RANCANG BANGUN PURWARUPA ELECTRICAL POWER SYSTEM UNTUK SATELIT NANO DALAM SKALA LABORATORIUM

Keberhasilan suatu misi dari sebuah satelit nano sangat bergantung pada sistem pengisian dan pengendalian daya nya. Apabila ditengah-tengah misi satelit nano kehabisan daya pada saat mengorbit di angkasa maka satelit nano tersebut jatuh ke bumi atau terlempar keluar angkasa dan misi satelit nano itu pun akan gagal. Oleh karena itu di dalam sebuah satelit nano perlu dibuat sebuah subsistem yang bertugas untuk mencatu daya, menyimpan daya, dan mendistribusikan daya, subsistem ini adalah Electrical Power System (EPS). Ada dua komponen yang berperan penting dalam perancangan EPS pada tugas akhir ini yaitu, battery charger ic dan load switch. Battery charger ic memiliki beberapa kegunaan. Selain untuk mengendalikan pengisian daya pada baterai, battery charger icmemiliki fitur seperti power path yang berfungsi untuk memilih antara solar panel dan baterai sebagai sumber catu daya ke sistem satelit nano. Pada sistem distribusi dan regulasi daya EPS ini digunakan komponen load switch yang dihubungkan dengan sebuah mikrokontroller untuk mengatur keluaran regulator mana yang akan diaktifkan dan dinonaktifkan. Fitur power path yang diaplikasikan pada purwarupa EPS ini memungkinkan untuk meminimalisir penggunaan baterai, karena daya baterai hanya digunakan sebanyak 4.8% pada saat tidak terkena cahaya matahari. Selain itu juga load switch dapat mematikan jalur daya ke beban jika kapasitas baterai mulai berkurang, sehingga dapat lebih menghemat daya baterai. Purwarupa EPS ini membutuhkan waktu 8 jam untuk mengisi 9.3% kapasitas baterai saat diuji di kondisi bumi. Sedangkan untuk pengosongan baterai dengan beban 0.765 Watt purwarupa EPS dapat bertahan selama 25 jam untuk menyuplai daya ke beban. Kata kunci: satelit nano, EPS, load switch, battery charger ic, power pat

Spastin mutations impair coordination between lipid droplet dispersion and reticulum.

Lipid droplets (LD) are affected in multiple human disorders. These highly dynamic organelles are involved in many cellular roles. While their intracellular dispersion is crucial to ensure their function and other organelles-contact, underlying mechanisms are still unclear. Here we show that Spastin, one of the major proteins involved in Hereditary Spastic Paraplegia (HSP), controls LD dispersion. Spastin depletion in zebrafish affects metabolic properties and organelle dynamics. These functions are ensured by a conserved complex set of splice variants. M1 isoforms determine LD dispersion in the cell by orchestrating endoplasmic reticulum (ER) shape along microtubules (MTs). To further impact LD fate, Spastin modulates transcripts levels and subcellular location of other HSP key players, notably Seipin and REEP1. In pathological conditions, mutations in human Spastin M1 disrupt this mechanism and impacts LD network. Spastin depletion influences not only other key proteins but also modulates specific neutral lipids and phospholipids, revealing an impact on membrane and organelle components. Altogether our results show that Spastin and its partners converge in a common machinery that coordinates LD dispersion and ER shape along MTs. Any alteration of this system results in HSP clinical features and impacts lipids profile, thus opening new avenues for novel biomarkers of HSP

Molecular codes and in vitro generation of hypocretin and melanin concentrating hormone neurons.

Hypocretin/orexin (HCRT) and melanin concentrating hormone (MCH) neuropeptides are exclusively produced by the lateral hypothalamus and play important roles in sleep, metabolism, reward, and motivation. Loss of HCRT (ligands or receptors) causes the sleep disorder narcolepsy with cataplexy in humans and in animal models. How these neuropeptides are produced and involved in diverse functions remain unknown. Here, we developed methods to sort and purify HCRT and MCH neurons from the mouse late embryonic hypothalamus. RNA sequencing revealed key factors of fate determination for HCRT (Peg3, Ahr1, Six6, Nr2f2, and Prrx1) and MCH (Lmx1, Gbx2, and Peg3) neurons. Loss of Peg3 in mice significantly reduces HCRT and MCH cell numbers, while knock-down of a Peg3 ortholog in zebrafish completely abolishes their expression, resulting in a 2-fold increase in sleep amount. We also found that loss of HCRT neurons in Hcrt-ataxin-3 mice results in a specific 50% decrease in another orexigenic neuropeptide, QRFP, that might explain the metabolic syndrome in narcolepsy. The transcriptome results were used to develop protocols for the production of HCRT and MCH neurons from induced pluripotent stem cells and ascorbic acid was found necessary for HCRT and BMP7 for MCH cell differentiation. Our results provide a platform to understand the development and expression of HCRT and MCH and their multiple functions in health and disease

Comparative expression of cell wall related genes in four maize RILs and one parental line of variable lignin content and cell wall degradability

