Sign Language Used By Deaf And Hearing Couple In Sign Duo Youtube Channel

Penelitian berjudul "Penggunaan Bahasa Isyarat Oleh Pasangan Tuli Dan Pendengar Di Saluran YouTube Sign Duo" bertujuan untuk mengungkap berbagai jenis elemen bahasa isyarat, dan komunikasi antara pasangan tuli dan pendengar juga dengan orang lain dalam kehidupan nyata. Dengan menggunakan metodologi kualitatif, penelitian ini menggunakan purposive sampling untuk memilih sampel yang relevan, dengan fokus pada ASL (American Sign Language) yang digunakan dalam saluran YouTube Sign Duo. Temuan mengungkapkan lima jenis elemen bahasa isyarat: handshape (33%), orientation (13%), location (21%), movement (20%), dan facial expression (13%). Komunikasi antara pasangan tuli dan pendengar menggunakan ASL (American Sign Language). Dalam kaitannya dengan unsur bahasa isyarat, di antara 88 data yang dianalisis, 46 data (33%), handshape adalah yang paling banyak ditemukan pada elemen bahasa isyarat sebagai cara termudah untuk berkomunikasi, terutama dengan ASL (American Sign Language) yang digunakan oleh pasangan tuli dan pendengar di saluran YouTube Sign Duo. Sebagian besar data yang digunakan adalah untuk nama seseorang, hewan, makanan, merek atau nama produk, akronim, lokasi atau tempat, nama acara, juga beberapa kalimat yang tidak memiliki tanda isyarat itu sendiri. Penelitian selanjutnya, orang perlu belajar bahasa isyarat dan ketika menggunakan bahasa isyarat, harus berhati-hati karena beberapa tanda memiliki arti yang berbeda, juga penggunaan bahasa isyarat di era digital

SLIDING MESH COMPUTATIONAL FLUID DYNAMICS SIMULATION OF A WIDE AND NARROW GAP INLINE ROTOR-STATOR MIXER

The FLUENT™ Computational Fluid Dynamics code was used to simulate the flow of water within an inline rotor-stator mixer. Two devices were simulated. Both had identical dimensions, except for the width of the shear gap: 4 mm for the 'wide gap' model and 0.5 mm for the 'standard gap' model. A two-dimensional approximation was used in conjunction with a RANS turbulence model and sliding mesh technique. Simulated turbulence intensities and mass flow rates are more evenly distributed in the standard gap model. Further, turbulence and mean shear levels within the gap are minimal and probably not important for the production of dispersions. The most intense turbulence is near the downstream stator slot wall, and it is due to fluid impingement. For the standard gap model, this region is more focused and of higher intensity. It is concluded that a narrow gap clearance is needed to produce high intensity stagnation flows on the stator teeth. Simulation results are also compared with previously reported measurements acquired via Laser Doppler Anemometry. With respect to mean velocity, qualitative agreement is good. Quantitatively, neither the mean velocities nor turbulence values are well predicted. This discrepancy is believed to be due in large part to leakage flow over the top of the rotor and stator teeth and to the three-dimensional nature of the flow. Future simulations should be carried out in three dimensions using more sophisticated turbulence models. Additionally, algorithms should be developed to decrease computation time by exploiting the periodic nature of rotor-stator flows

Phosphatidylserine is a critical modulator for Akt activation

Association of Akt with phosphatidylserine enhances binding to PIP3, inducing conformational changes in Akt that promote its phosphorylation-mediated activation

Depletion of brain docosahexaenoic acid impairs recovery from traumatic brain injury.

Omega-3 fatty acids are crucial for proper development and function of the brain where docosahexaenoic acid (DHA), the primary omega-3 fatty acid in the brain, is retained avidly by the neuronal membranes. We investigated the effect of DHA depletion in the brain on the outcome of traumatic brain injury (TBI). Pregnant mice were put on an omega-3 fatty acid adequate or deficient diet from gestation day 14 and the pups were raised on the respective diets. Continuation of this dietary regime for three generations resulted in approximately 70% loss of DHA in the brain. Controlled cortical impact was delivered to both groups of mice to produce severe TBI and the functional recovery was compared. Compared to the omega-3 adequate mice, the DHA depleted mice exhibited significantly slower recovery from motor deficits evaluated by the rotarod and the beam walk tests. Furthermore, the DHA deficient mice showed greater anxiety-like behavior tested in the open field test as well as cognitive deficits evaluated by the novel object recognition test. The level of alpha spectrin II breakdown products, the markers of TBI, was significantly elevated in the deficient mouse cortices, indicating that the injury is greater in the deficient brains. This observation was further supported by the reduction of NeuN positive cells around the site of injury in the deficient mice, indicating exacerbated neuronal death after injury. These results suggest an important influence of the brain DHA status on TBI outcome

