The Study of Near-Band-Edge Property in Oxygen-Incorporated ZnS for Acting as an Efficient Crystal Photocatalyst

A wide gap semiconductor material has attracted attention as a heterophotocatalyst because of its light harvesting nature to be used in alternative energy production for the next generation. We, herein, grow and synthesize ZnS_{(1–<i>x</i>)}O_<i>x</i> series compounds using the chemical vapor transport (CVT) method with I₂ serving as the transport agent. Different crystals, such as undoped ZnS and oxygen-doped ZnS_0.94O_0.06 and ZnS_0.88O_0.12, revealed different bright palette emissions that were presented in photoluminescence spectra in our previous report. To study the electron–hole pair interaction of this sample series, the near-band-edge transitions of the sample series were characterized in detail by photoconductivity (PC) experiments. Additional results from surface photovoltage (SPV) spectra also detected the surface and defect-edge transitions from the higher oxygen-doped ZnS crystals. PC measurement results showed a red-shift in the bandgap with increasing incorporation of oxygen on ZnS. Consequently, the samples were subjected to photoirradiation by xenon lamp for the degradation of methylene blue (MNB) by acting as heterophotocatalysts. Undoped ZnS emerged as the best photocatalyst candidate with the fastest rate constant value of 0.0277 min^–1. In cubic {111} ZnS [{111} c-ZnS], the polarized Zn⁺ → S^– ions may play a vital role as a photocatalyst because of their strong electron–hole polarization, which leads to the mechanism for degradation of the MNB solution

In-Plane Axially Enhanced Photocatalysis by Re₄ Diamond Chains in Layered ReS₂

Two-dimensional (2D) semiconductors play a crucial role in high-efficiency photocatalysts because of their high surface-to-volume ratio. The surface property is a key part of photocatalysis. In this work, the enhanced photocatalytic behavior of the layered ReS₂ with optical polarization along the Re₄ nano-diamond-chain (DC) direction (<i>b</i> axis) has been demonstrated. The unpolarized photoconductivity (PC) response of ReS₂ with an applied bias along the <i>b</i> axis is approximately 1 order higher than that of the applied bias perpendicular to the <i>b</i> axis. The polarization-dependent PC spectra of <i>E</i> ∥ <i>b</i> also reveal a higher photoresponsivity with respect to those measured along the <i>E</i> ⊥ <i>b</i> polarization for the layered ReS₂. This result indicates that stronger polarization dipoles as well as a larger amount of photogenerated carriers and surface states can contribute to the <i>C</i>-plane ReS₂ under the illumination of <i>E</i> ∥ <i>b</i> polarized photons. With the special axial effect, the layered ReS₂ 2D photocatalyst shows much faster degradation rates of 5.6 and 12.3 than the other transition-metal dichalcogenides of TaS₂ and MoS₂ for the degradation of methylene blue (MNB) solution. For the polarization-dependent photodegradation test, the degradation rate of illuminated <i>E</i> ∥ <i>b</i> polarized photons is also approximately 12 times faster than that of the illuminated <i>E</i> ⊥ <i>b</i> polarized light in a 25 μM MNB solution. The enhanced photocatalytic behavior of ReS₂ along the DC also shows a peak photoreponse of ∼25 μV detected in the polarized photovoltaic spectrum of the 0.5 μM MNB dye-sensitized solar cell positioned at ∼1.99 eV. The formation of a nano-DC and a one-layer trigonal crystalline phase is beneficial for the versatile energy applications of ReS₂

Protective Efficacy of VP1-Specific Neutralizing Antibody Associated with a Reduction of Viral Load and Pro-Inflammatory Cytokines in Human SCARB2-Transgenic Mice

<div><p>Hand-foot-mouth diseases (HFMD) caused by enterovirus 71 (EV71) and coxsackievirus 16 (CVA16) in children have now become a severe public health issue in the Asian-Pacific region. Recently we have successfully developed transgenic mice expressing human scavenger receptor class B member 2 (hSCARB2, a receptor of EV71 and CVA16) as an animal model for evaluating the pathogenesis of enterovirus infections. In this study, hSCARB2-transgenic mice were used to investigate the efficacy conferred by a previously described EV71 neutralizing antibody, N3. A single injection of N3 effectively inhibited the HFMD-like skin scurfs in mice pre-infected with clinical isolate of EV71 E59 (B4 genotype) or prevented severe limb paralysis and death in mice pre-inoculated with 5746 (C2 genotype). This protection was correlated with remarkable reduction of viral loads in the brain, spinal cord and limb muscles. Accumulated viral loads and the associated pro-inflammatory cytokines were all reduced. The protective efficacy of N3 was not observed in animals challenged with CVA16. This could be due to dissimilarity sequences of the neutralizing epitope found in CVA16. These results indicate N3 could be useful in treating severe EV71 infections and the hSCARB2-transgenic mouse could be used to evaluate the protective efficacy of potential anti-enterovirus agent candidates.</p></div

Administration of N3 reduced pro-inflammatory chemokines expression in CNS and muscle tissues of 5746-preinfected hSCARB2-transgenic mice.

