Effect of Some Risk Factors on Over-Anticoagulation Disorders and Bleeding in Patients Receiving Anticoagulant Therapy with Overdosage of Vitamin K Antagonist.

Objective: Study on effect of risk factors on over-anticoagulation in patients taking anticoagulant drugs with VKAs (vitamin K antagonists). Methods: Cross-sectional descriptive, prospective research. Study on 79 patients taking anticoagulant drugs with VKAs who had an INR (International Normalized Ratio) index of more than indicated anticoagulation dose with VKAs therapy. Results: A total of 79 patients, mean age 65.65 ± 12.17 years [33:85], the elderly group is common (73.4%). Patients had hemorrhage disorders account for 22.8%. The INR index had an average value was 5.88 ± 3.0 [3.02-23.95]; The INR> 5 level group is a higher risk of bleeding than the INR ≤5 level group, it's the statistical significance (p < 0.001). The risk factors such as drugs to treat dyslipidemia, hyperthyroid, amiodarone, beta blocker, prednisone, NSAIDs (Non-steroidal anti-inflammatory), BMI (Body Mass Index), smoke and alcohol that the risk factors of increasing of bleeding when receiving anticoagulants but it's not statistically significant yet (OR >1, p > 0.05); These patients using coenzyme Q10 and green vegetable nutrition such as cruciferous vegetables (Brassicaceae, Asteraceae) are quite common (31.6% and 35.4%), its effect on coagulation with vitamin K and cause of the increased in risk of bleeding was statistical significantly with OR = 5.28 (CI: 1.72-16.17, p < 0.01), and OR = 2.99 (CI: 1.01-8.80, p < 0.05) respectively. Conclusion: Most patients in over-anticoagulation were the elderly group. Patients had hemorrhage disorders account for 22.8%. The INR> 5 level group was a higher risk of bleeding than the INR ≤5 level group with statistical significance. Patients using Coenzyme Q10 and green vegetable nutrition such as cruciferous vegetables (Brassicaceae, Asteraceae) are quite common, its effect on coagulation and cause of the increased risk of bleeding complication with statistical significance.

Tongqiao Huoxue Decoction ameliorates traumatic brain injury-induced gastrointestinal dysfunction by regulating CD36/15-LO/NR4A1 signaling, which fails when CD36 and CX3CR1 are deficient.

AIMS: Gastrointestinal (GI) dysfunction, as a common peripheral-organ complication after traumatic brain injury (TBI), is primarily characterized by gut inflammation and damage to the intestinal mucosal barrier (IMB). Previous studies have confirmed that TongQiao HuoXue Decoction (TQHXD) has strong anti-inflammatory properties and protects against gut injury. However, few have reported on the therapeutic effects of TQHXD in a TBI-induced GI dysfunction model. We aimed to explore the effects of TQHXD on TBI-induced GI dysfunction and the underlying mechanism thereof. METHODS: We assessed the protective effects and possible mechanism of TQHXD in treating TBI-induced GI dysfunction via gene engineering, histological staining, immunofluorescence (IF), 16S ribosomal ribonucleic acid (rRNA) sequencing, real-time polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), Western blot (WB), and flow cytometry (FCM). RESULTS: TQHXD administration ameliorated TBI-induced GI dysfunction by modulating the abundance and structure of bacteria; reconstructing the destroyed epithelial and chemical barriers of the IMB; and improving M1/M2 macrophage, T-regulatory cell (Treg)/T helper 1 cell (Th1 ), as well as Th17 /Treg ratios to preserve homeostasis of the intestinal immune barrier. Notably, Cluster of Differentiation 36 (CD36)/15-lipoxygenase (15-LO)/nuclear receptor subfamily 4 group A member 1 (NR4A1) signaling was markedly stimulated in colonic tissue of TQHXD-treated mice. However, insufficiency of both CD36 and (C-X3-C motif) chemokine receptor 1 (CX3CR1) worsened GI dysfunction induced by TBI, which could not be rescued by TQHXD. CONCLUSION: TQHXD exerted therapeutic effects on TBI-induced GI dysfunction by regulating the intestinal biological, chemical, epithelial, and immune barriers of the IMB, and this effect resulted from the stimulation of CD36/NR4A1/15-LO signaling; however, it could not do so when CX3CR1 and CD36 were deficient. TQHXD might therefore be a potential drug candidate for treating TBI-induced GI dysfunction.

