Impact of Serious Games on Body Composition, Physical Activity, and Dietary Change in Children and Adolescents: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Over the past four decades, obesity in children of all ages has increased worldwide, which has intensified the search for innovative intervention strategies. Serious games, a youth-friendly form of intervention designed with educational or behavioral goals, are emerging as a potential solution to this health challenge. To analyze the effectiveness of serious games in improving body composition, physical activity, and dietary change, we performed a systematic review and meta-analysis of randomized controlled trials (RCTs) from PubMed, Web of Science, EMBASE, and Scopus databases. Pooled standardized mean differences (SMD) were calculated for 20 studies (n = 2238 the intervention group; n = 1983 in the control group) using random-effect models. The intervention group demonstrated a slightly better, although non-significant, body composition score, with a pooled SMD of -0.26 (95% CI: -0.61 to 0.09). The pooled effect tends to be stronger with longer duration of intervention (-0.40 [95% CI: -0.96, 0.16] for >3 months vs. -0.02 [95% CI: -0.33, 0.30] for ≤3 months), although the difference was not statistically significant (p-difference = 0.24). As for the specific pathways leading to better weight control, improvements in dietary habits due to serious game interventions were not significant, while a direct positive effect of serious games on increasing physical activity was observed (pooled SMD = 0.61 [95% CI: 0.04 to 1.19]). While the impact of serious game interventions on body composition and dietary changes is limited, their effectiveness in increasing physical activity is notable. Serious games show potential as tools for overweight/obesity control among children and adolescents but may require longer intervention to sustain its effect.

Circular RNA circSEPT9 Is Upregulated in Endometrial Cancer and Promotes Cell Invasion and Migration by Downregulating miR-186 through Methylation.

OBJECTIVE: MicroRNA-186 (miR-186) and circular RNA (circRNA) circSEPT9 are two crucial players in cancer biology, while their roles in endometrial cancer (EC) are unclear. Our preliminary sequencing analysis revealed the potential crosstalk between circSEPT9 and miR-186 in EC. MATERIALS AND METHODS: The expression levels of circSEPT9 and miR-186 in EC and paired non-tumor tissues from 64 EC patients were detected by RT-qPCRs. Correlation analysis was carried out with Pearson's correlation coefficient. The role of circSEPT9 in regulating the expression of miR-186 and the methylation of miR-186 gene was explored by RT-qPCR and methylation specific PCR (MSP), respectively. Cell invasion and migration were evaluated by Transwell assays. RESULTS: CircSEPT9 was upregulated in EC, and miR-186 was downregulated in EC. MiR-186 and circSEPT9 were inversely correlated across EC tissue samples, but not non-tumor samples. Overexpression of circSEPT9 decreased the expression levels of miR-186 and increased the methylation of miR-186 gene. CircSEPT9 increased cell invasion and migration and suppressed the role of miR-186 in inhibiting cell behaviors. CONCLUSION: Therefore, circSEPT9 is upregulated in EC and promotes cell invasion and migration by downregulating miR-186 through methylation.

Improve individual treatment by comparing treatment benefits: cancer artificial intelligence survival analysis system for cervical carcinoma.

