Reduced nitrogen fertilization under flooded conditions cut down soil N2O and CO2 efflux: An incubation experiment.

Unreasonable water (W) and inorganic nitrogen (N) fertilization cause an intensification of soil greenhouse gas (GHGs) emissions. W-N interactions (W × N) patterns can maximise the regulation of soil GHGs efflux through the rational matching of W and N fertilization factors. However, the effects of W × N patterns on soil GHGs efflux and the underlying mechanism remain unclear. In this study, urea fertilizers were applied to paddy soils in a gradient of 100 (N100), 80 (N80), and 60 mg kg-1 (N60) concentrations. Flooding (W1) and 60% field holding capacity (W2) was set for each N fertilizer application to observe the effects of W × N patterns on soil properties and GHGs efflux through incubation experiments. The results showed that W significantly affected soil electrical conductivity and different N forms (i.e., alkali hydrolyzed N, ammonium N, nitrate N and microbial biomass N) contents. Soil organic carbon (C) content was reduced by 14.40% in W1N60 relative to W1N100, whereas microbial biomass C content was increased by 26.87%. Moreover, soil methane (CH4) fluxes were low in all treatments, with a range of 1.60-1.65 µg CH4 kg-1. Soil nitrous oxide (N2O) and carbon dioxide (CO2) fluxes were significantly influenced by W, N and W × N. Global warming potential was maintained at the lowest level in W1N60 treatment at 0.67 g CO2-eq kg-1, suggesting W1N60 as the preferred W × N pattern with high environmental impact. Our findings demonstrate that reduced N fertilization contributes to the effective mitigation of soil N2O and CO2 efflux by lowering the soil total N and organic C contents and regulating soil microbial biomass C and N.

Identification and genetic analysis of alternative splicing of long non-coding RNAs in tomato initial flowering stage.

Alternative splicing (AS) is a key modulator of development in many eukaryotic organisms. Long non-coding RNAs (lncRNAs) are a class of non-coding RNAs that play essential regulatory roles in various developmental processes and stress responses. However, the functions of AS lncRNAs during the initial flowering of tomato are largely unknown. This study was designed to investigate the AS pattern of lncRNAs in tomato flower, leaf, and root tissues at the initial flowering stage. Using RNA-Seq, we found that 72.55% of lncRNAs underwent AS in these tissues, yielding a total of 16,995 AS events. Among them, the main type of AS event is alternative first exon (AFE), followed by retained intron (RI). We performed candidate target genes analysis on tissue-specific AS lncRNA, and the results indicated that the candidate target genes of these lncRNAs may be involved in the regulation of circadian rhythm, plant immunity, cellulose synthesis and phosphate-containing compound metabolic process. Moreover, a total of 73,085 putative SNPs and 15,679 InDels were detected, and the potential relationship between the AS of lncRNAs and interesting SNP and InDel loci, as well as their numbers, revealed their effects on tomato genetic diversity and genomic stability. Our data provide new insights into the complexity of the transcriptome and the regulation of AS.

The efficacy of magnesium supplementation for gestational diabetes: A meta-analysis of randomized controlled trials.

BACKGROUND: The efficacy of magnesium supplementation is unclear for the treatment of gestational diabetes. This meta-analysis aimed to study the efficacy of magnesium supplementation for glycemic control and pregnant outcomes in women with gestational diabetes. METHODS: Several databases including PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases have been systematically searched up to July 2023, and we included randomized controlled trials (RCTs) assessing the efficacy of magnesium supplementation for gestational diabetes. The meta-analysis was performed using the random-effect model or fixed-effect model based on the heterogeneity. RESULTS: Five RCTs and 266 patients were included in the meta-analysis. Overall, compared with control intervention for gestational diabetes, magnesium supplementation was able to significantly decrease FPG (MD = -7.33 mg/dL; 95 % CI = -7.64 to -7.02 mg/dL; P < 0.00001) and HOMA-IR (MD = -0.99; 95 % CI = -1.76 to -0.22; P = 0.01), but resulted in no obvious impact on serum insulin (MD = -4.17 µIU/mL; 95 % CI = -8.49 to 0.14 µIU/mL; P = 0.06), preterm delivery (OR = 0.42; 95 % CI = 0.06 to 2.95; P = 0.38), macrosomia (OR = 0.34; 95 % CI = 0.08 to 1.35; P = 0.13) or BMI change (MD = -0.01 kg/m2; 95 % CI = -0.06 to 0.04 kg/m2; P = 0.63). CONCLUSIONS: Magnesium supplementation may be effective for the treatment of gestational diabetes without taking insulin treatment.

