BACKGROUND AND OBJECTIVES:This study investigates the diagnostic value of YTHDF3 for abdominal aortic aneurysm (AAA) and further determines its regulatory mechanism in angiotensin II (Ang II)-induced vascular smooth muscle cells (VSMCs). METHODS:YTHDF3 expression in abdominal aortic tissues and adjacent non-aneurysm aortic tissues of AAA patients was tested via reverse transcription-quantitative polymerase chain reaction and Western blot. The diagnostic value of YTHDF3 protein expression for AAA was evaluated by receiver operating characteristic curve. VSMCs were stimulated by Ang II in vitro and transfected with sh-YTHDF3. Cell proliferation was assessed via 5-ethynyl-2'-deoxyuridine and cell counting kit-8 assays. Apoptosis was measured via caspase-3/9 activity and TUNEL assays. Tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were detected via enzyme-linked immunosorbent assay. The regulatory mechanism of YTHDF3/sirtuin 2 (SIRT2)/FOXO1 was determined via methylated RNA immunoprecipitation-qPCR, RNA immunoprecipitation, actinomycin D treatment, cycloheximide, and co-immunoprecipitation. RESULTS:YTHDF3 is highly expressed in AAA tissues and positively correlated with AAA diameter, TNF-α, IL-1-β, and IL-6 levels. YTHDF3 has certain diagnostic value for AAA. Knockdown of YTHDF3 alleviates the inhibitory effect of Ang II on VSMC proliferation, as well as its promoting effect on apoptosis and inflammation. Mechanistically, N6 methyladenosine reader YTHDF3 directly binds to SIRT2 mRNA and maintains its stability, facilitates the deacetylation of FOXO1, and reduces the stability of FOXO1 protein. CONCLUSIONS:YTHDF3 is highly expressed in AAA tissues and Ang II-induced VSMCs. YTHDF3 hinders the proliferation of Ang II-induced VSMCs while promoting apoptosis and inflammation. YTHDF3 deficiency exerts protective effect by interfering with SIRT2/FOXO1 axis.

Objective: Abdominal aortic aneurysms (AAA) involving branches of the visceral arteries mainly refer to AAA with flat renal artery (neck length ≤5 mm) or beyond the renal artery, and the branch of the visceral arteries needs to be reconstructed during treatment. Endoluminal repair (EVR) surgery refers to the isolation of AAA with less surgical trauma through vascular puncture, guidewire, catheter, stent and double suturer technology. However, postoperative endoleak is a complication specific to open surgery. This study aimed to analyze the efficacy of EVR for AAA involving visceral vessels (AAA-Vs) and the factors influencing the occurrence of postoperative endoleak. Methods: A total of 106 patients with AAA-Vs in our hospital during the period of January 2018 to January 2022 were distinguished as the observation group (received EVR, n = 48) and the control group (received laparotomy, n = 58). The operation time, intraoperative bleeding, intraoperative blood transfusion, postoperative intensive care unit (ICU) observation time, postoperative food-taking time, first time out of bed, hospital stay, complications and the one-year mortality of two groups were compared. According to the occurrence of postoperative endoleak, the patients underwent endoluminal repair surgery were graded as non-endoleak group (n = 39) and endoleak group (n = 9). The clinical data, including aneurysm anatomical conditions (proximal neck length, neck diameter, proximal neck angle), tumor shape (normal, calcification, mural thrombus), and internal iliac artery embolism of two groups were compared. Logistic regression analysis was employed to analyze the risk factors of endoleak after EVR of AAA. Results: The operation time, intraoperative blood loss, intraoperative blood transfusion, postoperative ICU observation time, postoperative food-taking time, first time out of bed and hospitalization days were sharply lower in the observation group than the control group (P < 0.001). There existed no significant difference in the proportion of pulmonary complications, cardiac complications and electrolyte disorders between two groups (P > 0.05). The observation group had much lower incidence of incision infection complications than the control group (P < 0.05). The one-year mortality rate in the observation group was 10.42 %, markedly lower than 25.86 % in the control group (P < 0.05). The incidence of endoleak in the observation group was 18.75 %, while no internal endoleak occurred in the control group (P < 0.05). The proportion of male patients, smoking history, internal iliac artery embolism, and the level of tumor neck length and proximal tumor neck angle in the endoleak group were memorably higher in comparison with the non-endoleak group (P < 0.05). Logistic regression analysis revealed that the length of the neck and the angle of the proximal neck were independent risk factors for postoperative endoleak of AAA (P < 0.05). In conclusion: EVR was effective for AAA-Vs with the advantages of small trauma, rapid recovery, low complication rate and high safety. The diameter of the aneurysm neck and the angle of the proximal aneurysm neck were the risk factors for the occurrence of endoleak after EVR. It was necessary to fully evaluate the aneurysm before operation to help reduce the incidence of endoleak.

