Factors as predictors for thoracic and thoracolumbar/lumbar structural curves in adolescent idiopathic scoliosis / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Recent studies have demonstrated that the Lenke system is relatively efficient and consistent in classifying scoliosis curves. Basically, fusion should include the main curve and the structural minor curve. The criteria for defining the structural minor curve were established to help guide these decision-making process. The present study was designed to investigate predictors of the structural curve, and see whether it was possible to prevent the formation of the structural curve by interfering with influencing factors to decrease the fusion level.</p><p><b>METHODS</b>Age, gender, Cobb angle, Perdriolle rotation, Risser sign and the number of vertebrae included in the curve, brace treatment, and curve location were recorded in 145 idiopathic scoliosis patients from July 2001 to January 2007. The patients were divided into two groups: structural and non-structural groups. Demographics and baseline characteristics were compared between the two groups as an initial screen. Logistic regression was used to analyze factors affecting the minor curve to become the structural curve.</p><p><b>RESULTS</b>Compared with the non-structural group, the structural group had a higher Cobb angle ((51.34 ± 13.61)° vs. (34.20 ± 7.21)°, P < 0.001), bending angle ((33.94 ± 9.92)° vs. (8.46 ± 5.56)°, P < 0.001) and curve rotation ((23.25 ± 12.86)° vs. (14.21 ± 8.55)°, P < 0.001), and lower flexibility ((33.48 ± 12.53)% vs. (75.50 ± 15.52)%, P < 0.001). There was no significant difference in other parameters between the two groups. The results of the Logistic regression analysis showed that the Cobb angle (OR: 9.921, P < 0.001) and curve location (OR: 4.119, P = 0.016) were significant predictors of structural curve in adolescent idiopathic scoliosis. Every 10° change of Cobb angle increased the possibility of turning the minor curve into the structural curve by 10-fold. And thoracic curve showed, on the average, the possibility of becoming the structural curve about 4-fold more often than did the thoracolumbar/lumbar curve.</p><p><b>CONCLUSIONS</b>Curve severity and curve location affect the minor curve's structural features in adolescent idiopathic scoliosis.</p>

Genetic characterization of HA1 gene of influenza H3N2 virus isolates during 2008-2009 in Zhuhai, China / 病毒学报

To understand the HA1 genetic variation characterization of influenza H3N2 virus isolates in Zhu-hai during 2008-2009, we selected 20 of H3N2 Influenza strains cultured in MDCK cell. Viral RNAs were extracted and amplified by using RT-PCR. The amplified products were purified after identified by gel electrophoresis and then the nucleotide sequences of the amplicons were determined. The results were analyzed by the software ClustalX and MEGA4. 1. When compared with the amino acid sequences of the epitopes of HA1 district of H3N2 influenza vaccine recommended by WHO in 2008, changes were found in those of H3N2 influenza strains in Zhuhai in 2008: K140I in all of H3N2 influenza strains, L157S in 08-0343 and 08-0677, K158R in 08-0466, 08-0620 and 08-0667, K173E in 08-0466 and 08-0620, K173N in 08-0667, and I192T in 08-0667. The epitopes of HA1 district of H3N2 influenza strains in Zhuhai in 2009 are different from that of H3N2 influenza vaccine during the same time: K173Q and P194L occur in all of H3N2 influenza strains, N144K, K158N, and N189K occur in the strains except the strain 09-0056. HA1 domain of H3N2 influenza strains in 2009 has lost a glycosylation site at amino acid position 144 while the glycosylation sites of HA1 domain of H3N2 influenza stains isolated in 2008 remained. This study suggested that H3N2 influenza virus in Zhuhai in 2008 was not evolved a novel variant and H3N2 influenza variant in 2009 was attributed to antigenic drift in HA1 district.

