Pengaruh Dimensi Benda Uji Terhadap Kuat Tekan Beton

Kuat tekan adalah karakteristik mekanik utama dari beton yang dapat diketahui melalui penelitian uji tekan di laboratorium terhadap benda uji. Baik dalam bentuk kubus ataupun silinder dengan ukuran standar: 10cm x 10cm x 10cm dan 15cm x 15cm untuk kubus dan 10cm x 20cm dan 15cm x 30cm untuk silinder. Untuk mendapatkan informasi mengenai kecendrungan harga kuat tekan beton dengan variasi dimensi benda uji, telah dilakukan penelitian-penelitian di laboratoriun untuk mendapatkan komposisi campuran tertentu pada umur beton 28 hari, variasi ukuran benda uji dibuat: 10cm x 10cm x 10cm, 12,5cm x 12,5cm x 12,5cm dan 15cm x 15cm x 15cm untuk kubus dan 10cm x 20cm, 12,5cm x 25cm dan 15cm x 30cm untuk silinder. Dengan jumlah benda uji masing-masing 20 buah untuk setiap ukuran benda uji. Melalui prosedur standar pengujian kuat tekan dan menggunakan formula-formula baku perhitungan tekan rata-rata diperoleh informasi bahwa peningkatan ukuran dimensi benda uji menghasilkan penurunan kuat tekan rata-rata, untuk benda uji kubus dengan ukuran masing-masing: 10cm x 10cm x 10cm, 12,5cm x 12,5cm x 12,5cm dan 15cm x 15cm x 15cm diperoleh kuat tekan rata-rata masing-masing: 32,86MPa, 31,26MPa dan 31,036MPa. Sedangkan untuk silinder dengan kururan 10cm x 20cm, 12,5cm x 25cm dan 15cm x 30cm diperoleh kuat tekan rata-rata masing-masing: 31,47MPa, 30,85MPa dan 30,44MPa

Time Course Analysis of Skeletal Muscle Pathology of GDE5 Transgenic Mouse

<div><p>Glycerophosphodiesterase 5 (GDE5) selectively hydrolyses glycerophosphocholine to choline and is highly expressed in type II fiber-rich skeletal muscles. We have previously generated that a truncated mutant of GDE5 (GDE5dC471) that lacks phosphodiesterase activity and shown that transgenic mice overexpressing GDE5dC471 in skeletal muscles show less skeletal muscle mass than control mice. However, the molecular mechanism and pathophysiological features underlying decreased skeletal muscle mass in GDE5dC471 mice remain unclear. In this study, we characterized the skeletal muscle disorder throughout development and investigated the primary cause of muscle atrophy. While type I fiber-rich soleus muscle mass was not altered in GDE5dC471 mice, type II fiber-rich muscle mass was reduced in 8-week-old GDE5dC471 mice. Type II fiber-rich muscle mass continued to decrease irreversibly in 1-year-old transgenic mice with an increase in apoptotic cell. Adipose tissue weight and blood triglyceride levels in 8-week-old and 1-year-old transgenic mice were higher than those in control mice. This study also demonstrated compensatory mRNA expression of neuromuscular junction (NMJ) components, including nicotinic acetylcholine receptors (α1, γ, and ε subunits) and acetylcholinesterase in type II fiber-rich quadriceps muscles in GDE5dC471 mice. However, we did not observe morphological changes in NMJs associated with skeletal muscle atrophy in GDE5dC471 mice. We also found that HSP70 protein levels are significantly increased in the skeletal muscles of 2-week-old GDE5dC471 mice and in mouse myoblastic C2C12 cells overexpressing GDE5dC471. These findings suggest that GDE5dC471 mouse is a novel model of early-onset irreversible type II fiber-rich myopathy associated with cellular stress.</p></div

RASSF6 Expression in Adipocytes Is Down-Regulated by Interaction with Macrophages

<div><p>Macrophage infiltration into adipose tissue is associated with obesity and the crosstalk between adipocytes and infiltrated macrophages has been investigated as an important pathological phenomenon during adipose tissue inflammation. Here, we sought to identify adipocyte mRNAs that are regulated by interaction with infiltrated macrophages <i>in vivo</i>. An anti-inflammatory vitamin, vitamin B6, suppressed macrophage infiltration into white adipose tissue and altered mRNA expression. We identified >3500 genes whose expression is significantly altered during the development of obesity in db/db mice, and compared them to the adipose tissue mRNA expression profile of mice supplemented with vitamin B6. We identified <i>PTX3</i> and <i>MMP3</i> as candidate genes regulated by macrophage infiltration. PTX3 and MMP3 mRNA expression in 3T3-L1 adipocytes was up-regulated by activated RAW264.7 cells and these mRNA levels were positively correlated with macrophage number in adipose tissue <i>in vivo</i>. Next, we screened adipose genes down-regulated by the interaction with macrophages, and isolated <i>RASSF6</i> (<i>Ras association domain family 6</i>). RASSF6 mRNA in adipocytes was decreased by culture medium conditioned by activated RAW264.7 cells, and RASSF6 mRNA level was negatively correlated with macrophage number in adipose tissue, suggesting that adipocyte RASSF6 mRNA expression is down-regulated by infiltrated macrophages <i>in vivo</i>. Finally, this study also showed that decreased RASSF6 expression up-regulates mRNA expression of several genes, such as <i>CD44</i> and <i>high mobility group protein HMGA2</i>. These data provide novel insights into the biological significance of interactions between adipocytes and macrophages in adipose tissue during the development of obesity.</p> </div

Two transcriptomes of quadriceps muscle in 2-week-old and 12-week-old of GDE5dC471 mice.

