Pengujian Kuat Tarik Lentur Beton Dengan Variasi Kuat Tekan Beton

Beton adalah campuran antara semen Portland atau semen hidraulik yang lain, agregat halus, agregat kasar, dan air dengan atau tanpa bahan tambah membentuk massa padat. Beton polos memiliki kekuatan tekan yang tinggi dibandingkan dengan kekuatan tariknya. Kuat tekan beban beton adalah besarnya beban per satuan luas, yang menyebabkan benda uji beton hancur bila dibebani dengan gaya tekan tertentu, yang dihasilkan oleh mesin tekan. Kuat tarik beton biasanya 8%-15% dari kuat tekan beton. Kuat tarik adalah suatu sifat yang penting yang mempengaruhi perambatan dan ukuran dari retak di dalam struktur. Sebuah balok yang diberi beban akan mengalami deformasi, oleh sebab itu timbul momen-momen lentur sebagai perlawanan dari material yang membentuk balok tersebut terhadap beban luar. Kuat tarik lentur adalah kemampuan balok beton yang diletakkan pada dua perletakan untuk menahan gaya dengan arah tegak lurus sumbu benda uji, yang diberikan padanya, sampai benda uji patah dan dinyatakan dalam Mega Pascal (MPa) gaya tiap satuan luas. Tujuan dari penelitian ini adalah, membandingkan hubungan antara kuat tarik lentur beton dan kuat tekan beton. Pada penelitian dilakukan perawatan selama 28 hari dengan benda uji yang digunakan adalah balok 100x100x400 mm sebanyak 32 buah untuk pengujian kuat tarik lentur dan silinder 10/20 mm sebanyak 20 buah untuk pengujian kuat tekan. Variasi kuat tekan yang digunakan yaitu 20,25,30 dan 35 MPa. Hasil pengujian menyatakan bahwa nilai kuat tarik lentur pada beton mengalami kenaikan yaitu semakin besar nilai kuat tekan maka nilai kuat tarik lentur yang dihasilkan semakin besar pula. Pada penelitian ini nilai fr/ berkisar 0,81 sampai 0,83

ANALISA PERBANDINGAN PANJANG ANTRIAN MENGGUNAKAN TEORI ANTRIAN DAN ANALISA GELOMBANG KEJUT DI LOKET KELUAR KENDARAAN KAWASAN MEGAMAS MANADO

In the science of traffic engineering, there are many methods of measuring queues and delays. Some of these methods are queuing theory and shockwave analysis. From these two methods will be compared the most ideal characteristics to analyze the queue and delay. The Methods in this research used primary data collected from Megamas Area through by manual survey method to analyze shockwave and queuing theory. The results obtained the following conclusions: (1) The shockwave analysis at the exit gateway counter are formed by Greenshields’s basic chart and  present the queue length, total duration of the counter opening for the last vehicle entering the queue, and total duration from opening of the counter to the normal condition will increase linearly with increasing incidence duration, while the delay will increase exponentially. (2) In queue theory analysis, existing counters are still capable for serving the vehicles, this is obtained from the average value ρ 1. Based on analysis, the service level on all counters are strongly influenced by the speed and accuracy of service door operators, readiness of reserve money for returns, readiness of drivers who will be out of the area, such as preparing money to pay retribution and admission ticket. (3) The queue theory analysis is easier to use to analyze the queue at the counter than the shock wave analysis. Shockwave analysis is more macro when using traffic parameters such as volume, speed of density and capacity of the road wherein the change of traffic flow due to the obstacle becomes a reference to analyze the shock waves. In the case of the exit gateway of the vehicle counter Megamas, the length of the road for queuing is very limited, and if the number of vehicle queue is too long until the intersection between segment A and segment B then speed in both segments will be affected due to queue. Eventually, queuing theory in analyzing the queue at vehicle counter in Megamas area is more effective and efficient to use. Keywords : shockwave, queue theory, queue lengt

The spectrum of neurodevelopmental, neuromuscular and neurodegenerative disorders due to defective autophagy

