TASK DEFINITION: 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".
PROBLEM: Paragraph: Human immunodeficiency virus type 1 (HIV-1) Tat plays an important role in HIV-associated neuropathogenesis; the underlying mechanisms are still evolving. We have recently shown that HIV-1 Tat induces expression of glial fibrillary acidic protein (GFAP), a characteristic of HIV-1 infection of the central nervous system (CNS). We have also shown that the Tat-induced GFAP expression in astrocytes is regulated by p300, and that deletion of the early growth response 1 (Egr-1) cis-transacting element within the p300 promoter abolishes Tat-induced GFAP expression. In this study, we further examined the relationship between Tat and Egr-1 in astrocytes. We found increased Egr-1 protein expression in Tat-expressing human astrocytoma cells and mouse primary astrocytes. Using the Egr-1 promoter-driven firefly luciferase reporter gene assay and the sitedirected mutagenesis, we demonstrated that Tat increased Egr-1 expression by transactivating the Egr-1 promoter and involving specific serum response elements (SRE) within the promoter. Consistent with these data, we showed that Tat transactivation of the Egr-1 promoter was abrogated when astrocytes were cultured in serum-reduced media. Taken together, these results reveal that Tat directly transactivates Egr-1 expression and suggest that Tat interaction with Egr-1 is probably one of the very upstream molecular events that initiate Tat-induced astrocyte dysfunction and subsequent Tat neurotoxicity. 
 Title: Activation of Egr-1 expression in astrocytes by HIV-1 Tat: new insights into astrocyte-mediated Tat neurotoxicity

SOLUTION: True

PROBLEM: Paragraph: It is not clear whether turning on the gaspers in the cabins of commercial airliners actually improves the air quality. To answer this question, this study first developed a hybrid turbulence model which was suitable for predicting the air distribution in an aircraft cabin with gaspers turned on. Next, the investigation validated the model using two sets of experimental data from a cabin mockup and an actual airplane. This study then used the validated model to systematically investigate the impact of gaspers on cabin air quality in a seven-row section of the fully-occupied, economy-class cabin of Boeing 767 and 737 airplanes. The CFD calculations formed a database consisting of 9660 data points that provide information about SARS infection risk. It was found that the distribution of opened gaspers can influence the infection risk for passengers. Even though the gasper supplies clean air, it is possible for it to have a negative impact on the passengers' health. Statistically speaking, the overall effect of turning on the gaspers on the mean infection risk for the general population was neutral. 
 Title: Investigating the impact of gaspers on cabin air quality in commercial airliners with a hybrid turbulence model

SOLUTION: True

PROBLEM: Paragraph: Multiple sclerosis (MS) afflicts genetically predisposed individuals and is associated with T lymphocyte-mediated damage to the myelin sheath of neurons in the central nervous system, resulting in severely impaired signal transmission. The mechanisms of the induction and manifestation of MS are not entirely understood. The control of autoimmune disorders is accomplished by both central tolerance in which autoreactive T lymphocytes are eliminated in the thymus and by tolerance mechanisms that operate in the periphery. Among the many mechanisms described, T regulatory (Treg) cells derived from the thymus (tTregs) and induced (iTregs) in the periphery as well as T regulatory type 1 cells (Tr1) are involved in many disease models. However, the precise details of the generation and perpetuation of these various Treg subsets and their relevance to the regulation of autoimmune diseases remain elusive. In this review, we critically analyze the current knowledge of the tolerance mechanisms involved in the regulation of MS and its animal model, experimental autoimmune encephalomyelitis. 
 Title: Immune Tolerance in Autoimmune Central Nervous System Disorders-brain barrier · Central nervous system · Cerebrospinal fluid · Foxp3 · GM-CSF · Human leukocyte antigen · Interferon-γ · Interleukin 17 · Myelin basic protein · Multiple sclerosis · Myelin oligodendrocyte glycoprotein · Neuromyelitis optica · Proteolipid protein · Th1 · Th17 · T regulatory cells · Trichostatin A · Tumor necrosis factor-α, Tolerance

SOLUTION:
False