Tricuspid annular plane systolic excursion (TAPSE) can predict the outcome of isolated tricuspid valve surgery in patients with previous cardiac surgery?

Background

Isolated tricuspid valve replacement is rare when performed as a re-operation after a left side operation. It is important to know the factors that determine mortality and morbidity. Tricuspid Annular Plane Systolic Excursion (TAPSE) is a scoring system that is used with non-invasive Doppler echocardiography to determine right ventricular (RV) function. This study analyzed TAPSE scores and adverse outcomes of isolated tricuspid valve surgery in patients with previous cardiac surgery.

Methods

All patients who underwent tricuspid valve replacement between January 2014 and December 2015 were retrospectively reviewed. Patients having concomitant mitral or aortic valve surgery were excluded. These patients were divided into two groups: TAPSE >14 mm and TAPSE ≤14 mm. In-hospital outcomes were compared.

Results

A total of 26 patients with severe tricuspid valve regurgitation underwent tricuspid valve replacement. There were 5 males (19.2%) and 21 females (80.8%). The average age at operation was 54.77±9.61 years (range, 27–69 years). There were 16 patients in the TAPSE >14 mm group and 10 patients in the TAPSE ≤14 mm group. The BNP in the TAPSE >14 mm group was significant (TAPSE >14 mm 672.34±229.98 versus TAPSE ≤14 mm 1,054.79±684.69, P=0.03). The median cardiopulmonary bypass (CPB) time and red blood cell (RBC) transfusions in the two groups were not different. The need for prolonged ventilatory support (>48 h) in the two groups was also not different (TAPSE> 14 mm 91.2±12.31 vs. TAPSE ≤14 mm 39.00±36.80, P=0.46). Moreover, hospital stays were similar between the two groups. No differences were found in postoperative renal and respiratory complications.

Conclusions

It is important to determine the right ventricule function quantitatively. The TAPSE score is an important parameter that determines the cardiac index and right ventricle function. It should be used for the prediction of mortality and morbidity with all the other parameters as a whole.     

Structure of Arabidopsis CESA3 catalytic domain with its substrate UDP-glucose provides insight into the mechanism of cellulose synthesis

Cellulose is synthesized by cellulose synthases (CESAs) from the glycosyltransferase GT-2 family. In plants, the CESAs form a six-lobed rosette-shaped CESA complex (CSC). Here we report crystal structures of the catalytic domain of Arabidopsis thaliana CESA3 (AtCESA3^CatD) in both apo and uridine diphosphate (UDP)-glucose (UDP-Glc)–bound forms. AtCESA3^CatD has an overall GT-A fold core domain sandwiched between a plant-conserved region (P-CR) and a class-specific region (C-SR). By superimposing the structure of AtCESA3^CatD onto the bacterial cellulose synthase BcsA, we found that the coordination of the UDP-Glc differs, indicating different substrate coordination during cellulose synthesis in plants and bacteria. Moreover, structural analyses revealed that AtCESA3^CatD can form a homodimer mainly via interactions between specific beta strands. We confirmed the importance of specific amino acids on these strands for homodimerization through yeast and in planta assays using point-mutated full-length AtCESA3. Our work provides molecular insights into how the substrate UDP-Glc is coordinated in the CESAs and how the CESAs might dimerize to eventually assemble into CSCs in plants.

