Left displacement of the third gastric compartment in an alpaca: the first case report in China.

BACKGROUND: Left displacement of the third gastric compartment (LDC3) in alpacas is an extremely rare condition and has not been reported thus far. Therefore, we describe the clinical diagnosis and treatment of LDC3 in an alpaca. CASE PRESENTATION: A 2-year-old brown female alpaca (Vicugna pacos) was presented to evaluate a 3-day history of abdominal distension causing loss of both appetite and thirst, along with oliguria and low to no defecation. Clinical examination, X-ray examination, surgical exploration, and determination of gastric pH (pH ~ 2.35) confirmed that LDC3 resulted in abdominal distension. The gastric wall of the displaced third gastric compartment was incised for the expulsion of pneumatosis, and a medical-grade silicone tube was inserted into the incision to remove the effusion by siphoning. Surgical treatment proved to effectively alleviate the abdominal distension caused by LDC3 without apparent side effects. CONCLUSIONS: To our knowledge, this case is the first known report of LDC3 in an alpaca in China. A similar condition, left displaced abomasum, has previously been described in cattle and sheep.

Degradable Photonic Synaptic Transistors Based on Natural Biomaterials and Carbon Nanotubes.

Artificial synaptic devices have potential for overcoming the bottleneck of von Neumann architecture and building artificial brain-like computers. Up to now, developing synaptic devices by utilizing biocompatible and biodegradable materials in electronic devices has been an interesting research direction due to the requirements of sustainable development. Here, a degradable photonic synaptic device is reported by combining biomaterials chlorophyll-a and single-walled carbon nanotubes (SWCNTs). Several basic synaptic functions, including excitatory postsynaptic current (EPSC), paired pulse facilitation (PPF), transition from short-term memory (STM) to long-term memory (LTM), and learning and forgetting behaviors, are successfully emulated through the chlorophyll-a/SWCNTs synaptic device. Furthermore, decent synaptic behaviors can still be achieved at a low drain voltage of -0.0001 V, which results in quite low energy consumption of 17.5 fJ per pulse. Finally, the degradability of this chlorophyll-a/SWCNTs transistor array is demonstrated, indicating that the device can be environmentally friendly. This work provides a new guide to the development of next-generation green and degradable neuromorphic computing electronics.

Periostin regulates osteogenesis of mesenchymal stem cells from ovariectomized rats through actions on the ILK/Akt/GSK-3ß Axis.

Osteoporosis is a condition of the skeleton that mainly results from estrogen deficiency. Periostin is a matricellular component in bone that is involved in osteoblast differentiation. However, how Periostin promotes osteogenesis remains largely unknown. Here, we isolated bone marrow skeletal stem cells (BMSCs) derived from an ovariectomy (OVX)-induced osteoporosis rat model and the effects of periostin on BMSCs derived from OVX rats (OVX-BMSCs) were assessed. Overexpression of periostin enhanced alkaline phosphatase (ALP) and alizarin red staining in OVX-BMSCs as well as the osteogenic genes OCN, BSP and Runx2. ILK is a downstream effector of signals from the extracellular matrix and participates in bone homeostasis. Overexpression of periostin also increased expression of protein levels for ILK, as well as the downstream targets pAkt and pGSK3ß. Suppression of ILK or Akt partially suppressed the enhancement of osteogenic ability induced by periostin overexpression in OVX-BMSCs. Thus, periostin may promote the osteogenic ability of OVX-BMSCs through actions on the ILK/Akt/GSK3ß axis.

[Network pharmacological analysis and experimental study of Pulsatilla chinensis against inflammatory injury caused by pneumonia in mice infected with influenza virus FM_1].

