Topological Quantum Walks in Momentum Space with a Bose-Einstein Condensate.

We report the experimental implementation of discrete-time topological quantum walks of a Bose-Einstein condensate in momentum space. Introducing stroboscopic driving sequences to the generation of a momentum lattice, we show that the dynamics of atoms along the lattice is effectively governed by a periodically driven Su-Schrieffer-Heeger model, which is equivalent to a discrete-time topological quantum walk. We directly measure the underlying topological invariants through time-averaged mean chiral displacements, which are consistent with our experimental observation of topological phase transitions. We then observe interaction-induced localization in the quantum-walk dynamics, where atoms tend to populate a single momentum-lattice site under interactions that are nonlocal in momentum space. Our experiment opens up the avenue of investigating discrete-time topological quantum walks using cold atoms, where the many-body environment and tunable interactions offer exciting new possibilities.

Tunable Nonreciprocal Quantum Transport through a Dissipative Aharonov-Bohm Ring in Ultracold Atoms.

We report the experimental observation of tunable, nonreciprocal quantum transport of a Bose-Einstein condensate in a momentum lattice. By implementing a dissipative Aharonov-Bohm (AB) ring in momentum space and sending atoms through it, we demonstrate a directional atom flow by measuring the momentum distribution of the condensate at different times. While the dissipative AB ring is characterized by the synthetic magnetic flux through the ring and the laser-induced loss on it, both the propagation direction and transport rate of the atom flow sensitively depend on these highly tunable parameters. We demonstrate that the nonreciprocity originates from the interplay of the synthetic magnetic flux and the laser-induced loss, which simultaneously breaks the inversion and the time-reversal symmetries. Our results open up the avenue for investigating nonreciprocal dynamics in cold atoms, and highlight the dissipative AB ring as a flexible building element for applications in quantum simulation and quantum information.

KCa3.1 channel mediates inflammatory signaling of pancreatic ß cells and progression of type 2 diabetes mellitus.

Chronic islet inflammation is associated with development of type 2 diabetes mellitus (T2DM). Intermediate-conductance calcium-activated K+ (KCa3.1) channel plays an important role in inflammatory diseases. However, the role and regulation of KCa3.1 in pancreatic ß cells in progression of T2DM remain unclarified. In the present study, we evaluated the effect of the specific KCa3.1 channel blocker 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34) on diabetic phenotype in the db/db model. In diabetic mice, blockade of KCa3.1 significantly improved glucose tolerance, enhanced secretion of postprandial insulin level, and reduced loss of ß-cell mass through attenuating the expression and secretion of inflammatory mediators. Furthermore, in cultured pancreatic ß cells, exposure to high levels of glucose or palmitic acid significantly increased expression and current density of the KCa3.1 channel as well as secretion of proinflammatory chemokines, and the effects were similarly reversed by preincubation with TRAM-34 or a NF-κB inhibitor pyrrolidinedithiocarbamate. Additionally, expression of KCa3.1 in pancreas islet cells was up-regulated by activation of NF-κB with IL-1ß stimulation. In summary, up-regulated KCa3.1 due to activation of NF-κB pathway leads to pancreatic inflammation via expression and secretion of chemokines and cytokines by pancreatic ß cells, thereby facilitating progression of T2DM.-Pang, Z.-D., Wang, Y., Wang, X.-J., She, G., Ma, X.-Z., Song, Z., Zhao, L.-M., Wang, H.-F., Lai, B.-C., Gou, W., Du, X.-J., Deng, X.-L. KCa3.1 channel mediates inflammatory signaling of pancreatic ß cells and progression of type 2 diabetes mellitus.

MiR-552 promotes the proliferation, migration and EMT of hepatocellular carcinoma cells by inhibiting AJAP1 expression.

