GABA signaling enforces intestinal germinal center B cell differentiation.

Recent compelling results indicate possible links between neurotransmitters, intestinal mucosal IgA+ B cell responses, and immunoglobulin A nephropathy (IgAN) pathogenesis. Here, we demonstrated that γ-amino butyric acid (GABA) transporter-2 (GAT-2) deficiency induces intestinal germinal center (GC) B cell differentiation and worsens the symptoms of IgAN in a mouse model. Mechanistically, GAT-2 deficiency enhances GC B cell differentiation through activation of GABA-mammalian target of rapamycin complex 1 (mTORC1) signaling. In addition, IgAN patients have lower GAT-2 expression but higher activation of mTORC1 in blood B cells, and both are correlated with kidney function in IgAN patients. Collectively, this study describes GABA signaling-mediated intestinal mucosal immunity as a previously unstudied pathogenesis mechanism of IgAN and challenges the current paradigms of IgAN.

Isoliquiritigenin limits inflammasome activation of macrophage via docking into Syk to alleviate murine non-alcoholic fatty liver disease.

Isoliquiritigenin (ISL) is a chalcone-type flavonoid derived from the root of licorice with antioxidant, anti-inflammatory, anti-tumour and neuroprotective properties. ISL has been proven to downregulate the productions of IL-1ß, TNF-α and IL-6 by macrophages. However, detailed molecular mechanisms of this modulation remain elusive. Here, ISL suppressed Syk phosphorylation and CD80, CD86, IL-1ß, TNF-α and IL-6 expressions in lipopolysaccharide-stimulated macrophages ex vivo. ApoC3-transgenic (ApoC3TG) mice had more activated macrophages. ISL was also able to downregulate the inflammatory activities of macrophages from ApoC3TG mice. Administration of ISL inhibited Syk activation and inflammatory activities of macrophages in ApoC3TG mice in vivo. The treatment of ISL further alleviated MCD-induced non-alcoholic fatty liver disease (NAFLD) in wild-type and ApoC3TG mice, accompanied by less recruitment and activation of liver macrophages. Due to the inhibition of Syk phosphorylation, ISL-treated macrophages displayed less production of cytoplasmic ROS, NLRP3, cleaved-GSDMD and cleaved-IL-1ß, suggesting less inflammasome activation. Finally, the molecular docking study demonstrated that ISL bound to Syk directly with the Kd of 1.273 × 10-8 M. When the Syk expression was knocked down by its shRNA, the inhibitory effects of ISL on activated macrophages disappeared, indicating that Syk was at least one of key docking-molecules of ISL. Collectively, ISL could alleviate MCD-induced NAFLD in mice involved with the inhibition of macrophage inflammatory activity by the blockade of Syk-induced inflammasome activation.

Liver transplantation for pediatric patients with congenital heart disease: A single-center study in mainland China.

BACKGROUND: Liver transplantation (LT) is a serious cardiovascular stressor for patients with end-stage liver disease (ESLD). Data on the effects of cardiovascular diseases on pediatric LT is limited. No study on LT for pediatric patients with ESLD combined with congenital heart disease (CHD) has been reported from mainland China. METHODS: A total of 1005 patients were included in this study. The Kaplan-Meier method with log-rank testing was used to evaluate survival outcomes between groups. Univariable and multivariable Cox regression models were used to determine the risk factors for patient and graft survival. RESULTS: The most common indication for LT was biliary atresia (BA 90.3%). The prevalence of CHD was 3.8% (38). 42 CHD were found in 38 patients. The incidence of death and graft loss was more common in the CHD group than in the no-CHD group (13.2% vs. 5.0%, p = .045 and 15.8% vs. 6.2%, p = .019, respectively). The 5-year patient survival and graft survival in the CHD group versus the no-CHD group was 86.8% versus 94.7% (log-rank p = .022) and 84.2% versus 93.5% (log-rank p = .015), respectively. No significant differences were observed in re-transplantation, hepatic artery thrombosis (HAT), and portal vein thrombosis (PVT). After adjusting for age, BMI, etiology of LT, and other confounding factors, we can still find that the presence of CHD was associated with patient and graft survival after LT. CONCLUSION: The presence of CHD was associated with higher mortality and lower graft survival after LT. If possible, the cardiac defects should be addressed prior to LT.

