MXRA7 is involved in monocyte-to-macrophage differentiation.

Macrophages are critical in mediating immune and inflammatory responses, while monocyte-to-macrophage differentiation is one of the main macrophage resources that involves various matrix proteins. Matrix remodeling associated 7 (MXRA7) was recently discovered to affect a variety of physiological and pathological processes related to matrix biology. In the present study, we investigated the role of MXRA7 in monocyte-to-macrophage differentiation in vitro. We found that knockdown of MXRA7 inhibited the proliferation of THP-1 human monocytic cells. Knockdown of MXRA7 increased the adhesion ability of THP-1 cells through upregulation the expression of adhesion molecules VCAM-1 and ICAM1. Knockdown of MXRA7 alone could promoted the differentiation of THP-1 cells to macrophages. Furthermore, the MXRA7-knockdown THP-1 cells produced a more significant upregulation pattern with M1-type cytokines (TNF-α, IL-1ß and IL-6) than with those M2-type molecules (TGF-ß1 and IL-1RA) upon PMA stimulation, indicating that knockdown of MXRA7 facilitated THP-1 cells differentiation toward M1 macrophages. RNA sequencing analysis revealed the potential biological roles of MXRA7 in cell adhesion, macrophage and monocyte differentiation. Moreover, MXRA7 knockdown promoted the expression of NF-κB p52/p100, while PMA stimulation could increase the expression of NF-κB p52/p100 and activating MAPK signaling pathways in MXRA7 knockdown cells. In conclusion, MXRA7 affected the differentiation of THP-1 cells toward macrophages possibly through NF-κB signaling pathways.

Interleukin-33 ameliorates perioperative neurocognitive disorders by modulating microglial state.

Perioperative neurocognitive disorders (PND) are cognitive dysfunctions that usually occur in elderly patients after anesthesia and surgery. Microglial overactivation is a key underlying mechanism. Interleukin-33 (IL-33) is a member of the IL-1 family that orchestrates microglial function. In the present study, we explored how IL-33, which regulates microglia, contributes to cognitive improvement in a male mouse model of PND. An exploratory laparotomy was performed to establish a PND model. The expression levels of IL-33 and its receptor ST2 were evaluated using Western blot. IL-33/ST2 secretion, microglial density, morphology, phagocytosis of synapse, and proliferation, and dystrophic microglia were assessed using immunofluorescence. Synaptic plasticity was measured using Golgi staining and long-term potentiation. The Morris water maze and open field test were used to evaluate cognitive function and anxiety. Hippocampal expression of IL-33 and ST2 were elevated on postoperative day 3. We confirmed that IL-33 was secreted by astrocytes and neurons, whereas ST2 mainly colocalized with microglia. IL-33 treatment induced microgliosis after anesthesia and surgery. These microglia had larger soma sizes and shorter and fragmented branches. Compared to the Surgery group, IL-33 treatment reduced the synaptic phagocytosis of microglia and increased microglial proliferation and dystrophic microglia. IL-33 treatment also reversed the impaired synaptic plasticity and cognitive function caused by anesthesia and surgery. In conclusion, these results indicate that IL-33 plays a key role in regulating microglial state and synaptic phagocytosis in a PND mouse model. IL-33 treatment has a therapeutic potential for improving cognitive dysfunction in PND.

Solution-Focused Group Counseling on Mental States in Hemodialysis Patients with Anxiety.

BACKGROUND: Hemodialysis patients usually suffer from anxiety due to physical and social factors, which belongs to a kind of psychological disorder, easily contributing to the decrease of patients' adherence to the treatment, and seriously affecting the patients' health status and quality of life. Solution-focused group counseling (SFGC) is a kind of psychotherapy proven to improve emotional problems in many fields. Still, the application of this therapy is rare in medical situations. This retrospective study aims to analyze the application of SFGC and probe into the effects on mental states in hemodialysis patients with anxiety. METHODS: From January 2022 to February 2023, 212 patients with hemodialysis and anxiety admitted to our hospital were selected, and 9 patients who did not meet the inclusion criteria were excluded. Finally, 203 patients were included in this retrospective study. According to different clinical management methods, 102 patients receiving routine management were classified as the control group (CG), and 101 patients receiving SFGC on the basis of routine management were included in the observation group (OG). The scores of the self-perceived burden scale (SPBS), medical coping modes questionnaire (MCMQ), and self-rating anxiety scale (SAS) of the two groups were collected. The data collected were calculated and processed by software SPSS 26.0, and the effects of different managements on the mental states of patients with hemodialysis and anxiety were compared. RESULTS: After management, the scores of SPBS in both groups were lower than those before management, and the score in OG was significantly lower than the CG (p < 0.001). After management, the confrontation scores increased, the avoidance and resignation scores decreased in the MCMQ of the two groups, and the scores in the OG changed significantly (p < 0.001). The SAS scores of the two groups after management were significantly lower than those before management, and the OG score was significantly lower than the CG (p < 0.001). CONCLUSION: SFGC has a positive effect on the mental states of patients with hemodialysis and anxiety, which is worthy of further clinical study.

