Impacts of continuous cropping on the rhizospheric and endospheric microbial communities and root exudates of Astragalus mongholicus.

Astragalus mongholicus is a medicinal plant that is known to decrease in quality in response to continuous cropping. However, the differences in the root-associated microbiome and root exudates in the rhizosphere soil that may lead to these decreases are barely under studies. We investigated the plant biomass production, root-associated microbiota, and root exudates of A. mongholicus grown in two different fields: virgin soil (Field I) and in a long-term continuous cropping field (Field II). Virgin soil is soil that has never been cultivated for A. mongholicus. Plant physiological measurements showed reduced fresh and dry weight of A. mongholicus under continuous cropping conditions (i.e. Field II). High-throughput sequencing of the fungal and bacterial communities revealed differences in fungal diversity between samples from the two fields, including enrichment of potentially pathogenic fungi in the roots of A. mongholicus grown in Field II. Metabolomic analysis yielded 20 compounds in A. mongholicus root exudates that differed in relative abundance between rhizosphere samples from the two fields. Four of these metabolites (2-aminophenol, quinic acid, tartaric acid, and maleamate) inhibited the growth of A. mongholicus, the soil-borne pathogen Fusarium oxysporum, or both. This comprehensive analysis enhances our understanding of the A. mongholicus microbiome, root exudates, and interactions between the two in response to continuous cropping. These results offer new information for future design of effective, economical approaches to achieving food security.

Salinity decreases the contribution of microbial necromass to soil organic carbon pool in arid regions.

Saline soils are widely distributed in arid areas but there is a lack of mechanistic understanding on the effect of salinity on the formation and biochemical composition of soil organic carbon (SOC). We investigated the effects of salinity on the accumulation of microbial necromass under natural vegetation and in cropland in salt-affected arid areas stretching over a 1200-km transect in northwest China. Under both natural vegetation and cropland, microbial physiological activity (indicated by microbial biomass carbon normalized enzymatic activity) decreased sharply where the electrical conductivity approached 4 ds m-1 (a threshold to distinguish between saline and non-saline soils), but microbial biomass was only slightly affected by salinity. These indicated that a larger proportion of microbes could be inactive or dormant in saline soils. The contribution of fungal necromass C to SOC decreased but the contribution of bacterial necromass C to the SOC increased with increasing soil salinity. Adding fungal and bacterial necromass C together, the contribution of microbial necromass C to SOC in saline soils was 32-39 % smaller compared with non-saline soils. Fungal necromass C took up 85-86 % of microbial necromass C in non-saline soils but this proportion dropped to 60-66 % in saline soils. We suggested that the activity, growth, and turnover rate of microbes slowed by salinity was responsible for the decreased accumulation of fungal necromass in saline compared with non-saline soils, while the increased accumulation of bacterial residue in saline soils could be induced mainly by its slower decomposition. Soil microbial biomass was a poor predictor for the accumulation of microbial necromass in saline soils. We demonstrated a reduced contribution of microbial necromass to SOC and a shift in its composition towards the increase in bacterial origin in saline relative to non-saline soils. We concluded that salinity profoundly changes the biochemistry of SOC in arid regions.

Energy metabolism: a new target for gastric cancer treatment

Gastric cancer is the fifth most common malignancy worldwide having the fourth highest mortality rate. Energy metabolism is key and closely linked to tumour development. Most important in the reprogramming of cancer metabolism is the Warburg effect, which suggests that tumour cells will utilise glycolysis even with normal oxygen levels. Various molecules exert their effects by acting on enzymes in the glycolytic pathway, integral to glycolysis. Second, mitochondrial abnormalities in the reprogramming of energy metabolism, with consequences for glutamine metabolism, the tricarboxylic acid cycle and oxidative phosphorylation, abnormal fatty acid oxidation and plasma lipoprotein metabolism are important components of tumour metabolism. Third, inflammation-induced oxidative stress is a danger signal for cancer. Fourth, patterns of signalling pathways involve all aspects of metabolic transduction, and many clinical drugs exert their anticancer effects through energy metabolic signalling. This review summarises research on energy metabolism genes, enzymes and proteins and transduction pathways associated with gastric cancer, and discusses the mechanisms affecting their effects on postoperative treatment resistance and prognoses of gastric cancer. We believe that an in-depth understanding of energy metabolism reprogramming will aid the diagnosis and subsequent treatment of gastric cancer (AU)

Neuroprotective effect of ketamine and sevoflurane against TNF-α induced cognitive impairment.