Interactions and effects of a stannous-containing sodium fluoride dentifrice on oral pathogens and the oral microbiome.

Numerous studies have investigated the effects of stannous ions on specific microbes and their efficacy in reducing dental plaque. Nonetheless, our understanding of their impact on the oral microbiome is still a subject of ongoing exploration. Therefore, this study sought to evaluate the effects of a stannous-containing sodium fluoride dentifrice in comparison to a zinc-containing sodium fluoride dentifrice and a control group on intact, healthy oral biofilms. Utilizing the novel 2bRAD-M approach for species-resolved metagenomics, and FISH/CLSM with probes targeting periodontal and caries associated species alongside Sn2+ and Zn2+ ions, we collected and analyzed in situ biofilms from 15 generally healthy individuals with measurable dental plaque and treated the biofilms with dentifrices to elucidate variations in microbial distribution. Although significant shifts in the microbiome upon treatment were not observed, the use of a stannous-containing sodium fluoride dentifrice primarily led to an increase in health-associated commensal species and decrease in pathogenic species. Notably, FISH/CLSM analysis highlighted a marked reduction in representative species associated with periodontitis and caries following treatment with the use of a stannous-containing sodium fluoride dentifrice, as opposed to a zinc-containing sodium fluoride dentifrice and the control group. Additionally, Sn2+ specific intracellular imaging reflected the colocalization of Sn2+ ions with P. gingivalis but not with other species. In contrast, Zn2+ ions exhibited non-specific binding, thus suggesting that Sn2+ could exhibit selective binding toward pathogenic species. Altogether, our results demonstrate that stannous ions could help to maintain a healthy oral microbiome by preferentially targeting certain pathogenic bacteria to reverse dysbiosis and underscores the importance of the continual usage of such products as a preventive measure for oral diseases and the maintenance of health.

IFN-γ-activated lymphocytes boost nitric oxide production in grass carp monocytes/macrophages.

It is well known that IFN-γ is a prime activator of nitric oxide (NO) production by monocytes/macrophages in mammals and fish. In parallel, whether IFN-γ-activated lymphocytes are associated with NO production remains unclear. In this study, grass carp monocytes/macrophages and lymphocytes from head kidney were isolated and effects of recombinant grass carp IFN-γ (rgcIFN-γ) on NO releases by these two cell populations were determined. Results showed that rgcIFN-γ time- and dose-dependently increased NO production by monocytes/macrophages but not lymphocytes, which are consistent with the findings in mammals. Interestingly, rgcIFN-γ displayed a greater stimulation on NO production in the co-cultures of monocytes/macrophages and lymphocytes when compared with that in the culture of monocytes/macrophages alone. Furthermore, the media harvested from rgcIFN-γ-treated lymphocytes were effective in boosting NO release in monocytes/macrophages. These data suggest that secretions from rgcIFN-γ-treated lymphocytes may be involved in the NO release by monocytes/macrophages. To address this hypothesis, effect of rgcIFN-γ on the gene expression of inflammatory cytokines in grass carp lymphocytes was examined, showing that it consistently stimulated the mRNA expression of grass carp TNF-α and IL-1ß but not IFN-γ. Furthermore, treatment of rgcIFN-γ combined with recombinant grass carp IL-1ß (rgcIL-1ß) induced a NO production by monocytes/macrophages, which was significantly higher than those induced by either cytokine alone. It provides the evidence that the cytokines secreted by the activated lymphocytes may facilitate the NO production by monocytes/macrophages. Taken together, our findings point out a new mechanism for the involvement of IFN-γ-activated lymphocytes in the NO production by monocytes/macrophages in fish. This knowledge not only strengthens the role of IFN-γ in immune system but also provides the evidence for the existence of a close relationship between lymphocytes and monocytes/macrophages in fish.

Evidence for pituitary adenylate cyclase-activating peptide as a direct immunoregulator in teleost head kidney.

