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Objective:To study the correlation between third lumbar skeletal muscle index(LSMI) and inflammatory factors and other factors in peripheral blood in gastric cancer patients.Methods:From October 2017 to December 2019, patients with gastric cancer admitted to West China Hospital Sichuan University were included. The LSMI of patients was obtained by dividing the area of skeletal muscle at the third lumbar vertebra level by the square of the height based on preoperative abdominal imaging data. The correlation between preoperative LSMI and inflammatory factors and other factors in peripheral blood were analyzed by person correlation analysis.Results:This study included 132 patients with gastric cancer. Among them, 39 were classified as stage Ⅰ, 36 were stage Ⅱ, and 57 were stage Ⅲ, respectively. Pearson correlation analysis suggested that the LSMI of gastric cancer patients was positively correlated with peripheral red blood cell count( P<0.01), hemoglobin( P<0.01), and prealbumin( P<0.01), and negatively correlated with interleukin-6(IL-6, P=0.027) and C-reactive protein(CRP, P= 0.014). Conclusion:Our study suggested that LSMI can be used as a nutritional index in gastric cancer patients and IL-6 and CRP played an important in the occurrence and development of sarcopenia in gastric cancer patients.
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The national famous TCM doctor, Professor LUO Quan considers that the key pathogeny of chronic heart failure (CHF) is deficiency of yang qi, blood blocking and liquid stagnation, and should be treated with the method of tonifying qi and warming yang, activating blood and expelling stasis and inducing diuresis to alleviate edema. Qiangxin Prescription was created based on the above treatments, with obvious efficacy. This article conducted a preliminary analysis on the essence of medication of Qiangxin Prescription, took some example of Professor LUO Quan's experiences in using this prescription, with a purpose to be helpful to the treatment of syndrome differentiation and treatment of CHF.
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AIM:R-spondin 2 (Rspo2), one member of R-spondin family which contains four secreted proteins , plays an important role in skeletal muscle development .However, the impact of Rspo2 on vascular smooth muscle cell ( SMC) differentiation is little known . This study aims at revealing the role and mechanism of Rspo 2 on SMC differentiation from embryonic stem cells (ESCs).METHODS:A well-established model for studying SMC differentiation from ESCs were used , in which mouse embryonic stem cells ( ES-D3) were seeded on collagen IV-coated flasks and cultured in differentiation medium (DM) for 2, 4, 6 and 8 days.Smooth muscle specific markers, includingα-smooth muscle actin (α-SMA), SM22 and smooth muscle myosin heavy chain (SM-MHC), were detected to in-sure the successful model by qRT-PCR and Western blot .After 3-day pre-differentiation, ESCs were treated with recombinant Rspo 2 protein, overexpression plasmid or shRNA plasmid for 96 h, and the mRNA and protein expression of smooth muscle markers was detected.To explore the role of Rspo2 on SMC differentiation in vivo, 3-day predifferentiated ESCs (106 in 50μLα-MEM) incubated with Rspo2-overexpression plasmid were mixed with 50 μL of Matrigel ( Becton Dickinson Labware ) and then subcutaneously injected into C57BL/6J mice.After 12 days, mice were sacrificed and the implants were harvested for immunofluorescence staining , qRT-PCR and Western blot.Furthermore, electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation assay (ChIP) and lucif-erase reporter assay were performed to investigate the transcriptional activity of SMC differentiation related transcription factors , inclu-ding serum response factor (SRF), myocardin (MYO), myocyte-specific enhancer factor 2C (MEF-2C).Involvement of Rspo2 re-ceptor, leucine-rich repeat-containing, G-protein-coupled receptors (Lgr)4,5,6, and β-catenin pathway during Rspo2-induced MSC differentiation were also uncovered by overexpression or inhibition of the respective protein .RESULTS:Our results showed that Rspo 2 mRNA and protein expression was significantly and consistently increased during ESC differentiation towards SMCs .Recombinant Rs-po2 protein and enforced Rspo 2 expression in ESCs resulted in up-regulation of smooth muscle markers and transcription factors , while knockdown decreased the expression of these genes .Expectedly , Rspo2 overexpression also promotes SMC differentiation in vivo. Mechanistically , our data showed that Rspo 2 could promote SRF binding to SM22 promoter region .Evidence also revealed that one of three Rspo2 receptors, LGR5, was up-regulated while the other two , LGR4 and LGR6, was down-regulated.Silencing of LGR5 inhibi-ted Rspo2-induced SMC differentiation, whereas knockdown of LGR4 had no impact.Finally, activation or inhibition of β-catenin could promote or inhibit SMC differentiation , respectively .CONCLUSION: Our findings demonstrate for the first time that Rspo 2 plays a positive role during smooth muscle cell differentiation from embryonic stem cells .We confirmed that Rspo 2 can up-regulate smooth muscle markers at transcription level .We also revealed Rspo promote smooth muscle cell differentiation through activation of LGR 5 re-ceptor and Wnt/β-catenin pathway .
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Objective To study the release of synthetic gene expression induced by vasopressin Ⅱ (U Ⅱ ) in hypoxic pulmonary hypertension. Methods Rat model of HPH was establish. RIA was used to observe the different time points of hypoxia in plasma and the dynamic changes of U Ⅱ , ADM content in bronchoalveolar lavage fluid (BALF). The impact of the release of U Ⅱ , as well as the relation-ship among U Ⅱ , ADM and HPH were explored to reveal the role of U Ⅱ in the pathophysiology of HPH. Results Rat HPH model was successfully established. Hypoxia promoted the expression, synthesis and release of U Ⅱ in lung tissue. U Ⅱ involved in the pathogenesis of HPH. HPH took place in the development of U Ⅱand was positive correlated with ADM. Conclusion The two peptides have opposite physiological effects on blood vessel, which suggest that these two peptides play an important role in maintaining the balance between the pul-monary circulation and lung ventilation as well as the stability of pulmonary artery pressure.