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Ulcerative colitis (UC) pathogenesis is largely associated with intestinal epithelial barrier dysfunction. A therapeutic approach to UC involves the repair of damaged intestinal barrier. Our study aimed to investigate whether aryl hydrocarbon receptor (AhR) mediated the intestinal barrier repair effects of quercetin to ameliorate UC. 3% dextran sulfate sodium was used to induce colitic mice, and quercetin (25, 50, and 100 mg/kg) was administered orally for 10 days to assess the therapeutic effects. In vitro, Caco-2 cells were used to explore the effect of quercetin on tight junction protein expression and AhR activation. The results showed that quercetin alleviated colitic mice by restoring tight junctions (TJs) integrity via an AhR-dependent manner (p < 0.05). In vitro, quercetin dose-dependently elevated the expressions of TJs protein ZO-1 and Claudin1, and activated AhR by enhancing the expression of CYP1A1 and facilitating AhR nuclear translocation in Caco-2 cells (p < 0.05). While AhR antagonist CH223191 reversed the therapeutic effects of quercetin (p < 0.05) and blocked quercetin-induced AhR activation and enhancement of TJs protein (p < 0.05). In conclusion, quercetin repaired intestinal barrier dysfunction by activating AhR-mediated enhancement of TJs to alleviate UC. Our research offered new perspectives on how quercetin enhanced intestinal barrier function., (© 2023 John Wiley & Sons Ltd.)

Berberine (BBR) is a natural alkaloid with multiple biotical effects that has potential as a treatment for fatty liver hemorrhagic syndrome (FLHS). However, the mechanism underlying the protective effect of BBR against FLHS remains unclear. The present study aimed to investigate the effect of BBR on FLHS induced by a high-energy, low-protein (HELP) diet and explore the involvement of the gut microbiota and bile acid metabolism in the protective effects. A total of 90 healthy 140-day-old Hy-line laying hens were randomly divided into three groups, including a control group (fed a basic diet), a HELP group (fed a HELP diet), and a HELP+BBR group (high-energy, high-protein diet supplemented with BBR instead of maize). Our results show that BBR supplementation alleviated liver injury and hepatic steatosis in laying hens. Moreover, BBR supplementation could significantly regulate the gut's microbial composition, increasing the abundance of Actinobacteria and Romboutsia. In addition, the BBR supplement altered the profile of bile acid. Furthermore, the gut microbiota participates in bile acid metabolism, especially taurochenodeoxycholic acid and α-muricholic acid. BBR supplementation could regulate the expression of genes and proteins related to glucose metabolism, lipid synthesis (FAS, SREBP-1c), and bile acid synthesis (FXR, CYP27a1). Collectively, our findings demonstrate that BBR might be a potential feed additive for preventing FLHS by regulating the gut microbiota and bile acid metabolism.

Background: In the context of global aging, the characteristics of chronic diseases seriously affect the quality of life of older adults. It is urgent to carry out continuous nursing basis for older adult patients with chronic diseases. In view of the remarkable efficacy of Chinese medicine in the treatment of chronic diseases, this study may help to understand the demand for "Internet + Chinese medicine" home care service and its influencing factors of older adult chronic disease patients, and to provide a reference basis for improving the quality of life of the older adult chronic disease population., Methods: This is a mixed study. The quantitative study adopted the convenience sampling method, and a total of 308 patients in a third-grade hospital in Shaanxi Province were investigated by general data questionnaire, traditional Chinese medicine service demand questionnaire, traditional Chinese medicine knowledge questionnaire, older adult Chinese medicine attitude questionnaire, and home care demand questionnaire from March to April 2022. In the qualitative study, semi-structured interviews were adopted, and patients were interviewed until the content was saturated. Colaizzi analysis method was used to analyze and summarize the topic of the interview data., Results: 308 valid questionnaires were collected, and the patients scored (58.42 ± 17.16) on the demand for TCM nursing services, (59.86 ± 11.54) on the knowledge of TCM, (73.03 ± 9.11) on the attitude toward TCM, and (136.84 ± 46.39) on the demand for home care. The results of multiple linear regression showed that learning about the nursing service pathway, knowledge of general knowledge of Chinese medicine, and attitude toward Chinese medicine among the older adult and home care demand were the influencing factors of the demand for Chinese medicine nursing services for older adult patients with chronic diseases ( p  < 0.05). The results of the in-depth interviews were summarized into three themes: facilitating factor, hindering factor, and the "Internet + Chinese medicine" multiple needs of home care., Conclusion: Older adult patients with chronic diseases have a high intention of home care demand and they are affected by multiple factors. Consequently, the actual demand situation of older adult patients with chronic diseases should be used as a guide to provide directed and diversified Chinese medicine home care services to meet the individualized needs of the older adult., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Wang, Chen, Feng, Zhuang, Wang, Zhang, Liu and Chen.)

