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".
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Question: Paragraph: Clinical metagenomics (CMg) is the discipline that refers to the sequencing of all nucleic acid material present within a clinical specimen with the intent to recover clinically relevant microbial information. From a diagnostic perspective, next-generation sequencing (NGS) offers the ability to rapidly identify putative pathogens and predict their antimicrobial resistance profiles to optimize targeted treatment regimens. Since the introduction of metagenomics nearly a decade ago, numerous reports have described successful applications in an increasing variety of biological specimens, such as respiratory secretions, cerebrospinal fluid, stool, blood and tissue. Considerable advancements in sequencing and computational technologies in recent years have made CMg a promising tool in clinical microbiology laboratories. Moreover, costs per sample and turnaround time from specimen receipt to clinical management continue to decrease, making the prospect of CMg more feasible. Many difficulties, however, are associated with CMg and warrant further improvements such as the informatics infrastructure and analytical pipelines. Thus, the current review focuses on comprehensively assessing applications of CMg for diagnostic and subtyping purposes. Crown
Title: Highlighting Clinical Metagenomics for Enhanced Diagnostic Decision-making: A Step Towards Wider Implementation

Answer: True

Question: 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 RA and City One Shatin 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

Answer: True

Question: Paragraph: The demyelinating canine distemper virus (CDV)-leukoencephalitis represents a translational animal model for multiple sclerosis. The present study investigated the expression of type I interferon (IFN-I) pathway members in CDV-induced cerebellar lesions to gain an insight into their role in lesion development. Gene expression of 110 manually selected genes in acute, subacute and chronic lesions was analyzed using pre-existing microarray data. Interferon regulatory factor (IRF) 3, IRF7, signal transducer and activator of transcription (STAT) 1, STAT2, MX protein, protein kinase R (PKR), 2 -5 -oligoadenylate synthetase (OAS) 1 and interferon-stimulated gene (ISG) 15 expression were also evaluated using immunohistochemistry. Cellular origin of STAT1, STAT2, MX and PKR were determined using immunofluorescence. CDV infection caused an increased expression of the antiviral effector proteins MX, PKR, OAS1 and ISG15, which probably contributed to a restricted viral replication, particularly in neurons and oligodendrocytes. This increase might be partly mediated by IRF-dependent pathways due to the lack of changes in IFN-I levels and absence of STAT2 in astrocytes. Nevertheless, activated microglia/macrophages showed a strong expression of STAT1, STAT2 and MX proteins in later stages of the disease, indicating a strong activation of the IFN-I signaling cascade, which might be involved in the aggravation of bystander demyelination. divided into acute (vacuolation of the white matter and mild astrogliosis), subacute (vacuolation and demyelination with mild or no inflammation) and chronic changes (demyelination with moderate to severe inflammation) [8] . The demyelinating distemper leukoencephalitis also represents a naturally occurring animal model for human multiple sclerosis (MS) due to similar histopathological findings and pathogenic mechanisms [3, 9, 10] . Interferons (IFNs) are signaling proteins, which can be classified into three major types based on their specific receptor binding: type I (IFN and IFN), type II (IFN) and type III (IFN) [11, 12] . Type I IFNs (IFN-I) play an important role in the innate immune response and have antiviral, antiproliferative and immunomodulatory capacities, which are already used in the therapy of human and animal disorders [13, 14] . IFN is primarily produced in later stages of the immune response by B cells, cytotoxic T cells and T helper (Th) cells and represents the main activator of macrophages [15] . IFN also has antiviral and antiproliferative effects but its role during canine distemper and therapeutic potential seems to be limited [14, [16] [17] [18] [19] [20] . While in human medicine administering IFN-I in MS is part of the standard therapy [21] , the therapeutic effect of IFN-I on the outcome of a CDV infection in dogs is still widely undetermined [14, 22] . The IFN-I pathway is initiated by the detection of typical structural elements of infectious agents (pathogen-associated molecular patterns; PAMPs), which can be recognized by so-called pattern recognition receptors (PRRs) [23] . Single-and double-stranded RNA produced during viral replication can be detected by toll-like receptors (TLRs), protein kinase R (PKR) and the family of the retinoic acid-inducible gene-I-like receptors (RLRs) including retinoic acid-inducible gene 1 (RIG1) and melanoma differentiation-associated gene 5 (MDA5), which are bound to endosomal membranes or localized in the cytoplasm [24] [25] [26] . After binding to viral RNA, these receptors recruit specific adapter proteins like Toll/IL-1 receptor domain containing adapter-inducing IFN (TRIF), myeloid differentiation primary response gene 88 (MyD88) and IFN promoter stimulator (IPS-1) as well as second messengers to activate IFN regulatory factor (IRF) 3 and IRF7, which induce the transcription of [27] [28] [29] [30] . IFN-I bind in an autocrine or paracrine fashion to their specific receptor, consisting of the subunits IFNAR1 and IFNAR2, to trigger signaling pathways that inhibit viral replication [31] . The receptor-associated kinases Janus kinase 1 (JAK1) and tyrosine kinase 2 (TYK2) phosphorylate the transcription factors, signal transducer and activator of transcription (STAT) 1 and STAT2, which then associate with IRF9 to form a heterotrimeric complex termed interferon-stimulated gene factor 3 (ISGF3) [32] [33] [34] [35] . After translocation into the nucleus, ISGF3 induces the transcription of numerous IFN-stimulated genes (ISGs), which have an IFN-stimulated response element (ISRE) in their promoter site [30, [35] [36] [37] . ISGs including MX proteins, 2 -5 -oligoadenylate synthetase (OAS), PKR and ISG15 play an important role in the resistance to viral infections due to their inhibitory effect on viral transcription, translation and release [30, 38, 39] . In addition, non-canonical aspects of JAK-STAT signaling are described, in which STAT2 homodimers mediate mechanisms of defense against pathogens that impede STAT1 signaling [40, 41] . The presence of IFN-I in the cerebrospinal fluid (CSF) of CDV-infected dogs has been known for a long time and was suggested to be used as a marker of virus persistence, but IFN-I CSF levels are generally low and not always present [42, 43] . An immunohistochemical study demonstrated strong expression of MX proteins in CDV-induced brain lesions [44] . Moreover, recent studies have shown that the virulence of CDV depends on the suppression of the IFN-I signaling pathway via interference with MDA5 and STAT2 signaling [45] . Interestingly, dogs exhibit a relatively high OAS serum activity compared to other animal species such as cats, rabbits and guinea pigs [46] . However, ISG expression has hardly been investigated in the CNS of CDV-infected dogs so far. The present study characterized the expression of several IFN-I pathway members on the gene and protein level in order to contribute to the understanding of the role of the innate immune response in the initiation and progression of CDV-infected cerebellar lesions.
Title: Interferon-Stimulated Genes-Mediators of the Innate Immune Response during Canine Distemper Virus Infection

Answer:
True