Evaluation of motion sickness susceptibility by motion sickness susceptibility questionnaire in adolescents with idiopathic scoliosis: a case–control study

Purpose

Adolescent idiopathic scoliosis (AIS) is a three-dimensional deformity of the spine, with unknown origin. Some studies have noted impaired postural balance in AIS, in particular, difficulty to manage situations with sensory conflict. The motion sickness susceptibility can be secondary to a sensory conflict, for example, between visual and vestibular information. Our hypothesis is: patients with AIS have difficulty in managing situations with sensory conflict and therefore have increased motion sickness susceptibility. The purpose of this study was to evaluate in AIS subjects by evaluating their susceptibility to motion sickness, as compared to a control group.

Methods

We conducted an analysis of data on motion sickness susceptibility collected prospectively from 2012, with the B score of motion sickness susceptibility questionnaire. This evaluation was completed for 65 adolescents (age 14.5 ± 1.6 year) with major right thoracic AIS (Cobb = 40.7° ± 13.1°) and 71 matched controls (14.6 ± 1.6 year).

Results

Adolescents with major right thoracic AIS were more susceptible to motion sickness (B score = 5.3 ± 5.8) than controls (B score = 3.4 ± 3.7) with significant difference (p = 0.025).

Conclusions

We interpret our results suggesting there is difficulty for patients with AIS to manage situations with sensory conflict. Previous studies focusing on situations with sensory conflict in AIS have required sophisticated technology. They are not accessible for routine patient management. Our research shows the same result with simple, non invasive, low-cost and quick method: B score of motion sickness susceptibility questionnaire.

     

Versatility of Hemisternotomy for Cardiac Surgery

Abstract   Background: Hemisternotomy has been suggested as a way to reduce morbidity by limiting the invasiveness of surgical interventions but it is often limited to aortic valve disease. This study reviews the experience of one center employing hemisternotomy and compares patient outcomes, both in-hospital and post-discharge, with a matched group of full sternotomy patients. Methods: Propensity scores were used to match all hemisternotomy valve cases (Hemi) to full sternotomy valve cases (Full) (1:2). An in-hospital composite outcome (COMP) was defined as mortality, stroke, deep sternal wound infection, sepsis, or return to operating room (OR) for bleeding or valve dysfunction. Provincial administrative health databases were used to determine freedom from mortality and hospital readmission for cardiac cause. Results: During the study period, 70 patients received hemisternotomy for various cardiac surgical interventions with only 38 patients undergoing isolated aortic valve replacement. Examining valve surgery exclusively, 65 Hemi were matched to 130 Full. In-hospital complications were low in both groups, with 1.0% mortality and a non-significant trend toward COMP in the Full group (Hemi = 4.6%; Full = 8.5%; p = 0.39). Ventilation time was significantly decreased in Hemi (median four vs. six hours; p = 0.002). At two years follow-up, survival was excellent for both (Hemi = 95.0%; Full = 93.6%) and freedom from cardiac morbidity (Hemi = 76.8%, Full = 73.2%) was comparable. Conclusion: Hemisternotomy appears to be a safe, effective, and versatile alternative for many cardiac surgical interventions. With a median follow-up of four years, this study represents the longest cardiac morbidity follow-up for hemisternotomy patients. However, we were unable to conclusively show a morbidity benefit with this incision.     

骨髓干细胞植入正常或慢性梗死心肌后短期内移植细胞的分布及可利用度

目的采用心肌内注射方法将骨髓间充质干细胞(BMSCs)植入到正常或慢性梗死心肌中后, 研究短期内植入细胞的分布和可利用度。方法采用选择性冠状动脉结扎方法建立大鼠慢性心肌梗死模型( n =9) 。1个月后, 采用心肌内注射方法将 111 铟 - 羟基喹啉 ( 111Indium- oxine, 111In) 同位素标记的自体 BMSCs (2×106/50μL)植入到慢性梗死心肌和正常对照心肌中( n =6) 。采用序列平面针孔闪烁扫描方法测定 BMSCs移植后 2 h、1 d、3 d、7 d 时的心肌 111In 的放射活性, 并计算植入细胞在心肌内的驻留率。于细胞移植术后第 7 天切取制备心脏横断面冷冻切片, 进行组织放射微成像(Micro- imaging)和组织病理学分析, 观察植入细胞在心肌内的分布情况。结果慢性心肌梗死(MI)组的心肌 111In 的放射活性在所有测定的时间点均显著高于正常对照组(P<0.01)。心肌放射强度实测值在经由各相应时间点 BMSCs细胞 111In 的自发泄漏率的体外标定值校正后, 计算得出植入的 BMSCs 细胞在慢性梗死心肌(MI 组)中的驻留率平均为 60%, 而在正常对照组心肌中细胞的驻留率只有 25%(P <0.01), 并在 7 d 的随访期中保持稳定。组织放射微成像和组织病理学分析都证实植入的 BMSCs 主要分布于由注射针头插入损伤或慢性心肌梗死所造成的纤维瘢痕组织中。结论心肌内细胞移植术后 7 d 内,被植入到慢性梗死心肌中的 BMSCs 细胞的可利用度高于被植入在正常心肌中的 BMSCs 细胞的可利用度。植入心肌内的 BMSCs 主要分布于由注射针头插入损伤和慢性心肌梗死导致的纤维瘢痕组织中。     

Respiratory oxygen uptake is associated with survival in a cohort of ventilated trauma and burn patients

Background

Little data is available in the literature about the role of end tidal oxygen in critically ill patients. We sought to identify the association between the level of respiratory oxygen and clinical outcomes in critically-ill ventilated trauma and burn patients.

