Efficacy of predictive pain intervention in patients with aortic dissection.

BACKGROUND: Aortic dissection is usually managed with interventional therapy, conservative therapy, and surgery to inhibit disease progression and improve prognoses. Nevertheless, the absence of meticulous and effective nursing during the treatment greatly increases the complication rates, which is detrimental to the recovery of patients. OBJECTIVE: This study aimed to explore the efficacy of predictive pain intervention in the nursing process of patients with aortic dissection. METHODS: Sixty patients with aortic dissection who were admitted to our hospital from December 2018 to December 2020 were observed in this study. Specifically, these patients were randomly and equally classified into Group A (patients who were given conventional nursing intervention) and Group B (patients who were given predictive pain intervention). Subsequently, the pain score, complication rates, and nursing satisfaction in the two groups were compared and analyzed. RESULTS: Compared with patients in Group A, patients in Group B had significantly lower pain scores (P< 0.05); complication rates were significantly lower in Group B than in Group A (6.67% vs. 23.33%, P< 0.05); patient satisfaction with care was significantly better in Group B compared to Group A (96.67% vs. 73.33%, P< 0.05). CONCLUSION: Predictive pain intervention is widely recognized as useful in the treatment of patients with aortic dissection. It has significant clinical application value as it can largely alleviate pain and is relatively safe for patients.

Effect of Early Exercise Rehabilitation on Cardiopulmonary Function and Quality of Life in Patients after Coronary Artery Bypass Grafting.

The purpose of this study was to analyze the effect of early exercise rehabilitation on cardiopulmonary function and quality of life in patients after coronary artery bypass grafting (CABG). Eighty patients with coronary heart disease who underwent CABG from April 2020 to April 2022 were divided into the study group (n = 40) and control group (n = 40). The control group was given conventional treatment and routine care after CABG, and the study group received early exercise rehabilitation according to the control group. The cardiac function indexes, 6-minute walking test (6MWT), and cardiopulmonary function indexes and quality of life of the two groups were compared before and after the intervention, and the length of hospitalization and hospital costs as well as the occurrence of pulmonary complications in both groups were recorded. Left ventricular ejection fraction (LVEF) was significantly higher (P < 0.05), and left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic diameter (LVESD) were significantly lower (P < 0.05) in the study group than in the control group after the intervention; 6MWT, maximal oxygen consumption (VO2max), and anaerobic threshold (AT) were significantly higher (P < 0.05) in the study group than in the control group after the intervention; physical function (PF), role physical (RP), general health (GH), and role emotional (RE) dimension scores were significantly higher (P < 0.05) in the study group compared with the control group after the intervention The differences in the scores of the remaining dimensions were not statistically significant (P > 0.05); the total hospitalization time in the test group was significantly shorter than that in the control group (P < 0.05), the hospitalization cost was significantly less than that in the control group (P < 0.05), and the total incidence of pulmonary infection and hypoxemia was significantly lower than that in the control group (P < 0.05). Early exercise rehabilitation can effectively improve cardiopulmonary function and exercise tolerance and improve the quality of life of patients after CABG.

Stable immobilization of uranium in iron containing environments with microbial consortia enriched via two steps accumulation method.

The stable stabilization of uranium (U) in iron (Fe) containing environments is restricted by the reoxidation of UO2. In the current study, based on air reoxidation tests, we propose a novel two steps accumulation method to enrich microbial consortia from paddy soil. The constructed microbial consortia, denoted as the Fe-U bacteria, can co-precipitate U and Fe to form stable Fe-U solids. Column experiments running for 4 months demonstrated the production of U(IV)-O-Fe(II) precipitates containing maximum of 39.51% uranium in the presence of Fe-U bacteria. The reoxidation experiments revealed the U(IV)-O-Fe(II) precipitates were more stable than UO2. 16S rDNA high throughput sequencing analysis demonstrated that Acinetobacter and Stenotrophomonas were responsible for Fe and U precipitation, while, Caulobacteraceae and Aminobacter were crucial for the formation of U(VI)-PO4 chemicals. The proposed two steps accumulation method has an extraordinary application potential in stable immobilization of uranium in iron containing environments.

In vivo genome editing in mouse restores dystrophin expression in Duchenne muscular dystrophy patient muscle fibers.

