Cell Content Research Articles

Novel Flavonol Derivatives Containing Quinoxaline: Insights into the Antifungal Mechanism against Sclerotinia sclerotiorum.

In this study, 12 pairs of tautomeric flavonol derivatives containing quinoxaline were synthesized. The results of antifungal activity showed that in the enol-keto tautomerism, the target compounds containing keto (YB series) had better inhibitory activity against Sclerotinia sclerotiorum (S.s.) than compounds containing enol (YA series). YB9 showed the strongest antifungal activity against S.s., and the median effective concentration (EC50) value was 1.0 μg/mL, which was better than azoxystrobin (Az, 35.3 μg/mL). In vivo fungal inhibition experiments showed that the protective activity of YB9 against rape leaves was 83.4% at 200 μg/mL, which was superior to that of Az (70.2%). The activity of succinate dehydrogenase and molecular docking results showed that YB9 had a stronger antifungal effect than YA9. The results of oxalic acid content determination showed that YB9 could reduce the pathogenic ability of S.s. Then, the inhibitory effect of YB9 against S.s. was further verified by scanning electron microscopy, fluorescence microscopy, cell membrane permeability, cell content leakage, and malondialdehyde content.

Experimental study on the causes of spontaneous osteogenesis of Masquelet technique induced membrane

To investigate the causes of spontaneous osteogenesis of Masquelet technique induced membrane. Forty-two male Sprague-Dawley rats aged 7-9 weeks were selected to establish a critical-sized bone defect of the right middle femur model. Then the rats were randomly divided into 4 groups, with 12 rats in groups A-C and 6 rats in group D. The bone defects in groups A-C were filled with vancomycin-loaded polymethyl methacrylate bone cement spacers. Then the Kirschner wires were used for intramedullary fixation in groups A and B, and the bone cement was used to connect the bone cement spacers and the bone ends in group B. The steel plate was used to fixation in group C. The bone defect in group D was only fixed with steel plate as a blank control group. The general condition was observed after operation. At 5 weeks after operation, 6 rats in groups A-C were selected for STRO-1 immunohistochemical staining to observe the content of mesenchyme stem cells (MSCs) in the induced membrane (STRO-1 + cells). At 12 weeks after operation, the remaining rats in groups A-D were taken for X-ray observation, gross observation, and histological observation (HE, safranin O-green staining) to observe the spontaneous osteogenesis of the membrane. All rats in the 4 groups survived until the completion of the experiment. At 5 weeks after operation, the immunohistochemical staining showed that group B was negative, while the contents of MSCs in the induced membrane in groups A and C were 14.20%±1.92% and 5.00%±0.71%, respectively, with a significant difference ( P<0.05). At 12 weeks after operation, group A showed that the new bone formed at the osteotomy site and growth towards the center of the bone defect, with an average length of 3.1 mm on one side; and the presence of bone, cartilage lesions, fibers, and a small amount of neovascularization were observed in the induced membrane. Group C only had a small amount of new bone at the osteotomy site, and a small amount of neovascularization in the induced membrane. Groups B and D did not have any new bone, but bone resorption or atrophy at the osteotomy site. Although the Masquelet technique induced membrane has osteogenesis, the key factor for the spontaneous osteogenesis is the bone marrow overflow from the bone marrow cavity providing MSCs. The spontaneous osteogenesis of the induced membrane belongs to endochondral ossification.

(E)-5-hydroxy-7-methoxy-3-(2-hydroxybenzyl)-4-chromanone, a Major Homoisoflavonoid, Attenuates Free Fatty Acid-Induced Hepatic Steatosis by Activating AMPK and PPARα Pathways in HepG2 Cells.

