Chondrogenic priming of human fetal synovium-derived stem cells in an adult stem cell matrix microenvironment

Cartilage defects are a challenge to treat clinically due to the avascular nature of cartilage. Low immunogenicity and extensive proliferation and multidifferentiation potential make fetal stem cells a promising source for regenerative medicine. In this study, we aimed to determine whether fetal synovium-derived stem cells (FSDSCs) exhibited replicative senescence and whether expansion on decellularized extracellular matrix (dECM) deposited by adult SDSCs (AECM) promoted FSDSCs\u27 chondrogenic potential. FSDSCs from passage 2 and 9 were compared for chondrogenic potential, using Alcian blue staining for sulfated glycosaminoglycans(GAGs), biochemical analysis for DNA and GAG amounts, and real-time PCR for chondrogenic genes including ACAN and COL2A1. Passage 3 FSDSCs were expanded for one passage on plastic flasks (PL), AECM, or dECM deposited by fetal SDSCs (FECM). During expansion, cell proliferation was evaluated using flow cytometry for proliferation index, stem cell surface markers, and resistance to hydrogen peroxide. During chondrogenic induction, expanded FSDSCs were evaluated for tri-lineage differentiation capacity. We found that cell expansion enhanced FSDSCs\u27 chondrogenic potential at least up to passage 9. Expansion on dECMs promoted FSDSCs\u27 proliferative and survival capacity and adipogenic differentiation but not osteogenic capacity. AECM-primed FSDSCs exhibited an enhanced chondrogenic potential

Chondrogenic priming of human fetal synovium-derived stem cells in an adult stem cell matrix microenvironment

Cartilage defects are a challenge to treat clinically due to the avascular nature of cartilage. Low immunogenicity and extensive proliferation and multidifferentiation potential make fetal stem cells a promising source for regenerative medicine. In this study, we aimed to determine whether fetal synovium-derived stem cells (FSDSCs) exhibited replicative senescence and whether expansion on decellularized extracellular matrix (dECM) deposited by adult SDSCs (AECM) promoted FSDSCs\u27 chondrogenic potential. FSDSCs from passage 2 and 9 were compared for chondrogenic potential, using Alcian blue staining for sulfated glycosaminoglycans(GAGs), biochemical analysis for DNA and GAG amounts, and real-time PCR for chondrogenic genes including ACAN and COL2A1. Passage 3 FSDSCs were expanded for one passage on plastic flasks (PL), AECM, or dECM deposited by fetal SDSCs (FECM). During expansion, cell proliferation was evaluated using flow cytometry for proliferation index, stem cell surface markers, and resistance to hydrogen peroxide. During chondrogenic induction, expanded FSDSCs were evaluated for tri-lineage differentiation capacity. We found that cell expansion enhanced FSDSCs\u27 chondrogenic potential at least up to passage 9. Expansion on dECMs promoted FSDSCs\u27 proliferative and survival capacity and adipogenic differentiation but not osteogenic capacity. AECM-primed FSDSCs exhibited an enhanced chondrogenic potential

Poly[di-μ2-azido-μ3-pyrazine-2-carboxyl­ato-cadmium(II)]

The title compound, [Cd(C5H3N2O2)(N3)]n, has been pre­pared by the reaction of pyrazine-2-carboxylic acid, cadmium(II) nitrate and sodium azide. In the structure, the CdII atom is six-coordinated by two azide anions and three pyrazine-2-carboxyl­ate ligands. Each pyrazine-2-carboxyl­ate ligand bridges three CdII atoms, whereas the azide ligand bridges two CdII atoms, resulting in the formation of a two-dimensional metal–organic polymer developing parallel to the (100) plane

Activity modulation and allosteric control of a scaffolded DNAzyme using a dynamic DNA nanostructure.

Recognition of the fundamental importance of allosteric regulation in biology dates back to not long after its discovery in the 1960s. Our ability to rationally engineer this potentially useful property into normally non-allosteric catalysts, however, remains limited. In response we report a DNA nanotechnology-enabled approach for introducing allostery into catalytic nucleic acids. Specifically, we have grafted one or two copies of a peroxidase-like DNAzyme, hemin-bound G-quadruplex (hemin-G), onto a DNA tetrahedral nanostructure in such a manner as to cause them to interact, modulating their catalytic activity. We achieve allosteric regulation of these catalysts by incorporating dynamically responsive oligonucleotides that respond to specific "effector" molecules (complementary oligonucleotides or small molecules), altering the spacing between the catalytic sites and thus regulating their activity. This designable approach thus enables subtle allosteric modulation in DNAzymes that is potentially of use for nanomedicine and nanomachines