Objective To compare the changes of volume and circumference of lymphedema before and after complete decongestive treatment(CDT)versus CDT+lymphaticovenular anastomosis(LVA)in patients with secondary lymphedema,and to investigate the efficacy of LVA on lymphedema.Methods Twenty-four patients with lower limb secondary lymphedema were diagnosed and treated in Henan Provincial People's Hospital from January to December 2021,among whom 11 patients received CDT(CDT group)and 13 patients received CDT+LVA(CDT+LVA group).The body mass index,tumor diagnosis time,lymphedema time,tumor treatment method,and affected limb condition were recorded.Before treatment and 1,3 and 6 months after treatment,the volume(△C)and the circumference of lymphedema(△C)were recorded and compared.Results There were no significant differences in the body mass index,tumor diagnosis time,lymphedema time,tumor treatment and affected limb between two groups(P＞0.05).Before treatment,there were no significant differences in the △V[(4 462±1 142)mL vs.(4 582±1 031)mL],△C(ankle)[(92±34)mm vs.(90±33)mm],△C(knee)[(98±39)mm vs.(96±38)mm]and △C(above knee)[(84±33)mm vs.(86±24)mm]between CDT+LVA group and CDT group(P＞0.05).In 1,3 and 6 months after treatment,△V[(2 438±597),(2 129±472),(1 765±422)mL],△C(ankle)[(54±19),(41±11),(36±8)mm],△C(knee)[(60±19),(49±15),(44±12)mm],and △C(above knee)[(68±19),(58±9),(51±10)mm]in CDT+LVA group were smaller than those in CDT group[1 month after treatment:(3 269±982)mL,(70±21)mm,(78±27)mm,(76±21)mm;3 months after treatment:(2 877±527)mL,(58±16)mm,(60±17)mm,(66±12)mm;6 months after treatment:(2 559±507)mL,(44±13)mm,(49±15)mm,(60±15)mm](P＜0.05).The △V,△C(ankle),△C(knee)and △C(above knee)in both groups decreased sequentially before treatment and in 1,3 and 6 months after treatment(P＜0.05).Conclusions Both CDT and CDT±LVA can effectively reduce the degree of limb swelling in patients with secondary lymphedema,and achieve good short-term efficacies.CDT±LVA has a better therapeutic efficacy.

造成门静脉血流梗阻的常见原因包括门静脉血栓形成(portal vein thrombosis,PVT)、腹部肿瘤侵犯或压迫门静脉,临床上以PVT最为常见[1].PVT的发病因素包括血管壁损伤、血流瘀滞和血液高凝状态,其发生、发展是一个多因素参与的过程,涉及局部因素和全身血栓前状态的协同作用[1],诊治具有一定的复杂性,若未及时诊治,可导致肠系膜缺血、门静脉海绵样变性(cavernous transformation of portal vein,CTPV)和门静脉高压症等.PVT合并非肝硬化性疾病与PVT合并肝硬化性疾病患者的临床表现不同.急性PVT经治疗后,若门静脉未能完全再通,将出现侧支循环代偿,当代偿不足时,可能出现消化道出血、腹腔积液等临床表现[2].临床上对于此类患者仅治疗消化道出血和腹腔积液,将病因误诊为肝硬化或漏诊骨髓增殖性肿瘤(myeloproliferative neoplasm,MPN)的情况时有发生.有研究显示,PVT合并肝硬化性疾病常见的潜在相关危险因素依次是MPN、凝血酶原基因G20210A突变和抗磷脂综合征[3-4].因而,有相当一部分急性或慢性门静脉高压症患者的疾病本质是MPN.

