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Interestingly, the expression of Wnt4, Wnt7a, and active β-catenin was increased, but not notch family members, in MSC-CM-treated organoid after irradiation. Treatment of recombinant mouse Wnt4 and Wnt7a after irradiation improved to some extent intestinal epithelial regeneration both in vitro and in vivo. Overall, these results suggested that intestinal organoids recapitulated the physiological stress response of the intestinal epithelium in vivo. Thus, our findings provided important insights into the physiology of intestinal organoids and may contribute to the development of strategies to enhance the functional maturation of engineered organoids.Hand, Foot, and Mouth disease (HFMD) is a mild exanthematous and febrile disease occurs in children aged ≤10 years old. The present study highlights clinical, epidemiological characteristics, distribution of enterovirus (EV) types, and sub genotypes in HFMD cases reported during 2017 to 2018 in Western India. A total of 93 clinical samples collected from 68 HFMD cases were included. The presence of EV-RNA was determined by 5'UTR based nested reverse transcription polymerase chain reaction followed by molecular typing, sub genotyping by VP1/2A junction or VP1, full VP1 gene amplification, and phylogenetic analysis. The study reports 80.64% (75/93) EV positivity and 94.66% (71/75) typing rate, with a predominant circulation of CVA16 and CVA6 strains. CD38 inhibitor 1 Sequence analysis revealed the presence of coxsackievirus (CV)A16 (57.7%), CVA6 (40.8%), and Echo1 (1.4%) strains. EV infections were predominantly observed in children aged 1 to 3 years old (43.9%). Although cases were reported throughout the year, peaked in July (15.8%) and August (24.6%) months and persisted till September (19.3%). All the CVA16 and CVA6 positive strains were genotyped using full VP1 gene amplification. All CVA16 Indian strains (n = 41) were clustered with rarely reported B1c sub genotype and CVA6 strains (n = 29) with E2 sub-lineage. The study highlights the genetic characteristics of circulating CVA16, CVA6, and Echo1 strains in HFMD cases from Western India. The emergence of CVA16 B1c genotype and sub-lineage E2 of CVA6 strains and their constant circulation further demands systemic surveillance studies on HFMD from different parts of India to facilitate the rapid diagnosis of CVA16 and CVA6 strains using the molecular and serological based approach and for intervention strategies.Preimplantation genetic testing for aneuploidy (PGT-A) by copy number analysis is now widely used to select euploid embryos for transfer. Whole or partial chromosome aneuploidy can arise in meiosis, predominantly female meiosis, or in the postzygotic, mitotic divisions during cleavage and blastocyst formation, resulting in chromosome mosaicism. Meiotic aneuploidies are almost always lethal, however, the clinical significance of mitotic aneuploidies detected by PGT-A is not fully understood and healthy live births have been reported following transfer of mosaic embryos. Here, we used single nucleotide polymorphism genotyping of both polar bodies and embryo samples to identify meiotic aneuploidies and compared copy number changes for meiotic and presumed mitotic aneuploidies in trophectoderm cells biopsied at the blastocyst stage and arrested embryos. PGT-A detected corresponding full copy number changes (≥70%) for 36/37 (97%) maternal meiotic aneuploidies. The number of presumed mitotic copy number changes detected exceeded those of meiotic origin. Although mainly in the mosaic range, some of these mitotic aneuploidies had copy number changes ≥70% and would have been identified as full aneuploidies. Interestingly, many arrested embryos had multiple mitotic aneuploidies across a broad range of copy number changes, which may have arisen through tripolar spindle and other mitotic abnormalities.
Dural arteriovenous fistula (DAVFs) in the transverse sinus (TS)/sigmoid sinus (SS) and cavernous sinus (CS) are observed frequently in the clinic. This study aimed to detect DAVFs with ultrasound and compare carotid ultrasound findings between these conditions.
We retrospectively reviewed 26 patients with either a TS/SS DAVF or a CS DAVF who were admitted to our hospital for evaluation of DAVFs from 2014 to 2018. The shunt site decision was made by neuroendovascular experts, whereas carotid ultrasound examinations were performed by ultrasound specialists. The flow velocity of the ipsilateral external carotid artery was reviewed in all 26 patients, whereas that of the occipital artery (OA) was examined in 20 patients. Blood flow velocities were compared between the TS/SS DAVF and CS DAVF groups.
The study included 18 patients with a TS/SS DAVF (11 women and 7 men; mean age ± SD, 65.3 ± 18.6 years) and 8 patients with a CS DAVF (7 women and 1 man; mean age, 70.4 ± 9.3 years). Evaluations of feeder arteries on cerebral angiography showed that all patients had dural branches from the internal carotid and middle meningeal arteries as feeders of CS DAVFs, whereas the OA was the major feeder source of all TS/SS DAVF cases. The end-diastolic velocity (EDV) of the external carotid artery was significantly higher in patients with a TS/SS DAVF compared with those with a CS DAVF (P = .004). The EDV of the OA was significantly elevated in TS/SS DAVF cases compared with CS DAVF cases (P < .001).
Duplex ultrasound parameters are significantly different between patients with TS/SS and CS DAVFs. An increased EDV of the OA can predict the presence of a TS/SS DAVF.