Network pharmacology and the mouse model of viral pneumonia caused by influenza virus FM_1 were employed to explore the main active components and the mechanism of Pulsatilla chinensis against the inflammatory injury of influenza virus-induced pneumonia. The components and targets of P. chinensis were searched from TCMSP, and the targets associated with influenza virus-induced pneumonia were searched from GeneCards. The common targets between P. chinensis and influenza virus-induced pneumonia were identified with Venn diagram established in Venny 2.1. The herb-component-disease-target(H-C-D-T) network was constructed by Cytoscape 3.7.2. The above data were imported into STRING for PPI network analysis. Gene Ontology(GO) enrichment and KEGG pathway enrichment were performed with DAVID. BALB/cAnN mice were infected with the influenza virus FM_1 by nasal drip to gene-rate the mouse model of pneumonia. Immunohistochemistry was adopted to the expression profiling of inflammatory cytokines in the lung tissues of mice in the blank group, model group, and P. chinensis group 1, 3, 5, and 7 days after infection. The pathological changes of lung and trachea of mice in blank group, model group, and P. chinensis group were observed with light microscope and scanning electron microscope at all the time points. The network pharmacological analysis indicated that 9 compounds of P. chinensis were screened out, with a total of 57 targets, 22 of which were overlapped with those of influenza virus-induced pneumonia. A total of 112 GO terms(P<0.05) were enriched, including 81 terms of biological processes, 11 terms of cell components, and 20 terms of molecular functions. A total of 53 KEGG signaling pathways(P<0.05) were enriched, including TNF signaling pathway, influenza A signaling pathway, NF-κB signaling pathway, MAPK signaling pathway and other signaling pathways related to influenza/inflammation. In the P. chinensis group, the expression of TNF-α and IL-1 in the lung tissue was down-regulated on the 3 rd day after infection, and that of IL-6 in the lung tissue was down-regulated on the 5 th day after infection. Light microscopy and scanning electron microscopy showed that P. chinensis significantly alleviated the pathological damage of lung and trachea compared with the model group. This study reflects the multi-components, multi-targets, and multi-pathways of P. chinensis against influenza virus-induced pneumonia. P. chinensis may reduce the production of proinflammatory cytokines and mediators and block the pro-inflammatory signaling pathways to alleviate viral pneumonia, which provides reference for future research.

Liver X receptor α participates in LPS-induced reduction of triglyceride synthesis in bovine mammary epithelial cells.

Lipopolysaccharides (LPS) could induce milk fat depression via regulating the body and blood fat metabolism. However, it is not completely clear how LPS might regulate triglyceride synthesis in dairy cow mammary epithelial cells (DCMECs). DCMECs were isolated and purified from dairy cow mammary tissue and treated with LPS. The level of triglyceride synthesis, the expression and activity of the liver X receptor α (LXRα), enzymes related to de novo fatty acid synthesis, and the expression of the fatty acid transporters were investigated. We found that LPS decreased the level of triglyceride synthesis via a down-regulation of the transcription, translation, and nuclear translocation level of the LXRα. The results also indicated that the transcription level of the LXRα target genes, sterol regulatory element binding protein 1 (SREBP1), fatty acid synthetase (FAS), acetyl-CoA carboxylase-1 (ACC1), were significantly down-regulated in DCMECs after LPS treatment. Our data may provide new insight into the mechanisms of milk fat depression caused by LPS.

The regulatory mechanism of chilling-induced dormancy transition from endo-dormancy to non-dormancy in Polygonatum kingianum Coll.et Hemsl rhizome bud.

