Molecular characterization of SPL gene family during flower morphogenesis and regulation in blueberry.

The SPL gene is a plant-specific transcription factor involved in the regulation of plant growth and development, which have been identified in woody plants. The process of floral bud differentiation affects the timing of flowering and fruit set and regulates plant growth, however, the mechanism of regulation of flower development by SPL genes is less studied. In this study, 56 VcSPL genes were identified in the tetraploid blueberry. The VcSPL gene family was classified into six subfamilies, and analysis of cis-elements showed that VcSPL genes were regulated by light, phytohormones (abscisic acid, MeJA), and low temperature. In the evolutionary analysis, segmental replication may play an important role in VcSPL gene amplification. Interestingly, we also studied diploid blueberry (Bilberry), in which 24 SPL genes were identified, and 36 homologous pairs were found, suggesting a high degree of convergence in the syntenic relationship between blueberry (Vaccinium corymbosum L) and bilberry (Vaccinium darrowii). Based on the expression profile, VcSPL genes were expressed at high levels in flowers, shoots, and roots, indicating a diversity of gene functions. Then we selected 20 differentially-expressed SPL genes to further investigate the role of VcSPL in floral induction and initiation. It showed that the genes VcSPL40, VcSPL35, VcSPL45, and VcSPL53 may play a crucial role in the blueberry floral transition phase (from vegetative growth to flower initiation). These results provided important information for understanding and exploring the role of VcSPLs in flower morphogenesis and plant growth.

Lycopene protects against ionizing radiation-induced testicular damage by inhibition of apoptosis and mitochondrial dysfunction.

Ionizing radiation (IR) is one of the key contributors that cause male infertility by disturbing spermatogenesis. Lycopene, a carotenoid with strong antioxidant properties, was shown to protect against oxidative damage induced by IR in several experimental models. The present study was designed to explore the possible protective effects of lycopene against IR-induced testicular damage in C57BL/6 mice. Mice were administered lycopene (20 mg/kg) by oral gavage for seven consecutive days prior to a single dose of whole-body X-ray irradiation (4 Gy, 1 Gy/min). We observed that lycopene remarkably augmented sperm motility and reduced sperm abnormalities in mice following IR exposure. Histopathological analyses also revealed that lycopene ameliorated the structural damage of seminiferous tubules and enhanced the regeneration of seminiferous epithelium following IR stress. Moreover, lycopene attenuated IR-induced oxidative stress, as evidenced by a decreasing lipid peroxidation level and an increase in the antioxidant enzyme superoxide dismutase activity. In addition, lycopene reduced the γH2AX expression and the number of TUNEL-positive cells in the germinal epithelium, as well as restoring the imbalance of Bax/Bcl-2 expression induced by IR exposure. Furthermore, lycopene prevented mitochondrial membrane potential depolarization and ATP reduction and preserved the activities of mitochondrial complexes I-IV in the testes of mice after exposure to IR. Lycopene also improved mitochondrial biogenesis in testes of mice exposed to IR, presenting as restored expressions of PGC-1α, Nrf1, and Tfam. Taken together, our results suggest that lycopene alleviates IR-induced testicular damage, and the underlying mechanism involves at least in part the inhibition of the mitochondrial apoptotic pathway and the maintenance of mitochondrial respiration and biogenesis. The beneficial effect of lycopene highlights the therapeutic potential of this plant-derived antioxidant against impaired spermatogenesis and male infertility induced by IR.

Significant improvement of procedural safety in stenting for basilar stenosis: A historically controlled study.

The basilar artery has the most perioperative complications in stenting compared to the other intracranial arteries. We aim to study whether the procedural safety in stenting for basilar stenosis has improved. This study was a single-arm, non-randomized trial that included historically controlled patients for comparison. Between January 2012 and March 2019, 147 consecutive patients with symptomatic basilar stenoses receiving elective stenting treatment were included in current basilar artery stenting (BAS) group. The prospectively collected and registered 120 patients by the same interventional team from September 2001 to November 2011 were set as historical BAS group for control. A total of 267 individuals were included in this study, with a mean age of 59.5 ±â€…8.1 years. The proportion of patients with lesion length >15 mm was 26.5% (39/147) in the current BAS group versus 4.2% (5/120) in the historical BAS group. We found significant differences between these 2 groups in Mori A (17.7% vs 42.5%) and Mori C patients (42.9% vs 13.3%). The proportion of patients receiving preoperative high-resolution magnetic resonance (HRMRI) evaluation was 83.0% (122/147) in the current BAS group versus 20.8% (25/120) in the historical group (P < .05). Balloon-expendable stent (BES) (n = 1), Wingspan (n = 34), and Enterprise (n = 112) stents were placed in the current BAS group. In contrast, only balloon-expendable stent (BES) (n = 48) and Wingspan (n = 72) were deployed in the historical BAS group. The incidence of the safety endpoint (SE) was 4.1% (involving 6 patients) in the current BAS group versus 11.7% (involving 14 patients) in the historical BAS group (P < .05). In multivariate analysis, no risk factor was associated with the occurrence of the safety endpoint (SE). When BAS cases operated by the surgical team accumulated to 120 to 150, the incidence of complications decreased significantly. This is the largest sample size study to discuss the safety of BAS. The significantly decreased incidence of complications indicates that the improving technical measures and the accumulation of operation experience are necessary.

