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Monilinia fructicola has been widely reported as the causal agent of brown rot disease on many Rosaceae family fruits worldwide. It has been reported on stone fruits, e.g., peach, plum, cherry, apricot and mume; as well as pome fruits, e.g., apple, pear and hawthorn. Loquat is a member of the Eriobotrya genus in subfamily Maloideae along with apple, pear and hawthorn. So far, loquat has not been reported as the host of any Monilia species. In June 2019, brown rot symptoms were observed on loquat fruits in an orchard in Wuhan, Hubei Province, China. Thirty single spore isolates were obtained and identified as M. fructicola based on morphological characteristics and molecular analysis. This is the first report of loquat brown rot disease caused by Monilia species in the world. Furthermore, upon artificial inoculation, all three Monilia species from peach in China, i.e., M. fructicola, M. mumecola and M. yunnanensis, could cause typical brown rot disease on loquat fruits. At the same time, M. fructicola isolates from loquat showed virulence similar to those isolates from peach when the pathogenicity test was conducted on peach fruits. These results suggested that loquat could be infected by other Monilia species and that isolates from loquat also have potential to damage other Rosaceae family fruits in practice.

This study aimed to investigate the effects of arachidonic acid metabolite epoxyeicosatrienoic acid (EETs) in the apoptosis of endothelial cells induced by tumor necrosis factor-alpha (TNF-α). After human umbilical vein endothelial cells were cultured, TNF-α/ActD, 14, 15-EET, and HMR-1098 were added, respectively, into the culture medium. The apoptosis level of endothelial cells was detected by flow cytometry. After TNF-α/ActD induced endothelial cell apoptosis, flow cytometry staining showed that endothelial cell apoptosis increased significantly, and the apoptotic cells were significantly reduced after the addition of 14, 15-EET. However, the apoptotic cells significantly increased after the addition of HMR-1098. Western Blot results showed that the phosphorylation levels of LC3-II and AMPK were increased after TNF-α/ActD induction, and the increase was noticeable after the addition of 14, 15-EET. However, the phosphorylation levels of LC3-II and AMPK significantly decreased after the addition of HMR-1098. The activity of Caspase-8 and -9 decreased significantly after the addition of 14, 15-EET but increased after the addition of HMR-1098. Arachidonic acid can inhibit TNF-α induced endothelial cell apoptosis by upregulating autophagy.

This paper presents a common-drain-based operational amplifier (OPAMP) fabricated by mono n-type indium-zinc-oxide (IZO) thin-film transistors (TFTs). Positive feedback technology is employed to the load TFTs by cross-coupled connection in order to boost the voltage gain of the common-drain differential pair. The OPAMP exhibits an open-loop voltage gain (Av) of 27 dB over a −3 dB bandwidth (BW) of 8.4 kHz at a DC supply voltage of 10 V. The measured unity-gain frequency (UGF), phase margin (PM) and DC power consumption are 119.4 kHz, 36° and 0.96 mW, respectively. Moreover, the chip area of the proposed OPAMP is as small as 0.37 mm $\times0.3$ mm since this concise topology needs only 10 TFTs.

This article presents a novel design of high-speed ring oscillator (RO) in ${n}$ -type-only indium-zinc-oxide (IZO) thin-film transistor (TFT) technology. The proposed ROs combine the advantage of the skewed delay (SD) scheme and the bootstrap inverter to achieve a higher oscillation frequency. The design of improved output buffers with stronger driving capability is also included. For comparison, the proposed seven-stage SD ROs and the conventional bootstrap RO are fabricated on the same glass. It is measured that the oscillation frequencies of the SD ROs with $-{t}_{{\text {pd}}}$ and 0 SD are improved by more than 45% and 25% within the supply voltage ranges from 6 V up to 20 V. In addition, the measured output swings of the proposed boost buffers are improved by more than 50% with input frequencies higher than megahertz.