Cellulose, a linear homopolymer of d-glucopyranose linked by β-1,4-glycosidic bonds, is the major structural component of the cell walls of plants, oomycetes, and algae and constitute the most abundant biopolymer on Earth (1). Cellulose is synthesized by cellulose synthases (CESAs) that belongs to the glycosyltransferase GT-2 superfamily (1, 2). In land plants, cellulose is produced at the plasma membrane by six-lobed rosette-shaped CESA complexes (CSCs) where each CESA is thought to synthesize one cellulose chain (3). The precise number of CESAs per CSC is unresolved but estimated to range between 18 and 36 (4–6).Plants contain multiple cesa genes, with 10 found in the Arabidopsis genome (7). Of these, CESA1, CESA3, CESA6, and the CESA6-like CESAs (i.e., CESA2, CESA5, and CESA9) are involved in primary cell wall formation, whereas CESA4, CESA7, and CESA8 participate in secondary cell wall formation (8–12). These two types of CSCs form heterotrimeric complexes with a ratio of 1:1:1 (13, 14). The Arabidopsis CESAs share an overall sequence identity of ∼60% and have seven transmembrane helices (15). In plants, the catalytic domain (CatD) of the CESAs is located between the second and third transmembrane helices and contains a canonical D, D, D, QxxRW motif (1). While there are similarities between the plant CatD and its counterpart in bacterial cellulose synthases, the CatD is flanked by two plant-specific domains, the so-called plant-conserved region (P-CR) and class-specific region (C-SR) (16). These domains are proposed to have important functions in cellulose synthesis and CESA oligomerization (17).The oligomerization of plant CESAs is thought to be important for the final CSC assembly, and multiple oligomeric states of CESAs, including homodimers, have been reported (18, 19). For example, immunoprecipitation assays using CESA7 fused to a dual His/STRP-tag demonstrated that CESA4, CESA7, and CESA8 could form independent homodimers, and it was hypothesized that the CESA homodimerization may contribute to early stages of CSC assembly. These homodimers might then be converted into CSC heterotrimeric configurations (19). This feature poses a marked difference from the bacterial cellulose synthase complex. However, how CESA homodimers are formed and how they function in cellulose synthesis are unknown.To comprehend the mechanisms behind plant cellulose synthesis, it is essential to acquire structural information about plant CESAs. Indeed, the BcsA–BcsB complex structure from Rhodobacter greatly aided our understanding of the cellulose synthesis in bacteria (20). Nevertheless, there are many differences between bacterial and plant CESAs and the corresponding protein complexes. Extensive efforts have been undertaken to acquire plant CESA structural information, including homology modeling and small-angle X-ray scattering analyses (5, 6, 16, 21, 22). While these efforts have been important to form new hypotheses, they did not reveal significant insights into substrate coordination, cellulose chain extrusion, and complex assembly. Recently, a homotrimeric CESA8 structure from Populus tremula × tremuloides was resolved by cryogenic electron microscopy (cryo-EM), which offered significant new molecular understanding of cellulose microfibril biosynthesis and CESA coordination within the CSC (15). Here we report the crystal structures of Arabidopsis CESA3 CatD (AtCESA3^CatD) in apo and uridine diphosphate (UDP)-glucose (UDP-Glc) bound forms and outline how the CatD might contribute to CESA homodimerization and substrate coordination.     

经十二指肠镜括约肌切开胆总管结石的处理(附168例报告)

目的：采用各种方法处理不同大小的胆总管结石。方法：于1986年3月至1996年9月经内镜括约肌切开（EST）治疗胆总管结石168例，其中单颗结石63例，2颗结石56例，3颗以上结石49例，最多一例8颗结石，结石的直径为5～25mm不等。结果：165例（98．2％）切开成功，3例失败。161例（95．8％）结石排出，其中96例（59．6％）结石自然排入肠道，57例（35．4％）采用网篮或气囊取出结石，6例（3．7％）采用碎石网篮碎石后排出，2例（1．2％）经震波碎石后排出。术后出现胃肠道出血1例（0．6％），胰腺炎1例（0．6％），胆管炎3例（1．8％）。48例术后行胃肠钡餐检查，43例胆道内无钡剂返流，2例胆道内有积气，3例有钡剂返流入胆道，但无临床症状。结论：EST是目前治疗胆管结石的重要手段之一。     

Different costimulation signals used by CD4(+) and CD8(+) cells that independently initiate rejection of allogenic hepatocytes in mice

The current study evaluated the role of CD40/CD40 ligand (CD40L) and CD28/B7 costimulation signals during alloimmune responses independently mediated by CD4(+) or CD8(+) T cells. Allogeneic hepatocytes were transplanted into CD8 or CD4 knock out (KO) mice under cover of costimulatory blockade. Rejection of FVB/N (H-2(q)) hepatocytes occurred by day 10 posttransplant in untreated CD8 or CD4 KO (H-2(b)) mice. Treatment of CD8 or CD4 KO mice with anti-CD40L monoclonal antibody (mAb; MR1) resulted in significant prolongation of hepatocyte survival indicating that CD40/CD40L interactions were critical in both CD4(+) and CD8(+) T-cell initiated hepatocyte rejection. Anti-CD40L mAb also prolonged hepatocyte survival in B-cell KO (H-2(b)) mice, indicating that the efficacy of CD40/CD40L blockade in preventing hepatocyte rejection was B-cell (and antibody) independent. In contrast, treatment with CTLA4 fusion protein (CTLA4Ig), prolonged hepatocyte survival in CD8 KO but not CD4 KO mice, showing that CD28/B7 interactions were important in CD4(+) but not CD8(+) T-cell initiated hepatocyte rejection. Under selected circumstances, such as in CD40 KO mice, both CD4(+) and CD8(+) T cells mediate hepatocyte rejection in the absence of CD40/CD40L costimulation and without a significant contribution from CD28/B7 costimulation signals. These results highlight the disparate roles of CD40/CD40L and CD28/B7 costimulation signals in CD4(+) versus CD8(+) T-cell mediated immune responses to allogeneic hepatocytes. The CD4(+) T-cell independent, CD40L-sensitive, CD28/B7-independent pathway of CD8(+) T-cell activation in response to transplantation antigens is novel.     