Objective:To study the treatment outcomes of transjugular intrahepatic portal shunt (TIPS) on refractory hepatic sinus obstruction syndrome (HSOS) caused by Gynura segetum.Methods:The clinical data of 15 patients with refractory HSOS caused by Gynura segetum treated at the Department of Vascular Surgery, Henan Provincial People's Hospital from January 2017 to April 2021 were retrospectively analyzed. There were 7 males and 8 females, with ages ranging from 30 to 85 years, mean ± s. d. (61.2±14.1) years. Albumin, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, glutamyl transferase, and portal vein pressure were compared before and after TIPS. The liver function and renal function of these patients were followed up.Results:When compared with pre-operation, the albumin, alanine aminotransferase, aspartate aminotransferase and other indexes were significantly improved after TIPS (all P<0.05). The portal vein pressure of 15 patients significantly decreased from the preoperative volume of (41.7±3.5) cmH 2O (1 cmH 2O=0.098 kPa) to (28.3±4.4) cmH 2O ( t=10.41, P<0.001). The preoperative liver function was Child-Pugh grade A in 1 patient, grade B in 8 patients, grade C in 6 patients. The postoperative Child-Pugh grading was grade A in 14 patients and grade B in 1 patient. Ascites, gastrointestinal bleeding, abdominal pain, abdominal distention and spontaneous peritonitis all disappeared in these 15 patients. Postoperative hepatic encephalopathy developed in 2 patients and hepatic myelopathy in 1 patient. Conclusion:TIPS for treatment of HSOS caused by Gynura segetum resulted in a rapid recovery of liver function, rapid symptomatic relief, with a low incidence of hepatic encephalopathy/hepatic myelopathy.

Oxidized low-density lipoprotein (ox-LDL) stimulation impairs the oxidation-reduction equilibrium in vascular endothelial cells (VECs) and contributes to atherosclerosis (AS). This study probed the mechanisms of extracellular vesicle (EV)-mediated transfer of lncRNA CLDN10 antisense RNA 1 (CLDN10-AS1) in ox-LDL-induced VEC injury. Initially, VEC injury models were established by treating human umbilical vein endothelial cells (HUVECs) with ox-LDL. EVs were isolated from HUVECs (HUVECs-EVs) and identified. CLDN10-AS1, microRNA (miR)-186, and Yin Yang 1 (YY1) expressions in ox-LDL-treated HUVECs and EVs derived from these cells (ox-EVs) were measured. HUVECs were incubated with EVs, after which the cell viability, apoptosis, and concentrations of proinflammatory cytokines and oxidative stress markers were measured. We discovered that CLDN10-AS1 and YY1 were upregulated in ox-LDL-treated HUVECs, whereas miR-186 was downregulated. ox-EVs treatment elevated CLDN10-AS1 expression in HUVECs and ox-EVs overexpressing CLDN10-AS1 promoted VEC injury. Besides, CLDN10-AS1 is competitively bound to miR-186 and promoted YY1 expression. Rescue experiments revealed that miR-186 overexpression or YY1 suppression partially reversed the roles of ox-EVs overexpressing CLDN10-AS1 in ox-LDL-induced VEC injury. Lastly, clinical serum samples were collected for verification. Overall, CLDN10-AS1 carried by HUVECs-EVs into HUVECs competitively bound to miR-186 to elevate YY1 expression, thereby aggravating ox-LDL-induced VEC injury.

Isoflurane has demonstrated to exert protective impacts against ischemia/reperfusion (I/R) injury in some organs. This research explored the role of emulsified isoflurane (EI) in myocardial I/R injury through the interaction with microRNA-21 (miR-21). The myocardial I/R injury mouse models established by coronary artery ligation were respectively treated with EI, miR-21 mimic/inhibitor or silenced secreted phosphoprotein 1 (SPP1) plasmids. Then, the pathology, fibrosis and cardiomyocyte apoptosis in mouse myocardial tissues were observed. Furthermore, the expression levels of miR-21, SPP1, oxidative stress indices, inflammatory factors and apoptotic proteins in mouse myocardial tissues were determined. The targeting relation between miR-21 and SPP1 was confirmed. MiR-21 was poorly expressed and SPP1 was highly expressed in myocardial I/R injury mice. EI treatment, elevated miR-21, or silenced SPP1 improved cardiac function and suppressed the oxidative stress, myocardial fibrosis, inflammatory reaction and cardiomyocyte apoptosis in myocardial I/R injury mice, thereby reliving the myocardial I/R injury. These therapeutic effects of EI were repressed by miR-21 inhibition. Additionally, SPP1 was targeted by miR-21. Results in our research indicated that miR-21 mediated the therapeutic effect of EI on myocardial I/R injury in mice by targeting SPP1. This study may provide a novel treatment strategy for myocardial I/R injury.

