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The decline in the stock of the narrow-barred Spanish mackerel in the Taiwan Strait has sparked interest in conservation efforts. To optimize conservation and restoration efforts, it is crucial to understand their habitat preference in response to changing environments. In this study, ensemble modeling was used to investigate the seasonal distribution patterns of Spanish mackerel. Winter was identified as the most productive season, followed by fall; productivity was the lowest in summer. Five single-algorithm models were developed, and on the basis of their performance, four were selected for inclusion in an ensemble species distribution model. The spatial distribution of Spanish mackerel was primarily along the latitudinal range 23°-25°N in spring and summer. However, in fall and winter, the geographical range increased toward the southern region. The findings of this study will contribute to the understanding of this specific species and the approach used in this study may be applicable to other fisheries stocks also., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Increasing the accuracy and reproducibility of subcortical brain segmentation is advantageous in various related clinical applications. In this study, we derived a segmentation method based on a convolutional neural network (i.e., U-Net) and a large-scale database consisting of 7039 brain T1-weighted MRI data samples. We evaluated the method by using experiments focused on three distinct topics, namely, the necessity of preprocessing steps, cross-institutional and longitudinal reproducibility, and volumetric accuracy. The optimized model, MX_RW-where "MX" is a mix of RW and nonuniform intensity normalization data and "RW" is raw data with basic preprocessing-did not require time-consuming preprocessing steps, such as nonuniform intensity normalization or image registration, for brain MRI before segmentation. Cross-institutional testing revealed that MX_RW (Dice similarity coefficient: 0.809, coefficient of variation: 4.6%, and Pearson's correlation coefficient: 0.979) exhibited a performance comparable with that of FreeSurfer (Dice similarity coefficient: 0.798, coefficient of variation: 5.6%, and Pearson's correlation coefficient: 0.973). The computation time per dataset of MX_RW was generally less than 5 s (even when tested without graphics processing units), which was notably faster than FreeSurfer. Thus, for time-restricted applications, MX_RW represents a competitive alternative to FreeSurfer., (© 2022 John Wiley & Sons Ltd.)

Background: Mitophagy plays essential role in the development and progression of colorectal cancer (CRC). However, the effect of mitophagy-related genes in CRC remains largely unknown., Aim: To develop a mitophagy-related gene signature to predict the survival, immune infiltration and chemotherapy response of CRC patients., Methods: Non-negative matrix factorization was used to cluster CRC patients from Gene Expression Omnibus database (GSE39582, GSE17536, and GSE37892) based on mitophagy-related gene expression. The CIBERSORT method was applied for the evaluation of the relative infiltration levels of immune cell types. The performance signature in predicting chemotherapeutic sensitivity was generated using data from the Genomics of Drug Sensitivity in Cancer database., Results: Three clusters with different clinicopathological features and prognosis were identified. Higher enrichment of activated B cells and CD4 + T cells were observed in cluster III patients with the most favorable prognosis. Next, a risk model based on mitophagy-related genes was developed. Patients in training and validation sets were categorized into low-risk and high-risk subgroups. Low risk patients showed significantly better prognosis, higher enrichment of immune activating cells and greater response to chemotherapy (oxaliplatin, irinotecan, and 5-fluorouracil) compared to high-risk patients. Further experiments identified CXCL3 as novel regulator of cell proliferation and mitophagy., Conclusion: We revealed the biological roles of mitophagy-related genes in the immune infiltration, and its ability to predict patients' prognosis and response to chemotherapy in CRC. These interesting findings would provide new insight into the therapeutic management of CRC patients., Competing Interests: Conflict-of-interest statement: The authors declare that they have no competing interests., (©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.)