KEY MESSAGE: We identified three dormant stages of Polygonatum kingianum and changes that occurred during dormancy transition in the following aspects including cell wall and hormones, as well as interaction among them. Polygonatum kingianum Coll.et Hemsl (P. kingianum) is an important traditional Chinese medicine, but the mechanism of its rhizome bud dormancy has not yet been studied systematically. In this study, three dormancy phases were induced under controlled conditions, and changes occurring during the transition were examined, focusing on phytohormones and the cell wall. As revealed by HPLC-MS (High Performance Liquid Chromatography-Mass Spectrometry) analysis, the endo- to non-dormancy transition was association with a reduced abscisic acid (ABA)/gibberellin (GA3) ratio, a decreased level of auxin (IAA) and an increased level of trans-zeatin (tZR). Transmission electron microscopy showed that plasmodesmata (PDs) and the cell wall of the bud underwent significant changes between endo- and eco-dormancy. A total of 95,462 differentially expressed genes (DEGs) were identified based on transcriptomics, and clustering and principal component analysis confirmed the different physiological statuses of the three types of bud samples. Changes in the abundance of transcripts associated with IAA, cytokinins (CTKs), GA, ABA, brassinolide (BR), jasmonic acid (JA), ethylene, salicylic acid (SA), PDs and cell wall-loosening factors were analysed during the bud dormancy transition in P. kingianum. Furthermore, nitrilase 4 (NIT4) and tryptophan synthase alpha chain (TSA1), which are related to IAA synthesis, were identified as hub genes of the co-expression network, and strong interactions between hormones and cell wall-related factors were observed. This research will provide a good model for chilling-treated rhizome bud dormancy in P. kingianum and cultivation of this plant.

[Application of numerical taxonomy in study of Dao-di herbs and their producing areas].

As a treasure of traditional Chinese medicine culture,Dao-di herbs are famous for their high quality and good effect.However,traditional characteristics of Dao-di herbs and their producing areas are mostly confined to qualitative description,lacking objective evaluation indicators. Numerical taxonomy,which uses mathematical methods to improve the research of taxonomy from qualitative description to quantitative comprehensive analysis,is objective and accurate,so is widely used in the field of biology and medicine.This paper reviews the concept and main research fields of numerical taxonomy,and summarizes its application status and development prospects in the study of Dao-di herbs and characteristics of production areas,in order to lay the foundation for the objectification and standardization of Dao-di herbs.

Gut microbiota and oral cavity cancer: a two-sample bidirectional Mendelian randomization study.

This study employs a two-sample bidirectional Mendelian randomization (MR) approach to systematically evaluate the causal relationship between gut microbiota and oral cavity cancer (OCC). Objective: To address the challenge in establishing the causal relationship between gut microbiota and OCC, we applied a systematic MR analysis. Methods: Utilizing GWAS data from the MiBioGen consortium (18,340 individuals) and UK Biobank (n = 264,137), we selected instrumental variables and employed MR-Egger, weighted median, IVW, and weighted mode analyses. Heterogeneity and pleiotropy were assessed using Cochran's Q test and MR-Egger intercept test. Results: Our findings indicate, at the order level, Bacteroidales (OR = 0.9990, 95% CI = 0.9980-1.0000, P = 0.046), Burkholderiales (OR = 1.0009, 95% CI = 1.0001-1.0018, P = 0.033), and Victivallales (OR = 0.9979, 95% CI = 0.9962-0.9995, P = 0.037) exhibit causality on OCC in the Weighted median, IVW, and MR-Egger analyses, respectively. At the family level, Alcaligenaceae (OR = 1.0012, 95% CI = 1.0004-1.0019, P = 0.002) and Clostridiaceae1 (OR = 0.9970, 95% CI = 0.9948-0.9992, P = 0.027) show causality on OCC in IVW and MR-Egger analyses. At the genus level, Clostridiumsensustricto1 (IVW, OR = 0.9987, 95% CI = 0.9980-0.9995, P = 0.001; MR-Egger, OR = 0.9978, 95% CI = 0.9962-0.9995, P = 0.035), Desulfovibrio (IVW, OR = 1.0008, 95% CI = 1.0001-1.0015, P = 0.016), Eggerthella (IVW, OR = 0.9995, 95% CI = 0.9990-1.0000, P = 0.048), Eubacterium fissicatena group (IVW, OR = 1.0005, 95% CI = 1.0000-1.0009, P = 0.032), and Holdemanella (IVW, OR = 0.9994, 95% CI = 0.9989-0.9999, P = 0.018) are implicated in causing OCC in related analyses. Conclusion: Our study identifies Burkholderiales order, Alcaligenaceae family, Desulfovibrio genus, and Eubacterium fissicatena group as causally increasing OCC risk. In contrast, Bacteroidales order, Victivallales order, Clostridiaceae1 family, Clostridiumsensustricto1 genus, Eggerthella genus, and Holdemanella genus are causally associated with a decreased OCC risk. However, further investigations are essential to delineate an optimal gut microbiota composition and unravel the underlying mechanisms of specific bacterial taxa in OCC pathophysiology.

