[Outcome comparison between LSA complete reconstruction and partial coverage with endovascular technique for patients with Stanford type B aortic dissection].

Objectives: To compare the short-term outcomes of branched stentgrafts for left subclavian artery (LSA) revascularization or partial LSA coverage without reconstruction in the treatment of type B aortic dissection with proximal tear close to LSA. Methods: A total of 125 type B aortic dissection patients were treated with thoracic endovascular aortic repair (TEVAR) in Xinqiao Hospital of the Army Medical University from January 2019 to March 2021. Their medical records were reviewed and the outcomes were followed up. According to the different treatment methodologies, the patients were divided into complete LSA coverage with reconstruction group (n=25) and partial LSA coverage without reconstruction group (n=100). The data of baseline characteristics, clinical outcomes, and incidence of postoperative in-hospital adverse events were collected and compared between the two groups. The adverse events during one-year follow-up were also compared between the two groups. Kaplan-Meier analysis and log-rank test were used to compare the cumulative survival rates between groups. Results: Compared with partial LSA coverage group, distance of proximal tear to LSA((8.69±2.32)mm vs. (13.77±1.71) mm) was shorter, in-hospital expenses[175 400(166 000-189 900) yuan vs. 143 700 (138 100-151 800) yuan] was higher, average length of stent [200.00 mm vs. 150.00 (150.00-150.00) mm] and operation time [155.00 (140.00-170.00) min vs. 95.00 (80.00-100.00) min] were longer, and volumes of contrast agent [300.00 (200.00-300.00) ml vs. 200.00 (200.00-300.00) ml] (P<0.05) were higher for patients in the complete LSA coverage with reconstruction group. The incidence of post-operative fever was significantly higher in complete LSA coverage with revascularization group than that in partial LSA partial coverage with reconstruction group (56% vs. 25%, P=0.003). There was no significant difference in the incidences of all-cause death, stroke, endoleak, paraplegia, and LSA branch vessel occlusion between the two groups during follow-up. Kaplan-Meier analysis showed that there was no significant difference in the cumulative survival rates between the two groups (log-rank test: P=0.572 5). Conclusion: The TEVAR with complete LSA revascularization or partial LSA coverage without reconstruction for type B aortic dissection close to LSA are safe and effective with high success rates. There is no significant difference between these two techniques in short-term outcomes.

[Risk factors of perivalvular leakage after transcatheter aortic valve replacement with Venus-A valve].

Objective: To investigate the risk factors of moderate or severe perivalvular leakage (PVL) after transcatheter aortic valve replacement (TAVR) with Veneus-A valve. Methods: This study was a single-center case-control study. The clinical data of patients with severe aortic stenosis, who underwent TAVR in the Department of Cardiology of Second Affiliated Hospital of Army Medical University from October 2017 to January 2021, were analyzed. According to the circumferential extent of prosthetic valve paravalvular regurgitation measured by transthoracic echocardiography before discharge (patients who died in hospital were referred to transesophageal echocardiography results after valve implanted), the patients were divided into moderate or severe PVL group and mild or non-PVL group. The clinical features, CT scan and analysis results of aortic root were compared between the two groups. Multivariate logistic regression analysis was used to identify the independent risk factors of postoperative moderate or severe PVL, and receiver operating characteristic (ROC) curve was used to explore the predictive value of related factors. Results: Eighty-two patients (mean age: (70.9±6.5) years, 46 males) were included in the analysis, there were 16 patients in the moderate or severe PVL group and 66 patients in the mild or non-PVL group. The proportion of male gender, depth of valve implantation, size of valve annulus and left ventricular outflow tract (LVOT), and coverage index of LVOT were significantly higher in moderate or severe PVL group than those in mild or non-PVL group (Pall<0.05). As there was a strong collinearity among the valve annular short diameter, LVOT short diameter and LVOT coverage index (partial correlation coefficient R 0.251-0.779, P<0.05), these parameters were not entered in regression model. Multivariate logistic regression analysis showed that valve implantation depth(OR=1.239,95%CI 1.036-1.442,P=0.023), aortic angulation(OR=1.128, 95%CI 1.044-1.312,P=0.038)and LVOT tract coverage index (OR=1.123, 95%CI1.003-1.315, P=0.032) were independent risk factors for moderate or severe PVL after TAVR. The ROC curve showed that the valve implantation depth could predict the occurrence of moderate or severe PVL after TAVR (area under ROC curve (AUC)=0.697, 95%CI 0.554-0.851, P=0.039). Conclusion: Among patients with severe aortic stenosis who undergo TAVR with Venus-A valve, the implantation depth, aortic angulation and LVOT coverage index are independent risk factors of moderate/severe PVL after TAVR, among which valve implantation depth could be used to predict the occurrence of moderate/severe PVL after TAVR.

