PENYALAHGUNAAN ASET NEGARA DALAM BENTUK JARINGAN SATELIT UNTUK KEPENTINGAN KORPORASI DIHUBUNGKAN DENGAN UNDANGUNDANG NOMOR 36 TAHUN 1999 TENTANG TELEKOMUNIKASI JO UNDANGUNDANG NOMOR 20 TAHUN 2001 TENTANG TINDAK PIDANA KORUPSI

telekomunikasi sebagaimana dilakukan oleh IM2. IM2 telah menyalahgunakan pita frekuensi 2.1 Ghz, dan secara melawan hukum beroperasi pada jaringan tersebut sehingga menimbulkan kerugian negara. Berdasarkan hal tersebut maka penulis tertarik meneliti, bagaimana Undang-Undang Telekomunikasi jo Peraturan Menteri Komunikasi dan Informatika dan Undang-Undang Tindak Pidana Korupsi mengatur mekanisme pemanfaatan aset negara berupa jaringan satelit, mengapa aset negara berupa jaringan satelit kerap kali disalahgunakan didalam pemanfaatannya oleh korporasi, serta bagaimana upaya yang dapat dilakukan untuk melindungi aset negara dalam bentuk jaringan satelit terhadap penyalahgunaan yang dilakukan oleh korporasi. Penelitian ini menggunakan spesifikasi penelitian yang bersifat deskriftif analitis dengan pendekatan yuridis normatif dibantu yuridis empiris, data yang diperlukan dalam penelitian ini dikumpulkan melalui studi kepustakaan dan studi lapangan, kemudian dianalisis menggunakan teknik analisis data berupa yuridis kualitatif. Pemanfaatan aset negara berupa jaringan satelit melalui pita frekuensi merupakan salah satu hak yang dalam pemanfaatannya diatur oleh peraturan perundang-undangan agar tercipta keadilan, kepastian dan ketertiban, keamanan, keseimbangan, perlindungan dan pemeliharaan dalam pemanfataannya. Jaringan satelit yang merupakan jaringan satelit aset negara pemanfaatannya mensyaratkan izin dan pembayaran tarif tertentu, sehingga konsekuensinya ketika terjadi penyalahgunaan pemanfaatan jaringan satelit, negara akan mengalami kerugian. Aset negara berupa jaringan satelit kerap kali disalahgunakan didalam pemanfaatannya oleh korporasi disebabkan beberapa faktor diantaranya faktor hukum itu sendiri dalam hal ini peraturan perundang-undangannya, faktor penegak hukum, faktor sarana atau fasilitas yang mendukung pengawasan dan penegakan hukum itu sendiri, faktor masyarakat, yakni lingkungan dimana hukum tersebut berlaku atau diterapkan, dalam hal ini yaitu lingkungan korporasi, faktor kebudayaan yakni kurangnya kesadaran hukum korporasi dalam upaya pemanfaatan aset negara secara berkeadilan dan tertib sesuai peraturan perundang-undangan yang berlaku, dimana pemanfaatan yang tidak secara berkeadilan akan membawa negara menuju kepada kehancuran. Upaya yang dapat dilakukan untuk melindungi aset negara dalam bentuk jaringan satelit terhadap penyalahgunaan yang dilakukan oleh korporasi harus berangkat dari beberapa faktor yang menjadi penyebab penyalahgunaan pemanfaatan jaringan satelit diantaranya yaitu melalui upaya preventif berupa revisi perunang-undangan, pengawasan, sosialisasi sert upaya represif berupa penegakan hukum. Penegakan hukum harus dilaksanakan tanpa pandang bulu, sebagai bentuk keyakinan atas doktrin hukum, bahwa setiap orang mempunyai kedudukan yang sama di depan hukum. Kata Kunci: Penyalahgunaan Aset Negara, Jaringan Sateli

Tau PET and relative cerebral blood flow in Dementia with Lewy bodies: A PET study

Purpose: Alpha-synuclein often co-occurs with Alzheimer’s disease (AD) pathology in Dementia with Lewy Bodies (DLB). From a dynamic [18F]flortaucipir PET scan we derived measures of both tau binding and relative cerebral blood flow (rCBF). We tested whether regional tau binding or rCBF differed between DLB patients and AD patients and controls and examined their association with clinical characteristics of DLB. / Methods: Eighteen patients with probable DLB, 65 AD patients and 50 controls underwent a dynamic 130-minute [18F]flortaucipir PET scan. DLB patients with positive biomarkers for AD based on cerebrospinal fluid or amyloid PET were considered as DLB with AD pathology(DLB-AD+). Receptor parametric mapping(cerebellar gray matter reference region) was used to extract regional binding potential (BPND) and R1, reflecting (AD-specific) tau pathology and rCBF, respectively. First, we performed regional comparisons of [18F]flortaucipir BPND and R1 between diagnostic groups. In DLB patients only, we performed regression analyses between regional [18F]flortaucipir BPND, R1 and performance on ten neuropsychological tests. / Results: Regional [18F]flortaucipir BPND in DLB was comparable with tau binding in controls (p>0.05). Subtle higher tau binding was observed in DLB-AD+ compared to DLB-AD- in the medial temporal and parietal lobe (both p<0.05). Occipital and lateral parietal R1 was lower in DLB compared to AD and controls (all p<0.01). Lower frontal R1 was associated with impaired performance on digit span forward (standardized beta, stβ=0.72) and category fluency (stβ=0.69) tests. Lower parietal R1 was related to lower delayed (stβ=0.50) and immediate (stβ=0.48) recall, VOSP number location (stβ=0.70) and fragmented letters (stβ=0.59) scores. Lower occipital R1 was associated to worse performance on VOSP fragmented letters (stβ=0.61), all p<0.05. / Conclusion: The amount of tau binding in DLB was minimal and did not differ from controls. However, there were DLB-specific occipital and lateral parietal relative cerebral blood flow reductions compared to both controls and AD patients. Regional rCBF, but not tau binding, was related to cognitive impairment. This indicates that assessment of rCBF may give more insight into disease mechanisms in DLB than tau PET

