general public and 526 nurses (i.e., 234 front-line nurses and 292 non-front-line nurses) to evaluate vicarious traumatization scores via a mobile appbased questionnaire. Front-line nurses are engaged in the process of providing care for patients with COVID-19. The results showed that the vicarious traumatization scores for front-line nurses including scores for physiological and psychological responses, were significantly lower than those of non-front-line nurses (P < 0.001). Interestingly, the vicarious traumatization scores of the general public were significantly higher than those of the front-line nurses (P < 0.001); however, no statistical difference was observed compared to the scores of nonfront-line nurses (P > 0.05). Therefore, increased attention should be paid to the psychological problems of the medical staff, especially non-front-line nurses, and general public under the situation of the spread and control of COVID-19. Early strategies that aim to prevent and treat vicarious traumatization in medical staff and general public are extremely necessary.

Since December 2019, more than 79,000 people have been diagnosed with infection of the Corona Virus Disease 2019 . A large number of medical staff were dispersed for Wuhan city and Hubei province to aid COVID-19 control. Psychological stress, especially vicarious traumatization (VT) caused by the COVID-19 pandemic, should not be ignored. To address this concern, the study employed a total of 214 general public (GP) and 526 nurses to evaluate VT scores via a mobile app-based questionnaire. Results showed that the VT scores slightly increased across periods of aiding COVID-19 control, although no statistical difference was noted (P = 0.083).However, the study found lower scores for VT in nurses [median = 69; interquartile range (IQR) = 56-85] than those of the GP (median = 75.5; IQR = 62-88.3) (P = 0.017). In addition, the VT scores for front-line nurses (FLNs; median = 64; IQR = 52-75), including scores for physiological and psychological responses, were significantly lower than those of non-front-line nurses (nFLNs; median = 75.5; IQR = 63-92) (P < 0.001). Interestingly, the VT scores of the GP were significantly higher than those of the FLNs (P < 0.001). However, no statistical difference was observed compared with those of nFLNs (P > 0.05). Importantly, nFLNs are more likely to suffer from VT, which might be related to two factors, namely, gender [odds ratio (OR) = 3.1717; 95% confidence interval (CI) = 4.247-18.808; P = 0.002] and fertility [OR = 2.072; 95%CI = 0.626-24.533; P = 0.039]. Therefore, increased attention should be paid to the psychological problems of the medical staff, especially nFLNs, and GP under the situation of the spread and control of COVID-19. Early strategies that aim . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. (which was not peer-reviewed)The copyright holder for this preprint . https://doi.org/10. 1101/2020 to prevent and treat VT in medical staff and GP are extremely necessary.

Neuritic plaques are a pathological hallmark of Alzheimer's disease (AD). However, the origin of extracellular amyloid peptide (Aβ) deposits and the process of plaque development remain poorly understood. The present study attempted to explore plaque pathogenesis by localizing β-secretase-1 (BACE1) elevation relative to amyloid peptide (Aβ) accumulation and synaptic/neuritic alterations in the forebrain using transgenic (Tg) mice harboring familial AD (FAD) mutations (5XFAD and 2XFAD) as models. In animals with fully-developed plaque pathology, locally elevated BACE1 immunoreactivity (ir) coexisted with compact-like Aβ deposition, with BACE1-ir occurring selectively in dystrophic axons of various neuronal phenotypes or origins (GABAergic, glutamatergic, cholinergic or catecholaminergic). Prior to plaque onset, localized BACE1/Aβ-ir occurred at swollen presynaptic terminals and fine axonal processes. These BACE1/Aβ-containing axonal elements appeared to undergo a continuing process of sprouting/swelling and dystrophy, during which extracellular Aβ-ir emerged and accumulated in surrounding extracellular space. These data suggest that BACE1 elevation and associated Aβ overproduction inside the sprouting/dystrophic axonal terminals coincide with the onset and accumulation of extracellular amyloid deposition during the development of neuritic plaques in transgenic models of AD. Our findings appear in harmony with an early hypothesis that axonal pathogenesis plays a key or leading role in plaque formation.

Reduced Anthocyanins in Petioles (RAP) encodes a glutathione S-transferase anthocyanin transporter that is essential for the foliage and fruit coloration in strawberry.

The genome of the wild diploid strawberry species Fragaria vesca, an ideal model system of cultivated strawberry (Fragaria × ananassa, octoploid) and other Rosaceae family crops, was first published in 2011 and followed by a new assembly (Fvb). However, the annotation for Fvb mainly relied on ab initio predictions and included only predicted coding sequences, therefore an improved annotation is highly desirable. Here, a new annotation version named v2.0.a2 was created for the Fvb genome by a pipeline utilizing one PacBio library, 90 Illumina RNA-seq libraries, and 9 small RNA-seq libraries. Altogether, 18,641 genes (55.6% out of 33,538 genes) were augmented with information on the 5′ and/or 3′ UTRs, 13,168 (39.3%) protein-coding genes were modified or newly identified, and 7,370 genes were found to possess alternative isoforms. In addition, 1,938 long non-coding RNAs, 171 miRNAs, and 51,714 small RNA clusters were integrated into the annotation. This new annotation of F. vesca is substantially improved in both accuracy and integrity of gene predictions, beneficial to the gene functional studies in strawberry and to the comparative genomic analysis of other horticultural crops in Rosaceae family.

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Alzheimer's disease (AD) is the most common dementia-causing disorder in the elderly, which may relate to multiple risk factors and is pathologically featured by cerebral hypometabolism, paravascular β-amyloid (Aβ) plaques, neuritic dystrophy and intra-neuronal aggregation of phosphorylated-tau. To explore potential pathogenic link among some of these lesions, we examined β-secretase-1 (BACE1) alteration relative to Aβ deposition, neuritic pathology and vascular organization in aged monkey and AD human cerebral cortex. Western blot analyses detected increased levels of BACE1 proteins and β-site-cleavage amyloid precursor protein Cterminal fragments in plaque-bearing human and monkey cortex relative to controls. In immunohistochemistry, locally elevated BACE1 immunoreactivity (IR) occurred in AD but not in control human cortex, with a trend of increased overall density among cases with greater plaque pathology. In double labeling preparations, BACE1 IR colocalized with immunolabeling for Aβ but not for phosphorylated tau. In perfusion-fixed monkey cortex, locally increased BACE1 IR coexisted with intra-axonal and extracellular Aβ IR among virtually all neuritic plaques ranging from primitive to typical cored forms. This BACE1 labeling localized to swollen/sprouting axon terminals that might co-express one or another neuronal phenotype marker (GABAergic, glutamatergic, cholinergic or catecholaminergic). Importantly, these BACE1-labeled dystrophic axons resided near or in direct contact with blood vessels. These finds implicate that plaque formation in AD or normal aging primates relate to a multisystem axonal pathogenesis that occurs

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