<p>The venn diagram shows genes that are altered in the quadriceps muscle of 2-week-old and 12-week-old GDE5dC471 mice. <i>A</i>, Of a total 96 genes up-regulated in quadriceps muscle of 2-week-old GDE5dC471 mice (<i>p</i><0.05), the expression of 18 genes were also increased in that of 12-week-old. On the contrary (<i>B</i>), the expression of 35 genes were also down-regulated in quadriceps muscle of 12-week-old GDE5dC471 mice.</p

Effects of RASSF6 siRNA on gene expression in 3T3-L1 adipocytes.

<p><i>A</i>–<i>C</i>, 3T3-L1 adipocytes were treated with MDI and differentiated into mature adipocytes as described under “Materials and Methods”. Differentiated 3T3-L1 adipocytes were transfected with luciferase siRNA (<i>Siluc</i>) or RASSF6 siRNA (<i>SiRassf6</i>). After 2 days of transfection, total RNAs were extracted and subjected to quantitative PCR analysis to examine expression levels of RASSF6, HMGA2 and CD44 mRNAs. The level of β-actin (<i>β-actin</i>) transcript was used as a control. *<i>P</i><0.05 compared with those of cells transfected with control siRNA (<i>Siluc</i>).</p

HSP70 protein expression in GDE5dC471 mice.

<p>Total protein from gastrocnemius muscle of 2-week-old and 4-week-old GDE5dC471 mice (Tg) and age-matched control mice (Wild) was subjected to SDS-PAGE followed by Western blotting using anti-GDE5 and anti-HSP70 antibodies. The filter was stained with Coomassie Brilliant Blue (CBB) as a control of protein loading.</p

Time course alterations of body weight and skeletal muscle weight in GDE5dC471 mice and age-matched control mice.

<p>Time course alterations of body weight and skeletal muscle weight in GDE5dC471 mice and age-matched control mice.</p

Time-course morphological alterations of type II fiber-rich muscles in GDE5dC471 mice.

<p><i>A</i>, Representative photographs of H&E staining in cross sections of gastrocnemius muscle, Left; 4-week-old GDE5dC471 mice (Tg) and age-matched control mice (Wild), center; 8-week-old, and right; 1-year-old. Central nuclei (arrow) appeared only in 1-year-old GDE5dC471 mice. <i>B</i>, Time-course alterations of fiber areas of gastrocnemius muscle of 4-week-old GDE5dC471 mice (Tg) and age-matched control mice (Wild). To visualize frequency of distribution of each myofibril, histogram images were analyzed. Both 8-week-old and 1-year-old Tg showed a leftward shift, indicating an evident increase in the percentage of small areas compared with age-matched Wild. <i>C</i>, Mean fiber areas of gastrocnemius muscle of 4-week-old GDE5dC471 mice (Tg) and age-matched control mice (Wild). 4-week-old: n = 4, 8-week-old: n = 3, and 1-year-old: n = 7 (Wild) and n = 10 (Tg). Data represent mean ± SD. *<i>p</i><0.05, **<i>p</i><0.01.</p

Effect of decreased RASSF6 expression on gene expression in 3T3-L1 adipocytes.

<p>DNA microarray analysis was repeated with the Cy3 and Cy5 dyes reversed (a dye swap), and fold change (<i>Fold</i>) represents the average of mRNA expression level in RASSF6-deprived 3T3-L1 adipocytes relative to control cells.</p

GDE5dC471 overexpression in skeletal muscle increases neuromuscular junctions-related mRNA expression.

<p><i>A</i>, Total RNA from gastrocnemius muscle of GDE5dC471 mice (Tg) and age-matched control mice (Wild) (4-week-old, n = 4; 8-week-old, n = 3; and 1-year-old, n = 5) was subjected to quantitative PCR to examine mRNA expression level of genes related to neuromuscular junctions. Data represent mean ± SE. *<i>p</i><0.05, **<i>p</i><0.01. <i>B</i>, Representative photographs of fluorescent α-bungarotoxin staining in transverse sections of gastrocnemius muscle, Left; 1-year-old of GDE5dC471 mice (Tg), and right; age-matched control mice (Wild). No morphological alteration of nicotinic acetylcholine receptor (nAchR) was observed between GDE5dC471 and control mice.</p