Photodynamic and nitric oxide therapy-based synergistic antimicrobial nanoplatform: an advanced root canal irrigation system for endodontic bacterial infections.

BACKGROUND: The main issues faced during the treatment of apical periodontitis are the management of bacterial infection and the facilitation of the repair of alveolar bone defects to shorten disease duration. Conventional root canal irrigants are limited in their efficacy and are associated with several side effects. This study introduces a synergistic therapy based on nitric oxide (NO) and antimicrobial photodynamic therapy (aPDT) for the treatment of apical periodontitis. RESULTS: This research developed a multifunctional nanoparticle, CGP, utilizing guanidinylated poly (ethylene glycol)-poly (ε-Caprolactone) polymer as a carrier, internally loaded with the photosensitizer chlorin e6. During root canal irrigation, the guanidino groups on the surface of CGP enabled effective biofilm penetration. These groups undergo oxidation by hydrogen peroxide in the aPDT process, triggering the release of NO without hindering the production of singlet oxygen. The generated NO significantly enhanced the antimicrobial capability and biofilm eradication efficacy of aPDT. Furthermore, CGP not only outperforms conventional aPDT in eradicating biofilms but also effectively promotes the repair of alveolar bone defects post-eradication. Importantly, our findings reveal that CGP exhibits significantly higher biosafety compared to sodium hypochlorite, alongside superior therapeutic efficacy in a rat model of apical periodontitis. CONCLUSIONS: This study demonstrates that CGP, an effective root irrigation system based on aPDT and NO, has a promising application in root canal therapy.

Determining nitrogen topdressing rates in accordance with actual seedling density and crop nitrogen status in direct-seeded rice.

BACKGROUND: Adjusting nitrogen (N) input based on actual seedling density (ASD) and plant N status is a practical approach for improving the yield stability of direct-seeded rice. However, the adjustment of topdressing N rates has been empirical in the past. This study aimed to establish a quantitative approach for determining N topdressing rates during tillering (Ntil ) and panicle development (NPI ) based on ASD and crop N status in direct-seeded rice. Field experiments were conducted involving 12 treatments, consisting of four Ntil and three seeding rates in 2017, and eight treatments combining seeding rate, Ntil , and NPI in 2020. RESULTS: Linear regression analysis revealed that the tiller number at panicle initiation (TILPI ) was predominantly influenced by ASD and Ntil . The determination coefficients (R2 ) of the regression models ranged from 0.887 to 0.936 across the four-season experiments. The results indicated that Ntil could be determined accurately using ASD and the target maximum tiller number. Similarly, grain yield was influenced significantly by the N uptake at panicle initiation (NUPPI ) and NPI , with R2 of 0.814 and 0.783 in the early and late seasons of 2020, respectively. This suggested that NPI could be calculated based on NUPPI and the target grain yield. CONCLUSION: The findings offer a quantitative method for establishing N topdressing rates for tillering and panicle development, relying on the monitoring of actual seedling density and plant N status in direct-seeded rice production. © 2023 Society of Chemical Industry.

Apolipoprotein C-III itself stimulates the Syk/cPLA2-induced inflammasome activation of macrophage to boost anti-tumor activity of CD8+ T cell.

Increased prevalence of cancer in obese individuals is involved with dyslipidemia- induced chronic inflammation and immune suppression. Although apolipoprotein C-III (ApoC3)-transgenic mice (ApoC3TG mice) or poloxamer 407 (P407)-treated mice had hyperlipidemia, CD8+ T cells with upregulated antitumor activities were observed in ApoC3TG mice, and decreased CD8+ T cell activities were observed in P407-treated mice. Increased ApoC3 expression in hepatocellular carcinoma was associated with increased infiltration of CD8+ T cells and predicted survival. Recombinant ApoC3 had no direct effects on CD8+ T cells. The upregulation of CD8+ T cells in ApoC3TG mice was due to cross-talk with context cells, as indicated by metabolic changes and RNA sequencing results. In contrast to dendritic cells, the macrophages of ApoC3TG mice (macrophagesTG) displayed an activated phenotype and increased IL-1ß, TNF-α, and IL-6 production. Coculture with macrophagesTG increased CD8+ T cell function, and the adoptive transfer of macrophagesTG suppressed tumor progression in vivo. Furthermore, spleen tyrosine kinase (Syk) activation induced by TLR2/TLR4 cross-linking after ApoC3 ligation promoted cellular phospholipase A2 (cPLA2) activation, which in turn activated NADPH oxidase 2 (NOX2) to promote an alternative mode of inflammasome activation. Meanwhile, mitochondrial ROS produced by increased oxidative phosphorylation of free fatty acids facilitated the classical inflammasome activation, which exerted an auxiliary effect on inflammasome activation of macrophagesTG. Collectively, the increased antitumor activity of CD8+ T cells was mediated by the ApoC3-stimulated inflammasome activation of macrophages, and the mimetic ApoC3 peptides that can bind TLR2/4 could be a future strategy to target liver cancer.