(E)-5-hydroxy-7-methoxy-3-(2-hydroxybenzyl)-4-chromanone (HMC), a homoisoflavonoid isolated from Portulaca oleracea, has significant anti-adipogenesis potential; it regulates adipogenic transcription factors. However, whether HMC improves hepatic steatosis in hepatocytes remains vague. This study investigated whether HMC ameliorates hepatic steatosis in free fatty acid-treated human hepatocellular carcinoma (HepG2) cells, and if so, its mechanism of action was analyzed. Hepatic steatosis was induced by a free fatty acid mixture in HepG2 cells. Thereafter, different HMC concentrations (10, 30, and 50 µM) or fenofibrate (10 µM, a PPARα agonist, positive control) was treated in HepG2 cells. HMC markedly decreased lipid accumulation and triglyceride content in free fatty acid-treated HepG2 cell; it (10 and 50 μM) markedly upregulated protein expressions of pAMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. HMC (10 and 50 μM) markedly inhibited the expression of sterol regulatory element-binding protein-1c, fatty acid synthase, and stearoyl-coA desaturase 1, which are the enzymes involved in lipid synthesis. Furthermore, HMC (10 and 50 μM) markedly upregulated the protein expression of peroxisome proliferator-activated receptor alpha (PPARα) and enhanced the protein expressions of carnitine palmitoyl transferase 1 and acyl-CoA oxidase 1. HMC inhibits lipid accumulation and promotes fatty acid oxidation by AMPK and PPARα pathways in free fatty acid-treated HepG2 cells, thereby attenuating hepatic steatosis.

FTO mediates the diabetic kidney disease progression through regulating the m6A modification of NLRP3

BackgroundThe objective of our research was to investigate the specific mechanism of FTO in diabetic kidney disease (DKD) progression.MethodsThe DKD model was established with renal tubular epithelial HK-2 cells and mice in vitro and in vivo. The N6-methyladenosine (m6A) content in cells was detected using dot plot assay and the m6A levels of NLRP3 was detected with the MeRIP assay. The mRNA and protein levels were tested with real-time reverse transcriptase-polymerase chain reaction (RT-qPCR) and western blot. The IL-1β and IL-18 levels were assessed with enzyme-linked immunosorbent assay (ELISA). The cell viability was measured by cell counting kit (CCK)-8 assay and cell pyroptosis was determined with Annexin V and propidium iodide (PI) double staining followed by flow cytometry analysis. RNA-binding protein immunoprecipitation (RIP) and dual luciferase reporter assays were conducted to detect the interaction between FTO and NLRP3. m6A levels were detected by Me-RIP assay. The renal injury was measured by observing the renal morphology and urine and blood levels of relevant indicators.ResultsThe results indicated that high glucose treatment induced HK-2 cell pyroptosis. m6A levels were prominently elevated in high glucose treated HK-2 cells while FTO expression were significantly down-regulated. FTO over-expression promoted cell viability but inhibited pyroptosis of HK-2 cells under high glucose (HG) treatment. Moreover, FTO could inhibit NLRP3 expression. RIP and Me-RIP assays indicated that FTO could bind with NLRP3 and regulate its m6A modification level. Further luciferase assay confirmed that FTO binds with the 233–237 bp region of NLRP3. NLRP3 neutralized the function of FTO in the HG stimulated HK-2 cells. In vivo, the H&E staining showed that FTO over-expression alleviated the kidney injury and suppressed the pyroptosis induced by DKD.ConclusionWe found that FTO could inhibit the DKD progression in vivo and in vitro by regulated the m6A modification of NLRP3.

Gastric Cancer Actively Remodels Mechanical Microenvironment to Promote Chemotherapy Resistance via MSCs-Mediated Mitochondrial Transfer.

