28 research outputs found

    Image_1_Alterations in the vaginal microbiota of patients with preterm premature rupture of membranes.png

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    BackgroundPreterm premature rupture of membranes (PPROM) is a common pregnancy complication. Yet, the main cause of PPROM remains poorly understood. In this study, we used 16S rRNA gene sequencing technology to identify the differences in vaginal microbiota between pregnant women with PPROM and those who delivered at term.MethodsVaginal samples were collected from 48 patients with PPROM and 54 age- and gestational age-matched pregnant women who delivered at term (controls). The vaginal microbiota of the two groups was compared using 16S rRNA gene sequencing of the V3-V4 regions.ResultsThe vaginal microbial composition of the PPROM group was significantly different from that of the control group. Our results showed that the diversity of vaginal microbiota in patients with PPROM increased compared with controls. The relative abundance of Lactobacillus iners, Gardnerella vaginalis, Prevotella bivia, Ochrobactrum sp., Prevotella timonensis, and Ureaplasma parvum were more abundant in patients with PPROM, while Lactobacillus crispatus and Lactobacillus gasseri were more abundant in controls. Ochrobactrum sp., Prevotella timonensis, and Gardnerella vaginalis, could serve as biomarkers for PPROM. Finally, we proposed several metabolic pathways, including PWY-6339, PWY-6992, and PWY-7295.ConclusionPPROM is characterized by vaginal microbial dysbiosis. The dysbiotic vaginal microbiota signatures in patients with PPROM include a higher bacterial diversity, decreased autochthonous bacteria, and increased pathogenic bacteria. These results may be beneficial for developing biomarkers for screening and early diagnosis of PPROM and may provide effective preventative treatments.</p

    Image_2_Alterations in the vaginal microbiota of patients with preterm premature rupture of membranes.jpeg

    No full text
    BackgroundPreterm premature rupture of membranes (PPROM) is a common pregnancy complication. Yet, the main cause of PPROM remains poorly understood. In this study, we used 16S rRNA gene sequencing technology to identify the differences in vaginal microbiota between pregnant women with PPROM and those who delivered at term.MethodsVaginal samples were collected from 48 patients with PPROM and 54 age- and gestational age-matched pregnant women who delivered at term (controls). The vaginal microbiota of the two groups was compared using 16S rRNA gene sequencing of the V3-V4 regions.ResultsThe vaginal microbial composition of the PPROM group was significantly different from that of the control group. Our results showed that the diversity of vaginal microbiota in patients with PPROM increased compared with controls. The relative abundance of Lactobacillus iners, Gardnerella vaginalis, Prevotella bivia, Ochrobactrum sp., Prevotella timonensis, and Ureaplasma parvum were more abundant in patients with PPROM, while Lactobacillus crispatus and Lactobacillus gasseri were more abundant in controls. Ochrobactrum sp., Prevotella timonensis, and Gardnerella vaginalis, could serve as biomarkers for PPROM. Finally, we proposed several metabolic pathways, including PWY-6339, PWY-6992, and PWY-7295.ConclusionPPROM is characterized by vaginal microbial dysbiosis. The dysbiotic vaginal microbiota signatures in patients with PPROM include a higher bacterial diversity, decreased autochthonous bacteria, and increased pathogenic bacteria. These results may be beneficial for developing biomarkers for screening and early diagnosis of PPROM and may provide effective preventative treatments.</p

    Image_3_Alterations in the vaginal microbiota of patients with preterm premature rupture of membranes.jpeg

    No full text
    BackgroundPreterm premature rupture of membranes (PPROM) is a common pregnancy complication. Yet, the main cause of PPROM remains poorly understood. In this study, we used 16S rRNA gene sequencing technology to identify the differences in vaginal microbiota between pregnant women with PPROM and those who delivered at term.MethodsVaginal samples were collected from 48 patients with PPROM and 54 age- and gestational age-matched pregnant women who delivered at term (controls). The vaginal microbiota of the two groups was compared using 16S rRNA gene sequencing of the V3-V4 regions.ResultsThe vaginal microbial composition of the PPROM group was significantly different from that of the control group. Our results showed that the diversity of vaginal microbiota in patients with PPROM increased compared with controls. The relative abundance of Lactobacillus iners, Gardnerella vaginalis, Prevotella bivia, Ochrobactrum sp., Prevotella timonensis, and Ureaplasma parvum were more abundant in patients with PPROM, while Lactobacillus crispatus and Lactobacillus gasseri were more abundant in controls. Ochrobactrum sp., Prevotella timonensis, and Gardnerella vaginalis, could serve as biomarkers for PPROM. Finally, we proposed several metabolic pathways, including PWY-6339, PWY-6992, and PWY-7295.ConclusionPPROM is characterized by vaginal microbial dysbiosis. The dysbiotic vaginal microbiota signatures in patients with PPROM include a higher bacterial diversity, decreased autochthonous bacteria, and increased pathogenic bacteria. These results may be beneficial for developing biomarkers for screening and early diagnosis of PPROM and may provide effective preventative treatments.</p

