Itaconate is a lysosomal inducer that promotes antibacterial innate immunity.

Lysosomes are the main organelles in macrophages for killing invading bacteria. However, the precise mechanism underlying lysosomal biogenesis upon bacterial infection remains enigmatic. We demonstrate here that LPS stimulation increases IRG1-dependent itaconate production, which promotes lysosomal biogenesis by activating the transcription factor, TFEB. Mechanistically, itaconate directly alkylates human TFEB at cysteine 212 (Cys270 in mice) to induce its nuclear localization by antagonizing mTOR-mediated phosphorylation and cytosolic retention. Functionally, abrogation of itaconate synthesis by IRG1/Irg1 knockout or expression of an alkylation-deficient TFEB mutant impairs the antibacterial ability of macrophages in vitro. Furthermore, knockin mice harboring an alkylation-deficient TFEB mutant display elevated susceptibility to Salmonella typhimurium infection, whereas in vivo treatment of OI, a cell-permeable itaconate derivative, limits inflammation. Our study identifies itaconate as an endogenous metabolite that functions as a lysosomal inducer in macrophages in response to bacterial infection, implying the potential therapeutic utility of itaconate in treating human bacterial infection.

Boosting Polysulfide Redox Kinetics by Temperature-Induced Metal-Insulator Transition Effect of Tungsten-Doped Vanadium Dioxide for High-Temperature Lithium-Sulfur Batteries.

The practical application of Li-S batteries is still severely restricted by poor cyclic performance caused by the intrinsic polysulfides shuttle effect, which is even more severe under the high-temperature condition owing to the inevitable increase of polysulfides' solubility and diffusion rate. Herein, tungsten-doped vanadium dioxide (W-VO2) micro-flowers are employed with first-order metal-insulator phase transition (MIT) property as a robust and multifunctional modification layer to hamper the shuttle effect and simultaneously improve the thermotolerance of the common separator. Tungsten doping significantly reduces the transition temperature from 68 to 35 °C of vanadium dioxide, which renders the W-VO2 easier to turn from the insulating monoclinic phase into the metallic rutile phase. The systematic experiments and theoretical analysis demonstrate that the temperature-induced in-suit MIT property endows the W-VO2 catalyst with strong chemisorption against polysulfides, low energy barrier for liquid-to-solid conversion, and outstanding diffusion kinetics of Li-ion under high temperatures. Benefiting from these advantages, the Li-S batteries with W-VO2 modified separator exhibit significantly improved rate and long-term cyclic performance under 50 °C. Remarkably, even at an elevated temperature (80 °C), they still exhibit superior electrochemical performance. This work opens a rewarding avenue to use phase-changing materials for high-temperature Li-S batteries.

Optimizing Surface State Electrons of Topological Semi-Metal by Atomic Doping for Enhanced Hydrogen Evolution Reaction.

Topological materials carrying topological surface states (TSSs) have extraordinary carrier mobility and robustness, which provide a new platform for searching for efficient hydrogen evolution reaction (HER) electrocatalysts. However, the majority of these TSSs originate from the sp band of topological quantum catalysts rather than the d band. Here, based on the density functional theory calculation, it is reported a topological semimetal Pd3Sn carrying TSSs mainly derived from d orbital and proposed that optimizing surface state electrons of Pd3Sn by introduction heteroatoms (Ni) can promote hybridization between hydrogen atoms and electrons, thereby reducing the Gibbs free energy (ΔGH) of adsorbed hydrogen and improving its HER performance. Moreover, this is well verified by electrocatalytic experiment results, the Ni-doped Pd3Sn (Ni0.1Pd2.9Sn) show much lower overpotential (-29 mV vs RHE) and Tafel slope (17 mV dec-1) than Pd3Sn (-39 mV vs RHE, 25 mV dec-1) at a current density of 10 mA cm-2. Significantly, the Ni0.1Pd2.9Sn nanoparticles exhibit excellent stability for HER. The electrocatalytic activity of Ni0.1Pd2.9Sn nanoparticles is superior to that of commercial Pt. This work provides an accurate guide for manipulating surface state electrons to improve the HER performance of catalysts.

