A visualized and scientometric analysis of research trends of weight loss in overweight/obese children and adolescents (1958-2021).

Background: Weight loss is an appropriate approach to reduce the health risks associated with overweight/obese children and adolescents, and the optimal method of weight loss requires further research. This study systematically explores scientific co-operation, disciplinary interaction, hotspots and trends in the field of weight loss in overweight/obese children and adolescents (WLOCA), and provides references for further research. Methods: Citespace 5.8.R1 (64-bit) was adopted to conduct a comprehensive visualization analysis of the literature on WLOCA from Web of Science Core Collection, including publication, institution, country/region, author, journal, keywords and reference. Results: 2,513 papers were found in the Web of Science Core Collection, and the annual number of papers published has increased significantly since 2003. Cincinnati Children's Hospital is the institution with the largest number of publications, while Washington University plays a pivotal role in the collaboration network. In terms of nations, USA has made greater contributions than the rest in terms of the number of publications and global co-operation research. The most influential authors in this field are Thomas H. Inge, Thomas Reinehr, Todd M. Jenkins, Epstein LH, Ogden CL, etc. The most active journals are "Obesity," "International Journal of Obesity," "Obesity Surgery," "Pediatrics," etc. which are characterized by interdisciplinary interactions. Research hot topics mainly include "assessment of obesity and pathophysiological mechanism," "comprehensive intervention," and "bariatric surgery," and there's a gradual shift from "lifestyle intervention" and "pathophysiological mechanism" to "clinical surgical application." In addition, disciplinary integration and comprehensive research, targeted intervention and treatment, and prospective research are the future research trends. Conclusion: The overall trend in WLOCA study is positive. The main contribution of this study is to reveal the overall picture of the research in this field with visual maps and detailed data by combining quantitative with qualitative approaches, which can provide valuable references for relevant researchers to quickly understand the status of studies on WLOCA, to seek co-operation, and grasp research hotspots and frontier trends.

Greenhouse gas reduction and nitrogen conservation during manure composting by combining biochar with wood vinegar.

The constant greenhouse gases (GHGs) and ammonia emissions during pig manure (PM) composting have made large contributions to air pollution and global temperature rise. This study aimed to evaluate the addition of biochar (B) and wood vinegar (WV) to reduce GHGs emissions and improve nitrogen retention and microbial activities during PM composting. Different treatments, carried out under a 1:2 ratio (dry weight) of PM and sawdust mixture with the addition of B (5%) and various proportions of WV, include a control treatment (CT) without the addition of B and WV and, B, B+0.5%WV, B+1.0%WV, B+1.5%WV, and B+2.0%WV treatments. The results indicated that the addition of B could accelerate the composting process in contrast to CT. In addition, various amounts of WV with B decreased NH3, CO2, CH4 and N2O emissions by 18.82-35.88%, 1.38-15.39%, 16.98-62.73%, and 4.47-19.91%, respectively. Furthermore, in contrast to the B treatment, WV addition was more effective in decreasing GHGs and NH3 emissions, and the B+1.0% WV treatment displayed the lowest nitrogen loss (2.12%) and GHGs emissions (11.62 g/kg). The bacterial community analysis demonstrated that synergistic application of WV and B can increase the relative abundance of Proteobacteria which can contribute to nitrogen fixation and reduction of nitrogen loss. The results proved that combining B with WV can be a feasible strategy to effectively reduce GHGs emissions and improve nitrogen conservation in the composting industry.

MiRNA-221-3p desensitizes pancreatic cancer cells to 5-fluorouracil by targeting RB1.

Pancreatic cancer is a highly lethal disease due to its rapid dissemination and resistance to conventional chemotherapy. MicroRNAs (miRNAs) are emerging as novel regulators of chemoresistance, which modulate the expression of drug resistance-related genes. MiRNA-221 has been reported to be associated with chemoresistance in various types of cancer. But the detailed molecular mechanism about miR-221-3p regulating 5-fluorouracil (5-FU) resistance in human pancreatic cancer remains to be clarified. In this study, we investigated the association between miR-221-3p expression and 5-FU sensitivity. Studies on pancreatic cancer cell lines suggested an increased 5-FU resistance with miR-221-3p over-expression. In addition, the results indicated that miR-221-3p down-regulated RB1 expression by directly binding to its 3'-UTR and therefore caused increased several aspects of pancreatic cancer pathogenesis, including proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Collectively, our findings revealed the important role of miR-221-3p in promoting 5-FU resistance of pancreatic cancer cells and provided a potential therapeutic target for pancreatic cancer.

MicroRNA-320a promotes 5-FU resistance in human pancreatic cancer cells.

