Depression and suicidal ideation among Chinese college students during the COVID-19 pandemic: the mediating roles of chronotype and sleep quality.

BACKGROUND: This study was intended to investigate the correlation between depression and suicidal ideation among Chinese college students during the COVID-19 pandemic and the potential mediating roles of chronotype and sleep quality in this relationship . METHODS: A sample of 4,768 college students was selected from four institutions in Anhui Province, China, and the study was conducted during the COVID-19 pandemic (November to December 2020) using a stratified, cluster, multi-stage sampling method. This study used the two-item Patient Health Questionnaire (PHQ-2) to assess depressive symptoms, the Morningness-Eveningness Questionnaire 19 (MEQ-19) to determine individual sleep chronotypes (i.e., morning or evening preference), and the Pittsburgh Sleep Quality Index (PSQI) to evaluate sleep quality. Participants were asked about suicidal ideation. MPLUS 8.3 software was used to analyze the mediating effect of chronotype and sleep quality on the relationship between depression and suicidal ideation. RESULTS: During the COVID-19 pandemic, the prevalence of suicidal ideation among Chinese college students was 5.4%. Depression was inversely correlated with chronotype (beta = - 0.346, P < 0.01) and positively correlated with sleep quality (beta = 0.846, P < 0.001), indicating that students experiencing depressive symptoms were more likely to have a later chronotype and poor sleep quality. A later chronotype (beta = - 0.019, P < 0.05) and poor sleep quality (beta = 0.066, P < 0.01) predicted suicidal ideation. Depression emerged as a direct and significant risk factor for suicidal ideation (effect value = 0.535, 95% confidence interval: 0.449 ~ 0.622). Chronotype and sleep quality were found to have potential mediating effects on the relationship between depression and suicidal ideation; however, the chain-mediating effect of chronotype and sleep quality was not statistically significant. CONCLUSIONS: Our findings suggest that during the COVID-19 pandemic, depression can precipitate suicidal ideation through its influence on sleep chronotype and quality. These compelling findings highlight the urgency of early intervention strategies intended to mitigate suicidal thoughts, particularly among students exhibiting depressive symptoms, who experience disrupted sleep patterns and poor sleep quality.

Aspartic proteases gene family: Identification and expression profiles during stem vascular development in tobacco.

Aspartic proteases (APs) constitute a large family in plants and are widely involved in diverse biological processes, like chloroplast metabolism, biotic and abiotic stress responses, and reproductive development. In this study, we focused on overall analysis of the APs genes in tobacco. Our analysis included the phylogeny and cis-elements in the cell wall-associated promoters of these genes. To characterize the expression patterns of APs genes in stem vascular development. The tissue expression analysis showed that NtAED3-like was preferentially expressed in the differentiating xylem and phloem cells of the vascular system. Based on histochemical staining analysis showed that the NtAED3-like gene was specifically expressed in stem vascular tissue, root vascular tissue, and petiole vascular tissue. The TdT-mediated dUTP nick-end labeling (TUNEL) assay illustrated a delayed progression of programmed cell death (PCD) within the xylem of the ko-ntaed3a-like mutant, relative to the wild type. The mutant ko-ntaed3a-like exhibited a phenotype of thinning stem circumference and changed in xylem structure and lignin content. In addition, the two-dimension heteronuclear single quantum coherent nuclear magnetic resonance (2D-HSQC) analysis of three milled wood lignins (MWLs) showed that the content of ß-O-4 connection in ko-ntaed3a-like decreased slightly compared with wild type. In conclusion, this study provides our understanding of the regulation of vascular tissue development by the NtAED3-like gene in tobacco and provides a better basis for determining the molecular mechanism of the aspartic protease in secondary cell wall (SCW) development.

Biocontrol of plant parasitic nematodes by bacteria and fungi: a multi-omics approach for the exploration of novel nematicides in sustainable agriculture.