BACKGROUND:Thoracic aortic aneurysm (TAA) is a serious disease usually happening in elder people and with high death rate. Accumulating studies have reported that long non-coding RNAs (lncRNAs) are implicated in the progression of various human diseases, including TAA.AIM:In our study, we intended to explore the function of elastin (Eln) and its upstream mechanism in TAA.METHODS:RT-qPCR determined gene expressions and western blot tested changes in protein levels. Ang Ⅱ treatment was implemented to induce cell apoptosis. Flow cytometry analysis, TUNEL assay and JC-1 assay were exploited to measure cell apoptosis. Meanwhile, mechanistic assays such as RIP, RNA pull down and luciferase reporter assays were employed to identify the interplay between RNAs.RESULTS:Eln inhibition was identified to protect rat arterial smooth muscle cells from apoptosis. Also, miR-29b-3p was identified to bind to Eln, and X inactive specific transcript (Xist) could boost Eln expression through absorbing miR-29b-3p. Meanwhile, Eln overexpression counteracted the suppression of silenced Xist on the apoptosis of rat arterial smooth muscle cells. More importantly, such ceRNA network was proved to aggravate the apoptosis of human aortic smooth muscle cells.CONCLUSION:LncRNA Xist contributes to arterial smooth muscle cell apoptosis through miR-29b-3p/Eln pathway, providing new potential roads for treating TAA.

Hemangioma (HA) is tumor formed by hyper-proliferation of vascular endothelial cells. The roles of interleukins on the progression of HA are not well illustrated. Our present study revealed that the expression of interleukin -6 (IL-6) and IL-8 in HA cells were significantly increased as compared with that in the human umbilical vein endothelial cell (HUVEC) cells. Targeted inhibition of IL-6, while not IL-8, can significantly suppress the proliferation and migration of HA cells. IL-6 treatment can increase the expression of vascular endothelial growth factor A (VEGFA), while had no significant effect on the expression of basic fibroblast growth factor (bFGF), in HA cells. Deletion of VEGFA can abolish IL-6 induced progression of HA, suggesting the essential role of VEGFA in IL-6 induced HA development. The specific inhibitor of hypoxia-inducible factor (HIF)-1α, while not Sp1, NF-κB, or AP1, abolished IL-6 induced VEGFA expression. Over expression of HIF-1α can attenuate anti-IL-6 suppressed expression of VEGFA in HA cells. Furthermore, IL-6 triggered the expression, nuclear translocation, and transcription activities of HIF-1α in HA cells via increasing its binding with the signal transducer and activator of transcription–3 (STAT3). STAT3 inhibitor CPA7 or si-STAT3 can abolish IL-6 induced upregulation of HIF-1α in HDEC cells. Collectively, our study revealed that IL-6 can trigger the malignancy of HA cells via induction of proliferation and migration. The activation of STAT3/HIF-1α/VEGFA signal was essential for this process. It suggested that IL-6/STAT3/HIF-1α/VEGFA signal may represent a novel therapeutic target for human HA treatment.

Atherosclerosis is a chronic inflammatory disease of arterial wall, and the proatherogenic molecules derived from endothelium and leukocyte recruitment are major contributors to its pathogenesis. The RNA-binding protein HuR plays several physiological roles in endothelial cells, but its relevance to atherosclerosis is not yet determined. Here, by utilizing the ApoE-/- mice depleted of endothelia HuR (ApoE-/-; HuRfl/fl; Cdh5-Cre), we observed that these mice exhibited attenuated atherosclerosis compared with wild-type littermates (ApoE-/-; HuRfl/fl). Mechanistically, this phenomenon may not be associated with systemic effects on lipid metabolism, however, we found that the expression levels of proatherogenic molecules, degree of local inflammation and extent of leukocyte recruitment to aortic endothelium were all decreased when endothelia HuR was absent. Collectively, our study uncovers the role of endothelia HuR deletion in attenuating atherosclerosis, and suggests that this effect is at least in part attributed to the decreased expression of proatherogenic molecules and suppressed local inflammation. Hence, our study might offer a potential strategy for atherosclerosis treatment via manipulating endothelia HuR.

