Review of Wireless RFID Strain Sensing Technology in Structural Health Monitoring.

Strain-based condition evaluation has garnered as a crucial method for the structural health monitoring (SHM) of large-scale engineering structures. The use of traditional wired strain sensors becomes tedious and time-consuming due to their complex wiring operation, more workload, and instrumentation cost to collect sufficient data for condition state evaluation, especially for large-scale engineering structures. The advent of wireless and passive RFID technologies with high efficiency and inexpensive hardware equipment has brought a new era of next-generation intelligent strain monitoring systems for engineering structures. Thus, this study systematically summarizes the recent research progress of cutting-edge RFID strain sensing technologies. Firstly, this study introduces the importance of structural health monitoring and strain sensing. Then, RFID technology is demonstrated including RFID technology's basic working principle and system component composition. Further, the design and application of various kinds of RFID strain sensors in SHM are presented including passive RFID strain sensing technology, active RFID strain sensing technology, semi-passive RFID strain sensing technology, Ultra High-frequency RFID strain sensing technology, chipless RFID strain sensing technology, and wireless strain sensing based on multi-sensory RFID system, etc., expounding their advantages, disadvantages, and application status. To the authors' knowledge, the study initially provides a systematic comprehensive review of a suite of RFID strain sensing technology that has been developed in recent years within the context of structural health monitoring.

A comparison between children and adolescents with autism spectrum disorders and healthy controls in biomedical factors, trace elements, and microbiota biomarkers: a meta-analysis.

Introduction: Autism spectrum disorder (ASD) is a multifaceted developmental condition that commonly appears during early childhood. The etiology of ASD remains multifactorial and not yet fully understood. The identification of biomarkers may provide insights into the underlying mechanisms and pathophysiology of the disorder. The present study aimed to explore the causes of ASD by investigating the key biomedical markers, trace elements, and microbiota factors between children with autism spectrum disorder (ASD) and control subjects. Methods: Medline, PubMed, ProQuest, EMBASE, Cochrane Library, PsycINFO, Web of Science, and EMBSCO databases have been searched for publications from 2012 to 2023 with no language restrictions using the population, intervention, control, and outcome (PICO) approach. Keywords including "autism spectrum disorder," "oxytocin," "GABA," "Serotonin," "CRP," "IL-6," "Fe," "Zn," "Cu," and "gut microbiota" were used for the search. The Joanna Briggs Institute (JBI) critical appraisal checklist was used to assess the article quality, and a random model was used to assess the mean difference and standardized difference between ASD and the control group in all biomedical markers, trace elements, and microbiota factors. Results: From 76,217 records, 43 studies met the inclusion and exclusion criteria and were included in this meta-analysis. The pooled analyses showed that children with ASD had significantly lower levels of oxytocin (mean differences, MD = -45.691, 95% confidence interval, CI: -61.667, -29.717), iron (MD = -3.203, 95% CI: -4.891, -1.514), and zinc (MD = -6.707, 95% CI: -12.691, -0.722), lower relative abundance of Bifidobacterium (MD = -1.321, 95% CI: -2.403, -0.238) and Parabacteroides (MD = -0.081, 95% CI: -0.148, -0.013), higher levels of c-reactive protein, CRP (MD = 0.401, 95% CI: 0.036, 0.772), and GABA (MD = 0.115, 95% CI: 0.045, 0.186), and higher relative abundance of Bacteroides (MD = 1.386, 95% CI: 0.717, 2.055) and Clostridium (MD = 0.281, 95% CI: 0.035, 0.526) when compared with controls. The results of the overall analyses were stable after performing the sensitivity analyses. Additionally, no substantial publication bias was observed among the studies. Interpretation: Children with ASD have significantly higher levels of CRP and GABA, lower levels of oxytocin, iron, and zinc, lower relative abundance of Bifidobacterium and Parabacteroides, and higher relative abundance of Faecalibacterium, Bacteroides, and Clostridium when compared with controls. These results suggest that these indicators may be a potential biomarker panel for the diagnosis or determining therapeutic targets of ASD. Furthermore, large, sample-based, and randomized controlled trials are needed to confirm these results.

Associations between rs3480 and rs16835198 gene polymorphisms of FNDC5 with type 2 diabetes mellitus susceptibility: a meta-analysis.

