预钙化加速类骨磷灰石在镍钛合金表面生长的电化学阻抗谱

通过酸碱处理活化NiTi合金表面,在模拟体液中仿生生长类骨磷灰石层以改善其生物相容性.采用电化学阻抗谱研究了预钙化对加速磷灰石沉积的影响,并基于双层模型建立了电子等效电路.结果表明:随着在模拟体液中浸泡时间的延长,化学处理的NiTi合金表面类骨磷灰石不断生长,并且添加预钙化试样浸泡3 d,即可在合金表面生长出均匀完整的类骨磷灰石层,而未预钙化试样表面沉积物稀少.对应电子等效电路中,预钙化试样电阻值明显大于未预钙化试样的,显示预钙化促进了活化NiTi合金表面类骨磷灰石的生长.     

The Regenerative Effects of c-Met Agonistic Antibodies in Vocal Fold Atrophy

Background: Atrophy of the vocal folds and the accompanying glottic insufficiency affect the quality of life. Although growth factors have been used to treat muscle atrophy, their effectiveness is limited by their short half-life. Methods: In total, 15 rabbits and 24 rats were used for the study. The right recurrent laryngeal nerves of all animals were transected. One month following nerve transection, PBS (PBS group), rHGF (HGF group), or a c-Met agonistic antibody (c-Met group) was injected into the paralyzed vocal folds. The larynges of the rabbits were harvested from each group for histologic examination and subjected to PCR analysis. Results: Cross-sectional areas (CSAs) of thyroarytenoid muscles were evaluated. The c-Met group had increased CSAs compared to the PBS and HGF groups, but there were no significant differences compared to normal controls. The expression levels of myogenesis-related genes were evaluated three weeks after the injection. The expression levels of myosin heavy chain IIa were significantly increased in the PBS group, while the expression levels of MyoD were increased in the c-Met group. Conclusions: The c-Met agonistic antibody showed promise for promoting muscle regeneration in a vocal fold palsy model.     

3′5-Dimaleamylbenzoic Acid Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by parenchymal scarring, leading progressively to alveolar architecture distortion, respiratory failure, and eventually death. Currently, there is no effective treatment for IPF. Previously, 3′5-dimaleamylbenzoic acid (3′5-DMBA), a maleimide, demonstrated pro-apoptotic, anti-inflammatory, and anti-cancer properties; however, its potential therapeutic effects on IPF have not been addressed. Bleomycin (BLM) 100 U/kg was administered to CD1 mice through an osmotic minipump. After fourteen days of BLM administration, 3′5-DMBA (6 mg/kg or 10 mg/kg) and its vehicle carboxymethylcellulose (CMC) were administered intragastrically every two days until day 26. On day 28, all mice were euthanized. The 3′5-DMBA effect was assessed by histological and immunohistochemical staining, as well as by RT-qPCR. The redox status on lung tissue was evaluated by determining the glutathione content and the GSH/GSSG ratio. 3′5-DMBA treatment re-established typical lung histological features and decreased the expression of BLM-induced fibrotic markers: collagen, α-SMA, and TGF-β1. Furthermore, 3′5-DMBA significantly reduced the expression of genes involved in fibrogenesis. In addition, it decreased reduced glutathione and increased oxidized glutathione content without promoting oxidative damage to lipids, as evidenced by the decrease in the lipid peroxidation marker 4-HNE. Therefore, 3′5-DMBA may be a promising candidate for IPF treatment.     

跳回失稳研究

本文以单元形函数作为单位分解函数，位移间断用富集节点的附加自由度表示，建立了允许单元内部位移非连续的统一位移场函数。结合粘结裂纹模型，研究了结构从延性到脆性失稳的特性以及引起脆性破坏的影响因素。数值计算表明：增加脆性指数可以提高结构的承载稳定性；初始预制缝可以增加结构延性但会降低极限承载力。     

PROPERTIES OF W/Cu FGMS CONTAINING 1%TiC OR 1%La2O3 PREPARED USING GSUHP

W / Cu functionally gradient materials (FGMs) containing 1%La_2O_3 and 1%TiC were prepared using graded sintering under ultra-high pressure (GSUHP). The specimens have been found to exhibit low porosity (11.57% and 11.35%, respectively). Shearing strength of the specimens between layers is good. Moreover, the specimens have still demonstrated good performance in testing thermal-shock resistance. When power density of laser is 200MWm~(-2), the specimens have been tested for thermal-shock resistance (1000 times); the specimens that contained 1%La_2O_3 were not subjected to damage, whereas those that contained 1%TiC began to crack. Finally, effect of additives on thermal-shock resistance was also preliminarily discussed.     