Objectives: This study aimed to select patients with cancer-related pain to further analyze the relationship between pain severity, fatigue severity, and quality of life., Methods: A cross-sectional study was conducted. A convenience sampling method was used to select 224 patients with cancer-related pain who were undergoing chemotherapy and met the inclusion criteria in two hospitals of two provinces from May to November 2019. All participants were invited to complete a general information questionnaire, the Brief Fatigue Inventory (BFI), the Numerical Rating Scale (NRS) for pain intensity, and the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30)., Results: In the 24 h before completing the scales, 85 patients (37.9%) had mild pain, 121 (54.0%) had moderate pain, and 18 (8.0%) had severe pain. In addition, 92 (41.1%) patients had mild fatigue, 72 (32.1%) had moderate fatigue, and 60 (26.8%) had severe fatigue. Most patients with mild pain only experienced mild fatigue, and their quality of life was also at a moderate level. Patients with moderate and severe pain mostly had moderate or higher levels of fatigue and a lower quality of life. There was no correlation between fatigue and quality of life in patients with mild pain ( r  = -0.179, P  = 0.104). There was a correlation between fatigue and quality of life in patients with moderate and severe pain ( r  = -0.537, P  < 0.01; r  = -0.509, P  < 0.05)., Conclusions: Patients with moderate and severe pain have more fatigue symptoms and lower quality of life than those with mild pain. Nurses should pay more attention to patients with moderate and severe pain, explore the interaction mechanism between symptoms, and carry out joint symptom intervention to improve the quality of life of patients., Competing Interests: The authors have declared no conflict of interest., (© 2022 The Authors.)

Proper regulation of epigenetic states of chromatin is crucial to achieve tissue-specific gene expression during embryogenesis. The lung-specific gene products, surfactant proteins B (SP-B) and C (SP-C), are synthesized in alveolar epithelial cells and prevent alveolar collapse. Epigenetic regulation of these surfactant proteins, however, remains unknown. Here we report that MCRIP1, a regulator of the CtBP transcriptional co-repressor, promotes the expression of SP-B and SP-C by preventing CtBP-mediated epigenetic gene silencing. Homozygous deficiency of Mcrip1 in mice causes fatal respiratory distress due to abnormal transcriptional repression of these surfactant proteins. We found that MCRIP1 interferes with interactions of CtBP with the lung-enriched transcriptional repressors, Foxp1 and Foxp2, thereby preventing the recruitment of the CtBP co-repressor complex to the SP-B and SP-C promoters and maintaining them in an active chromatin state. Our findings reveal a molecular mechanism by which cells prevent inadvertent gene silencing to ensure tissue-specific gene expression during organogenesis., Competing Interests: Competing interestsThe authors declare no competing financial or non-financial interests.

Fibroblasts are some of the major cells in tumour tissues that influence tumour progression and drug resistance. However, our understanding on fibroblast-mediated tumour malignancy remains incomplete. Munc18-1-interacting protein 3 (Mint3) is known as an activator of hypoxia-inducible factor-1 (HIF-1) even during normoxia in cancer cells, macrophages and fibroblasts. Although Mint3 promotes ATP production via glycolysis by activating HIF-1 in cancer cells and macrophages, the biological role of Mint3-mediated HIF-1 activation in fibroblasts remains unclear. To address this, we examined whether Mint3 in fibroblasts contributes to tumour growth. Mint3 depletion in mouse embryonic fibroblasts (MEFs) decreased tumour growth of co-injected human breast cancer cells, MDA-MB-231 and epidermoid carcinoma A431 cells in mice. In MEFs, Mint3 also promoted cancer cell proliferation in vitro in a cell-cell contact-dependent manner. Mint3-mediated cancer cell proliferation depended on HIF-1, and further gene expression analysis revealed that the cell adhesion molecule, L1 cell adhesion molecule (L1CAM), was induced by Mint3 and HIF-1 in fibroblasts. Mint3-mediated L1CAM expression in fibroblasts stimulated the ERK signalling pathway via integrin α5β1 in cancer cells, and promoted cancer cell proliferation in vitro and tumour growth. In cancer-associated fibroblasts (CAFs), knockdown of MT1-MMP, which promotes Mint3-mediated HIF-1 activation, or Mint3 decreased L1CAM expression. As MEFs, CAFs also promoted cancer cell proliferation in vitro, and tumour growth via Mint3 and L1CAM. In human breast cancer specimens, the number of fibroblasts expressing L1CAM, Mint3 and MT1-MMP was higher in cancer regions than in adjacent benign regions. In addition, more phospho-ERK1/2-positive cancer cells existed in the peripheral region surrounded by the stroma than in the central region of solid breast cancer nest. Thus, Mint3 in fibroblasts might be a good target for cancer therapy by regulating cancer cell-stromal cell communication.

