Efficient Implementation of Multiply Accumulate Operation Unit Using an Interlaced Partition Multiplier

2021 ◽  
Vol 18 (4) ◽  
pp. 1321-1326
Author(s):  
N. Bhuvaneswary ◽  
S. Prabu ◽  
K. Tamilselvan ◽  
K. G. Parthiban
Keyword(s):  
Vital Role ◽  
Efficient Implementation ◽  
Partial Sums ◽  
Array Multiplier ◽  
New Strategy ◽  
Operation Unit ◽  
Design Speed

A new strategy for quick multiplication of two numbers is introduced. Inputs are separated into segments, and one segment is replaced by two with zeros interlocking in each alternative segments. With zero carries between segments the product are computed, within the time needed to multiply the short partitions and add the partial sums. The multiplication of two numbers generated and adds that product to an accumulator by multiply accumulate operation (MAC unit). This operation is performed within the MAC unit. MAC is an advanced co-processor that plays a vital role in FFT, DFT, etc. The MAC unit is utilized for additional execution and its input is given to the proposed multiplier that provides a trivial speed increment over the array multiplier designs. This paper is utilized to design speed enhanced multiply Accumulate Unit by an Interlaced Partition Multiplier. This new multiplier design simulation is optimized with existing method.

scholarly journals Silence of NLRP3 Suppresses Atherosclerosis and Stabilizes Plaques in Apolipoprotein E-Deficient Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Fei Zheng ◽  
Shanshan Xing ◽  
Zushun Gong ◽  
Wei Mu ◽  
Qichong Xing
Keyword(s):  
Rna Interference ◽  
Apolipoprotein E ◽  
Nlrp3 Inflammasome ◽  
Vital Role ◽  
Nlrp3 Gene ◽  
New Strategy ◽  
Nlrp3 Inflammasomes ◽  
The Impact ◽  
Deficient Mice

Objectives. The role of the NLRP3 inflammasome in atherosclerosis remains controversial. The aim of this study was to determine whether inhibition of NLRP3 signaling by lentivirus-mediated RNA interference could reduce atherosclerosis and stabilizes plaques. We also tried to explore the mechanisms of the impact of NLRP3 inflammasome on atherosclerosis.Methods. Apolipoprotein E-deficient mice aged 8 weeks were fed a high-fat diet and were injected with NLRP3 interfering or mock viral suspension after 4 weeks. Lentivirus transfer was repeated in 2 weeks. Four weeks after the first lentivirus injection, we evaluated the effects of NLRP3 gene silencing on plaque composition and stability and on cholesterol efflux and collagen metabolism, by histopathologic analyses and real-time PCR.Results. Gene silence of NLRP3 prevented plaques progression and inhibited inductions of proinflammatory cytokines. Moreover, this RNA interference reduced plaque content of macrophages and lipid, and increased plaque content of smooth muscle cells and collagen, leading to the stabilizing of atherosclerotic plaques.Conclusions. NLRP3 inflammasomes may play a vital role in atherosclerosis, and lentivirus-mediated NLRP3 silencing would be a new strategy to inhibit plaques progression and to reduce local inflammation.

scholarly journals Autologous transplantation of thecal stem cells restores ovarian function in nonhuman primates

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Hong Chen ◽  
Kai Xia ◽  
Weijun Huang ◽  
Huijian Li ◽  
Chao Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Ovarian Function ◽  
Autologous Transplantation ◽  
Fertilization Rate ◽  
Vital Role ◽  
Ovarian Activity ◽  
New Strategy ◽  
First Time ◽  
Human Primate

AbstractPremature ovarian insufficiency (POI) is defined as the loss of ovarian activity under the age of 40. Theca cells (TCs) play a vital role during folliculogenesis and TCs dysfunction participate in the pathogenesis of POI. Therefore, transplantation of thecal stem cells (TSCs), which are capable of self-renewal and differentiation into mature TCs, may provide a new strategy for treating POI. To investigate the feasibility, safety, and efficacy of TSCs transplantation in clinically relevant non-human primate (NHP) models, we isolate TSCs from cynomolgus monkeys, and these cells are confirmed to expand continuously and show potential to differentiate into mature TCs. In addition, engraftment of autologous TSCs into POI monkeys significantly improves hormone levels, rescues the follicle development, promotes the quality of oocytes and boosts oocyte maturation/fertilization rate. Taken together, these results for the first time suggest that autologous TSCs can ameliorate POI symptoms in primate models and shed new light on developing stem cell therapy for POI.

