Blockade of the checkpoint receptor TIGIT prevents NK cell exhaustion and elicits potent anti-tumor immunity.

Checkpoint blockade enhances effector T cell function and has elicited long-term remission in a subset of patients with a broad spectrum of cancers. TIGIT is a checkpoint receptor thought to be involved in mediating T cell exhaustion in tumors; however, the relevance of TIGIT to the dysfunction of natural killer (NK) cells remains poorly understood. Here we found that TIGIT, but not the other checkpoint molecules CTLA-4 and PD-1, was associated with NK cell exhaustion in tumor-bearing mice and patients with colon cancer. Blockade of TIGIT prevented NK cell exhaustion and promoted NK cell-dependent tumor immunity in several tumor-bearing mouse models. Furthermore, blockade of TIGIT resulted in potent tumor-specific T cell immunity in an NK cell-dependent manner, enhanced therapy with antibody to the PD-1 ligand PD-L1 and sustained memory immunity in tumor re-challenge models. This work demonstrates that TIGIT constitutes a previously unappreciated checkpoint in NK cells and that targeting TIGIT alone or in combination with other checkpoint receptors is a promising anti-cancer therapeutic strategy.

NFS1 inhibits ferroptosis in gastric cancer by regulating the STAT3 pathway.

Cysteine desulfurase (NFS1) is highly expressed in a variety of tumors, which is closely related to ferroptosis of tumor cells and affects prognosis. The relationship between NFS1 and the development of gastric cancer (GC) remains unknown. Here we showed that NFS1 expression was significantly higher in GC tissues compared to adjacent normal tissues. Patients with high expression of NFS1 in GC tissues had a lower overall survival rate than those with low expression. NFS1 was highly expressed in cultured GC cells compared to normal gastric cells. Knockdown of NFS1 expression reduced the viability, migration and invasion of GC cells. In cultured GC cells, NFS1 deficiency promoted ferroptosis. Mechanistically, NFS1 inhibited ferroptosis by upregulating the signal transduction and activator of transcription 3 (STAT3) signaling pathway in cultured GC cells. NFS1 knockdown using siRNA inhibited the STAT3 pathway, reduced the expression of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11), and elevated intracellular levels of reactive oxygen species (ROS), ferrous ion (Fe2+), and malondialdehyde (MDA) in cultured GC cells. A specific STAT3 activator significantly reversed the inhibitory effect of NFS1 deficiency on ferroptosis in cultured GC cells. These in vitro results were further confirmed by experiments in vivo using a mouse xenograft tumor model. Collectively, THESE RESULTS INDICATE THAT NFS1 is overexpressed in human GC tissues and correlated with prognosis. NFS1 inhibits ferroptosis by activating the STAT3 pathway in GC cells. These results suggest that NFS1 may be a potential prognostic biomarker and therapeutic target to treat GC.

RORα inhibits gastric cancer proliferation through attenuating G6PD and PFKFB3 induced glycolytic activity.