Chemotherapy resistance is the main reason of treatment failure in gastric cancer (GC). However, the mechanism of oxaliplatin (OXA) resistance remains unclear. Here, we demonstrate that extracellular mechanical signaling plays crucial roles in OXA resistance within GC. We selected OXA-resistant GC patients and analyzed tumor tissues by single-cell sequencing, and found that the mitochondrial content of GC cells increased in a biosynthesis-independent manner. Moreover, we found that the increased mitochondria of GC cells were mainly derived from mesenchymal stromal cells (MSCs), whichcould repair the mitochondrial function and reduce the levels of mitophagy in GC cells, thus leading to OXA resistance. Furthermore, we investigated the underlying mechanism and found that mitochondrial transfer was mediated by mechanical signals of the extracellular matrix (ECM). After OXA administration, GC cells actively secreted ECM in the tumor microenvironment (TEM), increasing matrix stiffness of the tumor tissues, which promoted mitochondria to transfer from MSCs to GC cells via microvesicles (MVs). Meanwhile, inhibiting the mechanical-related RhoA/ROCK1 pathway could alleviate OXA resistance in GC cells. In summary, these results indicate that matrix stiffness could be used as an indicator to identify chemotherapy resistance, and targeting mechanical-related pathway could effectively alleviate OXA resistance and improve therapeutic efficacy.

Novel Insights into Ethanol-Soluble Oyster Peptide-Zinc-Chelating Agents: Structural Characterization, Chelation Mechanism, and Potential Protection on MEHP-Induced Leydig Cells.

Numerous studies have reported that mono-(2-ethylhexyl) phthalate (MEHP) (bioactive metabolite of Di(2-ethylhexyl) phthalate) has inhibitory effects on Leydig cells. This study aims to prepare an oyster peptide-zinc complex (PEP-Zn) to alleviate MEHP-induced damage in Leydig cells. Zinc-binding peptides were obtained through the following processes: zinc-immobilized affinity chromatography (IMAC-Zn2+), liquid chromatography-mass spectrometry technology (LC-MS/MS) analysis, molecular docking, molecular dynamic simulation, and structural characterization. Then, the Zn-binding peptide (PEP) named Glu-His-Ala-Pro-Asn-His-Asp-Asn-Pro-Gly-Asp-Leu (EHAPNHDNPGDL) was identified. EHAPNHDNPGDL showed the highest zinc-chelating ability of 49.74 ± 1.44%, which was higher than that of the ethanol-soluble oyster peptides (27.50 ± 0.41%). In the EHAPNHDNPGDL-Zn complex, Asn-5, Asp-7, Asn-8, His-2, and Asp-11 played an important role in binding to the zinc ion. Additionally, EHAPNHDNPGDL-Zn was found to increase the cell viability, significantly increase the relative activity of antioxidant enzymes and testosterone content, and decrease malondialdehyde (MDA) content in MEHP-induced TM3 cells. The results also indicated that EHAPNHDNPGDL-Zn could alleviate MEHP-induced apoptosis by reducing the protein level of p53, p21, and Bax, and increasing the protein level of Bcl-2. These results indicate that the zinc-chelating peptides derived from oyster peptides could be used as a potential dietary zinc supplement.

Effect of dalargin on the content of goblet cells and mucins in the colonic mucosa in experimental ulcerative colitis

Aim. To investigate the protective effect of dalargin on the content of goblet cells and mucins in the colonic mucosa in a mouse model of ulcerative colitis.Materials and methods. Ulcerative colitis was simulated in Balb/C mice by replacing drinking water with 5% sodium dextran sulfate in boiled water for 5 days. Dalargin was administered subcutaneously in a volume of 0.1 ml at a dose of 100 μg / kg of body weight once a day for 7 days from the beginning of ulcerative colitis simulation. Sulfasalazine as a reference-listed drug was administered intragastrically at a dose of 200 mg / kg once a day for 7 days. The mice were sacrificed on day 5, 7, and 28. The sections of the distal colon were prepared and stained with hematoxylin and eosin, alcian blue (pH = 1.0) according to Mowry or by PAS reaction. In the sections, the number of goblet cells and acid and neutral mucins was determined.Results. In the mouse model of ulcerative colitis, the number of goblet cells (mainly at the bottom of the crypts), acid and neutral mucins decreased. Dalargin administration increased the number of goblet cells and the content of acid and neutral mucins in the colonic mucosa more effectively than sulfasalazine.Conclusion. Dalargin has a protective effect in ulcerative colitis.

Single-cell heterogeneity in ribosome content and the consequences for the growth laws.