Metabolism of a fungicide propiconazole by Cunninghamella elegans ATCC36112.

The metabolic breakdown of propiconazole by fungi was examined, and it was found that the microbial model (Cunninghamella elegans ATCC36112) efficiently degrades the triazole fungicide propiconazole through the action of cytochrome P450. This enzyme primarily facilitates the oxidation and hydrolysis processes involved in phase I metabolism. We observed major metabolites indicating hydroxylation/oxidation of propyl groups of propiconazole. Around 98% of propiconazole underwent degradation within a span of 3 days post-treatment, leading to the accumulation of five metabolites (M1-M5). The experiments started with a preliminary identification of propiconazole and its metabolites using GC-MS. The identified metabolites were then separated and identified by in-depth analysis using preparative UHPLC and MS/MS. The metabolites of propiconazole are M1 (CGA-118245), M2(CGA-118244), M3(CGA-136735), M4(GB-XLIII-42-1), and M5(SYN-542636). To further investigate the role of key enzymes in potential fungi, we treated the culture medium with piperonyl butoxide (PB) and methimazole (MZ), and then examined the kinetic responses of propiconazole and its metabolites. The results indicated a significant reduction in the metabolism rate of propiconazole in the medium treated with PB, while methimazole showed weaker inhibitory effects on the metabolism of propiconazole in the fungus C. elegans.

Spontaneous isolated gastric intramural hematoma combined with spontaneous superior mesenteric artery intermural hematoma: a rare case.

BACKGROUND: Gastric intramural hematoma is a rare disease. Here we report a case of spontaneous isolated gastric intramural hematoma combined with spontaneous superior mesenteric artery intermural hematoma. CASE PRESENTATION: A 75-years-old man was admitted to our department with complaints of abdominal pain. He underwent a whole abdominal computed tomography (CT) scan in the emergency department, which showed extensive thickening of the gastric wall in the gastric body and sinus region with enlarged surrounding lymph nodes, localized thickening of the intestinal wall in the transverse colon, localized indistinct demarcation between the stomach and transverse colon, and a small amount of fluid accumulation in the abdominal cavity. Immediately afterwards, he was admitted to our department, and then we arranged a computed tomography with intravenously administered contrast agent showed a spontaneous isolated gastric intramural hematoma combined with spontaneous superior mesenteric artery intermural hematoma. Therefore, we treated him with anticoagulation and conservative observation. During his stay in the hospital, he was given low-molecular heparin by subcutaneous injection for anticoagulation therapy, and after discharge, he was given oral anticoagulation therapy with rivaroxaban. At the follow-up of more than 4 months, most of the intramural hematoma was absorbed and became significantly smaller, and the intermural hematoma of the superior mesenteric artery was basically absorbed, which also confirmed that the intramural mass was an intramural hematoma. CONCLUSION: A gastric intramural hematoma should be considered, when an intra-abdominal mass was found to be attached to the gastric wall. Proper recognition of gastric intramural hematoma can reduce the misdiagnosis rate of confusion with gastric cancer.

The potential role of differentially expressed tRNA-derived fragments in high glucose-induced podocytes.

The prevalence of diabetic kidney disease (DKD) is increasing annually. Damage to and loss of podocytes occur early in DKD. tRNA-derived fragments (tRFs), originating from tRNA precursors or mature tRNAs, are associated with various illnesses. In this study, tRFs were identified, and their roles in podocyte injury induced by high-glucose (HG) treatment were explored. High-throughput sequencing of podocytes treated with HG was performed to identify differentially expressed tRFs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed. The expression levels of nephrin, podocin, and desmin were measured in podocytes after overexpression of tRF-1:24-Glu-CTC-1-M2 (tRF-1:24) and concomitant HG treatment. A total of 647 tRFs were identified, and 89 differentially expressed tRFs (|log2FC| ≥ 0.585; p ≤ .05) were identified in the HG group, of which 53 tRFs were downregulated and 36 tRFs were upregulated. The 10 tRFs with the highest differential expression were detected by real-time quantitative polymerase chain reaction (RT-qPCR), and these results were consistent with the sequencing results. GO analysis revealed that the biological process, cellular component, and molecular function terms in which the tRFs were the most enriched were cellular processes, cellular anatomical entities, and binding. KEGG pathway analysis revealed that tRFs may be involved in signaling pathways related to growth hormones, phospholipase D, the regulation of stem cell pluripotency, and T-/B-cell receptors. Overexpression of tRF-1:24, one of the most differentially expressed tRFs, attenuated podocyte injury induced by HG. Thus, tRFs might be potential biomarkers for podocyte injury in DKD.