Viral infection and spread are inhibited by the polyubiquitination and downregulation of TRPV2 channel by the interferon-stimulated gene TRIM21.

Interferon (IFN) contributes to the host's antiviral response by inducing IFN-stimulated genes (ISGs). However, their functional targets and the mechanism of action remain elusive. Here, we report that one such ISG, TRIM21, interacts with and degrades the TRPV2 channel in myeloid cells, reducing its expression and providing host protection against viral infections. Moreover, viral infection upregulates TRIM21 in paracrine and autocrine manners, downregulating TRPV2 in neighboring cells to prevent viral spread to uninfected cells. Consistently, the Trim21-/- mice are more susceptible to HSV-1 and VSV infection than the Trim21+/+ littermates, in which viral susceptibility is rescued by inhibition or deletion of TRPV2. Mechanistically, TRIM21 catalyzes the K48-linked ubiquitination of TRPV2 at Lys295. TRPV2K295R is resistant to viral-infection-induced TRIM21-dependent ubiquitination and degradation, promoting viral infection more profoundly than wild-type TRPV2 when reconstituted into Lyz2-Cre;Trpv2fl/fl myeloid cells. These findings characterize targeting the TRIM21-TRPV2 axis as a conducive strategy to control viral spread to bystander cells.

Glutenin-chitosan 3D porous scaffolds with tunable stiffness and systematized microstructure for cultured meat model.

A glutenin (G)-chitosan (CS) complex (G-CS) was cross-linked by water annealing with aim to prepare structured 3D porous cultured meat scaffolds (CMS) here. The CMS has pore diameters ranging from 18 to 67 µm and compressive moduli from 16.09 to 60.35 kPa, along with the mixing ratio of G/CS. SEM showed the porous organized structure of CMS. FTIR and CD showed the increscent content of α-helix and ß-sheet of G and strengthened hydrogen-bondings among G-CS molecules, which strengthened the stiffness of G-CS. Raman spectra exhibited an increase of G concentration resulted in higher crosslinking of disulfide-bonds in G-CS, which aggrandized the bridging effect of G-CS and maintained its three-dimensional network. Cell viability assay and immuno-fluorescence staining showed that G-CS effectively facilitated the growth and myogenic differentiation of porcine skeletal muscle satellite cells (PSCs). CLSM displayed that cells first occupied the angular space of hexagon and then ring-growth circle of PSCs were orderly formed on G-CS. The texture and color of CMS which loaded proliferated PSCs were fresh-meat like. These results showed that physical cross-linked G-CS scaffolds are the biocompatible and stable adaptable extracellular matrix with appropriate architectural cues and natural micro-environment for structured CM models.

Non-canonical regulation of the reactivation of an oncogenic herpesvirus by the OTUD4-USP7 deubiquitinases.

Deubiquitinases (DUBs) remove ubiquitin from substrates and play crucial roles in diverse biological processes. However, our understanding of deubiquitination in viral replication remains limited. Employing an oncogenic human herpesvirus Kaposi's sarcoma-associated herpesvirus (KSHV) to probe the role of protein deubiquitination, we found that Ovarian tumor family deubiquitinase 4 (OTUD4) promotes KSHV reactivation. OTUD4 interacts with the replication and transcription activator (K-RTA), a key transcription factor that controls KSHV reactivation, and enhances K-RTA stability by promoting its deubiquitination. Notably, the DUB activity of OTUD4 is not required for K-RTA stabilization; instead, OTUD4 functions as an adaptor protein to recruit another DUB, USP7, to deubiquitinate K-RTA and facilitate KSHV lytic reactivation. Our study has revealed a novel mechanism whereby KSHV hijacks OTUD4-USP7 deubiquitinases to promote lytic reactivation, which could be potentially harnessed for the development of new antiviral therapies.