A 3-year experience of a simple, novel technique for accurate ostial/non-ostial coronary stenting: The buddy balloon anchor stent technique.

OBJECTIVE: To evaluate the safety and efficacy of a new technique for accurate ostial/non-ostial coronary stenting in percutaneous coronary intervention (PCI). BACKGROUND: Accurate stent localization is a key factor impacting the postoperative success of patients undergoing PCI. However, the accurate localization of some lesions, especially ostial lesions, is very difficult to achieve, because they are often complicated by bobbing or to-and-fro movement of the stent during cardiac contractions. METHODS: We report a novel technique of precise ostial/non-ostial stenting based on the buddy balloon anchor stent (BBAS) technique. Between May 2014 and July 2017, 47 patients with significant ostial/non-ostial coronary stenosis that required accurate stenting were included in this study. Of them, 23 patients were treated using the conventional method and the remaining 24 patients were treated using (BBAS) technique. Evaluation was then performed using intravascular ultrasound (IVUS) in the procedural, or coronary computed tomography angiography (CCTA) in the follow up. RESULTS: Using the BBAS technique, the procedural success was achieved in all 24 (100%) cases. IVUS was performed in seven patients (29.17%) and no procedural complications occurred. All six failed cases that occurred among patients with right coronary artery and left anterior descending artery ostial stenosis treated using the conventional method, the lesions were subsequently successfully re-stented using the BBAS technique. After a follow-up of 3-36 months, CCTA was performed in 11 patients (45.83%), all the stents were in the accurate position. There were no major cardiovascular events of death, myocardial infarction, or target lesion revascularization. CONCLUSION: BBAS is a simple, highly successful and safe technique for accurate stenting of difficult ostial/nonostial coronary stenosis lesions.

LncRNA MEG3 promotes the sensitivity of vincristine by inhibiting autophagy in lung cancer chemotherapy.

OBJECTIVE: Lung cancer is one of the most common malignancies worldwide, the morbidity and mortality of which have been on rising in recent years. Moreover, lncRNAs have been implicated in the development of various cancers, as well as cancer treatment and prognosis. In this study, long non-coding RNA (lncRNA) MEG3, an identified tumor suppressor, was explored for its role in the chemotherapy of lung cancer. MATERIALS AND METHODS: All cases were divided into (I+II) group and (III+IV) group according to different stages of tumor node metastasis (TNM), and were divided into sensitive group and insensitive group according to chemotherapy sensitivity. A549 and H292 cells were selected as the resistant cell and non-resistant lung cancer cells. Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was performed to detect the expression of MEG3. After transfection with overexpression plasmid pcDNA-MEG3 or/and different concentrations of vincristine, cell viability and proliferation were measured by cell counting kit-8 (CCK-8) assay and plate cloning assay, respectively. Western blotting was used to analyze the expressions of autophagy-related proteins. RESULTS: In vivo, lncRNA MEG3 was significantly lower in III+IV group and insensitive group than that in I+II group and sensitive group. In vitro, MEG3 expression in resistant cells was significantly lower than that in non-resistant cells. Overexpression of MEG3 significant inhibited the viability and proliferation of both resistant and non-resistant lung cancer cells. Western blot results showed that autophagy level was higher in resistant cells than that in non-resistant cells, while overexpression of MEG3 significantly reduced the expression of autophagy-related proteins. CCK-8 results also indicated that the cell viability was negatively correlated with the dose of vincristine, while the viability of drug-resistant cells was higher than that of non-drug resistant cells after the treatment of vincristine. The vitality of both cells decreased in a concentration-dependent manner after combined treatment with vincristine and MEG3. CONCLUSIONS: Our data indicated that lncRNA MEG3 showed a low expression in chemotherapy-sensitive lung cancer tissues, and overexpression of lncRNA MEG3 attenuated autophagy level, thus increasing the sensitivity of vincristine in chemotherapy of lung cancer.