Low-dose adropin stimulates inflammasome activation of macrophage via mitochondrial ROS involved in colorectal cancer progression.

Adropin is encoded by the energy homeostasis-associated (ENHO) gene and widely present in liver, pancreas, heart, kidney, brain, and vascular tissues. Abnormal adropin is associated with metabolic, inflammatory, immune, and central nervous disorders. Whether adropin is involved in the development of colorectal cancer (CRC) is still unclear. Here, decreased adropin expression of tumor-nest cells in advanced-stage CRC was demonstrated. Adropin expressed by carcinoma cells was negatively correlated with macrophage infiltration in the matrix of CRC tissues. However, tumor macrophages enhanced adropin expression and were positively correlated with tumor invasion and metastasis. ENHO gene transfection into colon cancer (MC38) cells inhibited tumor growth in vivo, accompanying the increase of M1 macrophages. Treatment with low-dose adropin (< 100 ng/mL) on macrophages ex vivo directly increased mitochondrial reactive oxygen species for inflammasome activation. Furthermore, ENHO-/- mice had less M1 macrophages in vivo, and ENHO-/- macrophages were inert to be induced into the M1 subset ex vivo. Finally, low-dose adropin promoted glucose utilization, and high-dose adropin enhanced the expression of CPT1α in macrophages. Therefore, variations of adropin level in carcinoma cells or macrophages in tumor tissues are differently involved in CRC progression. Low-dose adropin stimulates the antitumor activity of macrophages, but high-dose adropin facilitates the pro-tumor activity of macrophages. Increasing or decreasing the adropin level can inhibit tumor progression at different CRC stages.

Improving grain yield and nitrogen use efficiency of direct-seeded rice with simplified and nitrogen-reduced practices under a double-cropping system in South China.

BACKGROUND: Enhancing grain yield and nitrogen use efficiency (NUE) of rice is of great importance for sustainable agricultural development. Little effort has been made to increase grain yield and NUE of direct-seeded rice under the double-cropping system in South China. Field trials were conducted during 2018-2020 with four treatments, including nitrogen-free, farmers' fertilization practice (FP), 'three controls' nutrient management (TC), and simplified and nitrogen-reduced practice (SNRP). RESULTS: Grain yield under SNRP averaged 6.46 t ha-1 during the three years and was 23.0% higher than that of FP but comparable to that of TC. Recovery efficiency (REN ), agronomic efficiency (AEN ), and partial factor productivity (PFPN ) of nitrogen under SNRP increased by 12.0-22.7%, 159.3-295.0% and 94.6-112.5% respectively compared with FP. Harvest index and sink capacity increased by 7.3-10.8% and 14.9-21.3% respectively. Percentage of productive tillers (PPT) and biomass after heading increased by 24.0% and 104.5% respectively. Leaf nitrogen concentration at heading and nitrogen accumulation after heading increased by 16.3% and 842.0% respectively. Grain yield was positively correlated with PPT, sink capacity, harvest index, biomass and nitrogen accumulation after heading, REN , AEN , and PFPN . CONCLUSION: Grain yield and NUE under SNRP were superior to those under FP and comparable to those under TC. Increase in sink capacity, higher PPT, more biomass and nitrogen accumulation after heading, and greater harvest index were responsible for high grain yield and NUE in SNRP with reduced nitrogen fertilizer and labor input. SNRP is a feasible approach for direct-seeded rice under a double-cropping system in South China. © 2023 Society of Chemical Industry.