BACKGROUND: Mutations in the DMD gene encoding dystrophin-a critical structural element in muscle cells-cause Duchenne muscular dystrophy (DMD), which is the most common fatal genetic disease. Clustered regularly interspaced short palindromic repeat (CRISPR)-mediated gene editing is a promising strategy for permanently curing DMD. METHODS: In this study, we developed a novel strategy for reframing DMD mutations via CRISPR-mediated large-scale excision of exons 46-54. We compared this approach with other DMD rescue strategies by using DMD patient-derived primary muscle-derived stem cells (DMD-MDSCs). Furthermore, a patient-derived xenograft (PDX) DMD mouse model was established by transplanting DMD-MDSCs into immunodeficient mice. CRISPR gene editing components were intramuscularly delivered into the mouse model by adeno-associated virus vectors. RESULTS: Results demonstrated that the large-scale excision of mutant DMD exons showed high efficiency in restoring dystrophin protein expression. We also confirmed that CRISPR from Prevotella and Francisella 1(Cas12a)-mediated genome editing could correct DMD mutation with the same efficiency as CRISPR-associated protein 9 (Cas9). In addition, more than 10% human DMD muscle fibers expressed dystrophin in the PDX DMD mouse model after treated by the large-scale excision strategies. The restored dystrophin in vivo was functional as demonstrated by the expression of the dystrophin glycoprotein complex member ß-dystroglycan. CONCLUSIONS: We demonstrated that the clinically relevant CRISPR/Cas9 could restore dystrophin in human muscle cells in vivo in the PDX DMD mouse model. This study demonstrated an approach for the application of gene therapy to other genetic diseases.

Shikonin ameliorates lipoteichoic acid­induced acute lung injury via promotion of neutrophil apoptosis.

Shikonin is the major active component in Lithospermum erythrorhizon and has pharmacological effects including reducing inflammation, aiding resistance to bacteria and promoting wound healing. However, the effect of shikonin on lipoteichoic acid (LTA)­induced acute lung injury (ALI) remains to be elucidated. ALI is a serious illness resulting from significant pulmonary inflammation caused by various diseases, such as sepsis, acid aspiration and trauma. The present study found that shikonin significantly attenuated LTA­induced ALI. Following shikonin treatment, the accumulation of pulmonary neutrophils and expression of TNFα, IL­1ß and IL­6 were decreased in mice with LTA­induced ALI. Furthermore, Shikonin promoted neutrophil apoptosis by increasing the activation of caspase­3 and reducing the expression of the antiapoptotic myeloid cell leukemia­1 (Mcl­1) protein. However, shikonin treatment did not influence the expression of B­cell lymphoma­2. The findings of the present study demonstrated that shikonin protected against LTA­induced ALI by promoting caspase-3 and Mcl­1­related neutrophil apoptosis, suggesting that shikonin is a potential agent that can be used in the treatment of sepsis­mediated lung injury.

Engraftment of human induced pluripotent stem cell-derived myogenic progenitors restores dystrophin in mice with duchenne muscular dystrophy.

BACKGROUND: Duchenne muscular dystrophy (DMD) is a devastating genetic muscular disorder with no effective treatment that is caused by the loss of dystrophin. Human induced pluripotent stem cells (hiPSCs) offer a promising unlimited resource for cell-based therapies of muscular dystrophy. However, their clinical applications are hindered by inefficient myogenic differentiation, and moreover, the engraftment of non-transgene hiPSC-derived myogenic progenitors has not been examined in the mdx mouse model of DMD. METHODS: We investigated the muscle regenerative potential of myogenic progenitors derived from hiPSCs in mdx mice. The hiPSCs were transfected with enhanced green fluorescent protein (EGFP) vector and defined as EGFP hiPSCs. Myogenic differentiation was performed on EGFP hiPSCs with supplementary of basic fibroblast growth factor, forskolin, 6-bromoindirubin-3'-oxime as well as horse serum. EGFP hiPSCs-derived myogenic progenitors were engrafted into mdx mice via both intramuscular and intravenous injection. The restoration of dystrophin expression, the ratio of central nuclear myofibers, and the transplanted cells-derived satellite cells were accessed after intramuscular and systemic transplantation. RESULTS: We report that abundant myogenic progenitors can be generated from hiPSCs after treatment with these three small molecules, with consequent terminal differentiation giving rise to mature myotubes in vitro. Upon intramuscular or systemic transplantation into mdx mice, these myogenic progenitors engrafted and contributed to human-derived myofiber regeneration in host muscles, restored dystrophin expression, ameliorated pathological lesions, and seeded the satellite cell compartment in dystrophic muscles. CONCLUSIONS: This study demonstrates the muscle regeneration potential of myogenic progenitors derived from hiPSCs using non-transgenic induction methods. Engraftment of hiPSC-derived myogenic progenitors could be a potential future therapeutic strategy to treat DMD in a clinical setting.

