Background： Electroconvulsive therapy （ECT） can alleviate the symptoms of treatment-resistant depression （TRD）. Functional network connectivity （FNC） is a newly developed method to investigate the ...brain＇s functional connectivity patterns. The first aim of this study was to investigate FNC alterations between TRD patients and healthy controls. The second aim was to explore the relationship between the ECT treatment response and pre-ECT treatment FNC alterations in individual TRD patients. Methods： This study included 82 TRD patients and 41 controls. Patients were screened at baseline and after 2 weeks of treatment with a combination of ECT and antidepressants. Group information guided-independent component analysis （G1G-ICA） was used to compute subject-specific functional networks （FNs）. Grassmann maniibld and step-wise forward component selection using support vector machines were adopted to perform the FNC measure and extract the functional networks＇ connectivity patterns （FCP）. Pearson＇s correlation analysis was used to calculate the correlations between the FCP and ECT response. Results： A total of 82 TRD patients in the ECT group were successfully treated. On an average, 8.50 ~ 2.00 ECT sessions were conducted. After ECT treatment, only 42 TRD patients had an improved response to ECT （the Hamilton scores reduction rate was more than 50%）, response rate 51%. 8 FNs （anterior and posterior default mode network, bilateral frontoparietal network, audio network, visual network, dorsal attention network, and sensorimotor network） were obtained using GIG-ICA. We did not found that FCPs were significantly different between TRD patients and healthy controls. Moreover, the baseline FCP was unrelated to the ECT treatment response. Conclusions： The FNC was not significantly different between the TRD patients and healthy controls, and the baseline FCP was unrelated to the ECT treatment response. These findings will necessitate that we modify the experimental scheme to explore the mechanisms underlying ECT＇s effects on depression and explore the specific predictors of the effects of ECT based on the pre-ECT treatment magnetic resonance imaging.
Controlling toxigenic Fusarium graminearum (FG) is challenging. A bacterial strain (S76-3, identified as Bacillus amyloliquefaciens) that was isolated from diseased wheat spikes in the field ...displayed strong antifungal activity against FG. Reverse-phase high performance liquid chromatography and electrospray ionization mass spectrometry analyses revealed that S76-3 produced three classes of cyclic lipopeptides including iturin, plipastatin and surfactin. Each class consisted of several different molecules. The iturin and plipastatin fractions strongly inhibited FG; the surfactin fractions did not. The most abundant compound that had antagonistic activity from the iturin fraction was iturin A (m/z 1043.35); the most abundant active compound from the plipastatin fraction was plipastatin A (m/z 1463.90). These compounds were analyzed with collision-induced dissociation mass spectrometry. The two purified compounds displayed strong fungicidal activity, completely killing conidial spores at the minimal inhibitory concentration range of 50 mu g/ml (iturin A) and 100 mu g/ml (plipastatin A). Optical and fluorescence microscopy analyses revealed severe morphological changes in conidia and substantial distortions in FG hyphae treated with iturin A or plipastatin A. Iturin A caused leakage and/or inactivation of FG cellular contents and plipastatin A caused vacuolation. Time-lapse imaging of dynamic antagonistic processes illustrated that iturin A caused distortion and conglobation along hyphae and inhibited branch formation and growth, while plipastatin A caused conglobation in young hyphae and branch tips. Transmission electron microscopy analyses demonstrated that the cell walls of conidia and hyphae of iturin A and plipastatin A treated FG had large gaps and that their plasma membranes were severely damaged and separated from cell walls.
Intracerebral hemorrhage （ICH） leads to high rates of death and disability. The pronounced inflammatory reactions that rapidly follow ICH contribute to disease progression. Our recent clinical trial ...demonstrated that oral administration of an immune modulator fingolimod restrained secondary injury derived from initial hematoma, but the mechanisms remain unknown. In this study, we aim to investigate the effects of fingolimod on inflammatory mediators and vascular permeability in the clinical trial of oral fingolimod for intracerebral hemorrhage （ICH）. The results showed that fingolimod decreased the numbers of circulating CD4~ T, CD8~ T, CD19~ B, NK, and NKT cells and they recovered quickly after the drug＇ was stopped. The plasma ICAM level was decreased and IL-10 was increased by fingolimod. Interestingly, fingolimod protected vascular permeability as indicated by a decreased plasma level of MMP9 and the reduced rT1%. In conclusion, modulation of systemic inflammation by fingolimod demonstrates that it is an effective therapeutic agent for ICH. Fingolimod may prevent perihematomal edema enlargement by protecting vascular permeability.