Disulfiram ameliorates STING/MITA-dependent inflammation and autoimmunity by targeting RNF115.

STING (also known as MITA) is an adaptor protein that mediates cytoplasmic DNA-triggered signaling, and aberrant activation of STING/MITA by cytosolic self-DNA or gain-of-function mutations causes severe inflammation. Here, we show that STING-mediated inflammation and autoimmunity are promoted by RNF115 and alleviated by the RNF115 inhibitor disulfiram (DSF). Knockout of RNF115 or treatment with DSF significantly inhibit systemic inflammation and autoimmune lethality and restore immune cell development in Trex1-/- mice and STINGN153S/WT bone marrow chimeric mice. In addition, knockdown or pharmacological inhibition of RNF115 substantially downregulate the expression of IFN-α, IFN-γ and proinflammatory cytokines in PBMCs from patients with systemic lupus erythematosus (SLE) who exhibit high concentrations of dsDNA in peripheral blood. Mechanistically, knockout or inhibition of RNF115 impair the oligomerization and Golgi localization of STING in various types of cells transfected with cGAMP and in organs and cells from Trex1-/- mice. Interestingly, knockout of RNF115 inhibits the activation and Golgi localization of STINGN153S as well as the expression of proinflammatory cytokines in myeloid cells but not in endothelial cells or fibroblasts. Taken together, these findings highlight the RNF115-mediated cell type-specific regulation of STING and STINGN153S and provide potential targeted intervention strategies for STING-related autoimmune diseases.

Targeting METTL3 reprograms the tumor microenvironment to improve cancer immunotherapy.

The tumor microenvironment (TME) is a heterogeneous ecosystem containing cancer cells, immune cells, stromal cells, cytokines, and chemokines which together govern tumor progression and response to immunotherapies. Methyltransferase-like 3 (METTL3), a core catalytic subunit for RNA N6-methyladenosine (m6A) modification, plays a crucial role in regulating various physiological and pathological processes. Whether and how METTL3 regulates the TME and anti-tumor immunity in non-small-cell lung cancer (NSCLC) remain poorly understood. Here, we report that METTL3 elevates expression of pro-tumorigenic chemokines including CXCL1, CXCL5, and CCL20, and destabilizes PD-L1 mRNA in an m6A-dependent manner, thereby shaping a non-inflamed TME. Thus, inhibiting METTL3 reprograms a more inflamed TME that renders anti-PD-1 therapy more effective in several murine lung tumor models. Clinically, NSCLC patients who exhibit low-METTL3 expression have a better prognosis when receiving anti-PD-1 therapy. Collectively, our study highlights targeting METTL3 as a promising strategy to improve immunotherapy in NSCLC patients.

Solution-Focused Group Counseling on Mental States in Hemodialysis Patients with Anxiety

Background: Hemodialysis patients usually suffer from anxiety due to physical and social factors, which belongs to a kind of psychological disorder, easily contributing to the decrease of patients' adherence to the treatment, and seriously affecting the patients' health status and quality of life. Solution-focused group counseling (SFGC) is a kind of psychotherapy proven to improve emotional problems in many fields. Still, the application of this therapy is rare in medical situations. This retrospective study aims to analyze the application of SFGC and probe into the effects on mental states in hemodialysis patients with anxiety. Methods: From January 2022 to February 2023, 212 patients with hemodialysis and anxiety admitted to our hospital were selected, and 9 patients who did not meet the inclusion criteria were excluded. Finally, 203 patients were included in this retrospective study. According to different clinical management methods, 102 patients receiving routine management were classified as the control group (CG), and 101 patients receiving SFGC on the basis of routine management were included in the observation group (OG). The scores of the self-perceived burden scale (SPBS), medical coping modes questionnaire (MCMQ), and self-rating anxiety scale (SAS) of the two groups were collected. The data collected were calculated and processed by software SPSS 26.0, and the effects of different managements on the mental states of patients with hemodialysis and anxiety were compared. Results: After management, the scores of SPBS in both groups were lower than those before management, and the score in OG was significantly lower than the CG (p < 0.001). After management, the confrontation scores increased, the avoidance and resignation scores decreased in the MCMQ of the two groups, and the scores in the OG changed significantly (p < 0.001). ... (AU)

Proteomic and phosphoproteomic analysis of responses to enterovirus A71 infection reveals novel targets for antiviral and viral replication.