Engraftment of human induced pluripotent stem cell-derived myogenic progenitors restores dystrophin in mice with duchenne muscular dystrophy

BACKGROUND: Duchenne muscular dystrophy (DMD) is a devastating genetic muscular disorder with no effective treatment that is caused by the loss of dystrophin. Human induced pluripotent stem cells (hiPSCs) offer a promising unlimited resource for cell-based therapies of muscular dystrophy. However, their clinical applications are hindered by inefficient myogenic differentiation, and moreover, the engraftment of non-transgene hiPSC-derived myogenic progenitors has not been examined in the mdx mouse model of DMD. METHODS: We investigated the muscle regenerative potential of myogenic progenitors derived from hiPSCs in mdx mice. The hiPSCs were transfected with enhanced green fluorescent protein (EGFP) vector and defined as EGFP hiPSCs. Myogenic differentiation was performed on EGFP hiPSCs with supplementary of basic fibroblast growth factor, forskolin, 6-bromoindirubin-3'-oxime as well as horse serum. EGFP hiPSCs-derived myogenic progenitors were engrafted into mdx mice via both intramuscular and intravenous injection. The restoration of dystrophin expression, the ratio of central nuclear myofibers, and the transplanted cells-derived satellite cells were accessed after intramuscular and systemic transplantation. RESULTS: We report that abundant myogenic progenitors can be generated from hiPSCs after treatment with these three small molecules, with consequent terminal differentiation giving rise to mature myotubes in vitro. Upon intramuscular or systemic transplantation into mdx mice, these myogenic progenitors engrafted and contributed to human-derived myofiber regeneration in host muscles, restored dystrophin expression, ameliorated pathological lesions, and seeded the satellite cell compartment in dystrophic muscles. CONCLUSIONS: This study demonstrates the muscle regeneration potential of myogenic progenitors derived from hiPSCs using non-transgenic induction methods. Engraftment of hiPSC-derived myogenic progenitors could be a potential future therapeutic strategy to treat DMD in a clinical setting.

[Role of p53/p21 signal transduction pathway in the malignant transformation of human embryonic lung fibroblasts induced by quartz].

OBJECTIVE: To observe the expression of p53 protein and investigate the roles of p53 in the expressions and interactions of p21, cyclin D1 and cyclin dependent kinase 4(CDK4) proteins in malignant transformation of human embryonic lung fibroblasts(T-HELF) induced by quartz. METHODS: The cytosolic protein and nuclear protein of both HELF and T-HELF cells were extracted by the separation technique of cytoplasm and nuclei. The distribution and expression of p53, phosphorylated p53 and p21 proteins were detected by Western blot. Based on the RNA interference technique, p53 siRNA was transfected into T-HELF cells to observe the protein expression and change of p53, phosphorylated p53, p21, cyclin D1 and CDK4, while the control group was conducted by transfecting the CMV-neo blank vector into the plasmid. The expression levels of p21, cyclin D1 and CDK4 protein complex in HELF and T-HELF cells were detected by immunoprecipitation. After adding 20 µmol/L of p53 chemical inhibitor pifithrin-α(PFT-α) and 2 µg of p53 siRNA into T-HELF cells respectively, the effect of p53 protein inhibition on p21, cyclin D1 and CDK4 protein complex was also observed. RESULTS: Quartz stimulation of HELF caused a significant increase in the expression of p53 and phosphorylated p53 protein in the nucleus(P<0. 05). The protein expression of p53 in the nucleus of T-HELF was significantly lower than that of HELF(P<0. 05). After transfection of p53 siRNA, the expression of p53 protein was decreased and the expression of p21 and cyclin D1 protein was increased compared with the control group(P<0. 05), while the change of expression in CDK4 was not observed(P>0. 05). Additionally, the result of immunoprecipitation showed that the inhibition of p53 expression could down-regulate the expression level of the binding complex between p21 and cyclin D1 protein(P<0. 05). However, this effect on p21-CDK4 and cyclin D1-CDK4 protein complex was not observed(P>0. 05). CONCLUSION: By regulating the expression and protein-protein interaction between p21 and cyclin D1, p53 would participate in quartz-induced malignant transformation.

