Pulsed electromagnetic fields shows some potential in alleviating pain after mammaplasty. This systematic review and meta-analysis is conducted to investigate the analgesic efficacy of pulsed electromagnetic fields for pain control after mammaplasty.

Mitochondrial damage in airway epithelial cells plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Sirtuin 3 (Sirt3) is a mitochondrial deacetylase regulating mitochondrial function, but its role in the pathogenesis of COPD is still unknown. The aim of the present study was to investigate the effect of Sirt3 on airway epithelial mitochondria in cigarette smoke-induced COPD. Our present study has shown serious airway inflammation, alveolar space enlargement, and mitochondrial damage of the airway epithelium in COPD rats. Compared to the control rats, Sirt3 protein expression was significantly decreased in the airway epithelium and lung tissue homogenate from COPD rats. In airway epithelial cells (BEAS-2B), cigarette smoke extract (CSE) treatment significantly decreased mRNA and protein expression of Sirt3 and manganese superoxide dismutase (MnSOD), as well as MnSOD activity in a concentration and time-dependent manner. Sirt3 siRNA further significantly intensified the decreases in MnSOD expression and activity and aggravated mitochondrial oxidative stress and cell injury when airway epithelial cells were treated with 7.5% CSE. In contrast, Sirt3 overexpression significantly prevented the decrease of MnSOD expression and activity and improved mitochondrial oxidative stress and cell injury in CSE-treated airway epithelial cells. These data suggest that Sirt3 inhibits airway epithelial mitochondrial oxidative stress possibly through the regulation of MnSOD, thereby contributing to the pathogenesis of COPD.

Diarrhea is considered to be associated with microbial dysbiosis caused by infection of pathogens but poorly understood. We herein characterized the colonic microbiota of diarrheal early-weaning piglets infected with porcine circovirus type 2 (PCV2) and Campylobacter. Campylobacter infection significantly decreased species richness and Shannon diversity index of colonic microbiota together with a significant increase in the proportion of Campylobacter and Enterobacteriaceae, whereas no significant difference on the above indexes was observed in piglets infected with PCV2 compared with healthy piglets. PCV2 and Campylobacter infection could disturb the homeostasis of colonic microbiota through deterioration of ecological network within microbial community, and specially Campylobacter performed as a module hub in ecological networks. The microbial dysbiosis caused metabolic dysfunction and led to a remarkable reduction in production of short chain fatty acids, following by a higher pH level in colon cavity. Campylobacter infection disturbed the function of colonic tract barrier observed in terms of significant lower relative expression of claudin-1, occluding, and zonula occludens protein-1 genes, and PCV2 infection induced intestinal inflammation together with a higher permeability of colon. Generally, these results suggested that PCV2 and Campylobacter infection could induce microbial dysbiosis and metabolic dysfunction, and cause intestinal disorder, all of which finally were associated to contribute to the diarrhea of early-weaning piglets.

MicroRNAs (miRs) are short (ie, 18-26 nucleotide) regulatory elements of messenger RNA translation to amino acids.

Chronic pain often leads to cognitive impairment. Resveratrol (Res), a natural polyphenol existing in Polygonum cuspidatum, has been widely investigated for its antinociceptive, anti-inflammatory, and neuroprotective properties. Our aim was to explore the ameliorating effects of resveratrol on pain-related behaviors and learning and memory deficits induced by cobra venom-induced trigeminal neuralgia (TN). The TN model of rats was established by injecting cobra venom solution beneath the epineurium of the infraorbital nerve. Resveratrol was intragastrically administered at a dose of 40 mg/kg twice daily beginning on postoperative day 15. CREB inhibitor 666-15 was intraperitoneally administered at a dose of 10 mg/kg from POD 35-42 after morning resveratrol treatment. Mechanical allodynia was measured via von Frey filaments. Rat free movement was videotaped and analyzed. Spatial learning and memory were evaluated via the Morris water maze test. Ultrastructures of the hippocampal DG region and infraorbital nerve were observed by transmission electron microscopy. We found that resveratrol alleviated TN-induced allodynia, ameliorated learning and memory deficits, restored the ultrastructure of hippocampal neurons and synapses, repaired the damaged myelin sheath of the infraorbital nerve, and activated the CREB/BDNF pathway in the hippocampus of TN rats. CREB inhibitor administration suppressed the resveratrol-rescued abnormal hippocampal ultrastructural changes and aggravated spatial learning and memory impairment by inhibiting CREB/BDNF pathway activation in the hippocampus. Our findings indicated that resveratrol alleviated pain and improved cognitive deficits, probably by regulating neural ultrastructure remodelling and the CREB/BDNF pathway.

