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However, bees suffer from environmental pollution, parasites, and pathogens, including viruses. Outbreaks of virus infections cause the deaths of individual honeybees as well as collapses of whole colonies. Kashmir bee virus has been associated with colony collapse disorder in the US, and no cure of the disease is currently available. Here we report the structure of an infectious particle of Kashmir bee virus and show how its protein capsid opens to release the genome. Our structural characterization of the infection process determined that therapeutic compounds stabilizing contacts between pentamers of capsid proteins could prevent the genome release of the virus.Increasing evidence shows that Epstein-Barr virus (EBV) infection is closely related to various lymphoid and epithelioid malignancies. However, the underlying mechanisms are unclear. GCNT3 (core 2β-1,6-acetylglucosaminyltransferase) is a new type of core mucin synthase, and its expression in EBV-associated gastric cancer (EBVaGC) is lower than that in EBV-negative gastric cancer (EBVnGC). EBV-encoded latent membrane protein 2A (LMP2A) is a transmembrane protein with tumorigenic transformation properties. Here, we demonstrated that LMP2A inhibited the transcription of GCNT3 by inhibiting Smad2/3 and Smad4. LMP2A restrained the activation of the mTORC1 pathway by inactivating the TGF-β1/Smad pathway and then downregulated GCNT3 expression. The mTORC1-GCNT3 pathway promoted cell proliferation and migration and inhibited G0/G1 cell arrest. Related proteins involved in epithelial-mesenchymal transition (EMT) were downstream molecules of the TGF-β1/Smad-mTORC1-GCNT3 pathway. GCNT3 inhibited autophagy by inducing mTORC1 phosphorylation. These findings indicate that targeting the TGF-β1/Smad-mTORC1-GCNT3 axis may represent a novel therapeutic target in GC.ImportanceEpstein-Barr virus (EBV) is an opportunistic pathogen, and the latent membrane protein 2A (LMP2A) encoded by EBV plays a key role in ensuring the incubation period of EBV. Glycosylation modification is an important marker of cancer cells, and recent studies have reported that it is related to EBV. Our conclusions provide deeper theoretical support for the role of LMP2A and TGF/Smad-mTORC1-GCNT3 in EBVaGC and help to understand glycosylation abnormalities in cancer. Our results may provide novel therapeutic targets for the treatment of gastric cancer against the TGF/Smad-mTORC1-GCNT3 signaling cascade.The current SARS-CoV-2 pandemic has killed thousands across the world. SARS-CoV-2 is the latest but surely not the last such global pandemic we will face. The biomedical response to such pandemics includes treatment, vaccination, and so on. In this paper, though, we argue that it is time to consider an additional strategy the somatic (non-heritable) enhancement of human immunity. We argue for this approach and consider bioethics objections we believe can be overcome.This paper explores ethical issues raised by whole slide image-based computational pathology. find more After briefly giving examples drawn from some recent literature of advances in this field, we consider some ethical problems it might be thought to pose. These arise from (1) the tension between artificial intelligence (AI) research-with its hunger for more and more data-and the default preference in data ethics and data protection law for the minimisation of personal data collection and processing; (2) the fact that computational pathology lends itself to kinds of data fusion that go against data ethics norms and some norms of biobanking; (3) the fact that AI methods are esoteric and produce results that are sometimes unexplainable (the so-called ‘black box’problem) and (4) the fact that computational pathology is particularly dependent on scanning technology manufacturers with interests of their own in profit-making from data collection. We shall suggest that most of these issues are resolvable.For medical schools, the COVID-19 pandemic necessitated examination and curricular restructuring as well as significant changes to clinical attachments. With the available evidence suggesting that medical students’ mental health status is already poorer than that of the general population, with academic stress being a chief predictor, such changes are likely to have a significant effect on these students. This online, cross-sectional study aimed to determine the impact of COVID-19 on perceived stress levels of medical students, investigate possible contributing and alleviating factors, and produce recommendations for medical schools to implement during future healthcare emergencies. The majority (54.5%) of respondents reported levels of stress ranging from moderate to extreme. Higher levels of stress were significantly associated with female gender (p=0.039) and international status (p=0.031). A significant association was also noted between reported stress and the transition to online learning (p less then 0.0001) and online assessment formatting (p less then 0.0001), concerns for personal health (p less then 0.0001) and for the health of family members (p less then 0.0001). Students who reported higher stress levels were less confident in their government’s management of the crisis (p=0.041). Additionally, students who reported lower stress agreed highly that their medical school had an appropriate response to the crisis (p less then 0.0001), had provided sufficient information regarding the crisis (p=0.015), that they trust their school in handling the continuing of their education (p=0.020) and that their school had appropriate plans in place to support the continuing of education (p=0.017).The pandemic of COVID-19, caused by SARS-CoV-2, is a major global health threat. Epidemiological studies suggest that bats (Rhinolophus affinis) are the natural zoonotic reservoir for SARS-CoV-2. However, the host range of SARS-CoV-2 and intermediate hosts that facilitate its transmission to humans remain unknown. The interaction of coronavirus with its host receptor is a key genetic determinant of host range and cross-species transmission. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) as the receptor to enter host cells in a species-dependent manner. In this study, we characterized the ability of ACE2 from diverse species to support viral entry. By analyzing the conservation of five residues in two virus-binding hotspots of ACE2 (hotspot 31Lys and hotspot 353Lys), we predicted 80 ACE2 proteins from mammals that could potentially mediate SARS-CoV-2 entry. We chose 48 ACE2 orthologs among them for functional analysis, and showed that 44 of these orthologs-including domestic animals, pets, livestock, and animals commonly found in zoos and aquaria-could bind the SARS-CoV-2 spike protein and support viral entry.