Costing Systems and the Spare Capacity Conundrum: Avoiding the Death Spiral

2011 ◽  
Author(s):  
Ken Bates ◽  
John H. Bradshaw
Keyword(s):  
2012 ◽  
pp. 756-761 ◽  
Author(s):  
Miroslav Hutnan ◽  
Štefan Tóth ◽  
Igor Bodík ◽  
Nina Kolesárová ◽  
Michal Lazor ◽  
...  

The possibility of joint treatment of spent sugar beet pulp and wastewater from a sugar factory was studied in this work. Works focused on processing of spent sugar beet pulp separately or together with other substrates can be found in the literature. In the case of some sugar factories, which have spare capacity in the anaerobic reactor on an anaerobic-aerobic wastewater treatment plant, joint processing of spent sugar beet pulp and wastewater from the sugar factory might be an interesting option. The results of the operation of a pilot plant of an anaerobic reactor with a capacity of 3.5 m3 are discussed. Operation of the pilot plant confirmed the possibility of cofermentation of these materials. The organic loading rate achieved in the anaerobic reactor was higher than 6 kg/(m3·d) (COD), while more than half of the load was provided by spent sugar beet pulp. The addition of sugar beet pulp decreased the concentration of ammonia nitrogen in the anaerobic reactor and it was even necessary to add nitrogen. However, the nitrogen content in sludge water depends on the C:N ratio in the processed sugar beet pulp, therefore this knowledge cannot be generalized. About 1.5 to 2-fold biogas production can be expected from the cofermentation of wastewater with sugar beet pulp in an anaerobic reactor, compared with the biogas production from just wastewater treatment.


2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 309-310
Author(s):  
Yan Huang ◽  
Saeed Ghnaimawi ◽  
Yongjie Wang ◽  
Shilei Zhang ◽  
Jamie Baum

Abstract Muscle-derived stem cells (MDSCs, or myoblasts) play an important role in myotubes regeneration. However, these cells can differentiate into adipocytes once exposed to EPA and DHA, which are highly suggested during pregnancy. The objective of this study aims at determining the effect of isolated EPA and DHA on C2C12 cells undergoing white and brown adipogenic differentiation. Confluent cultured cells were treated with white and brown adipocyte induction medium (WIM and BIM respectively) with 50µM EPA and 50µM DHA separately. DHA treated groups differentiated into white-like adipocyte by down-regulating the expression of myogenic genes such as MyoD, MyoG, and Mrf4; but promoted white adipocyte marker genes(P < 0.05). Moreover, cells treated with WIM and DHA exhibited a decrease in mitochondrial biogenesis through suppressing PGC1a and TFAM expression (P < 0.05). Also, DHA promoted the expression of lipolysis regulating genes. DHA impaired C2C12 cells browning through reducing the mitochondrial biogenesis by significantly suppressing the expression of COX7a1, PGC1a, and UCP3 genes (P < 0.05). DHA treated groups showed an increased accumulation of lipid droplets and suppressed maximal mitochondrial respiration and spare capacity. EPA treatment reduced myogenesis regulating genes (P < 0.05) but did not affect adipogenic genes (P >0.05). Likewise, EPA suppressed the expression of WAT signature genes (P < 0.05), indicating its antagonism to DHA. EPA and WIM treatment suppressed the expression of TFAM and PGC1a, but did not affect PGC1a protein level. Although mitochondrial biogenic gene expression was reduced in EPA and BIDM treated group, no changes in mitochondrial function were observed. EPA supplementation did not affect the differential route of C2C12 into brown adipocytes. To conclude, EPA and DHA may similarly affect the integrity of muscle tissue, but DHA is a potent adipogenic and lipogenic factor that can change the metabolic profile of the body by increasing intramuscular fat.


2021 ◽  
Author(s):  
Hossa Almutairi ◽  
Axel Pierru ◽  
James L. Smith

2019 ◽  
Vol 12 (563) ◽  
pp. eaat9900 ◽  
Author(s):  
Souvarish Sarkar ◽  
Dharmin Rokad ◽  
Emir Malovic ◽  
Jie Luo ◽  
Dilshan S. Harischandra ◽  
...  

Chronic, sustained inflammation underlies many pathological conditions, including neurodegenerative diseases. Divalent manganese (Mn2+) exposure can stimulate neurotoxicity by increasing inflammation. In this study, we examined whether Mn2+activates the multiprotein NLRP3 inflammasome complex to promote neuroinflammation. Exposing activated mouse microglial cells to Mn2+substantially augmented NLRP3 abundance, caspase-1 cleavage, and maturation of the inflammatory cytokine interleukin-1β (IL-1β). Exposure of mice to Mn2+had similar effects in brain microglial cells. Furthermore, Mn2+impaired mitochondrial ATP generation, basal respiratory rate, and spare capacity in microglial cells. These data suggest that Mn-induced mitochondrial defects drove the inflammasome signal amplification. We found that Mn induced cell-to-cell transfer of the inflammasome adaptor protein ASC in exosomes. Furthermore, primed microglial cells exposed to exosomes from Mn-treated mice released more IL-1β than did cells exposed to exosomes from control-treated animals. We also observed that welders exposed to manganese-containing fumes had plasma exosomes that contained more ASC than did those from a matched control group. Together, these results suggest that the divalent metal manganese acts as a key amplifier of NLRP3 inflammasome signaling and exosomal ASC release.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A4-A4
Author(s):  
H Matthew Lehrer ◽  
Lauren Chu ◽  
Martica Hall ◽  
Kyle Murdock

Abstract Introduction Sleep is important for aging, health, and disease, but its cellular role in these outcomes is poorly understood. Basic research suggests that disturbed and insufficient sleep impair mitochondrial bioenergetics, which is involved in numerous aging-related chronic conditions. However, the relationship between sleep and bioenergetics has not been examined in humans. We examined associations of self-reported sleep with systemic bioenergetic function in peripheral blood mononuclear cells (PBMCs) of community-dwelling adults. Methods N = 43 adults (79% female) ages 48–70 (M = 61.63, SD = 5.99) completed the Pittsburgh Sleep Quality Index (PSQI) from which key components of sleep (satisfaction, alertness, timing, efficiency, and duration) were calculated. Participants provided blood samples from which PBMCs were isolated and measured for bioenergetics using extracellular flux analysis. Associations of sleep components with bioenergetic parameters, including the Bioenergetic Health Index (BHI), were examined. Results In bivariate analyses, lower sleep efficiency was associated with lower maximal respiration, spare capacity, and BHI (ps < 0.05). Longer sleep duration was associated with lower BHI (p < 0.01) and later sleep timing was associated with higher basal respiration, ATP-linked respiration, maximal respiration, spare capacity, and non-mitochondrial respiration (ps < 0.05). After adjustment for age, sex, and body mass index, lower sleep efficiency (β = 0.52, p < 0.01) and longer sleep duration (β = -0.43, p < 0.01) were associated with lower BHI. Conclusion Self-reported indices of sleep efficiency and duration are related to systemic bioenergetic function in humans, suggesting a possible cellular pathway linking sleep to health. Support (if any) T32HL082610


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