The present study investigated the incidence, causes, treatment and prevention of limb graft occlusion following endovascular aortic repair (EVAR). A total of 66 cases of abdominal aortic aneurysm receiving EVAR at our department from January 2005 to December 2013 were enrolled. After EVAR, patients received routine antiplatelet therapy of 75 mg PLAVIX for 6 months and then 100 mg Aspirin for another 6 months by oral administration. According to previous clinical experiences, antiplatelet therapy is able to effectively reduce the incidence of iliac occlusion after EVAR. A total of 61 bifurcated grafts and 5 aortauniilac grafts (127 limbs in total) were used. Physical examination, ankle-brachial-index and computer tomographic angiography were performed at 10 days, at 3, 6 and 12 months and annually thereafter. It was found that 7 limbs in 7 patients (10.6% of patients, 5.5% of limbs) were occluded between 20 days and 12 months (average, 7.8±5.3 months) after EVAR. Acute and severe ischemia was found in 2 cases, claudication was in found 3 cases, asthenia in both legs was found in 1 case and 1 case was asymptomatic. Femoral-femoral bypass, femoral-femoral bypass and stenting, aorto-iliac/femoral bypass, thrombectomy and conservative treatment were performed in 1 patient each and thrombectomy together with stenting was performed in 2 cases. Limb graft occlusion was not rare after EVAR. Treatment of this complication included surgery and endovascular therapy such as bypass, thrombectomy and thrombolysis. In conclusion, aggressive pre-emptive treatment including angioplasty and stenting prevented occlusion in certain cases.

Objective To investigate the effect of silencing epidermal growth factor receptor (EGFR) by small interfering RNA (siRNA) interference on the proliferation and migration of vascular smooth muscle cells (VSMCs),and the related mechanisms.Methods VSMCs of rats were isolated and cultured.VSMCs were infected with EGFR siRNA lentiviral vectors.The cells were divided into siRNA-EGFR group,siRNA-negative control group and blank control group.The cell proliferation abilities were detected by 5'-bromo-2'-deoxyuridine (5-BrdU) method.The cell migration abilities in different transfection groups were examined by Transwell chamber and scratch assays.The expression levels of EGFR,extracellular signal-regulated kinase (ERK),c-Jun N-terminal kinase (JNK) and p38 genes in different transfection groups were detected using real-time quantitative polymerase chain reaction (Real-time PCR) technology.The expression levels of EGFR,p-ERK,p-JNK and p-p38 proteins in different transfection groups were detected by Western blotting.Results The number of migration cells in the siRNA-EGFR group was 48.5 ± 6.1,which were significantly lower than the siRNA-negative control group and blank control group,which were 86.2 ± 7.2 and 88.3 ± 7.6;the difference was statistically significant (F =37.261,P =0.000).Compared with 0 h,after 24 h,the migration rate of VSMC in the siRNA-EGFR group was (35.7 ± 3.8) ％,which was significantly lower than that of siRNA-EGFR group and blank group,which were (74.2 ± 5.7) ％ and (75.5 ± 6.1) ％;the differences were statistically significant (F =40.315,P =0.000).The relative expression levels of ERK,JNK and p38 mRNA in the siRNA-EGFR group (0.53 ± 0.09,0.47 ± 0.11,0.41 ± 0.07) were lower than the siRNA-negative control group (0.82 ± 0.12,0.64 ± 0.10,0.68 ± 0.09) and blank control group (0.85 ± 0.14,0.66 ±0.13,0.70 ±0.12),the differences were statistically significant (F=15.391,12.817,ll.264,P =0.000,0.000,0.000).The relative expression levels of p-ERK,p-JNK and p-p38 proteins in the siRNA-EGFR group (0.46 ± 0.09,0.38 ± 0.06,0.33 ± 0.06) were lower than the siRNA-negative control group (0.71 ±0.12,0.57 ±0.08,0.52 ±0.07) and blank control group (0.73 ±0.13,0.56± 0.07,0.54± 0.09),the differences were statistically significant (F =20.152,14.375,13.843,P =0.000,0.000,0.000).Conclusion Specific inhibition of EGFR could effectively reduce prolifera tion and migration capacities of VSMCs,which might be related to inhibition of mitogen-activated protein kinase signaling pathway.