Hand, foot, and mouth disease (HFMD) is a common infectious disease in infants and children, especially those under five years of age. EV-A71 is a common pathogen that causes HFMD and the primary pathogen leading to severe or fatal HFMD, which is characterized by neurological complications. However, the underlying mechanisms of EV-A71 pathogenesis remain largely unknown. In this report, we used proteomic and phosphorylated proteomic methods to characterize the proteome and phosphoproteome profiles of EV-A71-infected human neuroblastoma SK-N-SH cells. More than 7744 host proteins and 10069 phosphorylation modification sites were successfully quantified. Among them, 974 proteins and 3648 phosphorylation modification sites were regulated significantly during EV-A71 infection. KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analysis revealed that EV-A71 altered cell biological processes, including protein synthesis, RNA splicing and metabolism in SK-N-SH cells. Notably, based on the prediction of upregulated kinases during EV-A71 infection, we identified specific kinase inhibitors approved by the FDA, with ceralasertib, bosutinib, flavin mononucleotide, minocycline, pimasertib and acetylcysteine inhibiting EV-A71 infection. Finally, EV-A71 proteins were found to be phosphorylated during infection, with one site (S184 on 3D polymerase) observed to be crucial for viral replication because a S184A mutation knocked out viral replication. The results improve our understanding of the host response to EV-A71 infection of neuroblastoma cells and provide potential targets for developing anti-EV-A71 strategies.

MXRA7 is involved in megakaryocyte differentiation and platelet production.

Matrix remodeling is a critical process in hematopoiesis. The biology of MXRA7, as a matrix remodeling associated gene, has still not been reported in hematopoietic process. Public databases showed that MXRA7 expressed in hematopoietic stem cells, suggesting that it may be involved in hematopoiesis. We found that the amounts of megakaryocytes were lower in bone marrow and spleen from Mxra7-/- mice compared with that from wild-type mice. Knock-out of MXRA7 also reduced the amount of platelet in peripheral blood and affected the function of platelets. Knock-out of MXRA7 inhibited hematopoietic stem/progenitor cells differentiate to megakaryocytes possibly through down-regulating the expression of GATA-1 and FOG-1. Moreover, knockdown of MXRA7 in MEG-01 cells could inhibit the cell proliferation and cell apoptosis. Knockdown of MXRA7 inhibited the differentiation of MEG-01 cells and proplatelet formation through suppressing the ERK/MAPK signaling pathway and the expression of ß-tubulin. In conclusion, the current study demonstrated the potential significance of MXRA7 in megakaryocyte differentiation and platelet production. The novel findings proposed a new target for the treatment of platelet-related diseases, and much more investigations are guaranteed to dissect the mechanisms of MXRA7 in megakaryocyte differentiation and platelet production.

Trend of Human Schistosomiasis Japonica Prevalence in China from 1990 to 2019.

Schistosomiasis (Schistosomiasis japonica) remains an important public health problem in China, and the Chinese government has set an ambitious goal of eliminating schistosomiasis by 2030. Based on the observational study of the Global Burden of Disease Study database in 2019 (GBD2019) and the World Bank database, this study aimed to analyze the prevalence trend of schistosomiasis in China from 1990 to 2019 by using the joinpoint regression model, and the relationship between economic and social development and schistosomiasis prevalence. The data of age-standardized infection rates (ASRs) from the Global Burden of Disease Study Global Health Data Exchange were collected, and Gross national product per capita (GDP) and people using safely managed sanitation services ((PPMS) % of population) were extracted from the World Bank database. Trends of ASR were analyzed using joinpoint regression analysis, the association of ASR with GDP, and PPMS using the Pearson correlation analysis. The results reveal that, from 1990 to 2019, the overall trend of ASR from schistosomiasis showed a decrease for both sexes, the decreases in men were relatively smaller compared with women. A larger decrease has been observed in the age groups from 15 to 49 years compared with other age groups. The ASR of schistosomiasis had a significant negative correlation with GDP and PPMS. This observational study identified decreasing prevalence rate of schistosomiasis in China since 1990. Continuous investment, optimization of control strategy, and economic development will help to achieve the goal of schistosomiasis elimination.

The clinical value of anal swabs for microbial detection in allogeneic haematopoietic stem cell transplantation.