Across species and environments, the ribosome content of cell populations correlates with population growth rate. The robustness and universality of this correlation have led to its classification as a "growth law." This law has fueled theories about how evolution selects for microbial organisms that maximize their growth rate based on nutrient availability, and it has informed models about how individual cells regulate their growth rates and ribosomal content. However, due to methodological limitations, this growth law has rarely been studied at the level of individual cells. While populations of fast-growing cells tend to have more ribosomes than populations of slow-growing cells, it is unclear whether individual cells tightly regulate their ribosome content to match their environment. Here, we employ recent groundbreaking single-cell RNA sequencing techniques to study this growth law at the single-cell level in two different microbes, S. cerevisiae (a single-celled yeast and eukaryote) and B. subtilis (a bacterium and prokaryote). In both species, we observe significant variation in the ribosomal content of single cells that is not predictive of growth rate. Fast-growing populations include cells exhibiting transcriptional signatures of slow growth and stress, as do cells with the highest ribosome content we survey. Broadening our focus to non-ribosomal transcripts reveals subpopulations of cells in unique transcriptional states suggestive that they have evolved to do things other than maximize their rate of growth. Overall, these results indicate that single-cell ribosome levels are not finely tuned to match population growth rates or nutrient availability and cannot be predicted by a Gaussian process model that assumes measurements are sampled from a normal distribution centered on the population average. This work encourages the expansion of growth law and other models that predict how growth rates are regulated or how they evolve to consider single-cell heterogeneity. To this end, we provide extensive data and analysis of ribosomal and transcriptomic variation across thousands of single cells from multiple conditions, replicates, and species.

Polycrystalline silicon photovoltaic cell defects detection based on global context information and multi-scale feature fusion in electroluminescence images

In photovoltaic (PV) cell inspection, electroluminescence (EL) imaging provides high spatial resolution for detecting various types of defects. The recent integration of EL imaging with deep learning models has enhanced the recognition of defects in PV cells. However, the high surface impurity content in polycrystalline silicon PV cells presents a challenge. Defect features can be similar to complex background textures, making highlighting features for small target defects difficult and leading to potential misclassification as background or other classes. To address these challenges, we propose a novel deep convolutional neural network (CNN) model for effectively identifying small target defects in polycrystalline PV cells. We first utilize a global context information (GCI) block to improve CNN’s modeling of global information, aiding in distinguishing PV cell defects with similar local details. Moreover, we design a channel weight feature pyramid (CWFP) that dynamically adjusts the channel weights of extracted features. We further achieve multi-scale feature fusion through the pyramid structure to enhance the resolution capability for small targets. The proposed model was evaluated on a publicly available dataset of 8 defect classes in polycrystalline PV cells, achieving an accuracy of 96.36 %. The experimental results show that the proposed model outperforms existing deep learning models in detecting small target defects with higher precision.

Portulaca oleracea (L.) essential oil inhibits Pestalotiopsis neglecta and controls black spot needle blight in Pinus sylvestris var. mongolica (Litv.)

Black spot needle blight in Pinus sylvestris var. mongolica is a common disease caused by Pestalotiopsis neglecta which leads to yellowing and withering of needles, eventually leading to the death of the affected trees. The study investigated the antifungal activity and mechanism of Portulaca oleracea essential oil (POEO) against P. neglecta and its efficacy in controlling black spot needle blight in Pinus sylvestris var. mongolica. In this study, we identified the main components of POEO as linalool and limonene. The antifungal assay proved that POEO could inhibit the growth of P. neglecta, 6 μL/mL of POEO inhibited P. neglecta by 100 % with an EC50 value of 1.16 μL/mL, and the results of scanning electron microscopy confirmed that POEO inhibited the growth of the P. neglecta mycelium. In addition, POEO treatment induced oxidative stress and exacerbated membrane lipid peroxidation of P. neglecta, which ultimately caused serious damage to P. neglecta cell membranes and cell contents leakage. POEO also reduced the activity and virulence of polygalacturonase (PG), endo-1,4-β-D-glucose hydratase (EG), and pectate lyase (PL) secreted by P. neglecta, thereby controlling black-spotted needle blight of Pinus sylvestris var. mongolica, which was able to control black spot needle blight in Pinus sylvestris var. mongolica. In summary, our results revealed the antifungal mechanism of POEO on P. neglecta and provided potential options for controlling black spot needle blight in Pinus sylvestris var. mongolica and other plant diseases.