In the present study, neuroprotective effect of sevoflurane in combination with ketamine was investigated on TNF-α induced necroptosis of neurons and cognitive impairment in the rat model. The results demonstrated that exposure to TNF-α/z-VAD led to a significant decrease in viability of HT-22 neuronal cells. However, incubation of HT-22 cells with ketamine plus sevoflurane inhibited decrease in viability induced by TNF-α/z-VAD exposure. The increase in production of ROS by TNF-α/z-VAD exposure in HT-22 cells was effectively suppressed on pre-treatment with ketamine plus sevoflurane. Moreover, suppression of TNF-α/z-VAD induced ROS production in HT-22 cells by ketamine plus sevoflurane pretreatment was higher in comparison to ketamine or sevoflurane treatment alone. Treatment of HT-22 cells with ketamine plus sevoflurane suppressed TNF-α/z-VAD induced increase in RIP1 and p-MLKL protein expression. Ketamine plus sevoflurane treatment effectively reversed decrease in movement speed as well as total distance traveled in TNF-α injected rats. The number of neurons in rat hippocampus injected with TNF-α showed a significant decrease more specifically in carbonic anhydrase-3 region. However, no significant change in the density of neurons was observed in the hippocampus of rats pretreated with ketamine plus sevoflurane by TNF-α injection. The increase in expression of p-MLKL and p-RIP3 by TNF-α injection was effectively reversed in rats on treatment with ketamine plus sevoflurane. In silico studies revealed that ketamine interacts with p-MLKL protein in different confirmations with the binding affinities ranging from -9.7 to -8.4 kcal/mol. It was found that ketamine binds to p-MLKL protein by interacting with alanine (ALA A:295), proline (PRO A:306), glutamine (GLN A: 307) and isoleucine (ILE A:293) amino acid residues. In summary, ketamine plus sevoflurane combination alleviates TNF-α/z-VAD induced decrease in viability of HT-22 cells in vitro and rat hippocampus neurons in vivo. Moreover, ketamine plus sevoflurane combination prevented TNF-α injection induced cognitive impairment in rats. Therefore, sevoflurane plus ketamine combination can be developed as a potential therapeutic regimen for treatment of isoflurone induced cognitive impairment.

The Role of LMP1 in Epstein-Barr Virus-associated Gastric Cancer.

EBV promotes many cancers such as lymphoma, nasopharyngeal carcinoma, and gastric; Latent Membrane Protein 1 (LMP1) is considered to be a major oncogenic protein encoded by Epstein- Barr virus (EBV). LMP1 functions as a carcinogen in lymphoma and nasopharyngeal carcinoma, and LMP1 may also promote gastric cancer. The expression level of LMP1 in host cells is a key determinant in tumorigenesis and maintenance of virus specificity. By promoting cell immortalization and cell transformation, promoting cell proliferation, affecting immunity, and regulating cell apoptosis, LMP1 plays a crucial tumorigenic role in epithelial cancers. However, very little is currently known about LMP1 in Epstein-Barr virus-associated gastric cancer (EBVaGC); the main reason is that the expression level of LMP1 in EBVaGC is comparatively lower than other EBV-encoded proteins, such as The Latent Membrane Protein 2A (LMP2A), Epstein-Barr nuclear antigen 1 (EBNA1) and BamHI-A rightward frame 1 (BARF1), to date, there are few studies related to LMP1 in EBVaGC. Recent studies have demonstrated that LMP1 promotes EBVaGC by affecting The phosphatidylinositol 3-kinase- Akt (PI3K-Akt), Nuclear factor-kappa B (NF-κB), and other signaling pathways to regulate many downstream targets such as Forkhead box class O (FOXO), C-X-C-motif chemokine receptor (CXCR), COX-2 (Cyclooxygenase-2); moreover, the gene methylation induced by LMP1 in EBVaGC has become one of the characteristics that distinguish this gastric cancer (GC) from other types of gastric cancer and LMP1 also promotes the formation of the tumor microenvironment (TME) of EBVaGC in several ways. This review synthesizes previous relevant literature, aiming to highlight the latest findings on the mechanism of action of LMP1 in EBVaGC, summarize the function of LMP1 in EBVaGC, lay the theoretical foundation for subsequent new research on LMP1 in EBVaGC, and contribute to the development of novel LMP1-targeted drugs.