Modulating d-Band Electronic Structures of Molybdenum Disulfide via p/n Doping to Boost Polysulfide Conversion in Lithium-Sulfur Batteries.

Polysulfide shuttle effect and sluggish sulfur reaction kinetics severely impede the cycling stability and sulfur utilization of lithium-sulfur (Li-S) batteries. Modulating d-band electronic structures of molybdenum disulfide electrocatalysts via p/n doping is promising to boost polysulfide conversion and suppress polysulfide migration in lithium-sulfur batteries. Herein, p-type V-doped MoS2 (V-MoS2 ) and n-type Mn-doped MoS2 (Mn-MoS2 ) catalysts are well-designed. Experimental results and theoretical analyses reveal that both of them significantly increase the binding energy of polysulfides on the catalysts' surface and accelerate the sluggish conversion kinetics of sulfur species. Particularly, the p-type V-MoS2 catalyst exhibits a more obvious bidirectional catalytic effect. Electronic structure analysis further demonstrates that the superior anchoring and electrocatalytic activities are originated from the upward shift of the d-band center and the optimized electronic structure induced by duplex metal coupling. As a result, the Li-S batteries with V-MoS2 modified separator exhibit a high initial capacity of 1607.2 mAh g-1 at 0.2 C and excellent rate and cycling performance. Moreover, even at a high sulfur loading of 6.84 mg cm-2 , a favorable initial areal capacity of 8.98 mAh cm-2 is achieved at 0.1 C. This work may bring widespread attention to atomic engineering in catalyst design for high-performance Li-S batteries.

A novel m7G regulator-based methylation patterns in head and neck squamous cell carcinoma.

Abnormal RNA N7-methylguanosine (m7G) modification is known to contribute to effects on tumor occurrence and development. Nevertheless, the mechanisms of its function in immunoregulation, tumor microenvironment (TME) modulation, and tumor promotion remain largely unknown. A series of computer-aided bioinformatic analyses were conducted based on transcriptomic, single-cell sequence, and spatial transcriptomic data to determine the m7G modification patterns in head and neck squamous cell carcinoma (HNSCC). Consensus clustering approach was employed according to the expressions of 33 m7G regulators. ESTIMATE, CIBERSORT, and single sample gene set enrichment analysis algorithms were adopted to investigate the immune cell infiltration features. A prognostic model named m7Gscore was established. Seurat, SingleR, and Monocle2 were used to analyze the single-cell sequence profiling. STUtility was used to integrate multiple spatial transcriptomic datasets. Quantitative reverse transcription polymerase chain reaction, transwell, and wound-healing assay were performed to verify the oncogenes. Here, three different m7G modification patterns were highlighted in HNSCC patients, which were also related to various clinical manifestations and three representative immunophenotypes: immune-excluded, immune-desert, and inflamed, separately. Patients with lower m7Gscore were highlighted by higher immune cell infiltrations, better overall survival rates, lesser tumor mutation burden (TMB), lower sensitivities to target inhibitors therapies, and better immunotherapeutic response. Moreover, DCPS, EIF4E, EIF4E2, LSM1, NCBP2, NUDT1, and NUDT5 were identified to play critical roles in T-cell differentiation. Knockdown of LSM1/NUDT5 could restrain the malignancy of HNSCC cells. Collectively, quantitative assessment of m7G modification patterns in individual HNSCC patients could contribute to identifying more efficient immunotherapeutic approaches and improve the clinical outcome of HNSCC.

