Konsepsi Penggantian Kerugian Atas Pemberian Izin Mendirikan Bangunan (Imb) yang Tidak Sesuai dengan Rtrw (Kajian terhadap Pasal 37 Undang-undang No.26 Tahun 2007 Tentang Penataan Ruang)

Pasal 37 Ayat (4),(5) dan (8) Undang-undang No.26 Tahun 2007 Tentang Penataan Ruang mengatakan bahwa IMB harus mengikuti konsep perencanaan yang tertera pada Rencana Tata Ruang Wilayah (RTRW) di setiap daerah dan apabila diketahui IMB tersebut melanggar RTRW maka harus dibatalkan dan dimungkinkan adanya pemberian ganti rugi atas pembatalan IMB tersebut. Fenomena yang terjadi saat ini adalah belum jelas dan belum konkretnya aturan yang ada terkait dengan konsepsi ganti rugi sehingga menyulitkan pihak-pihak yang ingin mengajukan upaya hukum melalui sarana hukum yang paling tepat dan efisien. Berdasarkan penelitian ini, penulis menawarkan sarana hukum administrasi karena dianggap yang paling efektif dan jelas dalam menyelesaikan permasalahan IMB yang dilakukan pembatalan, dikarenakan IMB merupakan Keputusan Tata Usaha Negara (KTUN) yang apabila bermasalah sudah terakomodasi di Pengadilan Tata Usaha Negara, sesuai dengan kompetensinya dan yang paling penting adalah gugatan yang dilakukan, terhadap subjek kewenangan yaitu pejabatnya bukan pribadi dari pejabat tersebut yang bertanggung jawab terhadap kesalahan-kesalahan yang berkaitan dengan ketidaksesuaiannya IMB dengan RTRW. Maka, penulis mengusulkan konsepsi penggantian atas kerugian yang diderita oleh investor atau masyarakat dengan melalui mekanisme penggantian yang dibebankan pada pemerintah daerah melalui Anggaran Pendapatan dan Belanja Daerah (APBD). Sehingga diharapkan dapat mengembalikan hakikat tujuan dan manfaat dari IMB.Kata Kunci : Izin Mendirikan Bangunan (IMB), Rencana Tata Ruang Wilayah (RTRW), Upaya Hukum Administrasi, Ganti Rugi

Benzo- and Naphthopentalenes: Syntheses, Structures, and Properties

Benzo- and naphthopentalene derivatives were synthesized, and the effects of structural variations on their antiaromaticity and optoelectronic and electrochemical properties were examined experimentally and theoretically in detail. The results unveiled that with increasing the bond order of the carbon–carbon bond ([5,6] junction) shared by the pentalene and aromatic moieties, the 8π antiaromatic character of pentalene is enhanced and the HOMO–LUMO gap is decreased, which accompanies both the elevation of the HOMO level and the lowering of the LUMO level. The ethynylene units between the pentalene skeleton and the phenyl groups proved to extend π-conjugation sufficiently

Benzo- and Naphthopentalenes: Syntheses, Structures, and Properties

Benzo- and naphthopentalene derivatives were synthesized, and the effects of structural variations on their antiaromaticity and optoelectronic and electrochemical properties were examined experimentally and theoretically in detail. The results unveiled that with increasing the bond order of the carbon–carbon bond ([5,6] junction) shared by the pentalene and aromatic moieties, the 8π antiaromatic character of pentalene is enhanced and the HOMO–LUMO gap is decreased, which accompanies both the elevation of the HOMO level and the lowering of the LUMO level. The ethynylene units between the pentalene skeleton and the phenyl groups proved to extend π-conjugation sufficiently

AAV9 vector-mediated GFP expression in the marmoset brain.

<p>AAV9 vectors expressing GFP under the control of the 0.3-kb cjGFAP promoter were injected into the cerebral and cerebellar cortices. (A and B) Bright field images of the marmoset whole brain overlaid with GFP fluorescence. (C and D) Bright field images of the sagittal sections of the cerebellar (C) and cerebral (D) hemispheres are presented with GFP fluorescence. Scale bars, 2 mm.</p

High specificity of the 0.3-kb cjGFAP promoter for astrocytes in the mouse cerebellum.

<p>(A) Shema depicting Purkinje cell (PC) and Bergmann glia (BG) in the cerebellar cortex. Cell bodies of Bergmann glia are present in the Purkinje cell layer (PCL) and extend processes into the molecular layer (ML). GCL; Granule cell layer. (B) A cerebellar section immunolabeled for parvalbumin. Arrows indicate molecular layer interneurons. (C) Cerebellar slices lentivirally expressing GFP under the control of the 1.5 kb mouse GFAP promoter were double-immunostained for GFP and S100 (an astrocyte marker). Arrows and arrowheads indicate cell bodies and the processes of Bergmann glia, respectively. GFP expression was observed in Bergmann glia, but not in Purkinje cells (P). (D-I) Cerebellar slices lentivirally expressing GFP under the control of different lengths of the marmoset GFAP promoter were double-immunostained for GFP and S100. Arrows in (I) indicate GFP-positive interneurons in the molecular layer. Scale bars, 50 μm. (J) Quantitative analysis of astrocyte specificity of the marmoset GFAP promoter fragments. More than 500 GFP-positive cells from 3 mice (3 slices/mouse) were randomly selected in each group, and the ratio of S100-labeled astrocytes was determined in these random selections. Asterisks and daggers indicate statistically significant differences compared with the cerebella expressing GFP under the control of the 2.0-kb promoter (asterisks) or the 0.3-kb promoter (daggers), as determined by one-way ANOVA followed by Tukey’s post hoc test, ***<i>p</i><0.001 and ††<i>p</i><0.01.</p

Absence of astrocyte specificity for the marmoset- and human-derived GFAP promoters in the mouse cerebrum.