The intestinal microbiota plays critical roles in allogeneic hematopoietic stem cell transplantation (allo-HSCT). Rapid and effective microbial detection methods have important guiding value for the selection of intervention strategies for allo-HSCT recipients. We evaluated the application of the anal swab test before transplantation in allo-HSCT recipients. A total of 120 patients who underwent anal swab testing before allo-HSCT were retrospectively analyzed and divided into 3 groups: sterile (aseptic growth-negative), G+ (gram-positive bacterial colonization), and G- (gram-negative bacterial colonization). On 16S rRNA sequencing, gram-negative bacteria predominated in the G- group before and after transplantation. Compared with the sterile group, the percentage of natural killer cells was higher and the percentage of T cells was lower after transplantation in the G- group at 1 month after transplantation. The percentage of CD4+ and CD4+CD8+ T cells was lower and the percentage of regulatory T cells was higher in the G- group. The plasma levels of proinflammatory cytokines (TNF-α, IFN-γ, IL-6, and IL-17A) at 2 weeks post-transplantation were lower in the G- group than in the sterile group, as was the cumulative incidence of grade III-IV acute graft-versus-host disease (GVHD). Gram-negative bacterial colonization before allo-HSCT was associated with low rates of bloodstream infections within 100 days post-transplantation and cytomegalovirus reactivation at 100 days to 2 years post-transplantation. Moreover, patients in the G- group had a higher rate of 2-year GVHD-free, relapse-free survival compared with patients in the sterile group. The detection results using anal swabs were consistent with the gram-negative or gram-positive bacteria abundance of 16S rRNA sequencing results and associated with immune homeostasis and clinical outcomes after allo-HSCT. Anal swab testing may have potential advantages as a simple and effective method for microbial detection in allo-HSCT.

Critical role of MXRA7 in differentiation blockade in human acute promyelocytic leukemia cells.

The biology of the matrix remodeling-associated 7 (MXRA7) gene has been ill defined. Bioinformatic analysis of public data sets revealed that MXRA7 messenger RNA (mRNA) was highly expressed in acute myeloid leukemia (AML), especially acute promyelocytic leukemia (APL). High expression of MXRA7 was associated with poor overall survival of patients with AML. We confirmed that MXRA7 expression was upregulated in patients with APL and cell lines. Knockdown or overexpression of MXRA7 did not affect the proliferation of NB4 cells directly. Knockdown of MXRA7 in NB4 cells promoted drug-induced cell apoptosis, whereas overexpression of MXRA7 had no obvious influence on drug-induced cell apoptosis. Lowering MXRA7 protein levels in NB4 cells promoted all-trans retinoic acid (ATRA)-induced cell differentiation possibly through decreasing the PML-RARα level and increasing PML and RARα levels. Correspondingly, overexpression of MXRA7 showed consistent results. We also demonstrated that MXRA7 altered the expression of genes involved in leukemic cell differentiation and growth. Knockdown of MXRA7 upregulated the expression levels of C/EBPB, C/EBPD, and UBE2L6, and downregulated the expression levels of KDM5A, CCND2, and SPARC. Moreover, knockdown of MXRA7 inhibited the malignancy of NB4 cells in a non-obese diabetic-severe combined immune-deficient mice model. In conclusion, this study demonstrated that MXRA7 influences the pathogenesis of APL via regulation of cell differentiation. The novel findings about the role of MXRA7 in leukemia not only shed light on the biology of this gene but also proposed this gene as a new target for APL treatment.

Transforming Growth Factor ß1 Ameliorates Microglial Activation in Perioperative Neurocognitive Disorders.