This paper presents a 50 dB high-gain operational amplifier (OPAMP), which is fabricated by unipolar n-type indium–zinc–oxide thin-film transistors. Different positive feedback technologies are employed to achieve sufficient voltage gain. The fabricated OPAMP exhibits an open-loop voltage gain (A v) of 50 dB over a −3 dB bandwidth of 15 kHz at the supply voltage of 20 V. The measured unity-gain frequency (f UG) and the DC power consumption are 500 kHz and 8.07 mW, respectively. In addition, an effective frequency compensation scheme is also introduced and simulated. The simulation results that the proposed OPAMP has a voltage gain of 50 dB with 60° phase margin at 150 kHz unity-gain frequency after compensation.

This paper presents an integrated operational amplifier (OPAMP) consisting of only n-type metal oxide thin-film transistors. In addition to using positive feedback in the input differential pair, a transconductance-enhancement topology is applied to improve the gain of the OPAMP. The OPAMP has a voltage gain ( $A_{v}$ ) of 29.54 dB over a 3-dB bandwidth of 9.33 kHz at a supply voltage of 15 V. The unity-gain frequency, phase margin (PM), and dc power consumption ( $P_{\mathrm{ DC}}$ ) are 180.2 kHz, 21.5° PM and 5.07 mW, respectively.

Bacillus Calmette‑Guérin (BCG) is considered to be a successful biotherapy for treating bladder cancer (BCa). However, the underlying mechanisms of BCG have not been completely clarified, to date. The role of macrophages in BCG therapy for BCa has still not been determined in vivo. In the present study, the role and potential mechanism of BCG (0.25, 1.25 and 6.25 µg/mouse; intravenous) immunotherapy for BCa was investigated in a NOD/scid IL2Rg‑/‑ (NSI) mouse model by targeting macrophages in vivo. Notably, it was observed that NSI mice with T24 BCa cells displayed high levels of the macrophage marker CD11b+ F4/80+ after injection via the tail vein of live BCG, as well as a significant reduction in tumor volume. The levels of the inflammatory and macrophage maturation cytokines, such as tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6, IL‑12P70, TNF superfamily member 11 and monocyte chemotactic protein 1, were significantly increased in the serum and the tumor supernatant compared to that in normal control subjects. Furthermore, BCG promoted the expression of the pro‑differential genes Spi‑1 proto‑oncogene, early growth response protein 1, nuclear factor (NF)‑κB and proto‑oncogene c‑Fos in bone marrow. In conclusion, these observations indicate that the injection of live BCG can target macrophages against bladder tumor growth in vivo. The mechanism is likely related to the promotion of macrophage maturation, immune activation and increased numbers of macrophages infiltrating the bladder tumor.

Background Epigallocatechin gallate (EGCG) has attracted increasing attention due to its beneficial effect on cardiovascular health. The aim of this study was to investigate the underlying mechanism by which EGCG protects against myocardial ischaemia/reperfusion injury (I/RI). Methods Murine myocardial I/RI and H2O2-induced cardiomyocyte injury models were established to evaluate the therapeutic effects of EGCG. In the myocardial I/RI mouse model, the echocardiographic parameters of ejection fraction (EF) and fraction shortening (FS) levels, infarct size, histological evaluation and transmission electron microscopy (TEM) were used to evaluate cardiac tissue damage and autophagy. MTT assays, TUNEL staining, flow cytometry and immunofluorescence (IF) were used to monitor cell viability, apoptosis and autophagy in vitro. qRT-PCR and western blotting were used to determine the mRNA and protein levels of key molecules, respectively. The epigenetic regulation of DUSP5 was assessed via RNA immunoprecipitation (RIP), RNA pull-down and chromatin immunoprecipitation (ChIP) assays. Results EGCG significantly improved cardiac function, reduced infarct size, enhanced cell viability and inhibited autophagic activity in both myocardial I/RI mouse models and H2O2-induced cardiomyocyte injury models. Moreover, EGCG suppressed H2O2- or myocardial I/R-increased Gm4419 expression, and Gm4419 overexpression dramatically abolished EGCG-mediated protective effects against myocardial I/RI. Mechanistically, Gm4419 epigenetically suppressed DUSP5 by recruiting EZH2, thus activating ERK1/2 pathway-mediated autophagy. Furthermore, the in vivo experiments further verified that the Gm4419-mediated disruptive effects of EGCG on myocardial I/RI were potentiated by DUSP5 knockdown but attenuated by DUSP5 overexpression. Conclusions In conclusion, our findings demonstrated that EGCG protected against myocardial I/RI by modulating Gm4419/DUSP5/ERK1/2-mediated autophagy.