scholarly journals NPI-0052 and gamma-radiation induce a synergistic apoptotic effect in the most aggressive medulloblastoma subgroup

2019 ◽  
Vol 21 (Supplement_4) ◽  
pp. iv16-iv16
Author(s):  
Eleni Frisira ◽  
Fatima Rashid ◽  
David Michod ◽  
Maria Victoria Niklison Chirou
Keyword(s):  
Gamma Radiation ◽  
Standard Of Care ◽  
Proteasome Inhibition ◽  
Vital Role ◽  
Novel Therapy ◽  
P53 Family ◽  
New Strategy ◽  
Apoptotic Effect ◽  
Group 3 ◽  
Preclinical Work

Abstract Group 3 medulloblastoma (MB) is the most aggressive and least characterised of all MB subgroups. These tumours are highly metastatic and patients undergo aggressive treatments leaving survivors with severe side effects. The standard of care for these patients consists of surgical resection followed by gamma-radiation and chemotherapy. Whilst this conventional therapy is successful in the majority of cases, however, many survivors are left with lifelong severe neurocognitive and physical sequelae. Interestingly, the proteasome plays a vital role in the pathogenesis of different tumours, therefore proteasome inhibition can be used as a new strategy for treating MB. NPI-0052 is a proteasome inhibitor that can penetrate the blood-brain barrier with a good safety profile, making it an appealing treatment for brain tumors. In the present study, we evaluate the anticancer activity of NPI-0052 in a range of MB patient derived MB cells and cell lines. Our preclinical work demonstrated that NPI-0052 can inhibit proteasome activity and activate apoptosis in MB cells. We also show that the p53-family plays a substantial role in NPI-0052’s mechanism of action. Moreover, we observe that NPI-0052 has a synergistic apoptotic effect with gamma-radiation, a component of the current MB therapy, in both cells and tumour organoids. Our work underscores the use of NPI-0052 as a novel therapy for reducing the doses of gamma-radiation in G3-MB patients.

scholarly journals Sirt1 Promotes the Restoration of Hepatic Progenitor Cell (HPC)-Mediated Liver Fatty Injury in NAFLD Through Activating the Wnt/β-Catenin Signal Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Qinjin Li ◽  
Yuqing Gong ◽  
Yi Wang ◽  
Bingbing Liu ◽  
Yi Chu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Fatty Liver ◽  
Glycogen Synthesis ◽  
Vital Role ◽  
Signal Pathway ◽  
Regeneration Ability ◽  
Mice Model ◽  
Ductular Reaction ◽  
Alcoholic Fatty Liver ◽  
New Strategy

Non-alcoholic fatty liver disease (NAFLD) has developed into the world's largest chronic epidemic. In NAFLD, hepatic steatosis causes hepatocytes dysfunction and even apoptosis. The liver has a strong restoration or regeneration ability after an injury, however, it is unclear through which pattern fatty liver injury in NAFLD is repaired and what the repair mechanism is. Here, we found that in the high-fat diet (HFD)-induced NAFLD mice model, fatty liver injury caused the significant ductular reaction (DR), which is a marker to promote the repair of liver injury. SOX9+ and HNF4α+ biphenotype also suggested that hepatic progenitor cells (HPCs) were activated by fatty liver injury in the HFD-elicited NAFLD mice model. Concurrently, fatty liver injury also activated the Wnt/β-catenin signal pathway, which is a necessary process for HPC differentiation into mature hepatocytes. However, Sirt1 knockdown weakened HPC activation and Wnt/β-catenin signal in Sirt1+/− mice with HFD feeding. In rat-derived WB-F344 hepatic stem cell line, Sirt1 overexpression (OE) or Sirt1 activator–Resveratrol promoted HPC differentiation via activating Wnt/β-catenin signal pathway. Glycogen PAS staining demonstrated that Sirt1 OE promoted WB-F344 cells to differentiate into mature hepatocytes with glycogen synthesis ability, while Sirt1 inhibitor EX527 or Wnt/β-catenin pathway inhibitor HF535 decreased glycogen positive cells. Together, our data suggested that Sirt1 plays a vital role in activating HPCs to repair fatty liver injury or promote liver regeneration through the Wnt/β-catenin signal pathway in NAFLD, which might provide a new strategy for fatty liver injury or NAFLD therapy.

