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.

Ex Input:
Purpose: Despite their controversial role, corticosteroids (CS) are frequently administered to patients with H1N1 virus infection with severe respiratory failure secondary to viral pneumonia. We hypothesized that invasive pulmonary aspergillosis (IPA) is a frequent complication in critically ill patients with H1N1 virus infection and that CS may contribute to this complication. Methods: We retrospectively selected all adult patients with confirmed H1N1 virus infection admitted to the intensive care unit (ICU) of two tertiary care hospitals from September 2009 to March 2011. Differences in baseline factors, risk factors, and outcome parameters were studied between patients with and without IPA. Results: Of 40 critically ill patients with confirmed H1N1, 9 (23 %) developed IPA 3 days after ICU admission. Five patients had proven and four had probable IPA. Significantly more IPA patients received CS within 7 days before ICU admission (78 versus 23 %, p = 0.002). IPA patients also received significantly higher doses of CS before ICU admission [hydrocortisone equivalent 800 (360-2,635) versus 0 (0-0) mg, p = 0.005]. On multivariate analysis, use of CS before ICU admission was independently associated with IPA [odds ratio (OR) 14.4 (2.0-101.6), p = 0.007]. Conclusions: IPA was diagnosed in 23 % of critically ill patients with H1N1 virus infection after a median of 3 days after ICU admission. Our data suggest that use of CS 7 days before ICU admission is an independent risk factor for fungal superinfection. These findings may have consequences for clinical practice as they point out the need for increased awareness of IPA, especially in those critically ill H1N1 patients already receiving CS.

Ex Output:
Invasive pulmonary aspergillosis is a frequent complication of critically ill H1N1 patients: a retrospective study

Ex Input:
The evolution of viral quasispecies can influence viral pathogenesis and the response to antiviral treatments. Mutant clouds in infected organisms represent the first stage in the genetic and antigenic diversification of RNA viruses, such as foot and mouth disease virus (FMDV), an important animal pathogen. Antigenic variants of FMDV have been classically diagnosed by immunological or RT-PCR-based methods. DNA microarrays are becoming increasingly useful for the analysis of gene expression and single nucleotide polymorphisms (SNPs). Recently, a FMDV microarray was described to detect simultaneously the seven FMDV serotypes. These results encourage the development of new oligonucleotide microarrays to probe the fine genetic and antigenic composition of FMDV for diagnosis, vaccine design, and to gain insight into the molecular epidemiology of this pathogen. A FMDV microarray was designed and optimized to detect SNPs at a major antigenic site of the virus. A screening of point mutants of the genomic region encoding antigenic site A of FMDV C-S8c1 was achieved. The hybridization pattern of a mutant includes specific positive and negative signals as well as crosshybridization signals, which are of different intensity depending on the thermodynamic stability of each probe-target pair. Moreover, an array bioinformatic classification method was developed to evaluate the hybridization signals. This statistical analysis shows that the procedure allows a very accurate classification per variant genome. A specific approach based on a microarray platform aimed at distinguishing point mutants within an important determinant of antigenicity and host cell tropism, namely the G-H loop of capsid protein VP1, was developed. The procedure is of general applicability as a test for specificity and discriminatory power of microarray-based diagnostic procedures using multiple oligonucleotide probes.

Ex Output:
BMC Genomics Microarray-based identification of antigenic variants of foot-and-mouth disease virus: a bioinformatics quality assessment

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infection , an animal model for multiple sclerosis (MS) , axonal injury precedes inflammatory demyelinating lesions , and the distribution of axonal damage present during the early phase of infection corresponds to regions where subsequent demyelination occurs during the chronic phase. We hypothesized that axonal damage recruits inflammatory cells to sites of Wallerian degeneration , leading to demyelination. Three weeks after TMEV infection , axonal degeneration was induced in the posterior funiculus of mice by injecting the toxic lectin Ricinus communis agglutinin (RCA) I into the sciatic nerve. Neuropathology was examined 1 week after lectin injection. Control mice , infected with TMEV but receiving no RCA I , had inflammatory demyelinating lesions in the anterior/lateral funiculi. Other control mice that received RCA I alone did not develop inflammatory lesions. In contrast, RCA I injection into TMEV-infected mice induced lesions in the posterior funiculus in addition to the anterior/lateral funiculi. We found no differences in lymphoproliferative responses or antibody titers against TMEV among the groups. This suggests that axonal degeneration contributes to the recruitment of inflammatory cells into the central nervous system by altering the local microenvironment. In this scenario, lesions develop from the axon (inside) to the myelin (outside) (Inside-Out model). Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). 1 Although its etiology is unknown, epidemiological data and clinical reports support the association of MS with environmental factors, particularly viral infection. In recent years, pathological and neuroimaging studies have re-emphasized the importance of axonal damage in MS. 2 Immunostaining studies have provided direct evidence for axonal damage using antibodies against two markers of injured axons: nonphosphorylated neurofilament protein (NFP) 3 and amyloid precursor protein. 4 Several groups have demonstrated that axonal damage occurred early during the course of MS and that damaged axons were found not only in active demyelinating lesions but also in periplaque white matter without demyelination, 5 remyelinating lesions and normal-appearing white matter. 6,7 Magnetic resonance spectroscopy analyses have also demonstrated gray matter lesions 8 and axonal injury in normal-appearing white matter in MS patients. 7, 9, 10 Axonal damage in normal-appearing white matter has also been found in an animal model for MS, coronavirus-induced demyelination. 11 Although axonal damage in MS is believed to occur secondarily after the destruction of the myelin sheath or oligodendrocytes, the myelin-forming cells, these findings suggest that axonal damage could be independent of demyelinating activity. 12 Wallerian degeneration is the anterograde degeneration of axons caused by injury to the proximal part of the axon or by death of the neuronal cell body. 13 In most cases, the demonstration of Wallerian degeneration in humans has been limited to compact neuronal tracts, such as the corticospinal tract and optic radiation. In MS, Wallerian degeneration was believed to be rare; this was probably attributable to a difficulty in detection because MS lesions are usually not confined to a single pathway or tract. However, more recently, magnetic resonance imaging, 14 -17 magnetic resonance spectroscopy, 18 and autopsy 19 studies have documented the presence of Wallerian degeneration in some patients with MS.

Ex Output:
Immunopathology and Infectious Disease Targeting Inflammatory Demyelinating Lesions to Sites of Wallerian Degeneration