N-acetylcysteine attenuates PM2.5-induced apoptosis by ROS-mediated Nrf2 pathway in human embryonic stem cells.

While the effects of fine particulate matter (PM2.5) on embryonic toxicity are widely accepted, its exact mechanisms have not yet been fully elucidated, which partially attribute to lack of ideal research model. Embryonic stem cells (ESCs) have the capacity to differentiate into all cell types of three germ layers. Thus, they are ideal resources for the reproductive toxicity assessment in vitro. In the present study, we investigated the effects of PM2.5 exposure on the oxidative stress and apoptosis of human ESCs (hESCs) and its possible mechanism. Our results showed that strong cytotoxicity high reactive oxygen species (ROS) level and fragmentation of nuclei were observed in the PM2.5-treated hESCs. Meanwhile, up-regulation of apoptosis as well as down-regulation of Nrf2 signaling pathway were also observed after PM2.5 treatment. However, we did not detect significant expression change or phosphorylation of Akt and Erk in PM2.5-treated hESCs. Interestingly, scavenging of PM2.5-induced ROS by N-acetylcysteine (NAC) could block cell apoptosis and rescue the activity of Nrf2 signaling pathway. In conclusion, we demonstrate that PM2.5 is toxic to hESCs by inhibition of ROS-mediated Nrf2 pathway activity. Our findings suggest activation of Nrf2 pathway will help develop new strategies for the prevention and treatment of PM2.5-associated disease.

Shexiang Tongxin Dropping Pill () Protects against Na2S2O4-Induced Hypoxia-Reoxygenation Injury in H9c2 Cells.

OBJECTIVES: To investigate the protective effects of Shexiang Tongxin Dropping Pill (, STP) on Na2S2O4-induced hypoxia-reoxygenation injury in cardiomyoblast H9c2 cells. METHODS: The cell viability and levels of mRNA and protein expression in H9c2 cells were determined following Na2S2O4-induced hypoxia using Hoechst staining, annexin V/propidium iodide (PI) flow cytometry, real-time polymerase chain reaction and Western blot analysis. RESULTS: STP pretreatment significantly increased the viability and inhibited aberrant morphological changes in H9c2 cardiomyoblast cells induced by Na2S2O4 treatment (P<0.05). In addition, STP pretreatment attenuated Na2S2O4-induced hypoxic damage, down-regulated the expression of pro-apoptotic Bax, and up-regulated the expression of anti-apoptotic Bcl-2 in H9c2 cells (P<0.05). CONCLUSIONS: STP was strongly cardioprotective in hypoxia-reoxygenation injury by preventing hypoxic damage and inhibiting cellular apoptosis. These results further support the use of STP as an effective drug for the treatment of ischemic heart disease.

Reversal of the Warburg effect with DCA in PDGF­treated human PASMC is potentiated by pyruvate dehydrogenase kinase­1 inhibition mediated through blocking Akt/GSK­3ß signalling.

