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]: Polymorphism of angiotensin converting enzyme (ACE) gene is reported to be associated with ischemic heart disease, hypertrophic cardiomyopathy, and idiopathic dilated cardiomyopathy. In this study, we investigated the relationship between Kawasaki disease and insertion/deletion polymorphism of ACE gene. Fifty five Kawasaki disease patients and 43 healthy children were enrolled. ACE genotype was evaluated from each of the subjects' DNA fragments through polymerase chain reaction (PCR). Frequencies of ACE genotypes (DD, ID, II) were 12.7%, 60.0%, 27.3% in Kawasaki group, and 41.9%, 30.2%, 27.9% in control group respectively, indicating low rate of DD and high rate of ID genotype among Kawasaki patients (p<0.01). Comparing allelic (I, D) frequencies, I allele was more prevalent in Kawasaki group than in control group (57.3% vs. 43.0%, p<0.05). In Kawasaki group, both genotype and allelic frequencies were not statistically different between those with coronary dilatations and those without. ACE gene I/D polymorphism is thought to be associated with Kawasaki disease but not with the development of coronary dilatations.
[A]: Address for correspondence Insertion/Deletion Polymorphism of Angiotensin Converting Enzyme Gene in Kawasaki Disease


[Q]: Background. Precise etiologic diagnosis in pediatric community-acquired pneumonia (CAP) remains challenging. Methods. We conducted a retrospective study of CAP etiology in 2 groups of pediatric patients who underwent flexible bronchoscopy (FOB) with bronchoalveolar lavage (BAL); children with acute nonresponsive CAP (NR-CAP; n 5 127) or recurrent CAP (Rec-CAP; n 5 123). Procedural measures were taken to limit contamination risk and quantitative bacterial culture of BAL fluid (significance cutoff point, R10 4 colony-forming units/mL) was used. Blood culture results, serological test results, nasopharyngeal secretion findings, and pleural fluid culture results were also assessed, where available. Results. An infectious agent was detected in 76.0% of cases. In 51.2% of infections, aerobic bacteria were isolated, of which 75.0%, 28.9%, and 13.3% were Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae, respectively. Most (97.9%) of the H. influenzae strains were nontypeable (NTHi). H. influenzae was detected in 26.0% of NR-CAP cases and 51.2% of Rec-CAP cases, whereas Mycoplasma pneumoniae was the predominant pathogen in the NR-CAP group (accounting for 34.9% of cases) but not in the Rec-CAP group (19.3%). Viruses were found in 30.4% of cases, with respiratory syncytial virus, parainfluenzaviruses, and influenzaviruses detected most frequently. Mixed infections were found in 18.9% of NR-CAP cases and 30.1% of Rec-CAP cases. Conclusions. A variety of microorganisms were isolated with frequent mixed infection. NTHi was one of the major pathogens found, especially in association with recurrent CAP, possibly because of improved detection with the FOB with BAL procedure. This suggests that the burden of pediatric CAP could be reduced by addressing NTHi as a major causative pathogen.
[A]: Microbiology of Bronchoalveolar Lavage Fluid in Children With Acute Nonresponding or Recurrent Community-Acquired Pneumonia: Identification of Nontypeable Haemophilus influenzae as a Major Pathogen


[Q]: Restriction factors are antiviral components of intrinsic immunity which constitute a first line of defense by blocking different steps of the human immunodeficiency virus (HIV) replication cycle. In immune cells, HIV infection is also sensed by several pattern recognition receptors (PRRs), leading to type I interferon (IFN-I) and inflammatory cytokines production that upregulate antiviral interferon-stimulated genes (ISGs). Several studies suggest a link between these two types of immunity. Indeed, restriction factors, that are generally interferon-inducible, are able to modulate immune responses. This review highlights recent knowledge of the interplay between restriction factors and immunity inducing antiviral defenses. Counteraction of this intrinsic and innate immunity by HIV viral proteins will also be discussed. of PAMPs by PRRs induces signaling cascades and leads to the transcription of pro-inflammatory cytokines and type I interferons (IFN-I), the most powerful antiviral effectors. Once produced by cells in which PRRs have been activated, IFN-I are secreted and bind, in an autocrine or paracrine manner, to the membrane receptor IFNAR (IFN-α/β receptor chain) to induce signal transduction driving the transcription of interferon-stimulated genes (ISGs). There are hundreds of ISGs encoding antiviral proteins such as the protein kinase R (PKR) or the 2 -5 -oligoadenylate synthetase 1 (OAS1) [13, 14] . Thus, ISGs are crucial to switch cells into an antiviral state. Interestingly, even if HIV restriction factors have been described as intrinsic immune effectors, most of them are IFN-inducible and can be defined as ISGs linking intrinsic and innate immunity. Moreover, by exerting their antiviral functions or by additional pathways, some restriction factors have been described to shape innate and adaptive immune responses highlighting an intimate relationship between restriction factors and immunity [15, 16] . In this review, we summarize the recent knowledge of the interplay between restriction factors and immunity focusing only on restriction factors that belong to the ISG family. After a description of restriction factors antiviral mechanisms and their induction by IFN, we will discuss how they can modulate immunity, in particular, innate immune responses. Moreover, since HIV-1 proteins are able to counteract many restriction factors, we will also mention viral mechanisms used to escape from intrinsic and innate immunity. Taken together, this review will allow a better understanding of the intricate interplay between restriction factors-mediated intrinsic immunity and innate immunity.
[A]:
cells Interplay between Intrinsic and Innate Immunity during HIV Infection