High boron stress leads to sugar beet (Beta vulgaris L.) toxicity by disrupting photosystem â ¡.

This sugar beet acts as a soil remediator in areas where there are high levels of boron (B) in the soil, since it has a high requirement of boron (B) for growth, and has strong resistance to high B levels. Although B toxicity in different plants has been widely researched, little is known about the response of photosystem II (PSII) activity in sugar beet leaves to B toxicity at present. To clarify the growth and photosynthetic physiological response of sugar beet to B toxicity, the effects of different concentrations of H3BO3 (0.05, 1.5, 2.5,3.5 mM) on the growth, photosynthetic characteristics and antioxidant defense system of sugar beet seedlings were investigated by hydroponic experiments. In the present study, high B stress inhibited the growth of sugar beet and significantly decreased the biomass of the plants. There was a remarkable increase in the accumulation of B in the shoots, which affected photosynthesis and decreased the photosynthetic pigments. As B toxicity increased, leaf PSII activities and maximum photochemical efficiency of PSII (Fv/Fm) showed a tendency to decrease; at the same time, the photosynthetic performance index based on absorbed light energy (PIABS) decreased as well. Meanwhile, the energy allocation parameters of the PSII reaction center were changed, the light energy utilization capacity and the energy used for electron transfer were reduced and the thermal dissipation was increased at the same time. Furthermore, B toxicity decreased catalase (CAT) activity, increased peroxidase (POD) and superoxide dismutase (SOD) activities, and increased malondialdehyde (MDA) accumulation. According to the results obtained in this study, high B concentrations reduced the rate of photosynthesis and fluorescence, thus weakened antioxidant defense systems, and therefore inhibited the growth of sugar beet plants. Thus, in high B areas, sugar beet possesses excellent tolerance to high B levels and has a high B translocation capacity, so it can be used as a phytoremediation tool. This study provides a basis for the feasibility of sugar beet resistant to high B environments.

Experimental Study on Danggui Shaoyao San Improving Renal Fibrosis by Promoting Autophagy.

Renal fibrosis could lead to chronic kidney disease (CKD) developing into the end-stage with its pathological manifestation is the deposition of extracellular matrix (ECM). Danggui Shaoyao San (DSS) is one of the widely used herbal formulas in ancient China, which has been proven to have efficacy in the treatment of CKD. The experiment employed TGF-ß1 to stimulate the NRK-52E cells to establish a renal fibrosis model. With rapamycin (RAPA) used as the positive control, we detected the expression of fibronectin (FN), caspase-3, and autophagy-related proteins in the NRK-52E cells treated with DSS by Western blot and immunofluorescence assay. In order to further verify autophagy-promoting effects of DSS, we adopted 3-MA to inhibit autophagy. The experiment has found that DSS can lower the protein levels of FN and caspase-3 in the NRK-52E cells induced by TGF-ß1. After TGF-ß1 stimulation, the expression of LC3 II/I and Beclin 1 has decreased, and the protein levels of mTOR and p62 have increased. Consistent with rapamycin, DSS has significantly reduced these effects of TGF-ß1. It has also been found that DSS can increase the expression of LC3 II/I and Beclin 1 proteins and can reduce the level of mTOR in cells treated with 3-MA, suggesting that DSS can promote autophagy. In conclusion, DSS has been proved to reduce the apoptosis and fibrosis of NRK-52E cells induced by TGF-ß1, which may be achieved by promoting autophagy.

Exogenous salicylic acid alleviates fomesafen toxicity by improving photosynthetic characteristics and antioxidant defense system in sugar beet.

Fomesafen herbicide application has become major pollution in the growth and production of crops. Spraying fomesafen on the target crops may drift out to non-target crops. In northeast China, sugar beets are always planted adjacent to soybeans. Salicylic acid (SA) plays an important role in crop growth and alleviating abiotic stress, however, the role of SA in relieving fomesafen stress in sugar beet growth has rarely been investigated. Therefore, a pot study was conducted to elucidate the effects of different concentrations (0.025, 0.25, 0.5, 1, 5, and 10 mM) of SA on morphological parameters, photosynthetic performance, and antioxidant defense system in sugar beet seedlings under fomesafen (22.5 g a.i. ha-1) stress. The results showed that fomesafen stress inhibited the growth of sugar beet seedlings, and photosynthetic performance, while increased membrane lipid peroxidation and oxidative stress. However, exogenous SA alleviated the fomesafen stress and increased plant height, biomass, photosynthetic pigment contents, net photosynthetic rate (Pn), and photochemical efficiency of PSⅡ (Fv/Fm) in sugar beet leaves. Meanwhile, exogenous SA maintained the cell membrane integrity by reducing the content of malondialdehyde (MDA) and electrolyte permeability and regulating the activities of antioxidant enzymes including superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and polyphenol (PPO). Therefore, it is concluded that exogenous SA ameliorated the adverse effects of fomesafen on the growth of sugar beet seedlings, with a pronounced effect at 1 mM SA. The present study results may have useful implications in managing other plants that are poisoned by herbicides.

Phytotoxicity response of sugar beet (Beta vulgaris L.) seedlings to herbicide fomesafen in soil.