Primary dysfunction of autophagy due to Mendelian defects affecting core components of the autophagy machinery or closely related proteins have recently emerged as an important cause of genetic disease. This novel group of human disorders may present throughout life and comprises severe early-onset neurodevelopmental and more common adult-onset neurodegenerative disorders. Early-onset (or congenital) disorders of autophagy often share a recognizable "clinical signature," including variable combinations of neurological, neuromuscular and multisystem manifestations. Structural CNS abnormalities, cerebellar involvement, spasticity and peripheral nerve pathology are prominent neurological features, indicating a specific vulnerability of certain neuronal populations to autophagic disturbance. A typically biphasic disease course of late-onset neurodegeneration occurring on the background of a neurodevelopmental disorder further supports a role of autophagy in both neuronal development and maintenance. Additionally, an associated myopathy has been characterized in several conditions. The differential diagnosis comprises a wide range of other multisystem disorders, including mitochondrial, glycogen and lysosomal storage disorders, as well as ciliopathies, glycosylation and vesicular trafficking defects. The clinical overlap between the congenital disorders of autophagy and these conditions reflects the multiple roles of the proteins and/or emerging molecular connections between the pathways implicated and suggests an exciting area for future research. Therapy development for congenital disorders of autophagy is still in its infancy but may result in the identification of molecules that target autophagy more specifically than currently available compounds. The close connection with adult-onset neurodegenerative disorders highlights the relevance of research into rare early-onset neurodevelopmental conditions for much more common, age-related human diseases.Peer reviewe

A full degree-of-freedom photonic crystal spatial light modulator

Harnessing the full complexity of optical fields requires complete control of all degrees-of-freedom within a region of space and time -- an open goal for present-day spatial light modulators (SLMs), active metasurfaces, and optical phased arrays. Here, we solve this challenge with a programmable photonic crystal cavity array enabled by four key advances: (i) near-unity vertical coupling to high-finesse microcavities through inverse design, (ii) scalable fabrication by optimized, 300 mm full-wafer processing, (iii) picometer-precision resonance alignment using automated, closed-loop "holographic trimming", and (iv) out-of-plane cavity control via a high-speed micro-LED array. Combining each, we demonstrate near-complete spatiotemporal control of a 64-resonator, two-dimensional SLM with nanosecond- and femtojoule-order switching. Simultaneously operating wavelength-scale modes near the space- and time-bandwidth limits, this work opens a new regime of programmability at the fundamental limits of multimode optical control.Comment: 25 pages, 20 figure

The spectrum of neurodevelopmental, neuromuscular and neurodegenerative disorders due to defective autophagy

Primary dysfunction of autophagy due to Mendelian defects affecting core components of the autophagy machinery or closely related proteins have recently emerged as an important cause of genetic disease. This novel group of human disorders may present throughout life and comprises severe early-onset neurodevelopmental and more common adult-onset neurodegenerative disorders. Early-onset (or congenital) disorders of autophagy often share a recognizable "clinical signature," including variable combinations of neurological, neuromuscular and multisystem manifestations. Structural CNS abnormalities, cerebellar involvement, spasticity and peripheral nerve pathology are prominent neurological features, indicating a specific vulnerability of certain neuronal populations to autophagic disturbance. A typically biphasic disease course of late-onset neurodegeneration occurring on the background of a neurodevelopmental disorder further supports a role of autophagy in both neuronal development and maintenance. In addition, an associated myopathy has been characterized in several conditions. The differential diagnosis comprises a wide range of other multisystem disorders, including mitochondrial, glycogen and lysosomal storage disorders, as well as ciliopathies, glycosylation and vesicular trafficking defects. The clinical overlap between the congenital disorders of autophagy and these conditions reflects the multiple roles of the proteins and/or emerging molecular connections between the pathways implicated and suggests an exciting area for future research. Therapy development for congenital disorders of autophagy is still in its infancy but may result in the identification of molecules that target autophagy more specifically than currently available compounds. The close connection with adult-onset neurodegenerative disorders highlights the relevance of research into rare early-onset neurodevelopmental conditions for much more common, age-related human diseases