Plant parasitic nematodes (PPNs) pose a significant threat to global crop productivity, causing an estimated annual loss of US $157 billion in the agriculture industry. While synthetic chemical nematicides can effectively control PPNs, their overuse has detrimental effects on human health and the environment. Biocontrol agents (BCAs), such as bacteria and fungi in the rhizosphere, are safe and promising alternatives for PPNs control. These BCAs interact with plant roots and produce extracellular enzymes, secondary metabolites, toxins, and volatile organic compounds (VOCs) to suppress nematodes. Plant root exudates also play a crucial role in attracting beneficial microbes toward infested roots. The complex interaction between plants and microbes in the rhizosphere against PPNs is mostly untapped which opens new avenues for discovering novel nematicides through multi-omics techniques. Advanced omics approaches, including metagenomics, transcriptomics, proteomics, and metabolomics, have led to the discovery of nematicidal compounds. This review summarizes the status of bacterial and fungal biocontrol strategies and their mechanisms for PPNs control. The importance of omics-based approaches for the exploration of novel nematicides and future directions in the biocontrol of PPNs are also addressed. The review highlighted the potential significance of multi-omics techniques in biocontrol of PPNs to ensure sustainable agriculture.

Analysis of Key Genes Related to Systemic Lupus Erythematosus and COVID-19.

BACKGROUND: Systemic Lupus Erythematosus (SLE) is a multifactorial and complex immune disease; however, the relevance of COVID-19 infection in SLE patients remains uncertain. AIM: This study aims to explore the key candidate genes and pathways in patients with SLE. It also seeks to employ bioinformatics analysis to unravel the molecular signatures inherent in both SLE and COVID-19 patients. The ultimate aim is to identify potential targets and markers specifically relevant to SLE patients who contract SARS-CoV-2. METHODS: Datasets (GSE12374, GSE20864, GSE61635, GSE81622, and GSE144390) from the Gene Expression Omnibus (GEO) database were analyzed using Robust Rank Aggregation (RRA) method to identify differential expression genes (DEGs) in SLE patients compared to healthy individuals. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, tissue-specific gene analysis, and Protein-protein interaction (PPI) network were performed. Finally, the Venn diagram was employed to identify the intersections of COVID-19 genes, serving as potential targets for SLE patients with COVID-19 infection. RESULTS: A total of 154 DEGs were discovered, with GO enrichment indicating a predominant involvement in the defense response against the virus (P<0.001). KEGG pathway analysis showed enrichment in the NOD-like receptor signaling pathway and coronavirus disease, specifically COVID-19 (P<0.001). Tissue-specific genes related to the hematological and immune systems were emphasized (74%). The PPI network highlighted 22 genes, and 5 key genes, namely, IFIT1, IFIT3, MX1, MX2, and OAS3, which were identified after intersecting with COVID-19 patients' data. CONCLUSION: IFIT1, IFIT3, MX1, MX2, and OAS3 exhibiting differential expression, as well as the pathways associated with COVID-19, could potentially function as biomarkers and therapeutic targets for individuals with SLE infected with COVID-19.

Modulatory effects of necroptosis: A potential preventive approach to control diseases in fish.

Necroptosis is a caspase-independent programmed cell death process characterized by morphological similarities to necrosis and the potential to cause significant inflammatory reactions. The initiation, execution, and inhibition of necroptosis involve a complex interplay of various signaling proteins. When death receptors bind to ligands, necroptosis is triggered through the receptor-interacting serine/threonine-protein kinase 1 (RIPK1)/RIPK3/Mixed Lineage Kinase Domain-Like (MLKL) axis, leading to inflammatory reactions in the surrounding tissues. This process encompasses numerous physiological regulatory mechanisms and contributes to the development and progression of certain diseases. The mechanisms of necroptosis were not well conserved across terrestrial and aquatic organisms, with differences in some components and functions. Given the significant challenges that aquatic animal diseases pose to aquaculture, research interest in necroptosis has surged recently, particularly in studies focusing on fish. Understanding necroptosis in fish can lead to interventions that offer potential breakthroughs in disease inhibition and fish health improvement.

Relationship between high-mobility group box-l and cognitive impairments induced by myocardial ischemia-reperfusion in elderly rats.

