Research Priorities for Childhood Apraxia of Speech: A Long View

This article introduces the Journal of Speech, Language, and Hearing Research Special Issue: Selected Papers From the 2022 Apraxia Kids Research Symposium. The field of childhood apraxia of speech (CAS) has developed significantly in the past 15 years, with key improvements in understanding of basic biology including genetics, neuroscience, and computational modelling; development of diagnostic tools and methods; diversity of evidence-based interventions with increasingly rigorous experimental designs; and understanding of impacts beyond impairment-level measures. Papers in this special issue not only review and synthesize the some of the substantial progress to date but also present novel findings addressing critical research gaps and adding to the overall body of knowledge. A second aim of this prologue is to report the current research needs in CAS, which arose from symposium discussions involving researchers, clinicians, and Apraxia Kids community members (including parents of children with CAS). Four primary areas of need emerged from discussions at the symposium. These were: (a) What questions should we ask? (b) Who should be in the research? (c) How do we conduct the research? and (d) How do we move from research to practice? Across themes, symposium attendees emphasized the need for CAS research to better account for the diversity of people with CAS and improve the timeliness of implementation of high-level evidence-based practice across the lifespan. It is our goal that the articles and prologue discussion in this special issue provide an appreciation of advancements in CAS research and an updated view of the most pressing needs for future research

C-reactive protein levels predict systolic heart failure and outcome in patients with first ST-elevation myocardial infarction treated with coronary angioplasty

Introduction: There is growing evidence that inflammation plays a pivotal role in the etiology and progression of atherosclerosis. High C-reactive protein (CRP) levels have been associated with high mortality in patients with acute myocardial infarction (AMI). Furthermore, in animal models CRP has been found to significantly increase infarct size. So there is growing evidence that CRP is not only a marker for cardiovascular disease but also might be pathogenic. The aim of our study was to test the hypothesis that peak CRP levels could predict heart failure (HF) in ST-elevation myocardial infarction (STEMI) patients. Material and methods: Eighty-one consecutive patients with STEMI were prospectively enrolled in the study. C-reactive protein concentrations were measured on admission and after 6, 12, 24, 30, 48, 72 and 96 h. We assessed the association between the elevation of CRP, heart failure and cardiovascular mortality following the first 12 months after STEMI. Results: C-reactive protein levels reached a peak after 48 h. Patients with STEMI and signs of HF showed significantly higher peak CRP levels. We found a positive correlation between maximum CK levels and peak CRP and a negative correlation between left ventricular ejection fraction (EF) and peak CRP. One year total mortality and HF mortality rates were found to be higher in patients with peak CRP > 47.5 mg/l than in those with CRP below that level (p < 0.001). Conclusions: Peak CRP levels in STEMI patients predict emergence of HF. Peak CRP is also a strong predictor of global and cardiovascular mortality during the following year after STEMI

Patients with acute coronary syndromes express enhanced CD40 ligand/CD154 on platelets

OBJECTIVE—To investigate whether CD40L/CD154 on platelets and soluble CD40L/CD154 may play a role in the inflammatory process of acute coronary syndromes.
DESIGN AND SETTING—Observational study in a university hospital.
PATIENTS—15 patients with acute myocardial infarction, 25 patients with unstable angina, 15 patients with stable angina, and 12( )controls.
MAIN OUTCOME MEASURES—CD40L/CD154 on platelets, P-selectin/CD62P on platelets, soluble CD40L/CD154 serum concentrations.
RESULTS—Mean (SD) CD40L/CD154 expression on platelets was 6.2 (2.8) MFI (mean fluorescence intensity) in the infarct group, 11 (3.3) MFI in the unstable angina group (p < 0.001 v infarction), 3.6( )(0.9) MFI in the stable angina group (p < 0.01 v infarction; p < 0.001 v unstable angina), and 3.2 (1.0) MFI in the controls (p < 0.01 v infarction; p < 0.001 v unstable angina; NS v stable angina). Soluble CD40L/CD154 concentration was 5.2 (1.1) ng/ml in the infarct group, 4.2 (0.7) ng/ml in the unstable angina group (p < 0.001 v infarction), 2.9 (1.0) ng/ml in stable angina group (p < 0.001 v infarction and unstable angina), and 3.0 (0.5) ng/ml in the controls (p < 0.001 v infarction and unstable angina; NS v stable angina). At a six months follow up, there was lower expression of CD40L/CD154 on platelets in patients with unstable angina (12.3( )(3.6) v 3.8 (1.2) MFI, p < 0.0001) and acute myocardial infarction (6.2 (2.8) v 3.5 (0.8) MFI, p < 0.01) compared with their admission values six months earlier. Patients with unstable angina who needed redo coronary angioplasty (PTCA) or who had recurrence of angina were characterised by increased CD40L/CD154 expression on platelets compared with the remainder of the study group (recurrence of angina: 12.7 (3.2) v 9.7 (1.6) MFI, p < 0.05; re-do PTCA: 14.3( )(4.2) v 10.3 (2.1) MFI, p < 0.05).
CONCLUSIONS—Both CD40L/CD154 on platelets and soluble CD40L/CD154 are raised in patients with unstable angina and myocardial infarction. These findings suggest that CD40-CD40L/CD154 interactions may play a pathogenic role in triggering and propagation of acute coronary syndromes.