Our goal was to explore the function of miR-552 and its potential target AJAP1 in hepatocellular carcinoma (HCC) oncogenesis and progression. In this study, bioinformatics analysis was performed to detect abnormally expressed miRNAs. The relationship between miR-552 and AJAP1 was validated using luciferase reporter assays. RT-qPCR and Western blot assays were applied to explore the expression level of miR-552, AJAP1 and epithelial-mesenchymal transition (EMT) markers. HCC cell proliferation was examined using CCK8 assays, while migration and invasion were investigated using Transwell assays. Nude mouse tumourigenesis models were established to facilitate observation of HCC progression in vivo. Finally, prognostic analysis was performed to discover how the prognosis of HCC patients correlated with miR-552 and AJAP1 expression. MiR-552 overexpression in HCC cells promoted HCC cell migration, invasion and EMT by targeting/suppressing AJAP1. Poorer prognosis appeared in HCC patients with higher miR-552 expression or lower AJAP1 levels. Our findings suggested that miR-552 promotes HCC oncogenesis and progression by inhibiting AJAP1 expression.

Fibrinopeptide A Induces Expression of C-Reactive Protein via the ROS-ERK1/2/ P38-NF-κB Signal Pathway in Vascular Smooth Muscle Cells.

BACKGROUND/AIMS: Atherosclerosis is a chronic inflammatory disease in the artery walls. Fibrinopeptide A (FPA) is a biomarker of the activation of coagulation system, and a high concentration of FPA in blood occurs in patients with ischemic heart disease etc. However, there exist few studies on the pathological effects of FPA in cardiovascular system. Therefore, the present study examined the effect of FPA on CRP expression in VSMCs and the molecular mechanisms. METHODS: mRNA and protein expression was identified by quantitative real-time PCR and Western blot, respectively. Reactive oxygen species (ROS) and the immunofluorescence staining were observed by a fluorescence microscope. Plasma FPA and CRP level was determined by ELISA. RESULTS: FPA induced the expressions of CRP, IL-1ß and IL-6 in VSMCs, and anti-IL-1ß and anti-IL-6 neutralizing antibodies partially reduced FPA-induced CRP expression in VSMCs. The subchronic administration of FPA to rats increased FPA level in plasma and CRP expression in the aortic artery walls. The further studies showed that FPA promoted superoxide anion generation in VSMCs. Antioxidant NAC antagonized FPA-stimulated superoxide anion generation and inhibited FPA-induced CRP expression in VSMCs. FPA activated ERK1/2 and p38 phosphorylation, and PD98059 and SB203580 reduced FPA-induced CRP expression. Moreover, NAC inhibited the activation of ERK1/2 and p38. In addition, FPA enhanced NF-κB level in the nuclei of VSMCs, and PDTC reduced FPA-induced expression of CRP. CONCLUSIONS: FPA induces CRP expression in VSMCs via ROS-ERK1/2/p38-NF-κB signal pathway. This finding for the first time provides an experimental evidence for pro-inflammatory effect of FPA.

Study of Staphylococcus aureus N315 Pathogenic Genes by Text Mining and Enrichment Analysis of Pathways and Operons.

BACKGROUND: Staphylococcus aureus (S. aureus) is a versatile pathogen found in many environments and can cause nosocomial infections in the community and hospitals. S. aureus infection is an increasingly serious threat to global public health that requires action across many government bodies, medical and health sectors, and scientific research institutions. METHODS: In the present study, S. aureus N315 genes that have been shown in the literature to be pathogenic were extracted using a bibliometric method for functional enrichment analysis of pathways and operons to statistically discover novel pathogenic genes associated with S. aureus N315. RESULTS: A total of 383 pathogenic genes were mined from the literature using bibliometrics, and subsequently a few new pathogenic genes of S. aureus N315 were identified by functional enrichment analysis of pathways and operons. CONCLUSIONS: The discovery of these novel S. aureus N315 pathogenic genes is of great significance to treat S. aureus induced diseases and identify potential diagnostic markers, thus providing theoretical fundamentals for epidemiological prevention.

