Soft chromophore featured liquid porphyrins and their utilization toward liquid electret applications

Optoelectronically active viscous liquids are ideal for fabricating foldable/stretchable electronics owing to their excellent deformability and predictable π-unit-based optoelectronic functions, which are independent of the device shape and geometry. Here we show, unprecedented 'liquid electret' devices that exhibit mechanoelectrical and electroacoustic functions, as well as stretchability, have been prepared using solvent-free liquid porphyrins. The fluidic nature of the free-base alkylated-tetraphenylporphyrins was controlled by attaching flexible and bulky branched alkyl chains at different positions. Furthermore, a subtle porphyrin ring distortion that originated from the bulkiness of alkyl chains was observed. Its consequences on the electronic perturbation of the porphyrin-unit were precisely elucidated by spectroscopic techniques and theoretical modelling. This molecular design allows shielding of the porphyrin unit by insulating alkyl chains, which facilitates its corona-charged state for a long period under ambient conditions

Apelin Deficiency Accelerates the Progression of Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the selective loss of motor neurons. Recent studies have implicated that chronic hypoxia and insufficient vascular endothelial growth factor (VEGF)-dependent neuroprotection may lead to the degeneration of motor neurons in ALS. Expression of apelin, an endogenous ligand for the G protein-coupled receptor APJ, is regulated by hypoxia. In addition, recent reports suggest that apelin protects neurons against glutamate-induced excitotoxicity. Here, we examined whether apelin is an endogenous neuroprotective factor using SOD1G93A mouse model of ALS. In mouse CNS tissues, the highest expressions of both apelin and APJ mRNAs were detected in spinal cord. APJ immunoreactivity was observed in neuronal cell bodies located in gray matter of spinal cord. Although apelin mRNA expression in the spinal cord of wild-type mice was not changed from 4 to 18 weeks age, that of SOD1G93A mice was reduced along with the paralytic phenotype. In addition, double mutant apelin-deficient and SOD1G93A displayed the disease phenotypes earlier than SOD1G93A littermates. Immunohistochemical observation revealed that the number of motor neurons was decreased and microglia were activated in the spinal cord of the double mutant mice, indicating that apelin deficiency pathologically accelerated the progression of ALS. Furthermore, we showed that apelin enhanced the protective effect of VEGF on H2O2-induced neuronal death in primary neurons. These results suggest that apelin/APJ system in the spinal cord has a neuroprotective effect against the pathogenesis of ALS

「抗菌薬含有脂肪由来幹細胞シート」を用いたバイオフィルム感染症への応用

金沢大学附属病院In this study, we investigated a new treatment method for periprosthetic joint infection (PJI) using adipose-derived stem cells (ADSCs). First, we established a treatment using "antibiotic-loaded ADSCs sheets" in combination with our original sheet technology, and then investigated the antibacterial effect of different administration methods. There were many difficulties in creating a sheet of ADSCs containing a certain amount of antibiotics due to technical problems, and furthermore, continuous research was necessary to create a stable sheet. In the study of different administration methods, ADSCs and intravenous antibacterial therapy showed a strong antibacterial effect on PJI model rats, with early recovery of body weight, reduction in bacterial counts, and suppression of bone mineral density loss. The antibacterial effect may be related to increased expression of cathelicidin.本研究では、脂肪由来幹細胞（ADSCs)を用いた人工関節周囲感染（PJI）に対する新たな治療法を検討した。そこで独自のシート化技術を併用し、「抗菌薬含有ADSCsシート」による治療の確立、さらに投与方法の違いによる抗菌効果を検討した。シート化に関しては技術的な問題から一定量の抗菌薬を含有させ、さらに安定した作成には継続した研究が必要であった。投与方法の違いを検討した結果、ADSCsと抗菌薬の静脈内投与はPJIモデルラットに対して、体重の早期回復、細菌数の減少、骨密度減少の抑制を示し、強い抗菌効果を認めた。この抗菌効果には、抗菌ペプチド(カテリシジン)の発現量増加に関連している可能性がある。研究課題/領域番号:20K17993, 研究期間(年度):2020-04-01 – 2022-03-31出典：研究課題「「抗菌薬含有脂肪由来幹細胞シート」を用いたバイオフィルム感染症への応用」課題番号20K17993（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） （https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-20K17993/20K17993seika/）を加工して作

Schwann cell derived-peroxiredoxin protects motor neurons against hydrogen peroxide-induced cell death in mouse motor neuron cell line NSC-34

Schwann cells and oligodendrocytes secrete proteins that promote neuron survival, but their role in amyotrophic lateral sclerosis (ALS) is unclear. To address this question, we evaluated the effect of molecules secreted by Schwann cells on reactive oxygen species (ROS)-induced motor neuronal cell death. We observed that in motor neuron cell line NSC-34 cultures, the conditioned medium (CM) from Schwann cell line YST-1 (YST-1 CM) cultures had a protective effect against hydrogen peroxide-induced cell death. However, this protective effect of YST-1 CM was abolished by removing peroxiredoxin 1–4 (PRDX1–4) from the CM. We found that the expression of PRDX1 mRNA was markedly downregulated in the lumbar spinal cord of the superoxide dismutase 1 (SOD1)G93A mouse model of ALS. We also found that transient transfection of YST-1 cells with G93A SOD1 resulted in reduced PRDX1 mRNA expression. Additionally, in the mutant transfected cells, YST-1 CM showed decreased neuroprotective effect against hydrogen peroxide-induced NSC-34 cell death compared to those transfected with WT SOD1. Our results suggest that Schwann cells protect motor neurons from oxidative stress by secreting PRDX1 and that the reduction of PRDX secreted from Schwann cells contributes to increased ROS and associated motor neuronal death in ALS