Biosynthesis of N-Docosahexanoylethanolamine from Unesterified Docosahexaenoic Acid and Docosahexaenoyl-Lysophosphatidylcholine in Neuronal Cells

We investigated the synthesis of N-docosahexaenoylethanolamine (synaptamide) in neuronal cells from unesterified docosahexaenoic acid (DHA) or DHA-lysophosphatidylcholine (DHA-lysoPC), the two major lipid forms that deliver DHA to the brain, in order to understand the formation of this neurotrophic and neuroprotective metabolite of DHA in the brain. Both substrates were taken up in Neuro2A cells and metabolized to N-docosahexaenoylphosphatidylethanolamine (NDoPE) and synaptamide in a time- and concentration-dependent manner, but unesterified DHA was 1.5 to 2.4 times more effective than DHA-lysoPC at equimolar concentrations. The plasmalogen NDoPE (pNDoPE) amounted more than 80% of NDoPE produced from DHA or DHA-lysoPC, with 16-carbon-pNDoPE being the most abundant species. Inhibition of N-acylphosphatidylethanolamine-phospholipase D (NAPE-PLD) by hexachlorophene or bithionol significantly decreased the synaptamide production, indicating that synaptamide synthesis is mediated at least in part via NDoPE hydrolysis. NDoPE formation occurred much more rapidly than synaptamide production, indicating a precursor–product relationship. Although NDoPE is an intermediate for synaptamide biosynthesis, only about 1% of newly synthesized NDoPE was converted to synaptamide, possibly suggesting additional biological function of NDoPE, particularly for pNDoPE, which is the major form of NDoPE produced

Composition of omega-3 fatty acid adequate and omega-3 fatty acid deficient diets¹.

<p>1 These diets were prepared by Dyets Inc. (Bethlehem, PA, USA) based on AIN-93G (18) and have been used to achieve DHA depletion in rodents (24,36).</p><p>2 DHASCO: DHA Algal Oil.</p><p>3 tBHQ: tert-butylhydroquinone.</p

Depletion of DHA does not affect the volume of the lesion induced by TBI.

<p>Lesion volumes of DHA depleted brains after TBI are not statistically different from those of the DHA adequate controls (<i>n</i> = 6).</p

DHA deficiency increases TBI-induced spectrin-αII breakdown products (SBDPs) and decreases synapsin 1.

<p>(A) SBDP levels differentially increased after TBI in the affected cortices of DHA adequate (Ade) and deficient mice (Def). The contralateral cortices were used as controls. The deficient TBI group showed a significantly greater increase in SBDP levels after TBI for both 145 kDa and 150 kDa fragments as compared to the adequate TBI group (<i>n = </i>4<i>)</i>. (B) Synapsin 1 level affected by TBI and DHA depletion. TBI significantly decreased the synapsin-1 level in both diet groups. DHA depletion lowered the synapsin significantly (<i>p</i><0.05) in the non-injured mouse cortices. Although statistical significance was not reached, a trend of further decrease in synapsin 1 level after TBI was observed with DHA deficiency. * <i>p</i><0.05; ** <i>p</i><0.01; *** <i>p</i><0.001 compared to the non-injured adequate group.</p

DHA deficiency decreases NeuN positive cells after TBI.

<p>DHA depleted mice showed decreased NeuN positive cells in the peri-contusional cortices relative to the DHA adequate mice as indicated by the representative micrographs (A) and quantitative analysis (B) of 25 brain sections from 5 mice. Scale bar  =  50µm. * <i>p</i><0.05.</p

Omega-3 fatty acid deficiency impairs recovery from TBI-induced motor deficits.

<p>(A) The rotarod test showing slower recovery from TBI in the DHA deficient group (Deficient TBI) as compared to the adequate (Adequate TBI) mice with statistically significant differences on day 2 and day 4 after TBI (* <i>p</i><0.05 and *** <i>p</i><0.001 vs. the respective O-3 adequate group; <i>n = </i>8). (B) The beam walk test showing greater hindlimb footslips in DHA deficient mice as compared to the respective adequate controls (* <i>p</i><0.05, ** <i>p</i><0.01 and *** <i>p</i><0.001 vs. adequate TBI group; <i>n = </i>7–8).</p