Arrhythmogenic right ventricular cardiomyopathy: use of a left ventricular assist device as a bridge to transplantation?

The principal characteristic of arrhythmogenic right ventricular cardiomyopathy (ARVC) is the tendency for ventricular arrhythmia and sudden death to occur without overt ventricular dysfunction. Current recommendations for management of patients with ARVC include insertion of an automated implantable cardioverter–defibrillator (AICD) to prevent sudden cardiac death. However, despite the use of AICD and/or anti-arrhythmic drugs some patients suffer recurrent ventricular arrhythmias unresponsive to optimum medical management. We present two cases of ARVC with refractory recurrent ventricular arrhythmias that were successfully managed by left ventricular assist device (LVAD) implantation, as a bridge to transplant (BTT). These two cases are unconventional examples of use of LVAD, given the predominant right ventricular pathology of ARVC and the arrhythmogenic nature of their presentation. The novelty of these cases should be taken in the context of increasing pressure to standardize indications for use of mechanical circulatory support.     

S6K1 controls pancreatic β cell size independently of intrauterine growth restriction

Type 2 diabetes mellitus (T2DM) is a worldwide heath problem that is characterized by insulin resistance and the eventual loss of β cell function. As recent studies have shown that loss of ribosomal protein (RP) S6 kinase 1 (S6K1) increases systemic insulin sensitivity, S6K1 inhibitors are being pursued as potential agents for improving insulin resistance. Here we found that S6K1 deficiency in mice also leads to decreased β cell growth, intrauterine growth restriction (IUGR), and impaired placental development. IUGR is a common complication of human pregnancy that limits the supply of oxygen and nutrients to the developing fetus, leading to diminished embryonic β cell growth and the onset of T2DM later in life. However, restoration of placental development and the rescue of IUGR by tetraploid embryo complementation did not restore β cell size or insulin levels in S6K1^–/– embryos, suggesting that loss of S6K1 leads to an intrinsic β cell lesion. Consistent with this hypothesis, reexpression of S6K1 in β cells of S6K1^–/– mice restored embryonic β cell size, insulin levels, glucose tolerance, and RPS6 phosphorylation, without rescuing IUGR. Together, these data suggest that a nutrient-mediated reduction in intrinsic β cell S6K1 signaling, rather than IUGR, during fetal development may underlie reduced β cell growth and eventual development of T2DM later in life.     

Myocardial migration by fibroblast progenitor cells is blood pressure dependent in a model of angII myocardial fibrosis

Activation of the renin-angiotensin system (RAS) is thought to promote myocardial fibrosis. However, it is unclear whether this physiological fibrotic response results from chronic hemodynamic stress or from direct cellular signaling. Male C57B/6 mice were randomly assigned to receive angiotensin II (AngII) (2.0?μg?kg(-1)?min(-1)), AngII+hydralazine (6.9?μg?kg(-1)?min(-1)) or saline (control) via osmotic pumps for 7 days. Blood pressure was measured via noninvasive plethysmography. Hearts were harvested and processed for analysis. Cellular infiltration and collagen deposition were analyzed using histological staining. Molecular mediators were assessed using quantitative RT-PCR. As previously described, animals that received AngII developed hypertension and multifocal cellular infiltration by SMA(+)/CD133(+) fibroblast progenitors followed by collagen deposition. The coadministration of hydralazine with AngII completely inhibited the hypertensive effects of AngII (P0.01) and resulted in minimal cellular infiltration and minimal collagen deposition. These findings were in the context of persistent RAS activation, which was evidenced by elevation in serum aldosterone levels in animals that received AngII or AngII+hydralazine compared with animals that received saline. At the molecular level, infusion of AngII resulted in the significant upregulation of profibrotic factors (connective tissue growth factor-7.8±0.7 fold), proinflammatory mediators (TNFα-4.6±0.8 fold; IL-1β-6.4±2.6 fold) and chemokines (CCL2-3.8±1.0 fold; CXCL12-3.2±0.4 fold), which were inhibited when hydralazine was also infused. We provide evidence that myocardial infiltration by fibroblast progenitor cells secondary to AngII and the resultant fibrosis can be prevented by the addition of hydralazine. Furthermore, the beneficial effects of hydralazine were observed while maintaining RAS activation, suggesting that the mechanism of fibrosis is blood pressure dependent.