Objective To analyze the mid-term outcomes of hybrid surgery for iliofemoral artery complex lesions. Methods We conducted a retrospective analysis of the clinical data on 16 patients with iliofemoral artery complex lesions who underwent hybrid technique treatment from September 2013 to December 2014. We evaluated the mid-term clinical efficacy in accordance with international standards. Results Technical and hemodynamic success rate were 100%. Mean ankle-brachial index increased from 0.42 ±0.15 to 0.85 ±0.11 (P<0.001). With a mean follow-up period of 19 months (ranged from 13 to 28 months), no severe perioperative complications and death were recorded. One case with dry gangrene of first toe of right foot was treated with toe amputation surgery, for the remaining cases, skin temperature improved obviously, intermittent claudication and rest pain disappeared or improved significantly after procedure and the foot ulcer healed. Eighteen months primary patency and primary-assisted patency rates were 83.2% and 91.4%, respectively. Conclusion Hybrid procedure for complex iliofemoral lesions can effectively avoid cross-joints stenting and preserve the deep femoral artery. It can also improve the chances and efficiency of opening occlusion, better solve the inflow and outflow tract hemodynamics problems and improve the long-term patency rate.

Objective To investigate the role of α7 nicotinic acetylcholine receptor (α7nAchR) agonist in myocardial fibrosis and its possible mechanism.Methods The cardiac fibroblasts were isolated and cultured from neonatal rats.The cardiac fibroblasts were divided into the following four groups: blank control group (cardiac fibroblasts without any intervention);model group [cardiac fibroblasts treated with 10-6 mol/L angiotensin Ⅱ (Ang Ⅱ) only];α7nAchR agonist group (cardiac fibroblasts treated with 5×10-6 mol/L PNU-282987, and 1 h later treated with 10-6 mol/L Ang Ⅱ);α7nAchR antagonist group (cardiac fibroblasts treated with 10-6 mol/L MLA, and 1 h later treated with 10-6 mol/L Ang Ⅱ).The proliferation abilities of cardiac fibroblasts in different treatment groups were measured using WST-1 method.The expression levels of α7nAchR genes in cardiac fibroblasts in different treatment groups were examined by real-time fluorescent quantitative polymerase chain reaction (FQ-PCR).The expression levels of α7nAchR, type Ⅰ and type Ⅲ collagen, α-smooth muscle actin (α-SMA), p38 mitogen activated protein kinase (p38MAPK) and phosphorylated p38MAPK (p-p38MAPK) proteins in cardiac fibroblasts were detected by Western blotting.Results (1) The final absorbance in the α7nAchR agonist group (0.50±0.13) was significantly lower than α7nAchR antagonist group and model group (0.75±0.10, 0.63±0.11, F=10.567, P=0.000).It suggested that activation of α7nAchR could inhibit the proliferation of cardiac fibroblasts.(2) The relative expression levels of α7nAchR mRNA and protein in α7nAchR agonist group (0.87±0.15, 0.76±0.08) were significantly higher than the α7nAchR antagonist group (0.45±0.09, 0.40±0.14), model group (0.62±0.11, 0.59±0.10) and blank control group (0.32±0.13, 0.30±0.07, F=25.402, P=0.000).It suggested that α7nAchR agonists can upregulate the expression of α7nAchR gene in cardiac fibroblasts.(3) The relative expression levels of type Ⅰ and type Ⅲ collagen proteins, α-SMA protein and p-p38MAPK protein in α7nAchR agonist group (0.53±0.09, 0.50±0.12, 0.38±0.08, 0.27±0.09) were lower than the model group (0.65±0.12, 0.62±0.10, 0.57±0.11, 0.45±0.11) and α7nAchR antagonist group (0.81±0.13, 0.71±0.11, 0.70±0.10, 0.68±0.08), while were higher than the blank control group (0.41±0.08, 0.35±0.06, 0.19±0.07, 0.16±0.07, F=29.647, 32.962, 30.549, 53.665, P=0.000, 0.000, 0.000, 0.000).The relative expression of p38MAPK protein in the α7nAchR agonist group (0.71±0.12) was higher than the model group (0.52±0.10) and α7nAchR antagonist group (0.35 ± 0.09), but was lower than the blank control group (0.85 ± 0.14, F=44.347, P=0.000).Conclusion α7nAchR agonists could inhibit the proliferation of cardiac fibroblasts and reduce the synthesis of collagen between cells.The mechanism might be related to inhibition of p38MAPK signaling pathway activation.

