Pengembangan Layanan Lembaga Sertifikasi Kompetensi (LSK) Berbasis Sinkronisasi Learning Management System (LMS)

Lembaga Sertifikasi Kompetensi (LSK) merupakan salah satu cara dalam meningkatkan skill individu maupun kelompok masyarakat di Indonesia. Dengan menciptakan LSK-LSK yang terdistribusi di daerah-daerah akan dapat menghilangkan kesenjangan skill antara masyarakat kota dan masyarakat desa. LSK yang dulunya melaksanakan ujian maupun pelatihan secara tradisional atau biasa disebut paper based akan dijadikan sistem yang modern (computer based) dengan mengimplementasikan LMS dalam hal ini adalah moodle. Pada buku ini akan dirancang testbed sebuah desain dan implementasi sistem sinkronisasi LSK server berbasis LMS secara bi-direksional yang terdistribusi pada jaringan. Kemudian dari hasil testbed tersebut akan dilakukan pengujian untuk didapatkan data unjuk kerja sistem sinkronisasi pada jaringan dan data unjuk kerja LSK server. Pengujian sistem sinkronisasi diamati dengan membandingkan perbedaan Perubahan course dan besar kecilnya file pada variasi bandwidth yang digunakan sedangkan pengujian unjuk kerja LSK server diamati dengan membandingkan jumlah user yang mengakses website LSK pada variasi bandwidth yang digunakan

Sensory profiles in women with neuropathic pain after breast cancer surgery

Purpose We performed a detailed analysis of sensory function in patients with chronic post-surgical neuropathic pain (NP) after breast cancer treatments by quantitative sensory testing (QST) with DFNS (German Research Network on Neuropathic Pain) protocol and bed side examination (BE). The nature of sensory changes in peripheral NP may reflect distinct pathophysiological backgrounds that can guide the treatment choices. NP with sensory gain (i.e., hyperesthesia, hyperalgesia, allodynia) has been shown to respond to Na+-channel blockers (e.g., oxcarbazepine). Methods 104 patients with at least "probable" NP in the surgical area were included. All patients had been treated for breast cancer 4-9 years ago and the handling of the intercostobrachial nerve (ICBN) was verified by the surgeon. QST was conducted at the site of NP in the surgical or nearby area and the corresponding contralateral area. BE covered the upper body and sensory abnormalities were marked on body maps and digitalized for area calculation. The outcomes of BE and QST were compared to assess the value of QST in the sensory examination of this patient group. Results Loss of function in both small and large fibers was a prominent feature in QST in the area of post-surgical NP. QST profiles did not differ between spared and resected ICBN. In BE, hypoesthesia on multiple modalities was highly prevalent. The presence of sensory gain in BE was associated with more intense pain. Conclusions Extensive sensory loss is characteristic for chronic post-surgical NP several years after treatment for breast cancer. These patients are unlikely to respond to Na+-channel blockers.Peer reviewe

The Kinetic of Cyclization-acetylation (R)-(+)-citronellal with Anhydride Acetic Acid Which Catalyzed of Zn2+-natural Zeolite

Reaction kinetic of acetylation-cyclization (R)- (+)-citronellal with acetic acid anhydride which catalyzed Zn2+-zeolite (Zn2+-Za) was analyzed by Langmuir- Hinshelwood Models. (R)-(+)-citronellal isolated from lemongrass oil with fractionation distillation reduced pressure and analyzed anantiomer ratio with GC chiral column β- DEX 225. Catalyst preparation of Zn2+-Za conducted by acid activation on natural zeolite Malang 100 mesh using 1% HF and 6 M HCl, then soaked on 0,1 M NH4Cl. Calcination was done at 450oC during 1 hour with N2 flow to achieved H-natural zeolite (HZa). Cation exchange H-Za with 0,1 M ZnCl2 conducted to obtain Zn2+-natural zeolit (Zn2+-Za). Reactions of Cyclization-acetylation (R )-(+)- citronellal using a catalyst of Zn2+-Za was done by varying molar ratio of (R )-(+)- citronellal with acetic acid anhydride, namely 0.25, 0.5, 1.0; 1 , 25; 1.5. During the reaction, into system, samples were taken each 1 mL of reaction with duration 10, 20, 30, 60, 120, 180 minutes. Reaction product was extracted with n-hexana. Structure elucidation was done by GC-MS, FTIR spectrophotometer, and 1H-NMR spectrometer. The result showed a greater molar ratio (R)-(+)-citronellal against quantity of acetic acid anhydride acetic, pulegil total was decline. Acetylation-cyclization catalyzed with Zn2+-Za on duration of 30 minutes and 80°C has k of 30.964 to 47.619 mmol (minute.gram catalyst)-1 and KSIT/KAA of 7.09

Metilasi Asam Galat Menggunakan Agen Metilasi Dimetil Sulfat (DMS) atau Dimetil Karbonat (DMC)