Background: Postoperative delirium (POD) is a common clinical complication in elderly patients after surgery and predicts poor outcomes., Aim: We researched whether postoperative infusion of dexmedetomidine (DEX) had prophylactic effect on POD in elderly patients., Methods: A total of 236 patients over the age of 60 years undergoing thoracoabdominal tumor surgery were enrolled in Zhejiang Cancer Hospital from November 2016 to October 2020. The patients were randomly assigned into DEX group (group D) and control group (Group C). DEX was provided via PCIA pump 1-3 days after surgery, which consisted of 3 ug/kg sufentanil and 3 ug/kg DEX in group D, and 3 ug/kg sufentanil without DEX in group C. The PCIA parameters were programmed as follows: total amount 150 ml, 2 ml bolus dose with a lock-out of 10 min and background infusion rate 2 ml/h. The primary endpoint was the incidence of POD, assessed twice daily within 7 days after surgery by Richmond Agitation-Sedation Scale (RASS) and the Confusion Assessment Method-Intensive Care Unit (CAM-ICU). The secondary endpoint was postoperative hospitalization days, ICU stay time, adverse events and non-delirium complications., Results: The incidence of POD in all patients was 7%. The incidence of POD in group C was significantly higher than that in group D (10.1% vs 3.4%, P = 0.042). There were no significant differences in length of hospital stay after operation, ICU stay time, the percentage of patients discharged within 7 days after surgery, non-delirium complications, and 30-day all-cause deaths between the two groups. The incidence of hypertension in group D was lower than that in group C (P = 0.003), and there were no differences in other adverse events., Conclusion: Patients aged over 60 years received DEX in addition to intravenous patient-controlled analgesia (PCIA) for major thoracoabdominal surgery experienced less delirium., (© 2023. The Author(s).)

