In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".

[Q]: Paragraph: The objectives of this study were to evaluate the effects of free-access acidified milk replacer feeding on the pre-and postweaning health of dairy and veal calves. Individually housed calves were systematically assigned at birth to 1 of 2 feeding programs: free-access feeding (ad libitum) of acidified milk replacer (ACD, n = 249) or traditional restricted feeding (3 L fed twice daily) of milk replacer (RES, n = 249). Calves were fed milk replacer containing 24% crude protein and 18% fat. Acidified milk replacer was prepared to a target pH between 4.0 and 4.5 using formic acid. Calves were weaned off milk replacer at approximately 6 wk of age. Weaning occurred over 5 d, and during this weaning period, ACD calves had access to milk replacer for 12 h/d and RES calves were offered only one feeding of milk replacer (3 L) daily. Calves were monitored daily for signs of disease. Fecal consistency scores were assigned each week from birth until weaning. A subset of calves was systematically selected for fecal sampling at 3 time points between 7 and 27 d of age. Fecal samples were analyzed for enterotoxigenic Escherichia coli F5, Cryptosporidium parvum, rotavirus, and coronavirus. Hip width, hip height, body length, heart girth, and body weight were measured at birth and weaning. Postweaning body weight measurements were collected from the heifers at approximately 8 mo of age. Postweaning body weight and carcass grading information was collected from the veal calves at slaughter once a live weight between 300 and 350 kg had been achieved. The odds of ACD calves being treated for a preweaning disease event tended to be lower than that of the RES calves (1.2 vs. 5.2%, respectively). Preweaning mortality, postweaning disease treatment, and postweaning mortality did not differ between feeding treatments. The ACD feeding treatment supported greater preweaning average daily gain (0.59 vs. 0.43 kg/d) and structural growth than RES feeding. Postweaning average daily gain and carcass characteristics were similar for ACD and RES calves. These results indicate that free-access acidified milk replacer feeding tended to support improved health, and greater body weight gain and structural growth during the preweaning period; these effects did not persist in the postweaning period. The growth advantage observed before weaning in the ACD calves likely disappeared due to the weaning methods used.
Title: Clinical trial on the effects of a free-access acidified milk replacer feeding program on the health and growth of dairy replacement heifers and veal calves
[A]: True

[Q]: Paragraph: Norovirus infection constitutes the primary cause of acute viral gastroenteritis. There are currently no vaccines or norovirus-specific antiviral therapeutics available for the management of norovirus infection. Norovirus 3C-like protease is essential for viral replication, consequently, inhibition of this enzyme is a fruitful avenue of investigation that may lead to the emergence of anti-norovirus therapeutics. We describe herein the optimization of dipeptidyl inhibitors of norovirus 3C-like protease using iterative SAR, X-ray crystallographic, and enzyme and cell-based studies. We also demonstrate herein in vivo efficacy of an inhibitor using the murine model of norovirus infection. . Accession Codes. The coordinates and structure factors for norovirus 3CL protease in complex with inhibitors have been deposited to the Protein Databank with the accession codes NVpro:17 (4XBB), NVPro:44-h (4XBC) and NVPro:44-o (4XBD). We initially focused on the design of peptidyl transition state inhibitors of NV 3CLpro that incorporate in their structure a recognition element (a peptidyl fragment) that is congruent with the known substrate specificity of the enzyme (vide supra) and a warhead (aldehyde or -ketoamide), latent warhead (bisulfite adduct) or transition state mimic (- Kankanamalage et al. The synthesized compounds were evaluated for their inhibitory activity against NV 3CLpro, as well as their anti-norovirus activity in a cell-based replicon system, as previously Kankanamalage et al. In order to evaluate the specific interactions between the enzyme and the hydroxyphosphonate inhibitors, inhibitor 17 was incubated with NV 3CLpro in Tris buffer, pH 8.0. Surprisingly, the enzyme-inhibitor complex formed corresponded to the complex formed between aldehyde 16 and 3CL protease. The formation of this complex indicates initial non-enzymatic (buffer)-or enzyme-catalyzed conversion of -hydroxyphosphonate 17 to the corresponding aldehyde 16, followed by the formation of a tetrahedral adduct with the active site cysteine (Cys139). Studies aimed at ascertaining the validity of this hypothesis are in progress. The ensemble of hydrogen bonding and hydrophobic interactions Kankanamalage et al.
Title: Structure-Guided Design and Optimization of Dipeptidyl Inhibitors of Norovirus 3CL Protease. Structure-Activity Relationships and Biochemical, X-ray Crystallographic, Cell- Based, and In Vivo Studies
[A]: False

[Q]: Paragraph: African swine fever virus (ASFV) infection induces apoptosis in the infected cell; however, the consequences of this activation on virus replication have not been defined. In order to identify the role of apoptosis in ASFV infection, we analyzed caspase induction during the infection and the impact of caspase inhibition on viral production. Caspases 3, 9 and 12 were activated from 16 h post-infection, but not caspase 8. Indeed, caspase 3 activation during the early stages of the infection appeared to be crucial for efficient virus exit. In addition, the inhibition of membrane blebbing reduced the release of virus particles from the cell. ASFV uses the endoplasmic reticulum (ER) as a site of replication and this process can trigger ER stress and the unfolded protein response (UPR) of the host cell. In addition to caspase 12 activation, indicators of ER stress include the upregulation of the chaperones calnexin and calreticulin upon virus infection. Moreover, ASFV induces transcription factor 6 signaling pathway of the UPR, but not the protein kinase-like ER kinase or the inositol-requiring enzyme 1 pathways. Thus, the capacity of ASFV to regulate the UPR may prevent early apoptosis and ensure viral replication.
Title: The ATF6 branch of unfolded protein response and apoptosis are activated to promote African swine fever virus infection
[A]:
False