Autographa californica multiple nucleopolyhedrovirus ac66 is required for the efficient egress of nucleocapsids from the nucleus, general synthesis of preoccluded virions and occlusion body formation

AbstractAlthough orf66 (ac66) of Autographa californica multiple nucleopolyhedrovirus (AcMNPV) is conserved in all sequenced lepidopteran baculovirus genomes, its function is not known. This paper describes generation of an ac66 knockout AcMNPV bacmid mutant and analyses of the influence of ac66 deletion on the virus replication in Sf-9 cells so as to determine the role of ac66 in the viral life cycle. Results indicated that budded virus (BV) yields were reduced over 99% in ac66-null mutant infected cells in comparison to that in wild-type virus infected cells. Optical microscopy revealed that occlusion body synthesis was significantly reduced in the ac66 knockout bacmid-transfected cells. In addition, ac66 deletion interrupted preoccluded virion synthesis. The mutant phenotype was rescued by an ac66 repair bacmid. On the other hand, real-time PCR analysis indicated that ac66 deletion did not affect the levels of viral DNA replication. Electron microscopy revealed that ac66 is not essential for nucleocapsid assembly, but for the efficient transport of nucleocapsids from the nucleus to the cytoplasm. These results suggested that ac66 plays an important role for the efficient exit of nucleocapsids from the nucleus to the cytoplasm for BV synthesis as well as for preoccluded virion and occlusion synthesis

Comparison of dynamic changes of endogenous hormones between calli derived from mature and immature embryos of maize

Mature and immature embryos of maize inbred lines 87-1 and 137 were used as explants to induce callus on improved N6 medium. The contents of endogenous hormones abscisic acid (ABA), indoleacetic acid (IAA), gibberellic acid (GA3) and cytokinins (ZR) of immature, mature embryos and their corresponding calli were detected by method of enzyme-linked immunosorbant assay (ELISA). At the beginning of culture, IAA and GA3 levels decreased rapidly and reached their lowest levels at day 7, indicating that large amounts of IAA and GA3 are needed for germination. Levels of IAA and GA3 were highest at the beginning of embryonic callus formation from immature embryos, suggesting high levels of IAA and GA3 were beneficial to induction of embryonic callus from immature embryos (CIME). The IAA, GA3 and ABA contents and ration of IAA to ABA (IAA/ABA), GA3 to ABA (GA3/ABA) in callus of mature embryos (CME) were higher than those of CIME after the 14th day from culture initiation and the changes of ratios IAA/ABA and GA3/ABA increased rapidly in CME while they remained low in CIME during the whole experimental period. This inferred that high levels of IAA, GA3 or ABA and large increases in IAA/ABA and GA3/ABA might hinder the induction and maintenance of embryonic calli from mature embryos

Taking PISA Seriously : How Accurate are Low Stakes Exams?

doi: 10.3386/w24930PISA is seen as the gold standard for evaluating educational outcomes worldwide. Yet, as it is a low-stakes exam, students may not take it seriously resulting in downward biased scores and inaccurate rankings. This paper provides a method to identify and account for non-serious behavior by leveraging information in computer-based assessments in PISA 2015. The authors show that this bias is large: a country can rise up to 15 places in rankings if its students took the exam seriously. The researchers ask where the bias is coming from and show that around half of it comes from the proportion of non-serious students, while 36% comes from their ability, with the remaining coming from the extent of non-seriousnes

Mitochondrial dysfunctions induce PANoptosis and ferroptosis in cerebral ischemia/reperfusion injury: from pathology to therapeutic potential

Ischemic stroke (IS) accounts for more than 80% of the total stroke, which represents the leading cause of mortality and disability worldwide. Cerebral ischemia/reperfusion injury (CI/RI) is a cascade of pathophysiological events following the restoration of blood flow and reoxygenation, which not only directly damages brain tissue, but also enhances a series of pathological signaling cascades, contributing to inflammation, further aggravate the damage of brain tissue. Paradoxically, there are still no effective methods to prevent CI/RI, since the detailed underlying mechanisms remain vague. Mitochondrial dysfunctions, which are characterized by mitochondrial oxidative stress, Ca2+ overload, iron dyshomeostasis, mitochondrial DNA (mtDNA) defects and mitochondrial quality control (MQC) disruption, are closely relevant to the pathological process of CI/RI. There is increasing evidence that mitochondrial dysfunctions play vital roles in the regulation of programmed cell deaths (PCDs) such as ferroptosis and PANoptosis, a newly proposed conception of cell deaths characterized by a unique form of innate immune inflammatory cell death that regulated by multifaceted PANoptosome complexes. In the present review, we highlight the mechanisms underlying mitochondrial dysfunctions and how this key event contributes to inflammatory response as well as cell death modes during CI/RI. Neuroprotective agents targeting mitochondrial dysfunctions may serve as a promising treatment strategy to alleviate serious secondary brain injuries. A comprehensive insight into mitochondrial dysfunctions-mediated PCDs can help provide more effective strategies to guide therapies of CI/RI in IS

Meta-analysis of MMP-9 levels in the serum of patients with epilepsy

BackgroundEpilepsy’s pathogenesis and progression are significantly influenced by neuroinflammation, blood–brain barrier function, and synaptic remodeling function. Matrix metalloproteinase 9 (MMP-9), as a critical factor, may contribute to the development of epilepsy through one or more of the above-mentioned pathways. This study aims to evaluate and quantify the correlation between MMP-9 levels and epilepsy.MethodsWe conducted a comprehensive search of Embase, Web of Science, PubMed, Cochrane Library, WanFang DATA, VIP, and the CNKI to identify studies that investigate the potential association between MMP-9 and epilepsy. The data were independently extracted by two researchers and assessed for quality using the Cochrane Collaboration tool. The extracted data were analyzed using Stata 15 and Review Manager 5.4. The study protocol was registered prospectively at PROSPERO, ID: CRD42023468493.ResultsThirteen studies with a total of 756 patients and 611 matched controls met the inclusion criteria. Eight of these studies reported total serum MMP-9 levels, and the other five studies were used for a further subgroup analysis. The meta-analysis indicated that the serum MMP-9 level was higher in epilepsy patients (SMD = 4.18, 95% confidence interval = 2.18–6.17, p < 0.00001) compared with that in the control group. Publication bias was not detected according to Begg’s test. The subgroup analysis of country indicated that the epilepsy patients in China, Poland, and Egypt had higher levels of serum MMP-9 than the control group, with the increase being more pronounced in Egypt. The subgroup analysis of the age category demonstrated that the serum MMP-9 levels of the adult patients with epilepsy were significantly higher than those of the matched controls. However, the serum MMP-9 levels did not significantly differ in children with epilepsy. The subgroup analysis of the seizure types demonstrated substantial difference in the MMP-9 levels between patients of seizure-free epilepsy (patients who have been seizure-free for at least 7 days) and the control group. Meanwhile, the serum MMP-9 level in patients with epileptic seizures was significantly higher than that in the control group. The subgroup analysis based on seizure duration in patients showed that the serum MMP-9 levels at 1–3, 24, and 72 h after seizure did not exhibit significant differences between female and male patients with epilepsy when compared with the control group. The serum MMP-9 levels at 1–3 and 24 h were significantly higher than those of the matched controls. Nevertheless, the serum MMP-9 level at 72 h was not significantly different from that in the control group.ConclusionThis meta-analysis presents the first comprehensive summary of the connection between serum MMP-9 level and epilepsy. The MMP-9 levels in epilepsy patients are elevated. Large-scale studies with a high level of evidence are necessary to determine the exact relationship between MMP-9 and epilepsy