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".

Ex Input:
Paragraph: It is known that the person-to-person spreading of certain infectious diseases is related with the transmission of human exhaled air in the indoor environments, and this is suspected to be the case with the severe acute respiratory syndrome (SARS) outbreak. This paper presents the numerical analysis of the human respiration process and the transport of exhaled air by breathing, sneezing, and coughing and their potential impact on the adjacent person in a modeled room with displacement ventilation. In order to account for the influence of the thermal plume around the human body, a three-dimensional computational thermal manikin (CTM) with an accurate description of body geometry was applied. Some of the results were compared with those from former simulations and experiments. It was found that personal exposure to the exhaled air from the normal respiration process of other persons is very low in a modeled room with displacement ventilation. Personal exposure to pollution caused by sneezing or coughing is highly directional. When two occupants face each other the cross-infection may happen due to the long transport distance of the exhalation. r 
 Title: Transient CFD simulation of the respiration process and inter-person exposure assessment

Ex Output:
False


Ex Input:
Paragraph: Introduction-HIV-1 uses a programmed -1 ribosomal frameshift to generate Gag-Pol, the precursor of its enzymes, when its full-length mRNA is translated by the ribosomes of the infected cells. This change in the reading frame occurs at a so-called slippery sequence that is followed by a specific secondary structure, the frameshift stimulatory signal. This signal controls the frameshift efficiency. The synthesis of HIV-1 enzymes is critical for the virus replication and therefore, the -1 ribosomal frameshift could be the target of novel antiviral drugs. Areas covered-This review examines various approaches used to select drugs interfering with the -1 frameshift of HIV-1. These include the selection and modification of chemical compounds that specifically bind to the frameshift stimulatory signal, the use of antisense oligonucleotides targeting this signal and the selection of compounds that modulate HIV-1 frameshift, by using bicistronic reporters where the expression of the second cistron depends upon HIV-1 frameshift. Expert opinion-The most promising approach is the selection and modification of compounds specifically targeting HIV-1 frameshift stimulatory signal. The use of antisense oligonucleotides binding to the frameshift stimulatory signal is still questionable. The use of bicistronic reporters preferentially selects compounds that modulate the frameshift by targeting the ribosomes, which is less promising. 
 Title: Targeting frameshifting in the human immunodeficiency virus

Ex Output:
True


Ex Input:
Paragraph: lung transplantation and thought to represent chronic rejection. Increased expression of Pentraxin 3 (PTX3), an acute phase protein, was associated with worse outcome in lung transplant patients. To determine the role of recipient PTX3 in development of chronic rejection, we used a minor alloantigen-mismatched murine orthotopic single lung transplant model. Male C57BL/10 mice were used as donors. Male PTX3 knockout (KO) mice and their wild type (WT) littermates on 129/SvEv/C57BL6/J background were used as recipients. In KO recipients, 7/13 grafted lungs were consolidated without volume recovery on CT scan, while only 2/9 WT mice showed similar graft consolidation. For grafts where lung volume could be reliably analyzed by CT scan, the lung volume recovery was significantly reduced in KO mice compared to WT. Interstitial inflammation, parenchymal fibrosis and bronchiolitis obliterans scores were significantly higher in KO mice. Presence of myofibroblasts and lymphoid aggregation was significantly enhanced in the grafts of PTX3 KO recipients. Recipient PTX3 deficiency enhanced chronic rejection-like lesions by promoting a fibrotic process in the airways and lung parenchyma. The underlying mechanisms and potential protective role of exogenous PTX3 as a therapy should be further explored. 
 Title: Pentraxin 3 deficiency enhances features of chronic rejection in a mouse orthotopic lung transplantation model

Ex Output:

True