Deficiency of miR-15a/16 upregulates NKG2D in CD8+ T cells to exacerbate dextran sulfate sodium-induced colitis.

The miR-15a/16 gene cluster is located in human chromosome 13 (13q14.3) and mouse chromosome 14 (14qC3). These genes are involved in cancer development and immune regulation. Our group has previously verified the binding of the 3'-untranslated region of NKG2D gene by miR-16 through dual-luciferase reporter assay. Herein, we found that miR-16 overexpression inhibited the NKG2D expression of CD8+ T cells, and that CD8+ NKG2D+ T cell frequency increased in miR-15/16-/- mice. CD8+ NKG2D+ T cells derived of miR-15/16-/- mice displayed activatory phenotype with enhanced IFN-γ production and cytotoxicity. The transfection of lentivirus containing antago-miR-16 sequences enhanced the NKG2D expression level of CD8+ T cells. However, no significant differences in CD8+ NKG2D+ T cell frequencies existed between wild-type and miR-15/16-transgenic mice because NKG2D was not expressed on the rest CD8+ T cells. When CD8+ T cells of miR-15/16-transgenic mice were treated with IL-2 in vitro, the magnitude of NKG2D expression and activation of CD8+ T cells was lower than that of wild-type mice. miR-15/16-/- mice showed that the exacerbation of colitis induced by dextran sulfate sodium (DSS) with more CD8+ T cells accumulated in inflamed colons, whereas miR-15/16-transgenic mice ameliorated DSS-induced colitis with less infiltration of CD8+ T cells. When NKG2D+ cells were depleted with NKG2D antibody in miR-15/16-/- mice, the aggravated colitis disappeared. All these results demonstrated that NKG2D could be upregulated by decreased miR-16 in CD8+ T cells to mediate inflammation. Thus, gene therapy based on the overexpression of miR-16 in CD8+ T cells can be used for patients with inflammatory diseases.

Periphytic Microbial Response to Environmental Phosphate (P) Bioavailability and Its Relevance to P Management in Paddy Fields.

Periphyton occurs widely in shallow-water ecosystems such as paddy fields and plays a critical part in regulating local phosphorus cycling. As such, understanding the mechanisms of biofilms' response to environmental phosphate (P) variability may lead to better perceptions of P utilization and retention in rice farms. The present study aims at exploring the biological and biochemical processes underlying periphyton's P buffering capability through examining changes in community structure, phosphorus uptake and storage, and molecular makeup of the exometabolome at different levels of P availability. Under stressed (both excessive and scarce) phosphorus conditions, we found increased populations of bacterial genera capable of transforming orthophosphate to polyphosphate, as well as mixotrophic algae, that can survive through phagotrophy. These results were corroborated by observed polyphosphate buildup under low- and high-P treatment. Exometabolomic analyses further revealed that periphytic organisms may substitute sulfur (S)-containing lipids for phospholipids, use siderophores to dissolve iron (hydr)oxides to scavenge adsorbed P, and synthesize auxins to resist phosphorus starvation. These findings not only shed light on the mechanistic insights responsible for driving the periphytic P buffer but attest to the ecological roles of periphyton in aiding plants such as rice to overcome P limitations in the natural environment. IMPORTANCE The ability of periphyton to buffer environmental P in shallow aquatic ecosystems may be a natural lesson on P utilization and retention in paddy fields. This work revealed the routes and tools through which periphytic organisms adapt to and regulate ambient P fluctuation. The mechanistic understanding further implicates that the biofilm may serve rice plants to alleviate P stress. Additional results from extracellular metabolite analyses suggest the dissolved periphytic exometabolome can be a valuable nutrient source for soil microbes and plants to reduce biosynthetic costs. These discoveries have the potential to improve our understanding of biogeochemical cycling of phosphorus in general and to refine P management strategies for rice farms in particular.

MiR-15a/16-1 deficiency induces IL-10-producing CD19+ TIM-1+ cells in tumor microenvironment.

