Algorithm for community security risk assessment and influencing factors analysis by back propagation neural network.

This paper aims to accurately assess and effectively manage various security risks in the community and overcome the challenges faced by traditional models in handling large amounts of features and high-dimensional data. Hence, this paper utilizes the back propagation neural network (BPNN) to optimize the security risk assessment model. A key challenge of researching community security risk assessment lies in accurately identifying and predicting a range of potential security threats. These threats may encompass natural disasters, public health crises, accidents, and social security issues. The intricate interplay of these risk factors, combined with the dynamic nature of community environments, presents difficulties for traditional risk assessment methodologies to address effectively. Initially, this paper delves into the factors influencing safety incidents within communities and establishes a comprehensive system of safety risk assessment indicators. Leveraging the adaptable and generalizable nature of the BPNN model, the paper proceeds to optimize the BPNN model, enhancing the security risk assessment model through this optimization. Subsequent comparison experiments with traditional models validate the rationality and effectiveness of the proposed model, with hidden layer nodes set at various levels like 10, 15, 20, 25, 30, and 35. These traditional models include Convolutional Neural Network (CNN), Long Short-Term Memory Network (LSTM), Bidirectional Encoder Representations from Transformers (BERT), Generative Pre-trained Transformer (GPT), and eXtreme Gradient Boosting (XGBOOST). Experimental findings demonstrate that with 20 hidden layer nodes, the optimized model achieves a remarkable final recognition accuracy of 99.1 %. Moreover, the optimized model exhibits significantly lower final function loss compared to models with different node numbers. Increasing the number of hidden layer nodes may diminish the optimized model's fit and accuracy. Comparison with traditional models reveals that the average accuracy of the optimized model in community risk identification reaches 98.5 %, with a maximum accuracy of 99.6 %. This marks an improvement of 9%-11 % in recognition accuracy across various risk factors compared to traditional models. Regarding system response time and resource utilization, the optimized model exhibits a response time ranging from 100 ms to 120 ms and consistently lower resource utilization rates across all scenarios, underscoring its efficiency in community security risk assessment. In conclusion, this experiment sheds light on the underlying mechanisms and patterns of community safety risk formation, offering novel perspectives and methodologies for researching community safety risk assessment. The paper concludes by presenting recommendations and strategies for addressing community safety risks based on experimental analysis.

Prognostic effect of atrial fibrillation on survival in patients with hypertrophic cardiomyopathy: a meta-analysis.

OBJECTIVE: To systematically evaluate the prognostic impact of atrial fibrillation (AF) in patients with hypertrophic cardiomyopathy (HCM). METHODS: The Chinese and English databases (PubMed, EMBASE, Cochrane Library, Chinese National Knowledge Infrastructure, and Wanfang database were systematically searched to include observational studies on the prognosis of AF in cardiovascular events or death in patients with HCM; these were evaluated using Revman 5.3. RESULTS: After systematic search and screening, a total of 11 studies with a high study quality were included in this study. Meta-analysis showed that patients with HCM accompanied by AF had a higher risk of all-cause death (odds ratio [OR] = 2.75; 95% confidence interval [CI]: 2.18-3.47; P < 0.001), heart-related death (OR = 2.62; 95%CI: 2.02-3.40; P < 0.001), sudden cardiac death (OR = 7.09; 95%CI: 5.77-8.70; P < 0.001), heart-failure-related death (OR = 2.04; 95%CI: 1.24-3.36; P = 0.005), and stroke death (OR = 17.05; 95%CI: 6.99-41.58; P < 0.001) compared with patients with HCM without AF. CONCLUSION: Atrial fibrillation is a risk factor for adverse survival outcomes in patients with HCM, and aggressive interventions are needed in this population to avoid the occurrence of adverse outcomes.

Evaluation of ABC Bleeding Score and SAMe-TT2R2 Score on the Risk of Bleeding after Anticoagulation in Patients with Nonvalvular Atrial Fibrillation Complicated with Coronary Heart Disease.

