55 research outputs found
Highly Stable Graphene-Based Nanocomposite (GO–PEI–Ag) with Broad-Spectrum, Long-Term Antimicrobial Activity and Antibiofilm Effects
Various
silver nanoparticle (AgNP)-decorated graphene oxide (GO) nanocomposites
(GO–Ag) have received increasing attention owing to their antimicrobial
activity and biocompatibility; however, their aggregation in physiological
solutions and the generally complex synthesis methods warrant improvement.
This study aimed to synthesize a polyethyleneimine (PEI)-modified
and AgNP-decorated GO nanocomposite (GO–PEI–Ag) through
a facile approach through microwave irradiation without any extra
reductants and surfactants; its antimicrobial activity was investigated
on Gram-negative/-positive bacteria (including drug-resistant bacteria)
and fungi. Compared with GO–Ag, GO–PEI–Ag acquired
excellent stability in physiological solutions and electropositivity,
showing substantially higher antimicrobial efficacy. Moreover, GO–PEI–Ag
exhibited particularly excellent long-term effects, presenting no
obvious decline in antimicrobial activity after 1 week storage in
physiological saline and repeated use for three times and the lasting
inhibition of bacterial growth in nutrient-rich culture medium. In
contrast, GO–Ag exhibited a >60% decline in antimicrobial
activity after storage. Importantly, GO–PEI–Ag effectively
eliminated adhered bacteria, thereby preventing biofilm formation.
The primary antimicrobial mechanisms of GO–PEI–Ag were
evidenced as physical damage to the pathogen structure, causing cytoplasmic
leakage. Hence, stable GO–PEI–Ag with robust, long-term
antimicrobial activity holds promise in combating public-health threats
posed by drug-resistant bacteria and biofilms
Stable Nanocomposite Based on PEGylated and Silver Nanoparticles Loaded Graphene Oxide for Long-Term Antibacterial Activity
The increasing occurrence
of antibiotic-resistant pathogens, especially superbugs, is compromising
the efficacy of traditional antibiotics. Silver nanoparticles (AgNPs)
loaded graphene oxide (GO) nanocomposite (GO-Ag) has drawn great interest
as a promising alternative antibacterial material. However, GO-Ag
nanocomposite often irreversibly aggregates in physiological solutions,
severely influencing its antibacterial capacity and practical application.
Herein, a PEGylated and AgNPs loaded GO nanocomposite (GO-PEG-Ag)
is synthesized through a facile approach utilizing microwave irradiation,
while avoiding extra reducing agents. Through PEGylation, the synthesized
GO-PEG-Ag nanocomposite dispersed stably over one month in a series
of media and resisted centrifugation at 10 000×<i>g</i> for 5 min, which would benefit effective contact between
the nanocomposite and the bacteria. In contrast, GO-Ag aggregated
within 1 h of dispersion in physiological solutions. In comparison
with GO-Ag, GO-PEG-Ag showed stronger bactericidal capability toward
not only normal Gram-negative/positive bacteria such as <i>E.
coli</i> and <i>S. aureus</i> (∼100% of <i>E. coli</i> and ∼95.3% of <i>S. aureus</i> reduction
by 10 μg/mL nanocomposite for 2.5 h), but also superbugs. Moreover,
GO-PEG-Ag showed lower cytotoxicity toward HeLa cells. Importantly,
GO-PEG-Ag presented long-term antibacterial effectiveness, remaining
∼95% antibacterial activity after one-week storage in saline
solution versus <35% for GO-Ag. The antibacterial mechanisms of
GO-PEG-Ag were evidenced as damage to the bacterial structure and
production of reactive oxygen species, causing cytoplasm leakage and
metabolism decrease. The stable GO-PEG-Ag nanocomposite with powerful
and long-term antibacterial capability provides a more practical and
effective strategy for fighting superbugs-including pathogen threats
in biomedicine and public health
Dendrogram displaying the PFGE profiles of the 43 isolates.
