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".

Q: Paragraph: Respiratory infectious diseases are mainly caused by viruses or bacteria that often interact with one another. Although their presence is a prerequisite for subsequent infections, viruses and bacteria may be present in the nasopharynx without causing any respiratory symptoms. The upper respiratory tract hosts a vast range of commensals and potential pathogenic bacteria, which form a complex microbial community. This community is assumed to be constantly subject to synergistic and competitive interspecies interactions. Disturbances in the equilibrium, for instance due to the acquisition of new bacteria or viruses, may lead to overgrowth and invasion. A better understanding of the dynamics between commensals and pathogens in the upper respiratory tract may provide better insight into the pathogenesis of respiratory diseases. Here we review the current knowledge regarding specific bacterial-bacterial and viral-bacterial interactions that occur in the upper respiratory niche, and discuss mechanisms by which these interactions might be mediated. Finally, we propose a theoretical model to summarize and illustrate these mechanisms. 
 Title: Viral and Bacterial Interactions in the Upper Respiratory Tract

A: False
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Q: Paragraph: Magnesium (Mg)-based biometal attracts clinical applications due to its biodegradability and beneficial biological effects on tissue regeneration, especially in orthopaedics, yet the underlying anabolic mechanisms in relevant clinical disorders are lacking. The present study investigated the effect of magnesium (Mg) and vitamin C (VC) supplementation for preventing steroid-associated osteonecrosis (SAON) in a rat experimental model. In SAON rats, 50 mg/kg Mg, or 100 mg/kg VC, or combination, or water control was orally supplemented daily for 2 or 6 weeks respectively. Osteonecrosis was evaluated by histology. Serum Mg, VC, and bone turnover markers were measured. Microfil-perfused samples prepared for angiography and trabecular architecture were evaluated by micro-CT. Primary bone marrow cells were isolated from each group to evaluate their potentials in osteoblastogenesis and osteoclastogenesis. The mechanisms were tested in vitro. Histological evaluation showed SAON lesions in steroid treated groups. Mg and VC supplementation synergistically reduced the apoptosis of osteocytes and osteoclast number, and increased osteoblast surface. VC supplementation significantly increased the bone formation marker PINP, and the combination significantly decreased the bone resorption marker CTX. TNFα expression and oxidative injury were decreased in bone marrow in Mg/VC/combination group. Mg significantly increased the blood perfusion in proximal tibia and decreased the leakage particles in distal tibia 2 weeks after SAON induction. VC significantly elevated the osteoblast differentiation potential of marrow cells and improved the trabecular architecture. The combination supplementation significantly inhibited osteoclast differentiation potential of marrow cells. In vitro study showed promoting osteoblast differentiation effect of VC, and antiinflammation and promoting angiogenesis effect of Mg with underlying mechanisms. Mg and VC supplementation could synergistically alleviate SAON in rats, indicating great translational potentials of metallic minerals for preventing SAON. 
 Title: Magnesium and vitamin C supplementation attenuates steroid-associated osteonecrosis in a rat model

A: False
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Q: Paragraph: Acute lung injury (ALI), and its more severe form, acute respiratory distress syndrome (ARDS), are syndromes of acute hypoxemic respiratory failure resulting from a variety of direct and indirect injuries to the gas exchange parenchyma of the lungs. The clinical syndrome is characterized by critical hypoxemia (partial pressure of oxygen in arterial blood/fraction of inspired oxygen <300 for ALI and <200 for ARDS), bilateral pulmonary infiltrates suggesting edema, no clinical or measured evidence of cardiac failure, and no other explanation for these findings. Pulmonary or nonpulmonary infections with sepsis are the most common causes of ALI and ARDS, although gastric aspiration, massive transfusions, trauma, and other factors contribute. 1 The diversity of causes and the stereotyped physiologic and pathologic responses have made modeling human ALI and ARDS difficult, but new themes are evolving from experimental studies, some of which are reviewed in this article. Most of what is known about the pathology of ALI and ARDS comes from the studies of patients who have died, although a limited number of patients have undergone open lung biopsy (Fig. 1) . The pathologic changes include an early phase of diffuse alveolar damage, with an increase in endothelial permeability, evidence of intravascular thrombi, severe epithelial injury with denudation of alveolar wall basement membranes, accumulation of protein and fibrin-rich alveolar infiltrates in the airspaces, and abundant alveolar neutrophilic infiltrates. If patients survive, these changes progress for days to a repair phase, characterized by hyaline membrane formation, transition from neutrophilic to mononuclear infiltrates, and the appearance of intra-alveolar and 
 Title: Experimental Models and Emerging Hypotheses for Acute Lung Injury Lung injury Animal model Respiratory distress

A:
True
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