青霉素G钠对阴生植物绿巨人愈伤组织诱导分化及试管苗生长的影响

报道了青霉素G钠对绿巨人愈伤组织诱导、分化及苗生长的初步结果 .试验表明 :青霉素G钠对诱导叶片愈伤组织的产生有抑制作用 ,而对愈伤组织的分化有促进作用 ,效果最好的浓度为 60万u·L- 1,平均每块愈伤组织可分化 7.0个不定芽 ;低浓度的青霉素G钠 ( 2 0万u·L- 1)对试管苗的生长有促进作用 ,同时也促进根系的发育 ;而高浓度的青霉素G钠对试管苗的生长有抑制作用 ,并随着浓度的提高而增强 ;在生根培养基中添加低浓度的青霉素G钠( 2 0万u·L- 1)比不加青霉素G钠的培养基的试管苗移栽成活率高 .

AFF1 and AFF4 differentially regulate the osteogenic differentiation of human MSCs

AFF1 and AFF4 belong to the AFF （AF4/FMR2） family of proteins, which function as scaffolding proteins linking two different transcription elongation factors, positive elongation factor b （P-TEFb） and ELL1/2, in super elongation complexes （SECs）. Both AFF1 and AFF4 regulate gene transcription through elongation and chromatln remodeling. However, their function in the osteogenic differentiation of mesenchymal stem cells （MSCs） is unknown. In this study, we show that small interfering RNA （siRNA）-mediated depletion of AFF1 in human MSCs leads to increased alkaline phosphatase （ALP） activity, enhanced mineralization and upregulated expression of osteogenic-related genes. On the contrary, depletion of AFF4 significantly inhibits the osteogenic potential of MSCs. In addition, we confirm that overexpression of AFF1 and AFF4 differentially affects osteogenic differentiation in vitro and MSC-mediated bone formation in vivo. Mechanistically, we find that AFFI regulates the expression of DKK1 via binding to its promoter region. Depletion of DKK1 in HA-AFFl-overexpressing MSCs abrogates the impairment of osteogenic differentiation. Moreover, we detect that AFF4 is enriched in the promoter region of ID1. AFF4 knockdown blunts the BRE luciferase activity, SP7 expression and ALP activity induced by BMP2 treatment. In conclusion, our data indicate that AFF1 and AFF4 differentially regulate the osteogenic differentiation of human MSCs.AFF1 and AFF4 belong to the AFF （AF4/FMR2） family of proteins, which function as scaffolding proteins linking two different transcription elongation factors, positive elongation factor b （P-TEFb） and ELL1/2, in super elongation complexes （SECs）. Both AFFI and AFF4 regulate gene transcription through elongation and chromatln remodeling. However, their function in the osteogenic differentiation of mesenchymal stem cells （MSCs） is unknown. In this study, we show that small interfering RNA （siRNA）-mediated depletion of AFF1 in human MSCs leads to increased alkaline phosphatase （ALP） activity, enhanced mineralization and upregulated expression of osteogenic-related genes. On the contrary, depletion of AFF4 significantly inhibits the osteogenic potential of MSCs. In addition, we confirm that overexpression of AFF1 and AFF4 differentially affects osteogenic differentiation in vitro and MSC-mediated bone formation in vivo. Mechanistically, we find that AFFI regulates the expression of DKK1 via binding to its promoter region. Depletion of DKK1 in HA-AFFl-overexpressing MSCs abrogates the impairment of osteogenic differentiation. Moreover, we detect that AFF4 is enriched in the promoter region of ID1. AFF4 knockdown blunts the BRE luciferase activity, SP7 expression and ALP activity induced by BMP2 treatment. In conclusion, our data indicate that AFF1 and AFF4 differentially regulate the osteogenic differentiation of human MSCs.

Correlation between receptor-interacting protein 140 expression and directed differentiation of human embryonic stem cells into neural stem cells

Overexpression of receptor-interacting protein 140（RIP140） promotes neuronal differentiation of N2 a cells via extracellular regulated kinase 1/2（ERK1/2） signaling.However,involvement of RIP140 in human neural differentiation remains unclear.We found both RIP140 and ERK1/2 expression increased during neural differentiation of H1 human embryonic stem cells.Moreover,RIP140 negatively correlated with stem cell markers Oct4 and Sox2 during early stages of neural differentiation,and positively correlated with the neural stem cell marker Nestin during later stages.Thus,ERK1/2 signaling may provide the molecular mechanism by which RIP140 takes part in neural differentiation to eventually affect the number of neurons produced.