DDIT4 promotes malignancy of head and neck squamous cell carcinoma.

This study investigated the cancer-promoting effect of ferroptosis regulator DNA damage-inducible transcript 4 (DDIT4) and its relevant mechanisms. Vital ferroptosis-related genes were identified using bioinformatic methods on the basis of data collected from TCGA and seven other online databases. Cell Counting Kit-8 (CCK8), colony formation, wound-healing and transwell assays, and western blot analysis were conducted for verifying the biological role of DDIT4 in vitro. The immune score and tumor purity were calculated using R package "estimate." The relationship was identified between DDIT4 expression and immune cell infiltration using ssGSEA and CIBERSORT algorithms. R package "Seurat" was used to perform unsupervised clustering of the single cells, and "SingleR" was utilized for annotation. R package "STUtility" was employed to plot the spatial expression of DDIT4. For trajectory analysis, monocle was used to predict cell differentiation and demonstrate the expression of DDIT4 at each state. Here, DDIT4 overexpression was observed in Head and Neck Squamous Cell Carcinoma (HNSCC) cohort, and DDIT4 upregulation showed a positive correlation with larger tumor size, lymph node metastasis, more advanced TNM stage and higher tumor mutational burden (TMB). Moreover, DDIT4 knockdown could markedly inhibit the proliferation, colony formation, invasion and migration of HNSCC cells, as well as suppress the expression of HIF-1a, VEGF and vimentin. In comparison, DDIT4 overexpression showed a negative correlation with immune score and infiltrations of several immune cells. DDIT4 played crucial roles in the differentiation of CAFs and T cells. Collectively, this study demonstrates that DDIT4 contributes a critical role in HNSCC progression. The positive feedback regulation between DDIT4 and HIF-1a may be a potential target for HNSCC treatment.

m7G-related genes-NCBP2 and EIF4E3 determine immune contexture in head and neck squamous cell carcinoma by regulating CCL4/CCL5 expression.

Aberrant N7 -methylguanosine (m7G) levels closely correlate with tumor genesis and progression. NCBP2 and EIF4E3 are two important m7G-related cap-binding genes. This study aimed to identify the relationship between the EIF4E3/NCBP2 function and immunological characteristics of head and neck squamous cell carcinoma (HNSCC). Hierarchical clustering was employed in classifying HNSCC patients into two groups based on the expressions of NCBP2 and EIF4E3. The differentially expressed genes were identified between the two groups, and GO functional enrichment was subsequently performed. Weighted gene co-expression network analysis was conducted to identify the hub genes related to EIF4E3/NCBP2 expression and immunity. The differential infiltration of immune cells and the response to immunotherapy were compared between the two groups. Single-cell sequence and trajectory analyses were performed to predict cell differentiation and display the expression of EIF4E3/NCBP2 in each state. In addition, quantitative real-time PCR, spatial transcriptome analysis, transwell assay, and western blotting were conducted to verify the biological function of EIF4E3/NCBP2. Here, group A showed a higher EIF4E3 expression and a lower NCBP2 expression, which had higher immune scores, proportion of most immune cells, immune activities, expression of immunomodulatory targets, and a better response to cancer immunotherapy. Besides, 56 hub molecules with notable immune regulation significance were identified. A risk model containing 17 hub genes and a prognostic nomogram was successfully established. Moreover, HNSCC tissues had a lower EIF4E3 expression and a higher NCBP2 expression than normal tissues. NCBP2 and EIF4E3 played a vital role in the differentiation of monocytes. Furthermore, the expression of CCL4/CCL5 can be regulated via EIF4E3 overexpression and NCBP2 knockdown. Collectively, NCBP2 and EIF4E3 can affect downstream gene expression, as well as immune contexture and response to immunotherapy, which could induce "cold-to-hot" tumor transformation in HNSCC patients.

Overexpression of Pasteurella multocida OmpA induces transcriptional changes and its possible implications for the macrophage polarization.

