Treatment of ischemic stroke caused by dissection and occlusion of internal carotid artery in a young patient

The type and etiology of stroke in young patients are known to differ from those in elderly patients, that influences the diagnosis and treatment. Dissection of cerebral arteries holds the top position in the structure of the causes of ischemic stroke in children and young people below 45 years. Currently no clear guideline on the proper treatment of this pathology exists. The article presents the case of acute ischemic stroke in a young patient (the stroke was caused by the occlusion due to dissection of the internal carotid artery) successfully treated with radiosurgical method - stenting of the cervical part of the artery with the transition to petrous segment of the left carotid artery using combined proximal and distal protection of cerebral vessels. The control of patient's state and results of angiography and ultrasound demonstrate the favourable immediate and medium-term prognosis for the patient

Clinical use of various endovascular stenting techniques in challenging coronary interventions

Aim. Development of an algorithm of actions for stenting of artery stenosis during challenging percutaneous coronary interventions (PCI) based on the analysis of the results of different endovascular techniques. Methods. We analyzed the experience of the department of radiologic endovascular diagnosis and treatment of Stavropol regional clinical hospital for endovascular surgical treatment of atherosclerosis of coronary arteries. The study included 317 cases of coronary interventions with technically impossible stent delivery to stenosis by standard method along the front-line guidewire and standard choice of the guide in case of distal TIMI 3 flow. For the study the patients were divided into 3 groups comparable by the number of subjects: 104, 113 and 100 respectively. For each group we determined different stages of enhancing support with consistent step-wise transition. The groups differed by the used methods of enhancing support and consistency of their use. Among other methods of support group 2 included the method of guide change and delivery of the second guidewire of enhanced support. At the same time groups 1 and 3 used these methods separately. Results. The smallest number of unsuccessful interventions was observed in group 2 compared to those of groups 1 and 3. The relative risk indicators also demonstrate the high effectiveness of tactics used in the group 2. Conclusion. The most preferable method for the necessary support when stent delivery distal to stenosis is impossible, is a choice of optimal guide and use of the second guidewire of enhanced support

Dilation of the Infarct-Related Coronary Artery to Reduce the Incidence of the No-Reflow Phenomenon in STEMI Patients

Background: The pathogenesis of slow/no-reflow phenomena is a critical socio-medical problem due to high mortality and work disability rates in patients with ST-segment elevation myocardial infarction (STEMI). Slow/no-reflow phenomena are multifactorial involving 4 key elements: 1) distal embolization of the coronary bed of the infarct-related coronary artery; 2) ischemic damage to the myocardium; 3) reperfusion injury of the heart muscle; 4) individual (genetic) susceptibility of the microcirculation to injury.   Objective: To analyze the outcomes of percutaneous coronary interventions (PCI) in patients with STEMI and TIMI 0 blood flow of an infarct-related coronary artery based on the strategy to restore antegrade blood flow (balloon predilation or dilation of an infarctrelated artery).   Materials and methods: We analyzed treatment outcomes of 209 patients with STEMI and TIMI 0 blood flow. The patients were grouped based on the PCI strategy: group 1 included 147 patients who underwent balloon angioplasty to restore antegrade blood flow, and group 2 included 62 patients who underwent dilation of an infarct-related coronary artery.   Results: Our study found that direct stenting in STEMI patients was associated with statistically significantly lower risk of slow/noreflow phenomena (P = 0.001, Pearson’s χ2) and, as a result, better functional outcomes of treatment (chronic heart failure grade classified according to Strazhesko-Vasilenko and by left ventricular ejection fraction) that were also statistically significant (P = 0.001, Pearson’s χ2).   Conclusions: Our study demonstrated that the risk of slow/no-reflow phenomena in patients with TIMI 0 blood flow of an infarctrelated coronary artery was statistically significantly lower (P = .001, Pearson’s χ2) in the group of patients who underwent dilation of an infarct-related coronary artery to restore antegrade blood flow. Functional outcomes (chronic heart failure grade and overall survival) were also better in this group of patients (P = .001, Pearson’s Chi-square). Moreover, dilation of an infarct-related coronary artery was associated with preserved left ventricular ejection fraction compared with the group of patients who underwent balloon angioplasty to restore antegrade blood flow (P < 0.001, Pearson’s χ2)

Uncoupling protein-1 (UCP1) contributes to the basal proton conductance of brown adipose tissue mitochondria

Proton leak pathways uncouple substrate oxidation from ATP synthesis in mitochondria. These pathways are classified as basal (not regulated) or inducible (activated and inhibited). Previously it was found that over half of the basal proton conductance of muscle mitochondria was catalyzed by the adenine nucleotide translocase (ANT), an abundant mitochondrial anion carrier protein. To determine whether ANT is the unique protein catalyst, or one of many proteins that catalyze basal proton conductance, we measured proton leak kinetics in mitochondria isolated from brown adipose tissue (BAT). BAT can express another mitochondrial anion carrier, UCP1, at concentrations similar to ANT. Basal proton conductance was measured under conditions where UCP1 and ANT were catalytically inactive and was found to be lower in mitochondria from UCP1 knockout mice compared to wild-type. Ablation of another abundant inner membrane protein, nicotinamide nucleotide transhydrogenase, had no effect on proton leak kinetics in mitochondria from liver, kidney or muscle, showing that basal proton conductance is not catalyzed by all membrane proteins. We identify UCP1 as a second protein propagating basal proton leak, lending support to the hypothesis that basal leak pathways are perpetrated by members of the mitochondrial anion carrier family but not by other mitochondrial inner membrane proteins