Aim： To examine the effects of anisomycin on glioma cells and the related mechanisms in vitro. Methods： The U251 and U87 human glioblastoma cell lines were tested. The growth of the cells was ...analyzed using a CCK-8 cell viability assay. Apoptosis was detected using a flow cytometry assay. The expression of proteins and phosphorylated kinases was detected using Western blotting. Results： Treatment of U251 and U87 cells with anisomycin （0.01-8 pmol/L） inhibited the cell growth in time- and concentration- dependent manners （the IC50 values at 48 h were 0.233±0.021 and 0.192±0.018 pmol/L, respectively）. Anisomycin （4 pmol/L） caused 21.5%±2.2% and 25.3%±3.1% of apoptosis proportion, respectively, in U251 and U87 cells. In the two cell lines, anisomycin （4 pmol/L） activated p38 MAPK and JNK, and inactivated ERK1/2. However, neither the p38 MAPK inhibitor SB203580 （10 pmol/L） nor the JNK inhibitor SP600125 （10μmol/L） prevented anisomycin-induced cell death. On the other hand, anisomycin （4 μmol/L） reduced the level of PP2A/C subunit （catalytic subunit） in a time-dependent manner in the two cell lines. Treatment of the two cell lines with the PP2A inhibitor okadaic acid （100 nmol/L） caused marked cell death. Conclusion： Anisomycin induces glioma cell death via down-regulation of PP2A catalytic subunit. The regulation of PP2A/C exression by anisomycin provides a clue to further study on its role in glioma therapy.
Chemical cross-linking coupled with mass spectroscopy （CXMS） is a powerful technique for investi- gating protein structures. CXMS has been mostly used to characterize the predominant structure for a ...protein, whereas cross-links incompatible with a unique structure of a protein or a protein complex are often discarded. We have recently shown that the so-called over-length cross-links actually contain protein dynamics information. We have thus established a method called DynaXL, which allow us to extract the information from the over-length cross-links and to visualize protein ensemble structures. In this protocol, we present the detailed procedure for using DynaXL, which comprises five steps. They are identification of highly confident cross-links, delineation of protein domains/subunits, ensemble rigid- body refinement, and final validation/assessment. The DynaXL method is generally applicable for analyzing the ensemble structures of multi-domain proteins and protein-protein complexes, and is freely available at www.tanglab.org/resources.
AIM： To investigate if there are changes in serotonin （5-HT） levels, enterochromaffin （EC） cells and mast cells in small intestinal mucosa of patients with irritable bowel syndrome （IBS）. METHODS： ...Diarrhea-predominant （IBS-D, n = 20）, or constipation-predominant （IBS-C, n = 18） IBS patients and healthy controls （n = 20） underwent colonoscopy and peroral small intestinal endoscopy, and mucosal samples were obtained at the descending part of the duodenum, proximal end of jejunum and terminal ileum. High-performance liquid chromatographyelectrochemistry and immunohistochemical methods were used to detect 5-HT content, EC cells and mast cells. RESULTS： （1） There were no differences in the number and distribution of EC cells between IBS patients and the normal group. （2） The mucosal 5-HT contents at the duodenum, jejunum and ileum in IBS-C patients were 182 ± 90, 122 ± 54, 61 ± 35 ng/mg protein, respectively, which were all lower than those in the normal group （256 ± 84, 188 ± 91, and 93 ± 45 ng/ mg protein, respectively）, with a significant difference at the jejunum （P 〈 0.05）. There were no differences in the small intestinal mucosal 5-HT contents between IBS-D patients and the normal group. The mucosal 5-HT contents at the duodenum were significantly higher than those at the ileum in the three groups （P 〈 0.001）. （3） The numbers of mast cells in patients with IBS-C and IBS-D at the ileum were 38.7 ± 9.4 and 35.8 ± 5.5/highpower field （hpf）, respectively, which were significantly more than that in the normal group （29.8 ± 4.4/hpf） （P 〈 0.001）. There was no significant difference in the numbers of mast cells at the other two parts between IBS patients and the normal group. The numbers of mast cells in IBS-C, IBS-D, and normal groups were all significantly higher at the ileum （38.7 ± 9.4, 35.8 ± 5.5, 29.8 ±4.4/hpf, respectively） than at the duodenum （19.6± 4.7, 18.5 ± 6.3, 19.2 ±3.3/hpf, respectively, P 〈 0.001）. CONCLUSION： The changes in the 5-HT signaling pathway at the jejunum of IBS-C patients and the increase in mast cells in patients with IBS at the terminal ileum may offer evidence to explain the pathogenesis of IBS.