Readthrough of nonsense mutation W822X in the SCN5A gene can effectively restore expression of cardiac Na+ channels W822X / 中华心血管病杂志

<p><b>OBJECTIVE</b>In this study we investigated the functional restoration of nonsense mutations in the SCN5A gene.</p><p><b>METHODS</b>The readthrough-enhancing reagents were introduced to HEK293 cells to suppress one nonsense mutation W822X in the SCN5A gene. Patch-clamp was used to record the whole-cell current and dynamics. Western blot and immunofluorescence staining were used to certify the expression and the location of the sodium channel.</p><p><b>RESULTS</b>In transfected HEK293 cells, the nonsense mutation in SCN5A inhibited the expression level of full-length protein, and the sodium currents from the mutant channels were less than 3% of the wild-type level. Readthrough enhancement by decreasing translation termination efficiency with a siRNA targeting eukaryotic release factor eRF3a (a GTPase that binds eRF1), the sodium current from the mutant cDNAs was restored to as much as 30% of the wild-type. After the treatment by the readthrough-enhancing reagents, the channels from cDNA carrying W822X remained the features of wild-type phenotype, and Western blot and immunochemical staining also showed the expression of full-length channel proteins.</p><p><b>CONCLUSION</b>Readthrough-enhancing reagents could effectively suppress nonsense mutations in SCN5A and partially restore the function of sodium channel and the expression of full-length channels.</p>

Clinical characteristics and outcome of 32 patients with long-QT syndrome accompanied with torsade de pointes / 中华心血管病杂志

<p><b>OBJECTIVE</b>To summarize the clinical characteristics and outcome of patients with long-QT syndrome (LQTs) accompanied with torsade de pointes.</p><p><b>METHODS</b>Thirty-two eligible patients were included in this study. Clinical and electrocardiographic data were analyzed and telephone or out-patient follow-up were made in all patients.</p><p><b>RESULTS</b>There were 15 patients with inherited LQTs (h-LQTs) and 17 patients with acquired LQTs (a-LQTs). There are more women (n = 24) than men (n = 8). β blockers, potassium and magnesium supplement were the basic therapy for h-LQTs patients, bivent pacemaker was implanted in 2 patients and implantable cardioverter defibrillator was implanted in 5 patients. Ventricular tachyarrhythmias and syncope occurred in 4 patients during (39.4 ± 25.1) months follow-up. In 17 a-LQTs patients, one patient with dilated cardiomyopathy died suddenly and another patient with implanted cardioverter defibrillator experienced one ventricular tachycardia during (30.9 ± 13.3) months follow-up.</p><p><b>CONCLUSIONS</b>The prognosis in h-LQTs and a-LQTs patients with structure heart disease is poor. ICD or CRT-D therapy is suggestive for a-LQTs patients with structure heart disease.</p>

Reasons for pacing leads abandonment during pacemaker replacement: a single center experience with 235 cases / 中华心血管病杂志

<p><b>OBJECTIVE</b>To analyse the reasons for pacing lead abandonment during pacemaker replacement.</p><p><b>METHOD</b>Clinical data of patients underwent permanent pacemaker replacement between Jan 1st, 1976 to Dec 31st 2006 in Fuwai Hospital were obtained and the reasons for pacing leads abandonment were analyzed.</p><p><b>RESULTS</b>Pacemaker was replaced in 1023 patients during this period and 235 pacing leads were abandoned, 131 leads (55.7%) were abandoned for leads malfunction, including leads body fracture (35, 14.9%), isolation defects (10, 4.3%), dislocations (10, 4.3%) and excessively high threshold values (76, 32.3%). Other reasons for leads abandonment were infection (50, 21.3%), incompatibility between the leads and new generator (30, 12.8%), need to degrade the pacing system (13, 5.5%) and other rare reasons (11, 4.7%).</p><p><b>CONCLUSION</b>The most often reason for leads abandonment during pacemaker replacement is lead malfunction, including lead body fracture, isolation defect, dislocation and excessively high threshold value of the leads.</p>