The basic helix-loop-helix(bHLH)transcription factor,DEC1,provides neuroprotection from apoptosis induced by MPP^+ through PI3K/Akt pathway in SHSY5Y cells

OBJECTIVE To determine the role of the basic helix-loop-helix(b HLH)transcription factor,differentiated embryonic chondrocyte gene 1(DEC1),in the apoptosis induced by 1-methyl-4-phenylpyridiniumion(MPP+)in SH-SY5Y cells.METHODS SH-SY5Y cells were treated with different concentrations of MPP+for 24or 48 h.The cell inhibition and apoptosis were measured by MTT and DAPI staining.DEC1,the apoptosis-related proteins and PI3K/Akt/GSK3β/β-catenin signaling were determined by Western blotting.The expression of DEC1was regulated by overexpression and sh RNA.RESULTS MPP+induces apoptosis along with decreasing of DEC1expression in SH-SY5Y cells.Overexpression or knockdown of DEC1 can alleviate or enhance the cell inhibition induced by MPP+.And overexpression of DEC1 can alleviate the increased cleaved caspase 3/caspase 3 but not alleviate Bax/Bcl-2 induced by MPP+.Meanwhile,MPP+represses PI3Kp110α,p-Akt/Akt,p-GSK-3β/GSK-3βandβ-catenin expression,which is accompanied by decreasing DEC1 expressions.It is confirmed that the activator or inhibitor of PI3K/Akt/GSK-3βpathway can alleviate or enhance the repression of PI3K/Akt/GSK3β/β-catenin signaling cascade induced by MPP+.Further study,we find that overexpression of DEC1 alone can increase PI3Kp110α,p-Akt/Akt,p-GSK-3β/GSK-3β,andβ-catenin expression.More importantly,overexpression of DEC1 significantly alleviates the decreased levels of PI3Kp110α,p-Akt/Akt,p-GSK-3β/GSK-3β,andβ-catenin induced by MPP+.CONCLUSION DEC1 provides neuroprotection from apoptosis induced by MPP+through PI3K/Akt pathway in SH-SY5Y cells.Promisingly,DEC1 is a candidate gene that may provide a novel therapeutic approach for the treatment of Parkinson disease.

Effects of GW5074 in the process of imDCs inducing differentiation of naive CD4^+ T cells into Treg cells in vitro

Objective To establish a stable and efficient method of culturing imDCs in vitro,and to explore the effect of GW5074,which blocks ERK1 /2 signal pathway in the process of immature dentritic cells ( imDCs) on inducing differentiation of the naive allogeneic CD4 + T

Further results on differentially 4-uniform permutations over F2^2m

We present several new constructions of differentially 4-uniform permutations over F22 mby modifying the values of the inverse function on some subsets of F22 m. The resulted differentially 4-uniform permutations have high nonlinearities and algebraic degrees, which provide more choices for the design of crytographic substitution boxes.

Electroacupuncture Attenuates Immune-Inflammatory Response in Hippocampus of Rats with Vascular Dementia by Inhibiting TLR4/MyD88 Signaling Pathway

Objective:To investigate whether electroacupuncture(EA)alleviates cognitive impairment by suppressing the toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)signaling pathway,which triggers immune-inflammatory responses in the hippocampus of rats with vascular dementia(VaD).Methods:The experiments were conducted in 3 parts and in total the Sprague-Dawley rats were randomly divided into 8 groups by a random number table,including sham,four-vessel occlusion(4-VO),4-VO+EA,4-VO+non-EA,sham+EA,4-VO+lipopolysaccharide(LPS),4-VO+LPS+EA,and 4-VO+TAK-242 groups.The VaD model was established by the 4-VO method.Seven days later,rats were treated with EA at 5 acupoints of Baihui(DV 20),Danzhong(RN 17),Geshu(BL 17),Qihai(RN 6)and Sanyinjiao(SP 6),once per day for 3 consecutive weeks.Lymphocyte subsets,lymphocyte transformation rates,and inflammatory cytokines interleukin-6(IL-6)and tumor necrosis factorα(TNF-α)were measured to assess immune function and inflammation in VaD rats.Transmission electron microscopy was used to observe the ultrastructure of nerve cells in the hippocampus.The levels of TLR4,MyD88,IL-6,and TNF-αwere detected after EA treatment.TLR4/MyD88 signaling and cognitive function were also assessed after intracerebroventricular injection of TLR4 antagonist TAK-242 or TLR4 agonist LPS with or without EA.Results:Compared with the 4-VO group,EA notably improved immune function of rats in the 4-VO+EA group,inhibited the protein and mRNA expressions of TLR4 and MyD88 in the hippocampus of rats,reduced the expressions of serum IL-6 and TNF-α(all P<0.05 or P<0.01),and led to neuronal repair in the hippocampus.There were no significant differences between the 4-VO+LPS+EA and 4-VO+EA groups,nor between the 4-VO+TAK-242 and 4-VO+EA groups(P>0.05).Conclusions:EA attenuated cognitive impairment associated with immune inflammation by inhibition of the TLR4/MyD88 signaling pathway.Thus,EA may be a promising alternative therapy for the treatment of VaD.

