Comminuted intraarticular calcaneal fractures: Multiplanar VA locked plating and interlocked nailing incorporate longitudinal strut and provide superior stability - a biomechanical cadaveric study.

Treatment of comminuted intraarticular calcaneal fractures remains controversial and challenging. The aim of this study was to investigate the biomechanical performance of three different methods for fixation of such fractures. Comminuted calcaneal fractures, including Sanders III AB fracture of the posterior facet and Kinner II B fracture of the calcaneocuboid joint (CCJ) articular calcaneal surface, were created in 18 human cadaveric lower legs by osteotomizing. The ankle joint, medial soft tissues and midtarsal bones along with their ligaments were preserved. The specimens were randomized to three groups for fixation with either (1) 2.7 mm variable-angle locking lateral calcaneal plate (Group 1), (2) 2.7 mm variable-angle locking anterolateral calcaneal plate in combination with one 4.5 mm and one 6.5 mm cannulated screws (Group 2), or (3) interlocking calcaneal nail with 3.5 mm screws in combination with three separate 4.0 mm cannulated screws (Group 3). All specimens were biomechanically tested to failure under axial loading in midstance foot position. Each test commenced with a quasi-static compression ramp from 50 to 200 N, followed by progressively increasing cyclic loading at 2 Hz. Starting from 200 N, the peak load of each cycle increased at a rate of 0.2 N/cycle. Interfragmentary movements were captured by motion tracking. In addition, mediolateral X-rays were taken every 250 cycles with a triggered C-arm. Böhler angle after 5000 cycles (1200 N peak load) increased significantly more in Group 1 compared to both other groups (P ≤ 0.020). Varus deformation of 10° between the calcaneal tuberosity and the lateral calcaneal fragments was reached at significantly lower number of cycles in Group 1 compared the other groups (P ≤ 0.017). Both cycles to 10° plantar gapping between the anterior process and the calcaneal tuberosity fragments, and 2 mm displacement at the CCJ articular calcaneal surface revealed no significant differences among the groups (P ≥ 0.773). From a biomechanical perspective, treatment of comminuted intraarticular calcaneal fractures using anterolateral variable-angle locking plate with additional longitudinal screws or interlocked nail in combination with separate transversal screws provides superior stability as opposed to lateral variable-angle locked plating only.

Effects of parity-time symmetry in nonlinear Klein-Gordon models and their stationary kinks.

In this work, we introduce some basic principles of PT-symmetric Klein-Gordon nonlinear field theories. By formulating a particular antisymmetric gain and loss profile, we illustrate that the stationary states of the model do not change. However, the stability critically depends on the gain and loss profile. For a symmetrically placed solitary wave (in either the continuum model or a discrete analog of the nonlinear Klein-Gordon type), there is no effect on the steady state spectrum. However, for asymmetrically placed solutions, there exists a measurable effect of which a perturbative mathematical characterization is offered. It is generally found that asymmetry towards the lossy side leads towards stability, while towards the gain side produces instability. Furthermore, a host of finite size effects, which disappear in the infinite domain limit, are illustrated in connection to the continuous spectrum of the problem.

Experimental demonstration of decoherence-free one-way information transfer.

We report the experimental demonstration of a one-way quantum protocol reliably operating in the presence of decoherence. Information is protected by designing an appropriate decoherence-free sub-space for a cluster state resource. We demonstrate our scheme in an all-optical setup, encoding the information into the polarization states of four photons. A measurement-based one-way information-transfer protocol is performed with the photons exposed to severe symmetric phase-damping noise. Remarkable protection of information is accomplished, delivering nearly ideal outcomes.

Ca2+-sensitivity and cGMP-independent effects of NO in vascular smooth muscle.