Objective: To explore the predictive value of ABC bleeding score and SAMe-TT2R2 score on the risk of bleeding in patients with nonvalvular atrial fibrillation (NVAF) complicated with coronary heart disease (CHD) after anticoagulation. Methods: 149 patients with NVAF complicated with CHD were followed up in our hospital for one year. The bleeding events during the follow-up period were observed, the ABC bleeding score and SAMe-TT2R2 score were calculated, the predictive value of the two scoring methods for the main bleeding risk was analyzed by the ROC curve, and the AUC area under the ROC curve of the two scoring methods was compared by the Delong test. Results: There were 32 bleeding events during the follow-up period. The AUC of ABC bleeding score and SAMe-TT2R2 score were 0.775 (P < 0.01) and 0.624 (P < 0.05), respectively. The Delong test showed that the AUC of ABC bleeding score was significantly higher than that of SAMe-TT2R2 score (d = 2.177, P < 0.05). Conclusion: Both the ABC bleeding score and SAMe-TT2R2 score can predict the risk of bleeding after anticoagulation in patients with NVAF and CHD. The critical value of the SAMe-TT2R2 score for predicting bleeding events in patients with NVAF and CHD may need to be increased to 4 or 5, and the prediction ability of ABC bleeding score is significantly better than that of the SAMe-TT2R2 score.

Clinical Observation of Helicobacter pylori Infection and Risk Factors and Cytotoxin-Associated Protein A in Patients with Coronary Heart Disease.

The aim was to analyze the infection, influencing factors, and clinical manifestations of Helicobacter pylori infection, coronary heart disease, and cytotoxin-associated protein A infection, so as to provide reference for the improvement of clinical diagnosis and treatment level of in-depth treatment. This paper presents a clinical observation method based on Helicobacter pylori infection, risk factors, and cytotoxin-associated protein A in patients with coronary heart disease. Methods. 237 patients with CHD diagnosed and tested by 14C breath test were selected from inpatients of cardiovascular diseases in a hospital for retrospective analysis. The clinical data, serum deepening indicators, Hcy, and other factors were analyzed through general condition investigation, previous history investigation, and physical examination. The patients were observed by the SPSS22.0 statistical data processing method. The results showed that among the respondents, 175 cases were HP-positive, the infection rate was 73.8%, 77 patients with stable angina pectoris were 64.9%, and 160 patients with acute coronary heart disease were 78.1%. The difference between the groups was statistically significant (P < 0.05). Conclusion. Helicobacter pylori cytotoxic-associated protein A can increase the risk of gastric cancer, and Helicobacter pylori eradication treatment is more conducive to reduce the incidence of gastric cancer and ensure the safety of patients.

Association between T-tau protein and Aß42 in plasma neuronal-derived exosomes and cognitive impairment in patients with permanent atrial fibrillation and the role of anticoagulant therapy and inflammatory mechanisms.

BACKGROUND: This study explores whether the differences in cognitive performance among individuals with permanent atrial fibrillation (AF) are attributable to the duration of AF and anticoagulant therapy and explores the possible inflammatory mechanism of cognitive dysfunction related to AF. METHODS: A total of 260 patients aged 50-75 years without previous cerebrovascular events were enrolled in this study. These 260 patients had been divided into the AF group (140 patients) and sinus rhythm group (120 patients). In the AF group, we divided participants into cognitive impairment (CI) group (90 patients) and cognitive normal (CN) group (50 patients). In the sinus rhythm group, we also divided participants into CI group (61 patients) and CN group (59 patients). The Mini-Mental State Examination (MMSE) was used to assess the cognitive function of all participants. Neuronal-derived exosomes were enriched in peripheral blood by immunoprecipitation and were confirmed by a transmission electron microscope, nanoparticle tracking analysis, and western blot. Alzheimer's disease-pathogenic exosomal proteins and inflammatory cytokines were quantified. The association between AF and cognitive function was estimated by logistic regression analysis. ANOVA or Welch's t-test compared the difference in protein concentrations between groups. RESULTS: Non-anticoagulant therapy in patients with AF was significantly associated with CI (OR = 13.99, 95% CI: 2.67-73.36, p < .01). The incidence of dementia in patients with AF > 3 years was significantly higher than in patients with AF ≤ 3 years, but there was no significant difference in total cognitive dysfunction (mild cognitive impairment [MCI] + dementia) (p = .126). The adjusted exosome concentrations of T-tau and amyloid-ß protein 42 (Aß42) in the CI group were significantly higher than in the CN group (p < .001). The serum concentrations of IL-6 and matrix metalloproteinase-9 (MMP-9) in patients with AF were higher than those in patients with sinus rhythm (p < .001). CONCLUSION: Aß42 and T-tau in peripheral blood neuronal-derived exosomes maybe be associated with the early diagnosis of CI in patients with permanent AF. However, the value of Aß42 and T-tau for CI in patients with permanent AF still needs to be confirmed in future randomized control trials.