IL-10-producing B cells (B10) are associated with autoimmune diseases, infection and tumours. MiR-15a/16 as a tumour-suppressive gene is down-regulated in several tumours, such as chronic lymphocytic leukaemia, pituitary adenomas and prostate carcinoma. Here, increased frequency of IL-10-producing CD19+ Tim-1+ cells was seen in both aged miR-15a/16-/- mice (15-18 months) with the onset of B cell leukaemia and young knockout mice (8-12 weeks) transplanted with hepatic cancer cells. CD19+ Tim-1+ cells down-regulated the function of effector CD4+ CD25low T cells ex vivo dependent on IL-10 production, and adoptive transfer of CD19+ Tim-1+ cells promoted tumour growth in mice. IL-10 production by CD19+ Tim-1+ cells was involved with the STAT3 activation. Bioinformatics analysis shows that miR-16 targets the 3'-untranslating region (3'-UTR) of STAT3 mRNA. Overexpression of miR-16 in CD19+ Tim-1+ cells inhibited STAT3 transcription and its protein expression. Thus, the loss of miR-15a/16 promoted induction of regulatory CD19+ Tim-1+ cells in tumour microenvironment. These results confirmed that miR-15a/16 could be used in tumour therapy due to its inhibition of tumour and regulatory B cells.

Heme oxygenase 1 facilitates cell proliferation via the B-Raf-ERK signaling pathway in melanoma.

BACKGROUND: Despite therapeutic advancements (e.g. B-RAF inhibitors) targeting cutaneous melanoma, many cellular processes, including inducible heme oxygenase 1 (HO-1), counteract treatments for malignancies. So there is an urgent need to find biological treatment targets, develop new therapeutic approaches and achieve longer responses. This study aimed to explore the relationship of HO-1 and B-Raf via mediating ERK1/2 signaling on cell cycle in melanoma. METHODS: Immunohistochemistry was applied to evaluate the levels of HO-1 and B-Raf expression in melanoma tissues and adjacent healthy tissues. Co-immunoprecipitation (Co-IP) assessed the interaction of HO-1 with B-Raf. Further study overexpression and knock-down of HO-1 in A375 cell lines, especially knockout HO-1 using CRISPR-Cas9, verified HO-1 regulate cell proliferation in vivo and in vitro. Finally, Western blot analysis and qRT-PCR were performed to investigate the mechanisms by which HO-1 mediates cell cycle by B-RAF-ERK1/2 signaling. RESULTS: First, histology and Co-IP show that HO-1 interacts with B-Raf directly in melanoma tissue. Further study illustrated that HO-1 overexpression promotes melanoma cell proliferation while HO-1 reduction represses melanoma cell proliferation because of HO-1 affects cell cycle. Mechanistic studies revealed that HO-1 was associated with a marked activation of B-RAF-ERK1/2 signaling and led to CDK2/cyclin E activation, thereby promoting melanoma proliferation. CONCLUSIONS: Our result reveals a previously unknown mechanism that the HO-1-B-RAF-ERK axis plays an important role in melanoma cell proliferation. Therapeutic target on HO-1 could be a novel method for treating melanoma.

The complex transmission seasonality of hand, foot, and mouth disease and its driving factors.

BACKGROUND: The transmission rate seasonality is an important index for transmission dynamics in many childhood infections, and has been widely studied in industrialized countries. However, it has been neglected in the study of pathogens in China. METHODS: To understand the transmission dynamics of hand, foot and mouth disease (HFMD), we examined the transmission rate seasonality of HFMD in three provinces, Henan, Anhui and Chongqing, in China, using a dynamical stochastic SIR model. We investigated potential driving factors, including school terms, the Chinese Spring Festival period, meteorological factors and population flux for their effects on the HFMD transmission seasonality using multiple regression models. RESULTS: The transmission rate of HFMD had complex seasonality with one large major peak in March and one small peak in autumn. School terms, the Chinese Spring Festival period, population flux and meteorological factors had combined effects on the HFMD transmission seasonality in mainland China. The school terms reflects the seasonal contact rate in Children, while the population flux and the Chinese Spring Festival period reflect the seasonal contact rate in population. They drove HFMD transmission rate seasonality in different time periods of the year in China. Contact rate seasonality in population dominated effects on HFMD transmission in February and March. The dramatic increase in transmission rate during February coincides with the Chinese Spring Festival period and high population flux in this month. The contact rate seasonality in children dominated effects on the transmission in the other months of the year in Chongqing. Meteorological factors can not solely explain the seasonality in HFMD transmission in mainland China; however, they may have combined effects with school terms and the highway passenger traffic on the transmission rate in Anhui during the fall semester. CONCLUSION: The transmission rate of HFMD in three provinces in China had complex seasonality. The Chinese Spring Festival period, population flux and (or) school terms explained the majority of the transmission rate seasonality of HFMD, and they drove HFMD transmission rate seasonality in different time periods of the year. The Chinese Spring Festival period dominantly caused the dramatic increase of the HFMD transmission rate during February.