Matrine inhibits production and actions of fibrogenic cytokines released by mouse peritoneal macrophages.

AIM: To study the effects of matrine (Mat) on production and actions of fibrogenic cytokines from mouse peritoneal macrophages. METHODS: Mouse peritoneal macrophages were primed with calcimycin 1 micromol/L for 8 h then elicited by lipopolysaccharides (LPS) 100 microg/L for 6 h to induce fibrogenic cytokines. Proliferative and collagen stimulating activity in the macrophage culture supernatants was determined by crystal violet staining assay and [3H]-proline incorporation assay using rat hepatic stellate HSC-T6 cell or mouse fibroblast NIH3T3 cell. Transforming growth factor beta (TGFbeta) activity was measured by [3H]-thymidine incorporation assay using Mv-1-Lu mink lung epithelial cell. RESULTS: Mat (0.5-2 mmol/L) was shown to significantly inhibit LPS-induced collagen stimulating activities and TGFbeta production (P < 0.01) whereas did not inhibit proliferative activities induced by macrophages. Macrophage conditioned medium (MCM)-driven proliferation and collagen synthesis of HSC-T6 cells as well as NIH3T3 cells were attenuated by Mat (0.5-2 mmol/L) in a concentration-dependent manner. CONCLUSION: Antifibrotic effects of Mat on hepatic stellate cells may be related to reduction of fibrogenic cytokine production and blockade of their actions.

Effect of six flavonoids on proliferation of hepatic stellate cells in vitro.

AIM: To study the effects of six flavonoids (fisetin, quercetin, apigenin, phloretin, hesperetin, and chalcone) on proliferation of hepatic stellate cell (HSC-T6 cells). METHODS: Cell proliferation was measured by crystal violet staining assay. RESULTS: Fisetin, quercetin, apigenin, phloretin, hesperetin, chalcone (6.25-50 mumol.L-1) inhibited the proliferation of HSC-T6 cells stimulated by serum, macrophage conditioned medium (MCM) and platelet-derived growth factor (PDGF) in a concentration-dependent manner. In the MCM-stimulated proliferation experiment, their IC50 were 21.48, 18.52, 19.75, 22.32, 30.32, and 30.85 mumol.L-1, respectively. In the PDGF-stimulated proliferation experiment, their IC50 were 9.47, 9.48, 9.25, 12.25, 25.22, and 30.40 mumol.L-1, respectively. CONCLUSION: The six flavonoids inhibited the proliferation of hepatic stellate cells.

Ro 31-8220 inhibits release of interleukin-1 and interleukin-6 from mouse peritoneal macrophages induced by fibrin fibrinogen degradation products.

AIM: To study the effect of fibrin fibrinogen degradation products (FFDP) on release of interleukin-1 (IL-1) and interleukin-6 (IL-6) from mouse peritoneal macrophages, and the effect of a new selectively potent protein kinase C inhibitor Ro 31-8220 (Ro). METHODS: IL-1 and IL-6 activities were measured by thymocyte proliferation assay and B9 cell proliferation methyl thiazolyl tetrazolium (MTT) colorimetric method, respectively. RESULTS: Ro 0.01-1 mumol.L-1 obviously inhibited FFDP-induced release of IL-1 and IL-6 from mouse peritoneal macrophages. CONCLUSION: Ro exerted inhibitory effects on FFDP-induced release of IL-1 and IL-6 in vitro.

Effects of Ro 31-8220 on lipopolysaccharides-induced hepatotoxicity and release of tumor necrosis factor from rat Kupffer cells.

