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.

Objective: To focus on the potential beneficial effects of the pleiotropic effects of dipeptidyl peptidase-4 inhibitors (DPP4is) on attenuating progression of diabetic kidney disease in reducing the long-term effect of the acute kidney injury (AKI) to chronic kidney disease (CKD) transition. , were analyzed, and patients with diabetes weaning from dialysis-requiring AKI were identified. Cox proportional hazards models and inverse-weighted estimates of the probability of treatment were used to adjust for treatment selection bias. The outcomes were incident end-stage renal disease (ESRD) and mortality, major adverse cardiovascular events, and hospitalized heart failure. Results: Of a total of 6165 patients with diabetes weaning from dialysis-requiring AKI identified, 5635 (91.4%) patients were DPP4i nonusers and 530 (8.6%) patients were DPP4i users. Compared with DPP4i nonusers, DPP4i users had a lower risk of ESRD (hazard ratio, 0.81; 95% CI, 0.70-0.94; P¼.04) and allcause mortality (hazard ratio, 0.28; 95% CI, 0.23-0.34; P<.001) after adjustments for CKD, advanced CKD, and angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker use. In contrast, the risk of major adverse cardiovascular events and hospitalized heart failure did not differ significantly between groups. Conclusion: Dipeptidyl peptidase-4 inhibitor users had a lower risk of ESRD and mortality than did nonusers among patients with diabetes after weaning from dialysis-requiring AKI. Therefore, a prospective study of AKI to CKD transitions after episodes of AKI is needed to optimally target DPP4i interventions.
Patients and Methods: Data from the National Health Insurance Research Database from

This study shows that the disease free equilibrium ( ) for COVID-19 coronavirus does not satisfy the criteria for a locally or globally asymptotic stability. This implies that as a pandemic as declared by WHO (2020) the COVID-19 coronavirus does not have a curative vaccine yet and precautionary measures are advised through quarantine and observatory procedures. Also, the Basic Reproductive number ( 0 < 1) by Equation (33) shows that there is a chance of decline of secondary infections when the ratio between the incidence rate in the population and the total number of infected population quarantined with observatory procedure. The effort to evaluate the disease equilibrium shows that unless there is a dedicated effort from government, decision makers and stakeholders, the world would hardly be reed of the COVID-19 coronavirus and further spread is eminent and the rate of infection will continue to increase despite the increased rate of recovery because of the absence of vaccine at the moment.
MATHEMATICAL PREDICTIONS FOR COVID-19 AS A GLOBAL PANDEMIC

Human astrovirus nonstructural protein nsP1a/4, located at the C-terminal end of 17 nsP1a, is thought to be involved in the regulation of RNA replication and capsid 18 maturation;however, its rolesviral growth and virulence are not well understood. 19 We investigated the intracellular host proteins that interact with nsP1a and 20 explored the potential roles of the interaction in the pathogenesis of human 21 astrovirus infection. We screened 14 independent proteins with a cDNA library 22 a nonstructural protein located at the C-terminal end of the human astrovirus 38 nsP1a polyprotein, interacts with the host protein CD63. Over expression of 39 CD63 promoted viral RNA replication, whereas knockdown of CD63 decreased 40 virus RNA replication, indicating that CD63 plays a critical role in the human 41 astrovirus life cycle. 42 43 KEYWORDS: human astrovirus, HAstV, protein-protein interaction, nsP1a, 44 nsP1a/4, CD63, virus replication 45 46 author/funder. All rights reserved. No reuse allowed without permission. The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/331835 doi: bioRxiv preprint Viruses are obligate intracellular pathogens thatutilize host-cell machinery to 47 infect cells, replicate themselves, and then exit the cells for another round of 48 infection. Human astroviruses (HAstVs) are a group of non-enveloped, 49 single-stranded, and positive-sense RNA viruses in the family Astroviridae. 50 HAstVs are causative agents of viral diarrhea in young children, 51 immunocompromised patients, and elderly individuals (1-5). The astrovirus 52 genome has three open reading frames (ORFs); ORF1a and ORF1b encode two 53 nonstructural polyproteins (nsPs), and ORF2 encodes the capsid protein (6). The 54 nsP1a polyprotein, transcribed from ORF1a, is involved in viral transcription 55 and replication. When HAstV infects a host cell, nsP1a is cleaved into at least 56 four products, named nsP1a/1, nsP1a/2, nsP1a/3 (protease), and nsP1a/4. The 57 nsP1a/4 protein is located at the C-terminal end of nsP1a.Several domains have 58 been identified in nsP1a/4, including two coiled-coil regions, a death domain 59 (DD), a nuclear localization signal (NLS), a putative viral genome-linked 60 protein(VPg), and a hypervariable region (HVR)(7-12). It was confirmed that 61 nsP1a/4 plays important roles in the activation of capsid maturation and the 62 regulation of RNA replication (13, 14). To better understand the roles of nsP1a 63 and nsP1a/4 in HAstV infection and replication, we characterized host proteins 64 that interact with nsP1a or nsP1a/4 by utilizing a yeast two-hybrid approach. We 65 identified at least 14 host proteins that could bind to nsP1a, one of which was 66 CD63. CD63, a member of the tetraspan transmembrane protein family, is a 68 author/funder. All rights reserved. No reuse allowed without permission.

Host protein CD63 enhances viral RNA replication by interacting with human astrovirus nonstructural protein nsP1a/4 2