Inhibition of apelin expression switches endothelial cells from proliferative to mature state in pathological retinal angiogenesis

The recruitment of mural cells such as pericytes to patent vessels with an endothelial lumen is a key factor for the maturation of blood vessels and the prevention of hemorrhage in pathological angiogenesis. To date, our understanding of the specific trigger underlying the transition from cell growth to the maturation phase remains incomplete. Since rapid endothelial cell growth causes pericyte loss, we hypothesized that suppression of endothelial growth factors would both promote pericyte recruitment, in addition to inhibiting pathological angiogenesis. Here, we demonstrate that targeted knockdown of apelin in endothelial cells using siRNA induced the expression of monocyte chemoattractant protein-1 (MCP-1) through activation of Smad3, via suppression of the PI3K/Akt pathway. The conditioned medium of endothelial cells treated with apelin siRNA enhanced the migration of vascular smooth muscle cells, through MCP-1 and its receptor pathway. Moreover, in vivo delivery of siRNA targeting apelin, which causes exuberant endothelial cell proliferation and pathological angiogenesis through its receptor APJ, led to increased pericyte coverage and suppressed pathological angiogenesis in an oxygen-induced retinopathy model. These data demonstrate that apelin is not only a potent endothelial growth factor, but also restricts pericyte recruitment, establishing a new connection between endothelial cell proliferation signaling and a trigger of mural recruitment. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10456-013-9349-6) contains supplementary material, which is available to authorized users

Influence of greater trochanteric bone density and three-dimensional morphology on perioperative greater trochanteric fracture following total hip arthroplasty via an anterolateral approach

Abstract Background Perioperative greater trochanteric fracture following total hip arthroplasty (THA) using the anterolateral approach is a recognized perioperative complication. There was no previous study to determine the relationship between bone mineral density (BMD) and three-dimensional greater trochanter morphology for perioperative greater trochanter fractures. The purpose of this study is to identify the influence of greater trochanteric bone density and three-dimensional morphology on perioperative greater trochanteric fracture following THA using the anterolateral approach. Methods We investigated 209 hips done primary THA using the anterolateral approach and preoperative BMD test for the proximal femoral bone with a minimum of 6 months follow-up. We picked up all patients who had perioperative greater trochanteric fractures. Multivariate analysis was done in order to investigate the influence of the greater trochanter young adult mean (YAM) and three-dimensional morphology on perioperative greater trochanteric fractures. Results There were 10 joints (10/209, 4.8%) with perioperative greater trochanteric fractures. Osteosynthesis was required only in one joint (1/209, 0.5%) because the bone fragments were significantly displaced proximally by the gluteus medius. Multivariate analysis showed the combination of Type B femoral shape (in cases where the top of the great trochanter was inside the longitudinal central axis of the planned femoral stem in computed tomography (CT)- based three-dimensional templating) and a YAM of < 80% was the only risk factor for fracture. Conclusions The preoperative greater trochanter BMD test (YAM < 80%) and three-dimensional femoral morphology (Type B femoral shape) provide useful information to mitigate the occurrence of perioperative greater trochanter fractures associated with THA using the anterolateral approach

Effect of apelin and VEGF on oxidative stress-induced neurotoxicity in rat primary neurons.

<p>(A) Representative picture shows the expression of APJ and apelin mRNA in primary cortical and hippocampal neuronal cultures (representatively, C and H). Culture medium was replaced with neurobasal media without B27 supplement for 24 hours. (B) Cell viability of hippocampal neuronal cultures treated with indicated concentration of apelin for 24 hours. The cultures were treated with the indicated concentration of apelin (C) or with VEGF (50 ng/ml) and apelin (indicated concentration) (D) for 15 min prior to exposure to H₂O₂ (10 µM) for 24 hours. Cell viability was assessed by MTT assay (n = 4). *<i>p</i><0.05 vs. control. Data represent mean ± SEM.</p

Effect of apelin deficiency on disease progression of ALS mice.

<p>(A) Motor signs (hind limb tremors) were measured as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0023968#pone-0023968-g003" target="_blank">Fig. 3B</a>. (B) Rotarod performance of SOD1^G93A littermates (open circles) and KO-SOD1^G93A (closed circles) mice was measured as described in the methods for 180 s. (C) The number of motorneurons was decreased in the lumbar spinal cord of KO-SOD1 ^G93A mice at 14 weeks-old (n = 3). Data represent mean ± SEM. *<i>p</i><0.05 vs. SOD1 ^G93A mice.</p