There is accumulating evidence indicating that the growth inhibitory effect of dichloroacetate (DCA) on pulmonary arterial smooth muscle cells (PASMCs) may be associated with the reversal of the Warburg effect and initiation of the mitochondria­dependent apoptotic pathway. Previous studies indicated that platelet­derived growth factor (PDGF) promoted the Warburg effect and resulted in apoptotic resistance of PASMCs, which was attributed to activation of the phosphatidylinositol 3­kinase (PI3K)/protein kinase B (Akt) signalling pathway. However, the mechanism underlying the pro­apoptotic effect of DCA on PDGF­treated PASMCs has not been thoroughly elucidated, and the effect of the Akt/glycogen synthase kinase­3ß (GSK­3ß) pathway inhibition concomitant with the effect of DCA on PASMC proliferation remains unclear. The growth of human PASMCs and the lactate concentration in extracellular medium of PASMCs were detected by Cell Counting Kit­8 assays and a Lactate Colorimetric Assay kit, respectively. Cell apoptosis was evaluated by fluorescence activated cell sorting. The mitochondrial membrane potential (ΔΨm) was assessed with 5,5',6,6'­tetrachloro­1,1',3,3'­tetraethylbenzimidazol­carbocyanine iodide assays. The expression levels of phosphorylated Akt and GSK­3ß, pyruvate dehydrogenase, cleaved caspase­3, pyruvate dehydrogenase kinase­1 (PDK­1), hypoxia inducible factor­1α (HIF­1α) and hexokinase­2 (HK­2) were measured with western blot analysis. Confocal analyses were employed to determine HK­2 co­localisation with the mitochondria. The results indicated that DCA inhibited human PASMC proliferation in a dose­dependent manner. DCA at 10 mM promoted apoptosis and the upregulation of activated caspase­3 in PASMCs pre­treated with 20 ng/ml PDGF­homeodimer BB (BB). Treatment with 5 µM LY294002 produced minimal anti­proliferative effects on human PASMCs and barely induced cellular apoptosis and caspase­3 activation. However, co­administration of 10 mM DCA with LY294002 significantly decreased the cell proliferation index and induced cell apoptosis and caspase­3 activation. The combined administration of LY294002 with DCA significantly decreased lactate concentration, promoted the depolarisation of the ΔΨm and repressed HIF­1α upregulation and HK­2 activation in PASMCs treated with PDGF, which was attributed to the potentiation of DCA­induced PDK­1 inhibition by LY294002 via blockade of the Akt/GSK­3ß/HIF­1α signalling pathway. In conclusion, inhibition of the Akt/GSK­3ß pathway improved the pro­apoptotic effect of DCA on human PASMCs, which may be attributed to a reversal of the Warburg effect by blocking the mutual interaction between HIF­1α and PDK­1, consequently downregulating HK­2. Therefore, combinatory treatment with DCA and PI3K inhibitors may represent a novel therapeutic strategy for the reversal of apoptosis resistance exhibited by PASMCs as a result of mitochondrial bioenergetic abnormalities, as well as the treatment of pulmonary vascular remodelling in pulmonary arterial hypertension.

Protective effects of Shexiang Tongxin Dropping Pill on pituitrin­induced acute myocardial ischemia in rats.

Shexiang Tongxin Dropping Pill (STP) is an established traditional Chinese medicine that is widely used for the treatment of ischemic heart disease (IHD), although its mechanisms remain unclear. The present study investigated the protective effects of STP following pituitrin (PTT)­induced myocardial ischemia in rats. ST­segment elevation, blood rheology, and the serum levels of creatine kinase­MB (CK­MB) and lactate dehydrogenase (LDH) were measured. Following heart excision, histological analysis using hematoxylin and eosin and terminal deoxynucleotidyl transferase dUTP nick end labeling were performed. The mRNA expression levels of B­cell lymphoma 2 (Bcl­2) and Bcl­2­associated X protein (Bax) were determined using reverse transcription­quantitative polymerase chain reaction, and their protein expression was detected using immunohistochemistry. The results demonstrated that STP treatment protected against ST elevation, lowered whole blood viscosity, and reduced the serum levels of CK­MB and LDH following acute myocardial ischemia. In addition, STP treatment restored the histopathological change following PTT­induced myocardial ischemia, and resulted in downregulated expression of Bax and upregulated expression of Bcl­2 in myocardial tissue. The present study demonstrates the cardioprotective ability of STP in a rat model of myocardial ischemic injury, which may be attributed to its anti­apoptotic properties. The cardioprotective properties of STP require further investigation to determine whether it may be used for the clinical treatment of IHDs.

Abnormal Neural Progenitor Cells Differentiated from Induced Pluripotent Stem Cells Partially Mimicked Development of TSC2 Neurological Abnormalities.

Tuberous sclerosis complex (TSC) is a disease featuring devastating and therapeutically challenging neurological abnormalities. However, there is a lack of specific neural progenitor cell models for TSC. Here, the pathology of TSC was studied using primitive neural stem cells (pNSCs) from a patient presenting a c.1444-2A>C mutation in TSC2. We found that TSC2 pNSCs had higher proliferative activity and increased PAX6 expression compared with those of control pNSCs. Neurons differentiated from TSC2 pNSCs showed enlargement of the soma, perturbed neurite outgrowth, and abnormal connections among cells. TSC2 astrocytes had increased saturation density and higher proliferative activity. Moreover, the activity of the mTOR pathway was enhanced in pNSCs and induced in neurons and astrocytes. Thus, our results suggested that TSC2 heterozygosity caused neurological malformations in pNSCs, indicating that its heterozygosity might be sufficient for the development of neurological abnormalities in patients.

[Anti-atherosclerotic Effects of Bear Bile Powder in Shexiang Tongxin Dripping Pill: a Mechanism Study].

