Kombinasi Format Factory, U-lead dan Microsoft Office Powerpoint dalam Upaya Meningkatkan Kualitas Media Pembelajaran

Peserta didik mempunyai gaya belajar yang berbeda-beda. Gaya belajar tersebut meliputi auditori, visual dan kinestetik (VAK). Seorang guru harus mampu memenuhi kebutuhan masing-masing gaya belajar peserta didik tersebut. Salah satu cara yang dapat dilakukan adalah dengan menggunakan media pembelajaran berbasis VAK. Media pembelajaran berbasis VAK dapat dipenuhi dengan menyisipkan file video di dalamnya. Selain itu, penggunaan file video sebagai media pembelajaran mendukung implementasi pembelajaran saintifik pada kurikulum 2013. Namun, belum semua guru memiliki kemampuan untuk mengemas file video tersebut dalam bentuk media pembelajaran. Tujuan penelitian ini adalah untuk meningkatkan kemampuan guru-guru di SMA Negeri 1 Teras dan SMA Negeri 1 Boyolali dalam membuat media pembelajaran berbasis VAK dengan kombinasi software Format Factory, U-Lead dan PowerPoint. Hasil penelitian menunjukkan bahwa terjadi peningkatan kemampuan para guru di SMA Negeri 1 Teras dan SMA Negeri 1 Boyolali dalam membuat media pembelajaran. Peningkatan kemampuan guru-guru tersebut berada di atas target yang direncanakan. Rerata peningkatan kemampuan guru-guru di SMA Negeri 1 Teras 7,87% di atas target, sedangkan di SMA Negeri 1 Boyolali 9,58% di atas target. Kata kunci: Media Pembelajaran, Format Factory, U-Lead, PowerPoint Students have different learning styles. Learning styles include visual learners, auditory learners, and kinesthetic learners. A teacher must be able to fulfill the needs of individual students\u27 learning styles. One way that can be applied is using Visual, Audio and Kinesthetic (VAK) learning media based. VAK-learning media based can be created by inserting video files on it. In addition, using video file as a learning media can support the implementation of scientific learning on the 2013 curriculum. However, not all teachers have the ability to use video files into a learning media. The purpose of this study is to improve the teachers\u27 ability at SMA Negeri 1 Teras and SMAN 1 Boyolali on making VAK-learning media based with a combination of Format Factory, U-Lead and PowerPoint software. The results showed that the teachers\u27 ability on making VAK-learning media based was increased. Increased the teachers\u27 ability was above planned target score. The mean score of the teachers\u27 ability at SMA Negeri 1 Teras 7.87% above the target, while at SMAN 1 Boyolali 9.58% above the target

Identification of Interleukin-1 by Functional Screening as a Key Mediator of Cellular Expansion and Disease Progression in Acute Myeloid Leukemia

Secreted proteins in the bone marrow microenvironment play critical roles in acute myeloid leukemia (AML). Through an ex vivo functional screen of 94 cytokines, we identified that the pro-inflammatory cytokine interleukin-1 (IL-1) elicited profound expansion of myeloid progenitors in ∼67% of AML patients while suppressing the growth of normal progenitors. Levels of IL-1β and IL-1 receptors were increased in AML patients, and silencing of the IL-1 receptor led to significant suppression of clonogenicity and in vivo disease progression. IL-1 promoted AML cell growth by enhancing p38MAPK phosphorylation and promoting secretion of various other growth factors and inflammatory cytokines. Treatment with p38MAPK inhibitors reversed these effects and recovered normal CD34+ cells from IL-1-mediated growth suppression. These results highlight the importance of ex vivo functional screening to identify common and actionable extrinsic pathways in genetically heterogeneous malignancies and provide impetus for clinical development of IL-1/IL1R1/p38MAPK pathway-targeted therapies in AML

Combined effect of TRAIL and doxorubicin in prostate carcinoma PPC-1 cells.