Pasteurella multocida (P. multocida) is a highly infectious, zoonotic pathogen. Outer membrane protein A (OmpA) is an important virulence component of the outer membrane of P. multocida. OmpA mediates bacterial biofilm formation, eukaryotic cell infection, and immunomodulation. It is unclear how OmpA affects the host immune response. We estimated the role of OmpA in the pathogenesis of P. multocida by investigating the effect of OmpA on the immune cell transcriptome. Changes in the transcriptome of rat alveolar macrophages (NR8383) upon overexpression of P. multocida OmpA were demonstrated. A model cell line for stable transcription of OmpA was constructed by infecting NR8383 cells with OmpA-expressing lentivirus. RNA was extracted from cells and sequenced on an Illumina HiSeq platform. Key gene analysis of genes in the RNA-seq dataset were performed using various bioinformatics methods, such as gene ontology enrichment analysis, Kyoto Encyclopedia of Genes and Genomes enrichment analysis, Gene Set Enrichment Analysis, and Protein-Protein Interaction Analysis. Our findings revealed 1340 differentially expressed genes. Immune-related pathways that were significantly altered in rat alveolar macrophages under the effect of OmpA included focal adhesion, extracellular matrix and vascular endothelial growth factor signaling pathways, antigen processing and presentation, nucleotide oligomerization domain-like receptor and Toll-like receptor signaling pathways, and cytokine-cytokine receptor interaction. The key genes screened were Vegfa, Igf2r, Fabp5, P2rx1, C5ar1, Nedd4l, Gas6, Cxcl1, Pf4, Pdgfb, Thbs1, Col7a1, Vwf, Ccl9, and Arg1. Data of associated pathways and altered gene expression indicated that OmpA might cause the conversion of rat alveolar macrophages to M2-like. The related pathways and key genes can serve as a reference for OmpA of P. multitocida and host interaction mechanism studies.

Metabolism of an insecticide fipronil by soil fungus Cunninghamella elegans ATCC36112.

In this study, the metabolic pathway of the phenylpyrazole insecticide fipronil in Cunninghamella elegans (C. elegans) was investigated. Approximately 92% of fipronil was removed within 5 days, and seven metabolites were accumulated simultaneously. The structures of the metabolites were completely or tentatively identified by GC-MS and 1H, 13C NMR. To determine the oxidative enzymes involved in metabolism, piperonyl butoxide (PB) and methimazole (MZ) were used, and the kinetic responses of fipronil and its metabolites were determined. PB strongly inhibited fipronil metabolism, while MZ weakly inhibited its metabolism. The results suggest that cytochrome P450 (CYP) and flavin-dependent monooxygenase (FMO) may participate in fipronil metabolism. Integrated metabolic pathways can be inferred from the control and inhibitor experiments. Several novel products from the fungal transformation of fipronil were identified, and similarities between C. elegans transformation and mammalian metabolism of fipronil were compared. Therefore, these results will help to gain insight into the fungal degradation of fipronil and potential applications in fipronil bioremediation. At present, microbial degradation of fipronil is the most promising approach and maintains environmental sustainability. In addition, the ability of C. elegans to mimic mammalian metabolism will assist in illustrating the metabolic fate of fipronil in mammalian hepatocytes and assess its toxicity and potential adverse effects.

Metabolic pathway of tebuconazole by soil fungus Cunninghamella elegans ATCC36112.

Tebuconazole is the most widely used fungicide in agriculture. Due to its long half-life, tebuconazole residues can be found in the environment media such as in soil and water bodies. Here, the metabolic pathway of tebuconazole was studied in Cunninghamella elegans (C. elegans). Approximately 98% of tebuconazole was degraded within 7 days, accompanied by the accumulation of five metabolites. The structures of the metabolites were completely or tentatively identified by gas chromatography-mass spectrometry (GC-MS) and ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). To identify representative oxidative enzymes that may be involved in the metabolic process, treatment with piperonyl butoxide (PB) and methimazole (MZ) was performed. PB had a strong inhibitory effect on the metabolic reactions, while MZ had a weak inhibitory effect. The results suggest that cytochrome P450 (CYP) and flavin-dependent monooxygenase are involved in the metabolism of tebuconazole. Based on the results, we propose a metabolic pathway for the fungal metabolism of tebuconazole. Data are of interest to gain insight into the toxicological effects of tebuconazole and for tebuconazole bioremediation.

