UPAYA MENINGKATKAN KEMAMPUAN BERPENDAPAT SISWA DALAM MATA PELAJARAN SEJARAH DENGAN MENGGUNAKAN TEKNIK TIME TOKEN : Penelitian Tindakan Kelas di Kelas XII MIA 2 SMA Negeri 1 Jalancagak

Penelitian ini dilatarbelakangi oleh kurangnya kemampuan berpendapat siswa dalam mata pelajaran sejarah. Padahal kemampuan mengemukakan pendapat merupakan suatu keterampilan yang perlu dimiliki oleh siswa, karena kemampuan ini merupakan salah satu dari aspek keterampilan berpikir. Penelitian ini dilaksanakan pada siswa Kelas XII MIA 2 SMA Negeri 1 Jalancagak Tahun Pelajaran 2017/2018. Peneliti mencoba menggunakan teknik time token yang dirasa cocok untuk meningkatkan kemampuan berpendapat siswa di kelas. Teknik time token ini dapat menjadikan siswa aktif dalam kegiatan pembelajaran, mengungkapkan pendapatnya, bertanya dan mendengarkan dalam kegiatan pembelajaran. Metode yang digunakan adalah Penelitian Tindakan Kelas (Classroom Action Research) yang merujuk pada desain penelitian Kemmis and Mc. Taggart terdiri dari tahapan perencanaan, tindakan, pengamatan atau observasi dan refleksi. Sumber data dapat diperoleh dari siswa, guru, interaksi antara siswa dengan guru, tempat dan peristiwa di mana aktivitas pembelajaran berlangsung. Teknik pengumpulan data menggunakan observasi, wawancara, dan dokumentasi. Berdasarkan hasil penelitian Tindakan Kelas yang telah dilaksanakan pada siswa kelas XII MIA 2 SMA Negeri 1 Jalancagak dengan teknik time token dalam pembelajaran sejarah maka dapat ditarik simpulan bahwa pembelajaran dengan teknik time token dapat meningkatkan kemampuan mengemukakan pendapat siswa pada pembelajaran sejarah kelas XII SMA Negeri 1 Jalancagak. Hal tersebut ditunjukkan berdasarkan indikator yang telah dirumuskan, selain itu teknik ini dapat dijadikan suatu alternatif solusi untuk mengatasi masalah pembelajaran sejarah yang ditemukan di kelas.;--- The background of this research is the lack of student’s ability in expressing their opinion in history subject. In fact the ability to express an opinion is a skill that should be owned by the students, because this ability is one of aspects of thinking skill. This research is conducted on students of XII MIA of Senior High School 1 Jalancagak School Year 2017/2018. Time token tecnic is used in this research which is considered suitable to improve students’ ability in expressing opinion in class. Time token tecnic can make students active in learning activities, expressed their opinions, ask questions and listen in learning activities. Classroom Action Research is used in this research which refers to design of Kemmis and McTaggart which consists of planning, action, observation and reflection. Data sources can be obtained from students, teacher, interaction between students and teacher, places and events in which learning activities take place. Data collection technique is used observation, interview and documentation. Based on the result of Classroom Action Research that is implemented on the students of XII MIA of Senior High School 1 Jalancagak uses Time Token tecnic in learning history, it can be concluded that learning activities with Time Token method can improve students’ ability in expressing their opinions on history subject of class XII MIA of Senior High School Jalancagak. It is shown based on of several indicators that have been formulated, in addition this method can be used as an alternative solution to overcome the problem of learning history found in the classroom

From signal transduction to targeted therapy : interference with TGF-_ and myostatin signaling for Duchenne muscular dystrophy