Keywords: acute coronary syndromes; unstable angina; CD40L/CD154; platelet

Electron beam irradiation enhanced of Hibiscus cannabinus fiber strengthen polylactic acid composites

This paper reported the effects of increasing Hibiscus canttabinus fiber (also known as kenaf fiber) loading level on properties of electron beam irradiated polylactic acid/low density polyethylene (PLA/LDPE). PLA and LDPE were compounded with 5-20 parts per hundred resins (phr) of kenaf respectively to enhance mechanical properties. The compounded kenaf added PLA/LDPE samples were electron beam irradiated from 15 to 60 kGy. The physical properties of kenaf added PLA/LDPE samples were characterized using gel content, X-Ray diffraction and scanning electron microscopy analysis. The results showed that the increasing of irradiation dosages in PLA/LDPE have gradually increased the gel content and tensile strength due to the formation of crosslinking networks in polymer matrix. However, the higher loading level of kenaf and irradiation dosages could decrease the elongation at break of PLA/LDPE samples. This is due to the restriction of polymer chains mobility as resulted by the poor interfacial adhesion between polymer matrix and kenaf particles as well as the formation of crosslinking networks in polymer matrix limits the sliding of polymer chains. Meanwhile, the increasing of kenaf loading level also has gradually increased the crystallinity of PLA/LDPE matrix. It is concluded that the electron beam irradiation dosages and amount of kenaf fiber in PLA/LDPE matrix should be kept at maximum 45 kGy and 15 phr, respectively for better combination to enhance the properties of the composites

Abdominal Aortic Endograft Implantation Immediately Induces Vascular Stiffness Gradients That May Promote Adverse Aortic Neck Dilatation: Results of A Porcine Ex Vivo Study

Purpose: Endovascular aortic repair (EVAR) is the method of choice for most abdominal aortic aneurysm (AAA) patients requiring intervention. However, chronic aortic neck dilatation (AND) following EVAR progressively weakens the structural seal between vessel and endograft and compromises long-term results of the therapy. This experimental ex vivo study seeks to investigate mechanisms of AND. Materials and Methods: Porcine abdominal aortas (n=20) were harvested from slaughterhouse pigs and connected to a mock circulation. A commercially available endograft was implanted (n=10) or aortas were left untreated as controls (n=10). Vascular circumferential strain was assessed via ultrasound in defined aortic segments as a parameter of aortic stiffness. Histology and aortic gene expression analysis were performed to investigate potential changes of aortic wall structure and molecular differences due to endograft implantation. Results: We found that endograft implantation acutely induces a significant stiffness gradient directly at the interface between stented and unstented aortic segments under pulsatile pressure. Comparing stented aortas with unstented controls, we detected increased aortic expression levels of inflammatory cytokines ( Il6 and Ccl2) and matrix metalloproteinases ( Mmp2 and Mmp9) after 6 hours of pulsatile pressurization. This effect, however, was abolished when repeating the same experiment under 6 hours of static pressure. Conclusions: We identified endograft-induced aortic stiffness gradients as an early trigger of inflammatory aortic remodeling processes that might promote AND. These results highlight the importance of adequate endograft designs to minimize vascular stiffness gradients and forestall late complications, such as AND. Clinical Impact AND may compromise the long-term results following endovascular aortic repair. However, the mechanisms behind the underlying detrimental aortic remodeling are still unclear. In this study we find that endograft-induced aortic stiffness gradients induce an inflammatory aortic remodeling response consistent with AND. This novel pathomechanistic insight may guide the design of new aortic endografts that minimize vascular stiffness gradients and forestall late complications such as AND.Deutsche Forschungsgemeinschaft https://doi.org/10.13039/501100001659Deutsche Forschungsgemeinschaft https://doi.org/10.13039/50110000165