AIM: To investigate protein kinase C (PKC) functions on lipopolysaccharide (LPS)-induced hepatotoxicity, a new potent PKC inhibitor Ro 31-8220 (Ro) was used to detect its effect on LPS-induced hepatotoxicity in rat hepatocytes and tumor necrosis factor (TNF) release from rat Kupffer cells (KC). METHODS: Hepatocytes (containing KC) were incubated with LPS (10 mg.L-1) and Ro (0.1-10 mumol.L-1) for 24 h, alanine aminotransferase (AlaA) leakage in the culture as indication of hepatotoxicity. The TNF activity in the supernatant of rat KC culture with LPS in the presence of Ro (0.1-10 mumol.L-1) was monitored by the L929 target cell lytic assay. RESULTS: Ro (0.1-10 mumol.L-1) reduced AlaA leakage in the hepatocyte culture. Ro inhibited dose-dependently the LPS-induced TNF production from rat KC. CONCLUSION: PKC inhibitor Ro protects the hepatocytes from LPS-induced cytotoxicity and inhibits the LPS-induced TNF production from rat KC.

[Inhibitory effect of matrine on lipopolysacchride-induced tumor necrosis factor and interleukin-6 production from rat Kupffer cells].

The effect of matrine on the lipopolysacchride (LPS)-induced tumor necrosis factor and interleukin-6 production from rat Kupffer cell was investigated. Results showed that matrine 125, 250 and 500 mg.L-1 suppressed TNF and IL-6 production from Cal-primed Kupffer cells in the presence of lipopolysacchrides (LPS, 100 micrograms.L-1) in a concentration-dependent manner. Treatment with matrine 50 and 100 mg.kg-1 before LPS injection(3.5 mg.kg-1) markedly decreased mouse serum TNF and IL-6. The results suggest that matrine may have protective effect on LPS-induced liver injury.

Effects of Ro 31-8220 on smooth muscle cell proliferation induced by fibrinogen degradation products.

AIM: To study the mitogenic activity of fibrin fibrinogen degradation products (FFDP) and the effect of a new selectively potent protein kinase C (PKC) inhibitor Ro 31-8220 (Ro). METHODS: Rat aortic smooth muscle cells (SMC) proliferation in culture was measured by crystal violet staining assay. RESULTS: FFDP stimulated the proliferation of SMC during the experimental period of 72 h, Ro 0.01-1 mumol.L-1 inhibited FFDP-induced cell proliferation in a concentration-dependent manner. CONCLUSION: Ro exerted inhibitory effect on cell proliferation induced by FFDP.

Effect of matrine on lipopolysaccharides/D-galactosamine-induced hepatitis and tumor necrosis factor release from macrophages in vitro.

AIM: To study the effects of matrine (Mat) on lipopolysaccharides (LPS)-induced fatal hepatitis in D-galactosamine (D-GalN)-sensitized mice and tumor necrosis factor (TNF) release from peritoneal macrophages (PMO). METHODS: Mice were pretreated with Mat (10, 50 mg.kg-1, i.p., bid x 3 d), and then injected i.p. LPS + D-GalN. Liver injury was assessed by quantifying plasma activity of alanine aminotransferase (ALT) and histopathological examination. The TNF activities in the supernatants of mouse PMO stimulated with LPS in the presence of Mat (32.5-500 mg.L-1) were monitored by the L929 target cells lytic assay. RESULTS: Mat pretreatment markedly diminished hepatic injury induced by LPS in combination with D-GalN. Mat inhibited LPS-induced TNF release from mouse PMO in vitro in a concentration-dependent manner. CONCLUSION: Mat protected the D-GalN-treated mice from the development of fatal hepatitis induced by LPS, and inhibited the LPS-induced TNF release from mouse PMO.

Effects of matrine on mouse splenocyte proliferation and release of interleukin-1 and -6 from peritoneal macrophages in vitro.

AIM: To investigate the mechanisms of anti-inflammatory effect of matrine (Mat), its effects on mouse splenocyte proliferation, and release of interleukin-1 (IL-1) and interleukin-6 (IL-6) from mouse peritoneal macrophages. METHODS: Splenocyte proliferation was assayed by [3H] TdR incorporation. IL-1 and IL-6 activities were measured by thymocyte proliferation assay and B9 cell proliferation MTT colorimetric method, respectively. RESULTS: Mat (125-500 mg.L-1) obviously inhibited concanavalin A (Con A, 5 mg.L-1)- and lipopolysaccarides (LPS, 10 mg.L-1)-induced splenocyte proliferation and LPS-induced release of IL-1 and IL-6 from mouse peritoneal macrophages. CONCLUSION: Mat inhibited splenocyte proliferation and release of IL-1 and IL-6 in vitro.