<p>RNAs were extracted from the brain, spinal cord, and muscle of 5746-infected 7-day old hSCARB2-transgenic mice treated with N3 or isotype antibody, and antibody-untreated mice as described in Fig. 6 and were subjected to quantitative RT-PCR specific to (<b>A</b>) CXCL10, (<b>B</b>) CCL3, and (<b>C</b>) IL-6. The number of PCR cycles (Ct) required for fluorescent detection of target genes was calculated and presented as the relative expression after normalization with the internal control of β-actin expression from the same tissue. Each normalized 2^Ct value was the ratio to the value from the mean of 2^Ct obtained from the antibody-untreated tissues. A schematic representation of the target gene expression and the statistical average from 10 mice per group is shown. Unpaired student <i>t</i> test with Welch correction was used for statistical analysis. (*<i>p</i>< = 0.05, **<i>p</i>< = 0.01).</p

Survival of N3 treated hSCARB2-transgenic mice preinfected with 5746.

<p>Seven-day old mice preinfected with 1×10⁵ pfu of 5746 were given 200 µg N3 at time points of 3 h (▾), 24 h (▴), 48 h (▪), and 48 h twice (•) post infection. Mice injected without N3 (O), with the same amounts of isotype antibody (♦), and mice treated with a low dose of N3 (70 µg) (□) 3 h post infection were included. Mice were monitored daily and survival rates were recorded. Each group consisted of 7 to 10 mice and the results were representative of 2 independent experiments. The Logrank test was used for statistical analysis.</p

N3 inhibited viral loads of the tissues from hSCARB2-transgenic mice preinfected with EV71 5746.

<p>7-day old hSCARB2-transgenic mice were challenged with 1×10⁵ pfu of 5746 and followed by receiving 200 µg N3 or isotype antibodies at 3 h post infection. Infected mice received no antibody were included. On day 6 post infection, mice were sacrificed and RNAs were extracted from the brainstem, spinal cord, muscle, skin, and intestine for quantitative RT-PCR using primers specific to VP1 region of P1 transcripts. Virus copy numbers were calculated using a standard curve shown by purified EV71. A schematic representation of the virus copy number and the statistical average from 11 mice per group is shown. The unpaired student <i>t</i> test with Welch correction was used for statistical analysis.</p

N3-mediated neutralization against B4 genotype of E59 and C2 genotype of 5746 viruses in vitro.

<p>(<b>A</b>) Both E59 and 5746 were pre-incubated (m.o.i. = 0.5) with various amounts of N3 for 1 h at 37°C before adding them to 3T3-SCARB2 cells. RNA was extracted 2 h after infection, and subjected to RT-PCR to detect the expression of viral genome P1. The amounts of N3 in different lanes were Lane 1∶50 µg, Lane 2∶10 µg, Lane 3∶2 µg, Lane 4∶0.4 µg, Lane 5: uninfected 3T3-SCARB2 cells as the negative control, and Lane 6: E59 viral cDNA as the positive control were included. The same loading scheme was applied to (<b>B</b>) where Lane 6 was replaced by 5746 virus for the control. Expression of cytosolic GADPH as the internal control of RT-PCR was detected. (<b>C</b>) and (<b>D</b>) The bar graph represents the densitometric quantification of the band intensities of viral genome P1 and GADPH from (<b>A</b>) and (<b>B</b>), respectively. The error bar of each group generated from three independent experiments was included.</p

N3 downregulated TNF-α and IL-1β in CNS and muscle tissues of 5746-infected hSCARB2-transgenic mice.

<p>RNA was extracted from the brain, spinal cord, and muscles of 5746-infected 7-day old hSCARB2-transgenic mice treated with N3 or isotype antibody, and antibody-untreated mice as described in Fig. 4 and were subjected to quantitative RT-PCR specific to (<b>A</b>) TNF-α and (<b>B</b>) IL-1β. The relative expression of target gene normalized with the internal control of β-actin expression from the same tissue was calculated as described in Fig. 7. Unpaired student <i>t</i> test with Welch correction was used for statistical analysis. (*<i>p</i>< = 0.05, **<i>p</i>< = 0.01).</p

N3 conferred the reduction of hair loss and scurf on E59-preinfected hSCARB2-transgenic mice.

<p>(<b>A</b>) and (<b>B</b>) 1-day old hSCARB2-transgenic mice (n = 9–10/group) were preinfected with a HFMD symptom-causing dose of E59 at 1×10⁷ pfu subcutaneously. After 3 h of infection, 200 µg of N3 or isotype antibody was injected i.p. Mice without any antibody treatment were included. The Experiments were repeated twice, and 100× magnification of pictures (<b>A</b>) shown the representative data were taken. The graph represents the scoring of severe hair loss and skin scurf (<b>B</b>) from each group of mice. The scores were monitored on a daily basis. One-way ANOVA and the Kruskal-Wallis test were used for statistical analysis (*<i>p</i>< = 0.05, **<i>p</i>< = 0.01).</p

N3 reduced the pathogenesis of EV71 in the limb muscles and in the intestinal mucosa and villi.

<p>(<b>A</b>) Brainstem and (<b>B</b>) limb muscle tissues were isolated from the 1×10⁵ pfu of 5746-infected 7-day old hSCARB2-Tg mice which treated i.p. with 200 µg of N3 or isotype antibodies (3 h post infection), and from antibody-untreated mice staining with anti-EV71 antibody on Day 4 post infection. The normal tissues (MOCK) with anti-EV71 staining were also prepared. (<b>C</b>) H/E staining of intestine (>8 days post infection) from the groups of mice described in (<b>A</b>) was shown. Observations were made at a magnification of x200 for (<b>A</b>) and x100 for (<b>B</b>) and (<b>C</b>).</p