scholarly journals SENP3-Mediated PPARγ2 DeSUMOylation in BM-MSCs Potentiates Glucocorticoid-Induced Osteoporosis by Promoting Adipogenesis and Weakening Osteogenesis

2021 ◽  
Vol 9 ◽  
Author(s):  
Yongxing Zhang ◽  
Yang Chen ◽  
Hangxiang Sun ◽  
Wenkan Zhang ◽  
Lingling Zhang ◽  
...  
Keyword(s):  
Bone Formation ◽  
Osteogenic Differentiation ◽  
Clinical Diagnosis ◽  
Pathological Change ◽  
Vital Role ◽  
Diagnosis And Treatment ◽  
Secondary Osteoporosis ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
New Strategy

Glucocorticoid-induced osteoporosis (GIOP) is the most common secondary osteoporosis and reduced bone formation was the main pathological change in GIOP. Our previous studies have shown that there was an imbalance between adipogenic and osteogenic differentiation in GIOP BM-MSCs and peroxisome proliferator-activated receptor γ2 (PPARγ2) played a vital role in this disorders. Here, we reported that there was an increase in ROS level and SENP3 expression in Dex-induced osteoporotic BM-MSCs, and enhanced adipogenesis and weakened osteogenesis in osteoporotic BM-MSCs might be caused by upregulated SENP3. Then we found that SENP3 de-SUMOylated PPARγ2 on K107 site to potentiate adipogenesis and weaken osteogenesis. These results may provide new strategy and target in the clinical diagnosis and treatment of GIOP.

scholarly journals An improved implementation of hierarchy array multiplier using CslA adder and full swing GDI logic

2017 ◽  
Vol 21 (1) ◽  
pp. 38
Author(s):  
Shoba Mohan ◽  
Nakkeeran Rangaswamy
Keyword(s):  
Energy Consumption ◽  
Power Consumption ◽  
Clock Cycle ◽  
Efficient Implementation ◽  
Multiplication Operation ◽  
Array Multiplier ◽  
Carry Select Adder ◽  
Simulation Results ◽  
Array Multipliers ◽  
Full Swing

In this paper, an efficient implementation of a 16 bit array hierarchy multiplier using full swing Gate Diffusion Input (GDI) logic is discussed. Hierarchy multiplier is attractive because of its ability to carry the multiplication operation withi one clock cycle. The existing hierarchical multipliers occupy more area and suffer from accumulation delay of base multiplier output bits. These issues can be addressed by incorporating carry select adder based addition and the multiplier implementation using full swing GDI logic. The basic computation blocks involved in the multiplier are AND gate and carry propagate adder. They are implemented with using full swing GDI logic. Due to their reduced transistor count and less power consumption, this multiplier implementation leads to significant improvement compared with the existing implementations. The designed and existing array multipliers are simulated at 45 nm technology model and their power consumption and delay are calculated from the simulation results. It is validated that the proposed hierarchy array multiplier based on full swing GDI logic has 27% less energy consumption than the existing design. The results confirmed that implemented multiplier has shown better performance and can be used for signal and im age processing.

Melatonin alleviates pyroptosis of retinal neurons following acute intraocular hypertension

2020 ◽  
Vol 19 ◽  
Author(s):  
Zhang Yu ◽  
Huang Yanxia ◽  
Guo Limin ◽  
Zhang Yun ◽  
Zhao Mingxuan ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Ganglion Cells ◽  
Vital Role ◽  
Retinal Ganglion ◽  
Retinal Neurons ◽  
Irreversible Loss ◽  
Inflammatory Reactions ◽  
New Strategy ◽  
High Risk Factor ◽  
Structural Loss

