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: Apelin is an inotropic and cardioprotective peptide that exhibits beneficial effects through activation of the APJ receptor in the pathology of cardiovascular diseases. Apelin induces the expression of angiotensin-converting enzyme 2 (ACE2) in failing hearts, thereby improving heart function in an angiotensin 1-7-dependent manner. Whether apelin antagonizes the over-activation of the renin-angiotensin system in the heart remains elusive. In this study we show that the detrimental effects of angiotensin II (Ang II) were exacerbated in the hearts of aged apelin-gene-deficient mice. Ang II-mediated cardiac dysfunction and hypertrophy were augmented in apelin knockout mice. The loss of apelin increased the ratio of angiotensin-converting enzyme (ACE) to ACE2 expression in the Ang II-stressed hearts, and Ang II-induced cardiac fibrosis was markedly enhanced in apelin knockout mice. mRNA expression of pro-fibrotic genes, such as transforming growth-factor beta (TGF-β) signaling, were significantly upregulated in apelin knockout hearts. Consistently, treatment with the ACE-inhibitor Captopril decreased cardiac contractility in apelin knockout mice. In vitro, apelin ameliorated Ang II-induced TGF-β expression in primary cardiomyocytes, accompanied with reduced hypertrophy. These results provide direct evidence that endogenous apelin plays a crucial role in suppressing Ang II-induced cardiac dysfunction and pathological remodeling. Int. J. Mol. Sci. 2019, 20, 239 2 of 12 dysfunctions [8, 10, 11] . By contrast, APJ was identified as a dual receptor to mediate cardiac hypertrophy [12, 13] via β-arrestin signaling [14, 15] . Thus, the precise role of endogenous apelin signaling in heart function remains elusive. Cardiac hypertrophy is an adaptive response to maintain cardiac function in the event of an increased workload, although prolonged cardiac hypertrophy can lead to heart failure via the ischemia of cardiomyocytes [16, 17] . In addition, cardiac fibrosis adversely increases tissue stiffness and impairs ventricular function. Consistently, cardiac hypertrophy and the development of fibrosis correlate with the deterioration of myocardial function in heart failure [18] [19] [20] . Thus, cardiac hypertrophy and fibrosis are key features of heart failure, and apelin's inotropic and protective roles in the heart are attractive as a potential therapeutic candidate for treating heart failure. Apelin has also been identified as a substrate for angiotensin-converting enzyme 2 (ACE2), which cleaves apelin with similar efficiency as its primary substrate angiotensin II (Ang II) [21] [22] [23] . ACE2 is a negative regulator of the renin-angiotensin system (RAS) that inactivates Ang II by converting it to angiotensin 1-7 (Ang 1-7) [21] [22] [23] , whereas angiotensin-converting enzyme 1 (or ACE1) activates RAS by converting Ang I to Ang II. ACE2 was also identified as a regulator of heart failure [24-26], diabetic nephropathy [27, 28] , acute lung failure [29, 30] , and the SARS (severe acute respiratory syndrome) coronavirus receptor [31, 32] . Apelin-APJ signaling has been shown to counteract the effects of Ang II on AT1R in defined physiological and pathophysiological settings. For instance, in hypertensive rat models, the continuous infusion of Ang II downregulates apelin and APJ expression [33] . We have shown that Apelin upregulates ACE2 expression. Apelin-induced ACE2 downregulates Ang II signaling while enhancing Ang 1-7-Mas receptor signaling in aged or failing hearts [34] . On the other hand, it has been suggested that the counter-balancing effects of the apelin-APJ axis on Ang II-AT1R signaling are mediated by receptor dimerization. The APJ receptor physically interacts with AT1 receptors, and exogenous apelin negatively regulates Ang II-AT1R signaling in in vitro cell culture systems and in an in vivo atherosclerosis model [35] . However, whether endogenous apelin counteracts the over-activation of RAS in the heart remains unexplored. In this study, we aimed to determine the effects of endogenous apelin on Ang II-induced pathology in the heart. We showed that Ang II-mediated cardiac dysfunction, hypertrophy, and fibrosis were augmented in apelin knockout (Apelin KO) mice. 
 Title: Loss of Apelin Augments Angiotensin II-Induced Cardiac Dysfunction and Pathological Remodeling