Repeated social defeat stress inhibits development of hippocampus neurons through mitophagy and autophagy.

The social defeat stress model is commonly used to study depression and anxiety disorder, which can significantly affect the structure and function of neurons in the hippocampus; however, the relevant mechanism in neuronal loss has not been clearly defined. In the present study, a social defeat stress model was established in mice to evaluate the impact of social defeat stress on the structure of neurons in the hippocampus using Western blotting, immunofluorescence, Nissl staining, Golgi staining and transmission electron microscopy. The results demonstrated that social defeat stress leads to disruption of homeostasis in the hippocampus and the integrity of mitochondria in hippocampal neurons was markedly affected by enhanced mitophagy and autophagy resulting in inhibition of development and growth. These findings provide new insights into the mechanisms of neuronal development and growth due to social defeat stress, which should help in the development of new strategies to combat the effects of depression and anxiety disorder.

GNAO1 as a Novel Predictive Biomarker for Late Relapse in Hepatocellular Carcinoma.

GNAO1, the alpha O1 subunit of G protein, was reported to be significantly downregulated in hepatocellular carcinoma (HCC), as well as being implicated in a variety of intracellular biological events; findings suggest that it may act as a tumor suppressor. Our goal was to further explore the expression of GNAO1 in HCC patients and its potential clinical significance. Oncomine and Kaplan-Meier plotter databases were used to assess the mRNA expression of GNAO1 in HCC tissues and patient survival time. Subsequently, immunohistochemistry (IHC) was used to measure GNAO1 protein level in tissue from 79 cases of HCC and paired adjacent tissues. The Kaplan-Meier survival analysis, Cox regression model, and prognostic nomogram were used to evaluate the prognostic role of GNAO1 in HCC. Results demonstrated that mRNA and protein expressions of GNAO1 were both lower in HCC tissues than in adjacent tissues (all p < 0.01). HCC patients with high expression of GNAO1 had better relapse-free survival (RFS) than those with low GNAO1 expression (all p < 0.05). A high expression of GNAO1, meanwhile, functioned as a good predictor of late relapse for HCC (p < 0.05). The nomogram consisting of GNAO1 expression and the tumor-node-metastasis (TNM) model presented good ability in predicting the 3-year relapse for HCC (C-index = 0.614). In conclusion, GNAO1 was a reliable biomarker of relapse prediction for HCC.

Synergistic Antioxidant Effects of Araloside A and L-Ascorbic Acid on H2O2-Induced HEK293 Cells: Regulation of Cellular Antioxidant Status.

Araloside A is a pentacyclic triterpenoid saponin, and L-ascorbic acid is a globally recognized antioxidant. In this study, coadministered araloside A and L-ascorbic acid were found to have a strong synergistic antioxidant effect, and correlations between cellular antioxidant indexes and free radical scavenging ability were found. Individual and combined pretreatment with araloside A and L-ascorbic acid increased both cell viability and antioxidant enzyme activity and inhibited the release of lactate dehydrogenase (LDH); the accumulation of malondialdehyde (MDA), lipid peroxidation (LPO) products, and H2O2; and the production of intracellular reactive oxygen species (ROS), protein carbonyls, and 8-hydroxy-2-deoxy guanosine (8-OHdG). Free radical scavenging ability was positively correlated with superoxide dismutase (SOD) and catalase (CAT) activity, the glutathione (GSH)/oxidized glutathione (GSSG) ratio, and total antioxidant capacity (T-AOC). Our study is the first investigation of araloside A and L-ascorbic acid coadministration for the treatment of diseases caused by oxidative stress. The synergistic antioxidant effects of araloside A and L-ascorbic acid support their potential as functional food ingredients for the elimination of oxidative stress-induced adverse reactions.

1-Methylcyclopropene (1-MCP) retards the senescence of Pteridium aquilinum var. latiusculum by regulating the cellular energy status and membrane lipid metabolism.

