were identified as an independent prognostic factor (P = 0.002) for the prediction of the responses to anti-PD-1 monotherapy with the AUC value of 0.791, which was further validated in another anti-PD-1 monotherapy cohort (P = 0.011, n = 70) whereas no significance was observed in patients receiving anti-PD-L1 monotherapy (P = 0.135, n = 30). Therefore, our data suggest the roles of peripheral IgM+ memory B cells in predicting the responses to anti-PD-1 treatment in Chinese advanced NSCLC patients.

LncRNA LINC00963 promotes osteogenic differentiation of hBMSCs and alleviates osteoporosis progression by targeting miRNA-760/ETS1 axis.

Although long non-coding RNA LINC00963 has been reported to play a crucial regulatory role in osteoporosis (OP), its specific mechanism has not been well studied. Cell viability of human bone marrow mesenchymal stem cells (hBMSCs) transfected with short hairpin RNA targeting LINC00963 (sh-LINC00963) and negative control (sh-NC) was analysed by cell counting kit-8 (CCK-8) assay. Alkaline phosphatase (ALP) activity in hBMSCs transfected with sh-LINC00963 and sh-NC after induction by osteogenic medium (OM) on day 7 was detected. The protein expression levels of osteocalcin (OCN) and osteopontin (OPN) in hBMSCs transfected with sh-LINC00963 and sh-NC during OM induction on day 3 were detected by western blot. The relationship among LINC00963, miR-760, and E26 transformation specific-1 (ETS1) was determined by bioinformatics analysis, luciferase reporter assay, and RNA-binding protein immunoprecipitation (RIP) assay. A rat model with OP was established to confirm the role of LINC00963 in vivo. The expression level of LINC00963 was much lower in hBMSCs isolated from the discarded femoral head tissues of OP patients compared with that in health patients. Meanwhile, the expression level of LINC00963 was significantly increased and the expression level of miR-760 was decreased in hBMSCs during osteogenic induction. LINC00963 could bind to the 3'-untranslated region (3'-UTR) of miR-760 and negatively regulate the expression of miR-760, then promote the osteogenic differentiation in hBMSCs. ETS1 was identified as a target of miR-760. Moreover, overexpression of LINC00963 obviously reduced bone mineral density (BMD) of the left femur in OP rats and alleviated OP progression in vivo. Our results demonstrated that LINC00963 positively regulated the expression of ETS1 by directly targeting miR-760, and then promoted osteogenic differentiation of hBMSCs in vitro, and also attenuated OP progression in vivo, suggesting that LINC00963 might be a potential therapeutic target for OP.

Phytochemical Profile and Anti-Inflammatory Activity of the Fraction from Artemisia lavandulaefolia.

Artemisia lavandulaefolia, a traditional herbal medicine, has been utilized as anti-inflammatory and analgesia agent in clinic. Bioassay-guided fractionation resulted in a fraction (ALDF) with anti-inflammatory effect obtained from A. lavandulaefolia. Its main constituents were analyzed and identified by UPLC-ESI-Q-TOF-MS technology. ALDF showed the strong inhibitory activity on the nitrogen oxide (NO) production in LPS-induced RAW 264.7 macrophages with an IC50 value of 1.64±0.41 µg/mL. Further results displayed that ALDF also significantly suppressed the secretion of key pro-inflammatory mediators, including tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2 ) and interleukin-1ß (IL-1ß), and the increase of the inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein expression induced by LPS stimulation. Mechanism study indicated that ALDF was able to block NF-κB signaling pathway through inhibiting IκB and p65 phosphorylation, as well as NF-κB p65 nuclear translocation. Furthermore, in vivo results in mice revealed that treatments with ALDF evoked significant inhibition on ear edema induced by xylene and on the writhing responses induced by acetic acid. These results suggest that ALDF holds great potential in the prevention and treatment of inflammatory disorders.

Polydopamine mediated modification of manganese oxide on melamine sponge for photothermocatalysis of gaseous formaldehyde.

It is an urgent need to develop environmentally friendly strategies with low energy consumption for gaseous formaldehyde (HCHO) purification. Herein, a sponge based MS/PDA/MnOx catalyst with plentiful 3D porosities was constructed. The dual-functional PDA layer not only promoted the MnOx loading (25 wt% MnOx in the composite), but also acted as a photothermal converter to absorb photo-irradiation to heat MnOx catalyst (~80 °C after 10 min irradiation). Moreover, the 3D network structure favored the mass transfer and effectively reduced the catalyst agglomeration to expose more active sites. As a result, the obtained MS/PDA/MnOx photothermocatalyst showed highly efficient performance for removal of HCHO within concentration of 40-320 ppm at room temperature under xenon light irradiation. This process followed a pseudo-second-order model, and the reaction rate of the MS/PDA/MnOx was 4.82 times of the MS/MnOx. Finally, a possible photothermocatalysis mechanism was proposed based on the intermediate examination via the in-situ DRIFTS investigation.