Development and Assessment of a Prediction Model for Alzheimer's Disease Diagnosis Based on Thermoregulation-Related Genes.

BACKGROUND: Alzheimer's disease (AD) is a prevalent neurodegenerative condition among the elderly population and the most common form of dementia, however, we lack potent interventions to arrest its inherent pathogenic vectors. Robust evidence indicates thermoregulatory perturbations during and before the onset of symptoms. Therefore, temperature-regulated biomarkers may offer clues to therapeutic targets during the presymptomatic stage. OBJECTIVE: The purpose of this study is to develop and assess a thermoregulation-related gene prediction model for Alzheimer's Disease diagnosis. METHOD: This study aims to utilize microarray bioinformatic analysis to identify the potential biomarkers of AD by analyzing four microarray datasets (GSE48350, GSE5281, GSE122063, and GSE181279) of AD patients. Furthermore, thermoregulation-associated hub genes were identified, and the expression patterns in the brain were explored. In addition, we explored the infiltration of immune cells with thermoregulation-related hub genes. Diagnostic marker validation was then performed at the single-cell level. Finally, the prediction of targeted drugs was performed based on the hub genes. RESULTS: Through the analysis of four datasets pertaining to AD, a total of five genes associated with temperature regulation were identified. Notably, CCK, CXCR4, SLC27A4, and SLC17A6 emerged as diagnostic markers indicative of AD-related brain injury. Furthermore, in the examination of peripheral blood samples from AD patients, SLC27A4 and CXCR4 were identified as pivotal diagnostic indicators. Regrettably, animal experimentation was not pursued to validate the data; rather, an assessment of temperature regulation-related genes was conducted. Future investigations will be undertaken to establish the correlation between these genes and AD pathology. CONCLUSION: Overall, CCK, CXCR4, SLC27A4, and SLC17A6 can be considered pivotal biomarkers for diagnosing the pathogenesis and molecular functions of AD.

Increased TMEM166 Level in Patients with Postoperative Stroke after Carotid Endarterectomy.

Postoperative stroke is a challenging and potentially devastating complication after elective carotid endarterectomy (CEA). We previously demonstrated that transmembrane protein 166 (TMEM166) levels were directly related to neuronal damage after cerebral ischemia-reperfusion injury in rats. In this subsequent clinical study, we aimed to evaluate the prognostic value of TMEM166 in patients suffering from post-CEA strokes. Thirty-five patients undergoing uncomplicated elective CEA and 8 patients who suffered ischemic strokes after CEA were recruited. We evaluated the protein level and expression of TMEM166 in patients diagnosed with postoperative strokes and compared it to those in patients who underwent uncomplicated elective CEA. Blood samples and carotid artery plaques were collected and analyzed. High expressions of TMEM166 were detected by immunofluorescence staining and Western Blot in carotid artery plaques of all patients who underwent CEA. Furthermore, circulating TMEM166 concentrations were statistically higher in post-CEA stroke patients than in patients allocated to the control group. Mean plasma concentrations of inflammatory markers, including interleukin 6 (IL-6) and C-reactive protein (CRP), were also elevated in patients with postoperative strokes. Therefore, based on these findings, we hypothesize that elevated TMEM166 levels, accompanied by a strong inflammatory response, serve as a useful biomarker for risk assessment of postoperative stroke following CEA.

[Preparation of Iron-modified Biochar and Its Application in Arsenic Contaminated Soil Remediation].