Fomesafen is the most widely used herbicide in the soybean field. However, there are urgent practical challenges with the long-term persistence of fomesafen in soil and its effects on the subsequent crops in agricultural production. Therefore, pot experiments were conducted to study the effects of fomesafen residues (0-0.05 mg kg-1) on growth, photosynthetic characteristics, and the antioxidant defense system of sugar beet seedlings. The results showed that with the increase of fomesafen residues, the phytotoxicity index increased, while the plant height, leaf area, root length, root volume, and dry weight of sugar beet decreased. Photosynthetic pigment content, net photosynthetic rate (Pn), maximum photosynthetic efficiency (Fv/Fm), and actual photosynthetic efficiency (Y(II)) declined with a dose-dependent manner of fomesafen, but the intercellular CO2 concentration (Ci) and non-photochemical quenching coefficient (NPQ) increased under fomesafen. On the other hand, the residues of fomesafen increased the content of malondialdehyde (MDA) and membrane permeability by aggravating oxidative stress and triggering the activities of superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), and polyphenol oxidase (PPO). In addition, sugar beet seedlings were significantly sensitive to fomesafen as the concentration of fomesafen in the soil was up to 0.025 mg kg-1. In conclusion, the present study showed that fomesafen residues in the soil could affect the morphophysiology and photosynthetic performance of sugar beet. This study is beneficial for understanding the effects of the herbicide fomesafen residues on non-target crops.

Therapeutic effects of probiotics on neonatal jaundice.

OBJECTIVE: To evaluate the therapeutic effects of probiotics on neonatal jaundice and the safety. METHODS: Sixty-eight neonates with jaundice were divided into a control group and a treatment group (n=34) randomly, and treated by blue light phototherapy and that in combination with probiotics. The serum bilirubin levels were detected before and 1, 4, 7 days after treatment. The time when therapy showed effects and jaundice faded, clinical outcomes as well as adverse reactions were recorded. The categorical data were expressed as (±s) and compared by t test. The numerical data were expressed as (case, %) and compared by χ² test. P<0.05 was considered statistically significant. RESULTS: Serum bilirubin levels of the two groups were similar before treatment (P>0.05). The levels significantly decreased 1, 4 and 7 days after treatment (P<0.05), but there was no significant inter-group difference on the post-treatment 1st day (P>0.05). The treatment group underwent more significant decreases on the 4th and 7th days than the control group did (P=0.002, 0.001). In the treatment group, the therapy exerted effects on (1.0±0.5) d and jaundice faded on (3.8±1.7) d, which were (2.6±0.6) d and (5.3±2.1) d respectively in the control group (P=0.001, 0.002). The effective rate of the treatment group significantly exceeded that of the control group (P=0.002). There were no obvious adverse reactions in either group. CONCLUSIONS: Probiotics lowered the serum bilirubin levels of neonates with jaundice rapidly, safely and significantly, and accelerated jaundice fading as well. This method is worthy of application in clinical practice.

Association between G6PD deficiency and hyperbilirubinemia in neonates: a meta-analysis.

Hyperbilirubinemia is prevalent in newborns and multiple factors are responsible for the occurrence of neonatal hyperbilirubinemia. G6PD (Glucose-6-Phosphate Dehydrogenase) deficiency is recognized as one of the risk factors. However, many pediatricians did not take into account the probable effect of G6PD-deficiency when severe neonatal hyperbilirubinemia occurred. The aim of the present study was to perform a meta-analysis to investigate whether G6PD-deficiency increases the risk of hyperbilirubinemia and phototherapy in newborn. We searched PubMed and Embase databases for eligible articles according to explicit study inclusion and exclusion criteria. Risk ratios (RRs) and 95% confidence interval (CI) were selected as the evaluation indexes. Cochrane Q and I(2) test were utilized to assess the heterogeneity among studies. A total of five cohort studies were included in this meta-analysis. There were 21,585 participants enrolled in these studies including 877 newborns with hyperbilirubinemia and 261 newborns receiving phototherapy. Comparison of the incidence of hyperbilirubinemia in newborns with G6PD-deficiency to the ones with normal G6PD in each study yielded a pooled RR of 3.92 (95% CI, 2.13-7.20; P <.0001). The pooled RR of receiving phototherapy in G6PD-deficiency neonates is 3.01 (95% CI, 2.20-4.12; P <.0001) when compared to G6PD normal neonates. This study revealed a significant correlation between G6PD-deficiency and neonatal hyperbilirubinemia, as well as G6PD-deficiency and phototherapy. G6PD-deficient newborns have higher risk of hyperbilirubinemia and phototherapy than the ones with normal G6PD. Monitoring the level of G6PD in newborns is important for predicting the occurrence of hyperbilirubinemia.

Calmodulin mediates Ca2+ sensitivity of sodium channels.

Ca2+ has been proposed to regulate Na+ channels through the action of calmodulin (CaM) bound to an IQ motif or through direct binding to a paired EF hand motif in the Nav1 C terminus. Mutations within these sites cause cardiac arrhythmias or autism, but details about how Ca2+ confers sensitivity are poorly understood. Studies on the homologous Cav1.2 channel revealed non-canonical CaM interactions, providing a framework for exploring Na+ channels. In contrast to previous reports, we found that Ca2+ does not bind directly to Na+ channel C termini. Rather, Ca2+ sensitivity appears to be mediated by CaM bound to the C termini in a manner that differs significantly from CaM regulation of Cav1.2. In Nav1.2 or Nav1.5, CaM bound to a localized region containing the IQ motif and did not support the large Ca(2+)-dependent conformational change seen in the Cav1.2.CaM complex. Furthermore, CaM binding to Nav1 C termini lowered Ca2+ binding affinity and cooperativity among the CaM-binding sites compared with CaM alone. Nonetheless, we found suggestive evidence for Ca2+/CaM-dependent effects upon Nav1 channels. The R1902C autism mutation conferred a Ca(2+)-dependent conformational change in Nav1.2 C terminus.CaM complex that was absent in the wild-type complex. In Nav1.5, CaM modulates the Cterminal interaction with the III-IV linker, which has been suggested as necessary to stabilize the inactivation gate, to minimize sustained channel activity during depolarization, and to prevent cardiac arrhythmias that lead to sudden death. Together, these data offer new biochemical evidence for Ca2+/CaM modulation of Na+ channel function.