Reduction of Hydrophilic Ubiquinones by the Flavin in Mitochondrial NADH:Ubiquinone Oxidoreductase (Complex I) and Production of Reactive Oxygen Species†

ABSTRACT: NADH:ubiquinone oxidoreductase (complex I) from bovine heart mitochondria is a complicated, energy-transducing, membrane-bound enzyme that contains 45 different subunits, a non-covalently bound flavin mononucleotide, and eight iron-sulfur clusters. The mechanisms of NADH oxidation and intramolecular electron transfer by complex I are gradually being defined, but the mechanism linking ubiquinone reduction to proton translocation remains unknown. Studies of ubiquinone reduction by isolated complex I are problematic because the extremely hydrophobic natural substrate, ubiquinone-10, must be substituted with a relatively hydrophilic analogue (such as ubiquinone-1). Hydrophilic ubiquinones are reduced by an additional, non-energy-transducing pathway (which is insensitive to inhibitors such as rotenone and piericidin A). Here, we show that inhibitor-insensitive ubiquinone reduction occurs by a ping-pong type mechanism, catalyzed by the flavin mononucleotide cofactor in the active site for NADH oxidation. Moreover, semiquinones produced at the flavin site initiate redox cycling reactions with molecular oxygen, producing superoxide radicals and hydrogen peroxide. The ubiquinone reactant is regenerated, so the NADH:Q reaction becomes superstoichiometric. Idebenone, an artificial ubiquinone showing promise in the treatment of Friedreich’s Ataxia, reacts at the flavin site. The factors which determine the balance of reactivity between the two sites of ubiquinone reduction (the energy-transducing site and the flavi

Functional Dissection of the Proton Pumping Modules of Mitochondrial Complex I

A catalytically active subcomplex of respiratory chain complex I lacks 14 of its 42 subunits yet retains half of its proton-pumping capacity, indicating that its membrane arm has two pump modules

Trophic status of Chlamydomonas reinhardtii influences the impact of iron deficiency on photosynthesis

To investigate the impact of iron deficiency on bioenergetic pathways in Chlamydomonas, we compared growth rates, iron content, and photosynthetic parameters systematically in acetate versus CO2-grown cells. Acetate-grown cells have, predictably (2-fold) greater abundance of respiration components but also, counter-intuitively, more chlorophyll on a per cell basis. We found that phototrophic cells are less impacted by iron deficiency and this correlates with their higher iron content on a per cell basis, suggesting a greater capacity/ability for iron assimilation in this metabolic state. Phototrophic cells maintain both photosynthetic and respiratory function and their associated Fe-containing proteins in conditions where heterotrophic cells lose photosynthetic capacity and have reduced oxygen evolution activity. Maintenance of NPQ capacity might contribute to protection of the photosynthetic apparatus in iron-limited phototrophic cells. Acetate-grown iron-limited cells maintain high growth rates by suppressing photosynthesis but increasing instead respiration. These cells are also able to maintain a reduced plastoquinone pool

Cryo-EM structures of complex I from mouse heart mitochondria in two biochemically defined states.

Complex I (NADH:ubiquinone oxidoreductase) uses the reducing potential of NADH to drive protons across the energy-transducing inner membrane and power oxidative phosphorylation in mammalian mitochondria. Recent cryo-EM analyses have produced near-complete models of all 45 subunits in the bovine, ovine and porcine complexes and have identified two states relevant to complex I in ischemia-reperfusion injury. Here, we describe the 3.3-Å structure of complex I from mouse heart mitochondria, a biomedically relevant model system, in the 'active' state. We reveal a nucleotide bound in subunit NDUFA10, a nucleoside kinase homolog, and define mechanistically critical elements in the mammalian enzyme. By comparisons with a 3.9-Å structure of the 'deactive' state and with known bacterial structures, we identify differences in helical geometry in the membrane domain that occur upon activation or that alter the positions of catalytically important charged residues. Our results demonstrate the capability of cryo-EM analyses to challenge and develop mechanistic models for mammalian complex I

Frequently asked questions about chlorophyll fluorescence, the sequel

[EN] Using chlorophyll (Chl) a fluorescence many aspects of the photosynthetic apparatus can be studied, both in vitro and, noninvasively, in vivo. Complementary techniques can help to interpret changes in the Chl a fluorescence kinetics. Kalaji et al. (Photosynth Res 122: 121-158, 2014a) addressed several questions about instruments, methods and applications based on Chl a fluorescence. Here, additionalChl a fluorescence-related topics are discussed again in a question and answer format. 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