Energy metabolism: a new target for gastric cancer treatment.

Gastric cancer is the fifth most common malignancy worldwide having the fourth highest mortality rate. Energy metabolism is key and closely linked to tumour development. Most important in the reprogramming of cancer metabolism is the Warburg effect, which suggests that tumour cells will utilise glycolysis even with normal oxygen levels. Various molecules exert their effects by acting on enzymes in the glycolytic pathway, integral to glycolysis. Second, mitochondrial abnormalities in the reprogramming of energy metabolism, with consequences for glutamine metabolism, the tricarboxylic acid cycle and oxidative phosphorylation, abnormal fatty acid oxidation and plasma lipoprotein metabolism are important components of tumour metabolism. Third, inflammation-induced oxidative stress is a danger signal for cancer. Fourth, patterns of signalling pathways involve all aspects of metabolic transduction, and many clinical drugs exert their anticancer effects through energy metabolic signalling. This review summarises research on energy metabolism genes, enzymes and proteins and transduction pathways associated with gastric cancer, and discusses the mechanisms affecting their effects on postoperative treatment resistance and prognoses of gastric cancer. We believe that an in-depth understanding of energy metabolism reprogramming will aid the diagnosis and subsequent treatment of gastric cancer.

Implication of Amyloid Precursor-like Protein 2 Expression in Cutaneous Squamous Cell Carcinoma Pathogenesis.

BACKGROUND/AIM: Regulatory functions of amyloid precursor-like protein 2 (APLP2) expression in intracellular trafficking of major histocompatibility complex class I (MHC-I) and biological behavior of tumor cells have been reported in various types of malignancies but not in cutaneous squamous cell carcinoma (CSCC). This study aimed to investigate the role of APLP2 expression in the pathogenesis of CSCC. PATIENTS AND METHODS: The expression of APLP2 and a key modulator of cancer immune escape, MHC-I, were determined in CSCC tissue samples obtained from 141 patients using immunohistochemistry. The regulatory effects of APLP2 expression on the biological behavior and surface expression of MHC-I in CSCC cells were investigated by trypan blue assay, Matrigel invasion assay, and in vivo xenograft analysis. RESULTS: APLP2 immunoreactivity was high in 73 (51.8%) tissue samples from patients with CSCC and was significantly related to subcutaneous fat invasion and poor prognosis in our cohort. Moreover, proliferation of and invasion by CSCC cells were significantly reduced after APLP2 knockdown in CSCC cells both in vitro and in vivo. A significant association was found between APLP2 and membrane MHC-I expression in patients with CSCC. In vivo xenograft analysis showed that APLP2 knockdown increased membrane MHC-I expression in CSCC cells. CONCLUSION: APLP2 not only acts as an oncogene in CSCC progression but also as a possible modulator of cancer immune escape by influencing MHC-I expression on the cell surface. APLP2 may serve as a novel molecular biomarker and therapeutic target for patients with CSCC.

Granular bacterial inoculant alters the rhizosphere microbiome and soil aggregate fractionation to affect phosphorus fractions and maize growth.