A comparison of gene expression in maize between the parental line F271 and four RILs derived from the cross F288 x F271 was investigated based on hybridization on the 17,555 probes Affymetrix micro-array, targeting nearly one third of the genes present in maize genomes. The parental line had unfavorable alleles for cell wall degradability traits at the major QTL position in bin 6.06, while the set of RILs had both the favorable allele and high cell wall degradability. 360 genes were differentially expressed in the four RIL in comparison to F271, including nine genes underlying the major QTL position and 36 underlying two other QTL positions. However, their proposed function (whenever is described) do not allow us to firmly consider their involvement in the observed variation of cell wall related traits. Only a few genes involved in monolignol biosynthesis or polymerization located elsewhere in the genome were differentially expressed between the four RILs and F271, corroborating with the fact that these genes are probably not involved in major determinants of cell wall degradability in the studied set of lines. Among the investigated regulation factors, three ZmMYB, one NAC and one C3HC4 zinc finger were differentially expressed between the four RILs and F271, but they were not located in bin 6.06. Notwithstanding, the obtained results especially strengthened the probable involvement of these genes in maize secondary wall assembly and/ or lignification

The evolutionarily conserved miRNA-137 targets the neuropeptide hypocretin/orexin and modulates the wake to sleep ratio.

SignificanceThe hypocretin (Hcrt, also known as orexin) neuropeptides regulate sleep and wake stability, and disturbances of Hcrt can lead to sleep disorders. MicroRNAs (miRNAs) are short noncoding RNAs that fine-tune protein expression levels, and miRNA-based therapeutics are emerging. We report a functional interaction between miRNA (miR-137) and Hcrt. We demonstrate that intracellular miR-137 levels in Hcrt neurons regulate Hcrt expression with downstream effects on wakefulness. Specifically, lowering of miR-137 levels increased wakefulness in mice. We further show that the miR-137:Hcrt interaction is conserved across mice and humans, that miR-137 also regulates sleep-wake balance in zebrafish, and that the MIR137 locus is genetically associated with sleep duration in humans. Together, our findings reveal an evolutionarily conserved sleep-wake regulatory role of miR-137

Comparative expression of cell wall related genes in four maize RILs and one parental line of variable lignin content and cell wall degradability

A comparison of gene expression in maize between the parental line F271 and four RILs derived from the cross F288 x F271 was investigated based on hybridization on the 17,555 probes Affymetrix micro-array, targeting nearly one third of the genes present in maize genomes. The parental line had unfavorable alleles for cell wall degradability traits at the major QTL position in bin 6.06, while the set of RILs had both the favorable allele and high cell wall degradability. 360 genes were differentially expressed in the four RIL in comparison to F271, including nine genes underlying the major QTL position and 36 underlying two other QTL positions. However, their proposed function (whenever is described) do not allow us to firmly consider their involvement in the observed variation of cell wall related traits. Only a few genes involved in monolignol biosynthesis or polymerization located elsewhere in the genome were differentially expressed between the four RILs and F271, corroborating with the fact that these genes are probably not involved in major determinants of cell wall degradability in the studied set of lines. Among the investigated regulation factors, three ZmMYB, one NAC and one C3HC4 zinc finger were differentially expressed between the four RILs and F271, but they were not located in bin 6.06. Notwithstanding, the obtained results especially strengthened the probable involvement of these genes in maize secondary wall assembly and/ or lignification

Distinct patterns of skeletal muscle mitochondria fusion, fission and mitophagy upon duration of exercise training.

Healthy ageing interventions encompass regular exercise to prevent mitochondrial dysfunction, key player in sarcopenia pathogenesis. Mitochondrial biogenesis has been well documented, but mitochondrial remodelling in response to exercise training is poorly understood. Here we investigated fusion, fission and mitophagy before and after an exercise intervention in older adults. Skeletal muscle biopsies were collected from 22 healthy sedentary men and women before and after 4 months of supervised training. Eight lifelong trained age- and gender-matched volunteers served as positive controls. Transmission electron microscopy was used to estimate mitochondrial content. Western blotting and qRT-PCR were used to detect changes in specific proteins and transcripts. After intervention, mitochondrial content increased to levels of controls. While enhancement of fusion was prevalent after intervention, inhibition of fission and increased mitophagy were dominant in controls. Similarly to PARKIN, BCL2L13 content was higher in controls. The observed molecular adaptations paralleled long-term effects of training on physical fitness, exercise efficiency and oxidative capacity. This study describes distinct patterns of molecular adaptations in human skeletal muscle under chronic exercise training. After 16 weeks of exercise, the pattern was dominated by fusion to increase mitochondrial content to the metabolic demands of exercise. In lifelong exercise, the pattern was dominated by mitophagy synchronized with increased fusion and decreased fission, indicating an increased mitochondrial turnover. In addition to these temporally distinct adaptive mechanisms, this study suggests for the first time a specific role of BCL2L13 in chronic exercise that requires constant maintenance of mitochondrial quality