Exosomes derived from EphB2-overexpressing bone marrow mesenchymal stem cells regulate immune balance and repair barrier function.

BACKGROUND: Disruption of intestinal barrier function and an imbalance in intestinal immunity are crucial for the occurrence and development of ulcerative colitis. Because of their important roles in regulating inflammation and immunity, exosomes (Exos) released from bone marrow mesenchymal stem cells (BMSCs) may be useful for treating ulcerative colitis. The EphB/EphrinB signaling pathway plays a crucial role in the inflammatory process and the development and function of immune cells, and can mediate long-distance intercellular communication through extracellular vesicles. This study was conducted to explore the effects of pre-modified BMSC-Exos expressing EphB2 (EphB2-Exos) on immunoregulation in vitro. METHODS: We transfected a lentivirus vector encoding EphB2 into BMSCs and isolated EphB2-Exos from the culture supernatant. Inflammation and oxidative damage in the human colon adenocarcinoma cell line (Caco-2) were induced by dextran sulfate sodium/hydrogen peroxide. In addition, spleen CD4+ T lymphocytes of rats were sorted in vitro. We conducted a series of experiments to explore the biological functions of EphB2-Exos. RESULTS: EphB2-Exos were successfully isolated and were found to significantly protect the activity, proliferation, and migration of Caco-2 cells that were inhibited by dextran sulfate sodium. EphB2-Exos alleviated inflammation and apoptosis and increased the activity of antioxidant enzymes while inhibiting oxidative stress in Caco-2 cells. EphB2-Exos restored intestinal barrier function by inhibiting the RhoA/ROCK pathway and regulated the polarization of CD4+T cells. CONCLUSION: EphB2-Exos enhanced intestinal barrier function and regulated the immune balance by inhibiting the RhoA/ROCK pathway in vitro. These findings suggest that EphB2-Exos can be applied as a cell-free therapy for ulcerative colitis.

Leukoencephalopathy in children with acute lymphoblastic leukemia after chemotherapy: a retrospective monocenter study.

Background: To investigate the clinical and neuroimaging characteristics of leukoencephalopathy among children with acute lymphoblastic leukemia (ALL), especially after chemotherapy. Methods: Clinical data for 17 pediatric patients with leukoencephalopathy and 17 matched controls were retrospectively analyzed. All participants were children with ALL admitted to the Children's Hospital of Soochow University from May 2011 to April 2021. The data mainly consisted of general information, laboratory studies, and imaging diagnostic results. Results: Overall, 94.12% of the patients experienced neurological symptoms. The most common symptoms were seizure (7/17, 41.18%), nausea (5/17, 29.41%), vomiting (5/17, 29.41%), paralysis (5/17, 29.41%), and numbness (4/17, 23.53%). On neuroimaging, multiple and irregular lesions were observed, distributed mainly in the periventricular area (9/17, 52.94%), parietal lobe (6/17, 35.29%), and basal ganglia (5/17, 29.41%). Moreover, there were significant differences in serum sodium (P=0.0001), C-reactive protein (P=0.0124) and blood pressure (P=0.0271) between patients with and without leukoencephalopathy. After aggressive treatment, the clinical symptoms (12/17, 70.59%) and imaging lesions (11/13, 84.62%) gradually improved in most patients. Conclusions: Chemotherapy is an important risk factor related to leukoencephalopathy. Although the clinical symptoms of leukoencephalopathy vary widely, there is a high degree of consistency in its radiological features. Abnormal laboratory results may also help the identification of leukoencephalopathy. Early detection and treatment can improve brain development in the long term.