PURPOSE: The current study aimed to construct a novel cancer artificial intelligence survival analysis system for predicting the individual mortality risk curves for cervical carcinoma patients receiving different treatments. METHODS: Study dataset (n = 14,946) was downloaded from Surveillance Epidemiology and End Results database. Accelerated failure time algorithm, multi-task logistic regression algorithm, and Cox proportional hazard regression algorithm were used to develop prognostic models for cancer specific survival of cervical carcinoma patients. RESULTS: Multivariate Cox regression identified stage, PM, chemotherapy, Age, PT, and radiation_surgery as independent influence factors for cervical carcinoma patients. The concordance indexes of Cox model were 0.860, 0.849, and 0.848 for 12-month, 36-month, and 60-month in model dataset, whereas it were 0.881, 0.845, and 0.841 in validation dataset. The concordance indexes of accelerated failure time model were 0.861, 0.852, and 0.851 for 12-month, 36-month, and 60-month in model dataset, whereas it were 0.882, 0.847, and 0.846 in validation dataset. The concordance indexes of multi-task logistic regression model were 0.860, 0.863, and 0.861 for 12-month, 36-month, and 60-month in model dataset, whereas it were 0.880, 0.860, and 0.861 in validation dataset. Brier score indicated that these three prognostic models have good diagnostic accuracy for cervical carcinoma patients. The current research lacked independent external validation study. CONCLUSION: The current study developed a novel cancer artificial intelligence survival analysis system to provide individual mortality risk predictive curves for cervical carcinoma patients based on three different artificial intelligence algorithms. Cancer artificial intelligence survival analysis system could provide mortality percentage at specific time points and explore the actual treatment benefits under different treatments in four stages, which could help patient determine the best individualized treatment. Cancer artificial intelligence survival analysis system was available at: https://zhangzhiqiao15.shinyapps.io/Tumor_Artificial_Intelligence_Survival_Analysis_System/ .

Comparative study of Cl,N-Cdots and N-Cdots and application for trinitrophenol and ClO- sensor and cell-imaging.

To understand the effect of Cl doping in carbon dots, nitrogen-doped carbon dots (N-Cdots) and nitrogen and chlorine dual-doped carbon dots (Cl,N-Cdots) were fabricated by high-temperature carbonization and low-temperature concentrated acid (HCl) acidification of dried shaddock peel, respectively. The quantum yield of Cl,N-Cdots is about four times of that of N-Cdots and the size of Cl,N-Cdots is smaller than that of N-Cdots. Furthermore, since trinitrophenol (PA) and ClO- could effectively quench the fluorescence of Cl,N-Cdots, the fluorescence sensors for determining PA and ClO- was constructed, respectively. The linear range of PA and ClO- are 0.9-90 µM and 3.24-216 µM with the limit of detection of 37.1 nM and 2.88 µM, respectively. The proposed sensor was used to detect PA in Taiyuan tap water, Wutai tap water, Wutai rain water and Wutai river water samples with encouraging results. The as-constructed sensor was also used to detect ClO- in Taiyuan tap water and commercial disinfectants. Last but not least, Cl,N-Cdots was employed as an agent for A549 and HeLa cell-imaging, possessing optimal imaging effect and ultra-low cytotoxicity. Our results suggested that Cl,N-Cdots has promising applications in sensing, water monitoring, commodity supervision and cell-imaging.

Carbon quantum dots doped with phosphorus and nitrogen are a viable fluorescent nanoprobe for determination and cellular imaging of vitamin B12 and cobalt(II).

Phosphorus and nitrogen dually-doped carbon quantum dots (PN-CQDs) were prepared from sucrose, 85% phosphoric acid and 1,2-ethylenediamine as the sources for carbon, phosphorus and nitrogen, respectively. The PN-CQDs possess good water solubility and favorable biocompatibility. The excitation/emission peaks are at 365/451 nm, but bright blue, green, or red emissions are found depending on whether the excitation wavelengths of the laser are set to 408 nm, 488 nm, or 543 nm, respectively. Fluorescence is quenched by both vitamin B12 (VB12) and Co(II) by a combination of inner filter effect and static quenching. The PN-CQDs are shown to be useful nanoprobes for determination of VB12 and Co(II). Response to VB12 is linear in the range of 2.0-31 µM. The response to Co(II) is linear in two ranges, viz. from 1.7-12 µM and from 28 to 141 µM. The limit of detection of VB12 and Co(II) are 3.0 nM and 29.4 nM, respectively. The nanoprobe was successfully applied to the analyses of VB12 in drug samples and of Co(II) in spiked water samples, and it gave satisfactory results. The nanoprobe was also applied to the determination of VB12 and Co(II) in human hepatocarcinoma cells (type SMMC7721), human pulmonary epithelial cells (type BEAS-2B), human adenocarcinoma cells (type A549), and human pheochromocytoma cells (type PC12), respectively. Graphical abstract Schematic presentation of the quenching of the fluorescence of phosphorus and nitrogen dually-doped carbon quantum dots (PN-CQDs) by vitamin B12 (VB12) and Co(II).