UNLABELLED: OBJECTIVE : To study the anti-atherosclerotic mechanism of bear bile powder (BBP) in Shexiang Tongxin Dripping Pill (STDP) , and to provide scientific evidence for treating atherosclerosis (AS) by its therapeutic characteristics of cool resuscitation. METHODS: AS model was duplicated using ApoE-/- gene knocked mice fed with high-fat diet. Thirty ApoE-/- deficient male mice were divided into four groups according to body weight using random digit table, i.e., the model group (A, n =9), the STDP group (B, n=E7), the STDP without BBP group (C, n =7), and the BBP group (D, n =9). Besides, another 9 C57BL/6J male mice of the same age were recruited as a normal control group (E). All mice in Group B, C, and D were respectively administered with corresponding drugs (30, 30, and 0. 33 mg/kg) by gastrogavage. Equal volume of normal saline was administered to mice in Group A and E. All medication lasted for 8 successive weeks. Serum levels of inflammatory cytokines such as interleukin 2 (IL-2), interleukin 6 (IL-6), tumor necrosis factor a (TNF-α), interferon y (IFNγ), and oxidized low-density lipoprotein (ox-LDL) were measured by ELISA. Serum levels of malondialdehyde (MDA), activities of glutathione (GSH) and superoxide dismutase (SOD) were determined using biochemical assay. Contents of reactive oxygen species (ROS) in the aortic root was detected by dihydroethidum (DHE) fluorescent probe. Expression levels of microRNAs (such as miR-20, miR-21, miR-126, and miR-155) were detected by real-time PCR. RESULTS: The fluorescence intensity of the aorta was obviously enhanced in Group A. But it was obviously attenuated in Group B, C, and D, and the attenuation was the most in Group B. Compared with Group E, serum levels of IL-2, IL-6, TNF-α, IFN-γ, oxLDL, and MDA all increased (P <0. 01), GSH contents and SOD activities decreased (P <0. 01), expression levels of miR-126, miR-21, and miR-155 in aorta increased (P <0. 01), and the expression level of miR-20 decreased in Group A (P<0. 01). Compared with Group A, serum levels of IL-2, IL-6, TNF-α, IFN-γ, oxLDL, and MDA were all down-regulated (P <0. 01), GSH contents and SOD activities were up-regulated (P <0. 01), expression levels of miR-126, miR-21, and miR-155 in aorta were down-regulated in Group B, C, and D (P <0. 01). The expression level of miR20 was up-regulated in Group B and D (P <0. 01). Compared with Group B, serum levels of IL-2, IL-6, TNF-α, IFN-γ increased (P <0.01); GSH contents and SOD activities decreased, levels of MDA and oxLDL increased (P <0. 01) in Group C and D. Expression levels of miR-20 and miR-155 were down-regulated in Group C and D (P <0. 01). CONCLUSIONS: STDP played roles in significantly regulating inflammatory factors and oxidative stress factors. Its mechanism might be possibly associated with regulating expressions of miR-126, miR-21, miR-155, and miR-20 in aorta. BBP played significant roles in STDP.

[Effect of jianpi tongluo jiedu recipe on expression levels of COX-2, NF-kappaBp65, and Bcl-2 in gastric mucosa of patients with precancerous lesions of gastric cancer].

OBJECTIVE: To explore the effect of Jianpi Tongluo Jiedu Recipe (JTJR) on protein expression levels of COX-2, NF-kappaBp65, Bcl-2, and Bax, mRNA expression levels of COX-2 and Bcl-2, and the apoptotic index (Al) in gastric mucosa of patients with precancerous lesions of gastric cancer (PL-GC). METHODS: Totally 65 PLGC patients were recruited and treated by JTJR (modified by syndrome typing), one dose per day for six successive months. Protein expression levels of COX-2, NF-KBp65, Bcl-2, and Bax were detected in 65 patients using immunohistochemical (IHC) assay before and after treatment. mRNA expression levels of COX-2 and Bcl-2 were detected in 54 patients using reverse transcription-polymerase chain reaction (RT-PCR). Meanwhile, changes of Al was detected in 65 patients using TdT-mediated dUTP-biotin nick end labeling (TUNEL) fluorescence method. RESULTS: After treatment with JTJR, positive protein expression levels of COX-2, NF-KBp65, and Bcl-2 were obviously decreased in the gastric mucosa of PLGC patients (P <0.01), but Bax positive protein expression was found to be higher (P < 0.05). At the same time mRNA expression levels of COX-2 and Bcl-2 were significantly lower after treatment than before treatment (P < 0.05, P < 0.01); Al also increased after treatment (P < 0.05). CONCLUSION: JTJR could promote apoptosis possibly via NF-kappaBp65/COX-2, COX-2/Bcl-2, and NF-kappaBp65/Bcl-2 signaling pathways, thereby affecting PLGC patients.

