APLIKASI BERBAGAI ZAT ANTIOKSIDAN SEBAGAI PENGHAMBAT BROWNING MEDIA TANAM EKSPLAN JATI PUTIH (Gmelina arborea Roxb) SECARA IN-VITRO

Browning is the most problem in plant tissue culture, both in growing media and explants. Browning is formed by oxidation process of phenolic compounds thatcan caused tissue death. The objective of this study were to analyze the effect of antioxidants addition against browning and to determine the best antioxidant toinhibited browning of Gmelina arborea explant growing media. The research was conducted by two steps, namely preparation of Murashige and Skoog (MS) media which are added 2,4-D growth regulators and addition of antioxidant PVP, ascorbic acid and activated charcoal. The results indicated that the addition ofantioxidants in the media were able to inhibit browning process of the media as well as in the explant. Moreover, the ascorbic acid performed better ability to inhibit browning process compared to the other antioxidants. &nbsp

Common carotid intima media thickness and ankle-brachial pressure index correlate with local but not global atheroma burden:a cross sectional study using whole body magnetic resonance angiography

Common carotid intima media thickness (CIMT) and ankle brachial pressure index (ABPI) are used as surrogate marker of atherosclerosis, and have been shown to correlate with arterial stiffness, however their correlation with global atherosclerotic burden has not been previously assessed. We compare CIMT and ABPI with atheroma burden as measured by whole body magnetic resonance angiography (WB-MRA).50 patients with symptomatic peripheral arterial disease were recruited. CIMT was measured using ultrasound while rest and exercise ABPI were performed. WB-MRA was performed in a 1.5T MRI scanner using 4 volume acquisitions with a divided dose of intravenous gadolinium gadoterate meglumine (Dotarem, Guerbet, FR). The WB-MRA data was divided into 31 anatomical arterial segments with each scored according to degree of luminal narrowing: 0 = normal, 1 = <50%, 2 = 50-70%, 3 = 70-99%, 4 = vessel occlusion. The segment scores were summed and from this a standardized atheroma score was calculated.The atherosclerotic burden was high with a standardised atheroma score of 39.5±11. Common CIMT showed a positive correlation with the whole body atheroma score (β 0.32, p = 0.045), however this was due to its strong correlation with the neck and thoracic segments (β 0.42 p = 0.01) with no correlation with the rest of the body. ABPI correlated with the whole body atheroma score (β -0.39, p = 0.012), which was due to a strong correlation with the ilio-femoral vessels with no correlation with the thoracic or neck vessels. On multiple linear regression, no correlation between CIMT and global atheroma burden was present (β 0.13 p = 0.45), while the correlation between ABPI and atheroma burden persisted (β -0.45 p = 0.005).ABPI but not CIMT correlates with global atheroma burden as measured by whole body contrast enhanced magnetic resonance angiography in a population with symptomatic peripheral arterial disease. However this is primarily due to a strong correlation with ilio-femoral atheroma burden

Calmodulin is responsible for Ca2+-dependent regulation of TRPA1 channels

TRPA1 is a Ca2+-permeable ion channel involved in many sensory disorders such as pain, itch and neuropathy. Notably, the function of TRPA1 depends on Ca2+, with low Ca2+ potentiating and high Ca2+ inactivating TRPA1. However, it remains unknown how Ca2+ exerts such contrasting effects. Here, we show that Ca2+ regulates TRPA1 through calmodulin, which binds to TRPA1 in a Ca2+-dependent manner. Calmodulin binding enhanced TRPA1 sensitivity and Ca2+-evoked potentiation of TRPA1 at low Ca2+, but inhibited TRPA1 sensitivity and promoted TRPA1 desensitization at high Ca2+. Ca2+-dependent potentiation and inactivation of TRPA1 were selectively prevented by disrupting the interaction of the carboxy-lobe of calmodulin with a calmodulin-binding domain in the C-terminus of TRPA1. Calmodulin is thus a critical Ca2+ sensor enabling TRPA1 to respond to diverse Ca2+ signals distinctly

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

ANALISIS PERLAKUAN AKUNTANSI DAN PELAPORAN PERTANGGUNGJAWABAN SOSIAL PERUSAHAAN (Studi Kasus Pada PT Bio Farma (Persero) Bandung)

Peneilitian ini bertujuan untuk mengetahui sejauh mana implementasi tanggung jawab sosial yang telah dilakukan PT Bio Farma (Persero). Peneliti juga menganalisis kepatuhan PT Bio Farma (Persero) dalam melaporkan tanggung jawab sosialnya sesuai dengan UU No. 40 tahun 2007 tentang Perseroan Terbatas dan PerMen BUMN No.9/MBU/2016 tentang Program Kemitraan dan Bina Lingkungan (PKBL). Selanjutnya peneliti menganalisis penerapan dan pelaporan akuntansi pertanggungjawaban sosial pada PT Bio Farma (Persero) serta apakah disajikan dalam sustainability report dan telah sesuai dengan Global Reporting Initiative (GRI). Metode Penelitian yang digunakan dalam penelitian ini adalah deskriptif kualitatif. Teknik pemilihan informan menggunakan metode purposive sampling sehingga informan dalam penelitian ini adalah Divisi PKBL, CSR & EHS, Divisi Anggaran dan Akuntansi, Divisi Keuangan dan Pajak serta Bagian Corporate Communication. Teknik pengumpulan data yang digunakan adalah kajian literatur, wawancara dan Observasi. Analisis data dilakukan secara deskriptif dengan menggunakan teknik analisis data model Alston dan Bowles. Tahap analisis data tersebut mencakup reduksi data, menggabungkan data, menjelaskan data. Hasil penelitian ini menunjukan bahwa PT Bio Farma (Persero) mengelola dua bentuk program tanggung jawab sosial perusahaan, sebagai perseroan adalah Program Corporate Social Responsibility (CSR) dan sebagai BUMN Program Kemitraan dan Bina Lingkungan (PKBL). Program Kemitraan dan Bina Lingkungan dilaporkan dalam Laporan Posisi Keuangan dan Laporan Aktivitas yang terpisah dari Laporan Keuangan Utama Perseroan menggunakan dasar PSAK 45-Pelaporan Keuangan Entitas Nirlaba. Sedangkan Program Corporate Social Responsibility (CSR) secara keseluruhan dilaporkan sebagai Beban pada Laporan Keuangan Utama Perseroan, dalam Laporan Laba-Rugi diklasifikasikan dalam pos Beban Administrasi dan Umum. Aktivitas tanggung jawab sosial perusahaan PT Bio Farma (Persero) juga dilaporkan dalam Sustainability Report dalam bentuk Narrative Reporting dan telah menggunakan Global Reporting Initiative (GRI G4) sebagai dasar pelaporannya, sehingga telah memenuhi semua indikator pelaporan

A regulatory variant at 3q21.1 confers an increased pleiotropic risk for hyperglycemia and altered bone mineral density

Nasa Sinnott-Armstrong and colleagues identify a pleiotropic risk locus at 3q21 that is associated with type 2 diabetes (T2D) and greater bone mineral density (BMD) and its associated cell-autonomous mechanisms in adipocytes and osteoblasts. Together, these findings provide a possible explanation for the perplexing finding that individuals with T2D have higher BMD but greater susceptibility to bone fracture