Biochar has a range of advantages including large porosity, high specific surface area, and strong adsorption capacity. It has been widely used in environmental pollution remediation, soil improvement, and carbon sequestration and emission reduction. Arsenic (As) is a highly toxic pollutant widely distributed throughout the soil. In typical surface soils, the most common forms of As are arsenite (AsO33-) and arsenate (AsO43-). Since most biochar surfaces are negatively charged, the adsorption efficiency of biochar to arsenic is usually low, and the biochar material needs to be modified to enhance its As adsorption performance. Iron-based materials, such as zero valent iron and iron oxide, are excellent As adsorption materials with wide environmental sources. They can be loaded to biochar to form iron-modified biochar via precipitation, pyrolysis, ball-milling, and micro-biological methods. The combined advantages of the iron-modified biochar will expand the application of biochar materials in environmental remediation. Based on a systematic analysis of the literature on iron-modified biochar in recent years, this study reviewed the common preparation methods of iron-modified biochars; analyzed biochar substrates, iron-modified biochar, and their synergistic mechanisms on As adsorption; and briefly expounded the application status of iron-modified biochar in soil pollution remediation. The prospects of the future research direction of iron-modified biochar were put forward as a reference for the large-scale application of biochar materials in the future.

Sex-Specific Associations between Serum IL-16 Levels and Sarcopenia in Older Adults.

Epidemiological studies of older adults have suggested a differential sex-specific prevalence of sarcopenia, which is a condition characterized by a progressive loss of skeletal muscle mass and function. Recently, we collected serum samples from 80 fully evaluated older adults and identified CXCL12α as a sex-independent serum marker of sarcopenia. Here, we used this serum collection to find potential sex-specific serum markers via the simultaneous quantification of 34 inflammatory cytokines/chemokines. The appendicular skeletal muscle index (ASMI) was used as a decisive criterion for diagnosing sarcopenia. A Pearson correlation analysis revealed a negative correlation between ASMI and serum IL-16 in females only (p = 0.021). Moreover, women with sarcopenia exhibited significantly higher IL-16 (p = 0.025) serum levels than women in a control group. In contrast, males with sarcopenia had lower IL-16 (p = 0.013) levels than males in a control group. The further use of Fisher's exact test identified obesity (p = 0.027) and high serum levels of IL-16 (p = 0.029) as significant risk factors for sarcopenia in females. In male older adults, however, malnutrition (p = 0.028) and low serum levels of IL-16 (p = 0.031) were the most significant risk factors for sarcopenia. The differential sex-specific associations of IL-16 in older adults may contribute to the development of more precise regression models for future research and elucidate the role of IL-16 in the progression of sarcopenic obesity.

Unsaturated Long-Chain Fatty Acids Activate Resident Macrophages and Stem Cells in a Human Skeletal Muscle Tissue Model.

Phenotypically heterogeneous populations of tissue-resident macrophages and stem cells play important roles in the regeneration of the skeletal muscle tissue. Previous studies using animal and cell culture models implied a beneficial effect of fatty acid (FA) species on tissue regeneration. Here, we applied a human experimental model using excised muscle tissues from reconstructive surgeries to study the effects of FAs on resident macrophages and stem cells in the natural environment of human skeletal muscle tissue. Muscle tissue samples from 20 donors were included in this study. The expression of 34 cytokines/chemokines was determined, using multiplex protein analysis. The phenotypes of macrophages and stem cells were determined immunohistochemically. The numbers of CD80+ macrophages correlated with the expression levels of IL-1α, IL-1RA, IL-8, IL-17A, and MCP-1, while the PAX7+ and MyoD+ stem cell counts were positively correlated with the expression level of CXCL12α, a recognized chemoattractant for muscle stem cells. Treatment of additional tissue sections with FAs revealed that CD80+ or MARCO+ macrophages- and PAX7+ or MyoD+ stem cells were simultaneously increased by unsaturated long-chain FAs. Taken together, this is the first experimental demonstration of a coordinated activation of macrophages and stem cells in human skeletal muscle tissue.

Construction of MIL-125-NH2@BiVO4 Composites for Efficient Photocatalytic Dye Degradation.