The constraint of phosphorus (P) fixation on crop production in alkaline calcareous soils can be alleviated by applying bioinoculants. However, the impact of bacterial inoculants on this process remains inadequately understood. Here, a field study was conducted to investigate the effect of a high-concentration, cost-effective, and slow-release granular bacterial inoculant (GBI) on maize (Zea mays L.) plant growth. Additionally, we explored the effects of GBI on rhizosphere soil aggregate physicochemical properties, rhizosphere soil P fraction, and microbial communities within aggregates. The outcomes showed a considerable improvement in plant growth and P uptake upon application of the GBI. The application of GBI significantly enhanced the AP, phoD gene abundance, alkaline phosphatase activity, inorganic P fractions, and organic P fractions in large macroaggregates. Furthermore, GBI impacted soil aggregate fractionation, leading to substantial alterations in the composition of fungal and bacterial communities. Notably, key microbial taxa involved in P-cycling, such as Saccharimonadales and Mortierella, exhibited enrichment in the rhizosphere soil of plants treated with GBI. Overall, our study provides valuable insight into the impact of GBI application on microbial distributions and P fractions within aggregates of alkaline calcareous soils, crucial for fostering healthy root development and optimal crop growth potential. Subsequent research endeavors should delve into exploring the effects of diverse GBIs and specific aggregate types on P fraction and community composition across various soil profiles.

Case report: Differential diagnosis of highly amplified anti-CD5 CAR T cells and relapsed lymphoma cells in a patient with refractory ALK positive anaplastic large cell lymphoma.

Background: Anaplastic Large Cell Lymphoma (ALCL) is one of the most common subtypes of T-cell lymphoma. Among these, refractory and relapsed (r/r) ALK positive ALCL lacks effective therapies. The chimeric antigen receptor-modified T (CAR-T) cell therapy holds great promise as a therapeutic strategy for this disease. However, it is not known yet whether anti-CD5 CAR-T cells are sufficient for the definitive treatment of relapsed ALK+ ALCL, nor the role of accurate laboratory-based diagnoses during CAR-T treatment. Case presentation: The adolescent patient received autologous T cells containing sequences encoding VH domains specific to CD5. Following the infusion, there was an increase in both the copy number and proportion of CAR-T cells in peripheral blood. IL-6 and ferritin levels in the patient exhibited significant fluctuations, with increases of 13 and 70 folds respectively, compared to baseline after the treatment. Additionally, adverse effects were observed, including grade 4 rash, grade 1 headache, nausea, and neck-pain. Surprisingly, a relapsed disease phenotype was identified based on the results of PET/CT and histopathological analysis of the inguinal lymph node biopsy. After conducting a thorough diagnostic assessment, which included flow cytometry, next-generation sequencing (NGS), examination of immune-related gene rearrangements, and analysis of the immune repertoire of T-cell receptors (TCR), we conclusively determined that the hyperplastic T cells identified in the lymph node were the result of an expansion of CAR-T cells. Ultimately, the patient has attained complete remission (CR) and has sustained a disease-free survival state for 815 days as of the cutoff date on August 30, 2023. Conclusion: Taken together, the results demonstrate that anti-CD5 CAR-T cells can induce a clinical response in r/r ALK+ ALCL patient. Furthermore, this case underscores the importance of utilizing advanced technologies with high sensitivity and accuracy for biological detection in clinical laboratory diagnosis and prognosis in CAR-T cell treatment. Trial registration number: NCT04767308.

Photoswitchable dynamic conjugate addition-elimination reactions as a tool for light-mediated click and clip chemistry.