Immortalized mesenchymal stromal cells overexpressing alpha-1 antitrypsin protect acinar cells from apoptotic and ferroptotic cell death.

Chronic pancreatitis (CP) is a progressive inflammatory disorder that impairs endocrine and exocrine function. Our previous work showed that mesenchymal stem/stromal cells (MSCs) and MSCs overexpressing alpha-1 antitrypsin (AAT-MSCs) could be therapeutic tools for CP. However, primary MSCs are predisposed to undergo senescence during culture expansion, which limits their therapeutic applications. We generated and characterized immortalized human MSCs (iMSCs) and AAT-MSCs (iAAT-MSCs) and tested their protective effect on 2,4,6-Trinitrobenzenesulfonic acid (TNBS)-induced acinar cell death in an invitro cell culture system. Primary MSCs were immortalized by transduction with simian virus 40 large T antigen (SV40LT), and the resulting iMSC and iAAT-MSC lines were analysed for proliferation, senescence, phenotype and multi-differentiation potential. Subsequently, apoptosis and ferroptosis pathways were investigated by assessing changes before and after TNBS treatment. Coculture of iMSCs and iAAT-MSCs with acinar cell lines inhibited early cell death induced by TNBS, reduced ER stress and reversed TNBS-induced protein reduction at tight junctions. Additionally, iMSCs and iAAT-MSCs exerted such protection by regulating mitochondrial respiration, ATP content and ROS production in TNBS-induced acinar cells. Furthermore, iMSCs and iAAT-MSCs ameliorated TNBS-induced ferroptosis by modulating iron generation and ROS production and regulating the ferritin heavy chain 1 (FTH1)/protein disulfide isomerase (PDI)/glutathione peroxide 4 (GPX4) signalling pathways in acinar cells. These findings identify ferroptosis as an unrecognized mechanism that leads to TNBS-induced cell death and offer mechanistic insights relevant to using stem cell therapy to treat acinar cell death associated with CP.

PAT exposure caused human hepatocytes apoptosis and induced mice subacute liver injury by activating oxidative stress and the ERS-associated PERK pathway

With the widespread use of antimony compounds in synthetic materials and processing, the occupational exposure and environmental pollution caused by antimony have attracted the attention of researchers. Studies have shown that antimony compounds can cause liver damage, but the mechanism has not yet been elucidated. In this study, we used the trivalent potassium antimony tartrate (PAT) to infect L02 hepatocytes and Kunming (KM) mice to establish an antimony-induced apoptosis model of L02 cells and a subacute liver injury model of KM mice. We found that PAT exposure caused hepatocyte apoptosis and was accompanied by oxidative stress and endoplasmic reticulum stress (ERS), and the ERS-associated PERK pathway was activated. Further experimental results showed that N-acetyl-l-cysteine (NAC) pretreatment or silencing of the PERK gene in L02 cells reduced PAT-induced apoptosis. The activity of SOD and CAT in treated L02 cells was increased, the malondialdehyde content in L02 cells and liver tissues was decreased, and the content of ERS-related proteins GRP78 and CHOP, as well as the content of PERK-pathway-related proteins p-PERK/PERK, p-eif2α/eif2α and ATF4 protein were significantly reduced. Overall, PAT exposure triggered hepatocyte apoptosis and liver injury by inducing oxidative stress and activating the ERS-associated PERK pathway; however, this effect could be alleviated by NAC intervention or silencing of PERK in hepatocytes.