Effectiveness and tolerability of adjunctive perampanel in pediatric patients (aged 4-12 years) with refractory epilepsy: An observational study.

Information on the effects of perampanel in Chinese children ≤12 years of age with refractory epilepsy is limited; thus, we conducted an observational study to assess the effectiveness, safety, and tolerability of adjunctive perampanel in this pediatric population. In this study, we reviewed the medical records of pediatric patients aged 4 to 12 years with refractory epilepsy who were admitted to Children's Hospital of Soochow University and prescribed perampanel between January 2020 and January 2021. Effectiveness of perampanel was measured by 50% responder rates, seizure-freedom rates, and retention rates for up to 48 weeks. Adverse events were monitored and recorded throughout the study. A total of 34 patients (male, n = 15) who exhibited refractory epilepsy were included in this study, and 64.71% of patients had focal-onset seizures combined with generalized epilepsy. The mean (± standard deviation) age of patients was 7.21 (± 2.12) years, with a mean (± standard deviation) age at seizure onset of 4.57 (± 2.59) years. After the addition of perampanel, the 50% responder rates at 4, 8, 12, 24, 36, and 48 weeks were 37.50% (12/32), 43.75% (14/32), 53.13% (17/32), 59.38% (19/32), 59.38% (19/32), and 62.07% (18/29). Two patients withdrew from perampanel treatment due to adverse events in the first 2 weeks. Adverse events were reported by 44.12% (15/34) of patients, and the retention rates at 36 and 48 weeks were 94.12% (32/34) and 85.29% (29/34), respectively. Overall, perampanel exhibited good effectiveness, safety, and tolerability in the treatment of pediatric patients (aged 4-12 years) with refractory epilepsy. These findings suggest that personalized treatment and better baseline seizure control may increase the responder rate and retention rate of perampanel.

BMSCs improve TNBS-induced colitis in rats by inducing Treg differentiation by expressing PD-L1.

OBJECTIVES: Bone marrow-derived mesenchymal stem cells (BMSCs) show promise in treating inflammatory bowel disease. We tested if BMSCs improve Trinitro-benzene-sulfonic acid (TNBS)-induced colitis by inducing Treg differentiation by modulating programmed cell death 1 ligand 1(PD-L1). RESULTS: BMSCs were isolated and transfected with PD-L1 siRNA. Sprague-Dawley rats were randomly divided into 4 groups: normal, model, BMSC control, and PD-L1 siRNA BMSC. Colitis was induced by TNBS, except in the normal group. On d4, the BMSC control and PD-L1 siRNA BMSC groups were intravenously injected with BMSCs at a dose of 5 × 106 cells in phosphate-buffered saline (PBS; volume matched). BMSCs were later verified to have reached the colon tissue. BMSC control showed significantly better clinical symptoms and reduced histopathological colitis severity; PD-L1 siRNA BMSC group showed no difference. PD-L1 siRNA reduced: spleen and mesenteric lymph node Tregs, PD-L1, interleukin-10 (IL10), phosphate and tension homology deleted on chromosome ten (PTEN); colon p-Akt and p-mTOR were increased. CONCLUSIONS: We found that BMSCs can induce Treg differentiation by inhibiting the Akt/mTOR pathway via PD-L1; this significantly improved symptoms and pathology in our ulcerative colitis rat models.

HSPA5 Inhibitor Meliorate DSS-Induced Colitis through HSPA1A/CHIP.

