تطوير المواد الدراسية في تعليم مهارة الكتاب في برنامج الخاض لتعليم اللغة العربية في جامعة مولانا مالك ابراهم الإسلامية الحكومية مالانج

ABSTRAK Perkembangan Universitas Islam Negeri Maulana Malik Ibrahim Malang sebagai salah satu Perguruan Tinggi Islam yang berkembang pesat membutuhkan terobosan- terobosan yang handal. Salah satu hal penting yang tidak bisa dipisahkan adalah peranan penting dari PKPBA (Program Khusus Pengembangan Bahasa Arab). PKPBA sebagai sebuah unit pengembangan bahasa, telah berperan penting dalam membantu meningkatkan kemampuan berbahasa mahasiswa khususnya bahasa arab. Banyak dari mahasiswa yang pertama kali masuk PKPBA belum mengetahui bahasa Arab. Namun setelah belajar di PKPBA mereka mampu mengenal ilmu bahasa arab. Namun, tidak hanya berhenti pada mengetahui bahasa arab saja, program ini juga berupaya agar semua mahasiswa mampu untuk menguasai salah satu dari 4 ketrampilan bahasa yakni ketrampilan menulis. Tujuan dari peneliyian ini adalah untuk melengkapi proses pengembangan penyusunan materi ajar menulis dan mengetahui ke-efektifan materi yang dikembangkan. Penelitian ini menggunakan prosedur eksperimen dimana peneliti mendisain Pre-test dan Postest terhadap dua kelompok yakni kelompok eksperimen dan kelompok kontrol. Hasil penelitian ini adalah bahwa pembelajaran ketrampilan menulis dengan menggunakan buku ajar lebih efektif dari pada tanpa menggunakan buku ajar. Dengan indikasi bahwa t-test kelas eksperimen (J3) lebih efektif dengan indikasi bahwa t-test kelas kontrol adalah 3,4. dimana hasil ini lebih besar dari pada tingkat t-table 5% 2,059 dan tingkat 1% 2,787. Dari hasil ini menunjukan bahwa pengajaran menulis bahasa Arab efektif dengan menggunakan materi ajar yang telah disusun oleh peneliti. Hasil penelitian ini adalah: (1) Penyusunan materi ajar untuk PKPBA dimulai dengan membatasi tujuan pengajaran, kemudian menentukan pembagian materi sesuai dengan jumlah hari yang digunakan untuk pembelajaran dalam satu minggu. (2) Pembelajaran menulis bahasa Arab dengan menggunakan Materi ajar ini dinyatakan efektif. Dari hasil yang disebutkan diatas, sudah semestinya materi pengajaran menulis bahasa Arab dapat dimanfaatkan dengan benar dalam proses pengajaran, selain itu penulis berharap agar penelitian ini menjadi referensi untuk penelitian lanjutan yang berhubungan dengan penelitian ini sehingga dapat dikembangkan ke dalam desain materi ajar menulis untuk tingkat selanjutnya. ABSTRACT The expansion of State Islamic University Maulana Malik Ibrahim need some powerful breakthrough. One of the important things is the role of Intensive Arabic Program as unit for improving Arabic, have played an important for helping Arabic language improvement. Most of the students when the first time they enter to this Program, they haven’t yet Arabic knowledge. But after studying in this program for several months they could understand about Arabic. But is not enough in knowing the Arabic only, but this program also try to make all students are mastering one of these four skills, that is writing skill. This research aims at designing process of writing teaching material and finding out the effectiveness of writing teaching material using in Intensive Arabic Program of State Islamic University of Maulana Malik Ibrahim Malang. This research uses the experimental method that the researcher design pre-test and post-test for both groups (Experiment and Control group). This research reach the degree of t-test 3,4 this biggest than t-table at the level of 5% (2,059) and at the level 1% (2,787). This indicates that the use of writing Teaching Material in Arabic for improving writing skill is effective. And the result of this research are obtained bellow: (1) Preparing this teaching material process started by determining the goals, finding out the learning material based on the days in a week which used for teaching (2) The use of writing Teaching Material in Arabic for improving writing skill is effective. Based on these results, teaching material must be used as good as possible in teaching process. Besides, the researcher hopes that the research becomes the reference for further researchers which have a relation with this chapter and could be developed to other teaching material for advance grade