BACKGROUND: Myocardial ischemia-reperfusion (MI/R) can lead to structural and functional abnormalities in the hippocampal neurons of the brain. High-mobility group box-l (HMGB1) is implicated in the activation of immune cells and the stimulation of inflammatory responses. However, the specific role of HMGB1 in cognitive impairment induced by MI/R in elderly rats has yet to be elucidated. METHODS: Elderly rats underwent surgical procedures to induce MI/R. To evaluate the learning and memory abilities of these rats, a water maze test and a new-object recognition test were administered. Nissl staining was utilised to examine hippocampal neuron damage. Enzyme-linked immunosorbent assay, western blotting, and real-time quantitative polymerase chain reaction (RT-qPCR) analyses were conducted to measure the expression levels of HMGB1, inflammatory cytokines, and molecular pathways. RESULTS: The study found that MI/R induced cognitive impairment in elderly rats. There was an observed increase in serum HMGB1 levels, along with elevated concentrations of pro-inflammatory cytokines in the plasma and hippocampus, accompanied by a decrease in anti-inflammatory cytokines. Moreover, substantial damage was evident in the hippocampal neurons of rats exposed to MI/R. In the brains of these rats, there was an increased expression of HMGB1, the receptor for advanced glycation end products (RAGE), toll-like receptor 4 (TLR4), phosphorylated p65, interleukin-1ß (IL-1ß), IL-6, IL-23, tumour necrosis factor-α (TNF-α), caspase-3, and Bax. In contrast, the expression of B-cell lymphoma 2 was decreased. The RT-qPCR analyses indicated elevated levels of HMGB1, RAGE, TLR4, IL-1ß, IL-6, IL-23, TNF-α, caspase-3, and Bax mRNA. CONCLUSION: The increased concentration of serum and hippocampal inflammatory factors in the brains of elderly rats subjected to MI/R suggests that cognitive impairment may be induced through the activation of the HMGB1/TLR4/NF-κB signalling pathway.

In Situ Pipe Prover Volume Measurement Method.

To improve the accuracy of in situ measurement of the standard volumes of pipe provers and to shorten the traceability chain, a new method of in situ pipe prover volume measurement was developed alongside a supporting measurement device. This method is based on the geometric dimension approach, which measures the inner diameter and length of a pipe prover to calculate its volume. For inner diameter measurement, a three-probe inner-diameter algorithm model was established. This model was calibrated using a standard ring gauge of Φ313 mm, with the parameters calculated through fitting. Another standard ring gauge of Φ320 mm was used to verify the inner diameters determined by the algorithmic model. A laser interferometer was employed for the segmented measurement of the pipe prover length. The comprehensive measurement system was then used for in situ measurement of the standard pipe prover. The newly developed system achieved an expanded uncertainty of 0.012% (k = 2) in volume measurement, with the deviation between the measured and nominal pipe prover volumes being merely 0.007%. These results demonstrate that the proposed in situ measurement method offers ultra-high-precision measurement capabilities.

CircUBA2 promotes the cancer stem cell-like properties of gastric cancer through upregulating STC1 via sponging miR-144-5p.

BACKGROUND: Cancer stem cells (CSCs) are critical factors that limit the effectiveness of gastric cancer (GC) therapy. Circular RNAs (circRNAs) are confirmed as important regulators of many cancers. However, their role in regulating CSC-like properties of GC remains largely unknown. Our study aimed to investigate the role of circUBA2 in CSC maintenance and the underlying mechanisms. METHODS: We identified circUBA2 as an upregulated gene using circRNA microarray analysis. qRT-PCR was used to examine the circUBA2 levels in normal and GC tissues. In vitro and in vivo functional assays were performed to validate the role of circUBA2 in proliferation, migration, metastasis and CSC-like properties of GC cell. The relationship between circUBA2, miR-144-5p and STC1 was characterised using bioinformatics analysis, a dual fluorescence reporter system, FISH, and RIP assays. RESULTS: CircUBA2 expression was significantly increased in GC tissues, and patients with GC with high circUBA2 expression had a poor prognosis. CircUBA2 enhances CSC-like properties of GC, thereby promoting cell proliferation, migration, and metastasis. Mechanistically, circUBA2 promoted GC malignancy and CSC-like properties by acting as a sponge for miR-144-5p to upregulate STC1 expression and further activate the IL-6/JAK2/STAT3 signaling pathway. More importantly, the ability of circUBA2 to enhance CSC-like properties was inhibited by tocilizumab, a humanised Interleukin-6 receptor (IL-6R) antibody. Thus, circUBA2 knockdown and tocilizumab synergistically inhibited CSC-like properties. CONCLUSIONS: Our study demonstrated the critical role of circUBA2 in regulating CSC-like properties in GC. CircUBA2 may be a promising prognostic biomarker for GC.