Phototriggered click and clip reactions can endow chemical processes with high spatiotemporal resolution and sustainability, but are challenging with a limited scope. Herein we report photoswitchable reversible covalent conjugate addition-elimination reactions toward light-addressed modular covalent connection and disconnection. By coupling between photochromic dithienylethene switch and Michael acceptors, the reactivity of Michael reactions was tuned through closed-ring and open-ring forms of dithienylethene, allowing switching on and off dynamic exchange of a wide scope of thiol and amine nucleophiles. The breaking of antiaromaticity in transition states and enol intermediates of addition-elimination reactions provides the driving force for photoinduced change in kinetic barriers. To showcase the versatile application, light-mediated modification of solid surfaces, regulation of amphiphilic assemblies, and creation/degradation of covalent polymers on demand were achieved. The manipulation of dynamic click/clip reactions with light should set the stage for future endeavors, including responsive assemblies, biological delivery, and intelligent materials.

Regulation of whole-transcriptome sequencing expression in COPD after personalized precise exercise training: a pilot study.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is one of the world's leading causes of death and a major chronic respiratory disease. Aerobic exercise, the cornerstone of pulmonary rehabilitation, improves prognosis of COPD patients; however, few studies have comprehensively examined the changes in RNA transcript levels and the crosstalk between various transcripts in this context. This study identified the expression of RNA transcripts in COPD patients who engaged in aerobic exercise training for 12 weeks, and further constructions of the possible RNAs networks were made. METHODS: Peripheral blood samples for all four COPD patients who benefited from 12 weeks of PR were collected pre- and post-aerobic exercises and evaluated for the expression of mRNA, miRNA, lncRNA, and circRNA with high-throughput RNA sequencing followed by GEO date validation. In addition, enrichment analyses were conducted on different expressed mRNAs. LncRNA-mRNA and circRNA-mRNA coexpression networks, as well as lncRNA-miRNA-mRNA and circRNA-miRNA-mRNA competing expression networks (ceRNAs) in COPD were constructed. RESULTS: We identified and analyzed the differentially expressed mRNAs and noncoding RNAs in the peripheral blood of COPD patients' post-exercise. Eighty-six mRNAs, 570 lncRNAs, 8 miRNAs, and 2087 circRNAs were differentially expressed. Direct function enrichment analysis and Gene Set Variation Analysis showed that differentially expressed RNAs(DE-RNAs) correlated with several critical biological processes such as chemotaxis, DNA replication, anti-infection humoral response, oxidative phosphorylation, and immunometabolism, which might affect the progression of COPD. Some DE-RNAs were validated by Geo databases and RT-PCR, and the results were highly correlated with RNA sequencing. We constructed ceRNA networks of DE-RNAs in COPD. CONCLUSIONS: The systematic understanding of the impact of aerobic exercise on COPD was achieved using transcriptomic profiling. This research offers a number of potential candidates for clarifying the regulatory mechanisms that exercise has on COPD, which could ultimately help in understanding the pathophysiology of COPD.

Comparative insight into the effects of different carbon source supplement on antibiotic resistance genes during whole-run and short-cut nitrification-denitrification processes.

Mature landfill leachate is known for nitrogen-removal challenging and meantime was considered as an important sink of antibiotic resistance genes (ARGs). The added external carbon sources, enabling the short-cut nitrification and denitrification, may facilitate the proliferation of bacteria that possibly carry ARGs. However, this speculation has yet to be studied. Here, we explored the effects of glucose, sodium acetate, and methanol supplements on ARGs during whole-run and short-cut treatment processes. The results showed that sodium acetate supplement during short-cut process efficiently reduced the abundances of total ARGs (0.84-1.99 copies/16S rRNA) and integrons (0.59-1.20 copies/16S rRNA), which were highly enhanced by methanol addition during whole-run treatment process (total ARGs: 3.60-11.01 copies/16S rRNA, integrons: 1.20-4.69 copies/16S rRNA). Indirect gradient analysis showed that the variation of ARGs was not correlated with the supplement of different external carbon source. Correlation analysis indicated that dominant intl1 (55.99 ± 17.61% of integrons) showed positively significant correlations with all detected ARGs expect for sul2 and ermB (p < 0.05), suggesting the significant role on ARGs dissemination. Redundancy analysis illustrated that the potential hosts of intl1, intl2, sul1, tetQ, tetM, mefA, and mexF were dominant Bacteroidetes and Actinobacteria. Interestingly, the numbers and significant extent of correlations under the supplement of sodium acetate during short-cut denitrification process were obviously declined, and it was in accordance with ARGs reduced by sodium acetate supplement, suggesting sodium acetate displayed the efficient ARGs reduction during short-cut process. In summary, this study provides a comparative understanding of the effects on ARGs by different carbon source supplements during nitrification-denitrification processes of leachate; sodium acetate is the optimal carbon source.