Nonsense mutations in the gene encoding dystrophin cause Duchenne muscular dystrophy (DMD), a lethal and debilitating neuromuscular disorder. Dystrophin is an important muscle structural protein that protects muscle membrane from contraction-induced damage. Therefore, in the absence of dystrophin, the integrity of muscle fibers will be compromised and severe degeneration will take place. When the regeneration process mediated by satellite cells can no longer compensate, muscle fibers is eventually replaced by connective or fibrotic tissue, leading to the loss of muscle function. Multiple stages in DMD pathology are associated with the Transforming Growth Factor (TGF)-_ signaling pathway (Chapter 1). The TGF-_ superfamily consists of more than 30 secreted proteins including TGF-_, bone morphogenetic protein (BMP), activin/inhibins and growth and differentiation factor (GDF). These proteins regulate many biological processes, such as cell growth and differentiation, and maintain homeostasis during development and in multiple adult tissues. To elicit these diverse physiological responses, a fairly simple and yet powerful signaling pathway is utilized by the TGF-_ family members. The basic signaling engine consists of two receptor serine/threonine kinases, termed receptor types I and II, and intracellular Smad proteins. The ligand assembles a receptor complex that activates Smad proteins, which will assemble multisubunit complexes that regulate transcription. Two general steps thus actually suffice to carry the TGF-_ stimuli to target genes. How can such a simple system mediate a variety of cell-specific gene response? It is now apparent that TGF-_ signaling pathways have equally important extracellular and intracellular control mechanism. This includes myostatin (GDF-8), one of the members that is highly expressed in skeletal muscle. In addition to being a negative regulator of myoblast differentiation, myostatin also plays role in adipogenesis, skeletal muscle fibrosis and myometrial cell proliferation. Genetic mutation of myostatin leads to a remarkable increase of muscle mass, but, as myostatin is found in the circulation, effects on other tissues are somehow expected. We hypothesized that such remarkable effects of myostatin in the muscle are controlled by a unique modulatory mechanism. Indeed, we found that myostatin signaling in myogenic and non myogenic cells are conferred by different utilization of type I receptors, which are also termed activin receptor-like kinases (ALKs), and co-receptor (Chapter 2). In myogenic cells, myostatin signaling is dependent on activin receptor-like kinase-4 (ALK4), whereas ALK5 is utilized in non myogenic cells. Furthermore, we found that the ALK4-dependent myostatin signaling in muscle is largely conferred by a membrane-associated co-receptor Cripto, which is predominantly expressed in myogenic cells but absent in non muscle cells. Moreover, Cripto has different influences on TGF-_ family members that play a role in muscle, i.e. myostatin, activin and TGF-_. As such, Cripto may also be an interesting therapeutic target to follow up in the future. As DMD is caused by the lack of dystrophin, one strategy is to bring back dystrophin in the dystrophic muscle. Antisense oligonucleotide (AON)-mediated exon skipping has been used to reframe the mutated DMD gene and restore dystrophin protein synthesis. It will, however, be less effective in the later stage of the disease where fibrosis is already extensive. This thesis explores the possibility of using exon skipping AONs to inhibit several components of the TGF-_ family signaling and blunt their inhibitory effects on muscle regeneration and fibrosis. In Chapter 3, we first used AONs to functionally knockdown myostatin expression. They efficiently downregulate myostatin in vitro, but induce only subtle exon skipping in vivo. Nevertheless, in a relatively straightforward manner, we were able to combine myostatin and dystrophin AONs and induce exon skipping of both genes without functional interference. This provides a conceptual foundation for a combinatorial therapeutic approach, which targets the primary genetic defect and attempts to improve muscle quality. We further sought to use AON to functionally knockdown myostatin and/or TGF-_ receptors ALK4 and/or ALK5 (Chapter 4). This strategy allowed us to target the activity of a broader spectrum of TGF-_ members, including but not limited to myostatin. Administration in dystrophic mice reduces fibrosis in the diaphragm, which is known to be the most affected muscle. Interestingly, combination of both ALK4 and ALK5 inhibition induces most pronounced effects. The beneficial response after targeting ALK4 or ALK5 separately demonstrates the involvement of TGF-_ and activin in DMD pathology. Overall, in addition to its therapeutic potential, the AON-mediated exon skipping approach also enables the dissection of the roles of TGF-_ family members in muscle regeneration and fibrosis, and potentially other aspects of DMD pathology. In summary, this thesis discusses how the inhibition of several members of the TGF-_ signaling pathway has been implicated in ameliorating DMD pathology. Furthermore, it also increases the awareness that more knowledge on how these family members actually play role in (dystrophic) muscle may still be needed. Finally, alteration of TGF-_ signaling components is involved in various diseases with multilayered pathophysiology, including but not limited to other neuromuscular disorders. Thus, the use of AONs has potential therapeutic value for other TGF-_-related disorders and is also important research tools to study the effect of modulation of TGF-_ receptor family members in the different facets of these diseases.Dutch Duchenne Parent Project, GeneTools, LLC., J.E. Jurriaanse Stichting and the Department of Human Genetics, LUMCUBL - phd migration 201