Why Pleiotropic Interventions are Needed for Alzheimer's Disease

Alzheimer's disease (AD) involves a complex pathological cascade thought to be initially triggered by the accumulation of β-amyloid (Aβ) peptide aggregates or aberrant amyloid precursor protein (APP) processing. Much is known of the factors initiating the disease process decades prior to the onset of cognitive deficits, but an unclear understanding of events immediately preceding and precipitating cognitive decline is a major factor limiting the rapid development of adequate prevention and treatment strategies. Multiple pathways are known to contribute to cognitive deficits by disruption of neuronal signal transduction pathways involved in memory. These pathways are altered by aberrant signaling, inflammation, oxidative damage, tau pathology, neuron loss, and synapse loss. We need to develop stage-specific interventions that not only block causal events in pathogenesis (aberrant tau phosphorylation, Aβ production and accumulation, and oxidative damage), but also address damage from these pathways that will not be reversed by targeting prodromal pathways. This approach would not only focus on blocking early events in pathogenesis, but also adequately correct for loss of synapses, substrates for neuroprotective pathways (e.g., docosahexaenoic acid), defects in energy metabolism, and adverse consequences of inappropriate compensatory responses (aberrant sprouting). Monotherapy targeting early single steps in this complicated cascade may explain disappointments in trials with agents inhibiting production, clearance, or aggregation of the initiating Aβ peptide or its aggregates. Both plaque and tangle pathogenesis have already reached AD levels in the more vulnerable brain regions during the “prodromal” period prior to conversion to “mild cognitive impairment (MCI).” Furthermore, many of the pathological events are no longer proceeding in series, but are going on in parallel. By the MCI stage, we stand a greater chance of success by considering pleiotropic drugs or cocktails that can independently limit the parallel steps of the AD cascade at all stages, but that do not completely inhibit the constitutive normal functions of these pathways. Based on this hypothesis, efforts in our laboratories have focused on the pleiotropic activities of omega-3 fatty acids and the anti-inflammatory, antioxidant, and anti-amyloid activity of curcumin in multiple models that cover many steps of the AD pathogenic cascade (Cole and Frautschy, Alzheimers Dement 2:284–286, 2006)

Structural neuroimaging of Alzheimer's disease and other dementias

This paper reviews the use of imaging techniques to aid in the clinical diagnosis of dementia. Two approaches are distinguished. One is the exclusionary approach in which imaging is used to rule out diseases that would mimic or cause dementia; based on the literature, this approach yields very little, if any, information that was not identified clinically. The more positive approach uses imaging as a diagnostic tool to identify changes specific for causes of dementia; any assessment of medial temporal lobe atrophy on Magnetic Resonance Imaging (MRI) will result in a reasonably high positive likelihood ratio distinguishing AD patients from non-demented individuals, but fails to distinguish AD patients from patients with other dementias. For a diagnosis of vascular dementia imaging is necessary, although not all vascular changes fulfill requirements of being relevant to dementia. Potentially of more importance, given the higher prevalence of AD, is the identification of concomitant vascular changes in AD that may be amenable to therapy, and may be used to identify subgroups. Structural and functional MRI techniques have great potential in identifying patients at risk for AD, which will allow for a very early treatment with drugs that slow or even halt progression

Dementia: The role of CT/MRI in clinical practice

This paper reviews that use of imaging techniques to aid in the clinical diagnosis of dementia. Using CT/MRI only for exclusion of treatable disease may yield very little, if any, information that was not identified clinically. Using MRI/CT as a diagnostic tool to identify changes specific for causes of dementia may be more productive. Any assessment of medial temporal lobe atrophy on MRI will result in a reasonably high positive likelihood ratio distinguishing AD patients from non-demented individuals but fails to distinguish AD patients from patients with other dementias. For a diagnosis of vascular dementia imaging is necessary, although not all vascular changes fulfil requirements of being relevant dementia. Potentially of more importance, given the higher prevalence of AD, is identifying concomitant vascular changes in AD that may be amenable to therapy and may be used to identify subgroups