In order to provide scientific basis for clinical selection of drugs, to compare and analyze the effective constitutes and the intestinal absorption in vivo in rats of the compound salvia tablets and compound salvia dropping pills (taken as the representatives). Determine the contents of tanshinol, protocatechuic aldehyde, salvianolic acid B and tanshinone II A, cryptotanshinone, ginseng saponin Rg1 and Rb1 in the compound salvia tablets and compound salvia dropping pills by High Performance Liquid Chromatography (HPLC). The intestinal absorption condition of the tanshinol, protocatechuic aldehyde, salvianolic acid B of the compound salvia tablets and compound salvia dropping pills in rats were detected by intestinal perfusion experiment. Only the intake of protocatechuic aldehyde in the compound salvia tablets was higher than in the compound dropping pills, the intake of the other 6 effective constitutes were all lower than in the compound dropping pills. The intestinal absorption of protocatechuic aldehyde was rather complete, while the intestinal absorption of tanshinol and salvianolic acid B were not significant. The duodenum was the main absorption region of these three components. The absorption of protocatechuic aldehyde was different in different regions of the intestines. Each intake of the effective constitutes in the tablets and dropping pills were significantly different, and the rat intestinal absorption of part of the components were different.

Objective: To study the changes in serum level of hyper-sensitive C-reactive protein (hs-CRP) in patients restenosis after internal carotid artery stent implantation (CAS) and its clinical value. Methods: The clinical data of 57 patients, who were readmitted to review stent condition by angiography after CAS, were retrospectively analyzed in this study. The rate of restenosis was measured using cerebral angiography. The patients were divided into restenosis group and non-restenosis group according to the criteria of stent restenosis. Venous blood was drawn at different time point (7 days, 3 months and 6 months) after CAS to measure hs-CRP level, and the results were analyzed by statistical method. Results: All the 57 patients, who underwent carotid artery stenting, were reviewed by cerebral angiography, among them, 11 cases (19.3%) had stent restenosis, including 5 patients (8.8%) with stenosis > 50% and 6 cases (10.5%) with stenosis of 30%-50%; 46 cases didn't have stent restenosis. Difference in preoperative hs-CRP level between restenosis group and non-restenosis group wasn't statistically significant (P > 0.05); however, the differences in hs-CRP level at postoperative 7 days, 3 months, and 6 months were statistically significant between the above two groups, the hs-CRP level in restenosis group was significantly higher than that of non-restenosis group (P < 0.001)..hs-CRP (the difference of hs-CRP between pre-operation and 6 months after stent implantation) in restenosis group was significantly lower than the non-restenosis group. Multivariate regression analysis showed that.hs-CRP is a risk factor for restenosis after CAS (OR=12.355, P=0.000). Conclusion: The increased serum hs-CRP level after stent implantation may participate in the pathological process of restenosis after stent implantation. Monitoring dynamic change in postoperative serum level of hs-CRP can better predict and evaluate the occurrence of restenosis after stent implantation.