Objective: Ulcerative colitis (UC) is closely related to immune response, in which Treg cells (Tregs) suppress the autoimmune response of effector T cells to maintain homeostasis. As a marker of endoplasmic reticulum stress (ERS), HSPA5 was highly expressed in the colon tissue of UC patients. This study is aimed at evaluating the therapeutic effect of HSPA5 inhibitor (HA15) on dextran sulfate sodium- (DSS-) induced ulcerative colitis in mice and explored the effect and related mechanism of HSPA5 inhibitor on the differentiation and function of Tregs. Methods: Thirty-two C57BL/6 mice were randomly divided into four groups (8 mice per group): normal control group, DSS model group, HSPA5 inhibitor (HA15) group (intraperitoneal injection), and dexamethasone (DXM) group (intraperitoneal injection). Except for the blank control group, the other groups were induced with 3% DSS for 7 days and then given corresponding intervention therapy for 7 days. Results: The disease activity index (DAI) score, colon length, histopathological changes, and scores of DSS-induced mice show that HA15 could significantly improve the degree of inflammation in ulcerative colitis. Moreover, HA15 can better inhibit the expression of HSPA5, HSPA1A, and CHIP in the colon and increase the level of FOXP3 mRNA. Finally, the content of Treg cells and the levels of IL-10 and TGF-ß1 were significantly increased, and the levels of IL-6 were significantly reduced. Conclusions: HA15 can improve the differentiation and function of Treg cells by inhibiting the HSPA1A/CHIP pathway, thereby improving ulcerative colitis. Therefore, inhibiting the expression of HSPA5 may serve as a new approach to treat ulcerative colitis.

Post-Traumatic Growth during COVID-19: The Role of Perceived Social Support, Personality, and Coping Strategies.

Although many studies on mental health have been conducted among various populations during the COVID-19 pandemic, few studies have focused on post-traumatic growth (PTG) in the general population. The current study aimed to explore whether perceived social support, personality, and coping strategies are associated with PTG in the COVID-19 pandemic period. The study also investigated whether coping strategies mediate the relations between perceived social support, personality, and PTG. A total of 181 participants (Mage = 24) completed the self-report questionnaire online, which was distributed via various online channels, mainly in China and Sweden. The relations between the study variables were examined with correlation analyses and a multiple mediation analysis. Results showed that more than half of the participants (60.8%) reported experiences of PTG during the pandemic. Additionally, perceived social support, personality traits (extraversion, emotional stability, agreeableness, and conscientiousness) and coping strategies (problem-focused coping, emotion-focused coping, and social support coping) were positively correlated with PTG. In addition, coping strategies (problem-focused coping, emotion-focused coping, and avoidance coping) mediated the relations between perceived social support, personality traits and PTG. Theoretical and practical implications of this study are discussed, concluding that the findings of this study have the potential to guide intervention efforts to promote positive change during the pandemic.

Extracellular vesicles derived from EphB2-overexpressing bone marrow mesenchymal stem cells ameliorate DSS-induced colitis by modulating immune balance.

BACKGROUND: The bone marrow mesenchymal stem cell (BMSCs)-derived extracellular vesicles (EVs) open up a new avenue for ulcerative colitis (UC) treatment recently, but they are not selectively enriched in targeted tissues. EphB2, a cell-to-cell signaling receptor, is identified as a regulator for inflammatory response, immune homeostasis and cell migration. In this study, we investigated the therapeutic potential and underlying mechanism for EphB2 over-expressing BMSCs derived EVs (EphB2-EVs) in the treatment of UC. METHODS: BMSCs and EVs were obtained and characterized by a series of experiments. Lentivirus vector encoding EphB2 was transfected into BMSCs and verified by qRT-PCR. We analyzed the EphB2-EVs ability of colonic targeting in a DSS-induced colitis model by using confocal microscope and WB. The protective effect of EphB2-EVs in vivo was systematically evaluated by using a series of function experiments. RESULTS: We successfully constructed EphB2-overexpressing BMSCs derived EVs (EphB2-EVs). Overexpression of EphB2 significantly enhanced the homing of EVs to the damaged colon. In addition, EphB2-EVs were effective to attenuate inflammation in intestinal mucosa and restore the damaged colon tissue by inhibiting the release of proinflammatory cytokines and upregulating the anti-inflammatory mediators. EphB2-EVs effectively reduced the oxidative stress and repaired the intestinal mucosal barrier in the UC rats. Moreover, EphB2-EVs demonstrated a robust immunomodulatory effect to restore immune homeostasis via modulating Th17/Treg balance and restraining STAT3 activation. CONCLUSIONS: Our results suggest that EphB2-EVs have high colonic targeting ability and could mitigate DSS-induced colitis via maintaining colonic immune homeostasis. These findings provide an effective therapeutic strategy for UC treatment in clinic.