丹蛭降糖胶囊对糖尿病大鼠肾组织NF-κB表达的影响*

Objective: To investigate the expression level of NF- κ B in renal tissue of diabetic rodent model and the regulating action of Danzhi Jiangtang Capsule (DJC) . Methods: 55 male SD rats were randomly divided into 2 groups, normal control group and experimental group. Normal control group was fed with basal diet, the experimental group were fed with high calorie diet. A single intraperitoneal injection of streptozotocin (STZ) of 35mg/kg to establish the animal model of diabetes mellitus, blood glucose was measured after 120h,when the diabetic rodent model was built, the experimental group were randomly divided into 4 groups, high does group of DJC, low does group of DJC , pioglitazone group and model group. In addition to the model group and control group, each group was kept with continuous intragastric administration of drugs for 8 weeks, high does group of DJC, low does group of DJC were treated with 1.08g/ (kg • d), 0.54 g/ (kg • d) by gavage, pioglitazone group was treated with 10mg/ (kg • d) by gavage, the blank group and the model group  were treated with physiological saline 5ml/ (kg • d)  by gavage. Then determined NF-κB by immunohistochemical method and detected blood glucose of rats . Results:  The expression of NF-κB in model group was strongly and significantly increased compared with the normal control group （P＜0.05 or P＜0.01）; after being given Danzhi Jiangtang Capsule for 8 weeks , high expression of NF-κB in high DJC group and low DJC group were significantly decreased (P＜0.05), much more than pioglitazone group . When the diabetic rodent model was built, the blood glucose of model group was increased significantly compared with the control group (P＜0.01).After the experimental group been given Danzhi Jiangtang Capsule for 2 weeks , the level of glucose was decreased significantly compared with model group (P＜0.01) , the blood glucose index declined steadily after 4~8 weeks（P＜0.01）. Conclusion: Danzhi Jiangtang Capsule can reduce blood sugar ,which delay the progression of diabetic nephropathy through inhibiting the high expression of NF- κ B in diabetic rats.目的  探讨NF-κB在糖尿病大鼠肾组织中的表达水平及丹蛭降糖胶囊（DJC）的调节作用。方法  取55只健康雄性大鼠随机分为两组，即正常对照组和实验组。正常对照组予普通饲料喂养，实验组予高脂饲料喂养。采用链尿佐菌素（STZ）单次腹腔注射35mg/kg，建立糖尿病动物模型，120h后测血糖，造模成功后，再将实验组随机分为丹蛭高、低剂量组,吡咯列酮组，模型组。除模型组和对照组外，各组连续灌胃药物8周，丹蛭高、低剂量组分别按1.08g/(kg•d)、0.54 g/(kg•d)灌胃，吡格列酮组按10mg/(kg•d)灌胃，正常对照组和模型组按5ml/(kg•d)给予生理盐水灌胃。免疫组化法检测NF-κB在肾脏中的表达水平，并测定各组大鼠血糖。结果 模型组的NF-κB的表达明显升高，多为强阳性，与正常对照组比较差异有显著性（P＜0.01）；丹蛭高、低剂量组灌胃8周后，两组NF-κB的高表达明显下降，多为弱阳性或不表达，与模型组比较有统计学意义（P＜0.01），疗效优于吡格列酮组。造模后，模型组血糖显著升高（P＜0.01），丹蛭降糖胶囊灌胃2周后，血糖显著下降，与模型组比较（P＜0.01），4~8周后血糖指标下降平稳（P＜0.01）。结论  丹蛭降糖胶囊可能通过抑制糖尿病大鼠NF-κB的高表达，降低血糖，延缓糖尿病肾病的进程

Special Libraries, November 1922

Volume 13, Issue 9https://scholarworks.sjsu.edu/sla_sl_1922/1008/thumbnail.jp

1-(2-Chloro­phenyl)-6-fluoro-2-methyl-1H-indole-3-carbonitrile

In the title compound, C16H10ClFN2, the dihedral angle between the indole ring system and the benzyl ring is 80.91 (5)°. The crystal packing features C—H⋯Cl, C—H⋯F and C—H⋯π inter­actions

Duplication and Remolding of tRNA Genes in the Mitochondrial Genome of \u3cem\u3eReduvius tenebrosus\u3c/em\u3e (Hemiptera: Reduviidae)

Most assassin bugs are predators that act as important natural enemies of insect pests. Mitochondrial (mt) genomes of these insects are double-strand circular DNAs that encode 37 genes. In the present study, we explore the duplication and rearrangement of tRNA genes in the mt genome of Reduvius tenebrosus, the first mt genome from the subfamily Reduviinae. The gene order rearranges from CR (control region)-trnI-trnQ-trnM-ND2 to CR-trnQ-trnI2-trnI1-trnM-ND2. We identified 23 tRNA genes, including 22 tRNAs commonly found in insects and an additional trnI (trnI2), which has high sequence similarity to trnM. We found several pseudo genes, such as pseudo-trnI, pseudo-CR, and pseudo-ND2, in the hotspot region of gene rearrangement (between the control region and ND2). These features provided evidence that this novel gene order could be explained by the tandem duplication/random loss (TDRL) model. The tRNA duplication/anticodon mutation mechanism further explains the presence of trnI2, which is remolded from a duplicated trnM in the TDRL process (through an anticodon mutation of CAT to GAT). Our study also raises new questions as to whether the two events proceed simultaneously and if the remolded tRNA gene is fully functional. Significantly, the duplicated tRNA gene in the mitochondrial genome has evolved independently at least two times within assassin bugs