The effects of NO on Ca2+-sensitivity of vascular smooth muscle (VSM) myofilaments have been the focus of this study. Simultaneous measurements of [Ca2+]i and force were carried out in rat tail artery segments. NO, 10(-7) M, evoked a transient decrease in [Ca2+]i accompanied by sustained relaxation (45.3+/-6.3 vs. 69.45+/-7.2%, P<0.05, respectively) of VSM precontracted with K+ (70 mM), suggesting a decrease in Ca2+-sensitivity of VSM. This decrease in Ca2+-sensitivity was completely abolished by preincubation of VSM with ODQ (10(-6) M) (63.9+/-7.8% for [Ca2+]i vs. 20.5+/-8.4% for relaxation, P<0.05). Ca2+-presensitization of VSM myofilaments with PE (10(-6) M) decreased the efficacy of NO to relax VSM (44.25+/-6.9% vs. 69.45+/-7.2%, P<0.05), but increased its ability to lower [Ca2+]i (70.5+/-6.8% vs. 45.3+/-6.3%, P<0.05). Application of DTT (10(-3) M) together with ODQ (10(-6) M) to subtract possible cGMP-independent effects revealed the total suppression of both the relaxant responses and [Ca2+]i of VSM under high-K+ preactivation of VSM. The data indicate that NO not only relaxes VSM and lowers [Ca2+]i in K+-preactivated VSM, but also decreases Ca2+-sensitivity of VSM myofilaments and these effects are strongly cGMP-dependent. In PE-induced contractions of VSM, NO relaxed VSM of rat tail artery and lowered [Ca2+]i, but failed to reverse Ca2+-presensitized myofilaments. We suggest that alternative cGMP-independent effects of NO are primarily manifested via activation of K+-channels and inhibition of Ca2+ current rather than to affect relaxation. An importance of reduced SH-groups within VSM myoplasm for both relaxation and [Ca2+]i disposal evoked by NO is evident whatever Ca2+-mobilization pathways are involved.

Arrhythmogenic peroxynitrite-induced alterations in mammalian heart contractility and its prevention with quercetin-filled liposomes.

The aim of the present study was to evaluate the effects of quercetin-filled phosphatidylcholine liposomes (PCLs) on peroxynitrite (ONOO-)-induced cardiac arrhythmias. Experiments were done using different experimental models, including isolated rat papillary muscle, Langendorff perfused rat hearts, and anesthetized animals. Being exogenously applied in a concentration greater than 50 microM, ONOO- caused inhibition of isometric twitch amplitude in isolated papillary muscles and led to an appearance of arrhythmias. Decomposed ONOO- had no similar effects and reversibly increased twitch amplitude. Authentic nitric oxide (NO, 100 microM) did not produce arrhythmias and had no significant effect on twitch amplitude. Verapamil and ruthenium red were with-out effect on ONOO- -induced arrhythmias, whereas tetrodotoxin and nicorandil effectively prevented arrhythmias development. Ouabain increased the arrhythmogenic effect of ONOO-. ONOO- significantly decreased coronary perfusion pressure (CPP) and mean left-ventricular pressure (MLVP) in the Langendorff perfused rat heart and produced severe arrhythmias. Authentic nitric oxide (NO) decreased CPP and MLVP insignificantly and resulted in a low incidence of arrhythmias. The NO donor SIN-1 in doses greater than 50 microM led to the appearance of low-incidence arrhythmias in anesthetized rats. Intraventricular injection of ONOO- promotes the appearance of a high incidence of arrhythmias in anesthetized rats and decreased MLVP. PCLs filled with the antioxidant quercetin restored normal cardiac contractility in both isolated tissues and anesthetizes animals. In conclusion, we hypothesized that ONOO-, but not its decomposed products, can initiate membrane lipid peroxidation and damage the phospholipid environment of ionic channels in myocardial cell plasma membranes inducing abnormal cardiac action potentials, arrhythmogenesis, and contractile dysfunction. Quercetin-filled PCL provide reliable protection against peroxynitrite-induced myocardial injury in isolated cardiac tissues and anesthetized animals primarily as a result of the decomposition of endogenously formed ONOO-.