Disulfidptosis-related long non-coding RNA signature predicts the prognosis, tumor microenvironment, immunotherapy, and antitumor drug options in colon adenocarcinoma.

This study aims to investigate the role and prognostic significance of long non-coding RNAs (lncRNAs) associated with disulfidptosis in colon adenocarcinoma (COAD). The TCGA database's clinical data and transcriptome profiles were employed. Analysis of previous studies identified 10 disulfidptosis-related genes (DRGs). We used these genes to construct a signature that could independently and accurately predict the prognosis of patients with COAD. The Kaplan-Meier (K-M) curve analysis showed that the lower-risk group had a better prognosis. With the help of multivariate Cox regression analysis, the risk score produced from the patient's signature might independently predict the outcomes. Utilizing a nomogram, the receiver operating characteristic (ROC) curve, and principal component analysis (PCA), the signature's predictive ability was also confirmed. It's interesting to note that immunotherapy, especially PD-1 immune checkpoint suppression, was more likely to benefit low-risk patients. The IC50 levels for certain anticancer agents were lower in the high-risk group. Finally, qRT-PCR analyses in colon cancer cell lines revealed elevated levels of lncRNAs CASC9, ZEB1-AS1, ATP2A1-AS1, SNHG7, AL683813.1, and AP003555.1, and reduced levels of FAM160A1-DT and AC112220.2, compared to normal cell lines. This signature offers insights into prognosis, tumor microenvironment, and options for immunotherapy and antitumor drugs in patients with COAD.

Changes in the correlation between substantia nigra hyperechogenicity area and Parkinson's disease severity at different Hoehn and Yahr stages.

BACKGROUND: It is debatable whether the area of substantia nigra hyperechogenicity (SN+) in transcranial sonography (TCS) is related to Parkinson's disease (PD) severity. Iron deposition, which is associated with the formation of SN+, may have different effects on dopamine nerve function as PD progresses. However, little research has explored the association between the SN + area and disease severity of PD in stages. METHODS: 612 PD patients with sufficient bone window were retrospectively included from a PD database, and disease severity was assessed by the Unified Parkinson's Disease Rating Scale (UPDRS) scores. Based on the Hoehn and Yahr (H-Y) scale, we classified the patients into seven groups (H-Y stage 1, 1.5, 2, 2.5, 3, 4, and 5) and then analyzed the correlations between the SN + area and the UPDRS scores separately. RESULTS: Our results indicated a U-shaped relationship between the initial-SN + area and disease severity in PD: In the H-Y stage 1 group, the initial-SN + area was negatively correlated with the UPDRS total score (r = - 0.456, p < 0.001) and UPDRS-III score (r = - 0.497, p < 0.001). No correlation was observed in the groups of H-Y stages 1.5, 2, and 2.5. In the groups of H-Y stage ≥ 3, the initial-SN + area was positively correlated with the UPDRS total score and UPDRS-III score, with strongest correlation in the H-Y stage 5 group (all p values < 0.05). Moreover, the larger SN + area and average SN + area showed a similar evolutionary trend of correlation with UPDRS total score and UPDRS-III score. CONCLUSIONS: Our study indicated a U-shaped correlation between the SN + area with the UPDRS total score and UPDRS-III score as H-Y stage progressed. The evolution of the correlation may reflect the evolution of underlying pathological mechanisms related to iron deposition in the substantia nigra.

