Pengembangan Suplemen Pembelajaran Fisika Gelombang Elektromagnetik Cahaya Sebagai Partikel Memanfaatkan Virtual Laboratorium

This research has been done to make a supplement for physics learning about light electromagnetic wave as a particle using virtual laboratory. The population of this research was the second year science-students at SMA Muhammadiyah 1 Metro. This development is begun by needs analysis, then identification of resource which is the background of this developmental research. The next step is, identifying the product specification then developing products which contained a tutorial book for teacher and a work sheet for student (LKS). The material and design expert test result is that those products were approved. The external test resulted by users show that the LKS was attractive, very easy to use, and useful. It also was effective to be used as a learning resource because 80% of students reached the passing grade.Telah dilakukan penelitian untuk mengembangkan suplemen pembelajaran fisika gelombang elektromagnetik cahaya sebagai partikel dengan memanfaatkan virtual laboratorium. Populasi penelitian pengembangan ini adalah siswa kelas XI IPA di SMA Muhammadiyah 1 Metro. Pengembangan ini diawali dengan analisis kebutuhan, kemudian identifikasi sumber daya yang melatar belakangi pengembangan. Langkah selanjutnya identifikasi spesifikasi produk yang dilanjutkan dengan mengembangkan produk berupa LKS untuk siswa dan buku panduan untuk guru. Hasil uji internal oleh ahli materi dan ahli desain menyatakan produk yang dikembangkan layak digunakan sebagai media pembelajaran. Hasil uji eksternal oleh pengguna menunjukkan kualitas media pembelajaran menarik, sangat mudah digunakan, dan bermanfaat serta efektif digunakan sebagai media pembelajaran dengan presentase hasil belajar sebesar 80% siswa telah memenuhi KKM

Anemia and Related Nutrient Deficiencies after Roux-en-Y Gastric Bypass Surgery

Study characteristics; Proportion of study participants with anemia before and after RYGB surgery; Proportion of study participants with low ferritin/ serum iron/ vitamin B12/ folate level before and after RYGB surgery; Hemoglobin/Hematocrit level among study participants; Ferritin/ serum Iron/ vitamin B12/ folate level among study participants before and after RYGB surgery before and after RYGB surgery; Literature search and study selection; Forest plot for proportion of study participants with anemia before RYGB and 12 months after RYGB; Forest plot for proportion of study participants with (A) ferritin (B) serum iron (C) vitamin B12 and (D) folate deficiencies before RYGB and 12 months after RYGB; Funnel plot comparing log(mean) and s.e. of log(mean) for proportion of study participants with anemia 12 months after RYGB; MEDLINE (via PubMed) search query with ‘All Fields’; Cochrane Library search query with ‘Search All Text

Inference of Cross-Level Interaction between Genes and Contextual Factors in a Matched Case-Control Metabolic Syndrome Study: A Bayesian Approach

<div><p>Genes, environment, and the interaction between them are each known to play an important role in the risk for developing complex diseases such as metabolic syndrome. For environmental factors, most studies focused on the measurements observed at the individual level, and therefore can only consider the gene-environment interaction at the same individual scale. Indeed the group-level (called contextual) environmental variables, such as community factors and the degree of local area development, may modify the genetic effect as well. To examine such <i>cross-level interaction</i> between genes and contextual factors, a flexible statistical model quantifying the variability of the genetic effects across different categories of the contextual variable is in need. With a Bayesian generalized linear mixed-effects model with an unconditional likelihood, we investigate whether the individual genetic effect is modified by the group-level residential environment factor in a matched case-control metabolic syndrome study. Such cross-level interaction is evaluated by examining the heterogeneity in allelic effects under various contextual categories, based on posterior samples from Markov chain Monte Carlo methods. The Bayesian analysis indicates that the effect of rs1801282 on metabolic syndrome development is modified by the contextual environmental factor. That is, even among individuals with the same genetic component of <i>PPARG</i>_Pro12Ala, living in a residential area with low availability of exercise facilities may result in higher risk. The modification of the group-level environment factors on the individual genetic attributes can be essential, and this Bayesian model is able to provide a quantitative assessment for such cross-level interaction. The Bayesian inference based on the full likelihood is flexible with any phenotype, and easy to implement computationally. This model has a wide applicability and may help unravel the complexity in development of complex diseases.</p> </div

Adipogenesis is regulated by PKCε-ALDH2 axis.