BACKGROUND: Glycolysis is critical for harvesting abundant energy to maintain the tumor microenvironment in malignant tumors. Retinoic acid-related orphan receptor α (RORα) has been identified as a circadian gene. However, the association of glycolysis with RORα in regulating gastric cancer (GC) proliferation remains poorly understood. METHODS: Bioinformatic analysis and retrospective study were utilized to explore the role of RORα in cell cycle and glycolysis in GC. The mechanisms were performed in vitro and in vivo including colony formation, Cell Counting Kit-8 (CCK-8), Epithelial- mesenchymal transition (EMT) and subcutaneous tumors of mice model assays. The key drives between RORα and glycolysis were verified through western blot and chip assays. Moreover, we constructed models of high proliferation and high glucose environments to verify a negative feedback and chemoresistance through a series of functional experiments in vitro and in vivo. RESULTS: RORα was found to be involved in the cell cycle and glycolysis through a gene set enrichment analysis (GSEA) algorithm. GC patients with low RORα expression were not only associated with high circulating tumor cells (CTC) and high vascular endothelial growth factor (VEGF) levels. However, it also presented a positive correlation with the standard uptake value (SUV) level. Moreover, the SUVmax levels showed a positive linear relation with CTC and VEGF levels. In addition, RORα expression levels were associated with glucose 6 phosphate dehydrogenase (G6PD) and phosphofructokinase-2/fructose-2,6-bisphosphatase (PFKFB3) expression levels, and GC patients with low RORα and high G6PD or low RORα and high PFKFB3 expression patterns had poorest disease-free survival (DFS). Functionally, RORα deletion promoted GC proliferation and drove glycolysis in vitro and in vivo. These phenomena were reversed by the RORα activator SR1078. Moreover, RORα deletion promoted GC proliferation through attenuating G6PD and PFKFB3 induced glycolytic activity in vitro and in vivo. Mechanistically, RORα was recruited to the G6PD and PFKFB3 promoters to modulate their transcription. Next, high proliferation and high glucose inhibited RORα expression, which indicated that negative feedback exists in GC. Moreover, RORα deletion improved fluorouracil chemoresistance through inhibition of glucose uptake. CONCLUSION: RORα might be a novel biomarker and therapeutic target for GC through attenuating glycolysis.

Young osteocyte-derived extracellular vesicles facilitate osteogenesis by transferring tropomyosin-1.

BACKGROUND: Bone marrow mesenchymal stem cells (BMSCs) can undergo inadequate osteogenesis or excessive adipogenesis as they age due to changes in the bone microenvironment, ultimately resulting in decreased bone density and elevated risk of fractures in senile osteoporosis. This study aims to investigate the effects of osteocyte senescence on the bone microenvironment and its influence on BMSCs during aging. RESULTS: Primary osteocytes were isolated from 2-month-old and 16-month-old mice to obtain young osteocyte-derived extracellular vesicles (YO-EVs) and senescent osteocyte-derived EVs (SO-EVs), respectively. YO-EVs were found to significantly increase alkaline phosphatase activity, mineralization deposition, and the expression of osteogenesis-related genes in BMSCs, while SO-EVs promoted BMSC adipogenesis. Neither YO-EVs nor SO-EVs exerted an effect on the osteoclastogenesis of primary macrophages/monocytes. Our constructed transgenic mice, designed to trace osteocyte-derived EV distribution, revealed abundant osteocyte-derived EVs embedded in the bone matrix. Moreover, mature osteoclasts were found to release osteocyte-derived EVs from bone slices, playing a pivotal role in regulating the functions of the surrounding culture medium. Following intravenous injection into young and elderly mouse models, YO-EVs demonstrated a significant enhancement of bone mass and biomechanical strength compared to SO-EVs. Immunostaining of bone sections revealed that YO-EV treatment augmented the number of osteoblasts on the bone surface, while SO-EV treatment promoted adipocyte formation in the bone marrow. Proteomics analysis of YO-EVs and SO-EVs showed that tropomyosin-1 (TPM1) was enriched in YO-EVs, which increased the matrix stiffness of BMSCs, consequently promoting osteogenesis. Specifically, the siRNA-mediated depletion of Tpm1 eliminated pro-osteogenic activity of YO-EVs both in vitro and in vivo. CONCLUSIONS: Our findings suggested that YO-EVs played a crucial role in maintaining the balance between bone resorption and formation, and their pro-osteogenic activity declining with aging. Therefore, YO-EVs and the delivered TPM1 hold potential as therapeutic targets for senile osteoporosis.

Microcystis viridis NIES-102 Cyanobacteria Lectin (MVL) Interacts with SARS-CoV-2 Spike Protein Receptor Binding Domains (RBDs) via Protein-Protein Interaction.