Sortase A-mediated chemoenzymatic synthesis of complex glycosylphosphatidylinositol-anchored protein.

Green fluorescent protein and a glycosylphosphatidylinositol (GPI) anchor containing the common core structure and a lipid chain were synthesized and then coupled together in the promotion of bacterial sortase A (SrtA), which was the first example for the synthesis of a full-size GPI-anchored protein by SrtA, demonstrating that this can be a generally useful method for GPI-anchored protein synthesis.

Chemoenzymatic synthesis of the human CD52 and CD24 antigen analogues.

Analogs of the human CD52 and CD24 antigens carrying the common core structure of glycosylphosphatidylinositol (GPI) anchors and the intact polypeptide sequences of CD52 and CD24 were chemoenzymatically synthesized. CD52 and CD24 proteins were obtained by solid-phase peptide synthesis and then coupled to chemically synthesized GPI anchors under the influence of a bacterial enzyme, sortase A, to afford the target molecules in good yields.

New method for site-specific modification of liposomes with proteins using sortase A-mediated transpeptidation.

A new method was developed for site-specific modifications of liposomes by proteins via sortase A (SrtA)-mediated transpeptidation reactions. In this regard, the enhanced green fluorescent protein (eGFP) was biologically engineered to carry at its polypeptide C-terminus the LPATG motif recognized by SrtA and used as the protein donor for linking to liposomes that were decorated with phospholipids carrying a diglycine motif as the other SrtA substrate and the eGFP acceptor. Under the influence of SrtA, eGFP was efficiently attached to liposomes, as proved by analyzing the enzymatic reaction products and the resultant fluorescent liposomes. It was observed that increasing the concentration and the distance of the diglycine motif on and from the liposome surface could significantly improve the efficiency of liposome modification by proteins. It is anticipated that this strategy can be widely useful for the modification of liposomes by other proteins.

Sortase A-catalyzed peptide cyclization for the synthesis of macrocyclic peptides and glycopeptides.

A chemoenzymatic method was developed for the synthesis of macrocyclic peptides and glycopeptides. Sortase A was found to mediate either head to tail cyclization or oligomerization and then head to tail cyclization of peptides and glycopeptides, depending on the peptide length, to produce 15-mer or higher cyclic peptides and glycopeptides.

Chemoenzymatic synthesis of glycosylphosphatidylinositol-anchored glycopeptides.

MUC1 glycopeptide was efficiently coupled to glycosylphosphatidylinositol (GPI) derivatives by sortase A (SrtA), verifying that SrtA can accept sterically hindered glycopeptide as substrate for ligation with GPIs. This work has established a practical method for the chemoenzymatic synthesis of GPI-linked glycopeptides.

Sortase A-catalyzed transpeptidation of glycosylphosphatidylinositol derivatives for chemoenzymatic synthesis of GPI-anchored proteins.

Several peptides/small proteins and glycosylphosphatidylinositol (GPI) derivatives were synthesized and compared as substrates of sortase A (SrtA), a bacterial transpeptidase, for enzymatic coupling. It was observed that peptides containing the LPKTGGS and LPKTGGRS sequences as sorting signals at the peptide C-terminus were effectively coupled to GPI derivatives having one or two glycine residues attached to the phosphoethanolamine group at the nonreducing end. This reaction was employed to prepare several analogues of the human CD52 and CD24 antigens, which are naturally GPI-anchored glycopeptides/glycoproteins. It was further observed that the trisaccharide GPI analogues 5 and 6 were better SrtA substrates than monosaccharide GPI analogue 4, suggesting that steric hindrance of the GPI analogues does not affect their peptidation reaction mediated by SrtA. Therefore, this synthetic strategy may be useful for the preparation of more complex GPI-anchored peptides, glycopeptides, proteins, and glycoproteins.

Sortase-catalyzed peptide-glycosylphosphatidylinositol analogue ligation.