<p>PPC-1 cells grown to subconfluency in 384 well plate were treated with TRAIL (0.1 ng/ml) and increasing concentrations of doxorubicin. The level of cytotoxicity was determined by an ATPLite reagent. T, TRAIL; Dox. doxorubicin. <i>P</i> < 0.01.</p

Combined treatment of NSC130362 and oxidative stress inducers ATO, Myr, and BSO efficiently induced apoptosis in a variety of cancer cells but not in primary human hepatocytes.

<p>The effect of NSC130362/ATO (A), NSC130362/Myr (B), and NSC130362/BSO (C) combined treatment in breast carcinoma cells and MDA-MB-435 melanoma cells. The effect of NSC130362/ATO and NSC130362/Myr (D) combined treatment in pancreatic, prostate, and lung carcinoma cells as well as in AML cells from cancer patients. Subconfluent cells in a 96-well plate were pre-incubated for 4 h with ATO (3 μM), Myr (100 μM), or BSO (10 μM) followed by treatment with NSC130362 (10 μM) for an additional 24 h. At the end of the treatment, the ratio of dead cells was determined by an ATPLite reagent. *, <i>P</i> < 0.05.</p

NSC130362 binds GSR in a concentration-dependent manner.

<p>(A) GSR and NSC130362 absorbance profile. (B) Absorbance of GSR + NSC130362 in the flow-through after desalting column. (C) <i>inset</i>. The structure of the GSH-NSC10362 adduct. Absorbance of GSR + NSC130362 +GSH in the flow-through after desalting column. All absorbance values in (B and C) were corrected for absorbance of individual NSC130362, GSH, and the GSH-NSC130362 adduct in the flow through. (D) GSR activity in the absence or presence of either NSC130362 or the GSH-NSC130362 adduct. *, <i>P</i> < 0.05.</p

Cell surface expression of DR5 and DcR1/DcR2 in MDA-MB-435 carcinoma cells.

<p>MDA-MB-435 cell were pretreated with either ML100 NSC130362 for 4 h and 24 h. Cells were then labeled with biotin and lysed. Labeled cell surface-associated DR5, DcR1, and DcR2 were captured by streptavidin-agarose beads. The precipitated samples were analyzed by Western blotting with the specific respective antibodies and horseradish peroxidase-conjugated secondary antibodies. The level of the cell surface DR4 was below the detection limits. Molecular weight markers are on the left.</p

Molecularly targeted drug combinations demonstrate selective effectiveness for myeloid- and lymphoid-derived hematologic malignancies

Translating the genetic and epigenetic heterogeneity underlying human cancers into therapeutic strategies is an ongoing challenge. Large-scale sequencing efforts have uncovered a spectrum of mutations in many hematologic malignancies, including acute myeloid leukemia (AML), suggesting that combinations of agents will be required to treat these diseases effectively. Combinatorial approaches will also be critical for combating the emergence of genetically heterogeneous subclones, rescue signals in the microenvironment, and tumor-intrinsic feedback pathways that all contribute to disease relapse. To identify novel and effective drug combinations, we performed ex vivo sensitivity profiling of 122 primary patient samples from a variety of hematologic malignancies against a panel of 48 drug combinations. The combinations were designed as drug pairs that target nonoverlapping biological pathways and comprise drugs from different classes, preferably with Food and Drug Administration approval. A combination ratio (CR) was derived for each drug pair, and CRs were evaluated with respect to diagnostic categories as well as against genetic, cytogenetic, and cellular phenotypes of specimens from the two largest disease categories: AML and chronic lymphocytic leukemia (CLL). Nearly all tested combinations involving a BCL2 inhibitor showed additional benefit in patients with myeloid malignancies, whereas select combinations involving PI3K, CSF1R, or bromodomain inhibitors showed preferential benefit in lymphoid malignancies. Expanded analyses of patients with AML and CLL revealed specific patterns of ex vivo drug combination efficacy that were associated with select genetic, cytogenetic, and phenotypic disease subsets, warranting further evaluation. These findings highlight the heuristic value of an integrated functional genomic approach to the identification of novel treatment strategies for hematologic malignancies