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: 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: Brazzein protein comes from an edible fruit, which has a long history of being a staple in the local human diet in Africa. The attractive features of brazzein as a potential commercial sweetener include its small size (53 amino acid residues), its stability over wide ranges of temperature and pH, and the similarity of its sweetness to sucrose. Heterologous production of brazzein is complicated by the fact that the protein contains four disulfide bridges and requires a specific N-terminal sequence. Our previous protocol for producing the protein from Escherichia coli involved several steps with low overall yield: expression as a fusion protein, denaturation and renaturation, oxidation of the cysteines, and cleavage by cyanogen bromide at an engineered methionine adjacent to the desired N-terminus. The new protocol described here, which is much faster and leads to a higher yield of native protein, involves the production of brazzein in E. coli as a fusion with SUMO. The isolated protein product contains the brazzein domain folded with correct disulfide bonds formed and is then cleaved with a specific SUMO protease to liberate native brazzein. This protocol represents an important advancement that will enable more efficient research into the interaction between brazzein and the receptor as well as investigations to test the potential of brazzein as a commercially viable natural low calorie sweetener. 
 Title: Efficient and rapid protein expression and purification of small high disulfide containing sweet protein brazzein in E. coli
[A]: True


[Q]: Paragraph: Humans are colonized after birth by microbial organisms that form a heterogeneous community, collectively termed microbiota. The genomic pool of this macro-community is named microbiome. The gut microbiota is essential for the complete development of the immune system, representing a binary network in which the microbiota interact with the host providing important immune and physiologic function and conversely the bacteria protect themselves from host immune defense. Alterations in the balance of the gut microbiome due to a combination of environmental and genetic factors can now be associated with detrimental or protective effects in experimental autoimmune diseases. These gut microbiome alterations can unbalance the gastrointestinal immune responses and influence distal effector sites leading to CNS disease including both demyelination and affective disorders. The current range of risk factors for MS includes genetic makeup and environmental elements. Of interest to this review is the consistency between this range of MS risk factors and the gut microbiome. We postulate that the gut microbiome serves as the niche where different MS risk factors merge, thereby influencing the disease process. (J. Ochoa-Repáraz). FEBS Letters 588 (2014) 4214-4222 j o u r n a l h o m e p a g e : w w w . F E B S L e t t e r s . o r g 2. Environmental, genetics and microbial risk factors associated with CNS demyelinating disease Environmental, genetic, immunological and infectious diseases have been associated with MS [2]. The genetic background is thought to be a critical epidemiologic risk factor. As reviewed by Compton and colleagues, the familial recurrence rate in MS is 20% [7] . Monozygotic twins, sharing the 100% of the genetic information, have an MS lifetime risk of approximately 25-30%, siblings with two affected parents approximately a 20%, whereas dizygotic twins have a 5% lifetime risk, frequencies that suggest that the genetic background could interact with other risk factors. Alterations in immuno-regulatory or structural genes might increase the susceptibility to MS. Differences in the human leukocyte antigen (HLA) system-genes in the chromosome 6 that serve as the major histocompatibility complex (MHC) in humans-haplotypes DRBl*1501 and DQ6 have been suggested as genetic risk factors [8] . Recent genome-wide association studies (GWAS) reveal an evident effect of these genetic risk factors, with particular importance of HLA class II region, but also class I [9,10]. Interestingly, the genetic factors associated with MS are involved in immunological processes [11] , providing strong theoretical support to the autoimmune nature of MS, and moreover, provides the potential framework that environmental factors may be intimately involved in the modulation and/or perhaps even the trigger for disease susceptibility. 
 Title: Gut microbiome and the risk factors in central nervous system autoimmunity
[A]:
False