<p>(A-C) Cerebral slices lentivirally expressing GFP under the control of the 0.3-kb marmoset-derived cjGFAP (A), 0.3-kb mouse-derived mGFAP (B) or 0.3-kb human-derived hGFAP (C) promoter were triple-immunostained for GFP (green), GFAP (magenta) and NeuN (a neuronal marker, cyan). Note the predominant expression of GFP in neurons (arrow) by the marmoset- and human-derived promoter, which is in sharp contrast to the astrocyte-specific expression (arrowhead) by the mouse-derived promoter. Scale bars, 50 μm. (D) Schema depicting morphology of neuron and astrocyte in the cerebral cortex. (E) Quantitative analysis of the astrocyte specificity for the cjGFAP, mGFAP and hGFAP promoters. More than 300 GFP-positive cells from 3 mice (3 slices/mouse) were randomly selected, and the ratio of GFAP-labeled astrocytes were determined in these random selections. Asterisks indicate statistically significant differences between the mouse promoter and the marmoset or human promoter, as determined by one-way ANOVA followed by Tukey’s post hoc test, ***<i>p</i><0.001.</p

Summary of hfMSC transplantation into the cerebellum of SCA1 mice.

<p>Summary of hfMSC transplantation into the cerebellum of SCA1 mice.</p

Degeneration of PC and molecular layer interneurons.

<p>(a, b) Fluorescence images of the cerebellar cortex immunostained for parvalbumin from a 6-month-old wild-type mouse (WT) (a) and an age-matched SCA1 mouse (B05) (b). Black and white arrows show examples of PCs and interneurons, respectively. Scale bar, 50 μm. (c, d) Graphs showing the size of cell bodies of interneurons (WT; n = 110 cells from 3 mice, B05; n = 140 cells from 4 mice) (c) and of PCs (WT; n = 81 PCs from 3 mice, B05; n = 80 PCs from 4 mice) (d). Asterisks indicate a statistically significant difference between the wild-type mice and SCA1 mice; ***<i>p</i><0.001 by unpaired <i>t</i>-test.</p

GFP expression in PCs and putative interneurons after grafting hfMSCs carrying the inverted GFP gene to the SCA1 mouse cerebellum.

<p>(a) Schema depicting the FLEx-Tet system, which permitted us to explore the fusion of hfMSCs with cerebellar neurons. An AAV9-SynImCMV-HA-mtTA-P2A-Cre vector expressing HA-tagged mtTA and Cre through a neuron-specific SynImCMV promoter was injected into the cerebella of 6–8-month-old SCA1 mice (1). A sequence with TRE and inverted GFP genes flanked by loxP and lox2272 was inserted into the genome of hfMSCs by using Lenti-TRE-FLEx-GFP vectors (2). Thus, GFP protein was never produced without Cre recombinase, and the expression increased drastically after co-provision with mtTA. The TRE-FLEx-GFP-hfMSCs (50,000 cells) were then injected into the SCA1 mice 2 weeks after injection of AAV9-SynImCMV-HA-mtTA-P2A-Cre vectors (3). (b-g) Emergence of GFP-expressing neurons in the cerebella of mice that were sacrificed 2 weeks after the TRE-FLEx-GFP-hfMSC injection. The cerebellar slices were immunolabeled for GFP and calbindin, a PC marker. GFP expression was detected in PCs (b, e-g) and cells in the molecular layer (c, d). Arrows in (e-g) indicate a GFP-expressing PCs co-immunostained for calbindin. Because we used a neuron-specific synapsin I promoter with a minimal CMV sequence, Cre and mtTA should have been expressed specifically in neurons, and thus the GFP-expressing cells in the molecular layer (c, d) were presumed to be basket cells (c) and stellate cells (d). Scale bar, 50 μm.</p

Emergence of GFP-expressing PCs in SCA1 mouse cerebella after transplantation of TRE-GFP-hfMSCs expressing GFP through the Tet-off system.

<p>(a) The TRE-GFP gene was introduced into hfMSCs through a lentivirus (1). The transduced TRE-GFP-hfMSCs were injected into the cerebella of 6–8-month-old SCA1 mice (2). Two weeks after the TRE-GFP-hfMSC injection, the SCA1 mice received an injection of AAV9-L7-HA-mtTA vectors expressing HA-tagged mtTA under the control of a PC-specific L7 promoter (3). (b) Schema depicting GFP expression in PCs expressing mtTA. TRE in the nucleus of TRE-GFP-hfMSCs initiated the transcription of the downstream GFP gene in the presence of mtTA, which was produced only in AAV9-L7-HA-mtTA-infected PCs. (c, d) Immunohistochemistry of cerebellar slices from SCA1 mice treated as shown in the schema (a). The mice were sacrificed 10 weeks after the hfMSC grafting. The slices were double immunolabeled for HA and GFP. HA-tagged mtTA (magenta) was efficiently expressed only in PCs, and some PCs co-expressed GFP (green). (e, f) Enlarged images of PCs immunostained for GFP. Scale bars, 200 μm (c) and 50 μm (d-f).</p