The Associations of Plasma/Serum Carotenoids with Alzheimer's Disease: A Systematic Review and Meta-Analysis.

BACKGROUND: Multiple lines of evidence indicate protective effects of carotenoids in Alzheimer's disease (AD). However, previous epidemiological studies reported inconsistent results regarding the associations between carotenoids levels and the risk of AD. OBJECTIVE: Our study aims to evaluate the associations of six major members of carotenoids with the occurrence of AD by conducting a systematic review and meta-analysis. METHODS: Following PRISMA guidelines, a comprehensive literature search of PubMed, Web of Science, Ebsco, and PsycINFO databases was conducted, and the quality of each included studies was evaluated by a validated scoring systems. Standardized mean differences (SMD) with 95% confidence intervals (CI) were determined by using a random effects model. Heterogeneity was evaluated by I2 statistics. Publication bias was detected using funnel plots and Egger's test. RESULTS: Sixteen studies, with 10,633 participants were included. Pooled analysis showed significantly lower plasma/serum levels of lutein (SMD = -0.86, 95% CI: -1.67 to -0.05, p = 0.04) and zeaxanthin (SMD = -0.59; 95% CI: -1.12 to -0.06, p = 0.03) in patients with AD versus cognitively intact controls, while α-carotene (SMD = 0.21, 95% CI: -0.68 to 0.26, p = 0.39), ß-carotene (SMD = 0.04, 95% CI: -0.57 to 0.65, p = 0.9), lycopene (SMD = -0.12, 95% CI: -0.96 to 0.72, p = 0.78), and ß-cryptoxanthin (SMD = -0.09, 95% CI: -0.83 to 0.65, p = 0.81) did not achieve significant differences. CONCLUSION: Of six major members of carotenoids, only lutein and zeaxanthin concentrations in plasma/serum were inversely related to the risk of AD. More high-quality longitudinal studies are needed to verify these findings.

Lycopene antagonizes lead toxicity by reducing mitochondrial oxidative damage and mitochondria-mediated apoptosis in cultured hippocampal neurons.

Lead (Pb) exhibits serious adverse effects on the central nervous system, and the major pathogenic mechanism of Pb toxicity is oxidative stress. As one of the carotenoid family members with potent antioxidant properties, lycopene has shown its protections by inhibiting oxidative stress damage in numerous models of neurotoxicity. The current study was designed to explore the possible protective property in primary cultured rat hippocampal neurons challenged with Pb. We observed that 5 µM lycopene pretreatment for 4 h efficiently ameliorated Pb-caused damage in cell viability, accumulation of reactive oxygen species (ROS), and apoptosis in a dose-dependent manner. Moreover, lycopene (5 µM) attenuated the 50 µM Pb-induced mitochondrial ROS production, improved the activities of mitochondrial respiratory chain enzymes and ATP production, and ameliorated the 50 µM Pb-induced depolarization of mitochondrial membrane potential as well as opening of mitochondrial permeability transition pores. In addition, 5 µM lycopene restored the imbalance of Bax/Bcl-2, inhibited translocation of cytochrome c, and reduced caspase-3 activation. Taken together, these findings indicate that lycopene antagonizes against Pb-induced neurotoxicity and the underlying mechanism probably involves reduction of mitochondrial oxidative damage and mitochondria-mediated apoptosis.

Protective effects of lycopene against methylmercury-induced neurotoxicity in cultured rat cerebellar granule neurons.

Methylmercury (MeHg) is a neurotoxin that induces neuronal degeneration in the central nervous system. Oxidative stress and mitochondrial dysfunction are widely accepted as central pathogenic mechanisms of MeHg-mediated neurotoxicity. Lycopene, a carotenoid compound, is a potent antioxidant with demonstrated neuroprotective properties in several experimental models of oxidative damage. The present study was designed to investigate whether lycopene could provide protective effects against MeHg-induced neurotoxicity in cultured rat cerebellar granule neurons (CGNs). The cultured CGNs were pretreated with different dose of lycopene for 2h, followed by the challenge with 500nM MeHg for 12h. It was found that MeHg exposure caused the loss of cell viability and the LDH release. Furthermore, we demonstrated that MeHg exposure significantly elevated intracellular reactive oxygen species generation and mitochondria-derived superoxide production, caused disruption of mitochondrial membrane potential and opening of mPTP, inhibited mitochondrial complex enzyme activities (complex III and complex IV), reduced ATP generation and decreased mtDNA copy numbers and mtDNA transcript levels. However, each of these oxidative damages was efficiently attenuated by lycopene pretreatment. Collectively, these results suggest that lycopene affords protection against MeHg-induced neurotoxicity in CGNs, and these beneficial effects of lycopene may be attributable to its roles in preventing mitochondrial dysfunction.