In December 2019, an outbreak of the severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection occurred in Wuhan, and rapidly spread to worldwide, which has attracted many people's concerns about the patients. However, studies on the infection status of medical personnel is still lacking.

No abstract

Callose is a β-l,3-glucan with diverse roles in the viral pathogenesis of plants. It is widely believed that the deposition of callose and hypersensitive reaction (HR) are critical defence responses of host plants against viral infection. However, the sequence of these two events and their resistance mechanisms are unclear. By exploiting a point inoculation approach combined with aniline blue staining, immuno-electron microscopy and external sphincters staining with tannic acid, we systematically investigated the possible roles of callose deposition during viral infection in soybean. In the incompatible combination, callose deposition at the plasmodesmata (PD) was clearly visible at the sites of inoculation but viral RNA of coat protein (CP-RNA) was not detected by RT-PCR in the leaf above the inoculated one (the upper leaf). In the compatible combination, however, callose deposition at PD was not detected at the site of infection but the viral CP-RNA was detected by RT-PCR in the upper leaf. We also found that in the incompatible combination the fluorescence due to callose formation at the inoculation point disappeared following the injection of 2-deoxy-D-glucose (DDG, an inhibitor of callose synthesis). At same time, in the incompatible combination, necrosis was observed and the viral CP-RNA was detected by RT-PCR in the upper leaf and HR characteristics were evident at the inoculation sites. These results show that, during the defensive response of soybean to viral infection, callose deposition at PD is mainly responsible for restricting the movement of the virus between cells and it occurs prior to the HR response.

to perform PDT. [7] PSs absorb laser energy in the presence of O 2 to produce cytotoxic reactive oxygen species (ROS) such as singlet oxygen ( 1 O 2 ) that causes the destruction of the genetic material in cancer cells, leading to cell apoptosis, or necrosis. [7][8][9][10] The O 2 involved in PDT improves tumor destruction and reduces the toxic side effects as compared with other conventional therapeutic modalities like radiotherapy, chemotherapy, and surgery. [11][12][13][14][15] However, hypoxia, one of the hallmarks of malignant tumors, [16][17][18] induces an unexpected resistance of tumors to PDT, since molecular O 2 plays an essential role during the process. Some types of nanocatalysts have been used to address this dilemma, such as manganese dioxide (MnO 2 ) nanoparticles, carbon dot, and single-atom ruthenium (Ru) for an in situ catalysis of the decomposition of H 2 O 2 to generate O 2 . [6,14,19] This could be an effective strategy to relieve hypoxia in the tumor microenvironment (TME), thus becoming a potential approach to improve the efficacy of PDT. [20] Additionally, the acidic TME with an excessive amount of H 2 O 2 is a natural activator of these nanocatalysts, making them intelligent nanocatalysts for tumor specific therapy. [21][22][23] Recently, MnO 2 nanostructures have received extensive attention in the field of bio-applications for their efficient O 2 production and easy synthesis, [24][25][26][27] enhancing the effect of radiation therapy, [27] chemotherapy, [28] and PDT. [29] In addition, MnO 2 is rapidly decomposed into water soluble Mn 2+ ion in an acidic condition, [6,[30][31][32][33][34] and excreted through the bile into the feces, avoiding unexpected accumulation and long-term toxicity in vivo. [6,29] However, MnO 2 nanostructures without surface coating have a poor structure stability under physiological conditions, [35] and it is difficult to control their size and morphology during the synthesis, thus, increasing the uncertainty of the reactivity of the nanomaterial. [25] Therefore, it is highly desirable to construct MnO 2 nanoparticles with uniform morphology, high stability and biocompatibility for biomedical applications.Ferritin (Ftn) is an endogenous iron storage protein composed of 24 subunits, with a hollow structure of 12 nm in the external diameter and an inner cavity of 8 nm. [36] Ftn has been widely used as a superior protein nanocage for the Hypoxia is a hallmark of the tumor microenvironment (TME) that promotes tumor development and metastasis. Photodynamic therapy (PDT) is a promising strategy in the treatment of tumors, but it is limited by the lack of oxygen in TME. In this work, an O 2 self-supply PDT system is constructed by co-encapsulation of chlorin e6 (Ce6) and a MnO 2 core in an engineered ferritin (Ftn), generating a nanozyme promoted PDT nanoformula (Ce6/ Ftn@MnO 2 ) for tumor therapy. Ce6/Ftn@MnO 2 exhibits a uniform small size (15.5 nm) and high stability due to the inherent structure of Ftn. The fluorescence imaging and immunofluorescence analysis dem...