Perioperative neurocognitive disorder (PND) is a common complication of surgery and anesthesia, especially among older patients. Microglial activation plays a crucial role in the occurrence and development of PND and transforming growth factor beta 1 (TGF-ß1) can regulate microglial homeostasis. In the present study, abdominal surgery was performed on 12-14 months-old C57BL/6 mice to establish a PND model. The expression of TGF-ß1, TGF-ß receptor 1, TGF-ß receptor 2, and phosphor-smad2/smad3 (psmad2/smad3) was assessed after anesthesia and surgery. Additionally, we examined changes in microglial activation, morphology, and polarization, as well as neuroinflammation and dendritic spine density in the hippocampus. Behavioral tests, including the Morris water maze and open field tests, were used to examine cognitive function, exploratory locomotion, and emotions. We observed decreased TGF-ß1 expression after surgery and anesthesia. Intranasally administered exogenous TGF-ß1 increased psmad2/smad3 colocalization with microglia positive for ionized calcium-binding adaptor molecule 1. TGF-ß1 treatment attenuated microglial activation, reduced microglial phagocytosis, and reduced surgery- and anesthesia-induced changes in microglial morphology. Compared with the surgery group, TGF-ß1 treatment decreased M1 microglial polarization and increased M2 microglial polarization. Additionally, surgery- and anesthesia-induced increase in interleukin 1 beta and tumor necrosis factor-alpha levels was ameliorated by TGF-ß1 treatment at postoperative day 3. TGF-ß1 also ameliorated cognitive function after surgery and anesthesia as well as rescue dendritic spine loss. In conclusion, surgery and anesthesia induced decrease in TGF-ß1 levels in older mice, which may contribute to PND development; however, TGF-ß1 ameliorated microglial activation and cognitive dysfunction in PND mice.

The deubiquitinase OTUD4 inhibits the expression of antimicrobial peptides in Paneth cells to support intestinal inflammation and bacterial infection.

Dysfunction of the intestinal epithelial barrier causes microbial invasion that would lead to inflammation in the gut. Antimicrobial peptides (AMPs) are essential components of the intestinal epithelial barrier, while the regulatory mechanisms of AMPs expression are not fully characterized. Here, we report that the ovarian tumor family deubiquitinase 4 (OTUD4) in Paneth cells restricts the expression of AMPs and thereby promotes experimental colitis and bacterial infection. OTUD4 is upregulated in the inflamed mucosa of ulcerative colitis patients and in the colon of mice treated with dextran sulfate sodium salt (DSS). Knockout of OTUD4 promotes the expression of AMPs in intestinal organoids after stimulation with lipopolysaccharide (LPS) or peptidoglycan (PGN) and in the intestinal epithelial cells (IECs) of mice after DSS treatment or Salmonella typhimurium (S.t.) infection. Consistently, Vil-Cre;Otud4fl/fl mice and Def-Cre;Otud4fl/fl mice exhibit hyper-resistance to DSS-induced colitis and S.t. infection compared to Otud4fl/fl mice. Mechanistically, knockout of OTUD4 results in hyper K63-linked ubiquitination of MyD88 and increases the activation of NF-κB and MAPKs to promote the expression of AMPs. These findings collectively highlight an indispensable role of OTUD4 in Paneth cells to modulate AMPs production and indicate OTUD4 as a potential target for gastrointestinal inflammation and bacterial infection.

The Impact of Flooding on Snail Spread: The Case of Endemic Schistosomiasis Areas in Jiangxi Province, China.

Flooding is the main natural factor in snail diffusion, and it has a negative impact on schistosomiasis transmission. There are few studies on the spread and migration of snails following a flood; therefore, we aimed to investigate the influence of flooding on snail diffusion and explore the characteristics and laws of snail diffusion in Jiangxi Province. By using a retrospective survey and cross-sectional survey, the data on snail spreading in Jiangxi Province from 2017 to 2021 were collected. The distribution, nature, and area of snail spread were systematically analyzed in combination with the hydrological situation, types of region, and types of flood. From 2017 to 2021, a total of 120 snail-spread environments were found, including in 92 hilly areas and in 28 lake areas. The areas caused by flood and by other means numbered 6 and 114, respectively. The proportions of recurrence, expansion, and first-time occurrences were 43.42%, 38.16%, and 18.42%, respectively, and the 14 new snail environments were only distributed in the hilly areas. With the exception of 2018, the ratio of snail-spread areas in the hilly region was higher than that in lake region in other years. The average density of live snails was 0.0184-1.6617 no./0.1 m2 and 0.0028-0.2182 no./0.1 m2 in the hilly region. Among the 114 environments affected by floods, 86 consisted of hilly environments, including 66 spreading environments affected by rainstorm floods, and 20 rainstorm debris flow environments. There were 28 lake areas, of which 10 were in the Jiangxi section of Yangtze River and were affected by rainstorm floods. Snail spread following flooding has a certain 'lag effect,' and = simple annual changes in hydrological characteristics have little effect on the diffusion of snails or on their density = in the affected environment, but it is more closely related to local floods. The hilly environments are more susceptible to floods than the lake region, and the risk of snail spread is much higher in the hilly than in the lake region.

