Quality and Quantity Control in Horse Feeding

2019 ◽  
pp. 274-277b
Author(s):  
Melvin Bradley
Keyword(s):  
Quantity Control

scholarly journals Quality and quantity control at the endoplasmic reticulum

2010 ◽  
Vol 22 (4) ◽  
pp. 437-446 ◽  
Author(s):  
Ramanujan S Hegde ◽  
Hidde L Ploegh
Keyword(s):  
Endoplasmic Reticulum ◽  
Quantity Control

scholarly journals Study on Profitable Shared Parking Management Based on Day-to-Day Evolution Model

2021 ◽  
Vol 33 (1) ◽  
pp. 17-33
Author(s):  
Duo Xu ◽  
Huijun Sun
Keyword(s):  
Urban Area ◽  
Optimal Allocation ◽  
Cost Minimization ◽  
Profit Maximization ◽  
Evolution Model ◽  
Residential Areas ◽  
Short Supply ◽  
Parking Lots ◽  
Morning Commute ◽  
Quantity Control

Parking problems are getting increasingly serious in the urban area. However, the parking spots in the urban area are underutilized rather than really scarce. There is a large number of private spots in the residential areas that have the potential of being shared. Due to its private nature, shared parking is usually operated by a profitable mode. To study the utilization of shared parking and its impact on the morning commute, this paper proposes an evolution model. The supply side is a profit-chasing manager who decides on the selling prices and the business scale, while the demand side refers to travellers who respond to costs and choose the trip mode. By analysing the behaviour (strategy) of both sides, the study covers: 1 - the attraction and competition between parking lots and trip modes, 2 - the utilization and user composition of the parking lots. By inducing two numerical examples, the conclusions are that 1 - managers can achieve maximum profit and optimal allocation through price adjustment and quantity control; 2 - publicity (system cost minimization) and profitability (profit maximization) are consistent under certain threshold conditions; 3 - competition exists between parking lots as well as trip modes; some parking lots are even in short supply; profitable management does not create a market monopoly.

Controlling quality and amount of mitochondria by mitophagy: insights into the role of ubiquitination and deubiquitination

2016 ◽  
Vol 397 (7) ◽  
pp. 637-647 ◽  
Author(s):  
Tao Tan ◽  
Marcel Zimmermann ◽  
Andreas S. Reichert
Keyword(s):  
Mammalian Cells ◽  
Mitochondrial Fission ◽  
Baker’S Yeast ◽  
Negative Regulator ◽  
Mitochondrial Outer Membrane ◽  
Baker's Yeast ◽  
Genome Wide ◽  
A Genome ◽  
Autophagy Pathway ◽  
Quantity Control

Abstract Mitophagy is a selective autophagy pathway conserved in eukaryotes and plays an essential role in mitochondrial quality and quantity control. Mitochondrial fission and fusion cycles maintain a certain amount of healthy mitochondria and allow the isolation of damaged mitochondria for their elimination by mitophagy. Mitophagy can be classified into receptor-dependent and ubiquitin-dependent pathways. The mitochondrial outer membrane protein Atg32 is identified as the only known receptor for mitophagy in baker’s yeast, whereas mitochondrial proteins FUNDC1, NIX/BNIP3L, BNIP3 and Bcl2L13 are recognized as mitophagy receptors in mammalian cells. Earlier studies showed that ubiquitination and deubiquitination occurs in yeast, yet there is no direct evidence for an ubiquitin-dependent mitophagy pathway in this organism. In contrast, a ubiquitin-/PINK1-/Parkin-dependent mitophagy pathway was unraveled and was extensively characterized in mammals in recent years. Recently, a quantitative method termed synthetic quantitative array (SQA) technology was developed to identify modulators of mitophagy in baker’s yeast on a genome-wide level. The Ubp3-Bre5 deubiquitination complex was found as a negative regulator of mitophagy while promoting other autophagic pathways. Here we discuss how ubiquitination and deubiquitination regulates mitophagy and other selective forms of autophagy and what argues for using baker’s yeast as a model to study the ubiquitin-dependent mitophagy pathway.