Ex Output:
True


Ex Input:
Paragraph: publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. Abstracts accepted for publication only Pathogenesis R2249 Effect of a probiotic dairy product containing Lactobacillus casei Shirota on the gut microbiota in irritable bowel syndrome: a randomised, placebo-controlled, double-blind study Objectives: It has been hypothesized that disturbances in the intestinal flora could be a factor in the onset and persistence of IBS complaints. The aim of the study was to analyse the effect of Lactobacillus casei Shirota (LcS) on the faecal flora of IBS patients. Methods: In a randomised, placebo controlled, double blind study, IBS patients fulfilling the Rome criteria II were included. Patients took 2 bottles daily for 8 weeks, containing either LcS or placebo. Faecal samples were collected before intervention (week −2/0,S1), at the end of intervention (week 6/8,S2) and during follow-up (week 14/16,S3). Microbial populations (Bacteroides, anaerobes, bifidobacteria, coliforms, clostridia, and lactobacilli) were enumerated using quantitative plating. Total bacterial counts were performed using FISH. Bacterial DNA was analysed by quantitative Real-Time PCR for the detection of Atopobium spp., Bacteroides-Prevotella-Porphyromonas group, Clostridium coccoides-Eubacterium rectale group, Clostridium leptum subgroup, Clostridium difficile, Clostridium perfringens, Desulfovibrio desulfuricans group, and Bifidobacterium spp. Statistical analysis was performed using Mann-Whitney U tests or Paired Wilcoxon tests. P < 0.05 was considered statistically significant. Results: No significant differences in total bacterial counts were seen between the treatment and placebo group. Using quantitative plating, no significant differences were seen for the different bacterial groups between both groups. Significantly lower bacterial counts were seen in both groups for clostridia for S2 compared to S1 and S3. In the placebo group, significantly higher amounts of bifidobacteria and lactobacilli were detected for S2 compared to S1. Using qRT-PCR, significantly lower counts for D. desulfuricans group were seen in the placebo group compared to the treatment group. In the treatment group significant differences were seen only for S2 compared to S3, whereas in the placebo group, no significant differences were detected for the different bacterial groups at the different sampling points. Analysis at the IBS subtype level revealed differences in microbiota between the different subtypes. Conclusions: Although significant changes in the microbiota were seen during intake of LcS in the treatment group, differences in microbial populations between both groups were not significant. Interestingly, specific findings are likely to be associated with a specific IBS subtype rather than with IBS in general. Objective: To asses the chest radiography findings of patients with H1N1 Influenza virus infection. Review of radiological findings of 110 patients with confirmed influenza A virus infection admitted to two Hospitals in Cantabria, Spain. The radiological findings were characterized by pattern of opacities, lung distribution and, presence or absence of pleural effusions or hiliar or mediastinal adenopahies. The initial radiography was abnormal in 39 (34%) patients, but only 28 (25%) were related exclusively to the influenza A virus infection. Characteristic imaging findings in these 28 patients included: parenchymal consolidation 68%, consolidation plus ground glass 25% and ground glass opacities in 7%. Seventeen patients had a diffuse distribution of the opacities, in 61% it was bilateral, and lower and middle zones were those most frequently affected. No pleural effusions or pathological mediastinal lymph nodes were seen in this initial radiography. Patients with abnormal chest X-ray were more frequently men, smokers, had dyspnoea, pleuritic pain and diarrhoea. Conclusions: Although more of patients with influenza virus A infection showed normal chest X-ray, those with abnormal chest radiographies, characteristically showed areas of consolidation with or without ground glass affectation, bilateral and diffuse distribution, and predilection for lower and middle zones. Pleural effusion or mediastinal adenopahty were not findings seen in the initial radiography. 
 Title: R2250 H1N1 virus infection: review of chest radiographic findings

Ex Output:
False


Ex Input:
Paragraph: Using six monoclonal antibodies to epitopes a-f on the glycoprotein E2 of Semliki Forest virus (SFV) we found antigenic differences between E2 in infected cells and in virus particles, respectively, if glycosylation was impaired by 2-deoxy-D-glucose or inhibited by N-methyl-l-deoxynojirimycin. Furthermore we concluded that a conformational change of E2 takes place on virus budding. The composition and structure of carbohydrate side chains attached to viral glycoproteins is important for virus maturation. They may influence virus adsorption and penetration, transport of viral glycoproteins [12] , proteolytic cleavage of precursor proteins [1, 7] , association of spike glycoproteins [13] or their antigenicities [5, 11] . With Semliki Forest virus (SFV), a togavirus containing the nucleocapsid protein C and three envelope glycoproteins El, E2 and E3, we previously observed that virus maturation could be inhibited by impairment of glycosylation, e.g. by treatment of infected cells with tunicamycin or 2-deoxy-D-glucose (2-DG) [5] . Using polyclonal antisera, we have shown in addition that antigenicities of glycoproteins with no carbohydrate side chains (after treatment with tunicamycin) or with truncated chains (after treatment with 2-DG) differed from those of virus particles [2, 4, 9-]. Using six monoclonal antibodies (mabs) specific for six epitopes a-f on virion E2 we recently found changes in antigenicity of virion E2, if SFV was propagated in cells in presence of N-methyl-l-deoxynojirimycin (MdN): released, infectious virus particles contained mannose-rich carbohydrate side chains of the composition GI%ManT.8,9(GlcNAc)2; epitope d reacted very well, epitopes c and e reacted less, and epitopes a, b and f only very slightly [6, 10-]. 
 Title: Differences in antigenicity of E2 in Semliki Forest virus particles and in infected cells Brief Report

Ex Output:

True