MicroRNA-92a-3p enhances functional recovery and suppresses apoptosis after spinal cord injury via targeting phosphatase and tensin homolog.

Spinal cord injury (SCI) is a neurological disease commonly caused by traumatic events on spinal cords. MiRNA-92a-3p is reported to be down-regulated after SCI. Our study investigated the effects of up-regulated miR-92a-3p on SCI and the underlying mechanisms. SCI mice model was established to evaluate the functional recovery of hindlimbs of mice through open-field locomotion and scored by Basso, Beattie, and Bresnahan (BBB) locomotion scale. Apoptosis of spinal cord cells was determined by flow cytometry. The effects of miR-92a-3p on SCI were detected by intrathecally injecting miR-92a-3p agomiR (agomiR-92) into the mice prior to the establishment of SCI. Phosphatase and tensin homolog (PTEN) was predicted as a target of miR-29a-3p by TargetScan. We further assessed the effects of agomiR-92 or/and overexpressed PTEN on apoptosis rates and apoptotic protein expressions in SCI mice. Moreover, the activation of protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling was determined by Western blot. The results showed that compared with the sham-operated mice, SCI mice had much lower BBB scores, and theapoptosis rate of spinal cord cells was significantly increased. After SCI, the expression of miR-92a-3p was down-regulated, and increased expression of miR-92a-3p induced by agomiR-92 further significantly increased the BBB score and decreased apoptosis. PTEN was specifically targeted by miR-92a-3p. In addition, the phosphorylation levels of Akt and mTOR were up-regulated under the treatment of agomiR-92. Our data demonstrated that the neuroprotective effects of miR-92a-3p on spinal cord safter SCI were highly associated with the activation of the PTEN/AKT/mTOR pathway.

RSK3 mediates necroptosis by regulating phosphorylation of RIP3 in rat retinal ganglion cells.

Receptor-interacting protein 3 (RIP3) plays an important role in the necroptosis signaling pathway. Our previous studies have shown that the RIP3/mixed lineage kinase domain-like protein (MLKL)-mediated necroptosis occurs in retinal ganglion cell line 5 (RGC-5) following oxygen-glucose deprivation (OGD). However, upstream regulatory pathways of RIP3 are yet to be uncovered. The purpose of the present study was to investigate the role of p90 ribosomal protein S6 kinase 3 (RSK3) in the phosphorylation of RIP3 in RGC-5 cell necroptosis following OGD. Our results showed that expression of RSK3, RIP3, and MLKL was upregulated in necroptosis of RGC-5 after OGD. A computer simulation based on our preliminary results indicated that RSK3 might interact with RIP3, which was subsequently confirmed by co-immunoprecipitation. Further, we found that the application of a specific RSK inhibitor, LJH685, or rsk3 small interfering RNA (siRNA), downregulated the phosphorylation of RIP3. However, the overexpression of rip3 did not affect the expression of RSK3, thereby indicating that RSK3 could be a possible upstream regulator of RIP3 phosphorylation in OGD-induced necroptosis of RGC-5 cells. Moreover, our in vivo results showed that pretreatment with LJH685 before acute high intraocular pressure episodes could reduce the necroptosis of retinal neurons and improve recovery of impaired visual function. Taken together, our findings suggested that RSK3 might work as an upstream regulator of RIP3 phosphorylation during RGC-5 necroptosis.

Impact of adjuvant therapy on survival for sinonasal mucosal melanoma.

Background: The optimal treatment modality for sinonasal mucosal melanoma (SNMM) remains controversial.Objectives: To investigate the impact of adjuvant therapy on SNMM.Material and methods: Ninety-two patients were retrospectively analyzed and were grouped into surgery alone (SA), surgery plus radiotherapy (SR), surgery plus chemotherapy (SC) and surgery plus radiochemotherapy (SRC) groups. Survival outcomes among different treatment modalities were analyzed using the Kaplan-Meier method and log-rank test.Results: Twenty-nine patients (31.5%) developed local recurrence, 10 patients (10.9%) had nodal metastasis, and 41 patients (44.6%) had distant metastasis. The overall survival time (OS) for SA, SR and SRC were 16, 29 and 27 months, respectively, and the disease-free survival time (DFS) were 10, 16 and 16 months, respectively. Significant differences were found between SA and SR (OS: p = .003; DFS: p = .016) and SA and SRC (OS: p = .002; DFS: p = .008). Superior outcomes were also found in SRC group compared to that in SA group for both OS (15 vs. 27 months, p = .012) and DFS (10 vs. 20 months, p = .017) in endoscopic approach.Conclusions and significance: SNMM had poor prognosis with high rates of local recurrence and metastasis. Adjuvant therapy improved survival outcomes for SNMM.