Combination antisense treatment for destructive exon skipping of myostatin and open reading frame rescue of dystrophin in neonatal <i>mdx</i> mice

The fatal X-linked Duchenne muscular dystrophy (DMD), characterized by progressive muscle wasting and muscle weakness, is caused by mutations within the DMD gene. The use of antisense oligonucleotides (AOs) modulating pre-mRNA splicing to restore the disrupted dystrophin reading frame, subsequently generating a shortened but functional protein has emerged as a potential strategy in DMD treatment. AO therapy has recently been applied to induce out-of-frame exon skipping of myostatin pre-mRNA, knocking-down expression of myostatin protein, and such an approach is suggested to enhance muscle hypertrophy/hyperplasia and to reduce muscle necrosis. Within this study, we investigated dual exon skipping of dystrophin and myostatin pre-mRNAs using phosphorodiamidate morpholino oligomers conjugated with an arginine-rich peptide (B-PMOs). Intraperitoneal administration of B-PMOs was performed in neonatal mdx males on the day of birth, and at weeks 3 and 6. At week 9, we observed in treated mice (as compared to age-matched, saline-injected controls) normalization of muscle mass, a recovery in dystrophin expression, and a decrease in muscle necrosis, particularly in the diaphragm. Our data provide a proof of concept for antisense therapy combining dystrophin restoration and myostatin inhibition for the treatment of DMD

New function of the myostatin/activin type I receptor (ALK4) as a mediator of muscle atrophy and muscle regeneration

Skeletal muscle fibrosis and impaired muscle regeneration are major contributors to muscle wasting in Duchenne muscular dystrophy (DMD). Muscle growth is negatively regulated by myostatin (MSTN) and activins. Blockage of these pathways may improve muscle quality and function in DMD. Antisense oligonucleotides (AONs) were designed specifically to block the function of ALK4, a key receptor for the MSTN/activin pathway in skeletal muscle. AON-induced exon skipping resulted in specific Alk4 down-regulation, inhibition of MSTN activity, and increased myoblast differentiation in vitro Unexpectedly, a marked decrease in muscle mass (10%) was found after Alk4 AON treatment in mdx mice. In line with in vitro results, muscle regeneration was stimulated, and muscle fiber size decreased markedly. Notably, when Alk4 was down-regulated in adult wild-type mice, muscle mass decreased even more. RNAseq analysis revealed dysregulated metabolic functions and signs of muscle atrophy. We conclude that ALK4 inhibition increases myogenesis but also regulates the tight balance of protein synthesis and degradation. Therefore, caution must be used when developing therapies that interfere with MSTN/activin pathways

Whole genome sequencing reveals a 7 base-pair deletion in DMD exon 42 in a dog with muscular dystrophy

Dystrophin is a key cytoskeletal protein coded by the Duchenne muscular dystrophy (DMD) gene located on the X-chromosome. Truncating mutations in the DMD gene cause loss of dystrophin and the classical DMD clinical syndrome. Spontaneous DMD gene mutations and associated phenotypes occur in several other species. The mdx mouse model and the golden retriever muscular dystrophy (GRMD) canine model have been used extensively to study DMD disease pathogenesis and show efficacy and side effects of putative treatments. Certain DMD gene mutations in high-risk, the so-called hot spot areas can be particularly helpful in modeling molecular therapies. Identification of specific mutations has been greatly enhanced by new genomic methods. Whole genome, next generation sequencing (WGS) has been recently used to define DMD patient mutations, but has not been used in dystrophic dogs. A dystrophin-deficient Cavalier King Charles Spaniel (CKCS) dog was evaluated at the functional, histopathological, biochemical, and molecular level. The affected dog’s phenotype was compared to the previously reported canine dystrophinopathies. WGS was then used to detect a 7 base pair deletion in DMD exon 42 (c.6051-6057delTCTCAAT mRNA), predicting a frameshift in gene transcription and truncation of dystrophin protein translation. The deletion was confirmed with conventional PCR and Sanger sequencing. This mutation is in a secondary DMD gene hotspot area distinct from the one identified earlier at the 5′ donor splice site of intron 50 in the CKCS breed. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00335-016-9675-2) contains supplementary material, which is available to authorized users