Effects of mirror therapy on walking ability, balance and lower limb motor recovery after stroke: a systematic review and meta-analysis of randomized controlled trials.

OBJECTIVE: To investigate the effects of mirror therapy on walking ability, balance and lower limb motor recovery in patients with stroke. METHOD: MEDLINE, EMBASE, Web of Science, CENTRAL, PEDro Database, CNKI, VIP, Wan Fang, ClinicalTrials.gov, Current controlled trials and Open Grey were searched for randomized controlled trials that investigated the effects of mirror therapy on lower limb function through January 2018. The primary outcomes included were walking speed, mobility and balance function. Secondary outcomes included lower limb motor recovery, spasticity and range of motion. Quality assessments were performed with the PEDro scale. RESULTS: A total of 13 studies ( n = 572) met the inclusion criteria. A meta-analysis demonstrated a significant effect of mirror therapy on walking speed (mean difference (MD) 0.1 m/s, 95% confidence interval (CI): 0.08 to 0.12, P < 0.00001), balance function (standard mean difference (SMD) 0.66, 95% CI: 0.43 to 0.88, P < 0.00001), lower limb motor recovery (SMD 0.83, 95% CI: 0.62 to 1.05, P < 0.00001) and passive range of motion of ankle dorsiflexion (MD 2.07°, 95% CI: 082 to 3.32, P = 0.001), without improving mobility (SMD 0.43, 95% CI: -0.12 to 0.98, P = 0.12) or spasticity of ankle muscles (MD -0.14, 95% CI: -0.43 to 0.15, P = 0.35). CONCLUSION: The systematic review demonstrates that the use of mirror therapy in addition to some form of rehabilitation appears promising for some areas of lower limb function, but there is not enough evidence yet to suggest when and how to approach this therapy.

Cloning and Functional Analysis of Phosphoethanolamine Methyltransferase Promoter from Maize (Zea mays L.).

Betaine, a non-toxic osmoprotectant, is believed to accumulate considerably in plants under stress conditions to maintain the osmotic pressure and promote a variety of processes involved in growth and development. Phosphoethanolamine N-methyltransferase (PEAMT), a key enzyme for betaine synthesis, is reported to be regulated by its upstream promoter. In the present investigation, by using the transgenic approach, a 1048 bp long promoter region of ZmPEAMT gene from Zea mays was cloned and functionally characterized in tobacco. Computational analysis affirmed the existence of abiotic stress responsive cis-elements like ABRE, MYC, HST, LST etc., as well as pathogen, wound and phytohormone responsive motifs. For transformation in tobacco, four 5'-deletion constructs of 826 bp (P2), 642 bp (P3), 428 bp (P4) and 245 bp (P5) were constructed from the 1048 bp (P1) promoter fragment. The transgenic plants generated through a single event exhibited a promising expression of GUS reporter protein in the leaf tissues of treated with salt, drought, oxidative and cold stress as well as control plants. The GUS expression level progressively reduced from P1 to P5 in the leaf tissues, whereas a maximal expression was observed with the P3 construct in the leaves of control plants. The expression of GUS was noted to be higher in the leaves of osmotically- or salt-treated transgenic plants than that in the untreated (control) plants. An effective expression of GUS in the transgenic plants manifests that this promoter can be employed for both stress-inducible and constitutive expression of gene(s). Due to this characteristic, this potential promoter can be effectively used for genetic engineering of several crops.