妊娠合并急性主动脉夹层是一种临床少见却严重威胁孕妇及胎儿生命的疾病。患者常合并有马凡综合征、主动脉瓣二瓣化畸形、慢性高血压、肥胖、梅毒或创伤性疾病。其通常发生在妊娠晚期、分娩时或产后早期，可能与妊娠期激素水平的变化以及血流动力学的改变有关，但确切的机制尚未明确[1-2]。本研究中，回顾性分析本中心2009年1月至2015年10月收治的5例妊娠合并急性主动脉夹层患者的病例资料，探讨其可能的发病原因、临床处理方法以及预防措施，旨在为降低该疾病的母婴病死率提供临床治疗经验。

Background: This study is to investigate the causes, treatment methods, and preventive measures of retrograde type A aortic dissection (RAAD) complicating thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD).Methods: From January 2005 to December 2013, 360 TBAD patients receiving TEVAR were enrolled in this study. Among them, 304 cases were male and 56 cases were female. They were from 19 to 85 years old, with a mean age of 52 +/- 12.8 years old. The average follow-up time was 32 +/- 11.3 months (3-63 months), the follow-up rate was 69.1% (249 cases), and the lost rate was 30.9% (111 cases). The reasons and the treatment methods of RAAD complicating TEVAR for TBAD were analyzed.Results: There were 5 cases of RAAD complicating TEVAR in TBAD (1.4%) patients, among them, 4 cases were male and 1 case was female. TEVAR operation failed in 1 case because of RAAD occurrence during TEVAR. This case was treated with open operation. In the other 4 cases, TEVAR operation was successfully carried out. During follow-up, RAAD was found in 3 cases within 1 month after TEVAR and in 1 case at 1 year after TEVAR. Conservative treatment was applied to 2 cases, whereas surgical operation treatment was performed in the other 3 cases. One case of conservative treatment patient was dead, and the other 4 cases are still alive.Conclusions: Incomplete design of stent-graft system, rough handling and presence of vascular wall lesions are the main reasons of RAAD complicating TEVAR for TBAD. Surgical operation is the most effective treatment measure for RAAD complicating TEVAR for TBAD.

Objective: To study the changes in serum level of hyper-sensitive C-reactive protein (hs-CRP) in patients restenosis after internal carotid artery stent implantation (CAS) and its clinical value. Methods: The clinical data of 57 patients, who were readmitted to review stent condition by angiography after CAS, were retrospectively analyzed in this study. The rate of restenosis was measured using cerebral angiography. The patients were divided into restenosis group and non-restenosis group according to the criteria of stent restenosis. Venous blood was drawn at different time point (7 days, 3 months and 6 months) after CAS to measure hs-CRP level, and the results were analyzed by statistical method. Results: All the 57 patients, who underwent carotid artery stenting, were reviewed by cerebral angiography, among them, 11 cases (19.3%) had stent restenosis, including 5 patients (8.8%) with stenosis > 50% and 6 cases (10.5%) with stenosis of 30%-50%; 46 cases didn’t have stent restenosis. Difference in preoperative hs-CRP level between restenosis group and non-restenosis group wasn’t statistically significant (P > 0.05); however, the differences in hs-CRP level at postoperative 7 days, 3 months, and 6 months were statistically significant between the above two groups, the hs-CRP level in restenosis group was significantly higher than that of non-restenosis group (P < 0.001). Δhs-CRP (the difference of hs-CRP between pre-operation and 6 months after stent implantation) in restenosis group was significantly lower than the non-restenosis group. Multivariate regression analysis showed that Δhs-CRP is a risk factor for restenosis after CAS (OR=12.355, P=0.000). Conclusion: The increased serum hs-CRP level after stent implantation may participate in the pathological process of restenosis after stent implantation. Monitoring dynamic change in postoperative serum level of hs-CRP can better predict and evaluate the occurrence of restenosis after stent implantation.

目的 探讨单纯下肢静脉曲张剥脱术后深静脉血栓形成(deep venous thrombosis,DVT)的治疗方法.方法 23例下肢静脉曲张术后DVT患者,其中15例行抗凝治疗(抗凝组),8例行导管直接溶栓治疗(溶栓组);观察2组近、远期治疗效果.结果 2组住院时间均为14d;抗凝组中5例周围型DVT患者出院时血栓完全溶解,6个月复查无静脉瓣膜功能不全,10例中央型或混合型DVT患者出院时5例血栓部分溶解,5例无明显变化,6个月复查均伴有深静脉瓣膜功能不全;溶栓组8例患者出院时血栓均完全溶解,6个月复查时无静脉瓣膜功能不全.结论 导管直接溶栓治疗可作为单纯下肢静脉曲张剥脱术后DVT首选治疗方法.