Inhibitory effect of quercetin on tumor necrosis factor and interleukin-1 beta pro-osteoclastic activities.

AIM: To study the effects of quercetin on tumor necrosis factor (TNF) and interleukin-1 beta (IL-1 beta) pro-osteoclastic activities. METHODS: [3H] TdR uptake by osteoblasts was used to measure cell proliferation, microspectrophotometer for cellular AIP activity using p-nitrophenyl phosphate as enzyme substrate, and radioimmunoassay for prostaglandin E2. RESULTS: Quercetin 5-40 mumol.L-1 reduced the inhibition of cell proliferation and AIP activity induced by TNF or IL-1 beta in a concentration-dependent manner. PGE2 production stimulated by either cytokines was also reduced by quercetin at 20 and 40 mumol.L-1. CONCLUSION: quercetin exerted a marked inhibitory effect on TNF and IL-1 activities, related to their pro-osteoclastic function.

[Effect of matrine on mouse hepatitis and tumor necrosis factor production induced by Propionibacterium acnes/lipopolysaccharides].

The effect of matrine (Mat) on lipopolysaccharides (LPS)-induced fatal hepatitis and tumor necrosis factor (TNF) production in Propionibacterium acnes (PA)-primed mice were studied. Mice were injected i.p. LPS (10 micrograms/mouse) 7 d after i.p. PA (0.5 ml/mouse) to induce fatal hepatitis. After i.p. LPS, serum TNF activity rose to 1657 +/- 406 kU.L-1 at 1.5 h and ALT activity increased up to 1,496 +/- 890 U.L-1 at 5 h. Six of 8 mice died within 5 h and the massive hemorrhagic necrosis of the liver was observed in all mice. Administration of Mat (10, 50 mg.kg-1, i.p., bid x 3 d) before the LPS injection markedly reduced the elevation of serum TNF and ALT activity in a dose-dependent manner, and diminished the mortality induced by LPS. Liver congestion and necrosis induced by LPS in PA-primed mice were ameliorated markedly by Mat pretreatment. Mat (62.5-250 mg.L-1) inhibited LPS-induced TNF release from PA-primed mouse peritoneal macrophage in vitro in a concentration-dependent manner. These results seggest that Mat protected PA-primed mice from the development of fatal hepatitis induced by LPS due to inhibition of TNF production.

[Inhibitory effects of protein kinase C inhibitors on tumor necrosis factor induced bovine pulmonary artery endothelial cell injuries].

The effects of protein kinase C(PKC) inhibitors 1-(5-isoquino-linylsulfonyl)-2-methylpeperazine (H-7) and quercetin on tumor necrosis factor (TNF) were studied in cultured bovine pulmonary artery endothelial cells (BPAEC) in vitro. Incubation of BPAEC with TNF caused a significant increase in percent lactate dehydrogenase (LDH) release, stimulation of EC-dependent neutrophils (PMN) adhesion to BPAEC and inhibition of BPAEC DNA synthesis and proliferation. All these were restored by both H-7 and quercetin. The IC50 of H-7 and quercetin was 9.7 and 10.8 mumol.L-1 for the inhibition of LDH% release; 19.5 and 16.7 mumol.L-1 for the inhibition of TNF-induced PMN-EC adhesion; 7.0 and 6.1 mumol.L-1 for TNF-induced inhibition of DNA synthesis and 8.7 and 11.36 mumol.L-1 for proliferation. These results suggest that PKC inhibitors H-7 and quercetin protect BPAEC from TNF induced injuries and PKC play an important role in EC activation by TNF.

[Effect of silymarin on mouse liver damage, production and activity of tumor necrosis factor].