Bladder cancer is one of the most malignant tumors closely associated with macrophages. Polyporus polysaccharide (PPS) has shown excellent efficacy in treating bladder cancer with minimal side effects. However, the molecular mechanisms underlying the effects of PPS in inhibiting bladder cancer remain unclear. In this study, we used macrophages cultured alone or with T24 human bladder cancer cell culture supernatant as study models. We found that PPS enhanced the activities of IFN-γ-stimulated RAW 264.7 macrophages, as shown by the release of inducible nitric oxide synthase (INOS), secretion of tumor necrosis factor (TNF)-α and interleukin (IL)-6, phagocytosis activity, as well as expression of M1 phenotype indicators, such as CD40, CD284 and CD86. PPS acted upstream in activation cascade of nuclear factor (NF)-κB signaling pathways by interfering with IκB phosphorylation. In addition, PPS regulated NF-κB (P65) signaling by interfering with Toll-like receptor (TLR)-4, INOS and cyclooxygenase (COX)-2. Our results indicate that PPS activates macrophages through TLR4/NF-κB signaling pathways.

In this paper, a blind demodulation scheme for chirp-binary orthogonal keying (BOK)-ultra wide band (UWB) system was proposed based on matching pursuit (MP) algorithm. The scheme was validated in additive white Gaussion noise (AWGN) and indoor multi-path channels that suggested by the IEEE P802.15 criterion. From the simulation results, it shows that the performance of the proposed MP method is consistent well with that of the traditional coherent method in communication circumstance with high quality requirement, and the performance difference of MP method and coherent method is less than 0.8 dB when the bit error rate (BER) is set as 0.001. As the requested BER getting small, the MP method has a comparable performance with the coherent method. It also presented an efficient way for spectrum sharing with other communication systems.

A new case of visceral leishmaniasis (kala-azar) was reported by Changzhi CDC of Shanxi Province in September 2011. The case was investigated clinically and epidemiologically. The patient was a two-year-old boy who lived in Huangnian Town of Changzhi County in Shanxi Province. Clinical examination showed hepatosplenomegaly, consistent decrease of blood cells and Leishman-Donovan body in the bone marrow smear. The rK39 immune diagnosis test showed strongly positive. The case was diagnosed as kala-azar. After one course treatment of sodium stibogluconate, the patient's condition improved markedly. There were no cases of kala-azar in this region historically. Blood samples of 17 individuals and 5 domestic animals including 3 dogs were all negative in the rK39 immunodiagnostic test. It is speculated that the potential risk of kala-azar transmission exists in this region.

Single-strand conformation polymorphism (SSCP) was used to characterize viroids. Eight cDNA clones, which showed identical profiles in preliminary existing SSCP analysis but had different sequences, were chosen to develop a sensitive SSCP technique for identifying the variability of Peach latent mosaic viroid (PLMVd). Polyacrylamide Gel Electrophoresis (PAGE) conditions were optimized to improve the sensitivity of the existing SSCP, and a modified SSCP protocol was developed. The results indicated that the modified SSCP protocol provided an overall sensitivity in identifying the variability of these clones, and showed higher resolution than the existing one and its improved versions. As shown by sequence analyses of cDNA clones of PLMVd and the modified SSCP profiles, there is no close correlation between the number of base changes and variation of the modified SSCP band patterns. The potential use of the modified SSCP analysis is discussed as a tool for viroids characterization.