We explored the effects of the media amended with different ration of hormones for inducing clustered buds with the embryo in vitro bearing cotyledon of Jatropha curcas.It showed that there were significant differences in bud inducement in MS basic medium in which different concentrations and types of hormone were made.For 3 concentrations with 3 hormones we used,the medium with Benzylaminopurine(6-BA) induced most buds however,it may be apt to variation into seedlings.The effect of Kinetin(KT) was mainly on stimulating the buds' growth in length.It showed that the less the concentration of it,the longer of the length,nevertheless,this hormone induced less buds.Thus we conclude that KT is not recommended in bud-inducement media.The hormone Ad had lest effect,it is not suitable in inducement media.
Abstract Teicoplanin, a glycopeptide antibiotic, is used for the treatment of severe staphylococcal infections. Teicoplanin is reported to have an ototoxic potential but its toxic effects on cochlea hair cells (HCs) remains unclear. TP53-induced glycolysis and apoptosis regulator (TIGAR) plays a key role to promote cell survival, our previous study shown that TIGAR protected inner ear spiral ganglion neuron against cisplatin injury. However, the role of TIGAR in mammalian HCs damage has not been explored yet. In this study, firstly, we found that teicoplanin induced significant cell loss of both HEI-OC1 cells and cochlea HCs in a dose-dependent manner in vitro . Next, we discovered that the expression of TIGAR was significantly decreased after teicoplanin treatment in HCs and HEI-OC1 cells. To explore the role of TIGAR in inner ear after teicoplanin damage, the expression of TIGAR was upregulated via recombinant adenovirus or knocked down by shRNA in HEI-OC1 cells, respectively. We found that the overexpression of TIGAR increased cell viability, decreased apoptosis and reduced intracellular reactive oxygen species (ROS) level after teicoplanin injury, whereas downregulation of TIGAR by shRNA decreased cell viability, exacerbated apoptosis and elevated ROS level. Finally, antioxidant treatment with N-acetyl-L-cysteine lowered ROS level, rescued cell loss as well as restored p38/phosphorylation-p38 expression levels induced by TIGAR deficiency in HEI-OC1 cells after teicoplanin injury. This study provides evidences that TIGAR might be a new potential target for prevention from the teicoplanin-induced ototoxicity.
Purpose: To assess the clinical and genetic characteristics of patients with Bietti crystalline dystrophy (BCD) with a focus on potential of microperimetry in monitoring macular function. Methods: A total of 208 genetically-confirmed BCD patients were enrolled in this retrospective study. The patients were categorized into subgroups based on their fundus characteristics (fovea sparing and fovea involved), optical coherence tomography (OCT) findings (presence/absence of retinal pigment epithelium [RPE] or ellipsoid zone [EZ] line at the fovea/parafovea), and genetic profiles (Mis/Mis, Tru/Mis, Tru/Tru). Fixation patterns were analyzed, and macular sensitivity (MS) parameters were compared among different groups. Longitudinal analysis was performed to calculate the annual changes in MS parameters. Correlation between genotype and phenotype were further investigated by analyzing cumulative incidence of vision impairment among different genotypic groups. Results: Patients with well-preserved RPE or EZ at the foveal/parafoveal region exhibited higher MS. Notably, there was a decline in sensitivity parameters, with a decrease of −2.193 dB/year (95% confidence interval [CI] −4.292 to −0.095, P = 0.041) at the fovea and −1.353 dB/year (95% CI −2.047 to −0.659, P < 0.001) in average sensitivity. An age-adjusted comparison of sensitivity among genotypic groups and cumulative incidence analyses showed no association between genotypic groups and vision loss. Conclusions: Microperimetry proves to be one of a credible tool for detecting macular functional changes in BCD patients. BCD patients with different genotypes may have similar disease progression.
Ionizing radiation (IR) can cause severe dysfunction of hematopoietic stem cells (HSCs), leading to acute or prolonged myelosuppression. In recent years, physical exercise has been recognized as a healthy lifestyle as it can fight a variety of diseases. However, whether it provides protection against IR is not fully understood. In this study, we revealed that long-term moderate exercise mitigated IR-induced hematopoietic injury by generating carnosine from skeletal muscles. We found that exercised mice displayed reduced loss of HSC number and function after IR, accompanied by alleviated bone marrow damage. Interestingly, these effects were largely abrogated by specific deletion of carnosine synthase Carns1 in skeletal muscles. In contrast, carnosine treatment protected HSCs against IR-induced injury. Mechanistically, we demonstrated that exercise-generated carnosine was specifically transported to HSCs via Slc15a2 and then inhibited p53 transcriptional activity by directly interacting with its core DNA-binding domain, which led to downregulation of the p53 target genes p21 and Puma, thus promoting the proliferation and survival and inhibiting the senescence of irradiated HSCs. More importantly, a similar role of the carnosine/Slc15a2-p53 axis was observed in human cord blood-derived HSCs. Collectively, our data reveal that moderate exercise or carnosine supplementation may be potential antiradiation strategies.
This paper studied the effect of polyethylene glycol (PEG) on regeneration and free proline accumulation of callus of Pogonatherum paniceum (Lam.) Hack. under motionless liquid culture condition and shake liquid culture condition. Callus of P. paniceum had the ability to resist the stress of PEG. The effects of PEG stress and culture conditions on the callus of P. paniceum appeared mainly in two aspects, delaying regeneration time and debasing regeneration rates. The shake liquid culture mainly delayed the regeneration time and PEG stress mainly debased the regeneration rates. Free proline accumulated in the two culture conditions, and the contents of proline were positively correlated with PEG concentrations and culture time. After stress removal, most of the callus could recover the ability of regeneration, and the free proline might pay an important part in the inhibition and recovery. So it must be chosen a more than 300 g x L(-1) PEG concentration and long than 3 weeks culture time in the selection of drought-resistant mutants of P. paniceum. The motionless liquid culture was more suitable for selection of drought-resistant mutants.
Abstract Oxidized human defensin 5 (HD5 OX ), a Paneth cell-secreted antibacterial peptide with three characteristic disulfide bonds, protects the host from invasion by morbigenous microbes in the small intestine. HD5 OX can be reduced by thioredoxin (Trx) in vitro , while the biochemical properties of the reduced linear peptide, HD5 RED , remain unclear. Here, we first confirm that HD5 RED does exist in vivo . Furthermore, we reveal that the recruitment of HD5 RED to the outer membrane of Gram-negative bacteria and to the anionic lipid A is lower than that of HD5 OX and HD5 RED is less efficient in penetrating bacterial outer and inner membranes and inducing membrane depolarization, which confers an attenuated antibacterial activity to HD5 RED . However, due to its higher structural flexibility, the binding of HD5 RED to bacterial lipopolysaccharide (LPS) is markedly stronger than that of HD5 OX . Consequently, HD5 RED is more effective in suppressing the production of the pro-inflammatory cytokine TNF-α in LPS-stimulated macrophages by blocking the interaction between LPS and LPS-binding protein, thus suggesting that HD5 RED might act as a scavenger to neutralize LPS in the gut. This study provides insights into the antibacterial and immunoregulatory effects of HD5 RED and expands the known repertoire of the enteric defensins.
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