Duplex ultrasound parameters are significantly different between patients with TS/SS and CS DAVFs. An increased EDV of the OA can predict the presence of a TS/SS DAVF.A nanometric revolution is underway, promising technical innovations in a wide range of applications and leading to a potential boost in environmental discharges. The propensity of nanoparticles (NPs) to be transferred throughout trophic chains and to generate toxicity was mainly assessed in primary consumers, whereas a lack of knowledge for higher trophic levels persists. The present study focused on a predatory fish, the European eel (Anguilla anguilla) exposed to gold NPs (AuNPs; 10 nm, polyethylene glycol-coated) for 21 d at 3 concentration levels in food 0 (NP0), 1 (NP1), and 10 (NP10) mg Au kg-1 . Transfer was assessed by Au quantification in eel tissues, and transcriptomic responses in the liver and brain were revealed by a high-throughput RNA-sequencing approach. Eels fed at NP10 presented an erratic feeding behavior, whereas Au quantification only indicated transfer to intestine and kidney of NP1-exposed eels. Sequencing of RNA was performed in NP0 and NP1 eels. A total of 258 genes and 156 genes were significantly differentially transcribed in response to AuNP trophic exposure in the liver and brain, respectively. Enrichment analysis highlighted modifications in the immune system-related processes in the liver. In addition, results pointed out a shared response of both organs regarding 13 genes, most of them being involved in immune functions. This finding may shed light on the mode of action and toxicity of AuNPs in fish. Environ Toxicol Chem 2020;392450-2461. © 2020 SETAC.
K
1.2 channels, encoded by the KCNA2 gene, regulate neuronal excitability by conducting K
upon depolarization. A new KCNA2 missense variant was discovered in a patient with epilepsy, causing amino acid substitution F302L at helix S4, in the K
1.2 voltage-sensing domain. Immunocytochemistry and flow cytometry showed that F302L does not impair KCNA2 subunit surface trafficking. Molecular dynamics simulations indicated that F302L alters the exposure of S4 residues to membrane lipids. Voltage clamp fluorometry revealed that the voltage-sensing domain of K
1.2-F302L channels is more sensitive to depolarization. Accordingly, K
1.2-F302L channels opened faster and at more negative potentials; however, they also exhibited enhanced inactivation that is, F302L causes both gain- and loss-of-function effects. Coexpression of KCNA2-WT and -F302L did not fully rescue these effects. The proband's symptoms are more characteristic of patients with loss of KCNA2 function. Enhanced K
1.2 inactivation could lead toof KV 1.2 function via accelerated inactivation onset, decelerated recovery and shifted inactivation voltage dependence to more negative potentials. These effects, which are not fully rescued by coexpression of wild-type and mutant KCNA2 subunits, probably result from the enhancement of VSD function, as demonstrated by optically tracking VSD depolarization-evoked conformational rearrangements. In turn, molecular dynamics simulations suggest altered VSD exposure to membrane lipids. Compared to other encephalopathy patients with KCNA2 mutations, the proband exhibits mild neurological impairment, more characteristic of patients with KCNA2 loss of function. Based on this information, we propose a mechanism of epileptogenesis based on enhanced KV 1.2 inactivation leading to increased synaptic release preferentially in excitatory neurons, and hence the perturbation of the excitatory/inhibitory balance of neuronal circuits.Understanding the complex growth and metabolic dynamics in microorganisms requires advanced kinetic models containing both metabolic reactions and enzymatic regulation to predict phenotypic behaviors under different conditions and perturbations. Most current kinetic models lack gene expression dynamics and are separately calibrated to distinct media, which consequently makes them unable to account for genetic perturbations or multiple substrates. This challenge limits our ability to gain a comprehensive understanding of microbial processes towards advanced metabolic optimizations that are desired for many biotechnology applications. Here, we present an integrated computational and experimental approach for the development and optimization of mechanistic kinetic models for microbial growth and metabolic and enzymatic dynamics. Our approach integrates growth dynamics, gene expression, protein secretion, and gene-deletion phenotypes. We applied this methodology to build a dynamic model of the growth kinetics in metabolic pathways to produce mechanistic models for the comprehensive understanding of enzymatic functions in multiple substrates.Pine wood nematode (PWN; Bursaphelenchus xylophilus), a destructive pest of Pinus massoniana, is causing a severe epidemic of pine wilt disease in China. When invaded by PWN, resistant P. massoniana secretes an abundance of oleoresin terpenoids as a defensive strategy. However, regulatory mechanisms of this defence in resistant P. massoniana have yet to be elucidated. Here, we characterized two terpene synthase genes, α-pinene synthase (PmTPS4) and longifolene synthase (PmTPS21), identified in resistant P. massoniana and investigate the contribution of these genes to the oleoresin defence strategy in resistant masson pines. Up-regulation of these two genes in the stem supported their involvement in terpene biosynthesis as part of the defence against PWN. Recombinant protein expression revealed catalytic activity for the two PmTPSs, with PmTPS4 primarily producing α-pinene, while PmTPS21 produced α-pinene and longifolene simultaneously. The major enzymatic products of the two terpene synthases had inhibitory effects on PWN in vitro.