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: Influenza viruses are a major public health problem worldwide. Although influenza has been extensively researched, there are still many aspects that are not fully understood such as the effects of within and between-hosts dynamics and their impact on behavior change. Here, we develop mathematical models with multiple infection stages and estimate parameters based on within-host data to investigate the impact of behavior change on influenza dynamics. We divide the infected population into three and four groups based on the age of the infection, which corresponds to viral load shedding. We consider within-host data on viral shedding to estimate the length and force of infection of the different infectivity stages. Our results show that behavior changes, due to exogenous events (e.g., media coverage) and disease symptoms, are effective in delaying and lowering an epidemic peak. We show that the dynamics of viral shedding and symptoms, during the infection, are key features when considering epidemic prevention strategies. This study improves our understanding of the spread of influenza virus infection in the population and provides information about the impact of emergent behavior and its connection to the within and between-hosts dynamics.

A: Connecting within and between-hosts dynamics in the influenza infection-staged epidemiological models with behavior change
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Q: Background: Proenkephalin (PENK) has been suggested as a novel biomarker for kidney function. We investigated the diagnostic and prognostic utility of plasma PENK in comparison with neutrophil gelatinase-associated lipocalin (NGAL) and estimated glomerular filtration rates (eGFR) in septic patients. Methods: A total of 167 septic patients were enrolled: 99 with sepsis, 37 with septic shock, and 31 with suspected sepsis. PENK and NGAL concentrations were measured and GFR was estimated by using the isotope dilution mass spectrometry traceable-Modification of Diet in Renal Disease (MDRD) Study and three Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations: CKD-EPICr, CDK-EPICysC, and CKD-EPICr-CysC. The PENK, NGAL, and eGFR results were compared according to sepsis severity, presence or absence of acute kidney injury (AKI), and clinical outcomes. Results: The PENK, NGAL, and eGFR results were significantly associated with sepsis severity and differed significantly between patients with and without AKI only in the sepsis group (all P < 0.05). PENK was superior to NGAL in predicting AKI (P = 0.022) and renal replacement therapy (RRT) (P = 0.0085). Regardless of the variable GFR category by the different eGFR equations, PENK showed constant and significant associations with all eGFR equations. Unlike NGAL, PENK was not influenced by inflammation and predicted the 30day mortality. Conclusions: PENK is a highly sensitive and objective biomarker of AKI and RRT and is useful for prognosis prediction in septic patients. With its diagnostic robustness and predictive power for survival, PENK constitutes a promising biomarker in critical care settings including sepsis.

A: Original Article Clinical Chemistry Proenkephalin, Neutrophil Gelatinase-Associated Lipocalin, and Estimated Glomerular Filtration Rates in Patients With Sepsis
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Q: The coronavirus, mouse hepatitis virus strain A59 (MHV), expresses a chymotrypsin-like cysteine proteinase (3CLpro) within the gene 1 polyprotein. The MHV 3CLpro is similar to the picornavirus 3C proteinases in the relative location of confirmed catalytic histidine and cysteine residues and in the predicted use of Q/(S, A, G) dipeptide cleavage sites. However, less is known concerning the participation of aspartic acid or glutamic acid residues in catalysis by the coronavirus 3Clike proteinases or of the precise coding sequence of 3CLpro within the gene 1 polyprotein. In this study, aspartic acid residues in MHV 3CLpro were mutated and the mutant proteinases were tested for activity in an in vitro trans cleavage assay. MHV 3CLpro was not inactivated by substitutions at Asp 3386 (D53) or Asp 3398 (D65), demonstrating that they were not catalytic residues. MHV 3CLpro was able to cleave at a glutamine-glycine (QG 3607-8 ) dipeptide within the 3CLpro domain upstream from the predicted carboxy-terminal QS 3635-6 cleavage site of 3CLpro. The predicted full-length 3CLpro (S 3334 to Q 3635 ) had an apparent mass of 27 kDa, identical to the p27 3CLpro in cells, whereas the truncated proteinase (S 3334 to Q 3607 ) had an apparent mass of 24 kDa. This 28-amino-acid carboxy-terminal truncation of 3CLpro rendered it inactive in a trans cleavage assay. Thus, MHV 3CLpro was able to cleave at a site within the putative full-length proteinase, but the entire predicted 3CLpro domain was required for activity. These studies suggest that the coronavirus 3CL-proteinases may have a substantially different structure and catalytic mechanism than other 3C-like proteinases. 1997 Academic Press

A:
Determinants of Mouse Hepatitis Virus 3C-like Proteinase Activity
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