Fusarium spp. are among the most important plant pathogens in the world. A survey on maize leaf blight was carried out in Heilongjiang province from 2019 to 2021. Based on morphological characteristics and a phylogenetic analysis on translation elongation factor (tef1) and second-largest subunit of RNA polymerase II (rpb2) genes, 146 Fusarium isolates were obtained and grouped into 14 Fusarium species, including F. ipomoeae (20.5%), F. compactum (17.1%), F. sporotrichioides (9.59%), F. graminearum (9.59%), F. citri (8.9%), F. asiaticum (6.85%), F. verticillioides (6.85%), F. acuminatum (5.48%), F. glycines (5.48%), F. temperatum (2.74%), F. armeniacum (2.74%), Fusarium sp. (2.05%), F. flagelliforme (1.4%), and F. annulatum (0.68%). The Fusarium incarnatum-equiseti species complex (FIESC, including F. ipomoeae, F. compactum, F. citri, and F. flagelliforme) was the most prevalent, indicating an evolving occurrence of the Fusarium species causing maize leaf blight. The typical symptoms observed on the maize leaves were oval to long strip lesions, with a gray to dark gray or brownish red coloration in the center and a chlorotic area at the edges. Based on the tef1 gene, seven haplotypes of FIESC were identified in Heilongjiang province, suggesting a population expansion. This is the first report of F. ipomoeae, F. compactum, F. flagelliforme, F. citri, F. sporotrichioides, F. graminearum, F. asiaticum, F. acuminatum, F. glycines, F. temperatum, F. armeniacum, Fusarium sp., and F. annulatum causing maize leaf blight in Heilongjiang province, China. The current research is informative for managing disease, exploring the phylogenetic relationship among Fusarium species, and clarifying the diversity of Fusarium species associated with maize leaf blight.

Rabies is a lethal zoonotic disease that kills approximately 60,000 people each year. Although inactivated rabies vaccines are available, multiple-dose regimensare recommended for pre-exposure prophylaxis or post-exposure prophylaxis,which cuts down the cost- and time-effectiveness, especially in low- and middle incomecountries.

Enterococcus faecalis (Efa) has been shown to be a "driver bacteria" in the occurrence and development of colorectal cancer (CRC). This study aims to explore the effect of specific metabolites of Efa on CRC.

Macrophage metabolic plasticity enables repurposing of electron transport from energy generation to inflammation and host defense. Altered respiratory complex II function has been implicated in cancer, diabetes, and inflammation, but regulatory mechanisms are incompletely understood. Here, we show that macrophage inflammatory activation triggers Complex II disassembly and succinate dehydrogenase subunit B loss through sequestration and selective mitophagy. Mitochondrial fission supported lipopolysaccharide-stimulated succinate dehydrogenase subunit B degradation but not sequestration. We hypothesized that this Complex II regulatory mechanism might be coordinated by the mitochondrial phospholipid cardiolipin. Cardiolipin synthase knockdown prevented lipopolysaccharide-induced metabolic remodeling and Complex II disassembly, sequestration, and degradation. Cardiolipin-depleted macrophages were defective in lipopolysaccharide-induced pro-inflammatory cytokine production, a phenotype partially rescued by Complex II inhibition. Thus, cardiolipin acts as a critical organizer of inflammatory metabolic remodeling.

Postoperative pain is a serious clinical problem with a poorly understood mechanism, and lacks effective treatment. Hydrogen (H2) can reduce neuroinflammation; therefore, we hypothesize that H2 may alleviate postoperative pain, and aimed to investigate the underlying mechanism.