The emergence of coronavirus disease 2019 (COVID-19) posed a major challenge to healthcare systems worldwide, especially as mutations in the culprit Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) complicated the development of vaccines and antiviral drugs. Therefore, the search for natural products with broad anti-SARS-CoV-2 capabilities is an important option for the prevention and treatment of similar infectious diseases. Lectins, which are widely recognized as antiviral agents, could contribute to the development of anti-SARS-CoV-2 drugs. This study evaluated the binding affinity of six lectins (including the cyanobacterial lectin from Microcystis viridis NIES-102 (MVL), and Jacalin, a lectin from the breadfruit, Artocarpus altilis) to the receptor binding domain (RBD) of the spike protein on the original (wild) SARS-CoV-2 and three of its mutants: Alpha, Delta, and Omicron. MVL and Jacalin showed distinct binding affinity to the RBDs of the four SARS-CoV-2 strains. The remaining four lectins (DB1, ConA, PHA-M and CSL3) showed no such binding affinity. Although the glycan specificities of MVL and Jacalin were different, they showed the same affinity for the spike protein RBDs of the four SARS-CoV-2 strains, in the order of effectiveness Alpha > Delta > original > Omicron. The verification of glycan-specific inhibition revealed that both lectins bind to RBDs by glycan-specific recognition, but, in addition, MVL binds to RBDs through protein-protein interactions.

Incidence and mortality trends in gastric cancer in the United States, 1992-2019.

Our study aimed to estimate the epidemiological trends of gastric cancer in the United States from 1992 to 2019. This population-based study used the US Surveillance, Epidemiology and End Results-12 database as a fundamental cohort to analyze gastric cancer incidence, incidence-based mortality (IBM), overall survival (OS) and cancer-specific survival (CSS) probabilities from 1992 to 2019. The Global Burden of Disease study (1990-2018) was used as a likely validation cohort. Age-period-cohort analyses were performed to explore the underlying causes of trend changes. We found that the incidence rate of gastric cancer decreased from 1992 to 2019. IBM also decreased significantly from 1997 to 2019. The 3-year OS and CSS of gastric cancer increased from 22.3% to 28.7% and 25.7% to 33.5%, respectively. However, the proportion of distant gastric cancer cases had unexpectedly increased rapidly from 33.1% in 1992 to 44.7% in 2019. Age-period-cohort modeling found that the incidence and IBM rates remained stable in the groups aged below 50 years, while that in all age groups older than 50 years showed a significant downward trend. High incidence and mortality risks were observed in the younger birth cohorts (birth year after 1990). To conclude, we observed a decline in incidence and mortality rates of gastric cancer in the United States in the past decades. We determined that progression of primary and tertiary preventive measures is the main reason for the reduction in the disease burden of gastric cancer. However, secondary preventive measures for gastric cancer still need to be strengthened.

Comprehensive analysis of the biological function and immune infiltration of SLC38A2 in gastric cancer.

BACKGROUND: Solute carrier family 38 member 2 (SLC38A2) has previously been reported to participate in carcinogenesis. However, its expression and function in gastric cancer (GC) remain unclear. The present study aimed to investigate the role of SLC38A2 in GC. METHODS: The prognostic value and expression of SLC38A2 in GC was analyzed by combining bioinformatics and experimental analyses. Colony formation, Cell Counting Kit-8, wound healing, Transwell and tumor formation assays were performed to assess the biological function of SLC38A2. The cBioPortal, GeneMANIA and LinkedOmics databases were mined to determine the underlying regulatory mechanisms of SLC38A2. The role of SLC38A2 in tumor immune infiltration was explored using the TIMER database. RESULTS: Our results demonstrated that SLC38A2 was upregulated and was correlated with a poor prognosis in GC patients. SLC38A2 downregulation significantly inhibited the proliferation, invasion and migration of GC cells. Abnormal genetic alteration and epigenetic regulation may contribute to the upregulation of SLC38A2 expression levels in GC. The results of enrichment analysis demonstrated that SLC38A2 was associated with 'hippo signaling' and 'ubiquitinyl hydrolase activity'. The results also indicated that SLC38A2 may be a key factor in GC immune infiltration and M2 macrophage polarization. CONCLUSION: Overall, these data identified that SLC38A2 may serve as a potential prognostic biomarker and therapeutic target in GC.

