Compensatory Mechanisms
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2021 ◽  
Vol 13 ◽  
Sonia Di Tella ◽  
Valeria Blasi ◽  
Monia Cabinio ◽  
Niels Bergsland ◽  
Giovanni Buccino ◽  

Aging is the major risk factor for chronic age-related neurological diseases such as neurodegenerative disorders and neurovascular injuries. Exploiting the multimodal nature of the Mirror Neuron System (MNS), rehabilitative interventions have been proposed based on motor-resonance mechanisms in recent years. Despite the considerable evidence of the MNS’ functionality in young adults, further investigation of the action-observation matching system is required in aging, where well-known structural and functional brain changes occur. Twenty-one healthy young adults (mean age 26.66y) and 19 healthy elderly participants (mean age 71.47y) underwent a single MRI evaluation including a T1-3D high-resolution and functional MRI (fMRI) with mirror task. Morphological and functional BOLD data were derived from MRI images to highlight cortical activations associated with the task; to detect differences between the two groups (Young, Elderly) in the two MRI indexes (BOLD and thickness z-scores) using mixed factorial ANOVA (Group∗Index analyses); and to investigate the presence of different cortical lateralization of the BOLD signal in the two groups. In the entire sample, the activation of a bilateral MNS fronto-parietal network was highlighted. The mixed ANOVA (pFDR-corr < 0.05) revealed significant interactions between BOLD signal and cortical thickness in left dorsal premotor cortex, right ventral premotor and prefrontal cortices. A different cortical lateralization of the BOLD signal in frontal lobe activity between groups was also found. Data herein reported suggest that age-related cortical thinning of the MNS is coupled with increased interhemispheric symmetry along with premotor and prefrontal cortex recruitment. These physiological changes of MNS resemble the aging of the motor and cognitive neural systems, suggesting specific but also common aging and compensatory mechanisms.

2021 ◽  
Vol 53 (8S) ◽  
pp. 264-264
Inês R. Correia ◽  
Megan Hetherington-Rauth ◽  
João P. Magalhães ◽  
Gil B. Rosa ◽  
Luís B. Sardinha

2021 ◽  
Vol 11 (1) ◽  
Anna Papazoglou ◽  
Christina Henseler ◽  
Karl Broich ◽  
Johanna Daubner ◽  
Marco Weiergräber

AbstractHigh voltage-activated Cav2.3 R-type Ca2+ channels and low voltage-activated Cav3.2 T-type Ca2+ channels were reported to be involved in numerous physiological and pathophysiological processes. Many of these findings are based on studies in Cav2.3 and Cav3.2 deficient mice. Recently, it has been proposed that inbreeding of Cav2.3 and Cav3.2 deficient mice exhibits significant deviation from Mendelian inheritance and might be an indication for potential prenatal lethality in these lines. In our study, we analyzed 926 offspring from Cav3.2 breedings and 1142 offspring from Cav2.3 breedings. Our results demonstrate that breeding of Cav2.3 deficient mice shows typical Mendelian inheritance and that there is no indication of prenatal lethality. In contrast, Cav3.2 breeding exhibits a complex inheritance pattern. It might be speculated that the differences in inheritance, particularly for Cav2.3 breeding, are related to other factors, such as genetic specificities of the mutant lines, compensatory mechanisms and altered sperm activity.

Ross Parry ◽  
Fabrice R Sarlegna ◽  
Nathanaël Jarrassé ◽  
Agnes Roby-Brami

The purpose of this study was to determine the contributions of feedforward and feedback processes on grip force regulation and object orientation during functional manipulation tasks. One patient with massive somatosensory loss resulting from large fibre sensory neuropathy, and ten control participants were recruited. Three experiments were conducted: 1) perturbation to static holding; 2) discrete vertical movement; and 3) functional grasp and place. The availability of visual feedback was also manipulated to assess the nature of compensatory mechanisms. Results from experiment 1 indicated that both the deafferented patient and controls used anticipatory grip force adjustments prior to self-induced perturbation to static holding. The patient exhibited increased grip response time, but the magnitude of grip force adjustments remained correlated with perturbation forces in the self-induced and external perturbation conditions. In experiment 2, the patient applied peak grip force substantially in advance of maximum load force. Unlike controls, the patient's ability to regulate object orientation was impaired without visual feedback. In experiment 3, the duration of unloading, transport and release phases were longer for the patient, with increased deviation of object orientation at phase transitions. These findings show that the deafferented patient uses distinct modes of anticipatory control according to task constraints, and that responses to perturbations are mediated by alternative afferent information. The loss of somatosensory feedback thus appears to impair control of object orientation, while variation in the temporal organization of functional tasks may reflect strategies to mitigate object instability associated with changes in movement dynamics.