Integrated photon sources for quantum information science applications

Ring resonators are used as photon pair sources by taking advantage of the materials second or third order non-linearities through the processes of spontaneous parametric downconversion and spontaneous four wave mixing respectively. Two materials of interest for these applications are silicon for the infrared and aluminum nitride for the ultraviolet through the infrared. When fabricated into ring type sources they are capable of producing pairs of indistinguishable photons but typically suffer from an effective 50% loss. By slightly decoupling the input waveguide from the ring, the drop port coincidence ratio can be significantly increased with the trade-off being that the pump is less efficiently coupled into the ring. Ring resonators with this design have been demonstrated having coincidence ratios of 96% but requiring a factor of ∼10 increase in the pump power. Through the modification of the coupling design that relies on additional spectral dependence, it is possible to achieve similar coincidence ratios without the increased pumping requirement. This can be achieved by coupling the input waveguide to the ring multiple times, thus creating a Mach-Zehnder interferometer. This coupler design can be used on both sides of the ring resonator so that resonances supported by one of the couplers are suppressed by the other. This is the ideal configuration for a photon-pair source as it can only support the pump photons at the input side while only allowing the generated photons to leave through the output side. Recently, this device has been realized with preliminary results exhibiting the desired spectral dependence and with a coincidence ratio as high as ∼ 97% while allowing the pump to be nearly critically coupled to the ring. The demonstrated near unity coincidence ratio infers a near maximal heralding efficiency from the fabricated device. This device has the potential to greatly improve the scalability and performance of quantum computing and communication systems.National Science Foundation (U.S.) (Grant ECCS- 1542081)National Science Foundation (U.S.) (Award No. ECCS14052481

The Functions of Auxilin and Rab11 in Drosophila Suggest That the Fundamental Role of Ligand Endocytosis in Notch Signaling Cells Is Not Recycling

Notch signaling requires ligand internalization by the signal sending cells. Two endocytic proteins, epsin and auxilin, are essential for ligand internalization and signaling. Epsin promotes clathrin-coated vesicle formation, and auxilin uncoats clathrin from newly internalized vesicles. Two hypotheses have been advanced to explain the requirement for ligand endocytosis. One idea is that after ligand/receptor binding, ligand endocytosis leads to receptor activation by pulling on the receptor, which either exposes a cleavage site on the extracellular domain, or dissociates two receptor subunits. Alternatively, ligand internalization prior to receptor binding, followed by trafficking through an endosomal pathway and recycling to the plasma membrane may enable ligand activation. Activation could mean ligand modification or ligand transcytosis to a membrane environment conducive to signaling. A key piece of evidence supporting the recycling model is the requirement in signaling cells for Rab11, which encodes a GTPase critical for endosomal recycling. Here, we use Drosophila Rab11 and auxilin mutants to test the ligand recycling hypothesis. First, we find that Rab11 is dispensable for several Notch signaling events in the eye disc. Second, we find that Drosophila female germline cells, the one cell type known to signal without clathrin, also do not require auxilin to signal. Third, we find that much of the requirement for auxilin in Notch signaling was bypassed by overexpression of both clathrin heavy chain and epsin. Thus, the main role of auxilin in Notch signaling is not to produce uncoated ligand-containing vesicles, but to maintain the pool of free clathrin. Taken together, these results argue strongly that at least in some cell types, the primary function of Notch ligand endocytosis is not for ligand recycling

EPG5-related Vici syndrome: a paradigm of neurodevelopmental disorders with defective autophagy

