9 results match your criteria: "Gunma Paz University Research Institute[Affiliation]"

Article Synopsis
  • The human parainfluenza virus type 4 (HPIV4) has two subtypes, 4a and 4b, which were analyzed through gene sequences from 48 strains collected between 1966 and 2022.
  • A phylogenetic study revealed that these subtypes separated around 1823, with common ancestors for subtype 4a and 4b existing until approximately 1940 and 1939, respectively.
  • The study indicates that while there are genetic differences among all strains, each subtype maintains genetic conservation with low evolutionary rates and identified potential B-cell epitopes on the virus's fusion protein.
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To better understand the evolution of the SARS-CoV-2 Omicron subvariants, we performed molecular evolutionary analyses of the spike () protein gene/S protein using advanced bioinformatics technologies. First, time-scaled phylogenetic analysis estimated that a common ancestor of the Wuhan, Alpha, Beta, Delta variants, and Omicron variants/subvariants diverged in May 2020. After that, a common ancestor of the Omicron variant generated various Omicron subvariants over one year.

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The identification of pathogens associated with respiratory symptoms other than the novel coronavirus disease 2019 (COVID-19) can be challenging. However, the diagnosis of pathogens is crucial for assessing the clinical outcome of patients. We comprehensively profiled pathogens causing non-COVID-19 respiratory symptoms during the 7th prevalent period in Gunma, Japan, using deep sequencing combined with a next-generation sequencer (NGS) and advanced bioinformatics technologies.

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Molecular evolutionary analyses of the fusion protein gene in human respirovirus 1.

Virus Res

August 2023

Department of Health Science, Gunma Paz University Graduate School of Health Sciences, Takasaki-shi, Gunma 370-0006, Japan; Advanced Medical Science Research Center, Gunma Paz University Research Institute, Shibukawa-shi, Gunma 377-0008, Japan. Electronic address:

Few evolutionary studies of the human respiratory virus (HRV) have been conducted, but most of them have focused on HRV3. In this study, the full-length fusion (F) genes in HRV1 strains collected from various countries were subjected to time-scaled phylogenetic, genome population size, and selective pressure analyses. Antigenicity analysis was performed on the F protein.

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Despite the increasing evidence of the clinical impact of -derived cephalosporinase (PDC) sequence polymorphisms, the molecular evolution of its encoding gene, , remains elusive. To elucidate this, we performed a comprehensive evolutionary analysis of . A Bayesian Markov Chain Monte Carlo phylogenetic tree revealed that a common ancestor of diverged approximately 4660 years ago, leading to the formation of eight clonal variants (clusters A-H).

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Article Synopsis
  • The exact causes of asthma are not fully understood, but respiratory infections, particularly those caused by rhinovirus (RV), may trigger or worsen the condition.
  • Understanding the connection between viral infections and asthma can help address differences in immune responses between viral infections and allergies.
  • The complexity of RV-induced asthma involves both the immune response to the virus and allergic reactions triggered by various cytokines, highlighting the need to explore both RV infections and host defense mechanisms for a clearer understanding.
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Molecular interactions between respiratory syncytial virus (RSV) fusion protein (F protein) and the cellular receptor Toll-like receptor 4 (TLR4) and myeloid differentiation factor-2 (MD-2) protein complex are unknown. Thus, to reveal the detailed molecular interactions between them, in silico analyses were performed using various bioinformatics techniques. The present simulation data showed that the neutralizing antibody (NT-Ab) binding sites in both prefusion and postfusion proteins at sites II and IV were involved in the interactions between them and the TLR4 molecule.

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Molecular Evolution of the DNA Gyrase Gene.

Microorganisms

August 2022

Infectious Disease Surveillance Center, National Institute of Infectious Diseases, Musashimurayama 162-8640, Tokyo, Japan.

Article Synopsis
  • DNA gyrase, specifically the GyrA protein encoded by the
  • gene
  • , is vital for DNA replication in bacteria and mutations in GyrA lead to resistance against quinolone antibiotics like ciprofloxacin.
  • A study used advanced bioinformatics to analyze the evolution of the
  • gene
  • , revealing a common ancestor over 760 years ago and that certain mutations (T83I and D87N) related to drug resistance became prevalent after clinical use of quinolones.
  • The research showed that these mutations reduce the effectiveness of ciprofloxacin, suggesting that the
  • gene
  • evolved to help bacteria survive antibiotic treatment post-1962 when quinolone use began.
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