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The use of stimulant medications for treatment of ADHD has raised concern as to whether they adversely impact linear growth. Previous studies have indicated that stimulant medications may suppress growth for a short period after treatment initiation; however, more information is needed to evaluate the long-term effects on final adult stature. This mini review aims to evaluate the effect of stimulant medications on final adult height in children with ADHD. We performed a literature review across PubMed/MEDLINE database. Only articles that included data on final adult height or near final adult height (age≥16 or 17 years) were included. Early studies investigating the long-term impacts of stimulant medications observed growth suppression during the active treatment period, but when comparing final adult height, there was no difference between the control and ADHD groups. A recent larger comprehensive study (Multimodal Treatment of ADHD study) has suggested that the long-term use of significant doses of stimulants during childhood may compromise final adult height to a clinically significant degree when comparing adult height across three long-term patterns of stimulant treatment (Consistent, Intermittent, Negligible). The consistent use subgroup was significantly shorter than other subgroups. For children with ADHD, a significant long-term dose of stimulant treatment should be used with caution to avoid diminishing adult height potential. Pediatric endocrinologists should consider chronic use of stimulants as a factor contributing to reduced adult height. [ABSTRACT FROM AUTHOR]

Abstract Background Mounting evidence has suggested that plasminogen activator inhibitor-1 (PAI-1) is a candidate for increased risk of diabetic retinopathy. Studies have reported that insertion/deletion polymorphism in the PAI-1 gene may influence the risk of this disease. To comprehensively address this issue, we performed a meta-analysis to evaluate the association of PAI-1 4G/5G polymorphism with diabetic retinopathy in type 2 diabetes. Methods Data were retrieved in a systematic manner and analyzed using Review Manager and STATA Statistical Software. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. Results Nine studies with 1, 217 cases and 1, 459 controls were included. Allelic and genotypic comparisons between cases and controls were evaluated. Overall analysis suggests a marginal association of the 4G/5G polymorphism with diabetic retinopathy (for 4G versus 5G: OR 1.13, 95%CI 1.01 to 1.26; for 4G/4G versus 5G/5G: OR 1.30, 95%CI 1.04 to 1.64; for 4G/4G versus 5G/5G + 4G/5G: OR 1.26, 95%CI 1.05 to 1.52). In subgroup analysis by ethnicity, we found an association among the Caucasian population (for 4G versus 5G: OR 1.14, 95% CI 1.00 to 1.30; for 4G/4G versus 5G/5G: OR 1.33, 95%CI 1.02 to 1.74; for 4G/4G versus 5G/5G + 4G/5G: OR 1.41, 95%CI 1.13 to 1.77). When stratified by the average duration of diabetes, patients with diabetes histories longer than 10 years have an elevated susceptibility to diabetic retinopathy than those with shorter histories (for 4G/4G versus 5G/5G: OR 1.47, 95%CI 1.08 to 2.00). We also detected a higher risk in hospital-based studies (for 4G/4G versus 5G/5G+4G/5G: OR 1.27, 95%CI 1.02 to 1.57). Conclusions The present meta-analysis suggested that 4G/5G polymorphism in the PAI-1 gene potentially increased the risk of diabetic retinopathy in type 2 diabetes and showed a discrepancy in different ethnicities. A higher susceptibility in patients with longer duration of diabetes (more than 10 years) indicated a gene-environment interaction in determining the risk of diabetic retinopathy.

New Findings: What is the topic of this review?Mechanisms regulating bone length and skeletal proportionsWhat advances does it highlight?The study of differential bone length between leg and finger bones, metatarsals of the Egyptian jerboa and genomic analysis of giraffes. Among mammalian species, skeletal structures vary greatly in size and shape, leading to a dramatic variety of body sizes and proportions. How different bones grow to different lengths, whether among different species, different individuals of the same species, or even in different anatomical parts of our the body, has always been a fascinating subject of research in biology and physiology. In the current review, we focus on some of the recent advances in the field and discuss how these provided important new insights into the mechanisms regulating bone length and skeletal proportions. [ABSTRACT FROM AUTHOR]

From the lungs to the central nervous system, cilia-driven fluid flow plays a fundamental role in many facets of life. Yet, there are few quantitative methods for analysing the function of ciliated surfaces. Here, we report a novel microfluidic approach for quantifying the performance of a ciliated surface using mixing performance as an integrated readout. [ABSTRACT FROM AUTHOR]

3D printing of a flexible polyurethane elastomer is highly demandable for its potential to revolutionize industries ranging from footwear to soft robotics thanks to its exceptional design flexibility and elasticity performance. Nevertheless, conventional methods like fused deposition modeling (FDM) and vat photopolymerization (VPP) polyurethane 3D printing typically limit material options to thermoplastic or photocurable polyurethanes. In this research, a water-borne polyurethane ink was synthesized for direct ink writing (DIW) 3D printing through the incorporation of cellulose nanofibrils (CNFs), enabling direct printing of complex, monolithic elastomeric structures at room temperature that can maintain the designed structure. Additionally, a solvent-induced fast solidification (SIFS) method was introduced to facilitate room-temperature curing and enhance mechanical properties. The 3D-printed WPU structures demonstrated strong interfacial adhesion, exhibiting high ultimate tensile strength of up to 22 MPa and an elongation at break of 951%. The 3D-printed WPU structures also demonstrated outstanding resilience and durability, capable of enduring more than 100 cycles of compression and tension as well as withstanding vehicle crushing and heavy lifting. This method also shows suitability for 3D printing complex structures such as a vase and an octopus.

Overgrowth syndromes can be caused by pathogenic genetic variants in epigenetic writers, such as DNA and histone methyltransferases. However, no overgrowth disorder has previously been ascribed to variants in a gene that acts primarily as an epigenetic reader. Here, we studied a male individual with generalized overgrowth of prenatal onset. Exome sequencing identified a hemizygous frameshift variant in Spindlin 4 (SPIN4), with X-linked inheritance. We found evidence that SPIN4 binds specific histone modifications, promotes canonical WNT signaling, and inhibits cell proliferation in vitro and that the identified frameshift variant had lost all of these functions. Ablation of Spin4 in mice recapitulated the human phenotype with generalized overgrowth, including increased longitudinal bone growth. Growth plate analysis revealed increased cell proliferation in the proliferative zone and an increased number of progenitor chondrocytes in the resting zone. We also found evidence of decreased canonical Wnt signaling in growth plate chondrocytes, providing a potential explanation for the increased number of resting zone chondrocytes. Taken together, our findings provide strong evidence that SPIN4 is an epigenetic reader that negatively regulates mammalian body growth and that loss of SPIN4 causes an overgrowth syndrome in humans, expanding our knowledge of the epigenetic regulation of human growth.