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.

[Q]: We tested the role of the "spring-loaded" conformational change in the fusion mechanism of the influenza hemagglutinin (HA) by assessing the effects of 10 point mutants in the region of high coiled-coil propensity, HA2 54-81. The mutants included proline substitutions at HA2 55, 71, and 80, as well as a double proline substitution at residues 55 and 71. Mutants were expressed in COS or 293T cells and assayed for cell surface expression and structural features as well as for their ability to change conformation and induce fusion at low pH. We found the following: Specific mutations affected the precise carbohydrate structure and folding of the HA trimer. All of the mutants, however, formed trimers that could be expressed at the cell surface in a form that could be proteolytically cleaved from the precursor, HA0, to the fusion-permissive form, HA1-S-S-HA2. All mutants reacted with an antibody against the major antigenic site and bound red blood cells. Seven out of ten mutants displayed a wild-type (wt) or moderately elevated pH dependence for the conformational change. V55P displayed a substantial reduction ( 60-80%) in the initial rate of lipid mixing. The other single mutants displayed efficient fusion with the same pH dependence as wt-HA. The double proline mutant V55P/ S71P displayed no fusion activity despite being well expressed at the cell surface as a proteolytically cleaved trimer that could bind red blood cells and change conformation at low pH. The impairment in fusion for both V55P and V55P/S71P was at the level of outer leaflet lipid mixing. We interpret our results in support of the hypothesis that the spring-loaded conformational change is required for fusion. An alternate model is discussed.
[A]: Specific Single or Double Proline Substitutions in the "Spring-loaded" Coiled-Coil Region of the Influenza Hemagglutinin Impair or Abolish Membrane Fusion Activity

[Q]: 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.
[A]: TSEN54 missense variant in Standard Schnauzers with leukodystrophy Author summary

[Q]: To determine the factors that predict in-hospital mortality among patients who require hospitalization for the treatment of community-acquired pneumonia (CAP). Study design: Prospective observational study of all patients who were admitted to six hospitals in Edmonton, AL, Canada, with a diagnosis of CAP from November 15, 2000, to November 14, 2002. Pneumonia was defined as two or more respiratory symptoms and signs and an opacity on a chest radiograph as interpreted by the attending physician. Results: A total of 3,043 patients were enrolled in the study, 246 of whom died (8.1%). On multivariate analysis, increasing pneumonia severity score, increasing age, site of care, consultation with a respirologist or infectious diseases physician, and functional status at the time of admission were all independently predictive of mortality. Increasing pneumonia severity risk score, increasing age, site of hospitalization, functional status, and consultation with an infectious diseases physician or a respirologist were independently associated with both early (< 5 days) and late (> 5 days) mortality. In contrast, partial or complete use of the pneumonia pathway was associated with decreased early mortality, but had no effect on late mortality. A low lymphocyte count and a high serum potassium level were associated with early but not with late mortality. The type of antibiotic therapy had an effect on late but not on early mortality. Conclusions: Functional status at the time of hospital admission is a powerful predictor of mortality and should be incorporated into any scores or models that are used to predict mortality. While there are some common predictors of early and late in-hospital mortality, early mortality is not affected by the timing or type of antibiotic therapy, whereas late mortality is influenced by the type of antibiotic therapy. Hyperkalemia and lymphopenia are associated with early mortality. Abbreviations: CAP community-acquired pneumonia; CI confidence interval; FSA forward sortation area; HRCT high-resolution CT; OR odds ratio C ommunity-acquired pneumonia (CAP) is a common illness with an incidence rate of approximately 11.6/1,000 adults per year, 1 of which approx-
[A]:
Factors Influencing In-hospital Mortality in Community-Acquired Pneumonia* A Prospective Study of Patients Not Initially Admitted to the ICU