The drug-resistance of pancreatic cancer cells results in poor therapeutic effect. To predict the therapeutic effect of the chemotherapy drugs to specific patients and to reverse the resistance of pancreatic cancer cells are critical for chemotherapy of pancreatic cancer. MicroRNAs (miRNAs) have been reported to play important roles in the genesis of drug-resistance of various cancer types. There are also many advantages of miRNAs in diagnosis and therapy of disease. Although several miRNAs regulating 5-Fluorouracil (5-FU) resistance in human pancreatic cancer have been reported, the detailed molecular mechanism remains to be determined. In this study, we found that miR-320a was significantly up-regulated in 5-FU resistant pancreatic cancer cells. Over-expression of miR-320a strongly contributed to pathogenesis of pancreatic cancer, which was represented by the increased proliferation, invasion, metastasis, drug-resistance characteristics and the epithelial-to-mesenchymal transition. Furthermore, we demonstrated that miR-320a was able to bind to 3'UTR of PDCD4 mRNA, and mediated its down-regulation in 5-FU resistance of human pancreatic cancer cells. Whereas restoration of PDCD4 expression could partially attenuate the function of miR-320a in pancreatic cancer. Taken together, our study demonstrated that miR-320a played important role in regulating 5-FU resistance by targeting PDCD4 and might be developed as new therapeutic target for pancreatic cancer.

MicroRNA-193b inhibits the proliferation, migration and invasion of gastric cancer cells via targeting cyclin D1.

MicroRNAs have been involved in RNA silencing and post-transcriptional regulation of gene expression and also play important roles in tumorigenesis and tumor progression. MiR-193b was previously reported to act as tumor suppressor in diverse cancers. However, little is known about the expression, function and mechanism of miR-193b in gastric cancer (GC). In this study, we investigated the expression of miR-193b in 50 GC cases and found that miR-193b was significantly reduced in GC tissues compared with the adjacent normal gastric tissues. Moreover, lower-level of miR-193b was also associated with a more aggressive GC phenotype. We further demonstrated that miR-193b can inhibit the proliferation, migration and invasion of HGC-27 and MGC-803 GC cells. Further mechanism study indicated that CCND1 was a direct target of miR-193b in GC. Overexpression of miR-193b inhibited the expression of CCND1, and knock-down of CCND1 inhibited the proliferation of GC cells, suggesting that miR-193b exerted its anti-tumorigenic role in GC cells through targeting CCND1 gene.

MicroRNA-21 induces 5-fluorouracil resistance in human pancreatic cancer cells by regulating PTEN and PDCD4.

Pancreatic cancer patients are often resistant to chemotherapy treatment, which results in poor prognosis. The objective of this study was to delineate the mechanism by which miR-21 induces drug resistance to 5-fluorouracil (5-FU) in human pancreatic cancer cells (PATU8988 and PANC-1). We report that PATU8988 cells resistant to 5-FU express high levels of miR-21 in comparison to sensitive primary PATU8988 cells. Suppression of miR-21 expression in 5-Fu-resistant PATU8988 cells can alleviate its 5-FU resistance. Meanwhile, lentiviral vector-mediated overexpression of miR-21 not only conferred resistance to 5-FU but also promoted proliferation, migration, and invasion of PATU8988 and PANC-1 cells. The proresistance effects of miR-21 were attributed to the attenuated expression of tumor suppressor genes, including PTEN and PDCD4. Overexpression of PTEN and PDCD4 antagonized miR-21-induced resistance to 5-FU and migration activity. Our work demonstrates that miR-21 can confer drug resistance to 5-FU in pancreatic cancer cells by regulating the expression of tumor suppressor genes, as the target genes of miR-21, PTEN and PDCD4 can rescue 5-FU sensitivity and the phenotypic characteristics disrupted by miR-21.

The up-regulation of miR-199b-5p in erythroid differentiation is associated with GATA-1 and NF-E2.

MicroRNAs (miRNAs) represent a class of small non-coding regulatory RNAs that play important roles in normal hematopoiesis, including erythropoiesis. Although studies have identified several miRNAs that regulate erythroid commitment and differentiation, we do not understand the mechanism by which the crucial erythroid transcription factors, GATA-1and NF-E2 directly regulate and control differentiation via miRNA pathways. In this study, we identified miR-199b-5p as a key regulator of human erythropoiesis, and its expression was up-regulated during the erythroid differentiation of K562 cells. Furthermore, the increase of miR-199b-5p in erythroid cells occurred in a GATA-1- and NF-E2-dependent manner during erythrocyte maturation. Both GATA-1 and NF-E2 bound upstream of the miR-199b gene locus and activated its transcription. Forced expression of miRNA-199b-5p in K562 cells affected erythroid cell proliferation and maturation. Moreover, we identified c-Kit as a direct target of miR-199b-5p in erythroid cells. Taken together, our results establish a functional link among the erythroid transcription factors GATA-1/NF-E2, miR-199b-5p and c-Kit, and provide new insights into the coupling of transcription and post-transcription regulation in erythroid differentiation.