The ERK pathway not only upregulates growth-promoting genes, but also downregulates anti-proliferative and tumor-suppressive genes. In particular, ERK signaling contributes to repression of the E-cadherin gene during epithelial-mesenchymal transition (EMT). The CtBP transcriptional co-repressor is also involved in gene silencing of E-cadherin. However, the functional relationship between ERK signaling and CtBP is unknown. Here, we identified an ERK substrate, designated MCRIP1, which bridges ERK signaling and CtBP-mediated gene silencing. CtBP is recruited to promoter elements of target genes by interacting with the DNA-binding transcriptional repressor ZEB1. We found that MCRIP1 binds to CtBP, thereby competitively inhibiting CtBP-ZEB1 interaction. When phosphorylated by ERK, MCRIP1 dissociates from CtBP, allowing CtBP to interact with ZEB1. In this manner, the CtBP co-repressor complex is recruited to, and silences, the E-cadherin promoter by inducing chromatin modifications. Our findings reveal a molecular mechanism underlying ERK-induced epigenetic gene silencing during EMT and its dysregulation in cancer., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Hypoxia-inducible factor 1 (HIF-1) plays a key role in the cellular adaptation to hypoxia. Although HIF-1 is usually strongly suppressed by posttranslational mechanisms during normoxia, HIF-1 is active and enhances tumorigenicity in malignant tumor cells that express the membrane protease MT1-MMP. The cytoplasmic tail of MT1-MMP, which can bind a HIF-1 suppressor protein called factor inhibiting HIF-1 (FIH-1), promotes inhibition of FIH-1 by Mint3 during normoxia. To explore possible links between HIF-1 activation by MT1-MMP/Mint3 and tumor growth signals, we surveyed a panel of 252 signaling inhibitors. The mTOR inhibitor rapamycin was identified as a possible modulator, and it inhibited the mTOR-dependent phosphorylation of Mint3 that is required for FIH-1 inhibition. A mutant Mint3 protein that cannot be phosphorylated exhibited a reduced ability to inhibit FIH-1 and promoted tumor formation in mice. These data suggest a novel molecular link between the important hub proteins MT1-MMP and mTOR that contributes to tumor malignancy.

Oxygen is a vital requirement for multi-cellular organisms to generate energy and cells have developed multiple compensatory mechanisms to adapt to stressful hypoxic conditions. Such adaptive mechanisms are intricately interconnected with other signaling pathways that regulate cellular functions such as cell growth. However, our understanding of the overall system governing the cellular response to the availability of oxygen remains limited. To identify new genes involved in the response to hypoxic stress, we have performed a genome-wide gene knockdown analysis in human lung carcinoma PC8 cells using an shRNA library carried by a lentiviral vector. The knockdown analysis was performed under both normoxic and hypoxic conditions to identify shRNA sequences enriched or lost in the resulting selected cell populations. Consequently, we identified 56 candidate genes that might contribute to the cellular response to hypoxia. Subsequent individual knockdown of each gene demonstrated that 13 of these have a significant effect upon oxygen-sensitive cell growth. The identification of BCL2L1, which encodes a Bcl-2 family protein that plays a role in cell survival by preventing apoptosis, validates the successful design of our screen. The other selected genes have not previously been directly implicated in the cellular response to hypoxia. Interestingly, hypoxia did not directly enhance the expression of any of the identified genes, suggesting that we have identified a new class of genes that have been missed by conventional gene expression analyses to identify hypoxia response genes. Thus, our genetic screening method using a genome-wide shRNA library and the newly-identified genes represent useful tools to analyze the cellular systems that respond to hypoxic stress.

