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: Pulmonary edema, a major manifestation of left ventricular heart failure, renal insufficiency, shock, diffuse alveolar damage and lung hypersensitivity states, is a significant medical problem worldwide and can be life-threatening. The proinflammatory cytokine tumor necrosis factor (TNF) has been shown to contribute to the pathogenesis and development of pulmonary edema. However, some recent studies have demonstrated surprisingly that TNF can also promote alveolar fluid reabsorption in vivo and in vitro. This protective effect of the cytokine is mediated by the lectin-like domain of the cytokine, which is spatially distinct from the TNF receptor binding sites. The TIP peptide, a synthetic mimic of the lectinlike domain of TNF, can significantly increase alveolar fluid clearance and improve lung compliance in pulmonary edema models. In this review, we will discuss the dual role of TNF in pulmonary edema. Abbreviations:-tumor necrosis factor (TNF); acute lung injury (ALI); acute respiratory distress syndrome (ARDS); positive end-expiratory pressure (PEEP);epithelial sodium channel (ENaC);neural precursor cell-expressed developmentally downregulated (gene 4) protein (Nedd4-2);serum and glucocorticoid dependent kinase (Sgk-1);insulin-like growth factor 1 (IGF-1);Protein Kinase C (PKC);reactive oxygen species (ROS);myosin light chain (MLC);pneumolysin (PLY);listeriolysin (LLO);interleukin (IL);bronchoalveolar lavage fluids (BALF);Bacillus Calmette-Guerin (BCG);TNF receptor type 1 (TNF-R1); TNF receptor type 2 (TNF-R2); 
 Title: Journal of Cardiovascular Disease Research OPEN ACCESS JCDR: Invited Review The Dual Role of TNF in Pulmonary Edema

A: True
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Q: Paragraph: The newborn calf's gastrointestinal tract is sterile at birth, but by 3 days of age coliforms, Lactobacilli, and Bifidobacteria are the predominant flora in the feces. During the preweaning period, calves are susceptible to diarrhea that can lead to high levels of morbidity and mortality. Diarrhea has been related with a decrease of beneficial microbiota and an increase of coliform counts in feces. Prebiotic supplements are believed to decrease diarrhea and positively affect some parameters of the immune system. In calves, these supplements have shown some promising effects on intestinal microbial populations but there is limited information about effects on immunity. The main objectives of this study were to evaluate effects of a prebiotic supplement containing fermentation products of lactic acid bacteria on the mucosal immune system by measuring fecal and salivary IgA and to evaluate calf health and growth performance. In this trial 40 Holstein calves were randomly assigned to receive milk replacer with a prebiotic supplement (20 g/day Prebio Support™; Meiji Feed Co., Ltd. Tokyo, Japan) or the same milk replacer with no prebiotic (control). Fecal and salivary IgA, calf health, plasma IgG, and lymphocyte counts were not affected by treatment. Lactobacilli count in feces was higher (P = 0.05) and Bifidobacteria tended to be higher (P = 0.07) in calves fed prebiotic. Prebiotic supplement increased beneficial bacteria in calves, but did not decrease overall incidence of diarrhea in this trial. Calves in this study were all affected by cryptosporidiosis and some were treated with antibiotics, so it is possible that this limited some of the effects of the prebiotic product. Fecal IgA seemed to be a good measure of mucosal immunity, and more studies are needed to develop methods to measure this type of immunity in calves. 
 Title: The effects of a prebiotic supplement (Prebio Support) on fecal and salivary IgA in neonatal dairy calves

A: True
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Q: Paragraph: The coronavirus replicase-transcriptase complex is an assembly of viral and cellular proteins that mediate the synthesis of genome and subgenome-sized mRNAs in the virus-infected cell. Here, we report a genetic and functional analysis of 19 temperature-sensitive (ts) mutants of Murine hepatitis virus MHV-A59 that are unable to synthesize viral RNA when the infection is initiated and maintained at the non-permissive temperature. Both classical and biochemical complementation analysis leads us to predict that the majority of MHV-A59 ORF1a replicase gene products (nonstructural proteins nsp1-nsp11) form a single complementation group (cistron1) while the replicase gene products encoded in ORF1b (non-structural proteins nsp12-nsp16) are able to function in trans and comprise at least three, and possibly five, further complementation groups (cistrons II-VI). Also, we have identified mutations in the non-structural proteins nsp 4, nsp5, nsp10, nsp12, nsp14, and nsp16 that are responsible for the ts phenotype of eight MHV-A59 mutants, which allows us to conclude that these proteins are essential for the assembly of a functional replicasetranscriptase complex. Finally, our analysis of viral RNA synthesis in ts mutant virus-infected cells allows us to discriminate three phenotypes with regard to the inability of specific mutants to synthesize viral RNA at the nonpermissive temperature. Mutant LA ts6 appeared to be defective in continuing negative-strand synthesis, mutant Alb ts16 appeared to form negative strands but these were not utilized for positive-strand RNA synthesis, and mutant Alb ts22 was defective in the elongation of both positive-and negative-strand RNA. On the basis of these results, we propose a model that describes a pathway for viral RNA synthesis in MHV-A59-infected cells. Further biochemical analysis of these mutants should allow us to identify intermediates in this pathway and elucidate the precise function(s) of the viral replicase proteins involved. Citation: Sawicki SG, Sawicki DL, Younker D, Meyer Y, Thiel V, et al. (2005) Functional and genetic analysis of coronavirus replicase-transcriptase proteins. PLoS Pathog 1(4): e39. 
 Title: Functional and Genetic Analysis of Coronavirus Replicase-Transcriptase Proteins

A:
False
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