AIM:To determine how the oncogene mi R-21 regulates the RAS signaling pathways and affects colon cancer cell behaviors.METHODS:RAS p21 GTPase activating protein 1(RASA1) protein expression in six ...colon cancer cell lines was assessed by Western blot.Colon cancer RKO cells were chosen for transfection because they are KRAS wild type colon cancer cells whose RASA1 expression is significantly decreased.RKO cells were transfected with vectors overexpressing or downregulating either mi R-21 or RASA1.Furthermore,a luciferase reporter assay was used to determine whether RASA1 is a gene target of mi R-21.Then,changes in m RNA and protein levels of RASA1,RASGTP,and other components of the RAS signaling pathways were assessed in transfected RKO cells by real-time quantitative reverse transcription-polymerase chain reaction,Western blot and immunoprecipitation.Finally,cell proliferation,apoptosis,invasion,and tumorformation ability w ere assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide dye assay,flow cytometry,transwell assay,and animal experiment,respectively.RESULTS:RASA1 protein levels were significantly decreased in RKO cells compared with the other 5 colon cancer cell lines,and RASA1 was confirmed as a target gene of mi R-21.Interestingly,RASA1 m RNA and protein levels in pre-mi R-21-LV(up-regulation of mi R-21) cells were lower than those in anti-mi R-21-LV(down-regulation of mi R-21) cells(P < 0.05).In addition,pre-mi R-21-LV or si RASA1(down-regulation of RASA1) cells showed higher cell proliferation,reduced apoptosis,increased expression of RAS-GTP,p-AKT,Raf-1,KRAS,and p-ERK1/2,and higher invasion and tumor formation ability,compared with control,antimi R-21-LV or pc DNA3.1-RASA1(up-regulation of RASA1) cells(P < 0.05).CONCLUSION:RASA1 is a target gene of mi R-21,which promotes malignant behaviors of RKO cells through regulation of RASA1 expression.
Ghosting artifacts caused by moving objects or misalignments is a key challenge in high dynamic range (HDR) imaging for dynamic scenes. Previous methods first register the input low dynamic range ...(LDR) images using optical flow before merging them, which are error-prone and cause ghosts in results. A very recent work tries to bypass optical flows via a deep network with skip-connections, however, which still suffers from ghosting artifacts for severe movement. To avoid the ghosting from the source, we propose a novel attention-guided end-to-end deep neural network (AHDRNet) to produce high-quality ghost-free HDR images. Unlike previous methods directly stacking the LDR images or features for merging, we use attention modules to guide the merging according to the reference image. The attention modules automatically suppress undesired components caused by misalignments and saturation and enhance desirable fine details in the non-reference images. In addition to the attention model, we use dilated residual dense block (DRDB) to make full use of the hierarchical features and increase the receptive field for hallucinating the missing details. The proposed AHDRNet is a non-flow-based method, which can also avoid the artifacts generated by optical-flow estimation error. Experiments on different datasets show that the proposed AHDRNet can achieve state-of-the-art quantitative and qualitative results.
Vanadium trioxide（V2O3） was directly prepared by NaVO3 electrolysis in Na Cl molten salts. Electrolysis products were characterized by X-ray diffraction（XRD）, scanning electron microscopy（SEM） and ...energy dispersive spectroscopy（EDS）. The existing state and electrochemical behavior of NaVO3 were also studied. The results indicated that V2O3 can be obtained from NaVO3. VC and C were also formed at high cell voltage, high temperature, and long electrolysis time. During electrolysis, NaVO3 was dissociated to Na＋ and VO3-in Na Cl molten salt. NaVO3 was initially electro-reduced to V2O3 on cathode and Na2O was released simultaneously. Na2CO3 was formed due to the reaction between Na2O and CO2. The production of C was ascribed to the electro-reduction of CO3（2-）. VC was produced due to the reaction between C and V2O3.
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