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Biomedical subjects

Qi Jin

Publications and source records attributed to Qi Jin.

8 recordsLinked to original sources

Avian Migration-Mediated Transmission and Recombination Driving the Diversity of Gammacoronaviruses and Deltacoronaviruses.

In the wake of pandemics like COVID-19, which have zoonotic origins, the role of wildlife as reservoirs for emerging infectious diseases has garnered heightened attention. Migratory birds, traversing continents, represent a potent but under-researched vector for the spread of infectious diseases, including novel coronaviruses. This study delves into the genetic diversity and transmission dynamics of coronaviruses in migratory birds, presenting pivotal findings. From April 2019 to April 2023, we screened 5,263 migratory bird samples collected from Shanghai, China, identifying 372 coronavirus-positive samples belonging to five avian-related coronavirus subgenera and subsequently obtaining 120 complete genome sequences. To facilitate further research with a global perspective, the study curated all available 19,000 avian-associated coronaviruses and expanded the original 12 species to 16, including three novel coronavirus species identified in our study and one re-classified species from the public domain. The study illuminates the intricate genetic evolution and transmission dynamics of birds-related coronaviruses on a global scale. A notable aspect of our research is the identification of complex recombination patterns within the spike protein across different virus species and subgenera, highlighting migratory birds as a reservoir of coronavirus. Notably, the coronaviruses found in migratory birds, predominantly from the orders Anseriformes, Charadriiformes, and Pelecaniformes, with domestic ducks from Anseriformes playing a key role in bridging the transmission of coronaviruses between migratory and non-migratory birds. These findings reveal the genetic and recombination characteristics of coronaviruses in migratory birds, emphasizing the critical role of ecologically pivotal bird species in coronavirus transmission and genetic diversity shaping.

Animals↗

Estimation of the optimal electrophoretic temperature of DNA single-strand conformation polymorphism by DNA base composition.

To explore the relation between DNA base composition and the optimal single-strand conformation polymorphism (SSCP) electrophoretic temperature (T(s)), we analyzed DNA base composition and T(s) of 24 DNA fragments from different genes and found that T(s) was positively correlative with the ratio of base C/base A. T(s) could be estimated by the formula T(s) = [80 x C/(A+1)]/[2.71 + [C/(A+1)]]. T(s) could be increased dramatically by the complementary sequences in both 5'-and 3'-ends of a DNA single-strand.

Base Composition↗

GenomeComp: a visualization tool for microbial genome comparison.

We have developed a software tool, GenomeComp, for summarizing, parsing and visualizing the genome sequences comparison results derived from voluminous BLAST textual output. With GenomeComp, the variation between genomes can be easily highlighted, such as repeat regions, insertions, deletions and rearrangements of genomic segments. This software provides a new visualizing tool for microbe comparative genomics.

Computational Biology↗

The Anti-HIV potency of cyclotriazadisulfonamide analogs is directly correlated with their ability to down-modulate the CD4 receptor.

9-Benzyl-3-methylene-1,5-di-p-toluenesulfonyl-1,5,9-triazacyclododecane (CADA) has been identified as a novel antiviral lead compound with significant anti-human immunodeficiency virus and anti-human herpesvirus 7 activity. Surprisingly, this compound selectively decreased the expression of the CD4 glycoprotein, the primary receptor needed for the entry of both viruses. Herein, we describe the CD4 down-modulating and antiviral potencies of more than 25 CADA derivatives. Flow cytometric evaluation of cellular CD4 receptor expression in T cells demonstrated the specific CD4 down-modulating capacity of the CADA derivatives, with IC(50) values similar to those obtained in the antiviral assays. The close correlation observed between the CD4 down-regulating and anti-HIV potencies of the CADA derivatives further points to CD4 receptor down-modulation as the primary mode of antiviral action for this group of compounds.

Anti-HIV Agents↗

A potent and selective nonpeptide antagonist of CXCR2 inhibits acute and chronic models of arthritis in the rabbit.