Background The renin-angiotensin system plays a crucial role in the development of heart failure, and Ang II (angiotensin II) acts as the critical effector of the renin-angiotensin system in regulating cardiac fibrosis. However, the mechanisms of cardiac fibrosis are complex and still not fully understood. IGF1R (insulin-like growth factor 1 receptor) has multiple functions in maintaining cardiovascular homeostasis, and low-dose IGF1 treatment is effective in relieving Ang II-induced cardiac fibrosis. Here, we aimed to investigate the molecular mechanism of IGF1R in Ang II-induced cardiac fibrosis. Methods and Results Using primary mouse cardiac microvascular endothelial cells and fibroblasts, in vitro experiments were performed. Using C57BL/6J mice and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated 9 (Cas9)-mediated IGF1R heterozygous knockout ( Igf1r +/- ) mice, cardiac fibrosis mouse models were induced by Ang II for 2 weeks. The expression of IGF1R was examined by quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot. Mice heart histologic changes were evaluated using Masson and picro sirius red staining. Fibrotic markers and signal molecules indicating the function of the Akt (protein kinase B)/ERK (extracellular signal-regulated kinase)/nuclear factor-κB pathway were detected using quantitative reverse transcription polymerase chain reaction and Western blot. RNA sequencing was used to explore IGF1R-mediated target genes in the hearts of mice, and the association of IGF1R and G-protein-coupled receptor kinase 5 was identified by coimmunoprecipitation. More important, blocking IGF1R signaling significantly suppressed endothelial-mesenchymal transition in primary mouse cardiac microvascular endothelial cells and mice in response to transforming growth factor-β1 or Ang II, respectively. Deficiency or inhibition of IGF1R signaling remarkably attenuated Ang II-induced cardiac fibrosis in primary mouse cardiac fibroblasts and mice. We further observed that the patients with heart failure exhibited higher blood levels of IGF1 and IGF1R than healthy individuals. Moreover, Ang II treatment significantly increased cardiac IGF1R in wild type mice but led to a slight downregulation in Igf1r +/- mice. Interestingly, IGF1R deficiency significantly alleviated cardiac fibrosis in Ang II-treated mice. Mechanistically, the phosphorylation level of Akt and ERK was upregulated in Ang II-treated mice, whereas blocking IGF1R signaling in mice inhibited these changes of Akt and ERK phosphorylation. Concurrently, phosphorylated p65 of nuclear factor-κB exhibited similar alterations in the corresponding group of mice. Intriguingly, IGF1R directly interacted with G-protein-coupled receptor kinase 5, and this association decreased ≈50% in Igf1r +/- mice. In addition, Grk5 deletion downregulated expression of the Akt/ERK/nuclear factor-κB signaling pathway in primary mouse cardiac fibroblasts. Conclusions IGF1R signaling deficiency alleviates Ang II-induced cardiac fibrosis, at least partially through inhibiting endothelial-mesenchymal transition via the Akt/ERK/nuclear factor-κB pathway. Interestingly, G-protein-coupled receptor kinase 5 associates with IGF1R signaling directly, and it concurrently acts as an IGF1R downstream effector. This study suggests the promising potential of IGF1R as a therapeutic target for cardiac fibrosis.

Hematoma-induced neuroinflammation is the cause of poor prognosis in intracerebral hemorrhage (ICH); therefore, promoting blood clearance and blocking overactivated inflammation are rational approaches for ICH treatment. β-site amyloid precursor protein (APP) lyase-1 (BACE1) is a key molecule regulating the microglial phenotype transition in neurodegenerative diseases. Therefore, the aim of this study was to investigate the role of BACE1 in microglial phagocytosis and inflammatory features in ICH. Here, we demonstrated the unique advantages of targeting BACE1 in microglia using an autologous blood model and primary microglia hemoglobin stimulation. When BACE1 was inhibited early in ICH, fewer residual hematomas remained, consistent with an increase in genetic features that favor phagocytosis and anti-inflammation. In addition, inhibition of BACE1 enhanced the secretion of anti-inflammatory cytokines and substantially reduced the expression of proinflammatory genes, which was regulated by signal transduction and phosphorylation of activator of transcription 3 (STAT3). Further pharmacological inhibition of STAT3 phosphorylation effectively blocked the proinflammatory and weak phagocytic phenotype of microglia due to BACE1 induction. In summary, BACE1 is the critical molecule regulating the inflammatory and phagocytic phenotypes of microglia after ICH, and targeted inhibition of the BACE1/STAT3 pathway is an important strategy for the future treatment of ICH-induced neurological injury.