Increased M1 macrophages in young miR-15a/16-/- mice with tumour grafts or dextran sulphate sodium-induced colitis.

M1 macrophages are involved in inflammation by producing proinflammatory cytokines, whereas M2 macrophages are associated with wound healing and tissue regeneration by producing anti-inflammatory cytokines. MicroRNAs are involved in macrophage polarization. To evaluate whether miR-15a/16 is involved in macrophage polarization under tumour or inflammation microenvironments, we observed the growth of transplanted hepatic cancer (H22) cells or severity of dextran sulphate sodium (DSS)-induced colitis in 8-week-old miR-15a/16 knockout (KO) mice. Compared with littermate controls, the miR-15a/16-/- mice exhibited retarded tumour growth and increased sensibility to DSS-induced colitis. Meanwhile, the M1 cell frequencies were higher in tumour tissues and inflamed colons of KO mice than of littermate controls. Macrophages with miR-15a/16 deletion revealed an enhanced NF-κB transcription under the physiological state and lipopolysaccharide (LPS) or high mobility group box 1 (HMGB1) stimulation. STAT3 expression was also significantly increased in miR-15a/16-/- macrophages under LPS or HMGB1 stimulation. The polarization of M1 macrophages can be associated with the coactivation of NF-κB and STAT3. Results indicated that miR-15a/16 deficiency in the macrophages directs M1 polarization for tumour suppression and proinflammation. Thus, miR-15a/16 deletion in macrophages holds a distinct biological significance from that of the microRNA deficiency in tumour cells.

MicroRNA let-7b inhibits keratinocyte differentiation by targeting IL-6 mediated ERK signaling in psoriasis.

BACKGROUND: The extensive involvement of microRNA (miRNA) in the pathophysiology of psoriasis is well documented. However, in order for this information to be useful in therapeutic manipulation of miRNA levels, it is essential that detailed functional mechanisms are elucidated. This study aimed to explore the effects of IL-6 targeting by let-7b and ERK1/2 mediated signaling on keratinocyte differentiation in psoriasis. METHODS: Following imiquimod cream (IMQ) application to let-7bTG (keratinocyte-specific let-7b overexpression mouse) and control mice for 7 days, we analyzed erythema, scaling and thickening of skin. A dual luciferase reporter assay and bioinformatics was carried out to detect target gene of let-7b. Additionally, the differentiation markers were measured. Immunohistochemistry analyses demonstrate a relationship of let-7b with IL-6 and ERK signaling. RESULTS: we found let-7bTG inhibits acanthosis and reduces the disease severity by treatment with IMQ compared to wild-type mice. Further study illustrated that let-7b promotes differentiation of keratinocytes in vivo and in vitro. Using bioinformatics and reporter gene assays, we found that IL-6 is a target gene of let-7b. In psoriasis, high expression levels of IL-6 lead to increased acivation of p-ERK1/2. High levels of let-7bTG transgene expression suppresses IL-6 expression and leads to increased keratinocyte differentiation. Moreover, let-7b acts as an upstream negative regulator of the ERK signaling pathway in keratinocytes of psoriasis. CONCLUSIONS: Our result reveals a previously unknown mechanism for regulation of IL-6 levels during psoriasis by let-7b and highlights a critical role for the ERK1/2 signaling pathway in epidermal differentiation during psoriasis. TRIAL REGISTRATION: The ethical approval for this study was from the Affiliated Hospital of Medical University of Anhui _ Fast_ PJ2017-11-14.

Cleaning of Fluid-Infused Surfaces in Microchannels.

When an immiscible fluid is flowing over a fluid-infused surface with transverse grooves in a microchannel, the infused fluid is either left in or cleaned away from the grooves by the flowing fluid. The cleaning status depends on the geometric parameters of the groove and the contact angle of the flowing fluids. The critical width of the grooves for the infused fluid enclosed in or driven out of the grooves is derived. This study helps to understand the stability of the Cassie status in a low-shear flow where the surface tension plays the key role.