A multicenter retrospective study of antidepressant use in outpatient clinics in China pre- and post-COVID.

BACKGROUND: Analyzing antidepressant prescribing in real-world settings can provide clinicians and health policymakers valuable information. AIM: This epidemiological study examined the status and trends in antidepressant prescribing among the Chinese population from July 1, 2017, to June 30, 2022. METHOD: A retrospective study was conducted in three hospitals. Data were collected 2.5 years before and 2.5 years after the onset of the COVID-19 pandemic. We analyzed the number of patients diagnosed with depression and their corresponding antidepressant prescriptions. Using the chi-square test, stratified analyses were performed to explore the characteristics of these prescriptions in different ages and sexes. RESULTS: The study included 124,355 patients and 400,840 antidepressant prescriptions. We observed fluctuating upward trends in the number of patients and antidepressant prescriptions. Post-COVID-19, the number of patients increased by 37.1% compared to the pre-pandemic period, and the number of antidepressant prescriptions rose by 88.3%. The three most frequently prescribed antidepressants for adolescents were sertraline, citalopram, and escitalopram. Among adults, citalopram, escitalopram, and sertraline were most common, while in older adults, citalopram, escitalopram, and mirtazapine were predominant. Male patients used mirtazapine, venlafaxine, paroxetine, bupropion, fluvoxamine, vortioxetine, and clomipramine more frequently compared to female patients, who were more likely to be prescribed citalopram, flupentixol/melitracen, agomelatine, and fluoxetine. Antidepressant monotherapy represented 76.6% of prescriptions, with the most common combination being antidepressants and anxiolytics. CONCLUSION: Over the past 5 years, both the number of patients and antidepressant prescriptions have shown upward trends, and the COVID-19 pandemic has impacted prescribing. Understanding the changes in antidepressant prescriptions can identify adherence to national guidelines.

Deliberation concerning the role of M1-type macrophage subset in oral carcinogenesis.

Over the last decade, accumulating evidence has suggested that tumor-associated macrophages (TAMs) play a significant role in the tumor development. This commentary wishes to highlight the findings by You, et al. that M1-like TAMs could cascade a mesenchymal/stem-like phenotype of oral squamous cell carcinoma (OSCC) via the IL6/Stat3/THBS1 feedback loop. These unprecedented findings identified M1-like TAMs-regulated processes as potentially tumor-promotion in the context of OSCC immunomicroenvironment.

Photoinduced Decarboxylative Thioacylation of N-Hydroxyphthalimide Esters with Tetraalkylthiuram Disulfides.

Dithiocarbamate is a key structural sequence in pharmaceuticals and agrochemicals, and its synthesis is crucial in organic chemistry. Although significant progress has been made in related synthesis research, developing a practical and universal synthesis method remains fascinating. Herein, we report a new visible-light-induced decarboxylation coupling reaction between N-hydroxyphthalimide esters and tetraalkylthiuram disulfides, which uses Ir(ppy)3 as a photocatalyst to promote the generation of corresponding decarboxylation thioacylation product-dithiocarbamates in high yields. This redox-neutral protocol uses inexpensive and readily available starting material under mild reaction conditions, exhibiting broad substrate scope and wide functional group compatibility. This method can be further used for post modification of complex natural products and bioactive drugs.

Association between transitions in metabolic health and colorectal cancer across categories of body size phenotype: a prospective cohort study.

