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".

[Q]: Paragraph: Cytokine expression patterns of T cells can be regulated by pre-commitment to stable effector phenotypes, further modification of moderately stable phenotypes, and quantitative changes in cytokine production in response to acute signals. We showed previously that the epidermal growth factor family member Amphiregulin is expressed by T cell receptor-activated mouse CD4 T cells, particularly Th2 cells, and helps eliminate helminth infection. Here we report a detailed analysis of the regulation of Amphiregulin expression by human T cell subsets. Signaling through the T cell receptor induced Amphiregulin expression by most or all T cell subsets in human peripheral blood, including naive and memory CD4 and CD8 T cells, Th1 and Th2 in vitro T cell lines, and subsets of memory CD4 T cells expressing several different chemokine receptors and cytokines. In these different T cell types, Amphiregulin synthesis was inhibited by an antagonist of protein kinase A, a downstream component of the cAMP signaling pathway, and enhanced by ligands that increased cAMP or directly activated protein kinase A. Prostaglandin E2 and adenosine, natural ligands that stimulate adenylyl cyclase activity, also enhanced Amphiregulin synthesis while reducing synthesis of most other cytokines. Thus, in contrast to mouse T cells, Amphiregulin synthesis by human T cells is regulated more by acute signals than precommitment of T cells to a particular cytokine pattern. This may be appropriate for a cytokine more involved in repair than attack functions during most inflammatory responses. 
 Title: The Acute Environment, Rather than T Cell Subset Pre- Commitment, Regulates Expression of the Human T Cell Cytokine Amphiregulin
[A]: False


[Q]: Paragraph: Using sequence data to infer population dynamics is playing an increasing role in the analysis of outbreaks. The most common methods in use, based on coalescent inference, have been widely used but not extensively tested against simulated epidemics. Here, we use simulated data to test the ability of both parametric and non-parametric methods for inference of effective population size (coded in the popular BEAST package) to reconstruct epidemic dynamics. We consider a range of simulations centred on scenarios considered plausible for pandemic influenza, but our conclusions are generic for any exponentially growing epidemic. We highlight systematic biases in non-parametric effective population size estimation. The most prominent such bias leads to the false inference of slowing of epidemic spread in the recent past even when the real epidemic is growing exponentially. We suggest some sampling strategies that could reduce (but not eliminate) some of the biases. Parametric methods can correct for these biases if the infected population size is large. We also explore how some poor sampling strategies (e.g. that over-represent epidemiologically linked clusters of cases) could dramatically exacerbate bias in an uncontrolled manner. Finally, we present a simple diagnostic indicator, based on coalescent density and which can easily be applied to reconstructed phylogenies, that identifies time-periods for which effective population size estimates are less likely to be biased. We illustrate this with an application to the 2009 H1N1 pandemic. Pandemic growth rates from sequences E. de Silva et al. 1799 Pandemic growth rates from sequences E. de Silva et al. 1807  
 Title: Inferring pandemic growth rates from sequence data
[A]: True


[Q]: Paragraph: Remyelination is a major therapeutic goal in human myelin disorders, serving to restore function to demyelinated axons and providing neuroprotection. The target disorders that might be amenable to the promotion of this repair process are diverse and increasing in number. They range primarily from those of genetic, inflammatory to toxic origin. In order to apply remyelinating strategies to these disorders, it is essential to know whether the myelin damage results from a primary attack on myelin or the oligodendrocyte or both, and whether indeed these lead to myelin breakdown and demyelination. In some disorders, myelin sheath abnormalities are prominent but demyelination does not occur. This review explores the range of human and animal disorders where myelin pathology exists and focusses on defining the myelin changes in each and their cause, to help define whether they are targets for myelin repair therapy. smooth ER in OLs in the myelin mutant taiep rat where it associates with accumulating microtubules. Golgi apparatus: This prominent organelle is involved in vesicular transport and trafficking and the site of post translational modifications of proteins such as PLP and myelin-associated glycoprotein (MAG). The rat mutant, vacuole formation (vf) may be the only myelin mutant with a specific defect in Golgi (see later). Microtubules: Microtubules are essential to the intracellular transport of protein and certain mRNAs (MBP and MAG mRNA) to the cell membrane and developing myelin sheath. The taiep rat has a specific defect in OL microtubules that result in both the initial failure of normal myelin production but also in its subsequent loss (see later). Lysosomes: This organelle is responsible for the intracellular degradation of effete organelles and extracellular materials through the action of hydrolytic enzymes that generate an acidic environment within the lysosome. A specific class of disorders, the lysosomal storage disorders result from a mutation in one of these enzymes that results in a build-up of the respective substrates. Two classic childhood lysosomal storage disorders, Krabbe's disease and metachromatic leukodystrophy result in severe CNS and peripheral nervous system (PNS) demyelination. Peroxisomes: They are involved in the metabolism of lipids in particular the β-oxidation of very long chain fatty acids. The primary example of a white matter disorder resulting from peroxisomal dysfunction is adrenoleukodystrophy. Unequivocal proof of myelin pathology and demyelination in the CNS requires definitive morphologic evidence that frequently can be hard to acquire, especially in human tissue. Tissue artifact following immersion fixation, poor perfusion (animals) or a delay in fixation after death is common and can lead to a de-compaction of myelin and misinterpretation of these and other changes. Paradoxically, the best fixation of CNS myelin is achieved where the density and thickness of myelin is less, i.e. in the genetic disorders. It is harder to achieve good fixation of myelin in the normal CNS because of the density and thickness of myelin sheaths perhaps leading to poor penetration of fixatives. The best fixation is achieved by cardiac or aortic perfusion with glutaraldehyde or Karnovsky fixative. In larger animal models, perfusion through the ascending and descending aorta is optimal. Using these methods and fixatives, tissue is processed for embedding in plastic resin that allows both light microscopy (1 micron, toluidine blue stained sections) or electron microscopy (ultrathin sections) to be performed. These sections provide superior resolution and quality to other histologic techniques and are the gold standard in myelin evaluation. Most recently, high pressure freezing of the CNS to avoid aldehyde fixation artifact has provided an alternative method to provide high quality ultrastructural resolution (Mobius et al., 2016) . 
 Title: Inherited and acquired disorders of myelin: the underling myelin pathology
[A]:
False