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: Biochar, that is, carbonized biomass similar to charcoal, has been used in acute medical treatment of animals for many centuries. Since 2010, livestock farmers increasingly use biochar as a regular feed supplement to improve animal health, increase nutrient intake efficiency and thus productivity. As biochar gets enriched with nitrogen-rich organic compounds during the digestion process, the excreted biochar-manure becomes a more valuable organic fertilizer causing lower nutrient losses and greenhouse gas emissions during storage and soil application. Scientists only recently started to investigate the mechanisms of biochar in the different stages of animal digestion and thus most published results on biochar feeding are based so far on empirical studies. This review summarizes the state of knowledge up to the year 2019 by evaluating 112 relevant scientific publications on the topic to derive initial insights, discuss potential mechanisms behind observations and identify important knowledge gaps and future research needs. The literature analysis shows that in most studies and for all investigated farm animal species, positive effects on different parameters such as toxin adsorption, digestion, blood values, feed efficiency, meat quality and/or greenhouse gas emissions could be found when biochar was added to feed. A considerable number of studies provided statistically non-significant results, though tendencies were mostly positive. Rare negative effects were identified in regard to the immobilization of liposoluble feed ingredients (e.g., vitamin E or Carotenoids) which may limit long-term biochar feeding. We found that most of the studies did not systematically investigate biochar properties (which may vastly differ) and dosage, which is a major drawback for generalizing results. Our review demonstrates that the use of biochar as a feed additive has the potential to improve animal health, feed efficiency and livestock housing climate, to reduce nutrient losses and greenhouse gas emissions, and to increase the soil organic matter content and thus soil fertility when eventually applied to soil. In combination with other good practices, co-feeding of biochar may thus have the potential to improve the sustainability of animal husbandry. However, more systematic multi-disciplinary research is definitely needed to arrive at generalizable recommendations. 
 Title: The use of biochar in animal feeding Distributed under Creative Commons CC-BY 4.0

Ex Output:
False


Ex Input:
Paragraph: Given the increased use of traditional medicines, possibilities that would ensure its successful integration into a public health framework should be explored. This paper discusses some of the links between biodiversity and traditional medicine, and addresses their implications to public health. We explore the importance of biodiversity and ecosystem services to global and human health, the risks which human impacts on ecosystems and biodiversity present to human health and welfare. 
 Title: Journal of Ethnobiology and Ethnomedicine Biodiversity, traditional medicine and public health: where do they meet?

Ex Output:

False