Assessment of the characteristics and quality of life of patients with uremic peripheral neuropathy
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OBJECTIVES: This study seeks to examine the characteristics and health-related quality of life (HRQL) of patients with uremic peripheral neuropathy. METHODS: Uremic patients undergoing maintenance hemodialysis (MHD) at our hospital were enrolled in this study. Data collection began in January 2011 and ended in June 2011. The patients were divided into two groups, the lesion group (110 cases) and the non-lesion group (168 cases), based on the presence or absence of peripheral neuropathy. To examine continuous changes in signs and symptoms in the lesion group, electromyography (EMG) was performed to measure sensory nerve conduction velocity (SCV), motor nerve conduction velocity (MCV), and distal latency (DL). Furthermore, HRQL was analyzed using the generic Short Form-36 (SF-36) questionnaire. RESULTS: Numbness and a burning sensation in the distal limbs were observed in the lesion group; in particular, these phenomena occurred in the upper limbs and the lower limbs in 3.6% (4/110) and 48.2% (53/110) of patients, respectively. With respect to motor symptoms, upper and lower limb weakness was observed in 1.8% (2/110) and 11.8% (13/110) of patients, respectively. Changes in physical signs were mainly evidenced by tendon reflexes, for example, areflexia, or tendon reflex loss was detected in the upper extremities, the knee tendon, and the Achilles tendon in 9.09% (10/110), 55.45% (61/110), and 35.5% (39/110) of patients, respectively. Relative to the non-lesion group, the lesion group had significantly slower average SCV and MCV as well as a longer average DL (p < 0.01 for all comparisons). Based on a clinical statistical analysis of SF-36 reports, scores on each scale were lower in the lesion group than in the non-lesion group. However, compared with the non-lesion group, the lesion group did not significantly differ with respect to overall SF-36 score (t = 1.896, p = 0.060) but did significantly differ with respect to bodily pain score (t = 5.301, p < 0.001). CONCLUSIONS: Typical symptoms of uremic peripheral neuropathy include numbness of the limbs and changes in tendon reflexes. In this study, sensory nerves were damaged more severely than motor nerves, and lower extremity lesions were more frequent than upper limb lesions. Clinicians should devote greater attention to patients with uremic peripheral neuropathy and strive to continuously improve these patients' quality of life.
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Exogenous application of urea and a urease inhibitor improves drought stress tolerance in maize (Zea mays L.).

Drought is believed to cause many metabolic changes which affect plant growth and development. However, it might be mitigated by various inorganic substances, such as nitrogen. Thus, the study was carried out to investigate the effect of foliar-applied urea with or without urease inhibitor N-(n-butyl) thiophosphoric triamide (NBPT) on a maize cultivar under drought stress simulated by 15% (w/v) polyethylene glycol 6000. Foliar-applied urea resulted in a significant increase in plant dry weight, relative water content, and photosynthetic pigments under water stress condition. Furthermore, the activities of superoxide dismutase (SOD), peroxidase (POD), and hydrogen peroxidase (CAT), were enhanced with all spraying treatments under drought stress, which led to decreases in accumulation of hydrogen peroxide (H2O2), superoxide anion ([Formula: see text]) and malondialdehyde (MDA). The contents of soluble protein and soluble sugar accumulated remarkably with urea-applied under drought stress condition. Moreover, a further enhancement in above metabolites was observed by spraying a mixture of urea and urease inhibitor as compared to urea sprayed only. Taken together, our findings show that foliar application of urea and a urease inhibitor could significantly enhance drought tolerance of maize through protecting photosynthetic apparatus, activating antioxidant defense system and improving osmoregulation.

Tislelizumab induced dual organs dysfunction in a patient with advanced esophageal squamous cell carcinoma: a case report.

Background: Tislelizumab, a humanized IgG4 anti-PD-1 monoclonal antibody has been approved in China and Europe. According to the published clinical research, tislelizumab shows satisfactory safety profile. No severe hepatotoxicity or acute kidney injury were reported. Case presentation: We presented a case study of a 74-year-old man who developed acute kidney injury (grade 3) and acute liver injury (grade 4) after being administered tislelizumab for the treatment of esophageal squamous cell carcinoma. We reviewed the patient's history, physical examination, and laboratory findings and provided comprehensive differentials of the possible causes of the toxicities. Immune Checkpoint Inhibitors (ICI) hepatotoxicity and nephrotoxicity were confirmed clinically. We also discussed the management of toxicities associated with ICIs and the need for a multidisciplinary approach to care. Conclusions: The case highlights the importance of close monitoring and prompt management of toxicities associated with ICIs and the need for further research to better understand the risk factors for these toxicities and to identify effective treatments for them.