Shexiang Tongxin dropping pill attenuates atherosclerotic lesions in ApoE deficient mouse model.

ETHNOPHARMACOLOGICAL RELEVANCE: Shexiang Tongxin dropping pill (STDP) is a formulation of Traditional Chinese Medicine mainly used for clinical treatment of stable angina pectoris in China. AIM OF THE STUDY: To investigate the effects and mechanisms of STDP treatment on atherosclerosis. MATERIALS AND METHODS: ApoE deficient (ApoE(-/-)) mice were utilized to evaluate the effect of STDP treatment (30 mg/kg/day) on atherosclerotic lesions. Histopathological features of atherosclerotic lesions, serum levels of lipid proteins, parameters of oxidative stress and pro-inflammatory cytokines were measured by H&E staining, Masson's trichrome staining and ELISA, respectively. Real-time PCR analyses were performed to examine the aortic expression of atherosclerosis-associated microRNAs. RESULTS: The STDP treatment resulted in attenuated atherosclerotic lesion manifested by reduced lipid deposition, fibrosis and oxidative stress. It also led to increase in serum levels of GSH and SOD, decrease in MDA, decrease in CHO, TG, LDL, ox-LDL and increase in HDL, respectively. Additionally, the levels of pro-inflammatory cytokines including IL-2, IL-6, TNF-α and γ-IFN were markedly reduced by STDP treatment. Furthermore, STDP treatment was associated with a significant reduction in the aortic expression of miR-21a, miR-132, miR-126a, miR-155 and increased expression of miR-20a. CONCLUSION: Our results demonstrated for the first time that STDP attenuated atherosclerotic lesions in ApoE(-/-) mouse model. Moreover, STDP treatment exhibited multi-targeting effects on pathological, biochemical and molecular aspects of atherosclerosis implicating lipid regulation, fibrosis, inflammation and oxidative stress. Findings from the current study warrant further evaluation of the clinical application of STDP in atherosclerosis treatment.

[Determination of tris (2-chloroethyl) phosphate in leather by gas chromatography-mass spectrometry coupled with mixed-mode sorbent solid phase extraction].

Leather is one of the important exporting products to European Union (EU), and tris(2-chloroethyl) phosphate (TCEP) is a commonly used flame retardant in leather and leather products. Recently, TCEP has been classified as a kind of substance of very high concern (SVHC) by EU for its carcinogenicity and reproductive toxicity. But to date, there is not a recognized method for the determination of TCEP in leather and leather products due to the serious matrix interferences and relatively low recovery of TCEP. In this work, a home-made mixed-mode sorbent (Silica-WCX) with carboxyl and alkyl groups was tested as the sorbent of solid phase extraction (SPE) to extract TECP from leather. The results demonstrated that, making the carboxyl groups protonized under acidic condition, Silica-WCX exhibited better extraction performance towards TCEP over some frequently used commercial sorbents tested. After the optimization of the SPE conditions based on Silica-WCX, a method of gas chromatography/mass spectrometry (GC-MS) was established for the determination of TCEP in leather samples. The linear range for TCEP ranged from 0.10 to 100.0 µg/L and the limit of quantification (LOQ, S/N = 10) was 44.46 ng/kg. The recoveries of TCEP spiked in samples at varied levels were in the range of 91.45%-99.98% with the relative standard deviations (RSDs) of 4.33%-5.97%. The method is simple, sensitive and reliable for the analysis of TCEP in leather and leather products.

Selections of appropriate regimen of high-dose chemotherapy combined with adoptive cellular therapy with dendritic and cytokine-induced killer cells improved progression-free and overall survival in patients with metastatic breast cancer: reargument of such contentious therapeutic preferences.