Background: Glaucoma is a multifactorial optic neuropathy progressive characterized by structural loss of retinal ganglion cells (RGCs) and irreversible loss of vision. High intraocular pressure (HIOP) is a high risk factor for glaucoma. It has been reported that the manners of RGCs’ loss are in-depth explored after acute HIOP injury, such as, apoptosis, autophagy and necrosis. However, pyroptosis, a novel type of pro-inflammatory cell programmed necrosis, rarely reported after acute HIOP injury. Researches also showed that melatonin (MT) possesses substantial anti-inflammatory properties. However, whether melatonin could alleviate retinal neurons death, especially pyroptosis, by acute HIOP injury is unclear. Objective: This study explored pyroptosis of retinal neurons and the effects of MT preventing retinal neurons form pyroptosis after acute HIOP injury. Method: Establish acute HIOP model in rat by increasing the IOP and then reperfusion. Western Blot (WB) was adopted to detect molecules related to pyroptosis at the protein level, such as GasderminD (GSDMD), GasderminDp32 (GSDMDp32), Caspase-1 (Casp-1) and Caspase-1p20 (Casp-1p20), and the products of inflammatory reactions, as interleukin-18 (IL-18) and interleukin-1β (IL-1β) as well. At the same time, Immunofluorescence (IF) was used to co-localize Casp-1with retinal neurons to determine the position of Casp-1 expression. Morphologically, Ethidium homodimer-III staining, a method commonly used for judging cell death, was carried out to stain dead cells. Subsequently, Lactate Dehydrogenase (LDH) cytotoxicity assay kit was used to quantitative analysis the LDH released after cell disruption. Results: The results suggested that pyroptosis played a vital role in retinal neurons death, especially in the ganglion cell layer, by acute HIOP injury and peaked at 6h after acute HIOP injury. Furthermore, it was found that MT might prevent retinal neurons from pyroptosis via NF-κB/NLRP3 axis after acute HIOP injury in rats. Conclusion: MT treatment might be considered a new strategy for protecting retinal neurons against pyroptosis following acute HIOP injury.

Ultrastructure of Lymphatic Capillaries in the Transport of Colloidal Particles

1967 ◽  
Vol 25 ◽  
pp. 186-187
Author(s):  
L. V. Leak ◽  
J. F. Burke
Keyword(s):  
Connective Tissue ◽  
Colloidal Particles ◽  
Ultrastructural Level ◽  
Vital Role ◽  
Time Intervals ◽  
Thorium Dioxide ◽  
Lymphatic Capillary ◽  
Tissue Area ◽  
Rapid Removal ◽  
Tissue Fluids

The vital role played by the lymphatic capillaries in the transfer of tissue fluids and particulate materials from the connective tissue area can be demonstrated by the rapid removal of injected vital dyes into the tissue areas. In order to ascertain the mechanisms involved in the transfer of substances from the connective tissue area at the ultrastructural level, we have injected colloidal particles of varying sizes which range from 80 A up to 900-mμ. These colloidal particles (colloidal ferritin 80-100A, thorium dioxide 100-200 A, biological carbon 200-300 and latex spheres 900-mμ) are injected directly into the interstitial spaces of the connective tissue with glass micro-needles mounted in a modified Chambers micromanipulator. The progress of the particles from the interstitial space into the lymphatic capillary lumen is followed by observing tissues from animals (skin of the guinea pig ear) that were injected at various time intervals ranging from 5 minutes up to 6 months.

Three-Dimensional reconstruction of isolated centrosomes by automated electron tomography

1994 ◽  
Vol 52 ◽  
pp. 310-311
Author(s):  
M.B. Braunfeld ◽  
M. Moritz ◽  
B.M. Alberts ◽  
J.W. Sedat ◽  
D.A. Agard
Keyword(s):  
Electron Tomography ◽  
Three Dimensional ◽  
Vital Role ◽  
Complex Nature ◽  
Animal Cells ◽  
Microtubule Organizing Center ◽  
Nucleation Sites ◽  
Dimensional Reconstruction ◽  
Organizing Center ◽  
Resolution Model

In animal cells, the centrosome functions as the primary microtubule organizing center (MTOC). As such the centrosome plays a vital role in determining a cell's shape, migration, and perhaps most importantly, its division. Despite the obvious importance of this organelle little is known about centrosomal regulation, duplication, or how it nucleates microtubules. Furthermore, no high resolution model for centrosomal structure exists.We have used automated electron tomography, and reconstruction techniques in an attempt to better understand the complex nature of the centrosome. Additionally we hope to identify nucleation sites for microtubule growth.Centrosomes were isolated from early Drosophila embryos. Briefly, after large organelles and debris from homogenized embryos were pelleted, the resulting supernatant was separated on a sucrose velocity gradient. Fractions were collected and assayed for centrosome-mediated microtubule -nucleating activity by incubating with fluorescently-labeled tubulin subunits. The resulting microtubule asters were then spun onto coverslips and viewed by fluorescence microscopy.

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