The design and construction of a photocatalyst with a heterostructure are a feasible and effective way to enhance the catalytic performance. Herein, a specially designed composite based on MIL-125-NH2 and BiVO4 was prepared and used for wastewater treatment. In the hybrid MIL-125-NH2@BiVO4, MIL-125-NH2 was uniformly dispersed on the BiVO4 surface. There is a high affinity between MIL-125-NH2 and BiVO4 due to the lattice defects. Under visible light irradiation, the catalytic activity of the as-prepared composite was evaluated by the degradation of various dyes such as malachite green, crystal violet, methylene blue, and Congo red. Nearly 98.7, 99.1, and 41.0% of the initial MG, MB and Cr(VI) were respectively removed over the optical sample of BVTN-5, demonstrating that the hybrid holds great promise for practical applications. Moreover, the composites can be recycled and reused with good stability after five consecutive cycles. The mechanism was proposed and discussed in detail. This work will shed light on the construction of MOF-based composites for efficient photocatalysis.

In Vitro Model of Human Skeletal Muscle Tissue for the Study of Resident Macrophages and Stem Cells.

Findings from studies of muscle regeneration can significantly contribute to the treatment of age-related loss of skeletal muscle mass, which may predispose older adults to severe morbidities. We established a human experimental model using excised skeletal muscle tissues from reconstructive surgeries in eight older adults. Muscle samples from each participant were preserved immediately or maintained in agarose medium for the following 5, 9, or 11 days. Immunofluorescence analyses of the structural proteins, actin and desmin, confirmed the integrity of muscle fibers over 11 days of maintenance. Similarly, the numbers of CD80-positive M1 and CD163-positive M2 macrophages were stable over 11 days in vitro. However, the numbers of PAX7-positive satellite cells and MYOD-positive myoblasts changed in opposite ways, suggesting that satellite cells partially differentiated in vitro. Further experiments revealed that stimulation with unsaturated fatty acid C18[2]c (linoleic acid) increased resident M1 macrophages and satellite cells specifically. Thus, the use of human skeletal muscle tissue in vitro provides a direct experimental approach to study the regulation of muscle tissue regeneration by macrophages and stem cells and their responses to therapeutic compounds.

Hydrogen sulphide inhibits cardiomyocyte hypertrophy by up-regulating miR-133a.

Hydrogen sulphide (H(2)S) has been shown to play a crucial role in cardiovascular physiology and disease. However, there is no information about the possible role of H(2)S in cardiomyocyte hypertrophy (CH). Our results showed that pretreatment with NaHS, an H(2)S donor, significantly reduced [(3)H]-leucine incorporation, cell surface area, mRNA expression of brain natriuretic peptide (BNP), intracellular reactive oxygen species (ROS), miR-21 and increased atrial natriuretic peptide (ANP) and miR-133a expression in hypertrophic cardiomyocytes. Anti-miR133a inhibitor transfection partly reduced the anti-hypertrophic effect of NaHS. In conclusion, H(2)S is a direct inhibitor of CH; it acts by increasing miR-133a and inhibiting the increase in intracellular ROS.

[Inhibitory effect of hydrogen sulfide on cardiac fibroblast proliferation].

The aim of the present study was to investigate the role of hydrogen sulfide (H(2)S) in the proliferation of neonatal rat cardiac fibroblasts (NRCFs). Proliferation of NRCFs was induced by the presence of fetal bovine serum (FBS) or angiotensin II (Ang II) at various concentrations. The concentration-dependent effect of NaHS (donor of H(2)S) on NRCFs proliferation was examined. NRCFs proliferation was assessed by 5'-bromo-2'-deoxyuridine (BrdU) incorporation method. Reactive oxygen species (ROS) level was measured using the dye probe, 2', 7'-dichlorofluorescein diacetate (DCFH-DA). The results showed that FBS- or Ang II-induced NRCFs proliferations were inhibited with the treatment of relatively high concentrations of NaHS (5 × 10(-5) mol/L, 1 × 10(-4) mol/L), but FBS-induced proliferation was increased by low concentration of NaHS (1 × 10(-5) mol/L). Two or 6 h of Ang II (1 × 10(-7) mol/L) treatment caused an increase of ROS level in NRCFs, while this increase was inhibited with NaHS (1 × 10(-4) mol/L) treatment. These results suggest that H(2)S is an inhibitor of cardiac fibroblast at a certain concentration range. This inhibitory effect may be mediated by a reduction in intracellular ROS production.

