Early versus Late Intravitreal Triamcinolone Acetonide for Macular Edema associated with Branch Retinal Vein Occlusion

PURPOSE: To compare the effect of early versus late intravitreal injection of triamcinolone in patients with macular edema due to branch retinal vein occlusion (BRVO). METHODS: Twenty eyes of 20 patients with macular edema from BRVO, including 10 with duration after onset of or 3 months, improvements in visual acuity and foveal thickness, though apparent at 1 month, were not maintained at 3 and 6 months post-triamcinolone. CONCLUSIONS: Intravitreal triamcinolone is more effective in patients with BRVO who are treated earlier

Altered expression of hypothetical proteins in hippocampus of transgenic mice overexpressing human Cu/Zn-superoxide dismutase 1

BACKGROUND: Cu/Zn-superoxide dismutase 1 (SOD1), encoded on chromosome 21, is a key enzyme in the metabolism of reactive oxygen species (ROS) and pathogenetically relevant for several disease states including Down syndrome (DS; trisomy 21). Systematically studying protein expression in human brain and animal models of DS we decided to carry out "protein hunting" for hypothetical proteins, i.e. proteins that have been predicted based upon nucleic sequences only, in a transgenic mouse model overexpressing human SOD1. RESULTS: We applied a proteomics approach using two-dimensional electrophoresis (2-DE) with in-gel digestion of spots followed by mass spectrometric (matrix-assisted laser desorption/ionization-time of flight) identification and quantification of hypothetical proteins using specific software. Hippocampi of wild type, hemizygous and homozygous SOD1 transgenic mice (SOD1-TGs) were analysed. We identified fourteen hypothetical proteins in mouse hippocampus. Of these, expression levels of 2610008O03Rik protein (Q9D0K2) and 4632432E04Rik protein (Q9D358) were significantly decreased (P < 0.05 and 0.001) and hypothetical protein (Q99KP6) was significantly increased (P < 0.05) in hippocampus of SOD1-TGs as compared with non-transgenic mice. CONCLUSIONS: The biological meaning of aberrant expression of these proteins may be impairment of metabolism, signaling and transcription machinery in SOD1-TGs brain that in turn may help to explain deterioration of these systems in DS brain

Visfatin exerts angiogenic effects on human umbilical vein endothelial cells through the mTOR signaling pathway

AbstractThe biologically active factors known as adipocytokines are secreted primarily by adipose tissues and can act as modulators of angiogenesis. Visfatin, an adipocytokine that has recently been reported to have angiogenic properties, is upregulated in diabetes, cancer, and inflammatory diseases. Because maintenance of an angiogenic balance is critically important in the management of these diseases, understanding the molecular mechanism by which visfatin promotes angiogenesis is very important. In this report, we describe our findings demonstrating that visfatin stimulates the mammalian target of the rapamycin (mTOR) pathway, which plays important roles in angiogenesis. Visfatin induced the expression of hypoxia-inducible factor 1α (HIF1α) and vascular endothelial growth factor (VEGF) in human endothelial cells. Inhibition of the mTOR pathway by rapamycin eliminated the angiogenic and proliferative effects of visfatin. The visfatin-induced increase in VEGF expression was also eliminated by RNA interference-mediated knockdown of the 70-kDa ribosomal protein S6 kinase (p70S6K), a downstream target of mTOR. Visfatin inactivated glycogen synthase kinase 3β (GSK3β) by phosphorylating it at Ser-9, leading to the nuclear translocation of β-catenin. Both rapamycin co-treatment and p70S6K knockdown inhibited visfatin-induced GSK3β phosphorylation at Ser-9 and nuclear translocation of β-catenin. Taken together, these results indicate that mTOR signaling is involved in visfatin-induced angiogenesis, and that this signaling leads to visfatin-induced VEGF expression and nuclear translocation of β-catenin

NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor

AbstractDNA damage induced apoptosis suppressor (DDIAS), or human Noxin (hNoxin), is strongly expressed in lung cancers. DDIAS knockdown induced apoptosis in non-small cell lung carcinoma A549 cells in response to DNA damage, indicating DDIAS as a potential therapeutic target in lung cancer. To understand the transcriptional regulation of DDIAS, we determined the transcription start site, promoter region, and transcription factor. We found that DDIAS transcription begins at nucleotide 212 upstream of the DDIAS translation start site. We cloned the DDIAS promoter region and identified NFAT2 as a major transcription factor (Im et al., 2016 [1]). We demonstrated that NFATc1 regulates DDIAS expression in both pancreatic cancer Panc-1 cells and lung cancer cells

CHANGES IN MUSCLE ACTIVITY PATTERN IN LOWER LIMB EXTREMITY DURING PEDALLING BY SADDLE HEIGHT

As a preliminary study for a preferential saddle height for cyclist, muscle activity pattern in lower limb extremity between preferred and higher saddle height during pedalling was compared. Seven cyclists performed 3 min sub-maximal pedalling under two different saddle heights. Range of motion (ROM) of muscle length, onset-timing of muscle activity, and amount of muscle activity in biceps femoris (BF), vastus lateralis (VL), gastrocnemius (GM), and tibialis anterior muscles (TA) were used to compare changes in muscle activity pattern due to saddle height. Results showed that there was a significant difference in ROM of VL and that of TA (