Analyzing MC-LR distribution characteristics in natural lakes by a novel fluorescence technology.

The death of aquatic and terrestrial organisms caused by cyanobacterial blooms has been a topic of considerable concern since the 19th century. Microcystin-LR (MC-LR) produced by cyanobacterial blooms threaten natural ecosystems and human health. Therefore, establishing an effective monitoring and early warning system to detect MC-LR in water bodies is crucial. However, rapidly and intuitively assessing the distribution traits of MC-LR in lakes is a challenging task due to the complexities and expenses associated with conventional detection methods. To overcome these technical limitations, we introduce a novel and effective method for evaluating the distribution of MC-LR in lakes. This method is achieved by using a fluorescence probe (BAD) technology, marking the first application of this technology in evaluating the distribution of MC-LR in natural lake environments. The probe BAD is endowed with unique functions through clever functionalization modification. Experimental results exhibit that BAD has different fluorescence signals at various lake sampling points. The correlation analysis of fluorescence data and physicochemical indicators determines that the fluorescence data of the probe exhibit good correlation with MC-LR, implying that BAD is capable of detecting MC-LR in lakes. Moreover, the introduction of fluorescence technology to achieve the intuitive distribution of MC-LR in the entire plateau lake. This study provides a new method for evaluating the distribution of MC-LR in plateau lakes. It opens a new avenue for exploring the relationship between cyanobacterial blooms and MC-LR in natural waters.

Differential evaluation of sulfur oxides in the natural lake water samples by carbazole-furan fluorescent probe.

Water bodies are frequently polluted, with sulfur oxides being the most common form of water pollution. Therefore, developing a detection mechanism for sulfur oxides in water bodies is particularly urgent. A new fluorescent probe YX-KZBD was designed and developed. This probe releases fluorescent signals with its own sulfurous acid recognition site, detects sulfurous acid based on the Michael addition reaction, and evaluates the pollution degree of sulfur oxides in the water environment through the transformation mode of the sulfur cycle. This probe has high energy transfer efficiency in aqueous solutions. In addition, the fluorescence data obtained by analyzing the water samples were linearly fitted with the gene abundance values of the functional genes of sulfur-producing bacteria, and a significant correlation was obtained. The Kriging interpolation model was used to evaluate the sulfate content distribution at each sampling point to understand the distribution of sulfur oxides in natural water intuitively. The fluorescence signal excited by the probe was also combined with a real-time quantitative polymerase chain reaction (qPCR), and sulfate-reducing and sulfur-oxidizing bacteria were introduced in the sulfur cycle, providing a new method to assess the extent of water pollution effectively.

Mycophagous Mite, Tyrophagus putrescentiae, Prefers to Feed on Entomopathogenic Fungi, except Metarhizium Generalists.

(1) Background: The mycophagous mite, Tyrophagus putrescentiae, was found to feed on entomopathogenic fungi (EPF) in our previous experiments, which seriously impacted the culture and preservation of fungal strains. Therefore, it is necessary to investigate the biological characteristics of the occurrence and damage to EPF. (2) Methods: The mite's growth and development and feeding preference were surveyed by comparative culture and observation; also, optical and electronic microscopies were employed. (3) Results: T. putrescentiae could survive normally after being fed on seven EPF species, including Purpureocillium lilacinum, Marquandii marquandii, Cordyceps fumosorosea, Beauveria bassiana, Metarhizium flavoviride, Lecanicillium dimorphum, and Metacordyceps chlamydosporia. The first four fungi were the mite's favorites with their greater feeding amount and shorter developmental duration. Interestingly, the mite could also feed on Metarhizium anisopliae and Metarhizium robertsii, but this led to the mite's death. After feeding on M. anisopliae and M. robertsii, the mites began to die after 24 h, and the mortality rate reached 100% by 72 h. Observation under optical microscopy and scanning electron microscopy revealed that the conidia of M. anisopliae and M. robertsii adhered to the mite's surface, but there was no evidence of penetration or invasion. However, dissection observation indicated that the two Metarhizium species germinate and grow within the mite's digestive tract, which implies that Metarhizium generalists with broad-spectrum hosts and the production of destruxins have acaricidal activity toward the mycophagous mites.