It is demonstrated that sortase A (SrtA) can catalyze efficient coupling of peptides to GPI analogues with a glycine residue attached to the phosphoethanolamine moiety at the nonreducing end to form GPI-linked peptides. This represents the first chemoenzymatic synthesis of GPI-peptide conjugates and is a proof-of-concept for the potential application of SrtA to the synthesis of more complex GPI-anchored peptides/glycopeptides and GPI-anchored proteins/glycoproteins.

Down-regulation of adenine nucleotide translocase 3 and its role in camptothecin-induced apoptosis in human hepatoma QGY7703 cells.

Adenine nucleotide translocase (ANT) is known as a core component of the mitochondrial permeability transition pore (MPTP) and a key player in cell death. However, its role in camptothecin (CPT)-induced apoptosis has not been examined. We showed that CPT-induced apoptosis in QGY7703 cells and down-regulated the expression of ANT3. Using ANT3 knock-out and overexpression experiments, we provide further evidence that ANT3 plays a contributive role in CPT-induced apoptosis through induction of MPTP. We speculate that the down-regulation of ANT3 upon stimulation with CPT may be part of the molecular basis underlying the mechanism of acquired resistance to CPT.

Analysis of common gene expression patterns in four human tumor cell lines exposed to camptothecin using cDNA microarray: identification of topoisomerase-mediated DNA damage response pathways.

Camptothecin (CPT) is a potent inhibitor of DNA topoisomerase I with a wide spectrum of anti-tumor activity. Relatively little information is available regarding the relation of known topoisomerase-mediated DNA damage with other intracellular pathways. To gain an insight into the intracellular molecular mechanisms of Topoisomerase I inhibitor camptothecin-mediated DNA damage leading to cell death, we used a high-density cDNA microarray to assess sensitive early gene expression profiles in SGC7901 (gastric cancer), Hela (cervical adenocarcinoma), K562 (chronic myelogenous leukemia) and HL60 (promyelocytic leukemia) tumor cells stimulated with camptothecin for 1 h at the concentrations of GI50 (50 % growth inhibition after 24 h of treatment). Analysis of the differentially expressed genes obtained 29 response genes common to all four cell lines. Moreover, these cell lines also shared the direction of regulation. Most of these common response genes were functionally related to cell proliferation or apoptosis, and some of them were involved in ATM (ataxia-telangiectasia mutated) and ATR (ATM-and Rad3 related) checkpoint pathways, JNK (c-Jun N-terminal kinase) pathway, the survival phosphatidylinositol (PI) 3 kinase-Akt-dependent pathway, mitochondrial cell death pathway, endoplasmic reticulum (ER)-related cell death pathway, and to ubiquitin/proteasome dependent protein degradation pathway. The data provides evidence for a linkage between topoisomerase-mediated DNA damage and intracellular signaling events, which may facilitate our understanding of the camptothecin mediated molecular mechanisms of action.

Effects of paclitaxel on proliferation and apoptosis in human acute myeloid leukemia HL-60 cells.

AIM: To investigate the regulatory effect of paclitaxel on proliferation and apoptosis in human acute leukemia HL-60 cells. METHODS: HL-60 cell growth was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tertrazolium bromide (MTT) colorimetric assay. Cell cycle kinetics and apoptosis were analyzed by flow cytometry and microscopic examination. In addition, DNA microarrays containing 14,400 EST elements were used to investigate the gene expression pattern of HL-60 cells exposed to paclitaxel 1 micromol/L. RESULTS: Paclitaxel inhibited HL-60 cell growth significantly in a dose-dependent and time-dependent manner (P<0.01). Marked cell accumulation in G2/M phase and multinucleated cells were also observed after treatment with paclitaxel 0.1 and 1 micromol/L. Among 14400 EST elements, 277 genes were found to be markedly up- or down-expressed in the HL-60 cells treated with paclitaxel 1 micromol/L for 0.5 h, comprising 210 known genes and 67 unknown genes. CONCLUSION: Paclitaxel suppresses the growth of HL-60 cells in vitro by causing cell-cycle arrest and apoptosis. The results of microarray suggest that paclitaxel initiates apoptosis through multiple mechanisms.