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.

Electron microscopy (EM) allows fast visualization of viruses in a wide range of clinical specimens. Viruses are grouped into families based on their morphology. Viruses from various families look distinctly and these morphological variances are the basis for identification of viruses by EM. The identification to the family level is often sufficient for the clinician or recognition of an unknown infectious agent. Diagnostic EM has two advantages over enzyme-linked immunosorbent assay and nucleic acid amplification tests. After a simple and fast negative staining, EM allows fast morphological identification and differential diagnosis of infectious agents contained in the specimen without the need for special considerations and/or reagents. Nevertheless, EM has the disadvantage of being unsuitable as a screening method. Abbreviations CSF cerebrospinal fluid PBS phosphate-buffered saline ELISA enzyme-linked immunosorbent assay PCR polymerase chain reaction EM electron microscopy PTA phosphotungstic acid IEM immune electron microscopy SARS severe acute respiratory syndrome NAT nucleic acid amplification (techniques) SPIEM solid phase immune electron microscopy NRL/ELM
The Role of Electron Microscopy in the Rapid Diagnosis of Viral Infections -review and Foreign Cell in Clinical Specimens CONTENTS

with the pathological structure of BPD, as seen in the lungs of preterm infants who died and in animal models (3, 7). As the authors note, this study was limited in that the subjects with BPD were stable outpatients younger than 3 years who did not require oxygen therapy at the time of the study. Whether their findings hold true in infants with persistent severe BPD, including those with chronic ventilator-dependent hypoxemic respiratory failure, is not clear. In addition, BPD classification was based on clinical decision making, rather than a physiologic assessment such as the oxygen reduction test (11). In an earlier article, members of this group studied DL CO and its components, DM and Vc, in full-term infants without lung disease and showed that DL CO and Vc (but not DM) correlated with the level of proangiogenic circulating hematopoietic stem/progenitor cells (pCHSPCs) (12). However, this study did not include preterm infants with or without BPD. Both pCHSPCs, also referred to as circulating progenitor cells, as well as late-outgrowth endothelial colony-forming cells, are decreased in the cord blood of preterm infants who later develop moderate or severe BPD (13, 14) . Together, these findings suggest that early disruptions in the number and function of angiogenic progenitor cells, possibly by maternal complications of pregnancy known to be associated with BPD risk, may lead to impaired development of the pulmonary vasculature and sustained impaired gas exchange in preterm infants with BPD. This study shows how a physiologic assessment, such as infant pulmonary function testing, may be used in the clinical setting to provide an estimation of impaired gas exchange in preterm infants with varying degrees of lung injury. Combining functional assays such as this with measurement of pCHSPCs and other angiogenic biomarkers in the cord blood, as well as novel imaging techniques such as quantitative pulmonary magnetic resonance imaging (15), will lead to improved disease phenotyping of preterm infants at risk for BPD. Given the spectrum of disease severity among infants with severe BPD (as determined by the currently accepted diagnostic criteria), novel methods such as these will help identify preterm neonates more accurately, permit targeted therapies for the most severely affected infants, and provide quantitative evidence of the efficacy of these interventions in young children after preterm birth (16). n
Jobe AH, Bancalari E. Bronchopulmonary dysplasia

The 5% nontranslated region (5%NTR) and nonstructural region nucleotide sequences of nine enzootic Venezuelan equine encephalitis (VEE) virus strains were determined, thus completing the genomic RNA sequences of all prototype strains. The full-length genomes, representing VEE virus antigenic subtypes I -VI, range in size from 11.3 to 11.5 kilobases, with 48-53% overall G + C contents. Size disparities result from subtype-related differences in the number and length of direct repeats in the C-terminal nonstructural protein 3 (nsP3) domain coding sequence and the 3%NTR, while G + C content disparities are attributable to strain-specific variations in base composition at the wobble position of the polyprotein codons. Highly-conserved protein components and one nonconserved protein domain constitute the VEE virus replicase polyproteins. Approximately 80% of deduced nsP1 and nsP4 amino acid residues are invariant, compared to less than 20% of C-terminal nsP3 domain residues. In two enzootic strains, C-terminal nsP3 domain sequences degenerate into little more than repetitive serine-rich blocks. Nonstructural region sequence information drawn from a cross-section of VEE virus subtypes clarifies features of alphavirus conserved sequence elements and proteinase recognition signals. As well, whole-genome comparative analysis supports the reclassification of VEE subtype-variety IF and subtype II viruses.

Sequencing of prototype viruses in the Venezuelan equine encephalitis antigenic complex