OBJECTIVE: We aimed to investigate the associations of changes in metabolic health across categories of body size phenotype with the risk of colorectal cancer in a community-based prospective cohort. METHODS: In the current study, a total of 70,987 participants were included. Changes in metabolic health across categories of body size phenotype were assessed between the health examination for the first time in the years 2006 through 2009 and a 2010/2011 health examination. A multivariate Cox proportional hazards model was used to assess the associations of changes in metabolic health across body size phenotype categories with risk of colorectal cancer. RESULTS: During the median follow-up time of 11.04 years, 428 (0.60%) participants developed colorectal cancer. Compared with metabolically healthy normal-weight (MHNW) participants who remained MH, the risk of colorectal cancer was increased by 144% (95% CI: 1.21-4.95) for participants with metabolically healthy obesity (MHO) who converted to a metabolically unhealthy (MU) phenotype. Participants who were MU at baseline were still at increased risk of colorectal cancer, regardless of obesity status. CONCLUSIONS: The MHO phenotype was a dynamic status over time, and converting to MU during follow-up and being initially MU were associated with having an increased risk of colorectal cancer, regardless of degree of obesity and body size phenotype.

Dissecting the emerging role of cancer-associated adipocyte-derived cytokines in remodeling breast cancer progression.

Breast cancer has been reported to transcend lung cancer as the most commonly diagnosed cancer in women all over the world. Adipocytes, serving as energy storage and endocrine cells, are the major stromal cells in the breast. Cancer-associated adipocytes (CAAs) are adjacent and dedifferentiated adipocytes located at the invasive front of human breast tumors. Adipocytes can transform into CAA phenotype with morphological and biological changes under the remodeling of breast cancer cells. CAAs play an essential role in breast cancer progression, including remodeling the tumor microenvironment (TME), regulating immunity, and interacting with breast cancer cells. CAAs possess peculiar secretomes and are accordingly capable to promote proliferation, invasiveness, angiogenesis, metastasis, immune escape, and drug resistance of breast cancer cells. There is a complex and coordinated crosstalk among CAAs, immune cells, and breast cancer cells. CAAs can release a variety of cytokines, including IL-6, IL-8, IL-1ß, CCL5, CCL2, VEGF, G-CSF, IGF-1, and IGFBP, thereby promoting immune cell recruitment and macrophage polarization, and ultimately stimulating malignant behaviors in breast cancer cells. Here, we aim to provide a comprehensive description of CAA-derived cytokines, including their impact on cancer cell behaviors, immune regulation, breast cancer diagnosis, and treatment. A deeper understanding of CAA performance and interactions with specific TME cell populations will provide better strategies for cancer treatment and breast reconstruction after mastectomy.

Synergistic Activation of LEPR and ADRB2 Induced by Leptin Enhances ROS Generation in TNBC Cells.

Purpose: Leptin interacts not only with leptin receptor (LEPR) but also engages with other receptors. While the pro-oncogenic effects of the adrenergic receptor ß2 (ADRB2) are well-established, the role of leptin in activating ADRB2 in triple-negative breast cancer (TNBC) remains unclear. Materials and Methods: The pro-carcinogenic effects of LEPR were investigated using murine TNBC cell lines, 4T1 and EMT6, and a tumor-bearing mouse model. Expression levels of LEPR, NOX4, and ADRB2 in TNBC cells and tumor tissues were analyzed via Western blot and qPCR. Changes in reactive oxygen species (ROS) levels were assessed using flow cytometry and MitoSox staining, while immunofluorescence double-staining confirmed the co-localization of LEPR and ADRB2. Results: LEPR activation promoted NOX4-derived ROS and mitochondrial ROS production, facilitating TNBC cell proliferation and migration, effects which were mitigated by the LEPR inhibitor Allo-aca. Co-expression of LEPR and ADRB2 was observed on cell membranes, and bioinformatics data revealed a positive correlation between the two receptors. Leptin activated both LEPR and ADRB2, enhancing intracellular ROS generation and promoting tumor progression, which was effectively countered by a specific ADRB2 inhibitor ICI118551. In vivo, leptin injection accelerated tumor growth and lung metastases without affecting appetite, while treatments with Allo-aca or ICI118551 mitigated these effects. Conclusion: This study demonstrates that leptin stimulates the growth and metastasis of TNBC through the activation of both LEPR and ADRB2, resulting in increased ROS production. These findings highlight LEPR and ADRB2 as potential biomarkers and therapeutic targets in TNBC.

Acidity-Responsive Fe-PDA@CaCO3 Nanoparticles for Photothermal-Enhanced Calcium-Overload- and Reactive-Oxygen-Species-Mediated Tumor Therapy.