Release kinetics and protective effect of novel curcumin-based nanoliposome modified with pectin, whey protein isolates and hyaluronic acid against oxidative stress

In the present study, a novel nanoliposome loaded with Curcumin (Cur) (NNLs-Cur) was established to overcome the gastrointestinal digestive barrier and enhance mitochondrial targeting capacity, exerting the antioxidant capacity of Cur. Noteworthy, NNLs-Cur was modified by pectin, whey protein isolates and hyaluronic acid. The results showed that the structure of traditional nanoliposomes loaded with Cur (NLs-Cur) was destroyed during digestion. However, NNLs-Cur maintained intact structural morphology, and the release of Cur in the stomach and intestines was consistent with zero-order and first-order kinetic models, respectively. Interestingly, the survival rate of HL-7702 cells after being damaged by H2O2 was 40.53 %, while the survival rate after treated with NNLs-Cur reached 99.87 %. Besides, the fluorescence localization indicated Cur in NNLs-Cur could escape lysosomal and achieve mitochondria targeting. Compared with NLs-Cur, the damaged cells treated with NNLs-Cur increased activities of catalase (CAT), glutathione peroxide (GSH-Px) and superoxide dismutase (SOD) from 16.16 ± 0.52, 16.92 ± 2.28 and 30.10 ± 0.93 U/mgprot to 19.09 ± 0.52, 20.41 ± 1.79 and 33.81 ± 0.29 U/mgprot, respectively. Malondialdehyde (MDA) content and reactive oxygen species (ROS) level of the oxidative damaged cells were reduced, mitochondrial membrane potential was restored, and cell apoptosis was reduced. This study provides theoretical guidance for realizing the industrial application of efficient targeted delivery Cur.

Mechanistic studies on the alleviation of lipid accumulation and oxidative stress by Majia pomelo seed oil

In this study, hot-pressed Majia pomelo seed oil (MPSO), which has high oxidative stability and antioxidant capacity, was used to study the effects and potential mechanisms of lipid accumulation and oxidative stress. The results indicated that the low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and triglycerides (TG) levels in HepG2 cells were lowest when the MPSO concentration was 0.5 mg/mL. At this concentration, MPSO could alleviate oleic acid (OA)-induced lipid accumulation, reduce intracellular lipid level, and decrease lipid and cholesterol synthesis by increasing AMPK phosphorylation and down-regulating the expression levels of genes and proteins of ACC, SREBP-1c, PPAR-γ, and FAS. Meanwhile, MPSO can reduce reactive oxygen species (ROS) and malondialdehyde (MDA) content and enhance superoxide dismutase (SOD) content in HepG2 cells by down-regulating the expression levels of Nrf2, γ-GCS, and HO-1 genes and proteins, thus acting as an anti-oxidative stress. In addition, molecular docking results indicated that the active ingredients of MPSO could effectively bind AMPK protein and Keap1 protein, which further demonstrated that MPSO could alleviate lipid accumulation and oxidative stress.

Inhibitory effects of phenylpropionamides from the hemp seed husk on tyrosinase

Tyrosinase is an enzyme involved in melanin production. To identify inhibitors of this enzyme in natural products, extracts and fractions of hemp seed husk were screened for tyrosinase inhibition. Phenylpropionamides 1–9, which were isolated from the ethyl acetate fraction, had inhibitory effects; compounds 3 and 4 had the greatest inhibitory effects. Cannabisin A (3) was a non-competitive and cannabisin B (4) was a competitive inhibitor. The binding site and interaction on tyrosinase of each inhibitor were calculated by computational chemistry. Potential inhibitor 3 decreased the melanin content and tyrosinase activity in B16F10 melanoma cells. Therefore, cannabisin A (3) has potential as a tyrosinase inhibitor.