CD137 deficiency because of two novel biallelic TNFRSF9 mutations in a patient presenting with severe EBV-associated lymphoproliferative disease.

Objectives: Increasing evidence indicates that some germline genetic mutations that impair pathways required for robust host immune surveillance against EBV infection may result in an extremely high susceptibility to EBV-associated lymphoproliferative disease (EBV+ LPD). TNFRSF9 encodes a vital costimulatory molecule that enhances CD8+ T-cell proliferation, survival and cytolytic activity. To date, no relevant case resulting from TNFRSF9 heterozygous mutations has been identified. Methods: Here, we report the first case of CD137 deficiency caused by two novel biallelic heterozygous TNFRSF9 mutations [NM_001561.5: c.208 + 1->AT and c.452C>A (p.T151K)] in a patient presenting with severe EBV+ LPD. Immunophenotyping and in vitro assays of lymphocyte function and NK cell activity were performed. Results: Biallelic TNFRSF9 mutations resulted in markedly reduced or abrogated expression of CD137 on activated T, B and NK cells. CD8+ T cells from the patient had impaired activation, reduced expression/release of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), perforin and granzyme B, and diminished cytotoxic activity. Functional experiments identified both variations were hypomorphic mutations and played a contributing role in CD137 deficiency and the development of EBV+ LPD. Conclusion: Our study expands the genetic spectrum and clinical phenotype of patients with CD137 deficiency and provides additional evidence that the TNFRSF9 gene plays a critical role in host immune responses to EBV infection.

Targeted therapy using larotrectinib and venetoclax for the relapsed/refractory T-cell acute lymphoblastic leukemia harboring a cryptic ETV6-NTRK3 fusion.

Outcomes for patients with relapsed and refractory (R/R) T-cell acute lymphoblastic leukemia (T-ALL) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) are dismal, with few available treatments. Recently, identification of cancer patients harboring neurotrophic tropomyosin receptor kinase (NTRK) gene fusions is constantly increasing, especially with the advent of NTRK inhibitors. However, the role of ETV6-NTRK3 in T-ALL has not been investigated. This case represented the first detailed report of T-ALL patient harboring a cryptic ETV6-NTRK3 fusion with an unfavorable prognosis, not only because of leukemia resistant to the standard multiagent chemotherapy but also early relapse after allo-HSCT. Acquired EP300 mutation was found at relapse, which could explain the cause of recurrence and affect the follow-up treatment. Combined targeted therapy like larotrectinib allied with pan-targeted BCL-2 inhibitor venetoclax, may be a potential maintenance treatment in R/R ETV6-NTRK3 positive leukemia after allo-HSCT. The leukemic clonal evolution might be revealed through transcriptome sequencing and overcome by drugs with universal targets. Our case demonstrated that both comprehensive profiling techniques (such as transcriptome sequencing, multiparameter flow cytometry, and digital droplet polymerase chain reaction) and a multimodality treatment strategy were critical for anticipating an early relapse and personalized therapy of R/R T-cell leukemia.

Characterization of clonal immunoglobulin heavy V-D-J gene rearrangements in Chinese patients with chronic lymphocytic leukemia: Clinical features and molecular profiles.