Analysis of Factors Influencing Prognosis and Assessment of 60 Cases of Decompensated Cirrhotic Patients with Portal Hypertension.

Objective: To investigate the risk factors for the development of portal hypertension in patients with decompensated cirrhosis and analyze their prognosis. Methods: Patients with decompensated cirrhosis who were admitted to our hospital and Qu fu People's Hospital from June 2022 to June 2023 were included in this study. Among them, there were 45 male and 15 female patients, with a median age of 56 (range: 35-77) years. A comparative analysis was performed between Group A (hepatic venous pressure gradient, HVPG <16 mmHg) and Group B (HVPG ≥16 mmHg) patients, along with various clinical outcomes. Multivariate analysis was conducted to explore the risk factors influencing the occurrence of portal hypertension and adverse prognosis in patients with cirrhosis. Results: In Group A patients with portal hypertension, we observed lower levels of aspartate aminotransferase, laminin, serum hyaluronic acid, type III procollagen N-terminal peptide, total bile acids, and cholylglycine acid compared to Group B. On the other hand, levels of alanine aminotransferase, white blood cells, and serum albumin were higher in Group A than in Group B. These differences between the groups were statistically significant (P < 0.05). Multivariate analysis of the aforementioned risk factors indicated that low white blood cell count, high cholylglycine acid levels, and high serum hyaluronic acid levels were identified as independent risk factors for the occurrence of difficult-to-control complications in decompensated portal hypertension among patients with liver cirrhosis (P < 0.05). Conclusion: Liver cirrhosis patients with portal hypertension and multiple risk factors like low white blood cell count and high liver transaminase levels should be cautious regarding the progression of portal hypertension when combined with splenomegaly, liver fibrosis, and bile stasis, as it often indicates a poor prognosis.

Detection of minimal hepatic encephalopathy in patients with cirrhosis based on the Stroop-CN model (NCRCID-CHESS 2106): a prospective multicenter study.

Minimal hepatic encephalopathy (MHE) has a substantial impact on the clinical outcomes and quality of life (QOL) of patients with cirrhosis. However, timely diagnosis and intervention are challenging due to sophisticated diagnostic methods. In this study, 673 healthy controls and 905 patients with cirrhosis were screened, and 660 healthy controls and 757 patients with cirrhosis, divided into the test (292 patients) and validation (465 patients) cohort, were analyzed after screening. A diagnostic model of the Stroop test (Stroop-CN) was constructed by multivariate linear regression based on the results of healthy controls. The prevalence of MHE and the comparison results with psychometric hepatic encephalopathy score through the Stroop-CN model were stable in the test and validation cohorts. Moreover, the prevalence of MHE remained significantly higher in patients with worse disease conditions marked as high Child-Pugh grades and the Model for End-stage Liver Disease and Sodium (MELD-Na) scores in the test and validation cohort. The EuroQol 5-D questionnaire revealed that patients with MHE had a worse QOL than those without MHE both in the test and validation cohort. In conclusion, an easy and practical Stroop-CN model for MHE diagnosis based on the EncephalApp is established. It is found that a considerable number of Chinese patients with cirrhosis experience MHE, which significantly impacts their QOL.

Carvedilol to prevent decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by liver stiffness: study protocol for a randomied, double-blind, placebo-controlled, multicentre trial in China.

