Genome Sequence Data of Leptosphaerulina arachidicola, a Causal Agent of Peanut Scorch Spot in China.

Peanut scorch spot caused by Leptosphaerulina arachidicola is one of the most severe leaf diseases of peanut that causes significant yield loss. Here, we report the first high-quality genome sequence of L. arachidicola JB313 isolated from an infected peanut leaf in China. The genome size is 47.66 Mb, consisting of 65 scaffolds (N50 length = 1.58 Mb) with a G+C content of 49.05%. The information in this report will provide a reference genome for future studies on the peanut scorch spot pathogen in peanut.

Establishment of a Faba Bean Banker Plant System with Predator Orius strigicollis for the Control of Thrips Dendrothrips minowai on Tea Plants under Laboratory Conditions.

The stick tea thrip Dendrothrips minowai (Priesner) (Thysanoptera: Thripidae) is a destructive pest in tea plantations in south and southwest China. To control this pest, a non-crop banker plant system was developed using a polyphagous predator Orius strigicollis (Poppius) (Heteroptera: Anthocoridae) with the black bean aphid Aphis fabae (Scopoli) (Hemiptera: Aphididae) as an alternative prey and the faba bean Vicia faba as the banker plant to support the predator in targeting the pest. The fitness of A. fabae on tea plants and faba bean was evaluated to determine its host specificity. Moreover, the control efficacy of the banker plant system on D. minowai on tea plants was tested in the laboratory and compared with that of direct release of O. strigicollis. The experiments showed that faba bean was an excellent non-crop host for A. fabae because, while the aphid population increased quickly on faba bean, it could only survive for up to 9 days on tea plants. Compared with direct release of O. strigicollis, lower densities of pest were observed when introducing the banker plant system. Our results indicate that this banker plant system has the potential to be implemented in the field to improve the control of the pest thrips.

Cullin 4B regulates cell survival and apoptosis in clear cell renal cell carcinoma as a target of microRNA-217.

Cullin 4B (CUL4B) was reported to be closely related to the progression of some tumors, but its function in clear cell renal cell carcinoma (ccRCC) has not been reported. Our present study found CUL4B was upregulated in ccRCC, and CUL4B knockdown markedly inhibited ccRCC cell growth and induced apoptosis. In addition, CUL4B knockdown markedly inhibited antiapoptotic proteins' expression in ccRCC cells, including Mcl-1 and Bcl-2, and silenced CUL4B also induced the cleavages of PARP, an important index of apoptosis. We also confirmed microRNA-217 (miR-217) was downregulated in ccRCC tumor tissues, and negatively correlated with CUL4B expression. Further investigations revealed miR-217 targeted CUL4B and markedly inhibited its expression in ccRCC cells. In addition, overexpression of miR-217 by mimics significantly suppressed ccRCC cell growth. In contrast, enforced expression of CUL4B significantly abolished miR-217-induced cell survival inhibition in ccRCC cells. In conclusion, our present results suggested targeting miR-217-CUL4B axis would be a promising strategy for ccRCC treatment.

Whey-based cheese provides more postprandial plasma leucine than casein-based cheese: A pig study.

With a long-term nutrition goal for healthy aging, the aim of this study was to compare the bioavailability of amino acids, in particular the leucine, after the ingestion of two solid and isocaloric dairy products (cheese) based either on whey or on caseins, by using pig as an in vivo digestion model. The whey-based cheese contained 25% more leucine than Mozzarella, however its digestion by pigs resulted in a concentration of postprandial plasma leucine between 2 h and 5 h30 twice higher than that produced during the digestion of Mozzarella. Noting that the dry matter of the duodenal effluents were similar after each of the two cheese meals, differences in gastric emptying would not explain the difference in leucine bioavailability. These results suggest the possibility of stimulating more efficiently the muscle synthesis in elderly people with cheese based on whey proteins rather than those based on caseins.

[Effects and mechanism of bFGF on rat myoblast oxidative injury induced by hydrogen peroxide].

