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.

Input: Consider Input: The renin-angiotensin system plays an important role in the maintenance of blood pressure homeostasis. The angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II. Angiotensin II, which binds the angiotensin II type-1 receptor (AT1R), is a potent vasoconstrictor. On a pathophysiological basis, both ACE I/D and AT1R A1166C polymorphism lead to an enhanced activity of the angiotensin II-AT1R axis, thereby possibly contributing to circulatory disturbances. A mutually facilitatory effect may be presumed between the two polymorphisms. We examined whether this synergistic effect is involved in the evolution of different types of ischemic stroke. Genetic and clinical data on 308 consecutive patients with acutely developing ischemic stroke were analyzed. A total of 272 stroke and neuroimaging alteration-free subjects served as a control group. Univariate and logistic regression statistical approaches were used. The ACE D allele combined with the AT1R 1166C allele did not yield a risk of ischemic stroke. However, the co-occurrence of the homozygous ACE D/D and at least one AT1R 1166C allele was more frequent in the ischemic stroke group than in the control group (22.4 vs 11%, p < 0.005, OR, 2.33; 95% CI, 1.46-3.7). After specific subgroup analysis, this synergistic association was even stronger for small-vessel ischemic stroke (OR, 3.44; 95% CI, 1.9-6.24; p < 0.0005). Multivariate logistic regression analysis of the data confirmed this association (adjusted OR, 3.54, 95% CI, 1.88-7.16; p < 0.0005). Our results demonstrate that ACE D/D and AT1R 1166C NeuroMolecular Medicine

Output: Coexistence of Angiotensin II Type-1 Receptor A1166C and Angiotensin-Converting Enzyme D/D Polymorphism Suggests Susceptibility for Small-Vessel-Associated Ischemic Stroke


Input: Consider Input: Recent years have seen several advances in our understanding of immunity to virus infection of the lower respiratory tract, including to influenza virus infection. Here, we review the cellular targets of viruses and the features of the host immune response that are unique to the lungs. We describe the interplay between innate and adaptive immune cells in the induction, expression and control of antiviral immunity, and discuss the impact of the infected lung milieu on moulding the response of antiviral effector T cells. Recent findings on the mechanisms that underlie the increased frequency of severe pulmonary bacterial infections following respiratory virus infection are also discussed. Viruses are highly evolved and ubiquitous pathogens. Although infection with many viruses results in a mild, self-limited disease, other viruses can produce severe and frequently fatal infections. The respiratory tract is a major portal through which viruses enter to initiate infection. Whereas some viruses can initiate infection in the respiratory tract and then disseminate to other sites in the body, other viruses typically remain localized to the respiratory tract, where they replicate and induce tissue injury (see Supplementary information S1 (table)). Various defence mechanisms have evolved in the respiratory tract to prevent and control infection by viruses and other pathogens. The respiratory tract can be divided anatomically into the upper respiratory tract (including the nose, mouth and pharynx) and the lower respiratory tract (which consists of the trachea, bronchi and lungs), with the lymphoid tissue of Waldeyer's ring (including the pharyngeal and palatine tonsils) representing the line of demarcation. Because of the crucial role of the lower respiratory tract in respiration, we limit the focus of this Review to recent advances in our understanding of the host immune response to virus infection at this site.

Output: Regulating the adaptive immune response to respiratory virus infection NIH Public Access


Input: Consider Input: To better understand the molecular epidemiology and genetic diversity of PEDV field isolates, in this study, we characterised the complete genome sequence of a novel PEDV variant JSCZ1601 from a outbreak in China in 2016. The PEDV isolate was 28,033 nucleotides (nt) in length without the polyadenylated sequences. Phylogenetic analysis based on the full-length genome sequence of JSCZ1601 grouped it with the pandemic variants determined post-2010 into group 2 (G2). However, the S gene of JSCZ1601 formed a new subgroup separated from the subgroups containing the other G2 strains. Comparative analysis of the amino acids encoded by the S genes revealed the N-terminal of the deduced JSCZ1601 S protein had a novel two-amino-acid deletion (N58 and S59) compared with all identified genogroups. Further, compared with the reference strains, a 'G' insertion was detected in the 5′ terminal of the 5′UTR of the JSCZ1601. The animal experiment revealed that this strain was high pathogenic to neonatal pigs. Taken together, a PEDV strain with the new molecular characterizations and phylogenies was found in mainland China. It is necessary to strengthen the monitoring of PEDV variations. Porcine epidemic diarrhoea (PED) is characterised by severe watery diarrhoea, leading to dehydration and high mortality among piglets. The disease is caused by the PED virus (PEDV), which belongs to family Coronaviridae, genus Alphacoronavirus, and has an envelope surrounding a single-stranded positive-sense RNA genome 1,2 . The PEDV genome is approximately 28 kb nucleotides (nt) long and contains a 5′ untranslated region (5′ UTR), a 3′ UTR with a polyadenylated tail, and at least seven open reading frames (ORFs) arranged in the following order: ORF1a, ORF1b, spike (S) glycoprotein gene, ORF3 hypothetical protein gene, envelope (E) gene, membrane (M) gene and nucleocapsid (N) gene 3,4 . The 5′ UTR is about 291-296 nt long and the 3′ UTR is about 334 nt long. Two long ORFs, ORF1a and ORF1b, occupy two-thirds of the genome and encode two nonstructural polyproteins (pp1a and pp1b) that direct genome replication and transcription 5 . PED was first reported in feeding and fattening pigs in England in 1971 2 . In China, PED was identified as a sporadic viral enteric disease in pig herds before 2010 6-8 . However, outbreaks of PED with increased severity of diarrhoea, vomiting, and dehydration have occurred in China since 2010. The disease approached a mobility rate as high as 100% and a mortality rate of 80-100% in piglets less than 10 days old, and has been recognised as a devastating illness causing death in neonatal piglets 9,10 . New outbreaks associated with a novel PEDV strain that is genetically distant from the prototype PEDV strain, CV777, have been reported in China 8,11,12 . Since then, PED outbreaks have increased markedly and have spread rapidly across countries. In late April 2013, PED was first confirmed in the United States and subsequently spread quickly across the country 13-15 .


Output: Characterization of Chinese Porcine Epidemic Diarrhea Virus with Novel Insertions and Deletions in Genome OPEN