Prognostic significance of NT-proBNP, 3D LA volume and LV dyssynchrony in patients with acute STEMI undergoing primary percutaneous intervention

Objectives

The aim of the present study was to assess the short term prognostic significance of N-terminal pro BNP (NT-proBNP), 3D left atrial volume (LAV) and left ventricular (LV) dyssynchrony in patients of acute ST-elevation myocardial infarction (STEMI) who underwent primary Percutaneous intervention (PCI).

Background

NT-proBNP, LV dyssynchrony and LAV in patients with acute coronary syndrome have been associated with PCI outcomes and predict the short and long-term prognosis.

Methods

This study consisted of 142 patients with a first STEMI who underwent primary PCI. Baseline echocardiographic data was collected at admission and at 6 months follow up. Left ventricular dyssynchrony was measured by tissue Doppler imaging and LAV by real time 3D-echocardiography, plasma NT-proBNP levels were estimated between 72 and 96 h of admission.

Results

During study period 3 patients expired and 4 developed congestive heart failure (CHF). Baseline NT-proBNP and LV dyssynchrony correlated with LV size and LV ejection fraction (LVEF) at baseline and during follow up. Patients with higher NT-proBNP levels and higher LV dyssynchrony showed significant increase in LV size with decrease in LVEF during follow-up. Baseline Left atrial volume index (LAVI) showed significant correlation with LV size but no association with LVEF at baseline and during follow-up.

Conclusions

Higher levels of NT-proBNP and higher LV dyssynchrony can predict patients with increase in LV size, worsening of LV systolic and diastolic function during follow-up. Patients with higher NT-proBNP levels at baseline developed CHF during follow-up.     

Three patients with structurally abnormal X chromosomes, each with Xq13 breakpoints and a history of idiopathic acquired sideroblastic anemia

Structural abnormalities of the X chromosome are rarely found in neoplastic disorders. We describe three patients with a history of idiopathic acquired sideroblastic anemia (IASA); each one had an abnormal clone of cells in the bone marrow, characterized by a structurally abnormal X chromosome. In two of these patients, the predominant karyotype was 47,X,2idic(X)(q13); in the other patient, it was 46,X,t(X;11)(q13;p15). Inasmuch as all three of these cases involved chromosome band Xq13, as did two previously published cases, we suggest that band Xq13 may be more prone to structural rearrangement than other X chromosome bands in hematologic disorders. The common Xq13 chromosome breakpoint and clinical presentation (IASA) among these three patients and the occurrence of an X-linked type of sideroblastic anemia may suggest that an association exists between X chromosome abnormalities and IASA. Perhaps alteration of a gene or chromosome structure in or near band Xq13 predisposes to development of IASA. The fact that two of these patients had preleukemia and the third had overt acute leukemia may imply that patients with IASA and X chromosome abnormalities have a poor prognosis. Cases of IASA without associated X chromosome abnormalities are known; thus, if an association between IASA and an abnormal X chromosome does exist, most likely it involves only some patients with IASA.     

Activation of the CPP32 protease in apoptosis induced by 1-beta-D- arabinofuranosylcytosine and other DNA-damaging agents

The response of human myeloid leukemia cells to treatment with 1-beta- arabinofuranosylcytosine (ara-C) includes the induction of apoptosis. Ara-C induced apoptosis is associated with proteolytic cleavage of poly(ADP-ribose) polymerase (PARP) and protein kinase C (PKC) delta. However, the signals involved in this response are unknown. The present studies show that ara-C treatment of U-937 cells is associated with induction of a protease activity that cleaves the tetrapeptides Ac-DEVD- pNA and Ac-DMOD-pNA found at the cleavage sites of PARP and PKC delta, respectively. The ara-C-induced protease activity was sensitive to overexpression of the anti-apoptotic protein Bcl-xL and the baculovirus protein p35. By contrast, overexpression of the cowpox virus protein CrmA blocked apoptosis induced by engagement of the Fas receptor but not that induced by ara-C. CrmA overexpression also had no detectable effect on ara-C-induced cleavage of PKC delta. The results further show that ara-C induces activation of the CPP32 protease by a CrmA- insensitive and p35-sensitive mechanism. Similar results were obtained with cisplatinum, etoposide, and camptothecin. These findings indicate that ara-C and other DNA-damaging agents activate a CrmA-insensitive apoptotic pathway involving CPP32 and that these signals differ from those associated with apoptosis induced by the Fas receptor.     

Synthesis of (+)-lariciresinol 3a-acetate, a lignan from Aglaia elaeagnoidea

(+)-Lariciresinol 3a-acetate [(+)-(3S)-acetyloxymethyl-(2S)-(4-hydroxy-3-methoxyphenyl)-(4R)-[(4-hydroxy-3-methoxyphenyl)methyl]tetrahydrofuran] (1), a metabolite of A. elaeagnoidea was synthesized starting from (-)-lariciresinol (2) in three steps with an overall yield of 66%.     

人ERRα基因小分子干扰RNA慢病毒载体构建及鉴定

目的构建并鉴定靶向人ERRα基因的小分子干扰RNA的慢病毒载体。方法针对ERRαmRNA设计了4条si RNA,并构建pGCSIL-GFP-siERRα慢病毒质粒,PCR扩增阳性克隆并测序鉴定。用pGCSIL-GFP-siERRα、pHelp-er1.0和pHelper2.0质粒共转染293T细胞包装产生慢病毒,测定病毒滴度。将慢病毒干扰RNA及含有ERRα过表达载体共转染293T细胞,Western-blot检测ERRα表达,观察蛋白表达抑制效果。结果 PCR和测序结果与设计的干扰序列一致,病毒滴度达2×109TU/ml。转染细胞中ERRα蛋白表达显著降低。结论成功构建高表达、高效率的人ERRα基因小分子干扰RNA慢病毒载体,为进一步研究ERRα在细胞核内转导中的作用机制和靶向ERRα治疗奠定基础。     

Cadmium-induced Oxidative Stress and Evaluation of Embilica Officinalis and Stressroak in Broilers

Cadmium (Cd) toxicity was studied in broilers, and efficacy of Emblica officinalis (500 ppm in feed), vitamin E (300 ppm in feed), and stressroak (1 g/kg feed) were evaluated for prophylactic and therapeutic management of Cd toxicity. One-day-old male broiler chicks were randomly divided into eight groups consisting of 10 chicks in each. Groups 1 and 2 were maintained as plain control and Cd (100 ppm in feed) toxic control (for six weeks). Groups 3, 4, and 5 were maintained on a combination of Cd (100 ppm in feed) and Emblica officinalis, vitamin E, and stressroak for six weeks. Groups 6, 7, and 8 were maintained with Cd for the first four weeks and on Emblica officinalis, vitamin E, and stressroak during the subsequent two weeks without Cd. Body weights, feed consumed, Feed conversion ratio (FCR), and glulathione (GSH) were significantly (P<0.05) decreased, whereas the activities of antioxidant enzymes (catalase and Superoxide dismutase (SOD)) and concentration of Thiobarbituric acid reacting substances (TBARS) were significantly (P<0.05) increased in toxic control group. After treatment with Emblica officinalis, vitamin E, and stressroak in groups 6, 7, and 8 during last two weeks and discontinuation of Cd, the parameters revealed improvement. From this study, it is concluded that Cd induces toxicity by oxidative stress, and supplementing Emblica officinalis, vitamin E, and stressroak in feed is useful in preventing and treating the toxicity.