Objective: To investigate the inhibiting effects of interleukin-10 (IL-10) on the expression of E-selectin and L-selectin in cerebral ischemia-reperfusions., Methods: Seventy-two adult male Sprague-Dawley rats were randomly divided into 4 equal groups, cerebral ischemia-reperfusion (I/R) group undergoing middle cerebral artery occlusion with Longa's thread method, IL-10 group undergoing lateral ventricle injection of IL-10 after the establishment of I/R model, Vehicle group undergoing lateral ventricle injection of normal saline after the establishment of I/R model, and sham operation (Sham) group. Twenty-four hours later the rats were killed with their brains taken out. Immunohistochemistry, RT-PCR and Western blotting were used to detect the mRNA and protein expression of E-selectin and L-selectin., Results: The E-selectin and L-selectin expression levels of the I/R group were significantly up-regulated compared with the Sham group (both P < 0.05). The numbers of E-selectin and L-selectin positive vessels of the IL-10 group were 18.8 +/- 1.9/10 HP fields and 15.8 + 2.4/10 HP fields respectively, both significantly less than those of the vehicle group (24.7 +/- 2.4/10 HP fields and 20.9 + 3.3/10 HP fields respectively, both P < 0.05). The E-selectin and L-selectin gene mRNA expression levels of the IL-10 group were (0.431 +/- 0.029) and (0.318 +/- 0.048) respectively, both significantly lower than those of the Vehicle group [(0.497 +/- 0.019) and (0.433 +/- 0.087) respectively, both P < 0.05]. The E-selectin and L-selectin protein expression levels of the IL-10 group were (0.349 +/- 0.037) and (0.296 +/- 0.035) respectively, both significantly lower than those of the Vehicle group [(0.421 +/- 0.043,) and (0.348 +/- 0.044) respectively, both P < 0.05]., Conclusions: IL-10 suppresses the expression of E-selectin and L-selectin in cerebral ischemia-reperfusion.

Aim: To investigate the effects of adipose-derived stem cell (ADSC) transplantation on the angiogenesis in the brain post focal cerebral ischemia in rats., Methods: 72 male adult Sprague-Dawley rats were randomly divided into 4 groups: sham-operated group, middle cerebral artery occlusion (MCAO) group, vehicle group and MCAO+ADSC-treated group (n=18). A permenant focal cerebral ischemia model was established with the modified Longa's method. ADSC were labeled by DAPI before transplantation. One day after right MCAO, 30 muL of cell suspension containing 1x10(6) cells were injected into the lateral ventricle of MCAO+ADSC-treated group and the same dose of PBS was given to the vehicle group. On D4, D7 and D14 after MCAO, the rats were killed to detect the regeneration of microvessel and the expression of bFGF and VEGF in ischemic region by immunohistochemistry and RT-PCR., Results: A lot of microvessel proliferate in the injured cortex reached peak in 2 weeks. The microvessel density in the brain tissues of rats treated with ADSC was higher than that in MCAO group and vehicle group (P<0.01). The expression of bFGF and VEGF in the brain tissues of MCAO+ADSC-treated group was higher than that in MCAO group and vehicle group on D4, D7 and D14 post MCAO., Conclusion: The transplantation of ADSC can promote the revascularization of cerebral ischemia in rats partly by enhancing bFGF and VEGF synthesis in brain.

Aim: To investigate the effects of bone marrow-derived mesenchymal stem cells (BMSC) transplantation on the recovery of neurological functions and the expression of synaptophysin in focal cerebral infarction in rats., Methods: 72 male adult Sprague-Dawley rats were randomly divided into 4 groups (18 in each group): shamoperated group, middle cerebral artery occlusion (MCAO) roup,vehicle group and MCAO+BMSC-treated group. A permanent focal cerebral ischemia model was established using modified Longa's method. BMSC was labeled by DAPI before the transplantation. One day after right middle cerebral artery occlusion(MCAO), 1 x 10(6) cells were injected into the lateral ventricle of rats in BMSCs-treated group and the same dose of PBS was given to the rats in vehicle group. Before sacrificed and at 4 d, 7 d and 14 d after MCAO, the neurological functions were tested by balance beam, rota-rod and screen prehensile and the synaptophysin was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemical method., Results: DAPI stained positive cells were observed around the cerebral infarcted area in the BMSC-treated group. Compared with the MCAO group and the vehicle group,the neurological functions in BMSC-treated group were better on 7 d and 14 d after MCAO (P<0.05 or P<0.01), and the synaptophysin around the cerebral infarcted area was significantly upregulated on 4 d, 7 d and 14 d after MCAO (all P<0.01)., Conclusion: BMSC transplantation can improve the neurological functions by upregulating the expression of synaptophysin after MCAO in rats.