INTRODUCTION: Patients with clinically significant portal hypertension (CSPH) are recommended to be treated with non-selective beta-blockers (ie, carvedilol) to prevent the first hepatic decompensation event by the renewing Baveno VII consensus. CSPH is defined by hepatic venous pressure gradient (HVPG)≥10 mm Hg; however, the HVPG measurement is not widely adopted due to its invasiveness. Liver stiffness (LS)≥25 kPa can be used as a surrogate of HVPG≥10 mm Hg to rule in CSPH with 90% of the positive predicting value in majority aetiologies of patients. A compelling argument is existing for using LS≥25 kPa to diagnose CSPH and then to initiate carvedilol in patients with compensated cirrhosis, and about 5%-6% of patients under this diagnosis criteria may not be benefited from carvedilol and are at risk of lower heart rate and mean arterial pressure. Randomised controlled trial on the use of carvedilol to prevent liver decompensation in CSPH diagnosed by LS remains to elucidate. Therefore, we aimed to investigate if compensated cirrhosis patients with LS≥25 kPa may benefit from carvedilol therapy. METHODS AND ANALYSIS: This study is a randomised, double-blind, placebo-controlled, multicentre trial. We will randomly assign 446 adult compensated cirrhosis patients with LS≥25 kPa and without any previous decompensated event and without high-risk gastro-oesophageal varices. Patients are randomly divided into two groups, with 223 subjects in group A and 223 subjects in group B. Group A is a carvedilol intervention group, while group B is a placebo group. All patients in both groups will receive aetiology therapies and are followed up at an interval of 6 months. The 3-year incidences of decompensated events of cirrhosis-related and liver-related death are the primary outcome. The secondary outcomes include development of each complication of portal hypertension individually (ascites, variceal bleeding or overt hepatic encephalopathy), development of spontaneous bacterial peritonitis and other bacterial infections, development of new varices, growth of small varices to large varices, delta changes in LS and spleen stiffness, change in hepatic dysfunction assessed by Child-Pugh and model for end-stage liver disease score, change in platelet count, development of hepatocellular carcinoma, development of portal vein thrombosis and adverse events with a 3-year follow-up. A predefined interim analysis will be performed to ensure that the calculation is reasonable. ETHICS AND DISSEMINATION: The study protocol has been approved by the ethics committees of the Sixth People's Hospital of Shenyang (2023-05-003-01) and independent ethics committee for clinical research of Zhongda Hospital, affiliated to Southeast University (2023ZDSYLL433-P01). The results from this trial will be submitted for publication in peer-reviewed journals and will be presented at international conferences. TRIAL REGISTRATION NUMBER: ChiCTR2300073864.

Carvedilol to prevent hepatic decompensation of cirrhosis in patients with clinically significant portal hypertension stratified by new non-invasive model (CHESS2306).

Background & Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvedilol-treating cohort. Results: In the meta-analysis with six studies (n = 819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new "CSPH risk" model. In the HVPG cohort (n = 151), the new model accurately predicted CSPH with cutoff values of 0 and -0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n = 1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <-0.68 (low-risk), -0.68 to 0 (medium-risk), and >0 (high-risk). In the carvedilol-treated cohort, patients with high-risk CSPH treated with carvedilol (n = 81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n = 613 before propensity score matching [PSM], n = 162 after PSM). Conclusions: Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Correlation of TNF-α, Cys C, and NLRP3 inflammasomes with venous ulcers in patients with lower extremity varicose veins.

