scholarly journals Warm Acclimation Increases Mitochondrial Efficiency in Fish: A Compensatory Mechanism to Reduce the Demand for Oxygen

2021 ◽  
Author(s):  
Y. Voituron ◽  
D. Roussel ◽  
L. Teulier ◽  
M. Vagner ◽  
Q. Ternon ◽  
...  
Keyword(s):  
Compensatory Mechanism ◽  
Mitochondrial Efficiency ◽  
Warm Acclimation

Comparison of Progressive Antithrombin Activity and the Concentration of Three Thrombin Inhibitors in Nephrotic Syndrome

1981 ◽  
Vol 46 (03) ◽  
pp. 623-625 ◽  
Author(s):  
B Boneu ◽  
F Bouissou ◽  
M Abbal ◽  
P Sie ◽  
C Caranobe ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Antithrombin Iii ◽  
Heparin Therapy ◽  
Thrombin Inhibitors ◽  
Compensatory Mechanism ◽  
Dramatic Reduction ◽  
Antithrombin Activity ◽  
Α2 Macroglobulin ◽  
At Iii ◽  
A Prospective Study

SummaryIn order to compare the plasmatic progressive antithrombin activity to the concentration of three thrombin inhibitors, antithrombin III (AT III), α2 macroglobulin (α2, M), α1 anti-trypsin (α1 AT) in nephrotic syndrome, a prospective study was carried out on a group of 28 children affected with the disease. A dramatic reduction of the level of AT III and of α1 AT, two inhibitors of molecular weight close to that of albumin, was observed. The decreased level of AT III was counterbalanced by an increase in α2 M. This phenomenon accounts for the increased progressive antithrombin activity observed in all the affected children. It is suggested that the above compensatory mechanism explains the absence of thrombotic accidents in this series and that the benefit of heparin therapy is doubtful in these conditions.

Mitochondrial Efficiency and Growth Rate in Sugarbeet 1

Crop Science ◽  
1975 ◽  
Vol 15 (1) ◽  
pp. 5-7 ◽  
Author(s):  
D. L. Doney ◽  
R. E. Wyse ◽  
J. C. Theurer
Keyword(s):  
Growth Rate ◽  
Mitochondrial Efficiency

Stew in its Own Juice: Protein Homeostasis Machinery Inhibition Reduces Cell Viability in Multiple Myeloma Cell Lines

2019 ◽  
Vol 19 (2) ◽  
pp. 112-119 ◽  
Author(s):  
Mariana B. de Oliveira ◽  
Luiz F.G. Sanson ◽  
Angela I.P. Eugenio ◽  
Rebecca S.S. Barbosa-Dantas ◽  
Gisele W.B. Colleoni
Keyword(s):  
Multiple Myeloma ◽  
Cell Death ◽  
Cell Viability ◽  
Cell Lines ◽  
Treatment Options ◽  
Compensatory Mechanism ◽  
Protein Homeostasis ◽  
Protein Response ◽  
Rpmi 8226

Introduction:Multiple myeloma (MM) cells accumulate in the bone marrow and produce enormous quantities of immunoglobulins, causing endoplasmatic reticulum stress and activation of protein handling machinery, such as heat shock protein response, autophagy and unfolded protein response (UPR).Methods:We evaluated cell lines viability after treatment with bortezomib (B) in combination with HSP70 (VER-15508) and autophagy (SBI-0206965) or UPR (STF- 083010) inhibitors.Results:For RPMI-8226, after 72 hours of treatment with B+VER+STF or B+VER+SBI, we observed 15% of viable cells, but treatment with B alone was better (90% of cell death). For U266, treatment with B+VER+STF or with B+VER+SBI for 72 hours resulted in 20% of cell viability and both treatments were better than treatment with B alone (40% of cell death). After both triplet combinations, RPMI-8226 and U266 presented the overexpression of XBP-1 UPR protein, suggesting that it is acting as a compensatory mechanism, in an attempt of the cell to handle the otherwise lethal large amount of immunoglobulin overload.Conclusion:Our in vitro results provide additional evidence that combinations of protein homeostasis inhibitors might be explored as treatment options for MM.