Sinorhodobacter populi sp. nov., isolated from the symptomatic bark tissue of Populus × euramericana canker.

We isolated five novel bacterial strains from symptomatic bark tissue of Populus × euramericana canker that were Gram-stain-negative, non-motile, aerobic oxidase-negative and catalase-positive. Growth occurred at 10-41 °C and at pH 5.0-7.0, with optimum growth at 30 °C and pH 7.0. Additionally, growth occurred in conditions of 0-5 % (w/v) salinity, but not above 7 % NaCl. The 16S rRNA gene sequences of the novel strains shared the highest similarity with Sinorhodobacter ferrireducens SgZ-3T (97.1 %). The average nucleotide identity values between the novel strains and two type strains (S.inorhodobacter ferrireducens CCTCC AB2012026T and 'Sinorhodobacter hungdaonensis' CGMCC 1.12963T) were 78.4-78.9 %, which were lower than the proposed species boundary cut-off (95-96 %). The main polar lipids were phosphatidylethanolamine, phosphatidylglycerol, diphosphatidylglycerol, an unidentified lipid and phosphatidylcholine. The main respiratory quinone was Q-10, and major fatty acids were C18 : 1ω7c and/or C18 : 1ω6c. Based on data from a polyphasic taxonomy study, the novel strains represent a novel species of the genus Sinorhodobacter, for which the name Sinorhodobacter populi sp. nov. is proposed. The type strain is sk2b1T (=CFCC 14580T=KCTC 52802T).

[Research progress on anti-inflammatory mechanism of natural sesquiterpenoids].

Sesquiterpenoid is a kind of compound widely distributed in nature, which has a wide range of biological activities, such as anti-inflammatory, anti-tumor and immunomodulatory activities. This paper would review the anti-inflammatory mechanism of sesquiterpenoid. The mechanism is mainly by inhibiting the activation of nuclear factor (NF-κB), mitogen-activated protein kinase (MAPKs) and signal transducers and activators of transcription (STAT) signaling pathways and down-regulating the inflammatory gene expression including tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), nitric oxide (NO), interleukin-1(IL-1), IL-6, IL-8 and other inflammatory factors. Thereby, the production and release of inflammatory cytokines are reduced to exert anti-inflammatory effect. This review is intended to provide reference for related research.

A Routine Laboratory Data-Based Model for Predicting Recurrence After Curative Resection of Stage II Colorectal Cancer.

Background: Use of chemotherapy in stage II colorectal cancer (CRC) is controversial because it improves survival only in some patients. We aimed to develop a statistical model using routine and readily available blood tests to predict the prognosis of patients with stage II CRC and to identify which patients are likely to benefit from chemotherapy. Methods: We divided 422 patients with stage II CRC into a training and a testing set. The association of routine laboratory variables and disease-free survival (DFS) was analyzed. A prognostic model was developed incorporating clinically relevant laboratory variables with demographic and tumor characteristics. A prognostic score was derived by calculating the sum of each variable weighted by its regression coefficient in the model. Model performance was evaluated by constructing receiver operating characteristic curves and calculating the area under the curve (AUC). Results: Significant associations were seen between 5 laboratory variables and patient DFS in univariate analyses. After stepwise selection, 3 variables (carcinoembryonic antigen, hemoglobin, creatinine) were retained in the multivariate model with an AUC of 0.75. Compared with patients with a low prognostic score, those with a medium and high prognostic score had a 1.99- and 4.78-fold increased risk of recurrence, respectively. The results from the training set were validated in the testing set. Moreover, chemotherapy significantly improved DFS in high-risk patients, but not in low- and medium-risk patients. Conclusions: A routine laboratory variable-based model may help predict DFS of patients with stage II CRC and identify high-risk patients more likely to benefit from chemotherapy.

Using drugs to target necroptosis: dual roles in disease therapy.

Necroptosis is programmed necrosis, a process which has been studied for over a decade. The most common accepted mechanism is through the RIP1-RIP3-MLKL axis to regulate necroptotic cell death. As a result of previous studies on necroptosis, positive regulation for promoting necroptosis such as HSP90 stabilization and hyperactivation of TAK1 on RIP1 is clear. Similarly, the negative regulation of necroptosis, such as through caspase 8, c-FLIP, CHIP, MK2, PELI1, ABIN-1, is also clear. Therefore, the promise of corresponding applications in treating diseases becomes hopeful. Studies have shown that necroptosis is involved in the development of many diseases, such as ischemic injury diseases in various organs, neurodegenerative diseases, infectious diseases, and cancer. Given these results, drugs that inhibit or trigger necroptosis can be discovered to treat diseases. In this review, we briefly introduce up to date concepts concerning the mechanism of necroptosis, the diseases that involve necroptosis, and the drugs that can be applied to treat such diseases.