Recent Advances in Experimental Burn Models.

Experimental burn models are essential tools for simulating human burn injuries and exploring the consequences of burns or new treatment strategies. Unlike clinical studies, experimental models allow a direct comparison of different aspects of burns under controlled conditions and thereby provide relevant information on the molecular mechanisms of tissue damage and wound healing, as well as potential therapeutic targets. While most comparative burn studies are performed in animal models, a few human or humanized models have been successfully employed to study local events at the injury site. However, the consensus between animal and human studies regarding the cellular and molecular nature of systemic inflammatory response syndrome (SIRS), scarring, and neovascularization is limited. The many interspecies differences prohibit the outcomes of animal model studies from being fully translated into the human system. Thus, the development of more targeted, individualized treatments for burn injuries remains a major challenge in this field. This review focuses on the latest progress in experimental burn models achieved since 2016, and summarizes the outcomes regarding potential methodological improvements, assessments of molecular responses to injury, and therapeutic advances.

Experimental Study of Burn Damage Progression in a Human Composite Tissue Model.

Comparative studies of human tissue damage caused by burns are challenging because precise information regarding the temperature, time, and duration of the exposure is often missing. Animal models cannot be fully translated to the human system due to interspecies differences in cutaneous tissues. We used a human composite tissue model to compare tissue damage caused by thermal burns with different dynamics. Equal subcutaneous/cutaneous composite tissue samples from six donors were first exposed to either preheated steel (100 °C) or a precision flame burner (300 °C) and were then maintained in vitro for seven days. Histological and immunohistochemical analyses revealed that flame burns instantly caused deep and stable damage to the subcutaneous tissue, which stayed constant for seven days. By contrast, contact burns inflicted tissue damage that was initially superficial but then expanded deeper into the adipose tissue. This spatiotemporal expansion of tissue damage was essentially accompanied by macrophage and fibroblast activation, which points towards inflammation resolution and wound healing. Our study suggests that thermal differences in burns directly influence the course of tissue damage, the cellular response and, consequently, the likely dynamics of repair processes days after burn injuries.

Circular RNA circ_0000423 promotes gastric cancer cell proliferation, migration and invasion via the microR-582-3p/Disheveled-Axin domain containing 1 axis.

For humans, gastric cancer (GC) is a common malignancy. Multiple circular RNAs (circRNAs) have been confirmed to be important cancer-promoting or tumor-suppressive factors. The present study discusses the roles and mechanisms of circ_0000423 in GC development. In this study, circ_0000423 expression in GC patient tissue samples and cell lines was detected via quantitative real-time polymerase chain reaction. Disheveled-Axin domain containing 1 (DIXDC1) expression in GC cells was examined via Western blot. Besides, cell counting kit-8 was utilized for detecting GC cell viability. GC cell migration and invasion were examined through Transwell assays. Bioinformatics and dual-luciferase reporter gene assays were employed to verify the regulatory relationships between microRNA-582-3p (miR-582-3p) and circ_0000423 or DIXDC1. In the present study, we demonstrated that circ_0000423 was highly expressed in GC. Circ_0000423 knockdown suppressed GC cell viability, migration and invasion. Moreover, miR-582-3p was confirmed as a direct target of circ_0000423, and an upstream regulator of DIXDC1. MiR-582-3p inhibition or DIXDC1 overexpression could reverse the above-mentioned effects of knocking down circ_0000423 on GC cells. In conclusion, circ_0000423 facilitates GC progression by modulating the miR-582-3p/DIXDC1 axis.