In mammals, pituitary adenylate cyclase activating polypeptide (PACAP) is a potent anti-inflammatory factor, showing that it inhibits the expression and release of proinflammatory cytokines and enhances the production of anti-inflammatory factors. However, whether fish PACAP plays similar regulatory roles as seen in mammals remains unclear. In the present study, expression of PACAP-specific receptor PAC1-R was shown in grass carp head kidney and spleen, supporting that PACAP may have a direct effect on fish immune cells. To test this hypothesis, the immunoregulatory role of grass carp PACAP (gcPACAP) was examined in head kidney leucocytes (HKLs). Results showed that gcPACAP inhibited basal and further attenuated lipopolysaccharide (LPS)-stimulated cell viability of HKLs, indicating that gcPACAP may possess similar inhibitory property at cellular level as seen in mammals. Curiously, in vitro and in vivo studies revealed that gcPACAP stimulated proinflammatory factors (IL-1ß and TNF-α) but not IL-10 mRNA expression in HKLs and head kidney. Moreover, bacterial infection and LPS enhanced IL-1ß, TNF-α and IL-10 mRNA expression in grass carp head kidney and HKLs, respectively, and these stimulatory effects were not influenced by gcPACAP. These findings suggest that PACAP plays distinct roles, at least does not function as an anti-inflammatory factor, in fish compared with that in mammals.

FNDC5 and AKR1B10 inhibit the proliferation and metastasis of adrenocortical carcinoma cells by regulating AMPK/mTOR pathway.

Being a rare malignancy, adrenocortical carcinoma (ACC) exhibits aggressiveness and poor prognosis. Fibronectin type III domain-containing protein 5 (FNDC5) is a transmembrane protein involved in multiple types of cancer. Aldo-keto reductase family 1 member B10 (AKR1B10) has a suppressive role in ACC. The present study aimed to investigate the role of FNDC5 in ACC cells as well as its mechanisms related to AKR1B10. The Gene Expression Profiling Interactive Analysis database predicted FNDC5 expression in tumour tissue of patients suffering from ACC and the overall survival rate. Western blotting as well as reverse transcription-quantitative PCR were used for the examination of the transfection efficiency of FNDC5-overexpression vector (Oe-FNDC5) and small interfering (si)RNA against AKR1B10. Cell Counting Kit-8 was employed for the assessment of cell viability. The proliferation, migration and invasion of the transfected cells were assessed by 5-ethynyl-2'-deoxyuridine staining, wound healing and Transwell assays. Additionally, cell apoptosis was evaluated by flow cytometry and caspase-3 activity was determined by ELISA. The levels of epithelial-mesenchymal transition- and 5'-AMP-activated protein kinase (AMPK)/mTOR signalling pathway-associated proteins were assessed by western blotting. The interaction between FNDC5 and AKR1B10 was confirmed by co-immunoprecipitation. FNDC5 levels in ACC tissue were reduced compared with normal tissue. After overexpressing FNDC5, proliferation, migration and invasion of NCI-H295R cells were suppressed, while cell apoptosis was promoted. FNDC5 interacted with AKR1B10 and AKR1B10 knockdown promoted proliferation, migration and invasion while inhibiting the apoptosis of NCI-H295R cells transfected with si-AKR1B10. The AMPK/mTOR signalling pathway was activated by FNDC5 overexpression, which was subsequently suppressed by AKR1B10 knockdown. Collectively, FNDC5 overexpression inhibited proliferation, migration and invasion while promoting apoptosis of NCI-H295R cells via triggering the AMPK/mTOR signalling pathway. These effects were counteracted by AKR1B10 knockdown.

A high efficiency CO2 concentration interval optimization method for lettuce growth.

The decline in carbon fertilization effects has shifted scientific focus toward the efficient and suitable regulation of CO2 concentration ([CO2]) for plant growth. In this study, the rapid A/CO2 response curve (RAC) data of lettuce were analyzed statistically under nine photosynthetic photon flux densities (PPFDs) and four temperatures. An efficient CO2 supplementation interval acquisition method based on the frequency distribution characteristics of RACs was proposed. The characteristic subsections of jumping were obtained depending on the frequency distribution of RACs. The cumulative contribution rate (CCR) of the characteristic subsections were >97 %, which showed the efficiency of the method. Additionally, U-chord curvature theory was used to simultaneously obtain the optimal regulated [CO2] for the same RAC curves, and the results showed that the [CO2] obtained by U-chord length were all within the interval obtained by the method, which proved the rationality of the method. The [CO2] interval supplement improved the daily CO2 exchange rate by 20.27 % and 21.64 % at 150 and 200 µmol·m-2·s-1, and increased the lettuce fresh biomass by 26.78 % at 150 µmol·m-2·s-1. Based on the interval of [CO2] efficient utilization regulation at various temperatures and PPFDs, a genetic algorithm-support vector regression model was built with R2 of the model was >0.84 and the root mean square error was <35.2256 µmol·mol-1. In conclusion, the [CO2] interval obtained by this method has a positive effect on lettuce growth. This work provides a new method for obtaining high-efficiency supplementary concentration of CO2 during the growth of lettuce.