Effects of nitric oxide donors on vascular smooth muscles depend on a type of vascular smooth-muscle preactivation.

The abilities of such therapeutic nitrovasodilators as sodium nitroprusside (SNP) and glyceryl trinitrate (GTN) to dilate vascular smooth muscles (VSM) and affect intracellular calcium concentration level ([Ca2+]i) in a rat tail artery were tested under different types of preactivation. To shed light on mechanisms underlying possible differences in the action of these two nitric oxide (NO) donors, simultaneous measurements of [Ca2+]i and contractile force were done. All vascular rings were precontracted either using a high-K+-Krebs solution or phenylephrine (PE). It was shown that the effect of both NO donors strongly depended on a type of VSM preactivation. The EC50 for GTN under K+ stimulation of VSM comprised (2.48 +/- 1.6) x 10(-5) M, whereas the mean EC50 under PE stimulation was (3.05 +/- 2.3) x 10(-4) M (p < 0.05, n = 9). The EC50 for SNP under K+ stimulation of VSM comprised (1.09 +/- 0.47) x 10(-7) M, whereas the EC(50) under PE stimulation was (8.01 +/- 2.4) x 10(-6) M (p < 0.05, n = 9). GTN demonstrated a significant discrepancy in the magnitude of changes in [Ca2+]i and related VSM relaxant responses, indicating the ability of GTN to relax VSM in the absence of a proportional decrease in [Ca2+]i. The main peculiarity of SNP action under K+ stimulation as compared to PE stimulation was the transient decrease in [Ca2+]i while relaxation was sustained. Therefore, both NO donors demonstrated their ability to produce vasorelaxation as a result of an alteration in myofilament calcium sensitivity. These data clearly indicate that the sensitivity of VSM to NO donors is higher under K+ depolarization than that seen under PE stimulation, indicating that Ca2+ entry through voltage-operated calcium channels is more sensitive to NO as compared to calcium mobilization by means of Ca2+ entry through receptor- operated calcium channels or intracellular Ca2+ release, or both.

Selected contribution: Lung hypoxia: antioxidant and antiapoptotic effects of liposomal alpha-tocopherol.

The aim of this study is to examine the antioxidant and antiapoptotic activity of liposomal alpha-tocopherol (LAT) in anesthetized rats exposed to severe hypoxia. It was shown that intratracheal application of LAT normalized lung phospholipid composition and inhibited lipid peroxidation in lung tissues, which in turn decreased lung edema and damage and improved breathing pattern, oxygen diffusion, and lung gas exchange. LAT also limited the overexpression of genes encoding hypoxia inducible factor-1alpha and both studied forms of phospholipase A(2), and it increased the power of cellular antioxidant and antiapoptotic defense by overexpressing genes encoding Mn- and Cu-Zn-cofactored superoxide dismutases, Bcl-2, and heat shock 70 proteins. The overexpression of studied caspases and their activity were downregulated, which significantly (1.6-2 times) limited apoptosis in lung cells. Finally, all these positive changes decreased mortality during hypoxia from approximately 60% in untreated animals to approximately 30% in the group of rats treated with LAT. The data obtained indicate that LAT may be useful for the correction of hypoxic lung injury.

Saline containing phosphatidylcholine liposomes possess the ability to restore endothelial function damaged resulting from gamma-irradiation.