Background: FNDC5 is a novel and important player in energy regulation related to glucose metabolism and insulin levels. Thus, it may affect the incidence of type 2 diabetes mellitus (T2DM). Nevertheless, the association between FNDC5 single nucleotide polymorphisms (SNPs) and susceptibility to T2DM remains unclear. The aim of this meta-analysis was to explore whether the SNPs, rs3480 and rs16835198, are associated with the risk of T2DM. Methods: Studies published before February 1st, 2022 were screened to identify the included studies. R software was also applied for calculation of odds ratio (OR), 95% confidence interval (95% CI), heterogeneity, and sensitivity analysis. Results: Seven studies for rs3480 (involving 5475 patients with T2DM and 4855 healthy controls) and five studies for rs16835198 (involving 4217 patients with T2DM and 4019 healthy controls) were included in this meta-analysis. The results revealed a statistically significant association of rs3480 with T2DM under homozygote (GG vs AA: OR = 1.76, 95% CI = 1.31-2.37, P = 0.0002, I2 = 59%) genetic model. However, there was no statistically significant correlation between rs16835198 and susceptibility to T2DM under allelic (G vs T: OR = 1.33, 95% CI = 0.94-1.89, P = 0.11, I2 = 84%), heterozygote (GT vs TT: OR = 1.17, 95% CI = 0.80-1.69, P = 0.42, I2 = 71%), homozygote (GG vs TT: OR = 1.35, 95% CI = 0.95-1.94, P = 0.10, I2 = 62%), recessive (GG+GT vs TT: OR = 1.25, 95% CI = 0.88-1.79, P = 0.22, I2 = 72%), and dominant (GG vs GT+GG: OR = 1.20, 95% CI = 0.96-1.50, P = 0.11, I2 = 46%) genetic models. Conclusions: The present meta-analysis revealed that rs3480 in FNDC5 is significantly associated with susceptibility to T2DM, while rs16835198 does not show such an association.

Consensus on potential biomarkers developed for use in clinical tests for schizophrenia.

Background: Schizophrenia is a serious mental illness affecting approximately 20 million individuals globally. Both genetic and environmental factors contribute to the illness. If left undiagnosed and untreated, schizophrenia results in impaired social function, repeated hospital admissions, reduced quality of life and decreased life expectancy. Clinical diagnosis largely relies on subjective evidence, including self-reported experiences, and reported behavioural abnormalities followed by psychiatric evaluation. In addition, psychoses may occur along with other conditions, and the symptoms are often episodic and transient, posing a significant challenge to the precision of diagnosis. Therefore, objective, specific tests using biomarkers are urgently needed for differential diagnosis of schizophrenia in clinical practice. Aims: We aimed to provide evidence-based and consensus-based recommendations, with a summary of laboratory measurements that could potentially be used as biomarkers for schizophrenia, and to discuss directions for future research. Methods: We searched publications within the last 10 years with the following keywords: 'schizophrenia', 'gene', 'inflammation', 'neurotransmitter', 'protein marker', 'gut microbiota', 'pharmacogenomics' and 'biomarker'. A draft of the consensus was discussed and agreed on by all authors at a round table session. Results: We summarised the characteristics of candidate diagnostic markers for schizophrenia, including genetic, inflammatory, neurotransmitter, peripheral protein, pharmacogenomic and gut microbiota markers. We also proposed a novel laboratory process for diagnosing schizophrenia in clinical practice based on the evidence summarised in this paper. Conclusions: Further efforts are needed to identify schizophrenia-specific genetic and epigenetic markers for precise diagnosis, differential diagnosis and ethnicity-specific markers for the Chinese population. The development of novel laboratory techniques is making it possible to use these biomarkers clinically to diagnose disease.

The Application of Polycaprolactone Scaffolds with Poly(ε-caprolactone)-Poly(ethylene glycol)-Poly(ε-caprolactone) Loaded on Kidney Cell Culture.

Human embryonic kidney cells are the host of adenovirus type-5 (Ad5) amplification. An Ad5-vector-based COVID-19 vaccine has been proven to be tolerated and immunogenic in healthy adults. Therefore, a rationally designed scaffold for culturing human embryonic kidney cells is useful for further studying its mechanism of action. Herein, a three-dimensional layered reticulated polycaprolactone (PCL) scaffold coated with poly(ε-caprolactone)-poly(ethylene glycol)-poly(ε-caprolactone) (PCEC) was developed to proliferate human embryonic kidney cells and to be used to amplify the Ad5 vector. The results indicate that PCEC improves the hydrophilicity and the cell culture ability of PCL cell culture scaffolds, resulting in a three times higher cell proliferation ratio of human embryonic kidney cells compared with those grown on bare PCL cell culture scaffolds. Meanwhile, the cytotoxicity test results showed that the scaffold material is noncytotoxic. This work provides an effective and scalable method for the in-depth study of adenoviruses.

The Development of Pharmacological Therapies for Alzheimer's Disease.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that currently has no cure. The aged population is growing globally, creating an urgent need for more promising therapies for this debilitating disease. Much effort has been made in recent decades, and the field is highly dynamic, with numerous trials. The main focus of these trials includes disease modification and symptomatic treatment. Some have shown beneficial outcomes, while others have shown no significant benefits. Here, we cover the outcome of recently published AD clinical trials, as well as the mechanism of action of these therapeutical agents, to re-think drug development strategies and directions for future studies.