Compound sophorae decoction enhances intestinal barrier function of dextran sodium sulfate induced colitis via regulating notch signaling pathway in mice.

BACKGROUND: Compound sophorae decoction (CSD), a Chinese Herbal decoction, is frequently clinically prescribed for patients suffered from ulcerative colitis (UC) characterized by bloody diarrhea. Yet, the underlying mechanism about how this formulae works is remain elusive. METHODS: In the present study, the experimental colitis in C57BL/6 J mice was induced by oral administration of standard diets containing 3% dextran sodium sulfate (DSS), and CSD was given orally for treatment at the same time. The clinical symptoms including stool and body weight were recorded each day, and colon length and its histopathological changes were observed. Apoptosis of colonic epithelium was studied by detecting protein expression of cleaved caspase-3, and cell proliferation by Ki-67 immunohistochemistry. Tight junction complex like ZO-1 and occludin were also determined by transmission electron microscope and immunofluorescence. The concentration of FITC-dextran 4000 was measured to evaluate intestinal barrier permeability and possible signaling pathway was investigated. Mucin2 (MUC2) and notch pathway were tested through western blot. The M1/M2 ratio in spleen and mesenteric lymph nodes were detected by flow cytometry. And the mRNA levels of iNOS and Arg1 were examined by qRT-PCR. RESULTS: CSD could significantly alleviate the clinical manifestations and pathological damage. Body weight loss and DAI score of mice with colitis were improved and shortening of colon was inhibited. The administration of CSD was able to reduce apoptotic epithelial cells and facilitate epithelial cell regeneration. Increased intestinal permeability was reduced in DSS-induced colitis mice. In addition, CSD treatment obviously up-regulated the expression of ZO-1 and occludin and the secretion of MUC2, regulated notch signaling, and decreased the ratio of M1/M2. CONCLUSIONS: These data together suggest that CSD can effectively mitigate intestinal inflammation, promote phenotypic change in macrophage phenotype and enhance colonic mucosal barrier function by, at least in part, regulating notch signaling in mice affected by DSS-induced colitis.

MiR-155 contributes to intestinal barrier dysfunction in DSS-induced mice colitis via targeting HIF-1α/TFF-3 axis.

Intestinal barrier dysfunction is a hallmark of inflammatory bowel disease (IBD). MiR-155 is increased in colitis and downregulates expression of hypoxia-inducible factor 1α (HIF-1α). Here, we investigated the effects of miR-155 on intestinal barrier dysfunction in dextran sulfate sodium (DSS)-induced colitis. We found that miR-155 antagomir treatment relieved weight loss and intestinal damage in IBD mouse models (P < 0.05). Furthermore, electron microscopy and immunofluorescence imaging showed that miR-155 increased intestinal barrier dysfunction and downregulated the expression of tight junction proteins in DSS-induced colitis. FG-4497, which upregulates HIF-1α expression, elicited protective effects on the intestinal barrier in DSS-induced colitis. Dual luciferase reporter assays also confirmed that miR-155 downregulated expression of HIF-1α. Finally, we discovered that HIF-1α levels were elevated by miR-155 antagomir treatment (P < 0.05) and that TFF-3 expression correlated positively with HIF-1α expression. These results suggest that miR-155 contributes to DSS-induced colitis by promoting intestinal barrier dysfunction and inhibiting the HIF-1α/TFF-3 axis.