Effects of age, elastin density, and glycosaminoglycan accumulation on the delamination strength of human thoracic and abdominal aortas

Aortic dissection is a life-threatening condition caused by layer separation. Despite extensive research, the relationship between the aortic wall's structural integrity and dissection risk remains unclear. Glycosaminoglycan (GAG) accumulation and elastin loss are suspected to play significant roles. We investigated how age-related changes in aortic structure affect dissection susceptibility. Peeling tests were performed on longitudinal and circumferential thoracic (TA) and abdominal aortic (AA) strips from 35 donors aged 13–76 years (mean 38 ± 15 years, 34 % female). GAG, elastin, collagen, and smooth muscle cell (SMC) contents were assessed using bidirectional histology. Young TAs resisted longitudinal peeling better than circumferential, with delamination strengths of 65.4 mN/mm and 44.2 mN/mm, respectively. Delamination strength decreased with age in both directions, more rapidly longitudinally, equalizing at ∼20–25 mN/mm in older TAs. Delamination strength in AAs was 22 % higher than in TAs. No sex differences were observed. GAG density increased, while elastin density decreased by 2.5 % and 4 % per decade, respectively. Collagen density did not change with age, while SMC density decreased circumferentially. GAGs partially mediated the reduction in longitudinal delamination strength due to aging, while circumferential strength reduction was not mediated by changes in either GAG or elastin densities. This study explains why aortic dissections are more common in TAs, especially in older individuals, and why they typically propagate spirally. TAs exhibit lower delamination strength compared to AAs and experience strength reduction with age, a phenomenon linked to increased GAG accumulation and elastin loss. These findings enhance our understanding of the pathophysiological mechanisms behind aortic dissection. Statement of significanceThis work explores the age-dependent relationships between delamination strength in human aortas and wall structural content. We investigated 35 human aortas from donors aged 13 to 76 years, providing new insights into the biomechanical and histological factors that influence aortic dissection risk. Our findings elucidate how variations in elastin, glycosaminoglycan, collagen, and smooth muscle cell densities impact the structural integrity of the aorta, contributing significantly to the understanding of aortic dissection mechanisms.

Anti-cytoplasmic performance of Zn/g-C3N4 photocatalysts in the battle against microcystis aeruginosa

Cyanobacterial blooms pose a serious challenge to ecosystems and human health. Photocatalysis, as an advanced green oxidation technology, has potential applications in cyanobacteria removal. In this paper, Zn/g-C3N4 photocatalysts with different mass ratios were prepared for algal inactivation. In 3 h, the best performance comes from the experiment using 10 % Zn/g-C3N4 photocatalyst, which inactivated 80 % of microcystis aeruginosa (9×106 ∼ 10×106 cells/mL) when exposed to visible light. Secondly, the potential mechanism of the photocatalytic inactivation of microcystis aeruginosa was proposed in combination with the generation of reactive oxygen species and the leakage of the algal cell contents. The photocatalyst first covered the surface of the algal cells to stop their movement; then the catalyst was excited under light and destroyed the outer protective structures of the cells (cell membrane, cell wall, and organic membrane, etc.) through the action of reactive oxygen species (1O2 and •OH) generated by Zn/g-C3N4, leading to structural changes in the outer layer of the cells. And then photocatalytic oxidation of the intracellular cytoplasm led to the loss of its physiological functions (via losing of inorganic ions and non-electrolytes, etc.). Finally the cell is inactivated or decomposed. This understanding may provide theoretical and practical implications for the prospects of harmful algal control.

Immune cells and tryptophan metabolism in the joint capsule tissue in rheumatoid arthritis