Effects of 1,25-(OH)(2)D (3) on the expressions of vitamin D receptor, STAT5 and cytoskeletal rearrangement in human monocytes incubated with sera from type 2 diabetes patients and diabetic nephropathy patients with uremia.

OBJECTIVE: To explore the effects of 1,25-(OH)(2)D(3) and lipopolysaccharide (LPS) plus human recombinant interleukin-15 (IL-15) on expression of vitamin D receptor (VDR) and STAT5, and cytoskeletal rearrangement in human monocytes incubated with sera from type 2 diabetes (T2DM) patients and diabetic nephropathy (DN) patients with uremia. MATERIALS AND METHODS: Peripheral sera were isolated from healthy volunteers (control group, T2DM patients and DN uremic non-dialysis patients). After incubation with or without 1,25(OH)(2)D(3), THP-1 monocytes were treated with LPS plus IL-15 prior to the collection of cells and supernatants. VDR mRNA transcription was examined by RT-PCR, whilst THP-1 monocytic VDR, STAT5 and p-STAT5 expressions were investigated by Western blotting. Concentrations of IL-6 and monocyte chemoattractant protein-1 (MCP-1) in supernatants were assessed by ELISA. Immunofluorescence and a laser confocal microscopy was used to examine the expression of VDR and cytoskeletal proteins. RESULTS: Compared to the normal control, LPS and IL-15 down-regulate monocytic VDR expression in T2DM patients and DN uremic patients, whilst with cytoskeletal rearrangement, they up-regulate p-STAT5 expression as well as IL-6 and MCP-1 activity. Such effects could be in part blocked by 1,25-(OH)(2)D(3). CONCLUSION: The above results suggest that the anti-inflammatory mechanism of 1,25-(OH)(2)D(3) may be related to cytoskeletal proteins, VDR and STAT5 signaling pathway.

Functional characterization of TNF-α in grass carp head kidney leukocytes: induction and involvement in the regulation of NF-κB signaling.

Tumor necrosis factor-alpha (TNF-α) is a potent regulatory cytokine, which serves as a key mediator of inflammation, immunity and apoptosis in mammals. Identification, expression and regulatory effects of TNF-α have been reported in various fish species, showing the structural and functional similarity or discrepancy between each other. In this study, TNF-α was identified from grass carp (Ctenopharyngodon idella) and the deduced grass carp TNF-α (gcTNF-α) protein possessed the TNF family signature motifs, a protease cleavage site, a transmembrane domain and two conserved cysteine residues. Further studies showed that gcTNF-α expression was induced with a rapid kinetics by immune challenge in vitro and in vivo. To characterize the function of gcTNF-α, recombinant gcTNF-α (rgcTNF-α) was prepared by using the Escherichia coli expression system. It was shown to enhance the mRNA expression of gcTNF-α and gcIL-1ß in head kidney leukocytes (HKLs), confirming the biological activity of rgcTNF-α. In the same model, NF-κB inhibitor (PDTC) was able to attenuate rgcTNF-α-induced gcTNF-α mRNA expression, implying the involvement of NF-κB pathway in fish TNF-α action. This notion was reinforced by the finding that rgcTNF-α could induce the phosphorylation of IκBα in a time-dependent oscillation in HKLs, indicating a dynamical variation of NF-κB activity as seen in mammals. In addition, rgcTNF-α could up-regulate the expression of two TNF receptor-associated factors (TRAF), TRAF1 and TRAF2, in a time- and dose-dependent manner, suggesting that gcTNF-α may function as a regulator of fish NF-κB pathway. These results for the first time reveal the link of gcTNF-α to the NF-κB pathway and provide a better understanding of TNF-α signaling in teleost immunity.

Treg/Th17 functional disequilibrium in Chinese uremia on hemodialysis: a link between calcification and cardiovascular disease.