Sepsis is a major contributor of intensive care units (ICUs) patient mortality. Prior investigations claimed that obesity enhances overall survival (OS) of septic patients. However, the reported results were inconsistent. This study examined the association between obesity and the 1-year mortality of septic patients.

Polysaccharides are important bioactive components of Nitraria retusa fruit (NRF). In this study, the ultrasonic-assisted extraction (UAE) conditions of polysaccharides from Nitraria retusa fruit (NRFPs) were optimized by response surface methodology (RSM). The structural characteristics and antioxidant activity were investigated. The maximum NRFPs yield of 3.35% was obtained under the following optimal conditions: temperature of 59.5 °C, time of 30.5 min, liquid-to-solid ratio of 19.5 mL/g. Three polysaccharide fractions, NRFP-1 (20.01 kDa), NRFP-2 (28.96 kDa), and NRFP-3 (67.45 kDa), were isolated. Glucose, galactose, and arabinose in different percentages were identified as the primary monosaccharide units. The Fourier transform infrared spectrometer (FT-IR) and nuclear magnetic resonance (NMR) analysis indicated the presence of α- and β-glycosidic bonds in NRFPs. The NRFP-3 exhibited the highest scavenging activities against DPPH, ABTS, -OH free radicals, and Fe+3-reducing activity.

Atopic dermatitis (AD) is a common, chronic inflammatory dermatosis with relapsing eruptions. Our study used bioinformatics to find novel candidate differentially expressed genes (DEGs) and predicted miRNAs between AD patients and healthy controls. The Mesh term "atopic dermatitis" was retrieved to obtain DEGs in GEO datasets. DEGs between AD patients and healthy controls were analyzed using GEO2R. Overlapping DEGs between different datasets were obtained with use of Draw Venn software. GO and KEGG enrichment analyses were conducted by the use of DAVID. STRING and miRWalk were used to individually analyze PPI networks, interactions of candidate genes and predicted miRNAs. A total of 571 skin samples, as retrieved from 9 databases were assessed. There were 225 overlapping DEGs between lesioned skin samples of AD patients and that of healthy controls. Nineteen nodes and 160 edges were found in the largest PPI cluster, consisting of 17 up-regulated and 2 down-regulated nodes. Two KEGG pathways were identified, including the cell cycle (CCNB1, CHEK1, BUB1B, MCM5) and p53 (CCNB1, CHEK1, GTSE1) pathways. There were 56 nodes and 100 edges obtained in the miRNA-target gene network, with has-miR-17-5p targeted to 4 genes and has-miR-106b-5p targeted to 3 genes. While these findings will require further verification as achieved with experiments involving in vivo and in vitro modles, these results provided some initial insights into dysfunctional inflammatory and immune responses associated with AD. Such information offers the potential to develop novel therapeutic targets for use in preventing and treating AD.

Podocyte injury is a common hallmark of chronic kidney disease (CKD). The podocin-nephrin complex localized in lipid rafts of podocyte is vital to reduce podocyte injury and proteinuria, however, the mechanism underlying its localization remains unclear. This study uncovers an important role of Flot2 in stabilizing the podocin-nephrin complex localized in lipid rafts. We first confirmed that Flot2 was expressed in podocyte and demenstrated that podocyte-specific Flot2 deletion worsen albuminuria, podocyte injury and glomerular pathology in LPS/ADR-induced nephropathy mouse models. Meanwhile, podocyte injury, albuminuria and pathologic aberrance were prevented in podocyte-specific Flot2 overexpression transgenic mice when challenged with LPS or ADR. Further found that Flot2 was vital to recruit podocin and nephrin into rafts and ameliorated podocyte injury. Flot2 and podocin directly interacted with each other via their SPFH domain. Meanwhile, we also showed that Flot-2 is a direct target of Krüppel-like factor (KLF15). Importanly, we observed that Flot2 was downregulated in renal biopsies from patients with podocytopathies and its expression negatively correlated with proteinuria and positively correlated with eGFR, indicating that Flot2 may be a novel therapeutic target for proteinuric kidney disease.