To the present day, many links in the pathogenesis of rheumatoid arthritis remain unclear, which leads to unsatisfactory results in its therapy.The aim. To study the cells involved in immune reactions and tryptophan metabolites in the joint capsule in rheumatoid arthritis.Materials and methods. The experiments were carried out on 40 Wistar rats. Rheumatoid arthritis was induced by intraperitoneal injection of a solution of type 2 collagen (Chondrex Inc., USA) in incomplete Freund’s adjuvant. On the days 7, 14 and 21, the content of tryptophan, kynurenine, 3-hydrokenurinine, L-5-hydrotryptophan in the joint capsule was determined using high-performance liquid chromatography. Cells with CD3, CD20 and CD68 in joint tissues were studied at the same time using the streptavidin-biotin-peroxidase method. We used enzyme-linked immunosorbent method to determine antibodies to citrulline-containing peptide. Statistical analysis was performed using the Jamovi, version 2.3 software.Results. The content of cells carrying CD3, CD20 and CD68 markers in the joint was high in experimental rheumatoid arthritis. In joint tissues, the content of tryptophan metabolites along the kynurenine pathway also increases and the concentration of metabolites along the serotonin pathway decreases. Direct positive correlations of cells carrying CD3, CD20 and CD68 differential clusters with the content of tryptophan metabolites along the kynurenine pathway and negative correlations with metabolites of the serotonin pathway were established.Conclusions. Cells carrying CD3, CD20 and CD68 markers and tryptophan metabolites – kynurenine and L-5-hydrotryptophan – play an important role in the pathogenesis of rheumatoid arthritis.

Three-dimensional reconstruction of insect chemosensory sensillum

The olfactory system is involved in food and mate recognition in insects. However, 3D structures of chemosensory sensilla in insects are unexplored yet. Here, the internal structures of an olfactory sensillum on the antenna of the brown planthopper, Nilaparvata lugens (Hemiptera: Delphacidae), one of the most important rice pests, are examined and imaged using focused ion beam scanning electron microscopy. Based on these images, a 3D structure is reconstructed in this study. We find that the trichoid olfactory sensillum possesses a multiporous wall encircling a lumen with one sensory cell. Besides, there are three accessory cells (ACs) and a glia cell with different cell contents surrounding the sensory cell. The abundant tubular membrane structures in the tormogen cell suggest its role in secreting proteins like odorant binding proteins into the receptor lymph, while three auxiliary cells with simpler cellular content closely enfold the sensory cell, probably to prevent leaking of the receptor lymph into the surrounding epidermis. In the sensory cell, the microtubules and two tandem basal bodies at the base of the microtubules are also reconstructed. They are considered as a propulsive engine to ensure dendrite vibration or spinning in the receptor lymph, so that the proteins and odorant molecules move faster in the receptor lymph, which improves recognition of environmental odors and enables the insect to immediately respond to this information.

Immunogram dynamics of students under the influence of dosed physical activity

Analysis of the dynamics of the state of blood leukocytes in muscular activity is relevant due to the development of methods of differentiation and assessment of the state of these cells. The purpose of the study is to study the dynamics of the phagocytic and NBT activity of neutrophils, as well as the content of CD lymphocytes of peripheral blood in students when moving on a treadmill. For students 18-20 years old involved in athletics (3 boys and 4 girls), blood was taken from the ulnar vein before and after a 15-minute jog, as well as after a 15-minute run of moderate intensity. The average level of physical performance of the examined PWC170 was 16.25±2.21 kGm/min/kg. Assessment of phagocytosis and NBT activity of neutrophils and determination of blood CD lymphocytes by immunophenotyping were performed using flow cytometry. It was found that in girls at rest, the relative content of lymphocytes and NK cells was significantly lower, and the level of induced NBT activity of neutrophils and the relative content of CD4-CD8- and CD4+CD8+ lymphocytes was significantly higher than in boys. At the same time, the dynamics of the leukogram parameters examined during the dosed physical activity fully corresponded to the development of the lymphocytic phase of myogenic leukocytosis. With an increase in the power of repeated exercise against the background of a general increase in the number of phagocytic neutrophils, the balance of spontaneous NBT-positive and reserve potentially active neutrophils significantly increased relative to the content of NBT-negative cells in the induced test. At the same time, the level of neutrocytes in girls was significantly higher, causing a higher level of phagocyte count and absolute content of NBT-positive neutrophils in a spontaneous and induced test. At the same time, against the background of an increase in the absolute content of CD4-CD8- and TNK lymphocytes, a statistically significant increase in the relative and absolute content of NK cells was observed. In contrast to the boys after the 2nd physical exercise, the relative and absolute content of NK cells, as well as the increase in the percentage of HBT-positive cells in the induced test, were significantly higher.