Treating Pediatric Neuromuscular Disorders: The future is now

Pediatric neuromuscular diseases encompass all disorders with onset in childhood and where the primary area of pathology is in the peripheral nervous system. These conditions are largely genetic in etiology, and only those with a genetic underpinning will be presented in this review. This includes disorders of the anterior horn cell (e.g., spinal muscular atrophy), peripheral nerve (e.g., Charcot-Marie-Tooth disease), the neuromuscular junction (e.g., congenital myasthenic syndrome), and the muscle (myopathies and muscular dystrophies). Historically, pediatric neuromuscular disorders have uniformly been considered to be without treatment possibilities and to have dire prognoses. This perception has gradually changed, starting in part with the discovery and widespread application of corticosteroids for Duchenne muscular dystrophy. At present, several exciting therapeutic avenues are under investigation for a range of conditions, offering the potential for significant improvements in patient morbidities and mortality and, in some cases, curative intervention. In this review, we will present the current state of treatment for the most common pediatric neuromuscular conditions, and detail the treatment strategies with the greatest potential for helping with these devastating diseases

From signal transduction to targeted therapy : interference with TGF-_ and myostatin signaling for Duchenne muscular dystrophy

Nonsense mutations in the gene encoding dystrophin cause Duchenne muscular dystrophy (DMD), a lethal and debilitating neuromuscular disorder. Dystrophin is an important muscle structural protein that protects muscle membrane from contraction-induced damage. Therefore, in the absence of dystrophin, the integrity of muscle fibers will be compromised and severe degeneration will take place. When the regeneration process mediated by satellite cells can no longer compensate, muscle fibers is eventually replaced by connective or fibrotic tissue, leading to the loss of muscle function. Multiple stages in DMD pathology are associated with the Transforming Growth Factor (TGF)-_ signaling pathway (Chapter 1). The TGF-_ superfamily consists of more than 30 secreted proteins including TGF-_, bone morphogenetic protein (BMP), activin/inhibins and growth and differentiation factor (GDF). These proteins regulate many biological processes, such as cell growth and differentiation, and maintain homeostasis during development and in multiple adult tissues. To elicit these diverse physiological responses, a fairly simple and yet powerful signaling pathway is utilized by the TGF-_ family members. The basic signaling engine consists of two receptor serine/threonine kinases, termed receptor types I and II, and intracellular Smad proteins. The ligand assembles a receptor complex that activates Smad proteins, which will assemble multisubunit complexes that regulate transcription. Two general steps thus actually suffice to carry the TGF-_ stimuli to target genes. How can such a simple system mediate a variety of cell-specific gene response? It is now apparent that TGF-_ signaling pathways have equally important extracellular and intracellular control mechanism. This includes myostatin (GDF-8), one of the members that is highly expressed in skeletal muscle. In addition to being a negative regulator of myoblast differentiation, myostatin also plays role in adipogenesis, skeletal muscle fibrosis and myometrial cell proliferation. Genetic mutation of myostatin leads to a remarkable increase of muscle mass, but, as myostatin is found in the circulation, effects on other tissues are somehow expected. We hypothesized that such remarkable effects of myostatin in the muscle are controlled by a unique modulatory mechanism. Indeed, we found that myostatin signaling in myogenic and non myogenic cells are conferred by different utilization of type I receptors, which are also termed activin receptor-like kinases (ALKs), and co-receptor (Chapter 2). In myogenic cells, myostatin signaling is dependent on activin receptor-like kinase-4 (ALK4), whereas ALK5 is utilized in non myogenic cells. Furthermore, we found that the ALK4-dependent myostatin signaling in muscle is largely conferred by a membrane-associated co-receptor Cripto, which is predominantly expressed in myogenic cells but absent in non muscle cells. Moreover, Cripto has different influences on TGF-_ family members that play a role in muscle, i.e. myostatin, activin and TGF-_. As such, Cripto may also be an interesting therapeutic target to follow up in the future. As DMD is caused by the lack of dystrophin, one strategy is to bring back dystrophin in the dystrophic muscle. Antisense oligonucleotide (AON)-mediated exon skipping has been used to reframe the mutated DMD gene and restore dystrophin protein synthesis. It will, however, be less effective in the later stage of the disease where fibrosis is already extensive. This thesis explores the possibility of using exon skipping AONs to inhibit several components of the TGF-_ family signaling and blunt their inhibitory effects on muscle regeneration and fibrosis. In Chapter 3, we first used AONs to functionally knockdown myostatin expression. They efficiently downregulate myostatin in vitro, but induce only subtle exon skipping in vivo. Nevertheless, in a relatively straightforward manner, we were able to combine myostatin and dystrophin AONs and induce exon skipping of both genes without functional interference. This provides a conceptual foundation for a combinatorial therapeutic approach, which targets the primary genetic defect and attempts to improve muscle quality. We further sought to use AON to functionally knockdown myostatin and/or TGF-_ receptors ALK4 and/or ALK5 (Chapter 4). This strategy allowed us to target the activity of a broader spectrum of TGF-_ members, including but not limited to myostatin. Administration in dystrophic mice reduces fibrosis in the diaphragm, which is known to be the most affected muscle. Interestingly, combination of both ALK4 and ALK5 inhibition induces most pronounced effects. The beneficial response after targeting ALK4 or ALK5 separately demonstrates the involvement of TGF-_ and activin in DMD pathology. Overall, in addition to its therapeutic potential, the AON-mediated exon skipping approach also enables the dissection of the roles of TGF-_ family members in muscle regeneration and fibrosis, and potentially other aspects of DMD pathology. In summary, this thesis discusses how the inhibition of several members of the TGF-_ signaling pathway has been implicated in ameliorating DMD pathology. Furthermore, it also increases the awareness that more knowledge on how these family members actually play role in (dystrophic) muscle may still be needed. Finally, alteration of TGF-_ signaling components is involved in various diseases with multilayered pathophysiology, including but not limited to other neuromuscular disorders. Thus, the use of AONs has potential therapeutic value for other TGF-_-related disorders and is also important research tools to study the effect of modulation of TGF-_ receptor family members in the different facets of these diseases