Biodegradation and metabolic pathway of quinalphos by Cunninghamella elegans ATCC36112.

Quinalphos is a long-term, wide-spectrum organophosphate insecticide with residual problems in the natural environment. Cunninghamella elegans (C. elegans) is a member of Mucoromycotina. Since the degradation products of its exogenous compounds are similar to those of mammals, it is often used to simulate the metabolism pathways of mammals. In this study, the detailed metabolic pathways of quinalphos were investigated with C. elegans. Quinalphos was degraded by 92% in 7 days, while ten metabolites were produced. The metabolites were analyzed and identified by GC-MS. To determine the responsible enzymes in quinalphos metabolism, piperonyl butoxide (PB) and methimazole included in the culture flasks, and the kinetic responses of quinalphos and its metabolites by C. elegans were measured. Results indirectly demonstrated that cytochrome P450 monooxygenases were involved in the metabolism of quinalphos, but that methimazole inhibited the metabolism less efficiently. Comprehensive metabolic pathways can be deduced from the detailed analysis of metabolite profiles in control and inhibitor assays.

Profiling Chromatin Accessibility Responses in Goat Bronchial Epithelial Cells Infected with Pasteurella multocida.

Pasteurella multocida can cause goat hemorrhagic sepsis and endemic pneumonia. Respiratory epithelial cells are the first line of defense in the lungs during P. multocida infection. These cells act as a mechanical barrier and activate immune response to protect against invading pathogenic microorganisms. Upon infection, P. multocida adheres to the cells and causes changes in cell morphology and transcriptome. ATAC-seq was conducted to determine the changes in the chromatin open region of P. multocida-infected goat bronchial epithelial cells based on transcriptional regulation. A total of 13,079 and 28,722 peaks were identified in the control (CK) and treatment (T) groups (P. multocida infection group), respectively. The peaks significantly increased after P. multocida infection. The specific peaks for the CK and T groups were annotated to 545 and 6632 genes, respectively. KEGG pathway enrichment analysis revealed that the specific peak-related genes in the T group were enriched in immune reaction-related pathways, such as Fc gamma R-mediated phagocytosis, MAPK signaling pathway, bacterial invasion of epithelial cells, endocytosis, and autophagy pathways. Other cellular component pathways were also enriched, including the regulation of actin cytoskeleton, adherent junction, tight junction, and focal adhesion. The differential peaks between the two groups were subsequently analyzed. Compared to those in the CK group, 863 and 11 peaks were upregulated and downregulated, respectively, after the P. multocida infection. Fifty-six known transcription factor motifs were revealed in upregulated peaks in the P. multocida-infected group. By integrating ATAC-seq and RNA-seq, some candidate genes (SETBP1, RASGEF1B, CREB5, IRF5, TNF, CD70) that might be involved in the goat bronchial epithelial cell immune reaction to P. multocida infection were identified. Overall, P. multocida infection changed the structure of the cell and caused chromatin open regions to be upregulated. In addition, P. multocida infection actively mobilized the host immune response with the inflammatory phenotype. The findings provide valuable information for understanding the regulatory mechanisms of P. multocida-infected goat bronchial epithelial cells.

Bovine skin fibroblasts mediated immune responses to defend against bovine Acinetobacter baumannii infection.

