In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Q: One word can be used to best describe the theme of each day that has transpired since the onset of the COVID-19 pandemic: uncertainty. Urologic surgical residents around the nation are faced with the unknown when they walk through the doors of the hospital each day. While experience has taught us navigational strategies to handle these circumstances, the COVID-19 pandemic has undoubtedly brought new meaning to this concept. Priorities have quickly transitioned from closely following our previously developed academic curriculum and enhancing our surgical skills, to limiting physician-patient encounters and ensuring the safety and health of our team. Normalcy within our professional and personal lives is completely lost. Yet, as health care providers, we must and will forge on. We review the techniques and guidelines that our institution has implemented in order to allow us to do just that. We believe that our leadership, both at an enterprise and program level, has taken the necessary and early measures to prepare our residency cohort for the uncertain future and challenges posed by COVID-19. This plan emphasizes social and professional distancing, allows residents and faculty to stay current on academic topics, and provides reasonable opportunities for personal wellness, all while emphasizing safety and rationalization. Most importantly, however, we have continued to provide our patients with exceptional urologic care at 2 adult hospitals and 1 children's hospital in the Greater Akron, Ohio area. While we understand each residency program has a unique curriculum with a different number of residents that cover a range of different hospitals, we hope to provide insight into our personal experience. We believe that this method of organization allows a residency program to continue to grow professionally, socially, academically, and personally during the uncertainty that is COVID-19. This framework could serve as an immediate action plan for future pandemics and natural disasters, especially for residency programs that cover multiple hospitals and health care settings.

A: Editorial Cleveland Clinic Akron General Urology Residency Program's COVID-19 Experience
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Q: Background: Complement proteins and activation products have been found associated with neuropathology in Alzheimer's disease (AD). Recently, a C5a receptor antagonist was shown to suppress neuropathology in two murine models of AD, Tg2576 and 3xTg. Previously, a genetic deficiency of C1q in the Tg2576 mouse model showed an accumulation of fibrillar plaques similar to the complement sufficient Tg2576, but reactive glia were significantly decreased and neuronal integrity was improved suggesting detrimental consequences for complement activation in AD. The goal of this study was to define the role of the classical complement activation pathway in the progression of pathology in the 3xTg mouse that develops tangles in addition to fibrillar plaques (more closely reflecting human AD pathology) and to assess the influence of complement in a model of AD with a higher level of complement hemolytic activity. Methods: 3xTg mice deficient in C1q (3xTgQ-/-) were generated, and both 3xTg and 3xTgQ-/-were backcrossed to the BUB mouse strain which has higher in vitro hemolytic complement activity. Mice were aged and perfused, and brain sections stained for pathological markers or analyzed for proinflammatory marker expression. Results: 3xTgQ-/-mice showed similar amounts of fibrillar amyloid, reactive glia and hyperphosphorylated tau as the C1q-sufficient 3xTg at the ages analyzed. However, 3xTg and 3xTgQ-/-on the BUB background developed pathology earlier than on the original 3xTg background, although the presence of C1q had no effect on neuropathological and pro-inflammatory markers. In contrast to that seen in other transgenic models of AD, C1q, C4 and C3 immunoreactivity was undetectable on the plaques of 3xTg in any background, although C3 was associated with reactive astrocytes surrounding the plaques. Importantly, properdin a component of the alternative complement pathway was associated with plaques in all models. Conclusions: In contrast to previously investigated transgenic models of AD, development of neuropathology in 3xTg mice, which progresses much slower than other murine models, may not be influenced by fibrillar amyloid mediated activation of the classical complement pathway, suggesting that the alternative complement pathway activation or a C3-independent cleavage of C5 could account for the detrimental effects in these mice that are prevented by the C5a receptor antagonist. Furthermore, the paucity of complement activation may be a factor in the slower kinetics of progression of pathology in the 3xTg model of this disease.

A: Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's disease
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Q: In the face of the worldwide threat of severe acute respiratory syndrome (SARS) to human life, some of the most urgent challenges are to develop fast and accurate analytical methods for early diagnosis of this disease as well as to create a safe anti-viral vaccine for prevention. To these ends, we investigated the antigenicity of the spike protein (S protein), a major structural protein in the SARS-coronavirus (SARS-CoV). Based upon the theoretical analysis for hydrophobicity of the S protein, 18 peptides were synthesized. Using Enzyme-Linked Immunosorbent Assay (ELISA), these peptides were screened in the sera from SARS patients. According to these results, two fragments of the S gene were amplified by PCR and cloned into pET-32a. Both S fragments were expressed in the BL-21 strain and further purified with an affinity chromatography. These recombinant S fragments were confirmed to have positive cross-reactions with SARS sera, either by Western blot or by ELISA. Our results demonstrated that the potential epitope regions were located at Codons 469-882 in the S protein, and one epitope site was located at Codons 599-620. Identification of antigenic regions in the SARS-CoV S protein may be important for the functional studies of this virus or the development of clinical diagnosis.

A:
A Strategy for Searching Antigenic Regions in the SARS-CoV Spike Protein
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