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: Several polypeptide products of MHV-A59 ORF 1 a were characterized in MHV-A59 infected DBT cells, using antisera directed against fusion proteins encoded in the first 6.5 kb of ORFla. These included the previously identified N-terminal ORF 1 a product, ~28, as well as 290-, 240-, and 50-kDa polypeptides. P28 was always detected as a discrete band without larger precursors, suggesting rapid cleavage of p28 immediately after its synthesis. Once p28 was cleaved there was little degradation of the protein over a 2-hr period. The intracellular cleavage of p28 was not inhibited by the protease inhibitor leupeptin, in contrast to results obtained during in vitro translation of genome RNA (Denison and Perlman, 1986). These data suggest that different protease activities may be responsible for the cleavage of p28 in vitro and in Go. The 290-kDa protein was an intermediate cleavage product derived from a precursor of greater than 400 kDa. The 290-kDa product was subsequently cleaved into secondary products of 50 and 240 kDa. The intracellular cleavage of the 290-kDa polypeptide was inhibited by leupeptin at concentrations which did not inhibit the early cleavage of p28 or the cleavage of the 290-kDa product from its larger polyprotein precursor. In the presence of zinc chloride, a product of >320 kDa was detected, which appears to incorporate p28 at its amino terminus. This suggests that at least two protease activities may be necessary for processing of ORFl a proteins, one of which cleaves p28 and is sensitive to zinc chloride but resistant to leupeptin, and the other which cleaves the 290-kDa precursor and is sensitive to both inhibitors. Both the 290-and 240-kDa proteins should contain sequences predicted to encode two papain-like prOtesS? activities. 0 1992 Academic PVE.S. Inc.

A: Intracellular Processing of the N-Terminal ORF la Proteins of the Coronavirus MHV-A59 Requires Multiple Proteolytic Events
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Q: In this paper, we analyze a delayed SEIR epidemic model in which the latent and infected states are infective. The model has a globally asymptotically stable disease-free equilibrium whenever a certain epidemiological threshold, known as the basic reproduction number R 0 , is less than or equal to unity. We investigate the effect of the time delay on the stability of endemic equilibrium when R 0 > 1. We give criteria that ensure that endemic equilibrium is asymptotically stable for all time delays and a Hopf bifurcation occurs as time delay exceeds the critical value. We give formulae for the direction of Hopf bifurcations and the stability of bifurcated periodic solutions by applying the normal form theory and the center manifold reduction for functional differential equations. Numerical simulations are presented to illustrate the analytical results.

A: Hopf bifurcation analysis of a delayed SEIR epidemic model with infectious force in latent and infected period
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Q: A characteristic feature of aggressive malignancy is the overexpression of lactic acid dehydrogenase-(LDH-) A, concomitant to pericellular accumulation of lactate. In a recent high-throughput screening, we identified Rhus chinensis (Mill.) gallnut (RCG) (also known as Galla Chinensis) extract as a potent (IC 50 < 1 g/mL) inhibitor of human LDH-A (hLDH-A). In this study, through bioactivity guided fractionation of the crude extract, the data demonstrate that penta-1,2,3,4,6-O-galloyl--D-glucose (PGG) was a primary constituent responsible for hLDH-A inhibition, present at ∼9.95 ± 0.34% dry weight. Theoretical molecular docking studies of hLDH-A indicate that PGG acts through competitive binding at the NADH cofactor site, effects confirmed by functional enzyme studies where the IC 50 = 27.32 nM was reversed with increasing concentration of NADH. Moreover, we confirm protein expression of hLDH-A in MDA-231 human breast carcinoma cells and show that PGG was toxic (LC 50 = 94.18 M), parallel to attenuated lactic acid production (IC 50 = 97.81 M). In a 72-hour cell proliferation assay, PGG was found to be a potent cytostatic agent with ability to halt cell division (IC 50 = 1.2 M) relative to paclitaxel (IC 50 < 100 nM). In summary, these findings demonstrate that PGG is a potent hLDH-A inhibitor with significant capacity to halt proliferation of human breast cancer cells.

A:
,6-Penta-O-galloylglucose within Galla Chinensis Inhibits Human LDH-A and Attenuates Cell Proliferation in MDA-MB-231 Breast Cancer Cells
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