AIM: To investigate the correlation of the functional disequilibrium of regulatory T cells (Treg)/T-helper (Th17) cells with calcification and to explore the significance of their influence on the outcome of cardiovascular disease (CVD) in uremic patients after hemodialysis (HD). METHODS: Out of 66 uremia patients, 36 patients had CVD after HD (maintenance hemodialysis (MHD) group1) and 30 patients did not have CVD (MHD group2). Twenty healthy volunteers were selected as normal control group. Peripheral blood mononuclear cells were isolated and treated with recombinant human bone morphogenetic protein-2 (rhBMP-2). Treg and Th17 frequencies were measured by flow cytometry. Forkhead/winged helix transcription factor (Foxp3) and retinoic acid receptor-related orphan receptor-γt (ROR-γt) mRNA expressions were measured by real-time quantitative polymerase chain reaction. Levels of interleukin (IL)-10 and IL-17 were detected by enzyme-linked immunosorbent assay. RESULTS: When compared with controls, rhBMP-2 upregulates Treg/Th17 functional disequilibrium in uremia patients, displaying higher Treg and Th17 frequencies, Foxp3 and ROR-γt expressions, and levels of cytokines (p < 0.05). These differences were also significant between MHD group1 and group2 (p < 0.05). It was also observed that Treg/Th17 functional disequilibrium was not only correlated with a calcification state but also consistent with the CVD. CONCLUSION: The Treg/Th17 cell function disequilibrium might act synergistically with calcification in the high incidence of CVD after HD.

SFRP2 is a Novel Diagnostic Biomarker and Suppresses the Proliferation of Pituitary Adenoma.

Pituitary adenoma (PA) constitutes one of the most common intracranial tumors. The present study was designed to identify potential diagnostic markers for PA. We used gene expression profiles (GEO: GSE26966 and GEO: GSE63357 datasets) derived from human PA and nontumor samples that were made freely accessible by the gene expression omnibus (GEO) datasets. Differentially expressed genes (DEGs) were screened between 14 normal specimens and 34 PA specimens by the use of the limma package of the R. The diagnostic genes were determined using a LASSO regression model and SVM-RFE analysis. SFRP2 expression in PA cells was analyzed using RT-PCR, and the effect of SFRP2 dysregulation on PA cell proliferation was measured using CCK-8 analysis. In this study, 361 DEGs were identified: 309 genes were downregulated and 52 genes were upregulated. The results of KEGG assays revealed that the 361 DEGs were mainly enriched in the PI3K-Akt signaling pathway, MAPK signaling pathway, growth hormone synthesis, secretion and action, and AGE-RAGE signaling pathway in diabetic complications. Results from the LASSO regression model and the SVM-RFE analysis indicated that LOC101060391 and SFRP2 were diagnostic genes. In contrast to normal tissue, the expressions of LOC101060391 and SFRP2 were much lower in PA samples. According to the ROC assays, high LOC101060391 and SFRP2 expression had an AUC value >0.9 for PA. Upregulation of SFRP2 distinctly inhibited the proliferative capacity of PA cells, as shown by CCK-8 analysis. Furthermore, knockdown of SFRP2 had an influence on cell growth in both the AtT-20 and HP75 cell lines. Taken together, our findings indicate that LOC101060391 and SFRP2 have diagnostic potential for PA. Furthermore, SFRP2 may be an antioncogene and a therapeutic target for PA.

Response analysis of fluorescence parameters of tomato seedlings oriented to vertical light environment adaptation.

Seedling quality greatly affects the subsequent survival, quality and yield of tomatoes. To explore the response of tomato seedlings on vertical light, we investigated the continuous trends of chlorophyll fluorescence parameters in six vertical light intensities and Pearson's correlation analysis of them. The results showed that the dark fluorescence parameters of Fm, Fv/Fm highly correlated with the photosynthetic photon flux density (PPFD) while NPQ, Y(NPQ), Y(NO) were highly correlated with the day of light processing (DLP). With increasing PPFD, the Fv/Fm decreased, the residual sum of curves increased and the scaling factor (S) was decreased. The photoinhibition phenomenon was relieved to different degrees on DLP 4. L4 (243.17 ± 4.37 µmol m-2 s-1) was the fastest light adaptation, L5 (295.34 ± 5.42 µmol m-2 s-1) was the second. ΦPSII accumulation was greatest in L4 and second in L5. Both L4 and L5 seedling health index and dry weight were significantly higher than L1 (53.20 ± 1.55 µmol m-2 s-1). L4 had the highest Chl a/b and total soluble sugar. It can be concluded that L4 was the best vertical PPFD with the highest light-adaption. The larger the PPFD, the greater the curve deviation, the greater the degree of data discretization, and the higher the photoinhibition. The more appropriate the light intensity is, the faster the seedlings light-adapted are. Therefore, the rapid and proper adjustment of light intensity is the key to obtain high quality tomato seedlings.