Acinetobacter baumannii (A. baumannii) is an opportunistic pathogen which can cause pneumonia, sepsis and infections of skin and soft tissue. The host mostly relies on innate immune responses to defend against the infection of A. baumannii. Currently, it has been confirmed that fibroblasts involved in innate immune responses. Therefore, to explore how bovine skin fibroblasts mediated immune responses to defend against A. baumannii infection, we analyzed the differential transcripts data of bovine skin fibroblasts infected with bovine A. baumannii by RNA-sequencing (RNA-seq). We found that there were 3014 differentially expressed genes (DEGs) at 14h with bovine A. baumannii infection, including 1940 up-regulated genes and 1074 down-regulated genes. Gene Ontology (GO) enrichment showed that ubiquitin protein ligase binding, IL-6 receptor complex, ERK1 and ERK2 cascade terms were mainly enriched. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment showed that innate immune pathways were significantly enriched, such as TNF, IL-17, NLR, MAPK, NF-κB, endocytosis, apoptosis and HIF-1 signaling pathways. Furthermore, Gene Set Enrichment Analysis (GSEA) revealed that GO terms such as chemokine receptor binding and Th17 cell differentiation and KEGG pathways such as TLR and cytokine-cytokine receptor interaction pathways were up-regulated. In addition, CASP3 and JUN were the core functional genes of apoptosis, while IL-6, ERBB2, EGFR, CHUK and MAPK8 were the core functional genes of immunity by Protein-Protein Interaction (PPI) analysis. Our study provided an in-depth understanding of the molecular mechanisms of fibroblasts against A. baumannii infection. It also lays the foundation for the development of new therapeutic targets for the diseases caused by A. baumannii infection and formulates effective therapeutic strategies for the prevention and control of the diseases caused by A. baumannii.

Dermatomal somatosensory evoked potentials and cortical somatosensory evoked potentials assessment in congenital scoliosis.

BACKGROUND: The aim of this study was to assess the value of dermatomal somatosensory evoked potentials (DSEPs) and cortical somatosensory evoked potentials (SSEPs) in monitoring spinal cord function for patients with congenital scoliosis (CS). METHODS: This retrospective study reviewed the medical records of patients (n = 102) who underwent DSEP (T2-S1 dermatome), of whom 60 were normal subjects and 62 with congenital scoliosis. The study analyzed the latencies and peaks of N1-L, N1-R, P1-L and P1-R recorded by DSEPs of patients' thoracolumbar dermatomes. To observe the incidence of abnormal DSEPs and SSEPs in CS patients and to analyze the difference in sensitivity and reliability between the two in the examination of scoliosis patients. SPSS 22.0 statistical software package was used to analyze the data, and χ2 test and correlation analysis were used to indicate that the difference was statistically significant, p < 0.05. RESULTS: Sixty two patients with CS were evaluated with total spine magnetic resonance imaging (MRI). Only 23 patients (37.09%) showed spinal cord malformations in the MRI findings. The DSEP recordings showed a relatively high sensitivity (97.8%) compared to the abnormality rate of SSEPs recordings, and the rates of waveform, latency and amplitude abnormalities were much higher in DSEPs recordings (36.6, 36.3, 24.8%) than in SSEPs recordings (3.2, 22.5, 14.5%). The abnormality rate of DSEP records with and without neurological symptoms was higher than the abnormality rate of SSEP records (100% vs 20, 96.2% vs 44.2%, p<0.05). And in 62 patients with CS, the rate of positive MRI (37.1%) was lower than that recorded by DSEP (79.6% / 57.9%). p < 0.05. CONCLUSION: DSEPs are more sensitive to microscopic posterior column dysfunction in patients with CS that cannot be detected by either radiology or routine clinical examination. Preoperative DSEPs assessment is recommended as a baseline examination for intraoperative monitoring and comparison with the postoperative situation. DSEPs recording complements the information obtained from routine clinical and radiological evaluation.

MicroRNA-382-5p Promotes Oral Squamous Cell Carcinoma Development and Progression by Negatively Regulating PTEN Expression.