1-MCP is an ethylene inhibitor which can delay the ripening and senescence of fruits and vegetables effectively. Pteridium aquilinum var. Latiusculum (PA) is one of the wild vegetables which is famous and nutrient in China. However, the mechanism of PA preservation treated with 1-MCP has not been reported. Consequently, the effects of postharvest 1-MCP treatment on the changes in quality, energy metabolism, and membrane lipid metabolism of PA were investigated in this study. The results indicated that 1-MCP treatment could effectively inhibit the decreases in firmness, titratable acid (TA) content and the increases in weight loss rate, malondialdehyde (MDA) content, membrane permeability, and membrane lipid metabolism-related enzymes in PA. The cellular energy charge (EC) and the levels of ATP, ATP/ADP, and ATP/AMP, the activities of energy metabolism-related enzymes, NAD+, and NADH were maintained, and the decreases in unsaturated fatty acids and the ratio of unsaturated-to-saturated fatty acids in the membrane of PA cells were effectively retarded by 1-MCP treatment. A positive correlation was observed between cellular ATP levels and the ratio of unsaturated-to-saturated fatty acids, while negative correlations were observed between the ratio of unsaturated-to-saturated fatty acids and both lipid peroxidation and membrane permeability. These results indicated that higher levels of energy status, unsaturated-to-saturated fatty acid ratios, and lipid metabolism in the membrane could preserve the membrane integrity of postharvest PA and effectively extend its shelf life.

Overexpression of lncRNA HULC Attenuates Myocardial Ischemia/reperfusion Injury in Rat Models and Apoptosis of Hypoxia/reoxygenation Cardiomyocytes via Targeting miR-377-5p through NLRP3/Caspase­1/IL­1ß Signaling Pathway Inhibition.

OBJECTIVE: Acute myocardial infarction (AMI) is characterized by myocardial tissue necrosis and activation of inflammatory response. This study aims to elucidate the potential mechanism underlying the protective effects of long non-coding RNA (lncRNA) highly up-regulated in liver cancer (HULC) against myocardial ischemia/reperfusion (I/R) injury in rat models and apoptosis of cardiomyocytes. METHODS: We firstly established rat models of myocardial I/R injury and rat cardiomyocyte (H9c2 cells) models of hypoxia/reoxygenation (H/R) injury. Sprague-Dawley (SD) neonatal rats were randomized into four groups: sham, I/R, I/R+ microRNA (miR) -377-5p mimic, and I/R+ miR-377-5p antagomir, respectively. Then, histopathological examination was applied. Apoptosis was evaluated by transferase-mediated dUTP nick end labeling (TUNEL) staining. Cell vitality was measured using MTT assay. The concentrations of creatine kinase MB (CK-MB), cardiac troponin I (cTnI), interleukin (IL) -6 (IL-6), and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA). The expression of Cleaved-Caspase-3, Caspase-3, NOD-like receptor P3 (NLRP3), Caspase-1, and IL-1ß was analyzed by immunohistochemical (IHC) or Western blot analysis. RESULTS: We found that HULC was downregulated and miR-377-5p was upregulated in IR-injured myocardial tissue and the H/R-induced H9c2 cell. Overexpression of miR-377-5p increased myocardial dysfunction and apoptosis and activated formation and secretion of IL-6 and TNF-α. The preprocessing of miR-377-5p silencing emerged opposite results. Strikingly, dual luciferase reporter assay showed that HULC was a sponge of miR-377-5p. Subsequently, mechanism experiments revealed that NLRP3/Caspase­1/IL­1ß was a target axis of miR-377-5p. In vitro, the protective effect of HULC overexpression on H9c2 cell viability and inflammation was offset by miR-377-5p silencing. Finally, rescue assay suggested that HULC-miR-377-5p -NLRP3/Caspase­1/IL­1ß axis regulated the apoptosis and inflammation of H/R-induced H9c2 cells. CONCLUSIONS: Overall, these results indicate that the protective effect of HULC against myocardial I/R injury and H/R cardiomyocyte apoptosis partially relies on the inhibition of NLRP3/Caspase­1/IL­1ß signaling pathway.

Existence of myodural bridge in the trachemys scripta elegans: indication of its important physiological function / Existencia del puente miodural en trachemys scripta elegans: indicación de su importante función fisiológica