Functional Synergy between Cholecystokinin Receptors CCKAR and CCKBR in Mammalian Brain Development

<div><p>Cholecystokinin (CCK), a peptide hormone and one of the most abundant neuropeptides in vertebrate brain, mediates its actions via two G-protein coupled receptors, CCKAR and CCKBR, respectively active in peripheral organs and the central nervous system. Here, we demonstrate that the CCK receptors have a dynamic and largely reciprocal expression in embryonic and postnatal brain. Using compound homozygous mutant mice lacking the activity of both CCK receptors, we uncover their additive, functionally synergistic effects in brain development and demonstrate that CCK receptor loss leads to abnormalities of cortical development, including defects in the formation of the midline and corpus callosum, and cortical interneuron migration. Using comparative transcriptome analysis of embryonic neocortex, we define the molecular mechanisms underlying these defects. Thus we demonstrate a developmental, hitherto unappreciated, role of the two CCK receptors in mammalian neocortical development.</p></div

Defects in cortical development in <i>Cckar/br</i> mutant mice.

<p>(A and B) Nissl staining of coronal sections of control and <i>Cckar/br</i> mutant brains at postnatal day 14 (P14) reveals thickening of the cingulate cortex, agenesis of the corpus callosum, and lateral displacement of the hippocampus. (C and D) In situ hybridization with <i>claudin 11</i>, which is expressed in myelinated oligodentrocytes thus highlighting white matter tracts, shows that the commissural axons of the corpus callosum do not cross to the contralateral hemisphere in <i>Cckar/br</i> mutants (D) compared to control (C). Of a total of 16 brains from <i>Cckar/br</i> mutants that were fully sectioned and analyzed for callosal development, 13 had complete and 3 had partial agenesis of the corpus callosum. Scale bar, 100 μm. (E and F) Labeling of callosal projections with DiI shows that colossal axons fail to cross the midline in <i>Cckar/br</i> double mutants (F). Green lines (in E,F) and asterisk (in F) indicate the midline and Probst bundles, respectively. Scale bar, 200 μm.</p

Pathway analysis (Ingenuity.com) of RNA-Seq data.

<p>Pathway analysis (Ingenuity.com) of RNA-Seq data.</p

Validation of comparative transcriptional profiling findings.

<p>(A-D) <i>Cxcl12</i>, encoding a chemokine that is a known attractant for tangentially migrating interneurons, is downregulated (fold change: -2.104, p = 6.14E-08) in <i>Cckar/br</i> mutants. In situ hybridization demonstrates a reduction in <i>Cxcl12</i> transcripts in the SVZ (arrows) of mutant embryos compared to controls at E14.5 (A,B) and E17.5 (C,D). (E and F) <i>Bmp7</i>, encoding a secreted protein, is also downregulated (fold change: -2.092, p = 2.13E-03) in <i>Cckar/br</i> mutants. Arrows indicate lower expression levels of <i>Bmp7</i> in the midline of the mutants. Scale bar, 200 μm. (G-L) <i>Nrp2</i>, encoding the neuropilin 2 receptor, is upregulated (fold change: 1.510, p = 3.29E-04) in the <i>Cckar/br</i> mutants (H,J,L) compared to controls (G,I,K). The sections shown are at three different rostro-caudal levels (G and H, I and J, K and L). Arrows point to areas of differential expression levels of <i>Nrp2</i>, expanded in the mutants. Scale bar, 200 μm.</p

Defects in tangentially migrating interneurons in <i>Cckar/br</i> mutants.

<p>(A,B,E,F) Interneuron progenitors are generated normally in <i>Cckar/br</i> mutant embryos compared to controls, as demonstrated by in situ hybridization with <i>Gad1</i> (A,B) and <i>Lhx6</i> (E,F). However their tangential migration appears delayed in the mutants. Arrows in (A,B) indicate the onset of tangential routes employed by migrating interneurons. Note a delay/reduction in tangential migration in <i>Cckar/br</i> mutants. Red marks in (E,F) indicate the extent of tangential migration (deep route) in the neocortex. Scale bar (B,D), 200 μm. (C,D,G,H) In situ hybridization with <i>Gad1</i> and <i>Lhx6</i> at birth (P0, C,D) or late embryogenesis (E17.5, G,H) demonstrates that despite the delay in migration, a majority of interneurons settle into the neocortex. Scale bar (F,H), 200 μm.</p

Neuronal migration defects in <i>Cckar/br</i> mutants.