PURPOSE: Oral squamous cell carcinoma (OSCC) local recurrence and distant metastasis remain a poorly understood clinical challenge. The objective of this study was to investigate how dysregulation of miR-382-5p impacts invasion and dissemination of OSCC. METHODS: Tissue samples were collected from 20 subjects with OSCC. Expression levels of miR-382-5p were determined by quantitative real-time polymerase chain reaction (qRT-PCR), and correlations with clinical characteristics were investigated. qRT-PCR was used to determine the miR-382-5p and peptidyl-prolyl cis/trans isomerase (PTEN) expression in tumor tissues, adjacent normal tissues, normal human oral keratinocyte line, and OSCC line (SCC-9). Cell proliferation, invasion, and migration of knock-in and knock-down miR-382-5p transfectants were assessed using cell counting kit-8 and Transwell assays. PTEN was confirmed to be a downstream target using a TargetScan prediction, dual-luciferase reporter assays, and western blot analysis. Statistical analysis of experimental data was performed with SPSS 22.0 software. RESULTS: We found high expression of miR-382-5p and significant downregulation of PTEN in tumor tissues and SCC-9 cells from OSCC patients (P < .05). miR-382-5p expression was lower in early stage (I + II) than in late stage (III + IV), while PTEN exhibited higher expression in early stage (I + II) instead of in late stage (III + IV) (P < .05). In addition, overexpression of miR-382-5p promoted the proliferation, invasion, and migration of OSCC cells. However, the proliferation, invasion, and migration of OSCC cells were inhibited after suppression of miR-382-5p. Finally, PTEN is downregulated by miR-382-5p. CONCLUSION: MiR-382-5p supports proliferation, invasion, and migration of OSCC cells through the PTEN pathway. Further investigation may improve our understanding of OSCC local recurrence and distant metastasis.

Rare variation: the absence of both the celiac trunk artery and the common hepatic artery.

BACKGROUND: Knowledge of celiac trunk anatomy is important in gastrointestinal surgery, hepatopancreatobiliary surgery, transplantation and interventional radiology. Variations in the celiac trunk are common and should be predicted prior to these interventions. METHODS: A 58-year-old woman was admitted to our department for surgical treatment of gastric cancer (GC) confirmed by gastroduodenoscopy and gastric antrum biopsy. In the contrast-enhanced computed tomography (CT), we found an absence of both the celiac trunk artery (CA) and the common hepatic artery (CHA). Therefore, we used computerized three-dimensional (3D) vascular reconstruction technology to reconstruct the abdominal trunk and its branch vessels before operation. RESULTS: Computerized 3D vascular reconstruction confirmed an extremely rare vascular anomaly: the absence of both CA and CHA. The splenic artery (SA) and gastroduodenal artery (GDA) originated from the abdominal aorta (AA). The left gastric artery (LGA) originated from the AA directly above the junction of SA and the GDA. The left hepatic artery (LHA) originated from the left gastric artery (LGA). The right hepatic artery (RHA) originated from the superior mesenteric artery (SMA). Laparoscopic radical resection of GC was performed. This anomaly was also confirmed intraoperatively. This patient was discharged on the 10th day after surgery without any postoperative complication. There were no signs of tumor recurrence during the 6-month follow-up. CONCLUSION: Correct identification of abnormal abdominal large blood vessels and their relationship with tumors before surgery is of great significance to avoid intraoperative blood vessel damage, major postoperative complications and the missing of lymph node dissection.

Monitoring thiophenols in both environmental water samples and bio-samples: A method based on a fluorescent probe with broad pH adaptation.

Thiophenol, which is a highly toxic sulfhydryl compound widely used in chemical industry, is an environmental pollutant that threatens human health significantly. It is of great importance to detect highly toxic thiophenols in both environmental and biological system. Thus, the need to develop rapid response, selective and sensitive probes is urgent. In this study, a novel probe was presented for the detection of thiophenols based on an intramolecular charge transfer (ICT) mechanism. This probe exhibits rapid response, broad pH adaptation (2-10), highly selectivity, a large Stokes shift (131 nm) and 40-fold enhancement in fluorescence. Besides, this probe showed low toxicity towards human cell HEK293 and could be applied to detect thiophenol both in living cells, zebrafish and environmental water samples with good recovery (over 94%). All the results indicated that this probe could be a promising sensor for applications for thiophenol derivatives detection in both environmental and biological sciences.