STRATEGI PESAN DALAM UPAYA MEMPERTAHANKAN CITRA PARIWISATA KABUPATEN BANTUL (Pesan pada Media Booklet, Leaflet, Company Profile, Kalender Event, Spanduk, Dinas Kebudayaan dan Pariwisata Kabupaten)

Perkembangannya kini Pariwisata menjadi suatu industri yang mengalami pertumbuhan pesat di seluruh dunia. Pariwisata berangsur-angsur telah mengalami perubahan dari suatu kebutuhan sekunder menjadi suatu kebutuhan pokok. Pariwisata Indonesia kini mulai banyak diminati oleh wisatawan, baik domestik maupun mancanegara. Pertumbuhan ini dimanfaatkan oleh Disbudpar Kabupaten Bantul dalam mengenalkan Pariwisata yang ada di Bantul. Disbudpar Kabupaten Bantul menggunakan media nirmassa sebagai alat membentuk, mempertahankan serta meningkatkan kunjungan wisatawan. Media nirmassa yang digunakan yaitu Booklet, company profile, dan kalender event. Penelitian ini merupakan penelitian deskriptif kualitatif. Tujuan dari penelitian ini untuk mengetahui strategi pesan pada media dan kaitannya dalam upaya mempertahankan citra. Menentukan sebuah strategi pesan haruslah mementingkan aspek- aspek dalam sebuah pesan seperti yang disampaikan oleh Cutlip, Center & Broom bahwa pesan dapat menghasilkan efek yang kuat, walaupun tidak dapat dijelaskan berdasarkan sebab- akibat langsung dan sederhana. Melalui beberapa bentuk metode pesan yaitu repetition, canalizing informative, persuasif, edukatif, coersive pesan disampaikan. Kemudian Susunan penyajian (order presentation), pernyataan kesimpulan (drawing conclusion) dan didukung oleh daya tarik visual yang meliputi warna, dan ilustrasi. Berdasarkan pada temuan lapangan dan analisis yang diperoleh dengan melakukan wawancara dan menganalisis media-media yang digunakan Disbudpar Kabupaten Bantul. Membuat sebuah strategi didalam sebuah pesan sudah dilakukan oleh Disbudpar secara sederhana dengan mengangkat sebuah pesan yang memiliki daya tarik kuat dan dapat menyentuh pada aspek sosial masyarakat menjadi strategi konsep pesan yang ingin disampaikan sebagai penguat citra yang sudah ada yaitu Bantul sebagai kota Budaya. Hasil penelitian menunjukan bahwa strategi pesan Disbudpar berupaya untuk dapat mempertahankkan citra budaya yang melekat pada Kabupaten Bantul dengan mengedepankan pesan yang mengangkat cerita legenda, sejarah, tradisi dan menyentuh pada aspek sosial masyarakat

STRATEGI PESAN DALAM UPAYA MEMPERTAHANKAN CITRA PARIWISATA KABUPATEN BANTUL

Perkembangannya kini Pariwisata menjadi suatu industri yang mengalami pertumbuhan pesat di seluruh dunia. Demikian juga dengan media sebagai sarana informasi wisata, saat ini banyak media yang dipakai untuk menyampaikan pesan-pesan tertentu seperti radio, televisi, maupun media non massa seperti billboard, leafleat, Company Profile, poster. Media- media tersebut menjadi sarana yang mudah di akses oleh khalayak. Citra Pariwisata yang dipertahankan oleh Dinas Kebudayaan dan Pariwisata Kabupaten Bantul melalui berbagai upaya yang dibuat dalam beberapa kegiatan. Kegiatan- kegiatan itulah yang nantinya membantu kinerja Disbudapar dalam mempertahankan citra. Strategi pesan oleh Disbudpar untuk citra dan menarik wisatawan adalah mengutamakan wisata- wisata bersejarah dan wisata yang memiliki keterkaitan erat dengan budaya Jawa dan Keraton Yogyakarta serta wisata alam. Selain itu dalam isi pesan juga terdapat sebuah gambar atau foto yang dimuat dalam media pastilah gambar yang dapat mewakili keindahan dan daya tarik dari sebuah tempat wisata tersebut Tujuan Kabupaten Bantul untuk mempertahankan citra Budaya yang dimiliki di bantu oleh citra yang dimiliki kota Yogyakarta, yang erat pula dengan budaya yang ada. Mengutamakan cerita dan sejarah yang melekat dimasyarakar dijadikan strategi sehingga mampu mempertahankan citra Budaya di Kabupaten Bantul