A NIR BODIPY dye bearing 3,4,4a-trihydroxanthene moieties.

A novel 3,4,4a-trihydroxanthene-fused pyrrole 2 was synthesized by the reaction of 2,3,4,4a-tetrahydro-1H-xanthen-1-one with 3-phenyl-2H-azirine in the presence of LDA. Utilizing this pyrrole 2, a NIR BODIPY 1 (λ(abs) = 732 nm, λ(em) = 747 nm) has been prepared. The new BODIPY 1 was stable, non-cytotoxic, and suited to labeling living cells for imaging assay in the NIR region.

Spatio-temporal expression of a novel neuron-derived neurotrophic factor (NDNF) in mouse brains during development.

BACKGROUND: Neuron-derived neurotrophic factor (NDNF) is evolutionarily well conserved, being present in invertebrate animals such as the nematode, Caenorhabditis elegans, as well as in the fruit fly, Drosophila melanogaster. Multiple cysteines are conserved between species and secondary structure prediction shows that NDNF is mainly composed of beta-strands. In this study, we aimed to investigate the function of NDNF. RESULTS: NDNF is a glycosylated, disulfide-bonded secretory protein that contains a fibronectin type III domain. NDNF promoted migration and growth and elicited neurite outgrowth of mouse hippocampal neurons in culture. NDNF also protected cultured hippocampal neurons against excitotoxicity and amyloid beta-peptide toxicity. Western blotting showed that NDNF was exclusively expressed in the brain and spinal cord. Immunostaining indicated that NDNF was expressed by neurons and not by astrocytes. Cajal-Retzius cells, cortex neurons, hippocampus neurons, olfactory mitral cells, cerebellar purkinje cells, cerebellar granular cells and spinal neurons were found to be NDNF-positive. NDNF expression was observed in the neurons during development. CONCLUSIONS: The results of this study indicated that NDNF is a novel neurotrophic factor derived from neurons that may be useful in the treatment of neuronal degeneration diseases and nerve injuries.

[Preventing steroid-induced osteonecrosis of the femoral head with Liuwei dihuang pills and molecular mechanism].

OBJECTIVE: To evaluate the effects and the molecular mechanism of Liuwei dihuang pills in preventing steroid-induced osteonecrosis of the femoral head (ONFH) so as to provide an experimental basis for preventing ONFH clinically. METHODS: Thirty-six adult Kunming mice (weighing 40-50 g, 46 g on average) were randomly divided into three groups (n=12): group A (control group), group B (model group) and group C (prevention group). In groups B and C, ONFH mice models were produced by intraperitoneal injection of horse serum at first (10 mL/kg) and a second injection of horse serum intraperitoneally (5 mL/kg) and prednisolone intramuscularly [45 mL/(kg x day), for 5 days] 2 weeks later. At the same time, the mice in group C were given Liuwei dihuang pills intragastrically [2 g/(kg x day)] and were given normal saline [10 mL/(kg x day)] in group B. In group A, mice were given normal saline intramuscularly and intragastrically as controls. The animals were sacrificed 2, 4, and 8 weeks after first treatment with prednisone, and femoral heads and livers were harvested to do histopathology analysis and apoptosis assay. RESULTS: Other mice survived throughout the experiment period except two death at 7 and 11 days after second injection of horse serum intraperitoneally in group B and one death at 24 hours after second injection of horse serum intraperitoneally in group C. The appearance and shape of the femoral head and the surface of cartilages were all normal. The histological observation showed: normal structures of liver and femoral head were seen in group A at each time point; swelling liver cells with small fat vacuole, unclear structure of hepatic cords and narrower sinus hepaticus were seen, the bone trabeculae of femoral head was thin, sparse and collapsed in some regions and the changes became more obvious with time in group B; group C had similar results to group A. The percentage of empty osteocyte lacunae was significantly higher in group B than in groups A and C (P < 0.01). The osteoprotegerin expression significantly decreased and the osteoprotegerin ligand expression significantly increased in group B when compared with groups A and C (P < 0.01). Apoptosis analysis showed that the apoptosis index in group B was significantly higher than that in groups A and C (P < 0.01). CONCLUSION: Liuwei dihuang pills can prevent steroid-induced ONFH by improving lipid metabolism, relieving bone lesion, and protecting against cell death.