BACKGROUND: We hypothesized that combination of dendritic cell (DC) with autologous cytokine-induced killer (CIK) immunotherapy in setting of high-dose chemotherapy (HDC) would be effective for selected metastatic breast cancer (MBC) patients. PATIENTS AND METHODS: Our previous work showed thiotepa could eradicate breast cancer stem cells. From 2004 to 2009, 79 patients received standard dose chemotherapy (SDC) of 75 mg/m(2) docetaxel and 75 mg/m(2) thiotepa versus 87 patients of HDC + DC/CIK: 120 mg/m(2) docetaxel to mobilize peripheral CD34(+) progenitor cells, a sequence of HDC (120 mg/m(2) docetaxel, plus 175 mg/m(2) thiotepa) + DC/CIK, with or without 400 mg/m(2) carboplatin depending upon bone marrow function. The endpoints were response rates (RR), progression-free survival (PFS), and overall survival (OS). RESULTS: Compared with SDC, PFS and OS were improved in HDC + DC/CIK (median PFS 10.2 vs. 3.7 months, P < 0.001; median OS 33.1 vs. 15.2 months, P < 0.001). Patients of pre-menopausal, HDC as first-line treatment after metastasis, or with visceral metastasis showed prolonged PFS and OS. SDC group also achieved the similar response as previous reports. CONCLUSION: Our study demonstrated the novel combination of HDC with DC/CIK to be an effective choice for the selected MBC population, in which choosing appropriate chemo regimens played important roles, and also specific HDC regimen plus DC/CIK immunotherapy showed the clinical benefits compared with chemotherapy alone.

[Effect of electric acupoint stimulation on shivering in cesarean section].

OBJECTIVE: To explore the efficacy of electric acupoint stimulation on shivering in cesarean section. METHODS: Eighty cases of parturients, under the America Society of Anesthesiologists (ASA) physical status II , were randomized into a transcutaneous electrical acupoint stimulation (TEAS) assisted anesthesia group (group A) and an anesthesia group (group B). Spinal-epidural anesthesia(CSEA) puncture was applied to both groups and 8 mg of 0. 75% bubivacaine was given by spinal injection, the block level was T4 T8. In group A, TEAS was applied before CSEA at paired acupoints-ipsilateral Hegu (LI 4)-Laogong (PC 8) and Sanyinjiao (SP 6)-Zusanli (ST 36) till ending the surgery. The 4 pair of bilateral acupoints were fixed with self-adhesive electrodes and connected with Han's acupoint and nerve stimulator (HANS, LH402H), the frequency was 2 Hz/ 15 Hz, the intensity was 10- 30 mA and the form was densedisperse wave within the patients' tolarance. The heart rate (HR), mean arterial pressure (MAP), oxyhemoglobin saturation (SPO) and shivering degree were recorded before anesthesia (To), 1 min after anesthesia puncture (Ti), 1 min after the delivery (Tz), during abdomen closure (T3) and at the end of surgery (T4). RESULTS: The occurrence rate of shivering was 35. 0% (14/40) in group A, which was lower to 67. 5% (27/40, P<0. 05) in group B; the degree of shivering was lighter in group A than that in group B at T2, T3 and T4 (all P<0. 01). In group A, HR was faster at T1 and T2 compared to that at To (all P<0. 05), while at T3 and T4, the HR was the same with that before anesthesia (all P>0. 05). In group B, the HR was faster at T1, T2, T3 and T4 compared to that at T0 (P<0. 05, P<0. 01). In both groups, the MAP was lower at T1, T2 (P<0.05,P<0.01) and resumed to that before anesthesia at T3 and T4 (all P>0.05); there was no statistical significance of SPO2 in both groups (all P>0.05). CONCLUSION: TEAS can reduce the occurrence rate of shivering and steady the heart rate in cesarean section.

Cigarette smoking in community-dwelling patients with schizophrenia in China.

This study examined the prevalence of cigarette smoking and its socio-demographic and clinical characteristics in Chinese schizophrenia patients. A sample of 540 community-dwelling patients (female/male: 50.4% vs. 49.6%) with schizophrenia was interviewed using standardized assessment instruments. The patients' basic socio-demographic and clinical data including smoking were collected. The prevalence of cigarette smoking was 28.5% in the whole sample, and 53.6% and 4.0% for men and women, respectively. In univariate analyses, male sex, use of first generation antipsychotics (FGAs) and alcohol consumption were significantly associated with smoking. In multiple logistic regression analysis, male sex, alcohol consumption, older age and lower level of education were independently associated with smoking. The prevalence of smoking in Chinese schizophrenia patients is considerably lower than most figures reported from Western settings. The dramatic differences between males and females underscore the influence of cultural norms on smoking.