Mitochondria and Heart Disease

Mitochondria play a key role in the normal functioning of the heart and in the pathogenesis and development of various types of heart disease. In addition, specific mitochondrial cardiomyopathies due to mutations in mitochondrial DNA have been identified. Increasing studies demonstrate that mitochondrial function has emerged as a therapeutic target in heart disease. This chapter addresses the recent studies of the role and the mechanism of mitochondria in the development of heart disease, and the progress in clinical diagnosis and treatments on a mitochondrial basis. Consequently, the aim of this chapter is to outline current knowledge about mitochondria in the heart disease

Vascular Smooth Muscle Cell

Vascular smooth muscle cells (VSMCs) are the stromal cells of the vascular wall and are responsible for regulating arterial tone, blood pressure, and blood supply of the tissues. VSMCs display diversity in function and phenotype depending on their location within the arterial tree (large conduit vs. small resistance vessels), their embryologic origin, and their organ-dependent microenvironment. The heterogeneity of VSMCs is regulated by multiple mechanisms including intracellular signaling and changes in the VSMC microenvironment. Genetic disorders and extrinsic stimuli-induced dysfunction in VSMCs are associated with age-related vascular pathogenesis and vascular diseases, and thus are considered as a potential therapeutic target

Non-Coding RNA in the Pathogenesis, Progression and Treatment of Hypertension

Hypertension is a complex, multifactorial disease that involves the coexistence of multiple risk factors, environmental factors and physiological systems. The complexities extend to the treatment and management of hypertension, which are still the pursuit of many researchers. In the last two decades, various genes have emerged as possible biomarkers and have become the target for investigations of specialized drug design based on its risk factors and the primary cause. Owing to the growing technology of microarrays and next-generation sequencing, the non-protein-coding RNAs (ncRNAs) have increasingly gained attention, and their status of redundancy has flipped to importance in normal cellular processes, as well as in disease progression. The ncRNA molecules make up a significant portion of the human genome, and their role in diseases continues to be uncovered. Specifically, the cellular role of these ncRNAs has played a part in the pathogenesis of hypertension and its progression to heart failure. This review explores the function of the ncRNAs, their types and biology, the current update of their association with hypertension pathology and the potential new therapeutic regime for hypertension

Evaluation of BKca channel expression in the normal cardiomyocyte and in heart disease

Atrial Fibrillation (AF) is the most common cardiac arrhythmia and a major cause ofheart failure, stroke and death. It occurs frequently in association with cardiac orsystemic disorders that increase left atrial pressure and/or volume. Recent datasuggest how genetic factors contribute to AF pathogenesis, but there is relatively littleknown about what the genetic variants are and how they cause AF. The first reportedfamilial AF locus was mapped to chr10q22‐q24 and has since been found to partiallyoverlap with loci for 3 other cardiac disorders, dilated cardiomyopathy (DCM),arrhythmogenic ventricular cardiomyopathy and hypoplastic left heart syndrome. Todate, no causative gene(s) for these mapped disorders has been identified. TheKCNMA1 gene, that encodes the α‐subunit of the large‐conductance Ca2+‐activated K+channel, BKCa, is positioned within the overlapping region of the chromosome 10cardiac loci. Before KCNMA1 can be considered as a candidate gene however, it iscrucial to demonstrate its cardiac expression and that it has relevant biologicalfunctions. Evaluation of BKCa expression in murine hearts confirmed Kcnma1 to bepresent in murine ventricular and atrial cardiomyocytes. Extensive alternativesplicing and multiple transcription start sites were present in both the ventricular andatrial cardiomyocyte with cardiac protein expression displaying multiple isoforms ofvarying size from 150‐50 kD. In ventricular cardiomyocytes, BKCa was shown to belocalised at the t‐tubules, scattered longitudinally along the myofibrils and at themitochondrial membrane. Kcnma1 expression was reduced in the hearts of mice withDCM and increased in mice with left ventricular hypertrophy induced by TAC banding.In a mouse embryonic atrial cell line (HL‐1), stretch application between 0.5 hr to 16hr, reduced the expression of Kcnma1. Mutation screening of the KCNMA1 gene in 118AF and 120 DCM probands identified 1 novel non‐synonymous variant, 6 synonymousvariants, 4 novel indels, and 27 intronic variants. One of the variant, 11‐12delSSinsG,due to disease segregation, absence in control populations and loss of a predictedphosphorylation site, was selected for detailed analysis. Electrophysiology analysis isunderway. These data imply that BKCa might have important roles in normal heartfunction and in heart disease