2021 ◽  
Vol 22 (13) ◽  
pp. 7220
Thuy-Hang Nguyen ◽  
Stephanie Conotte ◽  
Alexandra Belayew ◽  
Anne-Emilie Declèves ◽  
Alexandre Legrand ◽  

Muscular dystrophies (MDs) are a group of inherited degenerative muscle disorders characterized by a progressive skeletal muscle wasting. Respiratory impairments and subsequent hypoxemia are encountered in a significant subgroup of patients in almost all MD forms. In response to hypoxic stress, compensatory mechanisms are activated especially through Hypoxia-Inducible Factor 1 α (HIF-1α). In healthy muscle, hypoxia and HIF-1α activation are known to affect oxidative stress balance and metabolism. Recent evidence has also highlighted HIF-1α as a regulator of myogenesis and satellite cell function. However, the impact of HIF-1α pathway modifications in MDs remains to be investigated. Multifactorial pathological mechanisms could lead to HIF-1α activation in patient skeletal muscles. In addition to the genetic defect per se, respiratory failure or blood vessel alterations could modify hypoxia response pathways. Here, we will discuss the current knowledge about the hypoxia response pathway alterations in MDs and address whether such changes could influence MD pathophysiology.

2021 ◽  
Vol 13 ◽  
Rosaleena Mohanty ◽  
Lissett Gonzalez-Burgos ◽  
Lucio Diaz-Flores ◽  
J-Sebastian Muehlboeck ◽  
José Barroso ◽  

Neural compensatory mechanisms associated with broad cognitive abilities have been studied. However, those associated with specific cognitive subdomains (e.g., verbal fluency) remain to be investigated in healthy aging. Here, we delineate: (a) neural substrates of verbal (phonemic) fluency, and (b) compensatory mechanisms mediating the association between these neural substrates and phonemic fluency. We analyzed resting-state functional magnetic resonance imaging from 133 right-handed, cognitively normal individuals who underwent the Controlled Oral Word Association Test (COWAT) to record their phonemic fluency. We evaluated functional connectivity in an established and extended language network comprising Wernicke, Broca, thalamic and anti-correlated modules. (a) We conducted voxel-wise multiple linear regression to identify the brain areas associated with phonemic fluency. (b) We used mediation effects of cognitive reserve, measured by the Wechsler Adult Intelligence Scale—Information subtest, upon the association between functional connectivity and phonemic fluency tested to investigate compensation. We found that: (a) Greater functional connectivity between the Wernicke module and brain areas within the anti-correlated module was associated with better performance in phonemic fluency, (b) Cognitive reserve was an unlikely mediator in younger adults. In contrast, cognitive reserve was a partial mediator of the association between functional connectivity and phonemic fluency in older adults, likely representing compensation to counter the effect of aging. We conclude that in healthy aging, higher performance in phonemic fluency at older ages could be attributed to greater functional connectivity partially facilitated by higher cognitive reserve, presumably reflecting compensatory mechanisms to minimize the effect of aging.

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1072
Lucie Gerber ◽  
Kathy A. Clow ◽  
William R. Driedzic ◽  
Anthony K. Gamperl

The dynamic interactions between nitric oxide (NO) and myoglobin (Mb) in the cardiovascular system have received considerable attention. The loss of Mb, the principal O2 carrier and a NO scavenger/producer, in the heart of some red-blooded fishes provides a unique opportunity for assessing this globin’s role in NO homeostasis and mitochondrial function. We measured Mb content, activities of enzymes of NO and aerobic metabolism [NO Synthase (NOS) and citrate synthase, respectively] and mitochondrial parameters [Complex-I and -I+II respiration, coupling efficiency, reactive oxygen species production/release rates and mitochondrial sensitivity to inhibition by NO (i.e., NO IC50)] in the heart of three species of red-blooded fish. The expression of Mb correlated positively with NOS activity and NO IC50, with low NOS activity and a reduced NO IC50 in the Mb-lacking lumpfish (Cyclopterus lumpus) as compared to the Mb-expressing Atlantic salmon (Salmo salar) and short-horned sculpin (Myoxocephalus scorpius). Collectively, our data show that NO levels are fine-tuned so that NO homeostasis and mitochondrial function are preserved; indicate that compensatory mechanisms are in place to tightly regulate [NO] and mitochondrial function in a species without Mb; and strongly suggest that the NO IC50 for oxidative phosphorylation is closely related to a fish’s hypoxia tolerance.

2021 ◽  
Vol 4 (8) ◽  
pp. e202101055
Francesc X Guix ◽  
Ana Marrero Capitán ◽  
Álvaro Casadomé-Perales ◽  
Irene Palomares-Pérez ◽  
Inés López del Castillo ◽  

As neurons age, they show a decrease in their ability to degrade proteins and membranes. Because undegraded material is a source of toxic products, defects in degradation are associated with reduced cell function and survival. However, there are very few dead neurons in the aging brain, suggesting the action of compensatory mechanisms. We show in this work that ageing neurons in culture show large multivesicular bodies (MVBs) filled with intralumenal vesicles (ILVs) and secrete more small extracellular vesicles than younger neurons. We also show that the high number of ILVs is the consequence of the accumulation of cholesterol in MVBs, which in turn is due to decreased levels of the cholesterol extruding protein NPC1. NPC1 down-regulation is the consequence of a combination of upregulation of the NPC1 repressor microRNA 33, and increased degradation, due to Akt-mTOR targeting of NPC1 to the phagosome. Although releasing more exosomes can be beneficial to old neurons, other cells, neighbouring and distant, can be negatively affected by the waste material they contain.