The protective action of passive saline filled ("empty") phosphatidylcholine liposomes (PCL) on endothelial function was examined in thoracic aortas obtained from gamma irradiated (6 Gy) Chinchilla rabbits, and then verified in experiments on non-anesthetized and anesthetized rats. Acetylcholine (ACh)-induced vascular relaxant responses in isolated vascular tissues rats were used as the test of endothelial integrity and its functional ability. It was shown that when added to the bath solution (100 microg/ml), PCL effectively restored endothelium-dependent ACh relaxations of isolated vascular rings damaged resulting from gamma-irradiation but had no effect on endothelium-independent vascular responses to therapeutic nitric oxide (NO) donors. The liposomes were also without protective effect when injected to the rabbits intraperitoneally (30 mg/kg) 1 hour before irradiation. In contrast, PCL, being injected at the same dose 1 hour after radiation impact, promote normalization of both endothelium-dependent vascular responses to ACh and nitric oxide (NO) donors. PCL restored also the sensitivity of vascular tissues to authentic NO (aqueous NO solution) that was surprisingly increased after irradiation, and normalized relationship between ACh-stimulated NO release and relaxant response amplitudes in irradiated aortas. Experiments on non-anesthetized and anesthetized rats demonstrated that irradiation led to significant elevation in the level of arterial blood pressure without any changes in cardiac contractility. PCL administration (25 mg/kg, i.v.) effectively normalized an increased arterial blood pressure in irradiated animals. In conclusion, it appears that PCL due to its ability to normalize NO-dependent vascular tone control mechanisms might be worthwhile therapeutic approach in case of ionizing irradiation accident. These result support the concept that the depression of endothelium-dependent vascular responses after irradiation may be result of decreased NO bioavailability due to its conversion to less potent vasodilators during irradiation-induced oxidative attack.

Experimental entanglement distillation and 'hidden' non-locality.

Entangled states are central to quantum information processing, including quantum teleportation, efficient quantum computation and quantum cryptography. In general, these applications work best with pure, maximally entangled quantum states. However, owing to dissipation and decoherence, practically available states are likely to be non-maximally entangled, partially mixed (that is, not pure), or both. To counter this problem, various schemes of entanglement distillation, state purification and concentration have been proposed. Here we demonstrate experimentally the distillation of maximally entangled states from non-maximally entangled inputs. Using partial polarizers, we perform a filtering process to maximize the entanglement of pure polarization-entangled photon pairs generated by spontaneous parametric down-conversion. We have also applied our methods to initial states that are partially mixed. After filtering, the distilled states demonstrate certain non-local correlations, as evidenced by their violation of a form of Bell's inequality. Because the initial states do not have this property, they can be said to possess 'hidden' non-locality.

[Effect of biogenic stimulators--aloe extract and biotrite--on lipid peroxidation processes in saliva in inflammatory periodontal disease]. / Vliianie biogennykh stimuliatorov--ékstrakta aloé i biotrita--na protsessy peroksidatsii lipidov v sliune pri vospalitetl'nykh zabolevaniiakh parodonta.

The influence of biostimulators of vegetative origin, such as aloes and biotritis, on the process of lipid peroxidation in parodontium tissues, was studied. Biotritis has a more considerable parodontoprotective effect than aloes.

Evidence for the involvement of protein kinase C in depression of endothelium-dependent vascular responses in spontaneously hypertensive rats.

The goal of the present study was to evaluate the role of protein kinase C (PKC) in the depression of endothelium-dependent vacular response in spontaneously hypertensive Okamoto rats (SHR). Aortae from SHR demonstrated a decreased relaxant response to acetylcholine (Ach) as compared to aortae from normotensive Wistar-Kyoto (WKY) rats, while papaverine lowered the force of aorta to a similar degree in both strains of rats. PKC inhibitors, H-7 (5 x 10(-6) M) and chelerythrine chloride (10(-6) M), produced a greater decrease in the force developed by the aortae from SHR vs. WKY rats both in intact and chemically permeabilized tissues. In SHR aortae PKC inhibitors enhanced relaxation to Ach to a greater extent as compared to WKY aortae. Furthermore, in the presence of PKC inhibitors, the constrictor responses of SHR aortae to Ach were transformed into relaxant responses, and the concentration-response curve to Ach was shifted to the left. The sensitivity of aortae from SHR to authentic nitric oxide (NO) was lowere compared to WKY rats. EC50s for authentic NO in SHR and WKY rat aortae were different: -2.9 +/- 0.15 x 10(-6) M and 4.58 +/- 0.1 x 10(-7) M (n = 15, p < 0. 001), respectively. Bioassay experiments using SHR aortae showed that the addition of chelerythrine (10(-6) M) to the detector superfusate caused relaxation during treatment of the donor segment with Ach, indicating that the sensitivity of the aortae to NO had been restored. When SHR detector ring was substituted for denuded aortae from WKY rats and PKC inhibitors were not added to the detector superfusate, the relaxation of the detector aortae was also close to the normal Ach-induced relaxation. WKY aortae demonstrated a positive relationship between Ach-stimulated NO release and relaxant response amplitudes (correlation coefficient r = 0.905, p < 0.001, n = 10). In contrast, there was a significant negative correlation in SHR aortae (r = -0.712, p < 0.05, n = 10). Detection of NO release by chemiluminescence showed no significant difference in NO release in SHR and WKY aortae. Taken together, these data suggest that the blunted endothelium-dependent relaxations seen in SHR aortae are mainly due to a decreased sensitivity of vascular smooth muscle to EDRF/NO resulting from an increased PKC activity.