Adiponectin Deficiency Alters Placenta Function but Does Not Affect Fetal Growth in Mice

Adiponectin administration to pregnant mice decreases nutrient transport and fetal growth. An adiponectin deficiency, on the other hand, as seen in obese women during pregnancy, alters fetal growth; however, the mechanism is unclear. To determine the role of adiponectin on placenta function and fetal growth, we used adiponectin knockout, adiponectin heterozygote that displays reduced adiponectin levels, and wild-type mice on a control diet or high fat/high sucrose (HF/HS) diet. Triglycerides (TGs) in the serum, liver, and placenta were measured using colorimetric assays. Gene expression was measured using quantitative RT-PCR. Adiponectin levels did not affect fetal weight, but it reduced adiponectin levels, increased fetal serum and placenta TG content. Wildtype dams on a HF/HS diet protected the fetuses from fatty acid overload as judged by increased liver TGs in dams and normal serum and liver TG levels in fetuses, while low adiponectin was associated with increased fetal liver TGs. Low maternal adiponectin increased the expression of genes involved in fatty acid transport; Lpl and Cd36 in the placenta. Adiponectin deficiency does not affect fetal growth but induces placental dysfunction and increases fetal TG load, which is enhanced with obesity. This could lead to imprinting effects on the fetus and the development of metabolic dysfunction in the offspring.     

NGF Modulates Cholesterol Metabolism and Stimulates ApoE Secretion in Glial Cells Conferring Neuroprotection against Oxidative Stress

Cholesterol plays a crucial role in the brain, where its metabolism is particularly regulated by astrocytic activity. Indeed, adult neurons suppress their own cholesterol biosynthesis and import this sterol through ApoE-rich particles secreted from astrocytes. Recent evidence suggests that nerve growth factor (NGF) may exert neurotrophic activity by influencing cell metabolism. Nevertheless, the effect of NGF on glial cholesterol homeostasis has still not been elucidated. Thus, the aim of this project is to assess whether NGF could influence cholesterol metabolism in glial cells. To reach this objective, the U373 astrocyte-derived cell line was used as an experimental model. Immunoblot and ELISA analysis showed that proteins and enzymes belonging to the cholesterol metabolism network were increased upon NGF treatment in glial cells. Furthermore, NGF significantly increased ApoE secretion and the amount of extracellular cholesterol in the culture medium. Co-culture and U373-conditioned medium experiments demonstrated that NGF treatment efficiently counteracted rotenone-mediated cytotoxicity in N1E-115 neuronal cells. Conversely, neuroprotection mediated by NGF treatment was suppressed when N1E-115 were co-cultured with ApoE-silenced U373 cells. Taken together, these data suggest that NGF controls cholesterol homeostasis in glial cells. More importantly, NGF exerts neuroprotection against oxidative stress, which is likely associated with the induction of glial ApoE secretion.     

Serine Hydroxymethyltransferase 1 Is Essential for Primary-Root Growth at Low-Sucrose Conditions

Plant roots are essential organs for absorbing nutrients from the soil or medium. Sucrose functions as a vital carbon source in root development, and sucrose starvation interferes with the redox state of plant cells. However, the mechanism of root growth at sucrose starvation remains unclear. Here, we report that SHMT1 (serine hydroxymethyltransferase 1) plays a crucial role in primary-root growth. SHMT1 mutation caused decreased sugar levels, excessive H₂O₂ accumulation, and severe root-growth arrest at sucrose-free conditions, whereas plants with SHMT1 overexpression had increased sugar and decreased H₂O₂ levels, and longer primary roots. Sucrose supply fully restored root growth of shm1-2, but CO₂ alone could not, and SHMT1 is much more stable in roots than shoots at sucrose conditions, suggesting that SHMT1 accumulation in roots is critical for sucrose accumulation and root growth. Further ROS scavenging by GSH application or ROS synthesis inhibition by apocynin application or RBOHD mutation reduced H₂O₂ levels and partially restored the root-growth arrest phenotype of shm1-2 at low-sucrose conditions, suggesting that SHMT1 modulates root growth via sucrose-mediated ROS accumulation. Our findings demonstrated the role of SHMT1 in primary-root growth by regulating sucrose accumulation and ROS homeostasis in roots.     

Glioblastoma Stem Cells—Useful Tools in the Battle against Cancer

Glioblastoma stem cells (GSCs) are cells with a self-renewal ability and capacity to initiate tumors upon serial transplantation that have been linked to tumor cell heterogeneity. Most standard treatments fail to completely eradicate GSCs, causing the recurrence of the disease. GSCs could represent one reason for the low efficacy of cancer therapy and for the short relapse time. Nonetheless, experimental data suggest that the presence of therapy-resistant GSCs could explain tumor recurrence. Therefore, to effectively target GSCs, a comprehensive understanding of their biology and the survival and developing mechanisms during treatment is mandatory. This review provides an overview of the molecular features, microenvironment, detection, and targeting strategies of GSCs, an essential information required for an efficient therapy. Despite the outstanding results in oncology, researchers are still developing novel strategies, of which one could be targeting the GSCs present in the hypoxic regions and invasive edge of the glioblastoma.