2021 ◽  
Vol 6 (3) ◽  
pp. 263-268
I. V. Yaremena ◽  
М. B. Tarasuk ◽  
I. V. Palamar ◽  
S. E. Holovchanska-Pushkar ◽  

The purpose of the study. The article presents and substantiates the possibilities of reducing the risk of rehospitalization on the basis of a specially developed econometric model of behavior of the hospital doctor in conditions of different workload of patients using the schedule according to Slutsky. Materials and methods. The effects of the model showed that the growth of the competitive environment leads to: a) a decrease in the number of services provided by the hospital doctor; b) switching to perform functions that help improve the quality of the treatment process; c) an increase in the average duration of treatment. Modern tendencies are shown: a) reduction of the number of doctors of inpatient departments; b) increasing the workload of the hospital doctor with patients and bed-days; c) reducing the average length of stay in the hospital. Results and discussion. The economic mechanisms of reducing the risk of re-hospitalizations are substantiated, namely: a) compensation of the turn of the profit curve through compensatory mechanisms of payment for the quality of work of the hospital doctor; b) increasing the price elasticity of consumer demand for stationary services. That is, we chose the length of the period between regular hospitalizations of patients as a criterion for the quality of inpatient treatment. This criterion is essentially equivalent to the risk of re-hospitalization, in which hospitalization in a department of the same profile, which confirms the failure of the previous treatment. Thus, a link is expected between a longer stay of the patient in the hospital and a lower risk of re-hospitalization, provided that a longer stay will provide additional quality of treatment. Therefore, the discovery of such a connection is a confirmation of the hypothesis, which is based on the theoretical econometric model of physician behavior and relates to the reorientation to the additional quality of inpatient care in a competitive environment. That is, due to the increased load, the doctor reduces the length of the patient's stay in the hospital and therefore the quality of care deteriorates. Due to the fact that the discharge of the patient involves achieving a stable condition, doctors are sometimes forced to give an objective assessment of the condition at the time of discharge. The timeliness of evaluating effectiveness is the possibility of temporary relief when in fact the case of treatment is not over. It should be noted that in countries with a private health care system, reimbursement of hospital care costs is related to the number of bed-days spent by the patient in the hospital, where "day" is defined as the period from one midnight to the next, medical staff can manipulate the time of hospital discharge, as patients who are kept until midnight will have an additional day to reimburse. Conclusion. It follows from the research results that a reduction in the length of hospital stay in the existing situation significantly worsens the prognosis, increasing the risks of an uncontrolled course of the disease and, accordingly, subsequent hospitalizations

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Lisa Spiecker ◽  
Ines Witte ◽  
Julia Mehlig ◽  
Viral Shah ◽  
Markus Meyerhöfer ◽  

Background. Long-term hematopoietic stem cells (LT-HSCs) reside in bone marrow niches with tightly controlled reactive oxygen species (ROS) levels. ROS increase results into LT-HSC differentiation and stem cell exhaustion. Paraoxonase 2 (PON2) has been shown to be important for ROS control. Objectives. We investigate the effects of inactivation of the PON2 gene on hematopoietic cell differentiation and activity. Methods and Results. In young mice with inactivated Pon2 gene (Pon2-/-, <3 months), we observed an increase of LT-HSCs and a reduced frequency of progenitor cells. In competitive transplantations, young Pon2-/- BM outcompeted WT BM at early time points. ROS levels were significantly increased in Pon2-/- whole BM, but not in Pon2-/- LT-HSCs. In more differentiated stages of hematopoiesis, Pon2 deficiency led to a misbalanced erythropoiesis both in physiologic and stress conditions. In older mice (>9 months), Pon2 depletion caused an increase in LT-HSCs as well as increased levels of granulocyte/macrophage progenitors (GMPs) and myeloid skewing, indicating a premature aging phenotype. No significant changes in ROS levels in old Pon2-/- LT- and short-term (ST-) HSCs were observed, but a significant reduction of spontaneous apoptotic cell death was measured. RNA-seq analysis in Pon2-/- LT-HSCs identified overrepresentation of genes involved in the C-X-C chemokine receptor type 4 (Cxcr4) signaling, suggesting compensatory mechanisms to overcome ROS-mediated accelerated aging in hematopoietic progenitor cells. Conclusions. In summary, our current data indicate that PON2 is involved in the regulation of HSC functions.

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