The myodural bridge (MDB) is confirmed that connecting the most of suboccipital muscles to the cervical dura mater through the posterior intervertebral spaces and widely exists in mammals and birds. In order to reveal whether the MDB is universally existing in amniota of vertebrates, we explored the existence and the morphological features of the MDB in the Trachemys scripta elegans. Twenty fresh red-eared slider specimens were observed by the gross anatomy dissection and histological analysis. In the results, three kind of muscles in the postoccipital region of the red-eared slider were found. The rectus capitis dorsum minor muscle originated from the posterior margin of the occiput (C0) and terminated at the spinous process of the atlas (C1). The transversospinales muscle was attached to the vertebral arch and the postzygapophysis of the atlas and extended to the spinous process of the axis (C2). The C2-C3 intertransversales muscle were extended from the postzygapophysis of C2 and the one of C3. The three muscles covered the dorsal interspaces among C0-C3, and meantime they were closely connected with dense connective tissues, which filled in these interspaces. Each of these thick dense connective tissue membranes sent off several short and strong fibrous bundles ventrally to merge with the cervical spinal dura mater. Furthermore the connective tissues connecting these muscles with cervical spinal dura mater directly were revealed under the microscopy and they consisted of parallel and intensive collagen fibers with orientation from dorsal to ventral. In conclusion, this study for the first time demonstrated the existence of the MDB in the testudines, in all of the dorsal atlantooccipital, atlantoaxial and C2-C3 intervertebral spaces. Based on our results and comparative anatomical evidences in recent year, it could be inferred that the MDB might be its highly conserved structure in the evolution of amniota.

Se confirma que el puente miodural (PMD) conecta la mayoría de los músculos suboccipitales con la duramadre cervical a través de los espacios intervertebrales posteriores y existe ampliamente en mamíferos y aves. Para revelar si el MDB existe universalmente en la amniota de vertebrados, exploramos la existencia y las características morfológicas del PMD en Trachemys scripta elegans. Veinte muestras se observaron mediante disección anatómica y análisis histológico. En los resultados, se encontraron tres tipos de músculos en la región occipital. El músculo recto capitis dorsum minor se originó en el margen posterior del occipital (C0) y terminó en el proceso espinoso del atlas (C1). El músculo transverso espinal se unió al arco vertebral y el proceso del atlas y se extendió al proceso espinoso del axis (C2). El músculo intertransversario C2-C3 se extendió entre los procesos transversos de C2 y el de C3. Los tres músculos cubrían los espacios intermedios dorsales entre C0-C3 y, mientras tanto, estaban estrechamente conectados con tejidos conectivos densos, que rellenaban estos espacios. Cada una de estas membranas densas de tejido conectivo envían varios haces fibrosos cortos y fuertes ventralmente para fusionarse con la duramadre espinal cervical. Además, los tejidos conectivos que conectan estos músculos con la duramadre cervical y espinal se revelaron directamente bajo microscopía y consistían en intensas fibras de colágeno, paralelas, con orientación desde dorsal a ventral. En conclusión, este estudio demostró por primera vez la existencia del PMD en los estudios de prueba, en todos los espacios dorsales atlantooccipital, atlantoaxial e intervertebral C2-C3. Sobre la base de nuestros resultados y las evidencias anatómicas comparativas de los últimos años, se podría inferir que el PMD podría ser una estructura altamente conservada en la evolución de la amniota.

Simultaneous optimization of the acidified water extraction for total anthocyanin content, total phenolic content, and antioxidant activity of blue honeysuckle berries (Lonicera caerulea L.) using response surface methodology.

The purpose of this study was to optimize the total anthocyanin content (TAC), total phenolic content (TPC), and antioxidant activity of acidified water extract from blue honeysuckle berries by response surface methodology (RSM). The optimized conditions were HCl concentration of 0.35%, liquid-solid ratio of 49.42 ml/g, and extraction temperature of 41.56°C for total anthocyanin content (24.01 ± 0.37 mg/g), total phenolic content (207.03 ± 3.31 mg/g), DPPH radical scavenging activity (68.24 ± 1.13%), and ABTS radical scavenging activity (70.05 ± 0.84%). The experimental results are consistent with the predicted values. The results showed that acidified water extraction was an effective, simple, and green technique for the extraction of total anthocyanins, total phenol, and antioxidant activity from blue honeysuckle berries.

H19/miR-148a/USP4 axis facilitates liver fibrosis by enhancing TGF-ß signaling in both hepatic stellate cells and hepatocytes.