Vici syndrome is a progressive neurodevelopmental multisystem disorder due to recessive mutations in the key autophagy gene EPG5. We report genetic, clinical, neuroradiological, and neuropathological features of 50 children from 30 families, as well as the neuronal phenotype of EPG5 knock-down in Drosophila melanogaster. We identified 39 different EPG5 mutations, most of them truncating and predicted to result in reduced EPG5 protein. Most mutations were private, but three recurrent mutations (p.Met2242Cysfs*5, p.Arg417*, and p.Gln336Arg) indicated possible founder effects. Presentation was mainly neonatal, with marked hypotonia and feeding difficulties. In addition to the five principal features (callosal agenesis, cataracts, hypopigmentation, cardiomyopathy, and immune dysfunction), we identified three equally consistent features (profound developmental delay, progressive microcephaly, and failure to thrive). The manifestation of all eight of these features has a specificity of 97%, and a sensitivity of 89% for the presence of an EPG5 mutation and will allow informed decisions about genetic testing. Clinical progression was relentless and many children died in infancy. Survival analysis demonstrated a median survival time of 24 months (95% confidence interval 0–49 months), with only a 10th of patients surviving to 5 years of age. Survival outcomes were significantly better in patients with compound heterozygous mutations (P = 0.046), as well as in patients with the recurrent p.Gln336Arg mutation. Acquired microcephaly and regression of skills in long-term survivors suggests a neurodegenerative component superimposed on the principal neurodevelopmental defect. Two-thirds of patients had a severe seizure disorder, placing EPG5 within the rapidly expanding group of genes associated with early-onset epileptic encephalopathies. Consistent neuroradiological features comprised structural abnormalities, in particular callosal agenesis and pontine hypoplasia, delayed myelination and, less frequently, thalamic signal intensity changes evolving over time. Typical muscle biopsy features included fibre size variability, central/internal nuclei, abnormal glycogen storage, presence of autophagic vacuoles and secondary mitochondrial abnormalities. Nerve biopsy performed in one case revealed subtotal absence of myelinated axons. Post-mortem examinations in three patients confirmed neurodevelopmental and neurodegenerative features and multisystem involvement. Finally, downregulation of epg5 (CG14299) in Drosophila resulted in autophagic abnormalities and progressive neurodegeneration. We conclude that EPG5-related Vici syndrome defines a novel group of neurodevelopmental disorders that should be considered in patients with suggestive features in whom mitochondrial, glycogen, or lysosomal storage disorders have been excluded. Neurological progression over time indicates an intriguing link between neurodevelopment and neurodegeneration, also supported by neurodegenerative features in epg5-deficient Drosophila, and recent implication of other autophagy regulators in late-onset neurodegenerative disease

Wnt5a Regulates Ventral Midbrain Morphogenesis and the Development of A9–A10 Dopaminergic Cells In Vivo

Wnt5a is a morphogen that activates the Wnt/planar cell polarity (PCP) pathway and serves multiple functions during development. PCP signaling controls the orientation of cells within an epithelial plane as well as convergent extension (CE) movements. Wnt5a was previously reported to promote differentiation of A9–10 dopaminergic (DA) precursors in vitro. However, the signaling mechanism in DA cells and the function of Wnt5a during midbrain development in vivo remains unclear. We hereby report that Wnt5a activated the GTPase Rac1 in DA cells and that Rac1 inhibitors blocked the Wnt5a-induced DA neuron differentiation of ventral midbrain (VM) precursor cultures, linking Wnt5a-induced differentiation with a known effector of Wnt/PCP signaling. In vivo, Wnt5a was expressed throughout the VM at embryonic day (E)9.5, and was restricted to the VM floor and basal plate by E11.5–E13.5. Analysis of Wnt5a−/− mice revealed a transient increase in progenitor proliferation at E11.5, and a precociously induced NR4A2+ (Nurr1) precursor pool at E12.5. The excess NR4A2+ precursors remained undifferentiated until E14.5, when a transient 25% increase in DA neurons was detected. Wnt5a−/− mice also displayed a defect in (mid)brain morphogenesis, including an impairment in midbrain elongation and a rounded ventricular cavity. Interestingly, these alterations affected mostly cells in the DA lineage. The ventral Sonic hedgehog-expressing domain was broadened and flattened, a typical CE phenotype, and the domains occupied by Ngn2+ DA progenitors, NR4A2+ DA precursors and TH+ DA neurons were rostrocaudally reduced and laterally expanded. In summary, we hereby describe a Wnt5a regulation of Wnt/PCP signaling in the DA lineage and provide evidence for multiple functions of Wnt5a in the VM in vivo, including the regulation of VM morphogenesis, DA progenitor cell division, and differentiation of NR4A2+ DA precursors

Rho GTPase function in flies: insights from a developmental and organismal perspective.

Morphogenesis is a key event in the development of a multicellular organism and is reliant on coordinated transcriptional and signal transduction events. To establish the segmented body plan that underlies much of metazoan development, individual cells and groups of cells must respond to exogenous signals with complex movements and shape changes. One class of proteins that plays a pivotal role in the interpretation of extracellular cues into cellular behavior is the Rho family of small GTPases. These molecular switches are essential components of a growing number of signaling pathways, many of which regulate actin cytoskeletal remodeling. Much of our understanding of Rho biology has come from work done in cell culture. More recently, the fruit fly Drosophila melanogaster has emerged as an excellent genetic system for the study of these proteins in a developmental and organismal context. Studies in flies have greatly enhanced our understanding of pathways involving Rho GTPases and their roles in development