A new method for transcutaneous coaxial neuroendoscopy.

A new method of direct endoscopy of the subarachnoid space and a major part of the ventricles of the human central nervous system is presented. The technique was developed on more than 100 human bodies with the help of a bronchoscope. Percutaneous entry into the subarachnoidal space is performed from the dorsal side between vertebrae L5 and S1. The endoscope can be moved along the spinal cord on both the dorsal and the ventral side. From the dorsal side of spinal cord the cerebello-medullary cistern can be reached. The fourth ventricle is entered through the median aperture and then the third ventricle through the cerebral aqueduct. From the ventral side of the spinal cord the posterior cranial fossa is reached and the large arteries and the cranial nerves can be inspected. The main conclusion of the present report is that the subarachnoid space seems to be large enough for a coaxial exploration with a 3-5 mm diameter fibroscope if the investigator possesses a good knowledge of the subarachnoid anatomy. The technique provides new approaches in research and possibilities of clinical investigations and therapy.

[Effect of liposomes on lipid peroxidation in the brain in experimental cranio-cerebral trauma]. / Vliianie liposom na sostoianie perekisnogo okisleniia lipidov golovnogo mozga pri éksperimental'noi cherepno-mozgovoi travme.

Phospholipid liposomes were studied for their influence on accumulation of lipid peroxidation products at craniocerebral trauma. It was shown that injection of liposomes led to inhibition of lipid peroxidation processes in tissues and to decrease of the mortality from 70 to 10%.

[Effect of liposomes on lipid peroxidation in the heart and liver in crush syndrome]. / Vliianie liposom na perekisnoe okislenie lipidov v serdtse i pecheni pri sindrome dlitel'nogo razdavlivaniia.

The increased lipid peroxidation has been determined to be one of general mechanisms of disturbance in the functional state of the heart and liver fraction cells, regularities of inter-system disturbance in metabolic activity under the crush syndrome have been revealed. Administration of lecithin liposomes results in the decreased POL levels, increased antioxidant capacity of the organism. That permits recommending to include liposomes into complex therapeutics of the crush syndrome as detoxicating, antiinflammatory and antihypoxic drug.

Phospholipid vesicles (liposomes) restore endothelium-dependent cholinergic relaxation in thoracic aorta from spontaneously hypertensive rats.