Effect of Bisphenol A-Mediated RBP-4 on Pregnancy Outcomes in Nonobese Pregnant Female with Subclinical Hypothyroidism.

Hypothyroidism is a systemic hypometabolic syndrome caused by the thyroxine resistance or a reduction in its extent. It is an endocrinopathy secondary to gestational diabetes and occurs usually without significant symptoms. This study explored the effect of bisphenol A (BPA)-mediated retinol-binding protein 4 (RBP-4) on pregnancy outcomes in a nonobese pregnant female with subclinical hypothyroidism. Three hundred nonobese pregnant females who had that established pregnancy files and had regular obstetric examinations from January 2021 to March 2022 were enrolled and classified with 100 cases in each group as early pregnancy (6-12 weeks of gestation), second-trimester (13-24 weeks of gestation), and third-trimester groups (25-36 weeks of gestation). Thirty pregnant women with subclinical hypothyroidism were selected as subjects, and another thirty pregnant women with normal thyroid function were selected as the normal control group. Thyroid function (thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), free T4 (FT4), and thyroid peroxidase antibody (TPO-Ab)) was measured by immunoelectrochemiluminescence. The level of BPA in urine was determined by solid-phase extraction high-performance liquid chromatography-tandem mass spectrometry. Serum RBP4 levels were determined by enzyme-linked immunosorbent assay. The level of TSH in the third-trimester group was higher than that in the first- and second-trimester groups, while the levels of FT3, FT4, and TPO-Ab were lower than those in the other two groups (P < 0.05). TSH in the second-trimester group was higher than that in the first-trimester group, while FT3, FT4, and TPO-Ab levels were lower than those in the first-trimester group (P < 0.05). The levels of BPA and RBP4 in gestational diabetes mellitus and hypertension were higher than those in the nongestational period, and the levels of BPA and RBP4 in gestational intrahepatic cholestasis and anemia were higher than those in the nongestational period, and the levels of BPA and RBP4 in preterm delivery were higher than those in nongestational period (P < 0.05). Also, the level of urinary BPA in the hypothyroidism group was higher than that in the normal control group (P < 0.05) and the level of serum RBP4 in the hypothyroidism group was higher than that in the normal control group (P < 0.05). According to multivariate logistic regression analysis, age ≥30 years and the ascending BPA and RBP4 were risk factors for subclinical hypothyroidism during pregnancy in the nonobese female. BPA and RBP-4 are closely related to the pregnancy outcome of nonobese subclinical hypothyroidism in the pregnant female. The degree of BPA and RBP-4 in adverse pregnancy outcomes is increased, which is the risk factor for nonobese subclinical hypothyroidism.

Association between sleep-disordered breathing and periodontal diseases: A systematic review protocol.

Background: Sleep-disordered breathing (SDB) is a chronic sleep-related breathing disorder, considered associated with increased risk of cardiovascular disorders, metabolic disorders, cognitive dysfunction and behavior changes. Periodontal diseases are chronic infectious diseases that are also believed to be associated with cardiovascular diseases, metabolic syndrome and cognitive dysfunction. Several studies have indicated that SDB may be associated with periodontal diseases through certain mechanisms such as inflammation response, oxidative stress and oral dryness. The aim of this systematic review is to explore the association between SDB and periodontal diseases in an integrated approach. Materials and Methods: This systematic review will include cohort studies, cross-sectional studies and case-control studies that are identified by electronic and manual searches. Electronic searches will be conducted in the following databases: PubMed, Embase, Scopus and Web of Science. Our search will cover articles published from inception of databases to March 2022 without restrictions in language and settings. Pre-determined eligibility criteria include: participants (participants without a history of respiratory diseases, history of periodontal treatment within the past 6 months and history of medication that is known to influence SDB or periodontal diseases); exposure (participants who have been diagnosed with SDB or at high-risk for SDB); comparison (participants without SDB); and outcome (periodontal parameters, such as probing depth, clinical attachment level, bleeding on probing, radiographic bone loss). Two authors will perform study screening and data extraction independently and in duplicate. All discrepancies will be solved by discussion. The methodological quality of included studies will be assessed using the Newcastle-Ottawa Scale. Discussion: This systematic review will summarize the existing evidence on the association between SDB and periodontal diseases, a topic of controversy and clinical significance. Its findings can provide evidence for the development of relevant prevention and treatment strategies. The results will be disseminated through peer-reviewed journals. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/, identifier: CRD42022313024. Registered on March 28th 2022.