TEKNIK PERMAINAN “TEMPEL HURUF” UNTUK MENINGKATKAN PENGUASAAN HURUF HIRAGANA (Studi Eksperimen pada Siswa Kelas XI Ekstrakurikuler Bahasa Jepang SMK Negeri I Bandung Tahun Akademik 2007/ 2008)

Permasalahan awal diadakannya penulisan ini adalah adanya anggapan bahwa huruf hiragana dianggap sebagai materi pelajaran bahasa Jepang yang cukup sulit untuk dikuasai. Padahal huruf hiragana merupakan salah satu materi awal yang penting untuk dipelajari dalam bahasa Jepang. Dalam penelitian ini, agar pembelajaran huruf hiragana menjadi lebih menarik dan menyenangkan, penulis menerapkan permainan “Tempel Huruf”. Permainan ini merupakan permainan sederhana yang dapat memberikan dampak positif terhadap pembelajaran huruf hiragana. Huruf hiragana yang diulang untuk dipelajari dalam penelitian ini adalah huruf hiragana a - n. Penulisan ini bertujuan untuk mengetahui : tingkat kemampuan siswa dalam penguasaan huruf hiragana sebelum dan sesudah diterapkannya permainan ”Tempel Huruf”, hasil dari penerapan permainan ”Tempel Huruf” pada pembelajaran huruf hiragana, tanggapan dan kesan siswa terhadap permainan ”Tempel Huruf”. Penelitian ini menggunakan metode eksperimen. Jenis eksperimen yang digunakan adalah Pre Experimental Design, dengan model “One-group-before-after (Pre-test post-test design)”. Penelitian ini diadakan pada siswa kelas XI SMK Negeri I Bandung yang mengikuti ekstrakurikuler bahasa Jepang yang berjumlah 10 orang. Setelah menerapkan metode pembelajaran dengan menggunakan permainan ”Tempel Huruf” dan menganalisis data hasil penelitian, dapat diambil kesimpulan bahwa : nilai rata-rata siswa sebelum diterapkannya permainan ”Tempel Huruf” = 65,2, nilai rata-rata siswa sesudah diterapkannya permainan ”Tempel Huruf” = 88,8, hasil dari penerapan permainan ”Tempel Huruf” cukup memuaskan, siswa beranggapan bahwa permainan “Tempel Huruf” menyenangkan dan dapat membantu dalam mempelajari huruf hiragana, sehingga mereka pun beranggapan bahwa penerapan permainan “Tempel Huruf” penting dalam mempelajari huruf hiragana. Dari hasil penelitian tersebut, maka penulis beranggapan bahwa permainan ”Tempel Huruf” merupakan permainan yang cukup bagus, yang dapat memberikan dampak positif terhadap pembelajaran huruf hiragana, dapat menjadikan suasana belajar lebih enyenangkan dan dapat meningkatkan tingkat penguasaan siswa

