Maximal Reserve


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When the memory allocated for the vector falls short of storing new elements, a new memory block is allocated to vector and all elements are copied from the old location to the new location. This reallocation of elements helps vectors to grow when required. However, it is a costly operation and time complexity is involved in this step is linear. It indicates that the vector is created such that it can store at least the number of the specified elements without having to reallocate memory.

Each vector object has two parameters—size and capacity.

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The size denotes the number of elements currently stored in the vector while capacity is the maximum number of elements that the vector can store without reallocation. When the vector runs out of space to store new elements i. A call to the function reserve modifies the capacity parameter of the vector and so the vector requests sufficient memory to store the specified number of elements. In this new paper, the author limits to exchange total cost of reactive power by reactive power reserve, looking for maximizing reactive power reserves and minimizing active power losses.

The proposed procedure is very significant to eliminate violation constraints and give an optimal reactive power reserve for multi-operating conditions. The numerical results show that the proposed MFLP technique achieves a minimum real power loss with maximal reactive reserve for power systems for different operating conditions. Article :. DOI: Hence, a cohort of patients with more advanced or decompensated PH may reveal mitochondrial changes that are even more similar to those observed in animal models.

A recent study demonstrated that platelet activation induced by thrombin leads to increased platelet FAO and lipid mobilization through the actions of cytosolic phospholipase A 2 Although our data show upregulated FAO in PH platelets, we did not observe a significant increase in platelet activation markers. This is potentially due to the majority of our cohort being treated with PC, which have been demonstrated to directly inhibit platelet activation 41 — Further study is required to define the lipid profile of platelets from PH patients and to determine whether in the absence of medication altered platelet bioenergetics are linked to changes in platelet function in PH.

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This is particularly important since platelet activation has historically been thought to play a prominent role in PH pathogenesis. In addition to mediating thrombosis, activated platelets store and secrete vasoactive and mitogenic mediators, including thrombospondin-1, thromboxane A2, and serotonin, that together cause vasoconstriction and propagate smooth muscle proliferation reviewed in refs.

In contrast to the potential effects of medication on platelet activation, our data suggest that the altered mitochondrial bioenergetics observed in PH platelets is not significantly affected by the major classes of PH therapeutics.

However, this should be further examined in larger cohorts, as a potential limitation of our analysis was the small sample size of the subgroups on medication. Additionally, these data do not reveal whether the magnitude of bioenergetic change with disease progression is attenuated over the course of treatment. Studies evaluating these parameters over the course of disease treatment will be useful in determining whether changes in platelet bioenergetics can be utilized as markers to assess changes in systemic metabolic dysfunction in PH.

The finding that platelet respiratory reserve capacity correlates with mPAP and PVR presents a link between platelet mitochondrial function and disease severity. The association of increased RV SWI, a measure of ventricular workload and contractility, with mitochondrial energetics in this cohort of well-compensated patients may suggest a role for enhanced mitochondrial capacity as an adaptive mechanism.

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However, it is interesting to speculate that reserve capacity may diminish as the RV decompensates. Further investigation is required to determine whether this association persists in patients with very advanced PH and heart failure. Notably, we did not assess whether platelet bioenergetic alterations correlated with brain natriuretic peptide BNP levels, an established marker of disease severity Further, the majority of the current cohort were classified as WHO functional class 2 moderate PH , thus we were underpowered to compare bioenergetics between functional classes.

Additional investigation into the correlation of platelet reserve capacity and ECAR with other established markers of PH severity will be important to perform in larger future cohorts. Interestingly, associations have been demonstrated by utilizing [ 18 F]fluoro-d-glucose FDG PET imaging of the heart in which increased glucose uptake correlated with hemodynamic parameters 19 , While FDG-PET imaging has been proposed as a technique for assessing PAH severity and right heart failure 19 , 20 , measurement of bioenergetics in a simple blood draw as demonstrated here may provide similar information more efficiently and be more inclusive of a broader population of patients.

Lastly, it is important to consider the present findings in the context of BM pathology, a well-documented characteristic of PH 46 , Several cell types from the myeloid lineage, including mesenchymal stem cells, fibrocytes, and hematopoietic stem cells, have been implicated in the pathogenesis of PH For example, mast cells are known to be increased in vascular lesions of lungs explanted from PH patients 48 , 49 , and inhibition of mast cell degranulation in animal models of PH attenuates RV hypertrophy Similarly, depletion of fibrocytes in a mouse model of PH inhibited pulmonary artery thickening It is unclear whether these myeloid-derived cells are part of an adaptive response that leads to pathogenesis or whether they are dysfunctional.

Our data show that platelets, which are formed in the BM and retain the mitochondria of their megakaryocyte precursors, have altered bioenergetics.

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This presents a mechanistic link between altered myeloid function and metabolic dysregulation of the pulmonary vasculature. While the status of cellular metabolism in other BM-derived cells in PH is currently unknown, this represents an interesting avenue of future study. In summary, this study shows that patients with PH show aberrations in metabolism beyond the pulmonary artery and cardiac tissue, and that platelets from these patients can be used to assess mitochondrial changes.

This metabolic alteration is characterized by an increased mitochondrial reserve capacity that is dependent on increased FAO and linked to an increase in complex II activity. Notably, these changes are not affected by common therapeutics, and they correlate with clinical hemodynamic parameters.

The findings of this investigation warrant further study of platelet mitochondrial function in progression of PH and response to therapy, particularly in the context of emerging mitochondrial therapeutics. Study population.

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The control group consisted of healthy age and sex-matched participants without known cardiopulmonary or hematologic disease. In the PH group, hemodynamic parameters Table 1 were derived from right heart catheterization performed within 1 calendar year of bioenergetic assessment. Platelet isolation. Platelets were isolated by differential centrifugation and number quantified as previously described 23 , Briefly, venous blood was collected in citrate by standard venipuncture.

Measurement of platelet bioenergetics.


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Mitochondrial ROS generation. Platelet activation. Platelet activation was performed as previously described Platelets were identified by their characteristic light scatter and CD41a antibody binding. Mitochondrial enzyme expression.


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  4. Mitochondrial protein expression was measured by Western blot as previously described Antibody for PDK1 catalog ab was purchased from Abcam. ETC complex activity. Enzymatic activity of complexes I, II, and IV and citrate synthase were performed as previously described Statistics were performed on Graphpad Prism 7. Study approval. QLN and CC collected the experimental data.

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    QLN analyzed the data. All authors reviewed and approved the final version. Reference information: JCI Insight.

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