Lentiviral-mediated RNAi targeting p38MAPK ameliorates high glucose-induced apoptosis in osteoblast MC3T3-E1 cell line.

The p38 mitogen activated protein kinase (p38MAPK) pathway is an important signaling cascade involved in cell growth, differentiation and apoptosis. High glucose activates p38MAPK pathway in different cells, including osteoblasts. In the present study, role of p38MAPK in high glucose induced osteoblast apoptosis and potential of RNA interference (RNAi) targeting p38MAPK as a therapy strategy have been reported. Lentiviral-mediated RNAi effectively reduced p38MAPK and p-p38MAPK expressions in osteoblastic cell line (MC3T3-E1) following high glucose (22 mM) induction. Inhibition of p38MAPK activity significantly suppressed high glucose induced apoptosis of MC3T3-E1 cell and was confirmed by flow cytometry and ultra-structural examination by transmission electronic microscope. Inhibition of p38MAPK also significantly attenuates caspase-3 and bax protein expressions, but increased significantly bcl-2 expression as determined by Western blot analysis. The results suggested that p38MAPK mediates high glucose induced osteoblast apoptosis, partly through modulating the expressions of caspase-3, bax and bcl-2. Inhibition of p38MAPK with lentiviral-mediated RNAi or its specific inhibitor provides a new strategy to treat high glucose induced osteoblast apoptosis.

Maternal hypothyroidism during pregnancy alters the function of the retinol-binding protein 4-mediated mitochondrial permeability conversion pore in the kidneys of offspring rats.

OBJECTIVES: To determine the role of the RBP4/PiC/SIRT3 signaling pathway in the opening of the mitochondria permeability transition pore (mPTP) in offspring rats with hypothyroidism during pregnancy. METHODS: Sixty Sprague-Dawley (SD) rats were employed in this study. Pregnancy was deemed successful when a sperm was found in the uterus. After one week of pregnancy, offspring rats were divided into the following groups: overall hypothyroidism group (OH group), subclinical hypothyroidism group (SCH group), and normal control group (CON group). The establishment of the hypothyroidism model was confirmed when the serum thyroid stimulating hormone (TSH) levels were higher than normal value and TT4 level was within the normal range. The renal mitochondria of offspring rats were extracted on the 14th postnatal day (P14) and 35th postnatal day (P35). RESULTS: At P14, no significant differences in the degree of mPTP opening and expression of phosphoric acid carrier vector (PiC) were detected between the rats in the OH group and the SCH group. However, the expression level of silent mating-type information regulation 3 homolog (SIRT3) was markedly reduced. Retinol-binding protein 4 (RBP4) expression increased in the rats from the OH group, relative to that in those from the SCH group. At P35, the degree of mPTP opening and the expression levels of PiC and RBP4 in the OH group were higher than those in the SCH group. However, SIRT3 expression in the OH group was lower than that observed in the SCH group. CONCLUSION: RBP4 plays an important role in early renal mitochondrial damage and renal impairment in rats suffering from hypothyroidism during pregnancy. The RBP4/PiC/SIRT3 pathway is thus involved in the opening of the renal mPTP in offspring rats with hyperthyroidism.

Water-washed hydrochar in rice paddy soil reduces N2O and CH4 emissions: A whole growth period investigation.

Hydrochar (HC), an environment-friendly material, enhances soil carbon sequestration and mitigate greenhouse gases (GHGs) emissions in croplands. In this study, the water-washed HC (WW-HC) was applied to paddy soil to investigate effects on nitrous oxide (N2O) and methane (CH4) emissions during rice growth period. Four treatments, namely control (without N fertilizer and WW-HC), N fertilizer (WW-HC00), N fertilizer with 0.5 wt% WW-HC (WW-HC05) and N fertilizer with 1.5 wt% WW-HC (WW-HC15), were established. Results showed the WW-HC addition reduced N2O and CH4 emissions, global warming potential (GWP) and greenhouse gas intensity (GHGI) during the growing season. Moreover, the WW-HC application reduced N2O cumulative emission (P < 0.05) (by 28.6% and 23.8% for WW-HC05 and WW-HC15, respectively). It was mainly due to the reduced ratio of (nirK + nirS) to nosZ under WW-HC15 (P < 0.05). Compared with WW-HC00, the WW-HC05 reduced CH4 cumulative emissions by 14.8%, while the WW-HC15 increased by 9.7%. This might be ascribed to the significantly reduced expression of the methanogenic mcrA gene and ratio of mcrA to pmoA by WW-HC (P < 0.05). The WW-HC05 amendment decreased GWP and GHGI by 18.6% and 32.5%, respectively. Furthermore, the WW-HC application greatly improved nitrogen use efficiency by 116-145% compared with the control. Our study indicates the WW-HC application is a promising GHGs mitigation practice in paddy fields.