Taming transposable elements in livestock and poultry: a review of their roles and applications.

Livestock and poultry play a significant role in human nutrition by converting agricultural by-products into high-quality proteins. To meet the growing demand for safe animal protein, genetic improvement of livestock must be done sustainably while minimizing negative environmental impacts. Transposable elements (TE) are important components of livestock and poultry genomes, contributing to their genetic diversity, chromatin states, gene regulatory networks, and complex traits of economic value. However, compared to other species, research on TE in livestock and poultry is still in its early stages. In this review, we analyze 72 studies published in the past 20 years, summarize the TE composition in livestock and poultry genomes, and focus on their potential roles in functional genomics. We also discuss bioinformatic tools and strategies for integrating multi-omics data with TE, and explore future directions, feasibility, and challenges of TE research in livestock and poultry. In addition, we suggest strategies to apply TE in basic biological research and animal breeding. Our goal is to provide a new perspective on the importance of TE in livestock and poultry genomes.

Cloning, expression, and characterization of two pectate lyases isolated from the sheep rumen microbiome.

Pectate lyases (Pels) have a vital function in degradation of the primary plant cell wall and the middle lamella and have been widely used in the industry. In this study, two pectate lyase genes, IDSPel16 and IDSPel17, were cloned from a sheep rumen microbiome. The recombinant enzymes were expressed in Escherichia coli and functionally characterized. Both IDSPel16 and IDSPel17 proteins had an optimal temperature of 60 ℃, and an optimal pH of 10.0. IDSPel16 was relatively stable below 60 °C, maintaining 77.51% residual activity after preincubation at 60 °C for 1 h, whereas IDSPel17 denatured rapidly at 60 °C. IDSPel16 was relatively stable between pH 6.0 and 12.0, after pretreatment for 1 h, retaining over 60% residual activity. IDSPel16 had high activity towards polygalacturonic acid, with a Vmax of 942.90 ± 68.11, whereas IDSPel17 had a Vmax of only 28.19 ± 2.23 µmol/min/mg. Reaction product analyses revealed that IDSPel17 liberated unsaturated digalacturonate (uG2) and unsaturated trigalacturonate (uG3) from the substrate, indicating a typical endo-acting pectate lyase (EC 4.2.2.2). In contrast, IDSPel16 initially generated unsaturated oligogalacturonic acids, then converted these intermediates into uG2 and unsaturated galacturonic acid (uG1) as end products, a unique depolymerization profile among Pels. To the best of our knowledge, the IDSPel16 discovered with both endo-Pel (EC 4.2.2.2) and exo-Pel (EC 4.2.2.9) activities. These two pectate lyases, particularly the relatively thermo- and pH-stable IDSPel16, will be of interest for potential application in the textile, food, and feed industries. KEY POINTS: • Two novel pectate lyase genes, IDSPel16 and IDSPel17, were isolated and characterized from the sheep rumen microbiome. • Both IDSPel16 and IDSPel17 are alkaline pectate lyases, releasing unsaturated digalacturonate and unsaturated trigalacturonate from polygalacturonic acid. • IDSPel16, a bifunctional pectate lyase with endo-Pel (EC 4.2.2.2) and exo-Pel (EC 4.2.2.9) activities, could be a potential candidate for industrial application.

Donepezil attenuates inflammation and apoptosis in ulcerative colitis via regulating LRP1/AMPK/NF-κB signaling.