Objectives: To develop a novel analytical approach based on 18 F-fluorodeoxyglucose ([ 18 F]FDG) positron emission tomography (PET) metabolic parameters, serum inflammatory markers, and clinical variables to improve the outcome prediction in NSCLC., Methods: A total of 190 newly diagnosed NSCLC patients who underwent pretreatment [ 18 F]FDG PET/CT were retrospectively enrolled and divided into a training cohort (n = 127) and a test cohort (n = 63). Cox regression analysis was used to investigate the predictive values of PET metabolic parameters, inflammation markers, and clinical variables for progression-free survival (PFS) and overall survival (OS). Based on the results of multivariate analysis, PET-based, clinical, and combined models were constructed. The predictive performance of different models was evaluated using time-dependent ROC curve analysis, Harrell concordance index (C-index), calibration curve, and decision curve analysis., Results: The combined models incorporating SULmax, MTV, NLR, and ECOG PS demonstrated significant prognostic superiority over PET-based models, clinical models, and TNM stage in terms of both PFS (C-index: 0.813 vs. 0.786 vs. 0.776 vs. 0.678, respectively) and OS (C-index: 0.856 vs. 0.792 vs. 0.781 vs. 0.674, respectively) in the training cohort. Similar results were observed in the test cohort for PFS (C-index: 0.808 vs. 0.764 vs. 0.748 vs. 0.679, respectively) and OS (C-index: 0.836 vs. 0.785 vs. 0.726 vs. 0.660, respectively) prediction. The combined model calibrated well in two cohorts. Decision curve analysis supported the clinical utility of the combined model., Conclusions: We reported a novel analytical approach combining PET metabolic information with inflammatory biomarker and clinical characteristics, which could significantly improve outcome prediction in newly diagnosed NSCLC., Key Points: • The nomogram incorporating SULmax, MTV, NLR, and ECOG PS outperformed the TNM stage for outcome prediction in patients with newly diagnosed NSCLC. • The established nomogram could provide refined prognostic stratification., (© 2022. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

Background: Remimazolam is a novel ultrashort-acting intravenous benzodiazepine sedative−hypnotic that significantly reduces the times to sedation onset and recovery. This trial was conducted to confirm the recovery time from anesthesia of remimazolam-flumazenil versus propofol in patients undergoing endotracheal surgery under rigid bronchoscopy. Methods: Patients undergoing endotracheal tumor resection or stent implantation were randomly allocated into a remimazolam group (Group R) or a propofol group (Group P). The primary outcome was the recovery time from general anesthesia. The secondary outcomes were the time to loss of consciousness (LoC), hemodynamic fluctuations, and adverse events. Results: A total of 34 patients were screened, and 30 patients were enrolled in the study. The recovery time was significantly shorter for Group R (140 ± 52 s) than for Group P (374 ± 195 s) (p < 0.001). The times to LoC were 76 ± 40 s in Group R and 75 ± 25 s in Group P and were not significantly different. There were also no significant differences in hemodynamic fluctuations or adverse events between the two groups. Conclusions: The recovery time from general anesthesia in rigid bronchoscopy patients was shorter using remimazolam-flumazenil than with propofol, with no dramatic hemodynamic fluctuations and adverse events or differences between the agents. Remimazolam-flumazenil allows for faster recovery from anesthesia than propofol.

Background: Colorectal cancer is associated with ulcerative colitis (UC). The infiltration of neutrophils is the main cause of DNA damage produced by inflammation in the intestinal epithelium. Under the action of peptidyl arginine deaminase 4 (PAD4), neutrophils dissociate chromatin and form neutrophil extracellular traps (NETs), which can aggravate tissue inflammation and encourage tumor development. Although Huang Qin Decoction (HQD) was found to be useful in treating UC and was used to gradually prevent and treat digestive tract cancers, the underlying reasons were unclear., Methods: To demonstrate HQD could inhibits the initiation of colitis associated carcinogenesis by controlling NETs related inflammation, we first performed an AOM/DSS-generated colitis-associated carcinogenesis model to assess the efficacy of HQD in reducing neutrophil infiltration and anti-tumor activity. Then, using network pharmacology research, we investigated the potential mechanisms underlying those medicinal effects, as demonstrated by the detection of NETs aggregation and PAD4 expression changes in the colon., Results: HQD substantially reduced the number of colon cancers and the expression of Ki67, restored the level of intestinal tight junction protein occludin and ZO-1, and relieved the intestinal inflammation caused by TNF-α, IL-1β. At the same time, it inhibited neutrophil infiltration in the colon and improved the immunosurveillance of CD8 + T cells. The potential mechanisms of HQD intervention against UC and UC with neoplasia (UCN) were studied using network pharmacology, and 156 conjunct genes as well as numerous inflammation-related pathways were identified. Protein-protein interaction (PPI) analysis indicated that HQD inhibition of intestinal tumors might be related to the deactivation of PAD4, which was verified by the down-regulation of NETs, MPO-DNA complex levels, and PAD4 expression after HQD treatment., Conclusion: Huang Qin Decoction inhibits the initiation of colitis associated carcinogenesis by controlling PAD4-dependent neutrophil extracellular traps., Competing Interests: Declaration of Competing Interest The authors declared that they had no conflicts of interest to disclose., (Copyright © 2022. Published by Elsevier GmbH.)

