No abstract

<b><i>Background:</i></b> Although stroke is rare among the pediatric population, it is nevertheless associated with serious or life-threatening consequences. The etiologic factors of acute ischemic stroke (AIS) are likely to vary over the course of childhood development. The incidence rates of AIS, not previously systematically examined by pediatric age subgroup, could guide studies of its etiology. <b><i>Objective:</i></b> The aim of this study is to evaluate the incidence rate of AIS by age-group in the pediatric population (aged 0–17/18 years) and identify any common trends or sources of variability across different countries. <b><i>Methods:</i></b> Rates of pediatric AIS were collated from a systematic literature review of published studies globally (1983–2020) and hospitalization records from Europe and the USA (2015–2018). Records that were included in the analysis reported the code or description used for AIS diagnosis and age-specific data for children aged 0–17/18 years. AIS incidence rates were summarized by age-group, data source, country, and geographic region. A meta-analysis was conducted to assess the heterogeneity of AIS rates in neonates. <b><i>Results:</i></b> The pooled AIS incidence rate was 5.6 per 100,000 children across all records. When only records reporting the AIS incidence rates for children across the full age range (0–17/18 years) were analyzed, the pooled AIS incidence rate was 4.6 per 100,000 children and ranged from 7.0 per 100,000 (Germany) to 1.3 per 100,000 (Denmark). The highest pooled rates were observed in the 0–28-day age-group (24.6 per 100,000 live births), declining to the lowest rates in the 5–9-year age-group, and rising again in the 10–17/18-year age-group. AIS rates were the most heterogeneous in the 0–28-day age-group and across European countries. Significantly higher AIS rates in neonates were observed from hospital databases (35.9 per 100,000) than in the literature (19.4 per 100,000). AIS rates may be underestimated as pediatric AIS events are rare and challenging to diagnose, and limited age-specific data are available. <b><i>Conclusions:</i></b> Incidence rates of pediatric AIS by age-groups followed a consistent overall pattern of a reverse J-shaped curve, with the highest rates in neonates, across predominantly European and North American countries. Further research is warranted to examine if this pattern is observed in other geographic regions and to identify AIS risk factors specific to different phases of childhood development.

Current detection methods for contamination of aflatoxin and fumonisin used in the corn industry are based on bulk level. However, literature demonstrates that contamination of these mycotoxins is highly skewed and bulk samples do not always represent accurately the overall contamination in a batch of corn. Single kernel analysis can provide an insightful level of analysis of the contamination of aflatoxin and fumonisin, as well as suggest a possible remediation to the skewness present in bulk detection. Current literature describes analytical methods capable of detecting aflatoxin and fumonisin at a single kernel level, such as liquid chromatography, fluorescence imaging, and reflectance imaging. These methods could provide tools to classify mycotoxin contaminated kernels and study potential co-occurrence of aflatoxin and fumonisin. Analysis at a single kernel level could provide a solution to the skewness present in mycotoxin contamination detection and offer improved remediation methods through sorting that could impact food security and management of food waste.

No abstract

Long non-coding RNAs (lncRNAs) have been identified as critical regulators in gastric cancer (GC) progression. However, whether lncRNA small nucleolar host gene 4 (SNHG4) functions in GC development remains unknown. In this study, the bio-functional role of SNHG4 and its potential mechanism on GC progression were systematically dissected. To investigate the role of SNHG4 in GC, we silenced SNHG4 using short hairpin RNAs (shRNAs) to perform loss-of-function assays. The results showed that SNHG4 expression in GC cells was at a higher level compared to normal gastric mucosal epithelial cells. Knockdown of SNHG4 dramatically suppressed proliferation, migration and invasion, and blocked cell cycle progression of GC cells. Moreover, knockdown of SNHG4 upregulated microRNA-204-5p (miR-204-5p) expression, whereas downregulated ribonucleotide reductase subunit M2 (RRM2) expression in GC cells. Dua l-luciferase reporter assay results showed that miR-204-5p was a direct target of SN HG4. Additionally, knockdown of SHNG4 suppressed GC tumorigenesis in xenograft mouse models. Taken together, these data demonstrated that knockdown of SNHG4 suppressed GC development by targeting miR-204-5p.