MicroRNA-125b regulates Th17/Treg cell differentiation and is associated with juvenile idiopathic arthritis

Background Juvenile idiopathic arthritis(JIA)is the most common rheumatic disease in childhood driven by aberrant pathways of T-cell activation.T helper 17(Th17)/regulatory T cell(Treg)imbalance plays critical roles in the pathogenesis of arthritis.MicroRNA-125b(miR-125b)was upregulated after the activation of the initial CD4^+T cells,and could regulate the differentiation of CD4^+T cells.However,the effects of miR-125b on Th17/Treg imbalance and differentiation of Th 17/Treg cells remain unknown.Methods In this study,we evaluated the expression of miR-125b in the peripheral blood mononuclear cells(PBMCs)of children with JIA,and the relationship of miR-125b with Th17/Treg imbalance.Then,we used lentivirus vector-mediated overexpression technology to investigate the regulatory function of miR-125b in CD4^+T cells or dendritic cell/CD4^+T co-culture system.Results Decreased miR-125b expression in PBMCs and CD4^+T cells of JIA patients was negatively correlated with the ratio of Th17/Treg cells.It also correlated negatively with retinoic acid receptor-related orphan receptorγt but positively with Forkhead box protein 3 at transcriptional levels.Furthermore,we found that miR-125b overexpression inhibited Th17 cell differentiation,whereas facilitated the differentiation of Treg cells.MiR-125b upregulation led to the decrease of Th 17-secreting cytokines but the increase of the Treg-secreting cytokines.Conclusions Our results demonstrate that miR-125b participated in regulating Thl7/Treg cell differentiation and imbalance in JIA patients.These findings provide novel insight into the critical role of miR-125b in the Th17/Treg imbalance of JIA,and raise the distinct possibility that miR-125b may prove to be a potential therapeutic target for JIA.

Electrochemical determination of quercetin by self-assembled platinum nanoparticles/poly(hydroxymethylated-3,4-ethylenedioxylthiophene) nanocomposite modified glassy carbon electrode

A simple and sensitive platinum nanoparticles/poly（hydroxymethylated-3,4-ethylenedioxylthiophene） nanocomposite （PtNPs/PEDOT-MeOH） modified glassy carbon electrode （GCE） was successfully developed for the electrochemical determination of quercetin. Scanning electron microscopy and energy dispersive X-ray spectroscopy results indicated that the PtNPs were inserted into the PEDOT- MeOH layer. Compared with the bare GCE and poly（3,4-ethylenedioxythiophene） （PEDOT） electrodes, the PtNPs/PEDOT-MeOH/GCE modified electrode exhibited a higher electrocatalytic ability toward the oxidation of quercetin due to the synergic effects of the electrocatalytic activity and strong adsorption ability of PtNPs together with the good water solubility and high conductivity of PEDOT-MeOH. The electrochemical sensor can be applied to the quantification of quercetin with a linear range covering 0.04-91μmol L-1 and a low detection limit of 5.2 nmol L-1. Furthermore, the modified electrode also exhibited good reoroducibilitv and long-term stability, as well as high selectivity.

Existence of Exactly n+1 Simple 4-Periodic Solutions of the Differential Delay Equation x(t)=-f(x(t-1))

By discussing the zeros of periodic.solutions we give in this paper a criterion for the existence of exactly n+1 simple 4-periodic solutions of the differential delay equation x(T)= -f(x(t-1)).

Orbital dynamics satisfying the 4^(th)-order stationary extended Fisher-Kolmogorov equation

In this study,we discuss the central force problem by using the nonlocal-in-time kinetic energy approach.At low length scales,the system is dominated by the generalized 4^(th)-order extended Fisher-Kolmogorov stationary equation and by the 4^(th)-order stationary Swift-Hohenberg differential equation under explicit conditions.The energy is a conserved quantity along orbits of the extended Fisher-Kolmogorov stationary equation.The system is quantized,the system is stable,and the ground energy problem is solved.