[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.

[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 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.

[Effects of six naphthalenesulfonamide derivatives on LPS-induced release of tumor necrosis factor from mouse peritoneal macrophages].

The effects of six naphthalenesulfonamide derivatives were studied on the LPS-induced release of tumor necrosis factor (TNF) from mouse peritoneal macrophages primed with A23187. The calmodulin (CaM) antagonist, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) and its derivatives N-(6-aminobutyl)-5-chloro-1-naphthalenesulfonamide and N-(6-aminoethyl)-5-chloro-1-naphthalenesulfonamide (10-400 ng/ml) were found to inhibit LPS-induced TNF release in a dose-dependent manner, and the protein kinase C (PKC) activator, N-(n-heptyl)-5-chloro-1-naphthalenesulfonamide (SC-10) and its two derivatives, N-(n-quinyl)-5-chloro-1-naphthalenesulfonamide and N-(n-butyl)-5-chloro-1-naphthalenesulfonamide (1-16 micrograms/ml) were shown to increase LPS-induced TNF release at suboptimal doses in a dose-dependent manner. These results suggest that the LPS-induced release of TNF is CaM-dependent and PKC may play an important role in this process.

[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.

[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.

[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.

[Effects of protein kinase C activator and inhibitor on release of tumor necrosis factor from mouse peritoneal macrophages].

The effects of protein kinase C (PKC) activator 1-O-tetradecanoylphorbol-13-acetate (TPA) and inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) and quercetin were studied on release of tumor necrosis factor (TNF) from mouse peritoneal macrophages primed with Propionibacterium acnes (PA). The results showed that TPA (1-100 ng.ml-1) and lipopolysaccharides (LPS) (1-100 ng.ml-1) induced the release of TNF from PA-primed mouse peritoneal macrophages in dose- and time-dependent manners in vitro, and the effects of TPA and LPS were inhibited by H-7 (12.5-100 mumol.L-1) or quercetin (6.25-25 mumol.L-1) in a dose-dependent manner. After ip H-7 (50 mg.kg-1), LPS-induced release of TNF in vivo decreased significantly. These results suggest that PKC may play a critical role in release of TNF from PA-primed macrophages.

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.

Effects of cantharidin on interleukin-2 and interleukin-1 production in mice in vivo.

After cantharidin (0.75, 1.5 mg.kg-1) was given ip 3 times every other day in mice, Con A-induced spleen lymphocyte proliferation, as measured by [3H]TdR incorporation assay, was enhanced from 7,978 +/- 1,780 to 36,631 +/- 8,467 and 29,997 +/- 3,788 dpm in both doses. Interleukin-2 and interleukin-1 production were also increased from 11 +/- 4 to 52 +/- 18, 23 +/- 6 U.ml-1 and from 7,628 +/- 1,477 to 14,532 +/- 2,272, 11,515 +/- 2,862 dpm, respectively. These results suggest that cantharidin potentiates immune response through the release of interleukin-2 and interleukin-1.

[Effect of diethyldithiocarbamate on interleukin 2 production of patients with oral lichen planus and its clinical therapeutic efficacy].

Diethyldithiocarbamate (DTC), a biological augmenting agent specific for T cells, was applied to treat patients with incipient oral lichen planus (OLP) who had been refractory to traditional therapy. DTC was administered orally (5 mg.kg-1, twice a week) for at least 3 months. Interleukin 2 (IL-2) production and lymphocyte proliferation of peripheral blood mononuclear cells (PBMC) were measured before and after the treatment. The bioactivity of IL-2 was determined by the use of IL-2 dependent cell line CTLL-2 and human recombinant IL-2. The results indicated that both IL-2 production of PBMC and lymphocyte proliferation increased (P less than 0.01). Clinical symptoms were improved significantly. The effective rate in 30 patients was 86.7%. It is suggested that the mechanism involves that DTC improves the cellular immunity of the patients.

[Effects of Phytolacca acinosa polysaccharides I on cytotoxicity of macrophages and its production of tumor necrosis factor and interleukin 1].

The in vivo effects of Phytolacca acinosa polysaccharides I (PEP-I) on immunologic cytotoxicity of mouse peritoneal macrophages and its production of tumor necrosis factor (TNF) and interleukin 1 (IL-1) were studied. PEP-I 80, 160 mg/kg was given ip twice every 4 d. Both doses were found to have significant enhancing activity on macrophages cytotoxicity against S180 sarcoma cells and malignant transformed fibroblast L929 cells. Peritoneal activated macrophages were incubated with LPS for 2 and 24 h to induce TNF and IL-1, respectively. The TNF and IL-1 activities were tested from cytotoxicity against L929 cells in an absorbance assay of enzymatic reaction and proliferation of thymocytes co-stimulated assay separately. The optimal time for TNF production was found on d 8. Significant increases in TNF and IL-1 were observed. In comparison of the effect of PEP-I on TNF with that of known priming agent BCG, there was no difference between these two, but PEP-I had a high effect on IL-1. These results suggest that cytotoxicity of macrophages primed by PEP-I is closely related to its TNF and IL-1 production.