Liver fibrosis is a wound-healing response represented by excessive extracellular matrix deposition. Activation of hepatic stellate cell (HSC) is the critical cellular basis for hepatic fibrogenesis, whereas hepatocyte undergoes epithelial-mesenchymal transition (EMT) which is also involved in chronic liver injury. Long noncoding RNA H19 has been found to be associated with cholestatic liver fibrosis lately. However, the role of H19 in liver fibrosis remains largely to be elucidated. In this study, we found that the expression of H19 was significantly upregulated in the liver tissue of CCl4 -induced mice, a toxicant-induced liver fibrogenesis model. Overexpression of H19 significantly aggravated activation of HSC and EMT of hepatocyte both by stimulating transforming growth factor-ß (TGF-ß) pathway. In terms of mechanism, H19 functioned as a competing endogenous RNA to sponge miR-148a and subsequently sustained the level of ubiquitin-specific protease 4 (USP4), which was an identified target of miR-148a and was able to stabilize TGF-ß receptor I. In conclusion, our findings revealed a novel H19/miR-148a/USP4 axis which promoted liver fibrosis via TGF-ß pathway in both HSC and hepatocyte, indicating that H19 could become a promising target for the treatment of liver fibrosis.

DNMT1 mediated promoter methylation of GNAO1 in hepatoma carcinoma cells.

Hepatocellular carcinoma (HCC) is one of the most lethal and prevalent cancers worldwide and has recently become the second most common cause of cancer-related deaths in men of developing countries. Guanine nucleotide-binding protein (G protein) has been reported to be associated with the early process of HCC. In our previous study, GNAO1, one of members of G protein, was found to be down-regulated in HCC. Thus, the present study aimed to throw light upon the mechanism of the abnormal expression of GNAO1 in HCC. First, qPCR results from two HCC cell lines (SMMC-7721 and QGY-7703) confirmed the down-expression of GNAO1, followed by the validation of the methylation status of the promoter region by bisulfite sequence PCR (BSP). Moreover, 5-Aza-2'-deoxycytidine (DAC) with Trichostatin A (TSA) treatment made it much clear that GNAO1 transcription was inhibited by promoter hypermethylation, contributing to its low expression. It was further revealed that the silencing effect was regulated by methyltransferase 1 (DNMT1), and was further enhanced by transforming growth factor ß (TGF-ß). In addition, the up-regulation of GNAO1 with the help of recombinant plasmid was also found to accelerate cell apoptosis, confirmed by flow cytometry and western blotting analysis. All these results above indicated that the promoter hypermethylation of GNAO1 might play an important role in HCC, suggesting that it might be used as a promising biomarker for HCC diagnosis and targeted therapy.

Enhanced antitumor activity in A431 cells via encapsulation of 20(R)-ginsenoside Rg3 in PLGA nanoparticles.

OBJECTIVE: The objective of this study is to investigate the encapsulation of 20(R)-ginsenoside Rg3 (20(R)-Rg3) using polylactic-co-glycolic acid (PLGA) and promotion for its antitumor activity. SIGNIFICANCE: Preparation and evaluation of the antitumor efficacy of 20(R)-Rg3-loaded PLGA nanoparticles were the first reported. The data will be helpful to apply 20(R)-Rg3 efficiently and broadly in new drug form development and clinical cancer treatment. METHODS: The nanoparticles were prepared using emulsion and solvent evaporation methods. The uniform particle size and good dispersion were further confirmed by scanning electron microscopy. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was applied to detect cell proliferation after 20(R)-Rg3-loaded PLGA nanoparticles treatment. Western blotting and immunofluorescent staining were used for observation of key proteins related with proliferation and apoptosis. Cell cycle and apoptosis were analyzed by flow cytometer technology. RESULTS AND DISCUSSION: The results showed that the size of 20(R)-Rg3-loaded PLGA was 97.5 nm in diameter, and zeta potential was -28 mV detected by Malvern particle size analyzer. The encapsulation efficiency was 97.5%, and drug loading was 70.2% measured by high-performance liquid chromatography. The in vitro study showed that the encapsulated 20(R)-Rg3 was consecutively released and the release ratio reached to the highest value (19.36%) at the time point of 96 h. The encapsulated 20(R)-Rg3 significantly inhibited the proliferation and induced apoptosis in A431 cancer cells compared with the unencapsulated 20(R)-Rg3, control and PLGA alone. CONCLUSION: 20(R)-Rg3-loaded PLGA nanoparticles was well prepared and characterized. The antitumor activity was increased after PLGA encapsulation. The data will be beneficial to the development of new dosage forms of 20(R)-Rg3 and extensive application.

Investigation of the ischioanal fossa: Application to abscess spread.

