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".
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Question: Paragraph: microRNAs (miRNAs) represent a newly identified class of nonprotein-coding *22 nt small RNA that plays important roles in multiple biological processes by degrading targeted mRNA or repressing mRNA translation. This study observed the morphology of swine testicular tissue at different developmental stages (including 1-day old, 1-7 month old) by Hematoxylin-eosin staining. We also examined the expression of miR-499 and its target genes (CYLC1, DMRT1, QKI, XRN2, ZNF313) in samples of tissue slices using quantitative reversetranscription polymerase chain reaction, which showed that miR-499 had a significant negative correlation with QKI gene. Then, the proteins of QKI gene expression were determined by western blot, which were consistent with results of quantitative polymerase chain reaction (qPCR) detection. Therefore, the luciferase reporter gene system was used to verify correlation between miR-499 and QKI gene. Activity of luciferase was significantly lower in miR-499 co-transfected with pmiR-RB-REPORT-QKI-WT group than the miR-499 co-transfected with pmiR-RB-REPORT-QKI-mut/si groups, indicating that target sequence of miR-499 existed in 3UTR of QKI gene. Furthermore, the expressions of miR-499 and QKI were detected in testicular cells that were transfected with miR-499, miR-499 negative control and untreated. The results showed that the diameter of convoluted seminiferous tubule growth increased with age. Significantly different expressions of miR-499 and its target genes were found in swine testicular tissue at different developmental stages ( p < 0.05), overexpressing miR-499 analysis, suggesting that miR-499 was negatively correlated to the expression of QKI ( p < 0.05). In conclusion, QKI is a target gene of miR-499.
Title: Differential Expression of miR-499 and Validation of Predicted Target Genes in the Testicular Tissue of Swine at Different Developmental Stages

Answer: False

Question: Paragraph: This paper describes the molecular detection of respiratory viruses from nasopharyngeal flocked swabs (flocked swabs) and nasopharyngeal washes (washes) in a clinical setting. Washes and flocked swabs collected from children < 3 years old hospitalized with a lower respiratory tract infection were tested for parainfluenza virus 1-3, respiratory syncytial virus, influenza A and B and metapneumovirus (Group 1) and adenovirus, rhinovirus and coronavirus (Group 2) using realtime reverse transcriptase PCR (rRT-PCR). A consensuses standard was used to determine sensitivity and compare cycle thresholds (C T ) of washes and flocked swabs for each virus and group of viruses. Sensitivities ranged from 79 to 89% and 69 to 94% for flocked swabs and washes, respectively, excluding AdV which had a sensitivity of 35% for flocked swabs. When the flocked swabs and washes of Group 1 viruses were collected on the day of admission, the sensitivity of both sample types was 100%. Wash specimens had a lower C T value and higher sensitivity than flocked swabs; however there was no statistical difference in the sensitivity of a flocked swab (89%) versus wash (93%) for the detection of Group 1 viruses, particularly when samples were collected on the same day. Flocked swabs may be a useful alternative to washes for detection of respiratory viruses in clinical settings.
Title: Comparison of nasopharyngeal flocked swabs and nasopharyngeal wash collection methods for respiratory virus detection in hospitalized children using real-time polymerase chain reaction HHS Public Access

Answer: False

Question: Paragraph: cally active but which do not bind antibody 259 have been prepared recently; cells transformed by such mutants were not altered morphologically, nor did they show greatly inhibited thymidine incorporation, after injection of antibody 259 26 It is assumed that while viral oncogenes function without normal control, their mechanism of action is similar to that of related cellular genes. Here we have presented evidence to support this idea in the case of growth factor receptor-like molecules and related oncogenes. It is therefore possible that these data might aid in understanding the way in which cellular genes interact in the control of normal proliferation. Our results indicate that some receptor-like oncogenes depend on ras proteins while some cytoplasmic oncogenes do not. There are, of course, numerous oncogenes which we have not yet tested which might behave differently from those described here. With this limitation in mind and on the basis of our present data, we propose that an important class of proliferative signals are received at the cell surface by receptor molecules such as growth factor receptors, and the c-ras proteins are essential in the transfer of these signals to cytoplasmic effectors having serine kinase activity; the effectors then modify target molecules which are directly involved in initiating a proliferative cycle. Accordingly, if the cytoplasmic effector were mutated such that it functioned without activation, proliferation would continue independently of c-ras proteins. Receptor molecules, on the other hand, would always require c-ras to stimulate proliferation. While our data are consistent with the above scheme, they do not exclude many other possibilities involving multiple metabolic pathways and more complex interactions. For example, we have not reported results with nuclear oncogenes owing to their difficulty in transforming NIH 3T3 cells. The proposed scheme is primarily attractive because of its similarity to the carefully studied mechanism of signal transduction involving cyclic AMP. While it is unlikely that cyclic AMP itself regulates proliferation 27 , G-regulatory proteins with enzymatic similarities to c-ras proteins are involved. These regulatory proteins control signal transduction from cell-surface receptors to cytoplasmic serine kinase effector molecules by regulating adenyl cyclase activity28. While the present study has examined only one aspect of what is likely to be a highly complex system for regulating proliferation, it does provide a means of functionally comparing separate viral oncogenes. Injection of antibody has been used in other studies to characterize the types of molecules responsible for tumour cell proliferation. Like NIH 3T3 cells transformed by mos or raj genes, many tumour cells show no inhibition of proliferation when injected with anti-ras antibody. In this way their proliferation is distinct from that of the normal cell types studied, each of which was efficiently inhibited by the injected antibodyl6.
Title: Viral particles induce Ia antigen expression on astrocytes

Answer:
False