Soybean cyst nematode Heterodera glycines (SCN) is a major threat to global soybean production. Effective management of this disease is dependent on the development of resistant cultivars. Two SCN HG Types, 7 and 1.3.4.7. were previously identified as prevalent H. glycines populations in Northeast China. In order to evaluate soybean cultivars resistant to local SCN populations, 110 domestic commercial soybeans from different regions of Northeast China were assessed in the greenhouse to determine their potential as novel sources of resistance. The results suggested that cultivars responded differently to the two HG types. Of the 110 soybean cultivars evaluated, 24 accessions were classified as resistant or moderately resistant to HG Type 7, and five cultivars were classified as resistant or moderately resistant to HG Type 1.3.4.7. Among the tested cultivars, Kangxian 12 and Qingdou 13 had resistance response to both HG types 7 and 1.3.4.7. Thus, these broad-based SCN cultivars will be the valuable materials in the SCN resistance breeding program.

Extrachromosomal circular DNAs (eccDNAs) participate in tumorigenesis and tumor progression. However, the role and mechanism of eccDNAs have yet to be elucidated in non-small cell lung cancer (NSCLC). In our research, three surgically matched NSCLC tissue samples, NSCLC cell lines (H1299, A549, and H460), and a normal lung cell line (MRC-5) were used as study objects. High-throughput eccDNA sequencing and bioinformatics analysis were performed to study the distribution pattern and level of eccDNA expression. The upregulated candidate eccDNA-encoding PLCG2 was validated by routine PCR. Plasmid transfection, RNA interference, qRT‒PCR and western blotting experiments were used to verify the expression level of PLCG2. Our results showed that the chromosome distribution, length distribution, and genomic annotation of the eccDNAs were comparable between the NSCLC and normal groups. Nevertheless, there were no significant differences in eccDNAs between NSCLC tissues and matched normal lung tissues. The eccDNA derived from PLCG2 was upregulated in NSCLC cells. TCGA analysis and immunohistochemistry showed that PLCG2 was highly expressed in lung cancer tissues and tended to be associated with poor outcome. We also demonstrated that PLCG2 can promote metastasis through the regulation of mitochondrial respiration. These results suggested that PLCG2 identified by eccDNA sequencing acts as an oncogene and might be a new biomarker for NSCLC diagnosis and prognosis evaluation.

To detect the expression of Growth factor binding protein 2 associated binding protein 2 (Gab2) and CT10 regulator of kinase II (CrkII) in ovarian cancer and analyze their clinical significance. To explore the effects of Gab2 and CrkII on the biological behavior of ovarian cancer cells. To analyze the possible molecular mechanism of Gab2 in the development of ovarian cancer.

The TP53 tumor suppressor gene is one of the most mutated genes in lung adenocarcinoma (LUAD) and plays a vital role in regulating the occurrence and progression of cancer. We aimed to elucidate the association between TP53 mutations, response to immunotherapies and the prognosis of LUAD.

Type 2 diabetes (T2D) has an immense disease burden, affecting millions of people worldwide and costing billions of dollars in treatment. As T2D is a multifactorial disease with both genetic and nongenetic influences, accurate risk assessments for patients are difficult to perform. Machine learning has served as a useful tool in T2D risk prediction, as it can analyze and detect patterns in large and complex data sets like that of RNA sequencing. However, before machine learning can be implemented, feature selection is a necessary step to reduce the dimensionality in high-dimensional data and optimize modeling results. Different combinations of feature selection methods and machine learning models have been used in studies reporting disease predictions and classifications with high accuracy.

The Fourier transform infrared (FT-IR) signals obtained from bacterial samples are specific and reproducible, making FT-IR an efficient tool for bacterial typing at a subspecies level. However, the typing accuracy could be affected by many factors, including sample preparation and spectral acquisition. Here, we present a unified protocol for bacterial typing based on FT-IR spectroscopy. We describe sample preparation from bacterial culture and FT-IR spectrum collection. We then detail FT-IR spectrum preprocessing and multivariate analysis of spectral data for bacterial typing.