Calcium-overload-mediated tumor therapy has received considerable interest in oncology. However, its efficacy has been proven to be inadequate due to insufficient calcium ion concentration at the tumor site coupled with challenges in facilitating efficient calcium uptake by tumors, leading to unsatisfactory therapeutic outcomes. In the present study, calcium carbonate nanoshell mineralized ferric polydopamine nanoparticles (Fe-PDA@CaCO3 NPs) were prepared for achieving Ca2+-overload-mediated tumor therapy. Upon entering the tumor site, the pH-responsive CaCO3 layer, acting as a "Ca2+ storage pool", rapidly degraded and released high quantities of free Ca2+ within the weakly acidic environment. The Fe-PDA core, with its excellent photothermal conversion properties, could significantly increase the temperature upon exposure to near-infrared (NIR) light irradiation, thereby activating the TRPV1 channel and leading to a large influx of released Ca2+ into the cytoplasm. Furthermore, the exposed Fe-PDA core could react with the tumor-overexpressed hydrogen peroxide (H2O2) to efficiently produce hydroxyl radicals (•OH), significantly increasing intracellular reactive oxygen species (ROS) levels and thus inhibiting the activity of the Ca2+ efflux pump, resulting in a high intracellular Ca2+ concentration. Ultimately, the increase in calcium/ROS levels could disrupt mitochondrial homeostasis and activate the apoptosis pathway. The current work presents a promising approach for tumor therapy using photothermal-enhanced calcium-overload-mediated ion interference therapy and chemodynamic therapy.

Detecting the interaction between microparticles and biomass in biological wastewater treatment process with Deep Learning method.

Investigating the interaction between influent particles and biomass is basic and important for the biological wastewater treatment. The micro-level methods allow for this, such as the microscope image analysis method with the conventional ImageJ processing software. However, these methods are cost and time-consuming, and require a large amount of work on manual parameter tuning. To deal with this problem, we proposed a deep learning (DL) method to automatically detect and quantify microparticles free from biomass and entrapped in biomass from microscope images. Firstly, we introduced a "TU Delft-Interaction between Particles and Biomass" dataset containing labeled microscope images. Then, we built DL models using this dataset with seven state-of-the-art model architectures for a instance segmentation task, such as Mask R-CNN, Cascade Mask R-CNN, Yolact and YOLOv8. The results show that the Cascade Mask R-CNN with ResNet50 backbone achieves promising detection accuracy, with a mAP50box and mAP50mask of 90.6 % on the test set. Then, we benchmarked our results against the conventional ImageJ processing method. The results show that the DL method significantly outperforms the ImageJ processing method in terms of detection accuracy and processing cost. The DL method shows a 13.8 % improvement in micro-average precision, and a 21.7 % improvement in micro-average recall, compared to the ImageJ method. Moreover, the DL method can process 70 images within 1 min, while the ImageJ method costs at least 6 h. The promising performance of our method allows it to offer a potential alternative to examine the interaction between microparticles and biomass in biological wastewater treatment process in an affordable manner. This approach offers more useful insights into the treatment process, enabling further reveal the microparticles transfer in biological treatment systems.

Proteomics analysis of immune response-related proteins in Guillain-Barré Syndrome (GBS) and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP).

The objective is to characterize differentially expressed proteins (DEPs) in Guillain-Barré Syndrome (GBS) and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) through high-throughput analysis. Sera from 11 healthy controls (HCs), 21 GBS and 19 CIDP patients were subjected to Olink Proteomics Analysis. In the comparison between CIDP and GBS groups, up-regulation of ITM2A and down-regulation of NTF4 were observed. Comparing GBS with HCs revealed 18 up-regulated and 4 down-regulated proteins. Comparing CIDP with the HCs identified 15 up-regulated and 4 down-regulated proteins. Additionally, the correlation between clinical characteristics and DEPs were uncovered. In conclusion, the DEPs have significant potential to advance our understanding of the pathogenesis in these debilitating neurological disorders.