Tumor necrosis factor (TNF) has been well-characterized as a prominent mediator in the development of liver injury. Effects of silymarin (SB) on mouse liver damage, TNF production and activity were studied. Pretreatment with SB (25-50 mg.kg-1, i.p., bid x 3 d) before the lipopolysaccharides (LPS) injection markedly alleviated liver injury and diminished LPS-induced TNF production in Propionibacterium acnes (PA)-primed mice. SB (12.5-50 micrograms.ml-1) significantly inhibited LPS-induced TNF release from mouse peritoneal macrophage in a concentration-dependent manner. SB(12.5-100 micrograms.ml-1) was also shown to markedly reduce TNF cytotoxicity on human hepatic cell line GSG-7701 and mouse fibroblastic cell line L929 cells concentration-dependently. These results suggest that inhibition of TNF production and its actions may be involved in the mechanism of protective action of SB on liver damage.

[Effects of inhibitor of protein kinase C on brain edema formation evoked by experimental cerebral ischemia in gerbils and rats].

Recent studies have suggested that protein kinase C (PKC) may be involved in the formation of brain edema. In this paper, the effects of two kinds of PKC inhibitors, H-7 and matrine, were examined on the brain edema formation in experimental models. The results showed that pretreatment with H-7 6.25 and 12.5 mg.kg-1 prevented the accumulation of water and certain electrolytes in the unilateral hemisphere of the brain evoked by ligation of a single common carotid artery in Mongolian gerbil; pretreatment with matrine 25 and 50 mg.kg-1 reduced the extent of cerebral edema formation evoked by ligation of a single common carotid artery in gerbil and by middle cerebral artery occlusion in Sprague-Dawley rats. These results present new evidence for the involvement of PKC in the formation of brain edema.

Protein kinase C inhibitor H-7 blocks effects of tumor necrosis factor on bone cells.

AIM: To study the effects of tumor necrosis factor (TNF) on the neonatal mouse osteoblast-enriched calvarial cells and effects of protein kinase C (PK C) inhibitor, 1-(5-isoquinolinesulfonyl)-2 -methylpiperazine (H-7) on the TNF actions. METHODS: [3H]TdR uptake by the osteoblasts was used to measure cell proliferation. Cellular alkaline phosphatase (AIP) and tartrate resistant acid phosphatase (trAcP) activities were determined spectrophotometrically. RESULTS: TNF (1-100 kU . L-1) inhibited both proliferation and expression of AIP activity, but stimulated trAcP activity. These TNF-induced actions were blocked by simultaneous addition of H-7 (5-20 mumol . L-1). CONCLUSION: TNF has potent effects on the osteoblasts, and the blockade of TNF actions by H-7 suggests that TNF exert its effects through PK C.

[The infective state of cytomegalovirus in the infective disease of respiratory tract].

By means of molecular biology and serology, we detect the infective state of cytomegalovirus in 58 patients with infective disease of respiratory tract. The result shows that the infective state of cytomegalovirus exists in the RTID, but there is no virusemia in patients. The immune response of past-infection of cytomegalovirus in the patients of RTID is rather remarkable.

Antitumor activity and tumor necrosis factor production of Phytolacca acinosa polysaccharides I in mice.

The antitumor activities of Phytolacca acinosa polysaccharides I (PAP-I) and its effects on the induction of tumor necrosis factor (TNF) and immunological cytotoxicity of peritoneal macrophages were studied. PAP-I was given ip 5-20 mg.kg-1.d-1 x 7 d to ICR mice as priming agent with subsequent lipopolysaccharides (10 micrograms/mouse) iv for TNF production. TNF activity was measured by crystal violet staining assay using L929 cells. PAP-I showed priming activity for TNF production with hepto-splenic hyperplasia in a dose-dependent manner. The peritoneal macrophages treated with PAP-I 10 and 20 mg.kg-1 showed 67 and 74%, respectively, cytotoxicity (the control 34% cytotoxicity) against Meth A cells at effector:target = 40:1. PAP-I 10 and 20 mg.kg-1 prolonged the survival time of mice bearing ascites Meth A tumor from 21 +/- 4 to 32 +/- 10 and 38 +/- 8 d and inhibited the solid Meth A tumor growth with inhibition rate of 28.5 and 55.7%, respectively. These results suggested that the antitumor activities of PAP-I were based on the activation of macrophages and induction of TNF.