    Monitoring Nitric Oxide in Subcellular Compartments by Hybrid Probe Based on Rhodamine Spirolactam and SNAP-tag

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    By connection of <i>O</i><sup>6</sup>-benzylguanine (BG) to an “<i>o</i>-phenylenediamine-locked” rhodamine spirolactam responsive to nitric oxide (NO), a novel substrate (<b>TMR-NO-BG</b>) of genetically encoded SNAP-tag has been constructed. In living cells, labeling SNAP-tag fused proteins with <b>TMR-NO-BG</b> will <i>in</i> <i>situ</i> generate corresponding probe–protein conjugates (<b>TMR-NO-SNAP</b>) that not only inherit high NO sensitivity from the small-molecule parent but also guarantee the site-specificity to the designated subcellular compartments such as the mitochondrial inner membrane, nucleus, and cytoplasm. In two representative cellular processes, <b>TMR-NO-BG</b> demonstrates its applicability to monitor endogenous subcellular NO in the activated RAW264.7 cells stimulated by lipopolysaccharide and in the apoptotic COS-7 cells induced by etoposide

    A Novel Water-Soluble Heptaplatin Analogue with Improved Antitumor Activity and Reduced Toxicity

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    A novel water-soluble heptaplatin analogue, cis-[(4R,5R)-4,5-bis-(aminomethyl)-2-isopropyl-1,3-dioxolane](3-hydroxy-1,1-cyclobutanedicarboxylato)platinum(II), has been synthesized and biologically evaluated. The complex shows more activity and less toxicity than its parent drug heptaplatin, exhibiting the great potential for further development

    Multiplex PCR result of <i>L</i>. <i>monocytogenes</i>, <i>E</i>. <i>coli</i> O157:H7, and <i>S</i>. <i>aureus</i>, respectively.

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    <p>M: 1000 bp DNA marker. Lane 1 shows PCR amplicons, specific to <i>L</i>. <i>monocytogenes</i> (285 bp), <i>E</i>. <i>coli</i> O157:H7 (193 bp), and <i>S</i>. <i>aureus</i> (159 bp). Lanes 2–4 show individual PCR amplicons, specific to <i>S</i>. <i>aureus</i> (159 bp) (lane 2), <i>E</i>. <i>coli</i> O157:H7 (193 bp) (lane 3), and <i>L</i>. <i>monocytogenes</i> (285 bp) (lane 4). Lanes 5–6 show results for the negative control.</p

    Detection of multiplex PCR assay on fresh-cut cantaloupe inoculated with 10<sup>3</sup>–1 cfu/g following prior enrichment.

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    <p>Lane M shows 1000 bp DNA marker. Lanes 1 to 4, lanes 5 to 8, and lanes 9 to 12 show amplicon results after 0, 3, 6 h enrichment, respectively for <i>L</i>. <i>monocytogenes</i>, <i>E</i>. <i>coli</i> O157:H7, and <i>S</i>. <i>aureus</i> on fresh-cut cantaloupe that had been inoculated with 1.8 × 10<sup>3</sup>–1 cfu/g, 1.1 × 10<sup>3</sup>–1 cfu/g, and 1.4 × 10<sup>3</sup>–1 cfu/g.</p

    Primer specificity for <i>L</i>. <i>monocytogenes</i>, <i>E</i>. <i>coli</i> O157:H7, and <i>S</i>. <i>aureus</i>.

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    Lane M: 2000 bp DNA marker; Lanes 1, 12, and 23 show the PCR amplicons specific to L. monocytogenes (285 bp), E. coli O157:H7 (193 bp), and S. aureus (159 bp); Lanes 2–11 show PCR amplicons specific to Listeria ivanovii (ATCC 19119), Listeria grayi (ATCC 25401), Listeria seeligeri (ATCC 35967), Listeria welshimeri (ATCC 35897), Listeria innocua (ATCC 33090), Salmonella Typhimurium (ATCC 14028), Samonella enterica subspenterica (CMCC 50115), Salmonella paratyphi Type B (CMCC 50094), Salmonella enterica subsp. enterica (CICC 10871), and Salmonella Typhi (CMCC 50071); Lanes 12–22 show PCR amplicons specific to Micrococcus luteus (CMCC 28001), Proteus mirabilis (CMCC 49005), Bacillus cereus (CMCC 63301), Escherichia coli (CMCC 44102), Escherichia coli STEC (CICC10668), Escherichia coli ETEC (CICC10665), Escherichia coli ETEC O25:K19 (CICC 10414), Escherichia coli EPEC O127:K63 (CICC 10411), Escherichia coli EIEC (CICC 10661), and Vibrio parahemolyticus (CICC 21617); Lanes 23–32 show PCR amplicons specific to Vibrio cholera (CICC 23794), Enterobacter sakazakii (CICC 21560), Pseudomonas aeruginosa (CICC 20236), Campylobacter jejuni (CICC 22936), Shigella flexneri (CICC 10865), Shigella sonnei (CICC 21679), Pseudomonas fluorescens (CICC 20225), Yersinia enterocolitica (CICC 10869), and Bacillus subtilis (CICC 10275); Lane 33 is the negative control.</p
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