<p><i>A</i>, Expression of ALDH2 and PKCε protein during induced 3T3-L1 adipocyte differentiation (n = 3 independent experiments). The results shown are representative of an individual experiment. The ratio of intensity of bands corresponding to target protein per loading control was analyzed by densitometer software. The numbers indicate the means ± SE. <i>B</i>, Efficiency of shRNA control (shLuc), PKCε shRNA and ALDH2 shRNA targeted on mouse PKCε and ALDH2 protein levels of 3T3-L1 cells (n = 3 independent experiments). The results shown are representative of an individual experiment. <i>C</i>, 3T3-L1 preadipocytes expressing indicated lentiviral vectors were maintained in induction medium for 2 days. After 8 day of adipogenic stimulation, cells on the plates were stained with Oil-Red O. <i>D</i>, Quantification of Oil-Red O dye in shRNA control, PKCε-knockdown and double knockdown of PKCε and ALDH2 preadipocytes after 8 day induction. <i>E</i>, Determination of adipogenic gene (FABP4 and ADIPONECTIN) expression in shRNA control, PKCε-knockdown and double knockdown of PKCε and ALDH2 preadipocytes after 8 day induction. Data are shown as mean ± SE from 3 independent experiments. * P < 0.05 versus shLuc. <i>F</i>, shRNA control and ALDH2-knockdown preadipocytes were maintained in induction medium with or without 1 μM PKCε agonist for 2 days. After 8 day of adipogenic stimulation, cells on the plates were stained with Oil-Red O. <i>G</i>, Quantification of Oil-Red O dye in shRNA control, PKCε-knockdown and double knockdown of PKCε and ALDH2 preadipocytes with or without 1 μM PKCε agonist treatment after 8 day induction. <i>H</i>, Determination of adipogenic gene (FABP4 and ADIPONECTIN) expression in shRNA control, PKCε-knockdown and double knockdown of PKCε and ALDH2 preadipocytes with or without 1 μM PKCε agonist treatment after 8 day induction. Data are shown as mean ± SE from 3 independent experiments. * P < 0.05 versus shLuc.</p

The variance parameters represent the variability among areas for each SNP.

<p>Numbers are posterior means and standard deviations of variance components under the Bayesian conditional logistic regression model.</p

PKC-ALDH2 Pathway Plays a Novel Role in Adipocyte Differentiation

<div><p>The <i>ALDH2</i> gene encodes the mitochondrial aldehyde dehydrogenase 2 (ALDH2), a critical enzyme involved in ethanol clearance through acetaldehyde metabolism. ALDH2 also catalyzes the metabolism of other bioreactive aldehydes, including propionaldehyde, butyraldehyde, and 4-hydroxykenals (4-HNE). Increased levels of 4-HNE in adipose tissue positively correlate with obesity and insulin resistance. However, it remains unclear whether ALDH2 is involved in regulation of adipocyte differentiation. Here, we found that ALDH2 protein levels were lower in white adipose tissue of high-fat diet-fed mice and <i>ob/ob</i> mice relative to lean mice. Knockdown of ALDH2 expression in 3T3-L1 preadipocytes caused an increase in intracellular 4-HNE, thereby attenuated adipocyte differentiation. By contrast, an ALDH2 activator, Alda-1, significantly accelerated adipogenesis, which was accompanied by an increase in adipogenic gene expression. Consistently, adipogenesis was reduced when protein kinase C ε (PKCε), an ALDH2 phosphorylating activator, was silenced in 3T3-L1 preadipocytes, whereas treatment with a PKCε agonist in 3T3-L1 preadipocytes enhanced adipogenesis. Whole-genome microarray profiling of Alda-1-treated cells demonstrated several upregulated transcripts encoding proteins involved in metabolism and the majority of these transcripts are for proteins involved in PPAR signaling pathways. Furthermore, PKCε-ALDH2 interaction alleviates 4-HNE induced aberrant PPARγ regulation on adipogenesis. Taken together, these results demonstrate that ALDH2 activation enhances adipogenesis and signaling pathways involving PPARγ. Thus, activation of PKCε-ALDH2 regulatory axis may be a therapeutic target for treating obesity and type 2 diabetes.</p></div