The first de novo synthesis of 1-hydroxyl allogibberic methyl ester, en route to pharbinilic acid and other bioactive molecules, is accomplished in diastereoselective manner. Key reactions of the synthesis include a Pd-catalyzed Suzuki-Miyaura cross-coupling reaction, a Lewis acid-catalyzed reductive Prins cyclization reaction, and a SmI 2 -mediated transannular pinacol coupling reaction. The synthesis provides a new avenue to access diverse relevant bioactive molecules.

Purpose: Esophageal squamous cell carcinoma (ESCC) is one of the most common and serious malignancies in China. However, the exact mechanisms of tumor progression are still unclear. Thus, identifying biomarkers for early diagnosis, prognostic and recurrence assessment of ESCC is necessary., Experimental Design: iTRAQ was used to identify differentially expressed proteins (DEPs) in tumor tissues. N-alpha-acetyltransferase 10 (NAA10) is confirmed and validated by immunohistochemistry and western blotting. Furthermore, the effects of NAA10 on TE-1 cells were detected by CCK-8, colonies formation, anchorage-independent growth in soft agar, migration and transwell assays. LinkedOmics was used to identify differential gene expression with NAA10 and to analyze Gene Ontology and KEGG pathways. Coexpression gene network was conducted by the STRING database and Cytoscape software (MCODE plug-in)., Results: 516 DEPs were identified. NAA10 was downregulated in cancer tissues and selected for further confirmed. Furthermore, NAA10 can inhibit proliferation and tumorigenesis, and suppress migration and invasion of TE-1. Functional network analysis suggested that NAA10 regulates the ribosome pathways involving eight ribosomal proteins., Conclusion and Clinical Relevance: These findings clearly demonstrated that NAA10 is a tumor suppressor and novel potential biomarker for ESCC, laying a foundation for further study of the role of NAA10 in carcinogenesis., (© 2022 Wiley-VCH GmbH.)

Objective: This study aims to explore factors influencing metabolic and volumetric parameters of [ 18 F]fluorodeoxyglucose positron emission tomography/computed tomography ( 18 F-FDG PET/CT) imaging in non-small cell lung cancer (NSCLC) and the predictive value for prognosis of NSCLC., Methods: Retrospective analysis was performed on 133 NSCLC patients who received 18 F-FDG PET/CT imaging. After 18 F-FDG injection at 3.7 MBq/kg, 1 h early imaging and 2 h delayed imaging were performed. The metabolic and volumetric parameters such as SUVmax, SUVpeak, SULmax, SULpeak, MTV and TLG were measured. The tumor markers including CFYRA21-1, NSE, SCC-ag and the immunohistochemical biomarkers including Ki-67, P53 and CK-7 were examined. All patients were followed up for 24 months, and the 1-year and 2-year overall survival rate (OS) were recorded., Results: There were significant differences in metabolic and volumetric parameters (SUVmax, SUVpeak, SULmax, SULpeak and TLG) between adenocarcinoma and squamous cell carcinoma of NSCLC. SUVmax, SUVpeak, SULmax, SULpeak, MTV and TLG were correlated with tumor marker NSE and TNM stage. MTV and TLG were related to CYFRA21-1, and only MTV was associated with SCC-ag. SUVpeak and SULmax were related to P53. In addition, early SULpeak and delayed MTV were significant prognostic factors of 1-year OS, while early SUVpeak, delayed TLG and delayed MTV were predictive factors of 2-year OS in NSCLC., Conclusion: The metabolic and volumetric parameters of 18 F-FDG PET/CT were related to a variety of factors such as NSE, CFYRA21-1, SCC-ag, P53 and TNM stage, and have a predictive value in prognosis of NSCLC., Competing Interests: The authors declare no conflicts of interest., (© 2021 Zhang et al.)