Introduction: Several prognostic factors of chronic lymphocytic leukemia (CLL) have been identified, such as cytogenetic aberrations and recurrent gene mutations. B-cell receptor (BCR) signaling plays an important role in the tumorigenesis of CLL, and its clinical significance in predicting prognosis is also under study. Methods: Therefore, we assessed the already-known prognostic markers, immunoglobulin heavy chain (IGH) gene usage and the associations among these factors in 71 patients diagnosed with CLL in our center from October 2017 to March 2022. Sequencing of IGH gene rearrangements was performed using Sanger sequencing or IGH-based next-generation sequencing, and the results were further analyzed for distinct IGH/IGHD/IGHJ genes and the mutational status of the clonotypic IGHV (IGH variable) gene. Results: In summary, by analyzing the distribution of potential prognostic factors in CLL patients, we displayed a landscape of molecular profiles, confirmed the predictive value of recurrent genetic mutations and chromosome aberrations, and found that IGHJ3 was associated with favorable markers (mutated IGHV, trisomy 12), while IGHJ6 tended to correlate with unfavorable factors (unmutated IGHV, del17p). Discussion: These results provided an indication for IGH gene sequencing in predicting the prognosis of CLL.

Double n→π* Interactions with One Electron Donor: Structural and Mechanistic Insights.

Double n→π* interactions between one common electron donor of the carbonyl oxygen and two individual acceptor aldehyde/imine units are presented. The structural and mechanistic insights were revealed through a collection of experimental and computational evidence. The orientation and further energetic dependence of orbital interactions were facilely regulated by the size of cyclic urea scaffolds, the bulkiness of aldehydes/imines, and the flexibility of imine macrocycles.

Waste reclamation from municipal solid waste for the cost-efficient treatment of landfill leachate with a novel biological trickle reactor system.

Mature landfill leachate (MLL) would be a tough nut to crack, how to realize waste reclamation while deal with the intractable by-products deserves for more considerations. In this study, a novel system, equipped with two biological trickle reactors developed by inert wastes and a connected organic feeder using waste-recycling rotten banana powder, was established for treating MLL. Results indicated that superior pollutant removal performance and long-term stability were achieved by this system, with only COD and TN concentrations slightly higher than the relevant standard limits. But the shortage about poor resistance to shock pollution loads, was underlined by the fluctuation of water quality. Anaerobic condition and carbon source supplementation contributed to more microbial similarities but less community richness and diversity among inert fillings, and the selective enrichment of denitrification and organic-degrading strains simultaneously occurred. The comparisons with common processes demonstrated that this system was a cost-efficient choice for MLL treatment.

Calreticulin as a marker and therapeutic target for cancer.

Calreticulin (CRT) is a multifunctional protein found within the endoplasmic reticulum (ER). In addition, CRT participates in the formation and development of tumors and promotes the proliferation and migration of tumor cells. When a malignant tumor occurs in the human body, cancer cells that die from immunogenic cell death (ICD) expose CRT on their surface, and CRT that is transferred to the cell surface represents an "eat me" signal, which promotes dendritic cells to phagocytose the tumor cells, thereby increasing the sensitivity of tumors to anticancer immunotherapy. Expression of CRT in tumor tissues is higher than in normal tissues and is associated with disease progression in many malignant tumors. Thus, the dysfunctional production of CRT can promote tumorigenesis because it disturbs not only the balance of healthy cells but also the body's immune surveillance. CRT may be a diagnostic marker and a therapeutic target for cancer, which is discussed extensively in this review.

Photoswitchable Keto-Enol Tautomerism Driven by Light-Induced Change in Antiaromaticity.

The bidirectional interconversion between ketone and enol structures of 4-cyclopentene-1,3-dione derivatives was realized by photoswitching of fused dithienylethene using UV and visible light. A loss of antiaromaticity offered the driving force for light-triggered enolization and was supported by theoretical studies. Solvent and substituent effects provided additional means for regulating photoswitchable keto-enol tautomerism. Moreover, a significant change of acidity was revealed with light-induced keto-to-enol conversion, enabling control over base-catalyzed Michael addition.