This article focuses on the specific effects and mechanisms of donepezil (DNPZ) hydrochloride on inflammation and apoptosis in ulcerative colitis (UC). In vivo and in vitro models of UC were established using dextran sodium sulfate (DSS)-induced mice and NCM460 cells, respectively. Following oral administration of DNPZ, body weight, disease activity index (DAI) scores and colon lengths of mice were recorded. Histopathological damage was detected employing hematoxylin and eosin (H&E) staining. Inflammatory factors were tested using enzyme-linked immunosorbent assay and quantitative reverse transcription polymerase chain reaction, respectively. Apoptosis was estimated utilizing terminal deoxynucleotidyl transferase dUTP nick-end labeling and western blot. Low-density lipoprotein receptor-related protein 1 (LRP1)/AMP activated protein kinase (AMPK)/nuclear factor-κB (NF- κB) signaling proteins were detected utilizing western blot. NCM460 cell viability was assessed by cell counting kit (CCK)-8. We found that DNPZ partially restored body weight, reduced DAI scores and attenuated intestinal pathological damage in DSS-induced mice. Additionally, inflammatory factors decreased significantly after DNPZ treatment, accompanied by reduced apoptosis level. Phosphorylation (p)-AMPK increased and p-p65 decreased after DNPZ treatment, whereas LRP1 knockdown showed the opposite effect. Moreover, DNPZ treatment greatly restored NCM460 cell viability after DSS stimulation. DNPZ attenuated DSS-induced inflammation and apoptosis in NCM460 cells, which was reversed by LRP1 knockdown. In summary, DNPZ hydrochloride attenuates inflammation and apoptosis in UC via LRP1/AMPK/NF-κB signaling.

Comparison of the clinical and prognosis risk factors between endoscopic resection and radical gastrectomy for early-stage gastric cancer.

AIM: This study aimed to explore the efficacy and safety of endoscopic submucosal dissection/endoscopic mucosal resection (ESD/EMR), laparoscopic-assisted radical gastrectomy (LARG), and open radical gastrectomy (ORG) in early-stage gastric cancer. METHODS: A total of 417 patients with early-stage gastric cancer who were admitted in two hospitals from January 1, 2014 to July 31, 2017 were selected; the patients were divided into the ESD/EMR group (139 cases), LARG group (108 cases), and ORG group (170 cases) according to the operation methods used. The baseline data, economic cost of health, oncologic characteristics, postoperative complications, 5-year overall survival and disease-free survival, and risk factors of death were compared and analyzed. RESULTS: No significant difference was observed in the baseline data among the three patient groups (P > 0.05). The total hospitalization days, operation time, postoperative fluid intake time, hospitalization expenses, and proportion of antibiotic use rate in the ESD/EMR group were lesser than those in other groups (P < 0.05). The LARG group has a longer operation time and higher hospitalization expenses compared with the ORG group (P < 0.05), but the total hospitalization days, postoperative fluid intake time, proportion of antibiotic use, and lung infection status were consistent. The ESD/EMR group had a lower incidence of incision site infection and postoperative abdominal distension compared with that of the surgery groups (P < 0.05). Five patients required radical surgery after undergoing ESD/EMR (The patients had residual tissue margin cancer), while none of the patients had switched to ORG during LARG. Surgery had advantages over ESD/EMR in terms of lymph node dissection (P < 0.05). No significant differences were observed in the postoperative complications such as upper gastrointestinal bleeding, perforation, incision hernia, reoperation and recurrence (P > 0.05). The 5-year postoperative survival rates of patients in the three groups were 94.2% (ESD/EMR), 93.5% (LARG), and 94.7% (ORG), respectively, with no significant differences (P > 0.05). The binary logistics multivariate analysis showed that the tumor size, invasion depth, vascular invasion, and differentiated degree were risk factors for death in patients with gastric cancer. CONCLUSIONS: No significant difference was observed between ESD/EMR and radical surgery. However, standardized criteria for excluding metastatic lymph nodes should be established to promote ESD/EMR.

Harmine targets inhibitor of DNA binding-2 and activator protein-1 to promote preosteoclast PDGF-BB production.