Methylation of gallic acid has been conducted by the use of dimethyl sulfate (DMS) or dimethyl carbonate (DMC) as methylating agents. Methylation of gallic acid using DMS was carried out by various methods, i.e. mild condition at ambient temperature, reflux and sonication. The best method was achieved by methylation under reflux yielded 48.9% efficiency of 3,4,5-trimethoxybenzoic acid. Methylation of gallic acid with DMC was performed with several variations on the type and amount of base and phase transfer catalyst (PTC). In addition, green methods sonochemistry and microwave irradiation have also been done. Unfortunately, the methylation of gallic acid failed to give 3,4,5-trimethoxybenzoic acid. Methylation of gallic acid using green reagent DMC gave high yield at mole ratio of gallic acid : DMC : K2CO3 : KI : PTC of tetrabuthyl ammonium bromide (TBAB) = 5 : 320 : 20 : 5 : 8 under reflux for 10 hours and produced 75.96% of methyl 3,4,5-trimethoxybenzoate. Atom economy of gallic acid methylation method using DMC is 37.95%, which is not very different from that of DMS method (30.47%). However, the methylation method using DMC produced by products, which have the lower toxicity compared to that of methylation using DMS

POMC: The Physiological Power of Hormone Processing.

Pro-opiomelanocortin (POMC) is the archetypal polypeptide precursor of hormones and neuropeptides. In this review, we examine the variability in the individual peptides produced in different tissues and the impact of the simultaneous presence of their precursors or fragments. We also discuss the problems inherent in accurately measuring which of the precursors and their derived peptides are present in biological samples. We address how not being able to measure all the combinations of precursors and fragments quantitatively has affected our understanding of the pathophysiology associated with POMC processing. To understand how different ratios of peptides arise, we describe the role of the pro-hormone convertases (PCs) and their tissue specificities and consider the cellular processing pathways which enable regulated secretion of different peptides that play crucial roles in integrating a range of vital physiological functions. In the pituitary, correct processing of POMC peptides is essential to maintain the hypothalamic-pituitary-adrenal axis, and this processing can be disrupted in POMC-expressing tumors. In hypothalamic neurons expressing POMC, abnormalities in processing critically impact on the regulation of appetite, energy homeostasis, and body composition. More work is needed to understand whether expression of the POMC gene in a tissue equates to release of bioactive peptides. We suggest that this comprehensive view of POMC processing, with a focus on gaining a better understanding of the combination of peptides produced and their relative bioactivity, is a necessity for all involved in studying this fascinating physiological regulatory phenomenon

Maternal overnutrition programs epigenetic changes in the regulatory regions of hypothalamic Pomc in the offspring of rats.

Maternal overnutrition has been implicated in affecting the offspring by programming metabolic disorders such as obesity and diabetes, by mechanisms that are not clearly understood. This study aimed to determine the long-term impact of maternal high-fat (HF) diet feeding on epigenetic changes in the offspring's hypothalamic Pomc gene, coding a key factor in the control of energy balance. Further, it aimed to study the additional effects of postnatal overnutrition on epigenetic programming by maternal nutrition.Eight-week-old female Sprague-Dawley rats were fed HF diet or low-fat (LF) diet for 6 weeks before mating, and throughout gestation and lactation. At postnatal day 21, samples were collected from a third offspring and the remainder were weaned onto LF diet for 5 weeks, after which they were either fed LF or HF diet for 12 weeks, resulting in four groups of offspring differing by their maternal and postweaning diet.With maternal HF diet, offspring at weaning had rapid early weight gain, increased adiposity, and hyperleptinemia. The programmed adult offspring, subsequently fed LF diet, retained the increased body weight. Maternal HF diet combined with offspring HF diet caused more pronounced hyperphagia, fat mass, and insulin resistance. The ARC Pomc gene from programmed offspring at weaning showed hypermethylation in the enhancer (nPE1 and nPE2) regions and in the promoter sequence mediating leptin effects. Interestingly, hypermethylation at the Pomc promoter but not at the enhancer region persisted long term into adulthood in the programmed offspring. However, there were no additive effects on methylation levels in the regulatory regions of Pomc in programmed offspring fed a HF diet.Maternal overnutrition programs long-term epigenetic alterations in the offspring's hypothalamic Pomc promoter. This predisposes the offspring to metabolic disorders later in life

Common Variant Burden Contributes to the Familial Aggregation of Migraine in 1,589 Families

© 2018 Elsevier Inc. Complex traits, including migraine, often aggregate in families, but the underlying genetic architecture behind this is not well understood. The aggregation could be explained by rare, penetrant variants that segregate according to Mendelian inheritance or by the sufficient polygenic accumulation of common variants, each with an individually small effect, or a combination of the two hypotheses. In 8,319 individuals across 1,589 migraine families, we calculated migraine polygenic risk scores (PRS) and found a significantly higher common variant burden in familial cases (n = 5,317, OR = 1.76, 95% CI = 1.71–1.81, p = 1.7 × 10−109) compared to population cases from the FINRISK cohort (n = 1,101, OR = 1.32, 95% CI = 1.25–1.38, p = 7.2 × 10−17). The PRS explained 1.6% of the phenotypic variance in the population cases and 3.5% in the familial cases (including 2.9% for migraine without aura, 5.5% for migraine with typical aura, and 8.2% for hemiplegic migraine). The results demonstrate a significant contribution of common polygenic variation to the familial aggregation of migraine. Gormley et al. use polygenic risk scores to show that common variation, captured by genome-wide association studies, in combination contributes to the aggregation of migraine in families. The results may have similar implications for other complex traits in general