炎性相关细胞因子和心肌梗死微循环再灌注状态的关系

目的　观察急性心肌梗死 (AMI)患者梗死相关血管 (IRA)开通前后炎性细胞因子的动态变化及其与心肌组织水平灌注状态的关系。方法　 (1)测定 8例健康人和 2 2例AMI患者急诊冠状动脉介入治疗术 (PCI)前即刻 ,术后 12、2 4h ,血浆白细胞介素 (IL) 1β、肿瘤坏死因子 (TNF)α、IL 10的变化。 (2 )按照再灌注后 2h心电图ST段回落是否 >70 % ,将 2 2例AMI患者分为 :A组 (ST回落≥ 70 % )12例和B组 (ST回落 <70 % ) 10例 ,比较两组患者IL 1β、TNFα、IL 10的变化幅度。 结果　 (1)治疗前A、B两组AMI患者血浆TNFα、IL 10略高于健康对照组 ,但差异无统计学意义 (P >0 0 5 ) ;而IL 1β显著高于健康对照组 (P <0 0 5 ) ;再灌注后 12、2 4hA、B两组血浆IL 1β和TNFα均较术前显著增高 (P <0 0 1,P <0 0 5 ) ,B组血浆IL 10较术前显著增高 (P <0 0 5 ) ,A组则无此变化 (P >0 0 5 )。 (2 )A、B两组间比较 ,治疗前TNFα、IL 1β、IL 10差异均无显著性 (P >0 0 5 ) ;成功PCI、IRA血流达TIMI 3级者 ,B组患者血浆IL 1β、TNFα、IL 10 ,在再灌注 12h显著高于A组 (P <0 0 1,P <0 0 5 ,P <0 0 5 ) ,再灌注 2 4h ,IL 1β、IL 10仍然高于A组 (P <0 0 5 )。 (3)A、B两组患者抗炎因子IL 10的升高幅度均显著低于致炎     

顽固性室性早搏的导管标测与射频消融治疗

采用射频导管消融术对症状明显、药物无效的１０例顽固性室性早搏（简称室早）进行治疗。将消融电极送至右室流出道区域，以Ｓ１Ｓ１或ＲＳ２早搏刺激标测到与体表１２导联心电图记录的自发室早ＱＲＳ波群图形完全相同，并且激动标测时自发室早的局部电图较体表心电图ＱＲＳ波群提前３０ｍｓ以上的部位为消融靶点。以室早在放电后１０ｓ内消失，维持稳定窦性心律３０～６０ｍｉｎ为即刻成功标准。９例患者经１０～２０Ｗ、消融６０～１８０ｓ，早搏和短阵室速完全消失；１例失败。平均随访１１个月，未服任何抗心律失常药物症状消失，复查心电图和动态心电图，９例中８例无早搏、１例为偶发室早，均无并发症。提示射频导管消融术是治疗某些右室流出道早搏的可行方法。     

Mouse model of post-infarct ventricular rupture: time course, strain- and gender-dependency, tensile strength, and histopathology

OBJECTIVE: Recent studies on mice with surgically induced acute myocardial infarction (AMI) have documented the frequent occurrence of ventricular rupture, an event not previously reported in other laboratory species. We have examined the natural history, histopathology and myocardial mechanical strength in mice with AMI. METHODS: AMI was induced by coronary artery occlusion and animals were monitored for fatal events. Gross and histological examinations were undertaken. RESULTS: Rupture occurred in the left ventricular free wall at 2-6 days after AMI. Incidence of rupture in male mice varied among three strains studied (3% for FVB/N, 27% for C57B/6J, and 59% for 129sv, P<0.05) and was lower in female than male mice (23% vs. 59%, P<0.05). Histologically, ruptured hearts had rapid-occurring and severe infarct expansion, multifocal intramural hemorrhage and leucoyte infiltration at the border zone and infarcted zone. In vitro, infarcted left ventricles demonstrated a 50-60% reduction in muscle tensile strength. This reduction preceded the onset of rupture and was related to the time-window of rupture and to infarct size. CONCLUSION: LV wall rupture in the mouse occurs within a narrow time-window after AMI and is strain- and gender-dependent. Infarct expansion, regional hemorrhage with formation of hematoma and leuocyte accumulation are important pathological changes leading to reduced myocardial tensile strength.     

颈动脉支架置入术会取代颈动脉内膜切除术吗?

多年来,颈动脉内膜切除术(CEA)一直被视为重度颈动脉狭窄患者治疗的"金标准",但随着颈动脉支架置入术(CAS)的发展,逐渐使CEA的"金标准"地位受到挑战,甚至有人提出用CAS代替CEA.近年来陆续发表了有关两种治疗方式的对比研究,但对相关研究结果的解读,以及各项研究间的结果却并不一致.文章就这些方面的争议进行了分析.