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.

Example Input: strains of infectious bronchitis virus (IBV) were isolated from the vaccinated chicken flocks in Sichuan province, China. The S1 genes of the isolates were amplified and sequenced. Phylogenetic analysis revealed that the 19 isolates and 37 reference IBV strains can be grouped into eight genotypes. Although IBVs of Taiwan-I type, massachusetts type, and proventriculitis type were isolated, but most isolates were LX4 genotype. Homology analysis of the sequences of S1 genes of the 19 isolates and 37 reference IBV strains revealed that the identity of the nucleotides and amino acid sequences of the S1 genes between the 15 LX4-type isolates and other IBV strains were 71.9-99.3% and 72.1-99.1%, respectively, while those of the analyzed IBV of LX4 type were 96.0-99.9% and 94.3-99.8%, respectively. The results from this study and other published results in the GenBank database showed that isolates circulating in Sichuan province in recent years were mainly LX4 genotype, which is the predominant genotype circulated in China in recent years.
Example Output: Genetic analysis revealed LX4 genotype strains of avian infectious bronchitis virus became predominant in recent years in Sichuan area, China

Example Input: We report a hereditary leukodystrophy in Standard Schnauzer puppies. Clinical signs occurred shortly after birth or started at an age of under 4 weeks and included apathy, dysphoric vocalization, hypermetric ataxia, intension tremor, head tilt, circling, proprioceptive deficits, seizures and ventral strabismus consistent with a diffuse intracranial lesion. Magnetic resonance imaging revealed a diffuse white matter disease without mass effect. Macroscopically, the cerebral white matter showed a gelatinous texture in the centrum semiovale. A mild hydrocephalus internus was noted. Histopathologically, a severe multifocal reduction of myelin formation and moderate diffuse edema without inflammation was detected leading to the diagnosis of leukodystrophy. Combined linkage analysis and homozygosity mapping in two related families delineated critical intervals of approximately 29 Mb. The comparison of whole genome sequence data of one affected Standard Schnauzer to 221 control genomes revealed a single private homozygous protein changing variant in the critical intervals, TSEN54:c.371G>A or p.(Gly124Asp). TSEN54 encodes the tRNA splicing endonuclease subunit 54. In humans, several variants in TSEN54 were reported to cause different types of pontocerebellar hypoplasia. The genotypes at the c.371G>A variant were perfectly associated with the leukodystrophy phenotype in 12 affected Standard Schnauzers and almost 1000 control dogs from different breeds. These results suggest that TSEN54:c.371G>A causes the leukodystrophy. The identification of a candidate causative variant enables genetic testing so that the unintentional breeding of affected Standard Schnauzers can be avoided in the future. Our findings extend the known genotype-phenotype correlation for TSEN54 variants. Various hereditary diseases of the cerebral white matter occur in humans and dogs. We describe a new leukodystrophy in Standard Schnauzers. Genetic mapping and whole genome sequence analysis identified a likely candidate causative variant in the TSEN54 gene encoding tRNA splicing endonuclease 54. These results provide new information about the role of TSEN54 in cell metabolism and the development of the central nervous system in the late gestational and early post-natal period. The affected dogs potentially represent a translational large animal model for similar leukoencephalopathies in human medicine. The clinical phenotype in Schnauzers included multifocal central nervous system signs. A holistic pathogenically driven understanding of disease initiation and perpetuation requires a solid analysis of the underlying genetics and characterization of the disease phenotype at the clinical and cellular as well as sub-cellular level. In contrast to the canine phenotype with a predominant manifestation in the cerebrum white matter, other TSEN54 variants in humans have been reported to result in a different pathological phenotype characterized by pontocerebellar hypoplasia. The differences between humans and dogs underscore the need for comparative analysis at the clinical, pathological and molecular level to understand species-specific protein mediated pathways, interactions and outcomes.
Example Output: TSEN54 missense variant in Standard Schnauzers with leukodystrophy Author summary

Example Input: Next year will mark the 100th anniversary of the Michaelis-Menten equation [1], one of the most important and well known models in enzymology. Remarkable progress in enzymology over the past hundred years has not only provided deep insight into biological processes, but also has dramatically changed our lives. However, because of limitations in available techniques, enzymologists primarily investigate the in vitro properties and catalytic mechanisms of individual enzymes. Thus, they often fail to address a fundamental scientific question: how are biological processes, most of which are chemical reactions catalyzed by enzymes, coordinated in space and time to produce a living organism [2]? Fortunately, applications of new techniques and, in particular, wide acceptance of the idea of systems have enabled enzymologists to begin studying enzymes in the context of dynamic, complicated biological systems in recent years. Many excellent reviews and research articles on enzymology have been published in the past few years. These articles highlight the latest developments in enzymology, and should prove helpful for understanding how to best integrate the idea of systems into enzymology research. In living organisms, protein post-translational modification (PTM) pathways are large and interconnected networks. Via reversible or irreversible covalent modifications, allo-steric regulations of PTM enzymes and cross-talk of PTM pathways, PTM networks enable organisms to respond to stimuli faster than is possible through gene transcription regulation. Therefore, PTM enzymes, as key nodes of biological networks, are a recent focus of attention.
Example Output:
SCIENCE CHINA A glimpse of enzymology within the idea of systems