The location of perianal abscesses and the course of the fistula follow certain patterns, especially in the relationship between external and internal openings. However, it is still not clear how the contents of the ischioanal fossa, especially the fibrous network of fat tissue, affect the route for such diseases. Ten male adult cadavers were selected for the study. Seven horizontal transverse section planes from 1 cm above the pubic symphysis to the inferior border of the lesser trochanter of the femur were recorded after P45 sheet plastination. We observed characteristics of fiber distribution in the ischioanal fossa and its relationship with surrounding structures in every plane. There was a dense strip-type fiber connecting with junction fascia between the obturator internus and gluteus maximus muscles. Close to the levator ani, obturator internus, and gluteus maximus, the fibers were very dense and continuous with the fascia on the surfaces of these three muscles. The function of the fibrous network was considered to be not only the support of fat tissue in the fossa but also cushioning during physiological actions such as defecation. We hope that these morphological results could help to elucidate the passage of fistulae and the locations susceptible to perianal abscesses. Clin. Anat. 30:1029-1033, 2017. © 2017 Wiley Periodicals, Inc.

Inhibition of pro­collagen I expression by oxymatrine in hepatic stellate cells is mediated via nuclear translocation of Y­box binding protein 1.

Accumulating evidence indicated that oxymatrine (OMT), an alkaloid compound from the Chinese medicinal herb Sophora flavescens, exhibits activity against hepatic fibrosis. The present study attempted to explore the underlying mechanisms of OMT­mediated inhibition of collagen production. For this, the LX­2 human hepatic stellate cell line was treated with OMT (240, 480 or 960 mg/l) for 3­5 days. The endogenic expression of pro­collagen I was decreased by OMT in a dose­ and time­dependent manner, accompanied with the downregulation of Y­box binding protein 1 (YB­1), a vital transcription factor, particularly on the fourth day of incubation with a high concentration of OMT. To further explore the intracellular changes in YB­1 levels, nuclear/cytoplasmic proteins were extracted separately, and subsequent western blot analysis revealed a significant upregulation of YB­1 in the nucleus in parallel with its downregulation in the cytoplasm, indicating the nuclear translocation of YB­1 induced by OMT treatment. In another experiment, knockdown of YB­1 using small interfering RNA led to elevated mRNA levels of collagen I, thereby reversing the effects of OMT treatment. In conclusion, these present study suggested that the attenuation of pro­collagen I expression caused by OMT was, to a certain extent, mediated via nuclear translocation of YB­1.

New members of fluorescent 1,8-naphthyridine-based BF2 compounds: selective binding of BF2 with terminal bidentate N

Intensely luminescent 1,8-naphthyridine-BF2 complexes 1-9 containing terminal bidentate N^N^O and/or N^C^O groups are synthesized and structurally characterized by X-ray diffraction, electrospray ionization mass spectrometry, (1)H and (19)F NMR spectroscopy and elemental analysis. Complexes 1-4 are synthesized from 2-acetamino-1,8-naphthyridine derivatives by a facile route. Selective bonding modes and the chemical stability of complexes 5 and 6 obtained by reacting BF3·Et2O with 1,8-naphthyridine derivatives bearing dual-functional groups (N^C^O and N^N^O) are investigated by crystal structure analysis and time-dependent density functional theory calculations. The products containing a BF2 core bound to a N^C^O chelating group are energetically favorable and can expand the range of derivatives by substitution at the 2-position. In this regard, a free -NH2 group at the 2-position of complex 7 obtained from 5 can be functionalized under a variety of pH conditions to generate complexes 8 and 9, which bear flexible coordination arms that can be used to recognize certain transition metals. The photophysical properties of the complexes are examined in solution and solid state at room temperature. Compared with those of the starting naphthyridine-based compounds, the naphthyridine-BF2 complexes display desirable light-absorbing properties and intense solution and solid-state emission with large Stokes shifts. Complex 4 in solution exhibited an emission quantum yield of 0.98. In complexes 5-9, the binding sites for the BF2 core change from N^N^O to N^C^O, which leads to red shifts of absorption and emission, excellent chemical stability and high emission quantum yields.

Large Stokes shift induced by intramolcular charge transfer in N,O-chelated naphthyridine-BF2 complexes.

Novel N,O-chelated naphthyridine-BF(2) complexes with push-pull structures have been synthesized and characterized. Spectral investigations on these complexes reveal that photoinduced intramolecular charge transfer occurs and results in a large Stokes shift, which is further supported by density functional theory based theoretical calculations.