PENGARUH BEBAN PAJAK PENGHASILAN, ARUS KAS OPERASI, ARUS KAS INVESTASI DAN ARUS KAS PENDANAAN TERHADAP KEIKUTSERTAAN REVALUASI ASET TETAP (PMK RI NOMOR 191 DAN NOMOR 233 TAHUN 2015) (Studi Empiris pada BUMN yang terdaftar di Bursa Efek Indonesia Tahun 2013-2016)

Penelitian ini dilakukan untuk menguji secara empiris pengaruh variabel beban pajak penghasilan, arus kas aktivitas operasi, arus kas aktivitas investasi, dan arus kas aktivitas pendanaan perusahaan terhadap keikutsertaan revaluasi aset tetap (PMK RI Nomor 191 dan Nomor 233 Tahun 2015). Penelitian ini dilakukan terhadap perusahaan badan usaha milik negara yang terdaftar di Bursa Efek Indonesia. Penelitian ini menggunakan metode purposive sampling dengan kriteria perusahaan badan usaha milik negara yang terdaftar pada tahun 2013-2016 yang melakukan revaluasi aset tetap dan tidak melakukan revaluasi aset tetap. Berdasarkan data tersebut diperoleh sebanyak 7 perusahaan yang melakukan revaluasi aset tetap dari total sebanyak 20 perusahaan yang terdaftar. Data diperoleh dari data sekunder dari Bursa Efek Indonesia. Penelitian ini menggunakan analisis regresi logistik. Hasil analisis menunjukkan bahwa beban pajak penghasilan, arus kas aktivitas operasi, arus kas aktivitas investasi, dan arus kas aktivitas pendanaan tidak berpengaruh terhadap perusahaan dalam keikutsertaan revaluasi aset tetap untuk tujuan perpajakan

PENGGUNAAN MEDIA PEMBELAJARAN E-LEARNING BERBASIS GOOGLE CLASSROOM PADA MATA PELAJARAN EKONOMI

Penggunaan media pembelajaran yang kurang tepat merupakan salah satu faktor rendahnya hasil belajar peserta didik, rendahnya hasil belajar merupakan salah satu masalah dalam kegiatan belajar mengajar. Di lapangan sering dijumpai guru yang dapat menguasai materi belajar dengan baik tetapi tidak dapat melaksanakan kegiatan pembelajaran dengan baik. Penelitian ini dilakukan untuk mengetahui: 1) Perbedaan hasil belajar peserta didik yang menggunakan e-learning berbasis google classroom pada pengukuran awal (pretes) dan pengukuran akhir (posttest) di kelas Eksperimen, 2 Perbedaan hasil belajar peserta didik yang menggunakan media pembelajaran konvensional pada pengukuran awal (pretes) dan pengukuran akhir (posttest) di kelas kontrol. Dan 3) Perbedaan hasil belajar peserta didik yang menggunakan e-learning berbasis google classroom dengan peserta didik yang menggunakan media pembelajaran konvensional pada pengukuran akhir (posttest). Metode Penelitian yang digunakan adalah quasi eksperiment design tipe nonequival control group design. Penelitian dilakukan dengan objek penelitian yang terdiri dari 2 kelas. Adapun teknik analisis data yang digunakan adalah uji F dan uji t. Hasil penelitian menunjukkan bahwa: pertama, terdapat Perbedaan hasil belajar peserta didik yang menggunakan e-learning berbasis google classroom pada pengukuran awal (pretes) dan pengukuran akhir (posttest) di kelas Eksperimen. Kedua, terdapat perbedaan hasil belajar peserta didik yang menggunakan media pembelajaran konvensional pada pengukuran awal (pretes) dan pengukuran akhir (posttest) di kelas kontrol. Dan ketiga, terdapat perbedaan hasil belajar peserta didik yang menggunakan e-learning berbasis google classroom dengan peserta didik yang menggunakan media pembelajaran konvensional pada pengukuran akhir (posttest)