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: During viral entry, enveloped viruses require the fusion of their lipid envelope with host cell membranes. For coronaviruses, this critical step is governed by the virally-encoded spike (S) protein, a class I viral fusion protein that has several unique features. Coronavirus entry is unusual in that it is often biphasic in nature, and can occur at or near the cell surface or in late endosomes. Recent advances in structural, biochemical and molecular biology of the coronavirus S protein has shed light on the intricacies of coronavirus entry, in particular the molecular triggers of coronavirus S-mediated membrane fusion. Furthermore, characterization of the coronavirus fusion peptide (FP), the segment of the fusion protein that inserts to a target lipid bilayer during membrane fusion, has revealed its particular attributes which imparts some of the unusual properties of the S protein, such as Ca 2+ -dependency. These unusual characteristics can explain at least in part the biphasic nature of coronavirus entry. In this review, using severe acute respiratory syndrome coronavirus (SARS-CoV) as model virus, we give an overview of advances in research on the coronavirus fusion peptide with an emphasis on its role and properties within the biological context of host cell entry. 
 Title: Physiological and molecular triggers for SARS-CoV membrane fusion and entry into host cells

Ex Output:
True


Ex Input:
Paragraph: Middle East respiratory syndrome coronavirus MERS Healthcare-associated outbreaks S U M M A R Y Middle East respiratory syndrome coronavirus (MERS-CoV) is capable of causing acute respiratory illness. Laboratory-confirmed MERS-CoV cases may be asymptomatic, have mild disease, or have a life-threatening infection with a high case fatality rate. There are three patterns of transmission: sporadic community cases from presumed non-human exposure, family clusters arising from contact with an infected family index case, and healthcareacquired infections among patients and from patients to healthcare workers. Healthcareacquired MERS infection has become a well-known characteristic of the disease and a leading means of spread. The main factors contributing to healthcare-associated outbreaks include delayed recognition, inadequate infection control measures, inadequate triaging and isolation of suspected MERS or other respiratory illness patients, crowding, and patients remaining in the emergency department for many days. A review of the literature suggests that effective control of hospital outbreaks was accomplished in most instances by the application of proper infection control procedures. Prompt recognition, isolation and management of suspected cases are key factors for prevention of the spread of MERS. Repeated assessments of infection control and monitoring of corrective measures contribute to changing the course of an outbreak. Limiting the number of contacts and hospital visits are also important factors to decrease the spread of infection. 
 Title: Healthcare-associated infections: the hallmark of Middle East respiratory syndrome coronavirus with review of the literature

Ex Output:
True


Ex Input:
Paragraph: Methamphetamine (METH) is a psychostimulant with high abuse potential and severe neurotoxicity. Recent studies in animal models have indicated that METH can impair the blood-brain barrier (BBB), suggesting that some of the neurotoxic effects resulting from METH abuse could be due to barrier disruption. We report here that while chronic exposure to METH disrupts barrier function of primary human brain microvascular endothelial cells (HBMECs) and human umbilical vein endothelial cells (HUVECs), an early pro-survival response is observed following acute exposure by induction of autophagic mechanisms. Acute METH exposure induces an early increase in Beclin1 and LC3 recruitment. This is mediated through inactivation of the protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/p70S6K pathway, and upregulation of the ERK1/2. Blockade of Kappa opioid receptor (KOR), and treatment with autophagic inhibitors accelerated METH-induced apoptosis, suggesting that the early autophagic response is a survival mechanism for endothelial cells and is mediated through the kappa opioid receptor. Our studies indicate that kappa opioid receptor can be therapeutically exploited for attenuating METH-induced BBB dysfunction. Methamphetamine (METH) is a central nervous system (CNS) stimulant that is similar in structure to amphetamine. The escalating abuse of this drug in recent years and its longlasting neurotoxic effects have placed an increased burden upon health care costs. Previous studies have shown that METH-induced autophagy in neurons is associated with the formation of ubiquitin-positive aggregates and multilamellar bodies. 1,2 In addition to its direct effects on neurons, bloodbrain barrier (BBB) dysfunction could also contribute to METH-induced neurotoxicity. 3 The BBB is a specialized structure formed by brain endothelial cells that are tightly interconnected to form a boundary between the CNS and periphery . 4 Recent findings suggest that METH impairment of glucose transporter protein-1(GLUT1) at the brain endothelium may affect energy-associated disruption of tight junction assembly and loss of BBB integrity. 5 Furthermore, METH can act directly on cultured primary rat brain microvascular endothelial cells to compromise their barrier properties inducing eNOS activation and enhanced transcytosis. 3 The primary goal of the current study was to investigate whether METH treatment induces autophagy in endothelial cells. Macroautophagy (hereafter referred to as autophagy) is an intracellular lysosomal (vacuolar) degradation process that is characterized by the formation of a cytosolic doublemembrane vesicle, the autophagosome. During autophagy, cytoplasmic proteins, organelles or other materials are surrounded by phagophores, which expand and close to form double-membrane autophagosomes. These autophagosomes fuse with lysosomes (or vacuoles) to form autolysosomes, in which the cytoplasmic cargos are degraded by lysosomal enzymes. The primary role of autophagy is to ensure cell survival under stress conditions. 6 Most assays for autophagy modulators use the autophagy marker protein microtubule-associated protein 1 light chain 3 (LC3) as a readout for autophagic activity. LC3 is a mammalian orthologue of the yeast ATG 8 protein, a ubiquitin-like protein that becomes lipidated and tightly associated with the autophagosomal membranes. 7 Lysosomal-associated membrane protein1 (LAMP1) is among the most abundant lysosomal membrane protein. It is a heavily glycosylated protein creating a sugar coat or glycocalyx on the inner side of the lysosomal membrane which aids to the protection of the membrane from the hydrolytic enzymes and degradation. LAMP1 is expressed mainly in the endosome-lysosomal membrane of cells which is involved in maintaining lysosomal membrane integrity and phagolysosome formation. 8, 9 We show that METH exposure-induced autophagy early on and progressively changed into apoptosis in a time-dependent manner. The METH-induced autophagy was specific and initiated even in the presence of nutrient-rich medium. Inhibition of METH-induced autophagy accelerated apoptosis of endothelial cells. METH-induced autophagy was mediated 1 
 Title: Methamphetamine induces autophagy as a pro-survival response against apoptotic endothelial cell death through the Kappa opioid receptor

Ex Output:

False