COVID-19 patients benefit from early antiviral treatment: A comparative, retrospective study.

The outbreak of COVID-19, caused by severe acute respiratory syndrome coronavirus 2, started in December 2019, Wuhan, China. We aimed to figure out the time-point and duration of using antiviral drugs for receiving the maximal effects in patients with COVID-19. In this study, we enrolled 129 confirmed COVID-19 mild to moderate patients who had been treated with antiviral drugs during their hospitalization in Wuhan Union Hospital China. The patients were divided into an early antiviral treatment group and late antiviral treatment group. The demographic data, laboratory tests, the virus clearance time, chest computed tomography scans, and so forth were extracted, calculated, and compared between two groups. Our data showed that the median time from illness onset to initiation of antiviral treatment was 6 days in all patients. The group with early antiviral treatment demonstrated 7 days shorter in the virus clearance time when compared to the group with late antiviral treatment. After virus clearance, the group with early antiviral treatment showed milder illness than the group with late antiviral treatment. Early antiviral treatment could effectively shorten the virus clearance time, and prevent the rapid progression of COVID-19. Therefore, the COVID-19 patients should receive combined therapies with antiviral treatment at an early stage.

miR-155 antagomir protect against DSS-induced colitis in mice through regulating Th17/Treg cell balance by Jarid2/Wnt/ß-catenin.

BACKGROUND: Th subsets particularly T helper 17 and regulatory T cells play a critical role in immune balance in colonic mucosa of Inflammatory Bowel Disease. Recent studies have indicated miR-155 is overexpressed in the colonic mucosa in IBD patients. Thus, whether and how miR-155 influences Th17/Treg cell balance in IBD patients is worthy of researching. METHODS: We divided mice into four groups: the mice oral administration of 3.0 % DSS in fresh drinking water for 7 days except normal group. In this period, starting from the fifth day, the miR-155 and NC antagomir group were carried out by intraperitoneal injection of miR-155 antagomirs and corresponding negative controls. In vitro, we isolated naïve CD4+T cells and divided into two groups: the cells were transfected with mmu-miR-155-5p inhibitor or corresponding negative controls and then induced differentiation. RESULTS: We found miR-155 antagomir can reach colon tissues in DSS-induced colitis and indeed ameliorated DSS-induced experimental colitis. Subsequently, we proved the levels of Th17 cells in spleens and Mesenteric lymph nodes and its associated IL-6, IL-17A and RORγt in colonic tissues were dramatically decreased and TGF-ß1 raised in DSS + miR-155 antagomir group. However, miR-155 antagomir significantly increased the expression of Tregs. In vitro, we found miR-155 inhibitor could improve the Tregs but decrease Th17 cells. Finally, we dig out that Jarid2 was apparently improved by miR-155 antagomir, Wnt/ß-catenin and its associated T cell factor-4 (TCF-4) and Cyclin D1 expression were positively correlated with Jarid2. CONCLUSION: Silencing of miR-155 attenuates DSS-induced colitis by regulating Th17/Treg cell balance and Jarid2/Wnt/ß-catenin participated in the process.

Study on therapeutic mechanism of Rehmanniae Radix Praeparata- Corni Fructus in sequelae of ischemic stroke based on network pharmacology technology / 中国中药杂志