Background: A nationwide ban on family/replacement donation (FRD) went into effect on April 1, 2018 in China. To date, no reports relevant to the trend of plateletpheresis donations before and after a nationwide ban on FRD were found., Methods: We used two independent full samples, consisting of 135,851 and 82,129 plateletpheresis donors from Guangzhou and Chengdu between October 2012 and September 2019, respectively. A pseudo-panel data approach was applied by grouping three time-invariant covariates - gender, blood donation history, and birth year across 14 cross-sections (a 6-month interval each) to form a total of 24 cohort groups (14 × 24 = 336 cohorts, i.e., cells) with each having common covariates. The outcome was average apheresis platelet units per donor in each cell. We performed a two-piecewise linear mixed model with the cross-section (i.e., time) just right before the ban as a time breakpoint (i.e., 11th cross-section) to examine the trend of outcome with the adjustment of three time-invariant covariates. We removed the FRDs in each of the first 11 cross-sections to detect its possible influence on the trend., Results: The final model for the samples from Guangzhou presented a two-piecewise linear trend of the outcome over time with a horizontal line to the left of the breakpoint (β timeBefore11  = 0.0111, p = 0.0976) and a significantly positive linear trend to the right (β timeAfter11  = 0.0404, p < 0.0001). The male donors and the donors with plateletpheresis donation history had an increased baseline outcome and a significant outcome change over time after the ban. Such a two-piecewise linear trend pattern can be replicated using the samples from Chengdu with some minor variations. Removing the FRD before the ban can change the pattern., Conclusion: The significant increase of the average apheresis platelet units per donor over time after the FRD ban may be related to the implement of the FRD ban and the improved donation behavior of male donors and/or donors with platelet donation history after the ban. Our findings may potentially motivate the policymakers in other countries where the FRD for plateletpheresis donation is still legitimate to phase out their FRD strategy and ultimately achieve 100% voluntary plateletpheresis donation.

Hypertrophic cardiomyopathy (HCM) is a disease in which the heart muscle becomes abnormally thick making it difficult for the heart to pump blood. In this study an induced pluripotent stem cells (iPSC) line was derived from peripheral blood mononuclear cells of a 62-year-old male hypertrophic cardiomyopathy (HCM) patient with the mutation of heterozygous pathogenic myosin binding protein C (MYBPC3) c.3369-3370 insC using an episomal method. The generated iPSC line presented normal 46, XY male karyotypes, expressed pluripotent markers and could spontaneously differentiate into triblast cells. This HCM-specific iPSC line could act as a useful tool for studying and modeling hypertrophic cardiomyopathy., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

Objective: This study aimed to assess the clinical value of 4D fluorine-18-fluorodeoxyglucose PET/computed tomography (F-FDG PET/CT) in the differential diagnosis for lung lesions., Patients and Methods: Fifty-eight patients with lung lesions including lung cancer, pneumonia nodules, and benign pulmonary nodules were enrolled. The PET/CT scan was performed immediately (15 min of dynamic scan), at 60 min (early scan), and at 120 min (delayed scan) after the injection of F-FDG. The time-activity curves (TACs) were generated from the dynamic PET. The maximum standardized uptake value (SUVmax) of each lesion at early and delayed scans was measured, and the retention index of SUVmax (RI-SUVmax) was calculated. The cutoff values for SUVmax were determined., Results: Lung cancer lesions (27/31, 87.1%) exhibited a continuously rising slope of TAC, whereas pneumonia lesions (13/15, 86.66%) and benign pulmonary nodules (12/12, 100%) exhibited a continuously decreasing slope of TAC. The early-SUVmax and delayed-SUVmax in the pneumonia group were significantly lower than those in the lung cancer group, whereas notably higher than those in the benign pulmonary nodules group. The diagnostic accuracy was: delayed-SUVmax > early-SUVmax > RI-SUVmax., Conclusion: The 4D F-FDG PET/CT exhibited excellent performance with high accuracy in the dynamic PET/CT.