OBJECTIVE: To explore the protective role of basic fibroblast growth factor (bFGF) on attenuating hydrogen peroxide-induced injury in cultured rat myoblasts. METHODS: Cultured rat myoblasts at growth phase were randomly divided into four groups (n=6):control group (control), bFGF group (bFGF), model group(H2O2) and the treatment group (bFGF + H2O2). Model group was treated with 100 µmol/L hydrogen peroxide for 4h. B-cell lymphoma-2 (Bcl-2) positive particles were detected by immunohistochemistry; Reactive oxygen species (ROS) and expression for Bcl-2 associated X protein (Bax), Bcl-2 and Cytochrome C (Cyt. C) fluorescence were observed under the invented microscope; Cyt. C and Poly ADP-ribose polymerase(PARP)protein were assessed by Western blot. RESULTS: Compared with control group, the myoblats in the model group showed low expression of Bcl-2 positive particles, accompanied by high expression of ROS level and Cyt. C fuorescence (P < 0.05); Compared with model group, bFGF enhanced Bcl-2 activity of the myoblasts, and significantly downregulated Cyt. C and PARP expression (P < 0.05). CONCLUSIONS: bFGF could attenuate oxidative injury of rat myoblasts induced by hydrogen peroxide, which mechanism might be related to enhanced Bcl-2 and reduced ROS, Cyt. C levels.

DT-13 attenuates human lung cancer metastasis via regulating NMIIA activity under hypoxia condition.

Cancer metastasis plays a major role in tumor deterioration. Metastatic processes are known to be regulated by hypoxic microenvironment and non-muscle myosin IIA (NMIIA). DT-13, a bioactive saponin monomer isolated from Ophiopogon japonicus, has been reported to inhibit various cancer metastasis, but whether NMIIA is involved in the anti-metastatic activity of DT-13 under hypoxia remains to be determined. Thus, this study aims to clarify the role of DT-13 in regulating 95D cell metastasis under hypoxic microenvironment and to further investigate whether NMIIA is involved in the anti-metastatic mechanism of DT-13. We found that DT-13 significantly inhibited 95D cells metastasis in vitro and in vivo. Furthermore, hypoxia significantly inhibited the expression of NMIIA and redistributed NMIIA to the cell periphery, whereas DT-13 reversed the hypoxic effects by upregulating the expression of NMIIA. Moreover, DT-13 treatment redistributed NMIIA to the nuclear periphery and reduced the formation of F-actin in 95D cells. In addition, we found that the Raf-ERK1/2 signaling pathway is involved in regulation of NMIIA by DT-13. Collectively, these findings support NMIIA as a target of DT-13 to prevent lung cancer metastasis.

[The role of cell apoptosis mediated by endoplasmic reticulum stress (ERS) of deep tissue injury of pressure ulcer of rats].

OBJECTIVE: To observe the the expression of endoplasmic reticulum stress (ERS) related factors in deep tissue injury (DTI) at pressure ulcer rat and to investigate the ERS mechanism of DTI in muscle tissue and protective effect of 4-phenylbutyric acid (4-PBA) in local tissue. METHODS: Fifty male SD rats were randomly devided into control group, model group, experimental group NS group and PBA group, the experimental groups were divided into 4 d, 7 d, 14 d and 21 d group according to the observation time (n = 5). Rats in the PBA group were administrated with gastric perfusion of 4-PBA after the modeling; the NS group was given normal saline of the same quantity. Using HE staining to observe morphologic character. The expression of glucose regulated protein 78 (GRP78), CHOP, Caspase 12 were detected by immunohistochernical staining. Cell apoptosis was detected by TUNEL assay. RESULTS: HE staining results showed that each group demonstrated compression injury compared with control group: cellular swelling, ompaction of nuclear, and apoptosis in muscle tissue. The new muscle fiber in 4-PBA group fused faster than those in NS group. The number of TUNEL positive cells peaked at 4 day after compression, then got decreased on day 7 in muscle tissue, apoptosis positive cells were diminished after 4-PBA treatment. The immunohistochemical staining results showed that the expression of protein GRP78, CHOP, Caspase 12 peakd 4 d after modeling and decreased gradually. The GRP78, CHOP, Caspase 12 protein expression were significantly higher than those of PBA group at all time points (P < 0.05). CONCLUSION: Cell apoptosis induced by endoplasmic reticulum stress took part in deep tissue injury resulting of pressure ulcer, which mechanism might be related to reducing apoptosis mediated by CHOP, Caspase 12.