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".

Input: Consider Input: Paragraph: Factors affecting a residential unit's price are always of interest to homebuyers and building developers, especially in a city like Hong Kong which is known for expensive housing. Literature review indicates that the governing factors can be categorized into architectural and environmental attributes. Among different methods commonly used for pricing, the hedonic price approach is viewed as the most suitable. However, the successful use of this method requires that homebuyers know and choose the attributes. Whilst choosing architectural attributes are not a problem for homebuyers, the same does not apply to environmental attributes. Previous studies by the authors have proposed some simple indicators for quantifying the environmental attributes. Based upon the developed performance indicators and the transaction records of two representative housing estates (Royal Ascot ¼ RA and City One Shatin ¼ COS), details of the properties, including transaction prices, architectural particulars and environmental characteristics were numerically transformed for the hedonic price analysis. The analysis results revealed that the willingness to pay (percentage of house price in parenthesis) for architectural and environmental attributes was HK$302.3/ft 2 (5.8%) and HK$886.8/ft 2 (28.2%), respectively, for RA and HK$1672.7/ ft 2 (31.9%) and HK$111.5/ft 2 (3.5%) for COS. It was found that elasticity of substitution (ES) of environmental attributes contributed 3.4e13.3% of the property price, compared to 0.6e5.5% for architectural attributes. 
 Title: Development of price models for architectural and environmental quality for residential developments in Hong Kong

Output: True


Input: Consider Input: Paragraph: We have previously reported that the 3C-like proteinase of the coronavirus infectious bronchitis virus (IBV) is responsible for processing of the 1a and 1a/1b polyproteins to three mature products of 24, 10, and 100 kDa (Liu et al., 1994 (Liu et al., , 1997 Ng and Liu, 1998) . The C-terminal cleavage site of the 100-kDa protein was defined to be the Q 891(1b) -S 892(1b) dipeptide bond encoded by nucleotides 15, 129 to 15, 134 (Liu and Brown, 1995). In this report, other cleavage sites of the 3C-like proteinase in the polyprotein encoded by the ORF 1b region were mapped by coexpression, deletion, and site-directed mutagenesis studies. Using two ORF 1b-specific antisera, V58 and V17, three more Q-S(G) dipeptide bonds, encoded by nucleotides 16,929 to 16,934, 18,492 to 18,497, and 19,506 to 19,511, respectively, were demonstrated to be the cleavage sites of the 3C-like proteinase. Cleavage at these four positions would result in the release of four mature products with molecular masses of approximately 68, 58, 39, and 35 kDa. Among them, the 39-and 35-kDa proteins were specifically identified in IBV-infected cells. Taken together with the 100-kDa protein previously identified, these results suggest that the ORF 1b region of IBV mRNA1 may be able to encode five mature products. 
 Title: Proteolytic Mapping of the Coronavirus Infectious Bronchitis Virus 1b Polyprotein: Evidence for the Presence of Four Cleavage Sites of the 3C-like Proteinase and Identification of Two Novel Cleavage Products

Output: False


Input: Consider Input: Paragraph: and double-stranded (ds) RNA act as potent IFN inducing signals and we previously showed that E rns efficiently cleaves these substrates, thereby inhibiting an IFN response that is crucial for successful fetal infection. Considering that a large variety of RNases and DNases require dimerisation to cleave double-stranded substrates, the activity of E rns against dsRNA was postulated to depend on homodimer formation mediated by disulfide bonds involving residue Cys171. Here, we show that monomeric E rns is equally able to cleave dsRNA and to inhibit dsRNA-induced IFN synthesis as the wild-type form. Furthermore, both forms were able to degrade RNA within a DNA/RNA-as well as within a methylated RNA/RNA-hybrid, with the DNA and the methylated RNA strand being resistant to degradation. These results support our model that E rns acts as 'nicking endoribonuclease' degrading ssRNA within doublestranded substrates. This efficiently prevents the activation of IFN and helps to maintain a state of innate immunotolerance in persistently infected animals. Bovine viral diarrhea virus (BVDV), a pestivirus within the family Flaviviridae, occurs throughout the world with far-reaching consequences for animal health and the agricultural economy. Infection of pregnant cows within the first ∼120 days of gestation with a noncytopathic (ncp), but not cytopathic (cp), biotype of BVDV may result in the birth of persistently infected (PI) calves 1-6 . The early time point of fetal infection prior to the development of adaptive immunity and the distinct epitheliochorial placenta of ruminants that is impermeable to antibodies, however, cannot fully account for the successful establishment of persistent infection, because the innate immune defense is operative from the earliest time of fetal development. Therefore, in addition to the establishment of virus-specific B-and T-cell immunotolerance during ontogeny and to the lack of transfer of maternal antibodies to the fetus, the interplay of BVDV with the innate immune response of its host animals might be the most important aspect for the long-term survival of this virus in its host population (for review, see refs 1-6 ). Various pattern recognition receptors (PRR), such as the membrane-bound Toll-like receptors (TLR) or the cytoplasmic RIG-I-like receptors (RLR), activate the synthesis of interferon (IFN) type-I (IFN-α/β) upon detection of viral pathogen-associated molecular patterns (PAMP) 7-9 . IFN is a cytokine involved in the most important innate defense mechanism against virus infection, and most viruses, including the pestiviruses, have developed an enormous variety of strategies to bypass these antiviral effects 5,10-14 . The genome of the enveloped pestiviruses consists of a single-stranded (ss) RNA of positive polarity encoding for a single large polyprotein. Cap-independent translation is started by an internal ribosomal entry site (IRES), and the polyprotein is then further processed by cellular and viral proteases into four structural and at least eight non-structural viral proteins [15] [16] [17] . The N-terminal autoprotease N pro and the structural protein E rns are exclusively present in viruses of the pestivirus genus within the flaviviridae family, and both were implicated to be involved in the evasion of the host's type-I IFN defense 2,17,18 . N pro activates the proteasomal degradation of the interferon regulatory factor (IRF)-3 [19] [20] [21] [22] , and possibly also IRF-7 23 , thus preventing the transcriptional activation of the IFN genes. In this manner, the non-structural protein N pro is able in infected cells to prevent IFN synthesis that is induced by the activation Published: xx xx xxxx OPEN www.nature.com/scientificreports/ 
 Title: Homodimerisation-independent cleavage of dsRNA by a pestiviral nicking endoribonuclease OPEN


Output: False