<p>The strain number, origin, source, sequence type (ST), and H<sub>2</sub>S phenotype are shown for each strain. +, H<sub>2</sub>S-producing isolate; −, non-H<sub>2</sub>S-producing isolate.</p
Effect of various viruses on (A, B) IIP<sub>max</sub> and (C, D) IIP<sub>atoxic</sub> toward (A, C) HIV<sub>NL4-3</sub> and (B, D) mutant viruses.
<p>IIP was calculated using equation (1), with the concentrations used being peak plasma concentrations for IIP<sub>max</sub> and the maximum nontoxic concentration for IIP<sub>atoxic</sub>. Fractional changes in IIP were calculated using equation (3). The drugs tested are grouped by class: NRTIs, NNRTI, and PIs. Within each class, different shapes indicate the various mutants.</p
Epitope Binning Assay Using an Electron Transfer-Modulated Aptamer Sensor
Surface plasmon resonance and quartz crystal microbalance are workhorses
of protein–DNA interaction research for over 20 years, providing
ways to quantitatively determine the protein–DNA binding. However,
the cost, necessary technical expertise, and severe nonspecific adsorption
poses barriers to their use. Convenient and effective techniques for
the measurement of protein–DNA binding affinity and the epitope
binning between DNA and proteins for developing highly sensitive detection
platform remain challenging. Here, we develop a binding-induced alteration
in electron transfer kinetics of the redox reporter labeled (methylene
blue) on DNA aptamer to measure the binding affinity between prostate-specific
antigen (PSA) and aptamer. We demonstrate that the binding of PSA
to aptamer decreases the electron transfer rate of methylene blue
for ∼45%. Further, we identify the best pairwise selection
of aptamers for developing sandwich assay by sorting from 10 pairwise
modes with the PSA detection limit of 500 ng/mL. Our study provides
promising ways to analyze the binding affinity between ligand and
receptor and to sort pairwise between aptamers or antibodies for the
development of highly sensitive sandwich immunoassays
Sequence alignment of the <i>phs</i> gene and the protein.
<p>A nonsense mutation at position 208 of the <i>phsA</i> gene results in the replacement of a sense codon (CAG) with a termination codon (UAG) leading to the premature termination of <i>phsA</i>. The first sequence, <i>phsA</i>, is based on <i>S</i>. enterica serotype Typhimurium strain LT2 (GenBank AE006468). *, termination codon; +, H<sub>2</sub>S-producing isolate; −, non-H<sub>2</sub>S-producing isolate.</p
Curves of the dose-response of selected drugs.
<p>x axes indicate log of drug concentration (nM), y axes indicate the inhibitor rate of virus (%). (A) is the curve of the dose-response of 3 viruses (V179E\H221Y\T215Y, V179E\Y181C\T215Y and WT <sub>NL4.3</sub>) in d4T. (B) is the curve of the dose-response of 2 viruses (K103N\H221Y\Y181C\T215Y and WT <sub>NL4.3</sub>) in EFV. (C) is the curve of the dose-response of 3 viruses (G48V\I54V\V82A, M46I\N88S and WT <sub>NL4.3</sub>) in IDV. (D) is the curve of the dose-response of 3 viruses (G48V\I54V, V82A and WT <sub>NL4.3</sub>) in SQV.</p
The methodology of <i>Salmonella</i> detection procedure.
<p>The methodology of <i>Salmonella</i> detection procedure.</p
Effects of various resistance mutations on (A) IC50 and (B) slope, as calculated from dose-response curves.
<p>Fold changes in IC50 for mutants were relative to those for the wild-type virus, and fractional changes in slope were computed using equation (2). The drugs tested are grouped by class: NRTIs, NNRTI, and PIs. Within each class, different shapes indicate the various mutants.</p
Primers for PCR amplification of the <i>phsABC</i> genes.
<p>Primers for PCR amplification of the <i>phsABC</i> genes.</p
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