Effect of Common Genetic Variants of Growth Arrest-Specific 6 Gene on Insulin Resistance, Obesity and Type 2 Diabetes in an Asian Population

<div><p>Objectives</p><p>Growth arrest-specific 6 (Gas6), a vitamin K-dependent protein, has been implicated in systemic inflammation, obesity, and insulin resistance (IR). Data from recent studies suggest that polymorphisms in the <i>Gas6</i> gene are associated with cardiovascular disorders and type 2 diabetes (T2D). However, the association of <i>Gas6</i> gene variants with obesity, IR, and T2D development has not been explored.</p><p>Materials and Methods</p><p>Four common single nucleotide polymorphisms (SNPs) in the <i>Gas6</i> gene were genotyped in 984 participants from the Stanford Asia-Pacific Program for Hypertension and Insulin Resistance (SAPPHIRe) family cohort. An insulin suppression test was performed to determine IR based on steady-state plasma glucose (SSPG). Associations between IR indices and obesity, and SNP genotypes, based on previously-reported data for this cohort (Phase I), were analyzed. In the present follow-up study (Phase II), the effects of gene variants of <i>Gas6</i> on the progression to T2D were explored in individuals who were free of T2D in Phase I. The mean follow-up period for Phase II was 5.7 years.</p><p>Results</p><p>The mean age of the study population in Phase I was 49.5 years and 16.7% of individuals developed T2D during follow-up. After adjusting for covariates, three SNPs (rs8191973, rs8197974, and rs7323932) were found to be associated with SSPG levels (<i>p</i> = 0.007, <i>p</i> = 0.03, and <i>p</i> = 0.011, respectively). This association remained significant after multiple testing and showed a significant interaction with physical activity for SNP rs8191973. However, no other significant correlations were observed between <i>Gas6</i> polymorphisms and other indices of IR or obesity. A specific haplotype, AACG (from rs8191974, rs7323932, rs7331124, and rs8191973), was positively associated with SSPG levels (<i>p</i> = 0.0098). None of the polymorphisms were associated with an increased risk of T2D development.</p><p>Conclusions</p><p>Our results suggest that <i>Gas6</i> gene variants are associated with IR, although their effects on subsequent progression to T2D were minimal in this prospective Asian cohort.</p></div

Temporal expression profiles of the C/EBPs during differentiation of 3T3-L1 and NIH/3T3 cells.

<p>The mRNA levels and the standard errors (n = 3) of measurement of (A) C/EBPα, (B) C/EBPβ, and (C) C/EBPδ were determined by qPCR and normalized by Gapdh signal on day 0 (D0), 2 (D2) and 4(D4) in differentiation medium and day 8 in DMEM +10% FBS medium.</p

PKCε-ALDH2 interaction involves in regulation of PPARγ activity.