Left ventricular hypertrophy is a maladaptive response to pressure overload and an important risk factor for heart failure. Intermedin (IMD), a multi-functional peptide, plays important roles in cardiovascular protection. In this study, we revealed an autophagy-dependent mechanism involved in IMD’s protection against cardiac remodeling and cardiomyocyte death in heart hypertrophy. We observed that transverse aortic contraction (TAC) induction, Ang II or ISO exposure induced remarkable increase in the expression of endogenous IMD and its receptor components, CRLR, RAMP1 and RAMP3, in mouse hearts and H9c2 cell cultures, respectively. Furthermore, the heart size, heart weight/body weight ratios, cardiomyocyte size and apoptosis, interstitial collagen, hypertrophic markers including ANP and BNP expression were also significantly increased, which were effectively suppressed by IMD supplementation. In addition, IMD induced capillary angiogenesis and improved functions in hypertrophic hearts. We further observed that IMD induced strong autophagy in hypertrophic hearts and cultured cells, which was paralleling with the decrease in cardiomyocyte size and apoptosis. Furthermore, an autophagy inhibitor, 3-MA, was used to block the IMD-augmented autophagy level, and then the protection of IMD on cardiomyocyte hypertrophy and apoptosis was almost abrogated. We also observed that IMD supplementation stirred intracellular cAMP production, and augmented the ERK1/2 phosphorylation induced by Ang II/ISO exposure in H9c2 cells. In addition, we inhibited PI3K, PKA and MAPK/ERK1/2 signaling pathways by using wortamannin, H89 and PD98059, respectively, in H9c2 cells co-incubating with both IMD and Ang II or ISO, and observed that these inhibitors effectively reduced IMD-augmented autophagy level, but only H89 and PD98059 pre-incubation abrogated the anti-apoptotic action of IMD. These results indicate that the endogenous IMD and its receptor complexes are induced in hypertrophic cardiomyocytes and proposed to play an important role in the pathogenesis of cardiac hypertrophy, and the autophagy stirred by IMD supplementation is involved in its protection against cardiomyocyte hypertrophy and apoptosis through the activation of both cAMP/PKA and MAPK/ERK1/2 pathways.

This paper investigated ultraviolet A light-emitting diode (UVA-LED) irradiation to activate Fe­(VI) for the degradation of micropollutants (e.g., sulfamethoxazole (SMX), enrofloxacin, and trimethoprim). UVA-LED/Fe­(VI) could significantly promote the degradation of micropollutants, with rates that were 2.6–7.2-fold faster than for Fe­(VI) alone. Comparatively, UVA-LED alone hardly degraded selected micropollutants. The degradation performance was further evaluated in SMX degradation via different wavelengths (365–405 nm), light intensity, and pH. Increased wavelengths led to linearly decreased SMX degradation rates because Fe­(VI) has a lower molar absorption coefficient at higher wavelengths. Higher light intensity caused faster SMX degradation, owing to the enhanced level of reactive species by stronger photolysis of Fe­(VI). Significantly, SMX degradation was gradually suppressed from pH 7.0 to 9.0 due to the changing speciation of Fe­(VI). Scavenging and probing experiments for identifying oxidative species indicated that high-valent iron species (Fe­(V)/Fe­(IV)) were responsible for the enhanced degradation. A kinetic model involving target compound (TC) degradation by Fe­(VI), Fe­(V), and Fe­(IV) was employed to fit the TC degradation kinetics by UVA-LED/Fe­(VI). The fitted results revealed that Fe­(IV) and Fe­(V) primarily contributed to TC degradation in this system. In addition, transformation products of SMX degradation by Fe­(VI) and UVA-LED/Fe­(VI) were identified and the possible pathways included hydroxylation, self-coupling, bond cleavage, and oxidation reactions. Removal of SMX in real water also showed remarkable promotion by UVA-LED/Fe­(VI). Overall, these findings could shed light on the understanding and application of UVA-LED/Fe­(VI) for eliminating micropollutants in water treatments.

Oxidative stress induces serious tissue injury in cardiovascular diseases. Salidroside, with its strong antioxidative and cytoprotective actions, is of particular interest in the development of antioxidative therapies for oxidative injury in cardiac diseases. We examined the pharmacological effects of salidroside on H9c2 rat cardiomyoblast cells under conditions of oxidative stress induced by hydrogen peroxide (H2O2) challenge. Salidroside attenuated H2O2-impaired cell viability in a concentration-dependent manner, and effectively inhibited cellular malondialdehyde production, lethal sarcolemmal disruption, cell necrosis, and apoptosis induced by H2O2 insult. Salidroside significantly augmented Akt phosphorylation at Serine 473 in the absence or presence of H2O2 stimulation; wortmannin, a specific inhibitor of PI3K, abrogated salidroside protection. Salidroside increased the intracellular mRNA expression and activities of catalase and Mn-superoxide dismutases in a PI3K-dependent manner. Our results indicated that salidroside protected cardiomyocytes against oxidative injury through activating the PI3K/Akt pathway and increasing the expression and activities of endogenous PI3K dependent antioxidant enzymes.

Cardiac hypertrophy is the main cause of heart failure and sudden death in patients. But the pathogenesis is unclear. Angiotensin II may contribute to cardiac hypertrophy in response to pressure overload. In angiotensin II‐treated cardiomyocytes, there is a larger cross‐sectional area, more apoptosis cells, and a reduction of irisin expression. An increase in P62, an autophagy flux index, as well as LC3II, were observed in cardiomyocytes after angiotensin II‐induced injury. Surprisely, irisin supplementation increased LC3II expression and decreased P62 expression, consisted of results of RFP‐GFP‐LC3B adenovirus transfection, and reduced cardiomyocyte apoptosis, meanwhile, the protection of irisin was reversed by the autophagy inhibitor 3‐methyladenine. In animal experiments, overexpression of irisin reduced cardiomyocyte apoptosis and alleviated myocardial hypertrophy caused by pressure overload. The above results indicate that irisin‐induced protective autophagy and alleviated the apoptosis signaling pathway in cardiomyocytes, consequently reducing cardiomyocyte apoptosis after angiotensin II‐induced injury. Hence, increasing irisin expression may be a new way to improve cardiac function and quality of life in patients with cardiac hypertrophy.