Abnormal metabolic connectivity in default mode network of right temporal lobe epilepsy.

Aims: Temporal lobe epilepsy (TLE) is a common neurological disorder associated with the dysfunction of the default mode network (DMN). Metabolic connectivity measured by 18F-fluorodeoxyglucose Positron Emission Computed Tomography (18F-FDG PET) has been widely used to assess cumulative energy consumption and provide valuable insights into the pathophysiology of TLE. However, the metabolic connectivity mechanism of DMN in TLE is far from fully elucidated. The present study investigated the metabolic connectivity mechanism of DMN in TLE using 18F-FDG PET. Method: Participants included 40 TLE patients and 41 health controls (HC) who were age- and gender-matched. A weighted undirected metabolic network of each group was constructed based on 14 primary volumes of interest (VOIs) in the DMN, in which Pearson's correlation coefficients between each pair-wise of the VOIs were calculated in an inter-subject manner. Graph theoretic analysis was then performed to analyze both global (global efficiency and the characteristic path length) and regional (nodal efficiency and degree centrality) network properties. Results: Metabolic connectivity in DMN showed that regionally networks changed in the TLE group, including bilateral posterior cingulate gyrus, right inferior parietal gyrus, right angular gyrus, and left precuneus. Besides, significantly decreased (P < 0.05, FDR corrected) metabolic connections of DMN in the TLE group were revealed, containing bilateral hippocampus, bilateral posterior cingulate gyrus, bilateral angular gyrus, right medial of superior frontal gyrus, and left inferior parietal gyrus. Conclusion: Taken together, the present study demonstrated the abnormal metabolic connectivity in DMN of TLE, which might provide further insights into the understanding the dysfunction mechanism and promote the treatment for TLE patients.

Impact of the National Wetland Park in the Poyang Lake Area on Oncomelania hupensis, the Intermediate Host of Schistoma japonicum.

In this study, we aimed to understand the influence of ecotourism on the distribution of Oncomelania hupensis and to provide a scientific basis for formulating effective snail control methods in tourism development areas. Poyang Lake National Wetland Park was selected as the pilot area, and sampling surveys were conducted based on comprehensive and detailed investigations of all historical and suspected snail environments according to map data to determine the snail distribution and analyze the impact of tourism development. The results showed that from 2011 to 2021, the positive rates of blood tests and fecal tests tended to decrease among residents of the Poyang Lake area. The positive rates of blood tests and fecal tests in livestock also tended to decrease. The average density of O. hupensis snails decreased, and no schistosomes were detected during infection monitoring in Poyang Lake. The local economy rapidly grew after the development of tourism. The development of ecotourism projects in Poyang Lake National Wetland Park increased the transfer frequency of boats, recreational equipment, and people, but it did not increase the risk of schistosomiasis transmission or the spread of O. hupensis snails. Prevention and monitoring only need to be strengthened in low-endemic schistosomiasis areas to effectively promote economic development due to tourism activities without affecting the health of residents.

Gene sequencing and result analysis of balanced translocation carriers by third-generation gene sequencing technology.

Because the total gene copy number remains constant and all genes are normally expressed, carriers of balanced chromosomal translocations usually have a normal phenotype but are able to produce many different types of gametes during meiosis, and unbalanced gametes lead to increased risks of infertility, recurrent spontaneous abortion, stillbirth, neonatal death or malformations and intellectual abnormalities in offspring. The key to balanced translocations lies in finding the breakpoints, but current genetic testing techniques are all short-read sequencing, with the disadvantage of procedural complexity and imprecision for precisely identifying the breakpoints. The latest third-generation sequencing technology overcomes these drawbacks and uses robust long-read sequencing to accurately and rapidly detect genome-wide information and identify breakpoint locations. In this paper, we performed whole genome long-read sequencing using an Oxford Nanopore sequencer to detect the breakpoints of 4 balanced chromosomal translocation carriers. The results showed that employing about ~ 10× coverage confirmed 6 of the 8 breakpoints, of which, 2 had microdeletions/insertions identified near the breakpoints and 4 had breakpoints that disrupted the normal gene structure and were simultaneously tested for genome-wide structural variation (SV). The results show that whole genome long-read sequencing is an efficient method for pinpointing translocation breakpoints and providing genome-wide information, which is essential for medical genetics and preimplantation genetic testing.