<p><i>A</i>, Cytoplasmic and mitochondrial distribution of PKCε and ALDH2 protein throughout the differentiation process (n = 3 independent experiments). The results shown are representative of an individual experiment. The ratio of intensity of bands corresponding to target protein per loading control was analyzed by densitometer software. The numbers indicate the means ± SE. <i>B</i>, PKCε coimmunoprecipitates with ALDH2 during adipocyte differentiation. Cell extracts harvested from differentiating adipocytes were immunoprecipitated (IP) with either IgG, ALDH2 or PKCε antibody. The immunoblots (IB) were probed for either PKCε or ALDH2 antibody. Input is shown in the lower panels (n = 4 independent experiments). The results shown are representative of an individual experiment. <i>C</i>, shRNA control, ALDH2-knockdown and PKCε-knockdown preadipocytes were treated with or without 10 μM 4-hydroxynonenal (4-HNE) for 24 hours. Total cell extracts were harvested and analyzed by immunoblotting with anti-<a href="http://www.abcam.com/4-hydroxynonenal-antibody-ab46545.html" target="_blank">4-HNE antibody</a> (n = 4 independent experiments). The results shown are representative of an individual experiment. <i>D</i>, Effect of Alda-1 on 4-HNE formation. 3T3-L1 preadipocytes were maintained in induction medium with various dose of Alda-1 for 2 days. After 8 day of adipogenic stimulation, total cell extracts were harvested and analyzed by immunoblotting with anti-<a href="http://www.abcam.com/4-hydroxynonenal-antibody-ab46545.html" target="_blank">4-HNE antibody</a> (n = 4 independent experiments). The results shown are representative of an individual experiment. <i>E</i>, 4-HNE attenuates PPRE-driven luciferase activity in differentiating 3T3-L1 cells. Differentiating 3T3-L1 cells were transfected with reporter vectors (TK-LUC and PPRE-LUC) for 24 hour and then incubated cells in induction medium with or without treatments (10 μM 4-HNE) for 24 hour. The activity of firefly luciferase was determined and normalized to the activity of renilla luciferase. Data are shown as mean ± SE from 4 independent experiments. * P < 0.05 versus ethanol. <i>F</i>, PKCε agonist and Alda-1 trigger PPRE-driven luciferase activity in differentiating 3T3-L1 cells. Differentiating 3T3-L1 cells were transfected with reporter vectors (TK-LUC and PPRE-LUC) for 24 hour and then incubated cells in induction medium with or without treatments (1 μM PKCε agonist and 10 μM Alda-1) for 2 days. The activity of firefly luciferase was determined and normalized to the activity of renilla luciferase. Data are shown as mean ± SE from 4 independent experiments. * P < 0.05 versus ethanol. <i>G</i>, Silencing of ALDH2 or PKCε reduces PPRE-driven luciferase activity in differentiating 3T3-L1 cells. Differentiating shGFP, shALDH2 and shPKCε cells were transfected with reporter vectors (TK-LUC and PPRE-LUC) for 24 hour. The activity of firefly luciferase was determined and normalized to the activity of renilla luciferase. Data are shown as mean ± SE from 4 independent experiments. * P < 0.05 versus shGFP. <i>H</i>, PKCε-ALDH2 pathway potentiates PPARγ transcriptional activity. 293 cells were transiently transfected with expression vectors (Flag-ALDH2, Flag-PKCε and CMX-GAL4-PPARγ) and UAS_G×4-TK-LUC reporter plasmid for 24 hour and then incubated cells in growth medium with 1 μM PKCε agonist, 1 μM troglitazone and 10 μM 4-HNE for 2 days (n = 3 independent experiments). The results shown are representative of an individual experiment. <i>I</i>, The activity of firefly luciferase was determined and normalized to the activity of renilla luciferase. Data are shown as mean ± SE from 4 independent experiments. * P < 0.05 versus control cells. <i>J</i>, Proposed model for the mechanism by which PKCε-ALDH2 interaction involves in regulation of PPARγ activity by 4-HNE metabolism.</p

The observed genotype counts of metabolic cases (cs) and controls (cn) under each category of exercise facility availability.

<p>The observed genotype counts of metabolic cases (cs) and controls (cn) under each category of exercise facility availability.</p