In ischemic stroke sequela phase, Rehmanniae Radix Praeparata-Corni Fructus drug pair has the effect in protecting damaged neurons, but its mechanism has not been clear. In this study, network pharmacology was used to predict the mechanism of Rehmanniae Radix Praeparata-Corni Fructus in the treatment of ischemic stroke sequela. Through database search and literature retrie-val, 40 active ingredients of Rehmanniae Radix Praeparata and Corni Fructus were obtained, and their targets were obtained through STITCH and TCMSP databases. The targets of ischemic stroke sequela were obtained through OMIM,GAD,TTD and DrugBank databases. By screening the intersections of active ingredients targets and stroke treatment targets, 21 potential targets were obtained. The DAVID database was used for GO enrichment analysis and KEGG pathway analysis of potential targets. GO enrichment analysis showed that Rehmanniae Radix Praeparata-Corni Fructus were mainly involved in regulation of blood pressure, negative regulation of extrinsic apoptotic signaling and positive regulation of angiogenesis. KEGG pathway analysis showed that Rehmanniae Radix Praeparata-Corni Fructus could inhibit inflammatory response and apoptosis signaling pathway by regulating HIF-VEGFA signaling pathway in neural stem cell proliferation, TNF signaling pathway and NF-kappaB signaling pathway. Molecular docking technique was used to verify that Rehmanniae Radix Praeparata-Corni Fructus component has a good binding activity with potential targets. The results showed that in ischemic stroke sequela phase, Rehmanniae Radix Praeparata-Corni Fructus drug pair could play an important role in recovering neural function, promoting the proliferation of neural stem cells, angiogenesis, preventing neural cells apoptosis and regulating inflammatory factors.

[Effects of cornel iridoid glycoside on activity of cholinesterases in vitro].

The purpose of the present study was to investigate the effects of cornel iridoid glycoside (CIG) on the activity of cholinesterases in vitro, and to investigate the mechanism of CIG's treating Alzheimer's disease (AD). The sources of cholinesterases were prepared from human blood cells, rat brain homogenate and human blood plasma, respectively. The biochemical methods were used to detect the activity of acetylcholine esterase (AChE) and butyryl cholinesterase (BuChE) to investigate the influence of CIG on cholinesterases. The results showed that CIG inhibited the activity of AChE of human blood cells and rat brain homogenate, with the 50% inhibition rate (IC50) of 1.6 g . L-1 and 3.3 g . L-1, respectively; and the inhibition of AChE of CIG is reversible. CIG also inhibited the activity of BuChE of human blood plasma, with the IC50 of 2.9 g . L-1. In conclusion, CIG can inhibit the activity of AChE and BuChE in vitro, which may be one of the mechanisms of CIG to treat AD.

Effect of Bnxia Xexin Decoction and its disassembled recipes on somatostatin in rats with stress gastric ulcer / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore the acting mechanism of Banxia Xiexin Decoction (BXD) and its disassembled recipes on stress gastric ulcer, for providing references to the scientific researches on the assembling rule of BXD.</p><p><b>METHODS</b>The rat model of acute gastric ulcer was established by water immersion-restraint stress. The experimental rats were divided into the normal group, the model group and the treated groups treated with BXD and its disassembled recipes respectively to observe the therapeutic efficacy and the changes of somatostatin (SS) expression in brain and gastric tissues.</p><p><b>RESULTS</b>In the model group, the SS expression was 0.0237 +/- 0.0056 in brain and 0.0171 +/- 0.0053 in gastric tissue respectively, which was significantly lower than those in the normal group (0.0305 +/- 0.0024 and 0.0282 +/- 0.0037) respectively. Compared to the model group, the two indexes in rats treated with full BXD were 0.0294 +/- 0.0050 and 0.0288 +/- 0.0027, treated with sweet flavor portion were 0.0314 +/- 0.0027 and 0.0219 +/- 0.0059, all showed increase of SS expression, and the increment was more significant in the former.</p><p><b>CONCLUSION</b>BXD can increase the expression of SS to realize its therapeutic efficacy, and the recipe was assembled rationally.</p>

Chaological connotations of pulse tracings / 中华中医药杂志

Based on chaos theory,chaological connotations of pulse tracings and sphygmology were expounded and explained.Main contents included embodiments of four characteristics(inner randomness,sensitivity to initial value,chaos order and unpredictability of long-term behavior)of chaos in pulse tracings and sphygmology.