Association Between Magnesium and Oxidative Stress in Patients with Obesity

2020 ◽  
Vol 16 (5) ◽  
pp. 743-748
Author(s):  
Ana R.S. de Oliveira ◽  
Kyria J.C. Cruz ◽  
Jennifer B.S. Morais ◽  
Juliana S. Severo ◽  
Jéssica B. Beserra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thiobarbituric Acid ◽  
Magnesium Concentration ◽  
Control Group ◽  
Compensatory Mechanism ◽  
Thiobarbituric Acid Reactive Substances ◽  
Magnesium Intake ◽  
Significant Difference ◽  
Dietary Magnesium ◽  
And Control

Background: The role of minerals in preventing the generation of oxidative stress in obese individuals has been evaluated. Magnesium is an antioxidant nutrient and a cofactor of enzymes involved in the cell membrane stabilization, attenuating the effects of oxidative stress. Objective: To evaluate the association between magnesium and concentrations of thiobarbituric acid reactive substances (TBARS) in patients with obesity and eutrophic women. Methods: A cross-sectional study was conducted with 73 women, divided into two groups: case group (patients with obesity, n=27) and control group (eutrophic women, n=46). Measurements of body mass index and waist circumference were performed. Dietary magnesium intake was assessed by the three-day food record using the NutWin software. Urinary magnesium concentration was measured by atomic absorption spectrophotometry method. Plasma concentrations of thiobarbituric acid reactive substances (TBARS) were also determined. Results: Mean values of dietary magnesium intake were 161.59 ± 60.04 and 158.73 ± 31.96 for patients with obesity and control group, respectively, with no significant difference between the groups studied (p >0.05). The value of urinary excretion of magnesium was lower than the reference values in both groups, with no significant difference between the groups studied (p >0.05). The plasma concentration of thiobarbituric acid reactive substances was significantly higher in patients with obesity compared to the control group (p <0.001). There was no correlation between levels of magnesium biomarkers and the concentration of TBARS (p >0.05). Conclusion: Patients with obesity showed a reduced dietary magnesium intake which seems to induce hypomagnesuria as a compensatory mechanism. The marker of oxidative stress evaluated in this study was not influenced by magnesium.

Let-7e-5p Regulates GLP-1 Content and Basal Release From Enteroendocrine L Cells From DIO Male Mice

Endocrinology ◽  
2019 ◽  
Vol 161 (2) ◽  
Author(s):  
Sandra Handgraaf ◽  
Rodolphe Dusaulcy ◽  
Florian Visentin ◽  
Jacques Philippe ◽  
Yvan Gosmain
Keyword(s):  
Compensatory Mechanism ◽  
L Cells ◽  
Low Fat Diet ◽  
Obesity And Diabetes ◽  
Basal Release ◽  
Glucagon Like Peptide 1 ◽  
Cell Transcriptome ◽  
Microarray Analyses

Abstract Characterization of enteroendocrine L cells in diabetes is critical for better understanding of the role of glucagon-like peptide-1 (GLP-1) in physiology and diabetes. We studied L-cell transcriptome changes including microRNA (miRNA) dysregulation in obesity and diabetes. We evaluated the regulation of miRNAs through microarray analyses on sorted enteroendocrine L cells from control and obese glucose-intolerant (I-HFD) and hyperglycemic (H-HFD) mice after 16 weeks of respectively low-fat diet (LFD) or high-fat diet (HFD) feeding. The identified altered miRNAs were studied in vitro using the mouse GLUTag cell line to investigate their regulation and potential biological functions. We identified that let-7e-5p, miR-126a-3p, and miR-125a-5p were differentially regulated in L cells of obese HFD mice compared with control LFD mice. While downregulation of let-7e-5p expression was observed in both I-HFD and H-HFD mice, levels of miR-126a-3p increased and of miR-125a-5p decreased significantly only in I-HFD mice compared with controls. Using miRNA inhibitors and mimics we observed that modulation of let-7e-5p expression affected specifically GLP-1 cellular content and basal release, whereas Gcg gene expression and acute GLP-1 secretion and cell proliferation were not affected. In addition, palmitate treatment resulted in a decrease of let-7e-5p expression along with an increase in GLP-1 content and release, suggesting that palmitate acts on GLP-1 through let-7e-5p. By contrast, modulation of miR-125a-5p and miR-126a-3p in the same conditions did not affect content or secretion of GLP-1. We conclude that decrease of let-7e-5p expression in response to palmitate may constitute a compensatory mechanism contributing to maintaining constant glycemia in obese mice.

scholarly journals The effects of doxorubicin on left and right atrial mechanics in patients with lymphoma

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Vahabi ◽  
E Kharati-Koopaei ◽  
M Stewart ◽  
H Hancock ◽  
M Norouzi ◽  
...  
Keyword(s):  
Strain Rate ◽  
Left Atrial ◽  
Left Ventricular ◽  
Right Atrial ◽  
Lv Function ◽  
Compensatory Mechanism ◽  
Research Association ◽  
Anthracycline Cardiotoxicity ◽  
Diastolic Strain Rate ◽  
Significant Change