OBJECTIVE: The present study was designed to examine, using isolated preparations of thoracic aorta, the effects of artificial phosphatidylcholine vesicles (liposomes) on vascular endothelium-dependent responses in spontaneously hypertensive rats (SHR) compared with those in Wistar-Kyoto (WKY) normotensive rats. DESIGN: Phosphatidylcholine liposomes, which possess the ability to repair the plasma membrane of living cells, were used in these experiments. METHODS: Liposomes were prepared from egg phosphatidylcholine. A suspension of lipid was subjected to ultrasound treatment at 20 degrees C at a frequency of 44 kHz for 45 s. The contraction of vascular smooth muscle was recorded using a force-displacement transducer coupled with a physiograph. RESULTS: It was shown that aortic smooth muscle from SHR demonstrated a loss of endothelium-dependent relaxation in acetylcholine (10(-6) mol/l) compared with WKY rat aortic smooth muscle. Liposomes in a concentration of 100-125 micrograms/ml restored these endothelium-dependent responses more effectively than L-arginine (10(-5) to 10(-4) mol/l), which is known to be a precursor of endothelium-derived relaxing factor (EDRF). This effect was not observed in denuded aortic rings, and liposomes lost their ability of repairing endothelium-dependent vascular relaxant responses in the presence of methylene blue (5 x 10(-5) mol/l), which inhibits soluble guanylyl cyclase activation by nitric oxide (NO), and N omega-nitro-L-arginine (L-NNA, 5 x 10(-5) to 10(-4) mol/l), a potent and selective inhibitor of NO synthase. CONCLUSION: The present results suggest that the loss of vascular endothelium-dependent responses in SHR may be, at least partly, due to endothelial cells membrane damage, and that the phosphatidylcholine liposomes can repair the function of endothelial cells and restore synthesis or release, or both, of EDRF in hypertension.

[Liposomes in the combined treatment of patients with chronic obstructive bronchitis]. / Liposomy v kompleksnom lechenii bol'nykh s khronicheskim obstruktivnym bronkhitom.

Liposome inhalation was included into intensive combined treatment of 78 patients with chronic bronchitis exacerbation and preasthma. As shown by investigations of respiration, central hemodynamics, lipid and protein metabolism, vitamin E concentration, chemiluminescence before, during and after treatment, liposomes promote elimination of obstruction in the airways, pO2 normalization, correction of impaired lipid and protein metabolism, an increase in vitamin E level in peripheral blood leading to antioxidant system recovery and inhibition of lipid peroxidation. The use of lipin reduces the time of treatment of bronchitis chronics 2-fold. Lipin proved also to display a cardioprotective action.

[Prevention of postischemic lesions of the myocardium using liposomes]. / Preduprezhdenie postishemicheskikh povrezhdenii miokarda s pomoshch'iu liposom.

The experiments on dogs showed that 60-min blood flow restriction in the left coronary artery branch resulted in pumping and contractile heart dysfunctions. The removal of the blood flow barrier caused reinforcement of the above dysfunctions. The administration of 50 mg/kg liposome prior to reperfusion improved pumping and contractile heart functions and allowed maintenance of stable hemodynamics during the reperfusion.

[The physiological mechanisms of the antihypoxic action of the liposomes]. / Nekotorye fiziologicheskie mekhanizmy antigipoksicheskogo deistviia liposom.

The effect of phospholipids introduced into the vascular bed in the form of liposomes, was studied in pats in conditions of breathing with hypoxic gas mixture containing 7% of oxygen in nitrogen. The liposomes were shown to improve the oxygen diffusion from the blood into tissues and from air to the blood. In the result of this, the degree of the tissue hypoxia is considerably reduced, the process of peroxide oxidation of lipids is inhibited, and the efficacy of external respiration and gas exchange is increased.

[The enhancement under the action of a limited diet of the antimetastatic effect due to macrophage activation in mice with Lewis carcinoma]. / Usilenie pod vozdeistviem ogranichennogo ratsiona antimetastaticheskogo éffekta, obuslovlennogo aktivatsiei makrofagov, u myshei s kartsinomoi L'iuis.

An antimetastatic effect associated with macrophage activation by liposome-encapsulated glucosaminylmuramyldipeptide was found to enhance in malnourished mice with the Lewis lung carcinoma. These changes were not matched by further increase in the functional activity of macrophages. It has been suggested that enhancement of the antimetastatic effect in malnourished animals is due to the inhibition of neovascularization necessary for the beginning of metastatic exponential growth. The induction of neovascularization may be caused by the tumor necrosis factor, main product of activated macrophages.