Osteoporosis is one of the most common metabolic bone diseases affecting millions of people. We previously found that harmine prevents bone loss in ovariectomized mice via increasing preosteoclast platelet-derived growth factor-BB (PDGF-BB) production and type H vessel formation. However, the molecular mechanisms by which harmine promotes preosteoclast PDGF-BB generation are still unclear. In this study, we revealed that inhibitor of DNA binding-2 (Id2) and activator protein-1 (AP-1) were important factors implicated in harmine-enhanced preosteoclast PDGF-BB production. Exposure of RANKL-induced Primary bone marrow macrophages (BMMs), isolated from tibiae and femora of mice, to harmine increased the protein levels of Id2 and AP-1. Knockdown of Id2 by Id2-siRNA reduced the number of preosteoclasts as well as secretion of PDGF-BB in RANKL-stimulated BMMs administrated with harmine. Inhibition of c-Fos or c-Jun (components of AP-1) both reversed the stimulatory effect of harmine on preosteoclast PDGF-BB production. Dual-luciferase reporter assay analyses determined that PDGF-BB was the direct target of AP-1 which was up-regulated by harmine treatment. In conclusion, our data demonstrated a novel mechanism involving in the production of PDGF-BB increased by harmine, which may provide potential therapeutic targets for bone loss diseases.

miR-140-3p is involved in the occurrence and metastasis of gastric cancer by regulating the stability of FAM83B.

BACKGROUND: Gastric cancer (GC) is a malignant tumor and microRNAs (miRNAs) are closely connected to GC development. The purpose of this study is to investigate the effect of miR-140-3p on the occurrence and metastasis of GC. METHODS: We detected miR-140-3p expression in GC cells and tissues. The correlation between miR-140-3p and prognosis and clinicopathological features in GC was analyzed. The role of miR-140-3p in GC cell migration, invasion, and proliferation was analyzed. The model of tumor transplantation and metastasis in nude mice was established, and the effect of miR-140-3p on the development and metastasis of GC was assessed. The relation between miR-140-3p and SNHG12 and the relations among HuR, SNHG12, and FAM83B were analyzed. RESULTS: miR-140-3p was poorly expressed in GC. GC patients with low miR-140-3p expression had a poor prognosis and unfavorable clinicopathologic features. Overexpression of miR-140-3p inhibited GC cell migration, invasion, and proliferation, and inhibited the development and metastasis of GC. miR-140-3p directly bound to SNHG12 in GC tissues and downregulated SNHG12 expression. SNHG12 overexpression induced HuR nuclear transportation. HuR can bind to FAM83B and up-regulate the mRNA level of FAM83B. Overexpression of SNHG12 or FAM83B reduced the inhibition of overexpression of miR-140-3p on GC. CONCLUSION: miR-140-3p directly bound to SNHG12 in GC and down-regulated the expression of SNHG12, reduced the binding of SNHG12 and HuR, thus inhibiting the nuclear transportation of HuR and the binding of HuR and FAM83B, and reducing the transcription of FAM83B, and finally inhibiting the growth and metastasis of GC.

Regulation of ARHGAP19 in the endometrial epithelium: a possible role in the establishment of uterine receptivity.

