Pengembangan Media Pembelajaran Fisika Berupa Buletin Dalam Bentuk Buku Saku Untuk Pembelajaran Fisikakelas VIII Materi Gaya Ditinjau Dari Minat Baca Siswa

Tujuan dari penelitian ini untuk mengembangkan media pembelajaran berupa buletin dalam bentuk buku saku untuk pembelajaran Fisika kelas VIII pada materi Gaya ditinjau dari aspek materi, konstruk, dan bahasa serta minat baca siswa. Penelitian ini termasuk penelitian pengembangan yang menggunakan metode Research and Development (R&D). Penelitian ini menggunakan model pengembangan model prosedural yaitu model yang bersifat deskriptif yang menunjukkan tahapan-tahapan yang harus diikuti untuk menghasilkan produk berupa media pembelajaran.Jenis data yang diperoleh bersifat kualitatif dan kuantitatif yaitu angket dan wawancara. Teknik analisis data yang digunakan adalah analisis deskriptif kualitatif dan kuantitatif. Hasil penelitian menunjukkan bahwa media pembelajaran yang dikembangkan berupa buletin Fisika dalam bentuk buku saku memiliki kriteria sangat baik berdasarkan penilaian dari ahli materi, ahli bahasa Indonesia, dan ahli media memberikan rata-rata penilaian sebesar 86,56%. Media pembelajaran yang dikembangkan juga memiliki kriteria sangat baik bila ditinjau dari peningkatan minat baca siswa. Hal ini terbukti pada hasil angket minat baca awal dan akhir yang diberikan kepada siswa yang memberikan rata-rata peningkatan sebesar 11,13%. Selain itu juga dianalisis dengan menggunakan uji-t berpasangan terhadap data masing-masing kelompok uji coba untuk mengetahui signifikansi dari peningkatan minat baca siswa. Untuk uji coba perorangan diperoleh hasil perhitungan thitung = 6,957 > ttabel = 1,943 dan nilai Sig. = 0,001 < 0,05 yang berarti sangat signifikan. Untuk kelompok kecil didapatkan hasil perhitungan bahwa thitung = 7,848 > ttabel = 1,725 dan nilai Sig. = 0,000 < 0,05 yang berarti sangat signifikan. Untuk kelompok besar juga didapatkan hasil perhitungan bahwa thitung = 20,214 > ttabel = 1,725 dan nilai Sig. = 0,000 < 0,05 yang berarti sangat signifikan. Simpulan dari penelitian ini adalah media pembelajaran berupa buletin dalam bentuk buku saku memiliki kriteria sangat baik bila ditinjau dari aspek materi, konstruk, dan bahasa serta minat baca siswa

Transdifferentiation of lung adenocarcinoma in mice with Lkb1 deficiency to squamous cell carcinoma

Lineage transition in adenocarcinoma (ADC) and squamous cell carcinoma (SCC) of non-small cell lung cancer, as implicated by clinical observation of mixed ADC and SCC pathologies in adenosquamous cell carcinoma, remains a fundamental yet unsolved question. Here we provide in vivo evidence showing the transdifferentiation of lung cancer from ADC to SCC in mice: Lkb1-deficient lung ADC progressively transdifferentiates into SCC, via a pathologically mixed mAd-SCC intermediate. We find that reduction of lysyl oxidase (Lox) in Lkb1-deficient lung ADC decreases collagen disposition and triggers extracellular matrix remodelling and upregulates p63 expression, a SCC lineage survival oncogene. Pharmacological Lox inhibition promotes the transdifferentiation, whereas ectopic Lox expression significantly inhibits this process. Notably, ADC and SCC show differential responses to Lox inhibition. Collectively, our findings demonstrate the de novo transdifferentiation of lung ADC to SCC in mice and provide mechanistic insight that may have important implications for lung cancer treatment

Association analyses of the interaction between the ADSS and ATM genes with schizophrenia in a Chinese population