Much evidence implicates IL-8 as a major mediator of inflammation and joint destruction in rheumatoid arthritis. The effects of IL-8 and its related ligands are mediated via two receptors, CXCR1 and CXCR2. In the present study, we demonstrate that a potent and selective nonpeptide antagonist of human CXCR2 potently inhibits (125)I-labeled human IL-8 binding to, and human IL-8-induced calcium mobilization mediated by, rabbit CXCR2 (IC(50) = 40.5 and 7.7 nM, respectively), but not rabbit CXCR1 (IC(50) = >1000 and 2200 nM, respectively). These data suggest that the rabbit is an appropriate species in which to examine the anti-inflammatory effects of a human CXCR2-selective antagonist. In two acute models of arthritis in the rabbit induced by knee joint injection of human IL-8 or LPS, and a chronic Ag (OVA)-induced arthritis model, administration of the antagonist at 25 mg/kg by mouth twice a day significantly reduced synovial fluid neutrophils, monocytes, and lymphocytes. In addition, in the more robust LPS- and OVA-induced arthritis models, which were characterized by increased levels of proinflammatory mediators in the synovial fluid, TNF-alpha, IL-8, PGE(2), leukotriene B(4), and leukotriene C(4) levels were significantly reduced, as was erythrocyte sedimentation rate, possibly as a result of the observed decreases in serum TNF-alpha and IL-8 levels. In vitro, the antagonist potently inhibited human IL-8-induced chemotaxis of rabbit neutrophils (IC(50) = 0.75 nM), suggesting that inhibition of leukocyte migration into the knee joint is a likely mechanism by which the CXCR2 antagonist modulates disease.

Acute Disease↗

Genome sequence of Shigella flexneri 2a: insights into pathogenicity through comparison with genomes of Escherichia coli K12 and O157.

We have sequenced the genome of Shigella flexneri serotype 2a, the most prevalent species and serotype that causes bacillary dysentery or shigellosis in man. The whole genome is composed of a 4 607 203 bp chromosome and a 221 618 bp virulence plasmid, designated pCP301. While the plasmid shows minor divergence from that sequenced in serotype 5a, striking characteristics of the chromosome have been revealed. The S.flexneri chromosome has, astonishingly, 314 IS elements, more than 7-fold over those possessed by its close relatives, the non-pathogenic K12 strain and enterohemorrhagic O157:H7 strain of Escherichia coli. There are 13 translocations and inversions compared with the E.coli sequences, all involve a segment larger than 5 kb, and most are associated with deletions or acquired DNA sequences, of which several are likely to be bacteriophage-transmitted pathogenicity islands. Furthermore, S.flexneri, resembling another human-restricted enteric pathogen, Salmonella typhi, also has hundreds of pseudogenes compared with the E.coli strains. All of these could be subjected to investigations towards novel preventative and treatment strategies against shigellosis.

Amino Acid Sequence↗

Characterization of rpoB mutations in rifampicin-resistant Mycobacterium tuberculosis isolated in China.

The objective of this study was for the elucidation of the characteristics of the rpoB gene mutation in rifampicin (RIF)-resistant Mycobacterium tuberculosis strains isolated in China. The rifampicin resistance determination regions (RRDR) of the rpoB genes of 242 M. tuberculosis strains were sequenced, including 193 RIF-resistant, 46 RIF-sensitive clinical isolates and three manually induced RIF-resistant tuberculosis strains. Mutations in the 81 bp RRDR of the rpoB gene were identified in 89.6% (173/193) of RIF-resistant clinical isolates. No mutation was observed in RIF-sensitive strains. Ser531Leu mutations accounted for 46.1% (89/193) of RIF-resistant strains; the mutation frequency of 526-His was 17.6% (34/193) in RIF-resistant strains. Furthermore, a combination of 2-3 single-point mutations was observed in 24 RIF-resistant strains (12.4%; 24/193). Mutations in three manually induced RIF-resistant tuberculosis strains were located at codons 531 and 526, respectively. The results indicate that about 90% of rifampicin-resistant M. tuberculosis strains isolated in China had rpoB mutations;531-Ser and 526-His were the most common positions substituted; high-level rifampicin-resistant strains had a higher frequency of 531-Ser mutations than low-level rifampicin-resistant strains. Sequencing analysis of the 81 bp fragment in the rpoB gene is useful in predicting the rifampicin-resistant phenotype.

Antibiotics, Antitubercular↗

[Coxsackievirus B3 infection and Keshan disease].

To study the relationship between the infection of enteroviruses and the etiology of keshan disease, we examined the 30 blood samples from the latent-chronic KD patients from Mianning, Xider, Derchang county of Sichuan Province with LDE-PCR (long distance enterovirus-specific RT PCR), two sensitive and specific ELISAs (one for CVB1-6 IgM and the other for CVB1-6 IgG), and three-primer RT PCR specific for CVB3. Results show that: 1) The infection rate of enteroviruses in the samples from the latent-chronic KD patients is higher than from the control group (80% VS 0%, P < 0.01); 2) The CVB1-6 antibody positive rate in latent-chronic KD is higher than that of the control group (IgM, 33% VS 0%, P < 0.01; IgG, 23% VS 0%, P < 0.01); 3) 16.6% (4/24) of enteroviruses positive samples or 40% (4/10) of CVB1-6 IgM antibody positive samples can be identified as CVB3. So, the infection of enter viruses maybe involves in the cause and development of latent-chronic keshan disease, and at least we conclude that the mutation of CVB3 is not the only cause of KD.

Adolescent↗