PEDF relieves kidney injury in type 2 diabetic nephropathy mice by reducing macrophage infiltration.

INTRODUCTION: Pigment epithelium-derived factor (PEDF) is a multifunctional protein with anti-angiogenic, antioxidant and anti-inflammatory properties. PEDF is involved in the pathogenesis of diabetic retinopathy, but its exact role in diabetic kidneys remains unclear. P78-PEDF is an active peptide sequence consisting of 44 amino acids with biological activity similar to that of PEDF. The present study aimed to investigate whether PEDF can alleviate renal damage in type 2 diabetic nephropathy mice by inhibiting macrophage infiltration. MATERIAL AND METHODS: The db/db mice were randomly divided into a diabetes PEDF intervention group (DM-P78-PEDF), a diabetes empty carrier intervention group (DM-Vehicle), and a diabetes mellitus group (DM). Subsequently, they were injected subcutaneously P78-PEDF (0.3 µg/g/d) and PBS for 6 weeks. The ratio of kidney weight to body weight was observed in the mice. An automatic biochemical analyser was used to determine fasting blood glucose (GLU), blood urea nitrogen (UREA), serum creatinine (CREA), and haemoglobin (Hb) content. Histological and ultrastructural pathological changes in the kidneys were examined through H&E and PAS staining. Kidney tissue levels of interleukin-1ß (IL-1ß), interleukin 6 (IL-6), tumour necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ) were determined by ELISA. Expression of the macrophage infiltration and typing as well as that of PEDF, NF-kB, and TLR4 was evaluated in the kidneys. RESULTS: PEDF was located in glomeruli, and the expression of PEDF protein and mRNA in the kidney of diabetic mice declined significantly. Compared with diabetic mice treated with vehicle, continuous infusion of P78-PEDF could reduce blood urea nitrogen, serum creatinine (CREA), renal macrophage recruitment, inflammatory cytokines, and histological changes and restore the expression of TLR4/NF-κB signalling pathway-related factors in diabetic mice. CONCLUSION: These findings highlight the importance of P78-PEDF peptide as a potential treatment in the occurrence and development of diabetic renal injury.

Homeobox A5 activates p53 pathway to inhibit proliferation and promote apoptosis of adrenocortical carcinoma cells by inducing Aldo-Keto reductase family 1 member B10 expression.

Aldo-Keto Reductase Family 1 Member B10 (AKR1B10) and Homeobox A5 (HOXA5) are both down-regulated in adrenocortical carcinoma (ACC), and HOXA5 is predicted to bind to the promoter of AKR1B10. We aimed to investigate whether HOXA5 could bind to AKR1B10 to regulate ACC cells proliferation and apoptosis. The expression of AKR1B10 and HOXA5 in ACC patients and the relationship of their expression between ACC prognosis were evaluated by searching database. Then, NCI-H295R cells were overexpressed to detect the alteration of cell proliferation, apoptosis and the expression of p53 and p21 proteins. The interaction between AKR1B10 and HOXA5 was validated by luciferase report and chromatin immunoprecipitation. Finally, NCI-H295R cells were silenced with HOXA5 in the presence of AKR1B10 overexpression, and then cell proliferation and apoptosis were also assessed. Results revealed that AKR1B10 and HOXA5 are down-regulated in ACC patients and the low expression of it is correlated with low percent of overall survival (OS) and disease free survival (DFS). Compared with Y1 cells, SW-13 and NCI-H295R cells exerted lower expression of AKR1B10 and HOXA5. AKR1B10 significantly inhibited cell viability, colony formation and expression of Ki67 and PCNA, but promoted apoptosis and expression of p53 and p21 in NCI-H295R cells. HOXA5 could interact with AKR1B10 and enhance AKR1B10 expression. Furthermore, HOXA5 knockdown obviously blocked the effect of AKR1B10 overexpression on NCI-H295R cells proliferation and apoptosis. In conclusion, HOXA5 could bind to AKR1B10 promotor to increase its expression, activate p53 signaling, thereby inhibiting proliferation and promoting apoptosis of ACC cells.