Abstract Background Despite the associated dose-dependent cardiotoxicity, anthracyclines continue to form the backbone of modern chemotherapy regimens. Speckle Tracking Echocardiography (STE) has been a popular method of quantifying cardiac function but most studies have focused on left ventricular function. Research into the effects of anthracyclines on left atrial (LA) and right atrial (RA) function continues to be neglected. Purpose To investigate the effects of doxorubicin, a commonly used anthracycline, on both the LA and RA systolic and diastolic strain and strain-rate parameters in two groups of patients with lymphoma: Group 1 (G1) with a conventional drop in ejection fraction (EF &lt;53%), and Group 2 (G2) without. Methods We retrospectively studied 46 patients treated for lymphoma between 2015 and 2018; G1 (n=12) and G2 (n=34). Echocardiograms performed at baseline (T0), mid-chemotherapy (T1), and post-chemotherapy (T2), were analysed by using offline vendor-independent software (TomTec, 2D Cardiac Performance Analysis). Using 2D STE, LA and RA reservoir, conduit and contractile strains, systolic and diastolic strain-rates were measured. Multi-level longitudinal model was used for statistical analysis.This study was ethically approved by the Health Research Association (REC Reference 18/SS/0139). Results Median age was 64 years (IQR 51–74 years) in G1, and 65 years (IQR 57–73 years) in G2. In G1, there was no significant change in LA reservoir strain with time, however a significant decline with an average mean difference of −7.52 was seen between T0 to T2 (p=0.016) in G2. LA conduit strain did not significantly change in either group with incremental doses of doxorubicin. However, LA contraction strain was seen to significantly increase in G1 between T1 to T2 (p=0.045) with an average change of 7.23. LA peak systolic strain rate, and late diastolic strain rate did not show any significant change with time in both groups. Yet, a significant increase was seen in LA early diastolic strain rate between T0 to T2 (p=0.017) in G1 but not G2. No significant changes were seen in the RA strain parameters in both groups. Conclusion In patient with a reduction in LV function, a significant change was noted in the left atrial contraction strain and early diastolic strain rate with incremental doses of doxorubicin. These changes shows the close relationship between the LA and LV, and the importance of LA in providing a compensatory mechanism for a decline in LV function secondary to anthracycline cardiotoxicity. Funding Acknowledgement Type of funding source: None

scholarly journals Upregulation of COX4-2 via HIF-1α in Mitochondrial COX4-1 Deficiency

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 452
Author(s):  
Liza Douiev ◽  
Chaya Miller ◽  
Shmuel Ruppo ◽  
Hadar Benyamini ◽  
Bassam Abu-Libdeh ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Oxidative Phosphorylation ◽  
Nuclear Localization ◽  
Target Genes ◽  
Compensatory Mechanism ◽  
Terminal Electron Acceptor ◽  
Human Foreskin Fibroblasts ◽  
Mitochondrial Respiratory Complex ◽  
Mrna Transcripts ◽  
Oxphos System

Cytochrome-c-oxidase (COX) subunit 4 (COX4) plays important roles in the function, assembly and regulation of COX (mitochondrial respiratory complex 4), the terminal electron acceptor of the oxidative phosphorylation (OXPHOS) system. The principal COX4 isoform, COX4-1, is expressed in all tissues, whereas COX4-2 is mainly expressed in the lungs, or under hypoxia and other stress conditions. We have previously described a patient with a COX4-1 defect with a relatively mild presentation compared to other primary COX deficiencies, and hypothesized that this could be the result of a compensatory upregulation of COX4-2. To this end, COX4-1 was downregulated by shRNAs in human foreskin fibroblasts (HFF) and compared to the patient’s cells. COX4-1, COX4-2 and HIF-1α were detected by immunocytochemistry. The mRNA transcripts of both COX4 isoforms and HIF-1 target genes were quantified by RT-qPCR. COX activity and OXPHOS function were measured by enzymatic and oxygen consumption assays, respectively. Pathways were analyzed by CEL-Seq2 and by RT-qPCR. We demonstrated elevated COX4-2 levels in the COX4-1-deficient cells, with a concomitant HIF-1α stabilization, nuclear localization and upregulation of the hypoxia and glycolysis pathways. We suggest that COX4-2 and HIF-1α are upregulated also in normoxia as a compensatory mechanism in COX4-1 deficiency.

scholarly journals Pharmacological Blockade of PPARα Exacerbates Inflammatory Pain-Related Impairment of Spatial Memory in Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 610
Author(s):  
Jessica C. Gaspar ◽  
Catherine Healy ◽  
Mehnaz I. Ferdousi ◽  
Michelle Roche ◽  
David P. Finn
Keyword(s):  
Spatial Memory ◽  
Cognitive Processing ◽  
Inflammatory Pain ◽  
Dorsal Hippocampus ◽  
Memory Function ◽  
Intraperitoneal Administration ◽  
Compensatory Mechanism ◽  
Chronic Inflammatory Pain ◽  
Pharmacological Blockade ◽  
Innate Anxiety

Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent transcription factors that exist in three isoforms: PPARα, PPARβ/δ and PPARγ. Studies suggest that the PPAR signalling system may modulate pain, anxiety and cognition. The aim of the present study was to investigate whether endogenous signalling via PPARs differentially modulates innate anxiety responses and mnemonic function in the presence and absence of inflammatory pain. We examined the effects of intraperitoneal administration of GW6471 (PPARα antagonist), GSK0660 (PPARβ/δ antagonist), GW9662 (PPARγ antagonist), and N-palmitoylethanolamide (PEA) on rat behaviour in the elevated plus maze (EPM), open field (OF), light-dark box (LDB), and novel object recognition (NOR) tests in the presence or absence of chronic inflammatory pain. Complete Freund’s Adjuvant (CFA)-injected rats exhibited impaired recognition and spatial mnemonic performance in the NOR test and pharmacological blockade of PPARα further impaired spatial memory in CFA-treated rats. N-oleoylethanolamide (OEA) levels were higher in the dorsal hippocampus in CFA-injected animals compared to their counterparts. The results suggest a modulatory effect of CFA-induced chronic inflammatory pain on cognitive processing, but not on innate anxiety-related responses. Increased OEA-PPARα signalling may act as a compensatory mechanism to preserve spatial memory function following CFA injection.

scholarly journals De novo Neurosteroidogenesis in Human Microglia: Involvement of the 18 kDa Translocator Protein

2021 ◽  
Vol 22 (6) ◽  
pp. 3115
Author(s):  
Lorenzo Germelli ◽  
Eleonora Da Pozzo ◽  
Chiara Giacomelli ◽  
Chiara Tremolanti ◽  
Laura Marchetti ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
De Novo ◽  
Neuroactive Steroids ◽  
Translocator Protein ◽  
Compensatory Mechanism ◽  
Human Microglia ◽  
De Novo Biosynthesis ◽  
Murine Microglia ◽  
Synthetic Ligand ◽  
Tspo Expression

Neuroactive steroids are potent modulators of microglial functions and are capable of counteracting their excessive reactivity. This action has mainly been ascribed to neuroactive steroids released from other sources, as microglia have been defined unable to produce neurosteroids de novo. Unexpectedly, immortalized murine microglia recently exhibited this de novo biosynthesis; herein, de novo neurosteroidogenesis was characterized in immortalized human microglia. The results demonstrated that C20 and HMC3 microglial cells constitutively express members of the neurosteroidogenesis multiprotein machinery—in particular, the transduceosome members StAR and TSPO, and the enzyme CYP11A1. Moreover, both cell lines produce pregnenolone and transcriptionally express the enzymes involved in neurosteroidogenesis. The high TSPO expression levels observed in microglia prompted us to assess its role in de novo neurosteroidogenesis. TSPO siRNA and TSPO synthetic ligand treatments were used to reduce and prompt TSPO function, respectively. The TSPO expression downregulation compromised the de novo neurosteroidogenesis and led to an increase in StAR expression, probably as a compensatory mechanism. The pharmacological TSPO stimulation the de novo neurosteroidogenesis improved in turn the neurosteroid-mediated release of Brain-Derived Neurotrophic Factor. In conclusion, these results demonstrated that de novo neurosteroidogenesis occurs in human microglia, unravelling a new mechanism potentially useful for future therapeutic purposes.

The role of PKMζ in the maintenance of long-term memory: a review

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Hamish Patel ◽  
Reza Zamani
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Long Term Potentiation ◽  
Global Memory ◽  
Long Term Memory ◽  
Compensatory Mechanism ◽  
Term Memory ◽  
Kinase C

Abstract Long-term memories are thought to be stored in neurones and synapses that undergo physical changes, such as long-term potentiation (LTP), and these changes can be maintained for long periods of time. A candidate enzyme for the maintenance of LTP is protein kinase M zeta (PKMζ), a constitutively active protein kinase C isoform that is elevated during LTP and long-term memory maintenance. This paper reviews the evidence and controversies surrounding the role of PKMζ in the maintenance of long-term memory. PKMζ maintains synaptic potentiation by preventing AMPA receptor endocytosis and promoting stabilisation of dendritic spine growth. Inhibition of PKMζ, with zeta-inhibitory peptide (ZIP), can reverse LTP and impair established long-term memories. However, a deficit of memory retrieval cannot be ruled out. Furthermore, ZIP, and in high enough doses the control peptide scrambled ZIP, was recently shown to be neurotoxic, which may explain some of the effects of ZIP on memory impairment. PKMζ knockout mice show normal learning and memory. However, this is likely due to compensation by protein-kinase C iota/lambda (PKCι/λ), which is normally responsible for induction of LTP. It is not clear how, or if, this compensatory mechanism is activated under normal conditions. Future research should utilise inducible PKMζ knockdown in adult rodents to investigate whether PKMζ maintains memory in specific parts of the brain, or if it represents a global memory maintenance molecule. These insights may inform future therapeutic targets for disorders of memory loss.

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