Objective To investigate the therapeutic effect and mechanism of paeoniflorin on dextran sulphate sodium (DSS)-induced ulcerative colitis (UC) mice. Methods C57BL/6 male mice were randomly divided into control group, model group, 600 mg/(kg.d) mesalazine treatment group, (12.5, 25, 50) mg/(kg.d) paeoniflorin treatment group, with 10 mice in each. All mice were treated with 30 g/L DSS for 5 days except the control group. Meanwhile, the mice in the other groups were orally administrated corresponding drugs for 10 days, while the mice in the control and model groups were given equivalent volumes of distilled water. Body mass, fecal characteristics and hematochezia of the mice were observed and recorded daily, and then disease activity index (DAI) was evaluated and calculated. Pathological changes in the colon were observed by HE staining. The levels of anti-flagellin antibody, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in the serum were measured by ELISA. The expression levels of Toll-like receptor 5 (TLR5), myeloid differentiation factor 88 (MyD88) and nuclear factor kappa-Bp65 (NF-κBp65) in the colon tissues were evaluated by Western blot analysis and the activation of lymphocytes in mesenteric lymph node (MLN) was detected by flow cytometry. Results Compared with the control group, DAI scores in the model group were significantly raised, the colon length was significantly shortened, and the epithelium and intestinal gland disappeared. In addition, the serum levels of anti-flagellin antibody, IL-6, TNF-α and the protein levels of TLR5, MyD88, NF-κBp65 in the colon significantly increased, and the activation of T lymphocytes in MLN went up in the model group. All symptoms above were alleviated in the mesalazine and paeoniflorin groups compared with the model group. Conclusion Paeoniflorin can attenuate UC in mice by inhibiting the expression of flagellin and TLR5, and the activation of T cells.

Human gait identification aims to identify people by a sequence of walking images. Comparing with fingerprint or iris based identification, the most important advantage of gait identification is that it can be done at a distance. In this paper, silhouette correlation analysis based human identification approach is proposed. By background subtracting algorithm, the moving silhouette figure can be extracted from the walking images sequence. Every pixel in the silhouette has three dimensions: horizontal axis (x), vertical axis (y), and temporal axis (t). By moving every pixel in the silhouette image along these three dimensions, we can get a new silhouette. The correlation result between the original silhouette and the new one can be used as the raw feature of human gait. Discrete Fourier transform is used to extract features from this correlation result. Then, these features are normalized to minimize the affection of noise. Primary component analysis method is used to reduce the features' dimensions. Experiment based on CASIA database shows that this method has an encouraging recognition performance.

The difference between adjacent frames of human walking contains useful information for human gait identification. Based on the previous idea a silhouettes difference based human gait recognition method named as average gait differential image (AGDI) is proposed in this paper. The AGDI is generated by the accumulation of the silhouettes difference between adjacent frames. The advantage of this method lies in that as a feature image it can preserve both the kinetic and static information of walking. Comparing to gait energy image (GEI), AGDI is more fit to representation the variation of silhouettes during walking. Two-dimensional principal component analysis (2DPCA) is used to extract features from the AGDI. Experiments on CASIA dataset show that AGDI has better identification and verification performance than GEI. Comparing to PCA, 2DPCA is a more efficient and less memory storage consumption feature extraction method in gait based recognition.