BACKGROUND: The establishment of uterine receptivity is essential for embryo implantation initiation and involves a significant morphological transformation in the endometrial epithelial cells (EECs). The remodeling of junctional complexes and membrane-associated cytoskeleton is crucial for epithelial transformation. However, little is known about how this process is regulated in EECs during the receptive phase. ARHGAP19 is a Rho GTPase-activating protein that participates in various cytoskeletal-related events, including epithelial morphogenesis. Here, we investigated the role of ARHGAP19 in endometrial epithelial transformation during the establishment of uterine receptivity. The upstream regulator of ARHGAP19 was also investigated. METHODS: ARHGAP19 expression was examined in mouse uteri during early pregnancy and in human EEC lines. The role of ARHGAP19 was investigated by manipulating its expression in EECs. The effect of ARHGAP19 on junctional proteins in EECs was examined by western blotting and immunofluorescence. The effect of ARHGAP19 on microvilli was examined by scanning electron microscopy. The upstream microRNA (miRNA) was predicted using online databases and validated by the dual-luciferase assay. The in vivo and in vitro effect of miRNA on endogenous ARHGAP19 was examined by uterine injection of miRNA agomirs and transfection of miRNA mimics or inhibitors. RESULTS: ARHGAP19 was upregulated in the receptive mouse uteri and human EECs. Overexpression of ARHGAP19 in non-receptive EECs downregulated the expression of junctional proteins and resulted in their redistribution. Meanwhile, upregulating ARHGAP19 reorganized the cytoskeletal structure of EECs, leading to a decline of microvilli and changes in cell configuration. These changes weakened epithelial cell polarity and promoted the transition of non-receptive EECs to a receptive phenotype. Besides, miR-192-5p, a miRNA that plays a key role in maintaining epithelial properties, was validated as an upstream regulator of ARHGAP19. CONCLUSION: These results suggested that ARHGAP19 may contribute to the transition of EECs from a non-receptive to a receptive state by regulating the remodeling of junctional proteins and membrane-associated cytoskeleton.

Online Color Classification System of Solid Wood Flooring Based on Characteristic Features.

Solid wood flooring has good esthetic properties and is an excellent material for interior decoration. To meet the artistic effects of specific interior decoration requirements, the color of solid wood flooring needs to be coordinated. Thus, the color of the produced solid wood flooring needs to be sorted to meet the individual needs of customers. In this work, machine vision, deep learning methods, and ensemble learning methods are introduced to reduce the cost of manual sorting and improve production efficiency. The color CCD camera was used to collect 108 solid wood floors of three color grades provided by the company and obtained 108 18,000 × 2048 pixel wood images. A total of 432 images were obtained after data expansion. Deep learning methods, such as VGG16, DenseNet121, and XGBoost, were compared. After using XGBoost to filter the features, the accuracy of solid wood flooring color classification was 97.22%, the training model time was 5.27 s, the average test time for each picture was 51 ms, and a good result was achieved.

A Sawn Timber Tree Species Recognition Method Based on AM-SPPResNet.

Sawn timber is an important component material in furniture manufacturing, decoration, construction and other industries. The mechanical properties, surface colors, textures, use and other properties of sawn timber possesed by different tree species are different. In order to meet the needs of reasonable timber use and product quality of sawn timber products, sawn timber must be identified according to tree species to ensure the best use of materials. In this study, an optimized convolution neural network was proposed to process sawn timber image data to identify the tree species of the sawn timber. The spatial pyramid pooling and attention mechanism were used to improve the convolution layer of ResNet101 to extract the feature vector of sawn timber images. The optimized ResNet (simply called "AM-SPPResNet") was used to identify the sawn timber image, and the basic recognition model was obtained. Then, the weight parameters of the feature extraction layer of the basic model were frozen, the full connection layer was removed, and using support vector machine (SVM) and XGBoost classifier which were commonly used in machine learning to train and learn the 21 × 1024 dimension feature vectors extracted by feature extraction layer. Through a number of comparative experiments, it is found that the prediction model using linear function as the kernel function of support vector machine learning the feature vectors extracted from the improved convolution layer performed best, and the F1 score and overall accuracy of all kinds of samples were above 99%. Compared with the traditional methods, the accuracy was improved by up to 12%.

Protecting healthcare workers from SARS-CoV-2 and other infections.

