Enhanced photosynthetic efficiency by nitrogen-doped carbon dots via plastoquinone-involved electron transfer in apple.

Artificially enhancing photosynthesis is critical for improving crop yields and fruit qualities. Nanomaterials have demonstrated great potential to enhance photosynthetic efficiency; however, the mechanisms underlying their effects are poorly understood. This study revealed that the electron transfer pathway participated in nitrogen-doped carbon dots (N-CDs)-induced photosynthetic efficiency enhancement (24.29%), resulting in the improvements of apple fruit qualities (soluble sugar content: 11.43%) in the orchard. We also found that N-CDs alleviated mterf5 mutant-modulated photosystem II (PSII) defects, but not psa3 mutant-modulated photosystem I (PSI) defects, suggesting that the N-CDs-targeting sites were located between PSII and PSI. Measurements of chlorophyll fluorescence parameters suggested that plastoquinone (PQ), the mobile electron carrier in the photosynthesis electron transfer chain (PETC), was the photosynthesis component that N-CDs targeted. In vitro experiments demonstrated that plastoquinone-9 (PQ-9) could accept electrons from light-excited N-CDs to produce the reduced plastoquinone 9 (PQH2-9). These findings suggested that N-CDs, as electron donors, offer a PQ-9-involved complement of PETC to improve photosynthesis and thereby fruit quality. Our study uncovered a mechanism by which nanomaterials enhanced plant photosynthesis and provided some insights that will be useful in the design of efficient nanomaterials for agricultural/horticultural applications.

Determination of Protein Interactions among Replication Components of Apple Necrotic Mosaic Virus.

Apple mosaic disease is one of the most widely distributed and destructive diseases in apple cultivation worldwide, especially in China, whose apple yields account for more than 50% of the global total. Apple necrotic mosaic virus (ApNMV) is a newly identified ilarvirus that is closely associated with apple mosaic disease in China; however, basic viral protein interactions that play key roles in virus replication and the viral life cycle have not been determined in ApNMV. Here, we first identify an ApNMV-Lw isolate that belongs to subgroup 3 in the genus Ilarvirus. ApNMV-Lw was used to investigate interactions among viral components. ApNMV 1a and 2apol, encoded by RNA1 and RNA2, respectively, were co-localized in plant cell cytoplasm. ApNMV 1a interacted with itself at both the inter- and intramolecular levels, and its N-terminal portion played a key role in these interactions. 1a also interacted with 2apol, and 1a's C-terminal, together with 2apol's N-terminal, was required for this interaction. Moreover, the first 115 amino acids of 2apol were sufficient for permitting the 1a-2apol interaction. This study provides insight into the protein interactions among viral replication components of ApNMV, facilitating future investigations on its pathogenicity, as well as the development of strategies to control the virus and disease.

Establishment of reference intervals and transfusion criterion for Sonoclot analysis.

Sonoclot analyzer has been widely used in many countries. But the reference intervals provided by the manufacturer were derived from only 45 participants, and there was no cut-off value for transfusion for Sonoclot analysis. This study aimed to establish reference intervals and transfusion criterion for Sonoclot analysis. Volunteers were recruited from healthy Chinese adults and patients undergoing cardiac surgery. Blood samples were withdrawn from forearm vein and measured for activated clotting time (ACT), clot rate (CR), platelet function (PF), activated partial thromboplastin time (APTT), fibrinogen concentration (FIB), and platelet count (PLT). The reference intervals were determined by the nonparametric method. Cut-off values were determined by the receiver operating characteristics curve. A total of 135 healthy volunteers and 281 patients were enrolled. The 95% reference intervals were 96-195 s, 22-51 signal U/min, >1.6 for ACT, CR, PF respectively. In the 281 patients, the results of APTT, FIB, PLT, ACT, CR, and PF ranged from 20.5-300.0 s, 0.28-4.11 g/L, (19.0-387.3)×109/L, 80-514 s, 2.9-74 signal U/min, and 0.1-5.1 respectively. The cut-off values for transfusion were >208, ≤14, and ≤1.3 for ACT, CR, PF respectively. The cut-off values of Sonoclot analysis were within the manufacturer's reference intervals, while they were outside the reference intervals established in this study. The results suggested that the manufacturer's reference intervals were not suitable for Chinese. The reference intervals and cut-off values established in this study will be helpful to Chinese patients.

Effect of Jinguo Weikang Capsule on proto-oncogene expression of gastric mucosa in rats with gastric precancerous lesions.

OBJECTIVE: To study the effect of Jinguo Weikang Capsule [see text] on the gene expression of H-ras, epidermal growth factor receptor (EGFR), P53 and C-myc of the gastric mucosa in rats with gastric precancerous lesions, and to investigate the action mechanism of JWC on gastric precancerous lesions. METHODS: A rat model with paratypical proliferation of the gastric epithelium mucosa was established by using 60Co irradiation. Rats were divided into the normal group, model group, high-, medium-, low-dose JWC treatment groups, and the vitacoenzyme control group, and were treated for 30 days. The expression of H-ras, EGFR, P53 and C-myc genes of the gastric mucosa was detected by using immunohistochemical methods. RESULTS: The expression and over-expression rates of H-ras, EGFR, P53 and C-myc gene in the high-and medium-dose JWC treatment groups were significantly lower (P<0.05) as compared with those of the model group. CONCLUSION: JWC can inhibit the expression of the H-ras, EGFR, P53 and C-myc genes expression of the gastric mucosa in rats, which may be one of mechanisms involved in suppressing or reversing gastric carcinogenesis.

[The effects of somatostatin on serum interleukin-6 and tumor necrosis factor-alpha in lipopolysaccharide-induced septic shock: experiment with rats].

OBJECTIVE: To explore the effect of somatostatin on serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in lipopolysaccharide (LPS)-induced septic shock. METHODS: 24 male Wistar rats were randomly divided into 2 groups: intervention group (injected with LPS of Escherichia coli via femoral vein to induce septic shock) and control group (injected with LPS of Escherichia coli and then injected with somatostatin). The mean arterial pressure (MAP), heart rate, respiration rater, and mortality rate were observed before the injection of LPS, and 30, 90, and 360 min after the injection, and the serum IL-6 and TNF-alpha level were detected before the injection of LPS, 30, 90, and 360 min after the injection, or after the death. RESULTS: The IL-6 levels 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 233 +/- 47, 212 +/- 33, and 217 +/- 26 mg/L respectively, all significantly lower then those of the control group (308 +/- 56, 260 +/- 32, and 230 +/- 92 mg/L, all P < 0.05). The TNF-alpha level 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 450 +/- 82, 417 +/- 92, and 440 +/- 49 mg/L, all significantly lower than those of the control group (607 +/- 149, 517 +/- 74, and 474 +/- 219 mg/L, all P < 0.05). In addition, compared with the control group, the MAP of the somatostatin intervention group increased after 90 min. Two rats in the control group died 30 to 90 min later and 4 rats died 90 to 360 min later, however, 360 min later all rats in the somatostatin intervention group were alive (P = 0.0054). CONCLUSION: Somatostatin can inhibit the level of serum IL-6 and TNF-alpha in septic shock induced by LPS and improve the survival rate.