<p>Abstract</p> <p>Background</p> <p>The blood-derived RNA levels of the adenylosuccinate synthase (<it>ADSS</it>) and ataxia telangiectasia mutated (<it>ATM</it>) genes were found to be down- and up-regulated, respectively, in schizophrenics compared with controls, and <it>ADSS </it>and <it>ATM </it>were among eight biomarker genes to discriminate schizophrenics from normal controls. ADSS catalyzes the first committed step of AMP synthesis, while ATM kinase serves as a key signal transducer in the DNA double-strand breaks response pathway. It remains unclear whether these changes result from mutations or polymorphisms in the two genes.</p> <p>Methods</p> <p>Six SNPs in the <it>ADSS </it>gene and three SNPs in the <it>ATM </it>gene in a Chinese population of 488 schizophrenics and 516 controls were genotyped to examine their association with schizophrenia (SZ). Genotyping was performed using the Sequenom platform.</p> <p>Results</p> <p>There was no significant difference in the genotype, allele, or haplotype distributions of the nine SNPs between cases and controls. Using the Multifactor Dimensionality Reduction (MDR) method, we found that the interactions among rs3102460 in the <it>ADSS </it>gene and rs227061 and rs664143 in the <it>ATM </it>gene revealed a significant association with SZ. This model held a maximum testing accuracy of 60.4% and a maximum cross-validation consistency of 10 out of 10.</p> <p>Conclusion</p> <p>These findings suggest that the combined effects of the polymorphisms in the <it>ADSS </it>and <it>ATM </it>genes may confer susceptibility to the development of SZ in a Chinese population.</p

GDF11 Forms a Bone Morphogenetic Protein 1-Activated Latent Complex That Can Modulate Nerve Growth Factor-Induced Differentiation of PC12 Cells

All transforming growth factor β (TGF-β) superfamily members are synthesized as precursors with prodomain sequences that are proteolytically removed by subtilisin-like proprotein convertases (SPCs). For most superfamily members, this is believed sufficient for activation. Exceptions are TGF-βs 1 to 3 and growth differentiation factor 8 (GDF8), also known as myostatin, which form noncovalent, latent complexes with their SPC-cleaved prodomains. Sequence similarities between TGF-βs 1 to 3, myostatin, and superfamily member GDF11, also known as bone morphogenetic protein 11 (BMP11), prompted us to examine whether GDF11 might be capable of forming a latent complex with its cleaved prodomain. Here we demonstrate that GDF11 forms a noncovalent latent complex with its SPC-cleaved prodomain and that this latent complex is activated via cleavage at a single specific site by members of the developmentally important BMP1/Tolloid family of metalloproteinases. Evidence is provided for a molecular model whereby formation and activation of this complex may play a general role in modulating neural differentiation. In particular, mutant GDF11 prodomains impervious to cleavage by BMP1/Tolloid proteinases are shown to be potent stimulators of neurodifferentiation, with potential for therapeutic applications

α3 chains of type V collagen regulate breast tumour growth via glypican-1

Abstract Pericellular α3(V) collagen can affect the functioning of cells, such as adipocytes and pancreatic β cells. Here we show that α3(V) chains are an abundant product of normal mammary gland basal cells, and that α3(V) ablation in a mouse mammary tumour model inhibits mammary tumour progression by reducing the proliferative potential of tumour cells. These effects are shown to be primarily cell autonomous, from loss of α3(V) chains normally produced by tumour cells, in which they affect growth by enhancing the ability of cell surface proteoglycan glypican-1 to act as a co-receptor for FGF2. Thus, a mechanism is presented for microenvironmental influence on tumour growth. α3(V) chains are produced in both basal-like and luminal human breast tumours, and its expression levels are tightly coupled with those of glypican-1 across breast cancer types. Evidence indicates α3(V) chains as potential targets for inhibiting tumour growth and as markers of oncogenic transformation