Coronavirus disease 2019 (COVID-19) has had a tremendous impact in China and abroad since its onset in December 2019 and poses a major threat to human health. Healthcare workers (HCWs) are at the forefront of the response to outbreaks. This study reviewed literature data and found that HCWs were at high risk of infection during the COVID-19 pandemic, especially at the early stage of the epidemic, and many factors greatly affected their occupational safety. Although SARS-CoV-2 transmission was controlled in China, the Chinese experience can help protect HCWs from COVID-19 and other respiratory diseases.

H-type blood vessels participate in alveolar bone remodeling during murine tooth extraction healing.

OBJECTIVES: We aimed to investigate whether skeletal-specific H-type blood vessels exist in alveolar bone and how they function in alveolar bone remodeling. MATERIALS AND METHODS: H-type vessels with high expression of CD31 and Endomucin (CD31hi Emcnhi ) were immunostained in alveolar bone. Abundance and age-related changes in CD31hi Emcnhi endothelial cells (H-ECs) were detected by flow cytometry. Osteoprogenitors association with H-type vessels and bone mass were detected in tooth extraction model of alveolar bone remodeling by immunohistofluorescence and micro-CT, respectively. Transcription and expression of H-EC feature genes during in vitro Notch inhibition were measured by RT-qPCR and immunocytofluorescence. RESULTS: We verified that H-type vessels existed in alveolar bone, the abundance of which was highest at infancy age, then decreased but maintained a constant level during aging. In tooth extraction model, H-ECs significantly increased with concomitant perivascular accumulation of Runx2+ osteoprogenitors and gradually augmentation of bone mass. Notch inhibition of in vitro cultured H-ECs resulted in decreased expression levels of Emcn and hes1, but not Pecam1 or Kdr genes, with decreased expression levels of H-EC numbers, accordingly. CONCLUSIONS: The present study suggests that H-type vessels promote osteogenesis during alveolar bone remodeling. Notch signaling pathway regulates expression of Emcn and possibly determines fate and functions of alveolar H-ECs.

Detecting Defects on Solid Wood Panels Based on an Improved SSD Algorithm.

Wood is widely used in construction, the home, and art applications all over the world because of its good mechanical properties and aesthetic value. However, because the growth and preservation of wood are greatly affected by the environment, it often contains different types of defects that affect its performance and ornamental value. To solve the issues of high labor costs and low efficiency in the detection of wood defects, we used machine vision and deep learning methods in this work. A color charge-coupled device camera was used to collect the surface images of two types of wood from Akagi and Pinus sylvestris trees. A total of 500 images with a size of 200 × 200 pixels containing wood knots, dead knots, and checking defects were obtained. The transfer learning method was used to apply the single-shot multibox detector (SSD), a target detection algorithm and the DenseNet network was introduced to improve the algorithm. The mean average precision for detecting the three types of defects, live knots, dead knots and checking was 96.1%.

Interleukin-1ß/nuclear factor-κB signaling promotes osteosarcoma cell growth through the microRNA-181b/phosphatase and tensin homolog axis.

So far, microRNA has attracted plenty of interest due to its role in tumorigenesis. Reportedly, miR-181b may be involved in the tumorigenesis of osteosarcoma (OS). In the current study, we attempted to investigate the detailed function and mechanism of miR-181b in OS carcinogenesis. Herein, miR-181a, miR-181b, miR-181c, and miR-181d expressions in OS tissues were higher than that in nontumor tissue samples as examined real-time polymerase chain reaction. Via direct targeting, miR-181b negatively regulated the expression of phosphatase and tensin homolog (PTEN), a well-known tumor suppressor. Furthermore, a small interfering RNA strategy was used to find that interleukin (IL)-1B and nuclear factor-κB (NF-κB) regulate miR-181b and PTEN expression. Consequently, the repression of PTEN by miR-181b promotes OS cell proliferation. In summary, our data support a critical role for NF-κB-dependent upregulation of miR-181b, which further inhibited PTEN expression and promoted the cell proliferation of OS cell lines. The above findings represent a new pathway for the repression of PTEN and the promotion of cell proliferation upon IL-1ß induction.