<p>(A-F) In situ hybridization with markers of cortical interneurons at P7: <i>Gad1</i> (A,B) (a general interneuron marker); <i>Lhx6</i> (C,D) (a marker of MGE-derived interneurons); and <i>reelin</i> (E,F) (a marker of CGE- and pre-optic area derived interneurons) indicates a significant overall reduction of interneurons in <i>Cckar/br</i> mutants, irrespective of their origin. Scale bar, 200 μm. (G) Quantification of <i>Lhx6-</i>expressing interneurons. <i>Cckar/br</i> mutants have a 26% reduction in MGE-derived cortical interneurons at P7 (p = 0.0160, n = 3). (H) Distribution of <i>Lhx6-</i>expressing interneurons. Despite the reduction in their number, cortical interneurons are distributed in a similar fashion in control and <i>Cckar/br</i> mutant neocortex, suggesting that interneurons that successfully completed tangential migration are able to respond to local cues in the neocortex and settle into their final position. The fraction of <i>Lhx6-</i>positive interneurons per bin is similar in control and <i>Cckar/br</i> mutant neocortices (p is at least > 0.15 for all comparisons, n = 3). (I) Quantification of <i>reelin</i>-expressing interneurons. <i>Cckar/br</i> mutants have a 15% reduction in CGE- and POA-derived cortical interneurons at P7 (p = 0.0226, n = 4). Error bars represent s.e.m.</p

Abnormal differentiation of the midline in <i>Cckar/br</i> mutant embryos.

<p>(A-F) In situ hybridization with <i>Gfap</i>, a marker of midline glia at perinatal stages, reveals that two midline cell populations, the induseum griseum (IG) and midline zipper glia (mzg), are reduced in <i>Cckar/br</i> double mutants (D-F) compared even with <i>Cckar^+/-;Cckbr^+/-</i> double heterozygous embryos (A-C) at E17.5. Expression of <i>Gfap</i> at the glial wedge (gw) does not appear to be affected to the same extent, suggesting defective differentiation of the midline. Scale bar, 200 μm. (G and H) In situ hybridization with <i>Tag1</i>, a marker of commissural neurons, which also marks the subcallosal sling (scs), demonstrates that a continuous sling is present in control <i>Cckbr^+/-</i> pups (G) at P0, but it fails to transverse the gap between the two hemispheres in <i>Cckar/br</i> mutants (H). Scale bar, 200 μm. (I-N) In situ hybridization demonstrates a modest increase in <i>Cckbr</i> transcripts in the ventral hypothalamus of <i>Cckar</i> single mutants (J,L,N) compared with wild type (I,K,M) at P14. The sections shown are at three different rostro-caudal levels. Scale bar, 0.5 mm.</p

Select transcripts identified by comparative transcriptional profiling.

<p>Select transcripts identified by comparative transcriptional profiling.</p

Expression of CCK and its receptors in mouse and human brain.

<p>(A, B) <i>Cckar</i> is highly expressed in the developing mouse brain at E13.5, contrary to <i>Cckbr</i> mRNA, which is barely detectable at this stage. Scale bar, 200 μm. (C) Select embryonic cells express <i>Cck</i> at E15.5. Scale bar, 500 μm (D and E) Expression of <i>CCKBR</i> (D) and <i>CCK</i> (E) in human fetal neocortex at 20 gestational weeks. Both transcripts are detected in the developing cortical plate (cp); <i>CCK</i> is also expressed in the marginal zone (mz). Scale bar, 0.5 mm. (F-H) By the second postnatal week, <i>Cckar</i> becomes restricted to the hippocampus and select extracortical sites, whereas <i>Cckbr</i> is highly expressed in the neocortex; <i>Cck</i> is also robustly expressed in the neocortex, hippocampus and thalamic nuclei. Scale bar, 100 μm. Note the opposite trends in expression levels of the two receptors at embryonic and postnatal stages. (I and J) Expression of <i>CCKBR</i> (I) and <i>CCK</i> (J) in human adult cortex (temporal lobe). Both transcripts are detected throughout all cortical layers with <i>CCK</i> being more robustly expressed. Scale bar, 0.5 mm.</p