Abstract 152: Mitochondrial Fission Inhibitor Mdivi-1 Attenuates Angiotensin II-Induced Cardiovascular Remodeling

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Steven J Forrester ◽  
Tatsuo Kawai ◽  
Katherine J Elliott ◽  
Kunie Eguchi ◽  
Victor Rizzo ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Er Stress ◽  
Mitochondrial Fission ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Heart Weight ◽  
Cardiovascular Remodeling ◽  
Target Organs ◽  
Quantity Control ◽  
Affect Heart Rate

Mitochondrial dysfunction has been implicated in various types of cardiovascular diseases which may involve overload and de-compensation in mitochondrial quality/quantity control. However, limited mechanistic insight is available regarding the contribution and mechanism of mitochondrial quality control in hypertension. In the present study, we tested our hypothesis that enhancement of mitochondrial fission in vascular cells is involved in hypertensive vascular remodeling. 8 week old male C57/Bl6 mice were infused with angiotensin II (1000 ng/kg/min) for 2 weeks with or without treatment of mitochondrial fission inhibitor Mdivi-1 (25 mg/kg ip every other day). Mdivi-1 significantly inhibited AngII-induced left ventricular hypertrophy assessed by heart weight body weight ratio as well as by echocardiogram. Histological assessment of the Mdivi-1-treated mouse hearts further demonstrated significant suppression of vessel hypertrophy and fibrosis induced by AngII. However, Mdivi-1 did not affect heart rate or hypertension induced by AngII assessed by telemetry. KDEL and VCAM1 staining of the heart and aorta suggest attenuation of vascular ER stress and inflammation, respectively. In cultured rat vascular smooth muscle cell (VSMCs), AngII induced mitochondrial fission promoting Drp1 phosphorylation at Ser616 and Ser637. Pretreatment of Mdivi-1 (5 microM 30 min) attenuated 100 nM AngII-induced mitochondrial fission in VSMCs assessed by mito-tracker staining. Mdivi-1 also attenuated extracellular collagen accumulation induced by AngII in VSMCs assessed by Sirius Red staining quantification kit. In conclusion, this data suggests that Mdivi-1 treatment prevents AngII-induced cardiovascular remodeling independently of hypertension via suppression of mitochondrial fission and attenuation of ER stress and inflammation in target organs.

Determination of the Content of Ultra-Low Sulphur in PM Superalloy FGH96 by Infrared Carbon-Sulphur Detector

2013 ◽  
Vol 634-638 ◽  
pp. 1821-1825
Author(s):  
Jian Huan Wei ◽  
Wei Cao ◽  
Yong Zhang
Keyword(s):  
Grain Boundary ◽  
Fatigue Property ◽  
Market Demand ◽  
Analysis Techniques ◽  
Test Conditions ◽  
Turbine Disc ◽  
Quantity Control ◽  
Impurity Elements ◽  
Pm Superalloy

PM Superalloy FGH96 is usually used as turbine disc materials. It is a kind of alloy with high purity, which has strict demands of the content of impurity elements, especially the element of sulphur. Because sulphur is accumulated in the grain boundary of manganese or iron, with the form of sulfide, it has great impact on the performance of PM Superalloy FGH96, such as toughness and fatigue property. Therefore, it is an important part of quantity control to detect accurately of the content of ultra-low sulphur in PM Superalloy FGH96. As the market demand of PM Superalloy FGH96 and quality becomes varied, it is a trend that PM Superalloy FGH96 has ultra-low content of sulphur (S: 0.0001%-0.0020%). Hence, the related analysis techniques are needed. A new method of analyzing Ultra-low Sulphur (S: 0.0001%-0.0020%) in PM Superalloy FGH96 is established in the article by selective experiments with relevant test conditions, such as combustion conditions and blank test, using infrared carbon-sulphur detector.

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