In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Ex Input:
Influenza viruses are a major public health problem worldwide. Although influenza has been extensively researched, there are still many aspects that are not fully understood such as the effects of within and between-hosts dynamics and their impact on behavior change. Here, we develop mathematical models with multiple infection stages and estimate parameters based on within-host data to investigate the impact of behavior change on influenza dynamics. We divide the infected population into three and four groups based on the age of the infection, which corresponds to viral load shedding. We consider within-host data on viral shedding to estimate the length and force of infection of the different infectivity stages. Our results show that behavior changes, due to exogenous events (e.g., media coverage) and disease symptoms, are effective in delaying and lowering an epidemic peak. We show that the dynamics of viral shedding and symptoms, during the infection, are key features when considering epidemic prevention strategies. This study improves our understanding of the spread of influenza virus infection in the population and provides information about the impact of emergent behavior and its connection to the within and between-hosts dynamics.

Ex Output:
Connecting within and between-hosts dynamics in the influenza infection-staged epidemiological models with behavior change


Ex Input:
Middle east respiratory syndrome coronavirus International travel Pilgrims a b s t r a c t Objective: We aimed to evaluate the level of knowledge of Middle East respiratory syndrome coronavirus (MERS-CoV) among Hajj pilgrims before and after an education health programme during international vaccine consultations in France. Methods: Consecutive adults (>18 years old) who attended for pre-Hajj meningococcal vaccination were eligible to complete an anonymous questionnaire with closed answers to evaluate their level of knowledge about MERS-CoV. To evaluate the effectiveness of the information given during the consultation, the same questionnaire was completed by the Hajj pilgrim before and after the consultation, where the information about MERS-CoV was provided. Results: Among 82 Hajj pilgrim adults enrolled in the study, less than 25% were aware of the routes of transmission, symptoms and preventive behaviours to adopt abroad or in case of fever. Pilgrims had a higher rate of correct responses on each question at the time they completed the second questionnaire, as compared with the first, with 11 of 13 questions answered significantly better after delivery of educational information about MERS-CoV. However, although the rate of correct answers to the questions about routes of transmission, symptoms, preventive behaviours to adopt in case of fever and time delay between return and potential MERS-CoV occurrence increased significantly after receiving the information, the rates remained below 50%. Conclusion: Information given during travel consultations significantly increases the general level of knowledge, but not enough to achieve epidemic control.

Ex Output:
Effectiveness of an education health programme about Middle East respiratory syndrome coronavirus tested during travel consultations Public Health


Ex Input:
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

Ex Output:

Methamphetamine induces autophagy as a pro-survival response against apoptotic endothelial cell death through the Kappa opioid receptor