OBJECTIVE: To explore the correlation of tumor necrosis factor α (TNF-α), cystatin C (Cys C), and NLR family pyrin domain containing 3 (NLRP3) inflammasomes with venous ulcers from lower extremity varicose veins. METHODS: In this retrospective analysis, 135 patients with primary varicose veins of lower extremities were selected and divided into a varicose ulcer group (n=32) and a non-varicose ulcer group (n=103) according to clinical ulcer presence. Healthy adults with similar general information during the same period were included as a healthy controls (n=30). The levels of TNF-α, interleukin-1ß (IL-1ß), Cys C, and NLRP3 inflammasomes were statistically analyzed among the three groups. Logistic regression was used for analyzing the risk factors for venous ulcers in patients with varicose veins of the lower extremities. Spearman correlation was applied for correlation analysis. The area under the receiver operating characteristic (ROC) curve (AUC) was found to disclose the predictive value of TNF-α, Cys C, and NLRP3 inflammasomes for venous ulcers. RESULTS: (1) Logistic regression analysis showed that TNF-α, IL-1ß, and NLRP3 inflammasomes were risk factors for venous ulcers in patients with varicose veins of the lower extremity, and Cys C in ulcer wound tissue was a protective factor. (2) TNF-α was significantly correlated with IL-1ß and Cys C in ulcer wound tissue, and NLRP3 in plasma (r=0.256, -0.290, 0.305; P=0.003, 0.001, <0.001). IL-1ß was significantly correlated with CysC in ulcer wound tissue and plasma (r=-0.251, -0.193; P=0.003, 0.025). (3) The AUC, sensitivity, and specificity of TNF-α and NLRP3 inflammasomes for predicting varicose veins were high, with AUC of 0.881 and 0.712, sensitivity of 0.875% and 0.875%, and specificity of 0.893% and 0.738%, respectively. CONCLUSION: TNF-α in plasma, Cys C in ulcer wound tissue and plasma, and NLRP3 inflammasomes in plasma were closely related to the occurrence of venous ulcers in patients with varicose veins of the lower and may serve as new targets for treatment.

Effects of Liver Fibrosis on Islet Function in Patients with Chronic Hepatitis B Complicated with Impaired Fasting Glucose.

Background: Patients with chronic hepatitis B (CHB) and cirrhosis often have impaired fasting glucose (IFG). This study sought to investigate the impact of liver fibrosis on islet function in individuals diagnosed with CHB and IFG. Material and Methods: Patients with chronic hepatitis B (CHB) and impaired fasting glucose (IFG) were selected for this study. They were divided into low-risk (L-R), intermediate-risk (M-R), and high-risk (H-R) liver fibrosis groups based on the FIB-4 score. The study compared islet function among different risk groups of liver fibrosis and analyze the correlation between liver fibrosis and islet function. Additionally, the patients were divided into a diabetes mellitus (DM) group and a non-DM (NDM) group based on the development of DM. The cumulative risk of progression to DM in patients with L-R, M-R, and H-R liver fibrosis was analyzed using the Kaplan-Meier method. Hazard ratios (HRs) and confidence intervals (CIs) were calculated for DM development through Cox regression analysis. Results: In this study of 228 individuals, higher FIB-4 scores were observed in the DM group compared to the NDM group. Patients with H-R liver fibrosis displayed lower islet function and had a significantly higher risk of developing DM. The FIB-4 score and fasting plasma glucose (FPG) were identified as independent risk factors for DM progression in CHB patients with IFG. Conclusion: Among patients with CHB and IFG, the severity of liver fibrosis is associated with islet function, and the FIB-4 score is a significant risk factor for DM development.

Validation and analysis of the geographical origin of Angelica sinensis (Oliv.) Diels using multi-element and stable isotopes.

BACKGROUND: Place of origin is an important factor when determining the quality and authenticity of Angelica sinensis for medicinal use. It is important to trace the origin and confirm the regional characteristics of medicinal products for sustainable industrial development. Effectively tracing and confirming the material's origin may be accomplished by detecting stable isotopes and mineral elements. METHODS: We studied 25 A. sinensis samples collected from three main producing areas (Linxia, Gannan, and Dingxi) in southeastern Gansu Province, China, to better identify its origin. We used inductively coupled plasma mass spectrometry (ICP-MS) and stable isotope ratio mass spectrometry (IRMS) to determine eight mineral elements (K, Mg, Ca, Zn, Cu, Mn, Cr, Al) and three stable isotopes (δ13C, δ15N, δ18O). Principal component analysis (PCA), partial least square discriminant analysis (PLS-DA) and linear discriminant analysis (LDA) were used to verify the validity of its geographical origin. RESULTS: K, Ca/Al, δ13C, δ15N and δ18O are important elements to distinguish A. sinensis sampled from Linxia, Gannan and Dingxi. We used an unsupervised PCA model to determine the dimensionality reduction of mineral elements and stable isotopes, which could distinguish the A. sinensis from Linxia. However, it could not easily distinguish A. sinensis sampled from Gannan and Dingxi. The supervised PLS-DA and LDA models could effectively distinguish samples taken from all three regions and perform cross-validation. The cross-validation accuracy of PLS-DA using mineral elements and stable isotopes was 84%, which was higher than LDA using mineral elements and stable isotopes. CONCLUSIONS: The PLS-DA and LDA models provide a theoretical basis for tracing the origin of A. sinensis in three regions (Linxia, Gannan and Dingxi). This is significant for protecting consumers' health, rights and interests.