Nesprin-1 and actin contribute to nuclear and cytoskeletal defects in lamin A/C-deficient cardiomyopathy

Lamin A/C mutations are the most common cause of familial dilated cardiomyopathy (DCM) but the pathogenetic mechanisms are incompletely understood. Nesprins are spectrin repeat-containing proteins that interact with lamin A/C and are components of the linker-of-nucleoskeleton-and-cytoskeleton (LINC) complex that connects the nuclear envelope to the actin cytoskeleton. Our aim was to determine whether changes in nesprin-1 and actin might contribute to DCM in homozygous Lmna knockout (Lmna-/-) mice. Here we find that Lmna-/- cardiomyocytes have altered nuclear envelope morphology, disorganization of nesprin-1 and heterogeneity in the distribution of nuclear and cytoskeletal actin. Functional interactions of nesprin-1 with nuclear G-actin and with the cytoskeletal γ-actin, α-cardiac actin and α-smooth muscle actin (α-SMA) isoforms were shown by immunoprecipitation and Western blotting. At 4-6weeks of age, Lmna-/- mice had normal levels of γ-actin and α-cardiac actin, but α-SMA expression was increased by 50%. In contrast to the predominant vascular distribution of α-SMA in WT ventricular sections, α-SMA had a diffuse staining pattern in Lmna-/- sections. Osmotic swelling studies showed enhanced radial swelling in Lmna-/- cardiomyocytes indicative of cytoskeletal instability. The distensibility of Lmna-/- cardiomyocytes with osmotic stress was reduced by addition of α-SMA-specific fusion peptide. Our findings support a model in which uncoupling of the nucleus and cytoskeleton associated with disruption of the LINC complex promotes mechanical instability and defective force transmission in cardiomyocytes. Changes in the distribution and expression patterns of nuclear and cytoskeletal actin suggest that diverse transcriptional and structural defects may also contribute to DCM in Lmna-/- mice

Conserved Role of the Large Conductance Calcium-Activated Potassium Channel, KCa1.1, in Sinus Node Function and Arrhythmia Risk

BACKGROUND: KCNMA1 encodes the α-subunit of the large-conductance Ca(2+)-activated K(+) channel, K(Ca)1.1, and lies within a linkage interval for atrial fibrillation (AF). Insights into the cardiac functions of K(Ca)1.1 are limited, and KCNMA1 has not been investigated as an AF candidate gene. METHODS: The KCNMA1 gene was sequenced in 118 patients with familial AF. The role of K(Ca)1.1 in normal cardiac structure and function was evaluated in humans, mice, zebrafish, and fly. A novel KCNMA1 variant was functionally characterized. RESULTS: A complex KCNMA1 variant was identified in 1 kindred with AF. To evaluate potential disease mechanisms, we first evaluated the distribution of K(Ca)1.1 in normal hearts using immunostaining and immunogold electron microscopy. K(Ca)1.1 was seen throughout the atria and ventricles in humans and mice, with strong expression in the sinus node. In an ex vivo murine sinoatrial node preparation, addition of the K(Ca)1.1 antagonist, paxilline, blunted the increase in beating rate induced by adrenergic receptor stimulation. Knockdown of the K(Ca)1.1 ortholog, kcnma1b, in zebrafish embryos resulted in sinus bradycardia with dilatation and reduced contraction of the atrium and ventricle. Genetic inactivation of the Drosophila K(Ca)1.1 ortholog, slo, systemically or in adult stages, also slowed the heartbeat and produced fibrillatory cardiac contractions. Electrophysiological characterization of slo-deficient flies revealed bursts of action potentials, reflecting increased events of fibrillatory arrhythmias. Flies with cardiac-specific overexpression of the human KCNMA1 mutant also showed increased heart period and bursts of action potentials, similar to the K(Ca)1.1 loss-of-function models. CONCLUSIONS: Our data point to a highly conserved role of K(Ca)1.1 in sinus node function in humans, mice, zebrafish, and fly and suggest that K(Ca)1.1 loss of function may predispose to AF