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Biological evidence technology plays an important role in the field of crime scene investigation. DNA technology is known as one of the important ways to make a breakthrough in the resolution of a criminal case. Nonetheless, there are some problems in on-site experiment-based teaching during the COVID-2019 pandemic, which limits the students' incentives to acquire knowledge about DNA. Under these conditions, the goals and requirements of the Biological Evidence Technology course cannot be achieved. A virtual simulation experiment can solve these problems online. The students can gain a deeper understanding of the process and method of human DNA extraction and identification, and thus, the impact of experiment-based teaching improves. In this paper, we discuss the contents of DNA experiments, specifications of the simulation system, system requirements, the implementation process, and other parameters of the design. We investigated the early teaching effect. A virtual simulation experiment with DNA can overcome the limitations of devices (and other equipment) and spatial and temporal limitations during the COVID-2019 pandemic. Students can participate in the whole process of experiment-based teaching. Teaching mode “Internet + laboratory” increases the open access and sharing of experiment-based teaching resources.

In this study, a sensitive and rapid magnetic solid-phase microextraction (MSPE) procedure based on Fe3O4 nanoparticle-modified, multi-walled carbon nanotubes combined with a gas chromatography/electron capture detector (GC/ECD) was developed to quantify pyrethroids in human blood samples. This study compared liquid–liquid extraction and solid-phase extraction methods and found that the MSPE-GC/ECD method had many advantages, such as high recovery rate, high extraction efficiency, high detection sensitivity, low limit of detection, and simple operation. It can meet the actual requirements for the determination of synthetic pyrethroids in human blood.

Objectives: The present study mainly focused on the assessment of developmental toxicity induced by exposure to brodifacoum (BDF) in zebrafish at early life stages. Material and Methods: Zebrafish embryos were exposed to 0.2, 0.4, and 0.8 mg/L of BDF from 6 to 96 hr post‐fertilization (hpf), and the toxic effects of BDF on early embryonic development were investigated in terms of morphological changes, oxidative stress, and alterations in heart development‐related genes. Results: The experimental results showed that BDF significantly decreased the heart rate, survival rate, body length, and spontaneous movements of zebrafish embryos at 0.8 mg/L, and the morphological developmental abnormalities were also observed at 96 hpf. In addition, exposure to BDF significantly increased oxidative stress levels in zebrafish embryos by increasing the enzymatic activities of catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA) levels, and decreased glutathione (GSH) levels. Furthermore, BDF treatment‐induced alterations in the expression levels of the heart development‐related genes (gata4, sox9b, tbx2b, and nppa). Conclusion: Results from this study indicated that exposure to BDF could lead to marked growth inhibition and significantly alter the activities of antioxidant enzymes in zebrafish embryos. Moreover, BDF exposure exhibited severe cardiotoxicity and significantly disrupted heart development‐related genes. The results indicated that BDF could induce developmental and cardiac toxicity in zebrafish embryos. [ABSTRACT FROM AUTHOR]

Anisodamine is one of the major components of the tropine alkaloid family and is widely used in the treatment of pain, motion sickness, pupil dilatation, and detoxification of organophosphorus poisoning. As a muscarinic receptor antagonist, the low toxicity and moderate drug effect of anisodamine often result in high doses for clinical use, making it important to fully investigate its toxicity. In this study, zebrafish embryos were exposed to 1.3‐, 2.6‐, and 5.2‐mM anisodamine for 7 days to study the toxic effects of drug exposure on pigmentation, mineral density, craniofacial area, and eye development. The results showed that exposure to anisodamine at 1.3 mM resulted in cranial malformations and abnormal pigmentation in zebrafish embryos; 2.6‐ and 5.2‐mM anisodamine resulted in significant eye development defects and reduced bone density in zebrafish embryos. The associated toxicities were correlated with functional development of neural crest cells through gene expression (col1a2, ddb1, dicer1, mab21l1, mab21l2, sox10, tyrp1b, and mitfa) in the dose of 5.2‐mM exposed group. In conclusion, this study provides new evidence of the developmental toxicity of high doses of anisodamine in aqueous solutions to organisms and provides a warning for the safe use of this drug. We studied the early developmental toxicity of anisodamine in zebrafish. The results showed that anisodamine exposure resulted in toxicity such as increased pigmentation, decreased mineral density, smaller craniofacial area, and smaller eyes. Alterations in related genes were associated with the functional development of neural crest cells. [ABSTRACT FROM AUTHOR]

Acetylcholinesterase (AChE) is the crucial enzyme in the central nervous system. It is the target of various organophosphorus nerve agents and pesticides, and the inhibition of AChE is a therapeutic strategy for the treatment of various neurological‐related diseases. The Glu202 is a key residue adjacent to the catalytic His447 and plays important role in catalysis. Although the Glu202 has long been considered as negatively charged in many studies, more and more evidences support a protonated Glu202. However, Glu202 is freely accessible by solvent, and thus it seems more reasonable for Glu202 to majorly take the deprotonated state. In the present work, we carried out a series of molecular dynamics simulations with the Glu202 adopting different protonation states. Our results show that the protonated Glu202 is important in maintaining the key hydrogen bond network that supports the catalytic triad, whereas the deprotonated Glu202 results in the collapse of the key hydrogen bond network which consequently destabilizes the catalytic His447. We also notice that different protonation states of Glu202 merely alters the binding mode of ACh. However, since the catalytic His447 is disrupted if Glu202 is deprotonated, His447 cannot facilitate the nucleophilic attack performed by Ser203. Therefore, the catalytic efficiency of ACh hydrolysis should be remarkably decreased if Glu202 is deprotonated. Our findings suggest that, when designing and developing highly active AChE inhibitors or proposing mechanistic hypotheses for AChE‐catalyzed reactions, the protonated state of Glu202 should be considered. [ABSTRACT FROM AUTHOR]