New insights into the phylogeny of Sinocarum (Apiaceae, Apioideae) based on morphological and molecular data.

Sinocarum is a Sino-Himalayan endemic genus of Apiaceae and distributed in high-elevations from Nepal to SW China. In this study, morphological characteristics were combined with nuclear internal transcribed spacer (ITS) and two chloroplast DNA (cpDNA) intron sequences (rpl16 and rps16) to determine the phylogenetic placement of Sinocarum and the infrageneric relationships between five Sinocarum species. The results confirmed that Sinocarum was a polyphyletic group separated into two clades, Acronema and East Asia clades. S. coloratum, the generic type of Sinocarum, S. cruciatum, S. vaginatum and S. filicinum are in the Acronema clade. Among them, the first three species are clustered into a subclade and are closely related to the genus Acronema. While S. filicinum has a close affinity with Meeboldia. S. schizopetalum did not ally with its congeners we collected and is allied closely with members of the distantly related East Asia clade. In addition, the fruit of the Acronema clade Sinocarum species is usually oblong-ovoid or ovoid, and the pollen is super-rectangular, while the Sinocarum species in the East Asia clade have broad-ovoid fruit and sub-rhomboidal pollen. This study has furnished cumulative evidence to reduce phylogenetic uncertainty and provide a more comprehensive description of the plant morphology, fruit morphology and anatomy, and pollen morphology of these five Chinese Sinocarum species.

Caulophine protects cardiomyocytes from oxidative and ischemic injury.

Caulophine is a new fluorenone alkaloid isolated from the radix of Caulophyllum robustum MAXIM and identified as 3-(2-(dimethylamino) ethyl)-4,5-dihydroxy-1,6-dimethoxy-9H-fluoren-9-one. Due to its new chemical structure, the pharmacological activities of caulophine are not well characterized. The present study evaluated the protective effect and the primary mechanisms of caulophine on cardiomyocyte injury. Viability of cardiomyocytes was assayed with the MTT method, and cell apoptosis was detected by flow cytometry. Myocardial infarction was produced by ligating the coronary artery, and myocardial ischemia was induced by isoproterenol in rats. Myocardial infarction size was estimated with p-nitro-blue tetrazolium staining. Lactate dehydrogenase (LDH), creatine kinase (CK), superoxide dismutase (SOD), malondialdehyde (MDA), and free fatty acid (FFA) were spectrophotometrically determined. Histopathological and ultrastructural changes of ischemic myocardium were observed. The results showed that pretreatment with caulophine increased the viability of H(2)O(2)- and adriamycin-injured cardiomyocytes; decreased CK, LDH, and MDA; increased SOD; and inhibited H(2)O(2)-induced cellular apoptosis. Caulophine reduced myocardial infarct size and serum CK, LDH, FFA, and MDA; raised serum SOD; and improved histopathological and ultrastructural changes of ischemic myocardium. The results demonstrate that caulophine has the ability to protect cardiomyocytes from oxidative and ischemic injury through an antioxidative mechanism that provides a basis for further study and development of caulophine as a promising agent for treating coronary heart disease.