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ABSTRACT The effectiveness of reinforced plasters and Composite Reinforced Mortars (CRM) for increasing the inplane shear capacity of masonry walls was investigated on a series of 32 single-leaf tuff masonry [...]

IMPORTANCE: Dual thrombolytic treatment with small bolus alteplase and mutant prourokinase has the potential to be a safer and more efficacious treatment for ischemic stroke than alteplase alone because mutant prourokinase is designed to act only on degraded fibrin without affecting circulating fibrinogen. OBJECTIVE: To assess the safety and efficacy of this dual thrombolytic treatment compared with alteplase. DESIGN, SETTING, AND PARTICIPANTS: This controlled, open-label randomized clinical trial with a blinded end point was conducted from August 10, 2019, to March 26, 2022, with a total follow-up of 30 days. Adult patients with ischemic stroke from 4 stroke centers in the Netherlands were enrolled. INTERVENTIONS: Patients were randomized (1:1) to receive a bolus of 5 mg of intravenous alteplase and 40 mg of an intravenous infusion of mutant prourokinase (intervention) or usual care with 0.9 mg/kg of intravenous alteplase (control). MAIN OUTCOMES AND MEASURES: The primary outcome was any intracranial hemorrhage (ICH) on neuroimaging at 24 hours. Secondary outcomes included functional outcome at 30 days, symptomatic ICH, and fibrinogen levels within 24 hours. Analyses were by intention to treat. Treatment effects were adjusted for baseline prognostic factors. RESULTS: A total of 268 patients were randomized, and 238 (median [IQR] age, 69 [59-77] years; 147 [61.8%] male) provided deferred consent and were included in the intention-to-treat population (121 in the intervention group and 117 in the control group). The median baseline score on the National Institutes of Health Stroke Scale was 3 (IQR, 2-5). Any ICH occurred in 16 of 121 patients (13.2%) in the intervention group and 16 of 117 patients (13.7%) in the control group (adjusted odds ratio, 0.98; 95% CI, 0.46-2.12). Mutant prourokinase led to a nonsignificant shift toward better modified Rankin Scale scores (adjusted common odds ratio, 1.16; 95% CI, 0.74-1.84). Symptomatic ICH occurred in none of the patients in the intervention group and 3 of 117 patients (2.6%) in the control group. Plasma fibrinogen levels at 1 hour remained constant in the intervention group but decreased in the control group (β = 65 mg/dL; 95% CI, 26-105 mg/dL). CONCLUSIONS AND RELEVANCE: In this trial, dual thrombolytic treatment with small bolus alteplase and mutant prourokinase was found to be safe and did not result in fibrinogen depletion. Further evaluation of thrombolytic treatment with mutant prourokinase in larger trials to improve outcomes in patients with larger ischemic strokes is needed. Overall, in patients with minor ischemic stroke who met indications for treatment with intravenous thrombolytics but were not eligible for treatment with endovascular therapy, dual thrombolytic therapy with intravenous mutant prourokinase was not superior to treatment with intravenous alteplase alone. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT04256473

It is nowadays recognized that the building sector causes the greatest environmental impact in terms of both waste production and carbon emissions. Within the context of ecologically sustainable development (ESD), the construction sector is looking for more eco-friendly materials, such as natural fibres. Natural fibers are worldwide recognized as ideal replacement for traditional construction materials, providing excellent thermal and acoustic insulation for building but also for adoption as reinforcement fibers in cement mortars, composite materials, solid boards/panels, raw biomasses, multi-layers, filled loosen/foaming types, particles, slurry types, coils, bricks, etc. The aim of this work is to provide a clear overview on the natural fibers currently employed in the green production of building components, with the main focus on wool fibers deriving from the livestock sector, where wool waste disposal is a crucial problem. This article is a review conducted using the Systematic Literature Review (SLR) approach, a globally recognized method that is not inherently innovative. The innovation of this article lies in the addressed topic, which is relatively new and has only recently gained significant attention, resulting in a limited number of highly relevant articles in the literature.

Translation of acute ischemic stroke research to the clinical setting remains limited over the last few decades with only one drug, recombinant tissue-type plasminogen activator, successfully completing the path from experimental study to clinical practice. To improve the selection of experimental treatments before testing in clinical studies, the use of large gyrencephalic animal models of acute ischemic stroke has been recommended. Currently, these models include, among others, dogs, swine, sheep, and nonhuman primates that closely emulate aspects of the human setting of brain ischemia and reperfusion. Species-specific characteristics, such as the cerebrovascular architecture or pathophysiology of thrombotic/ischemic processes, significantly influence the suitability of a model to address specific research questions. In this article, we review key characteristics of the main large animal models used in translational studies of acute ischemic stroke, regarding (1) anatomy and physiology of the cerebral vasculature, including brain morphology, coagulation characteristics, and immune function; (2) ischemic stroke modeling, including vessel occlusion approaches, reproducibility of infarct size, procedural complications, and functional outcome assessment; and (3) implementation aspects, including ethics, logistics, and costs. This review specifically aims to facilitate the selection of the appropriate large animal model for studies on acute ischemic stroke, based on specific research questions and large animal model characteristics.

PURPOSE AND METHODS: We analyzed the clinical, laboratory, and radiologic data in nine patients who sustained an intracranial hemorrhage (ICH) after receiving intravenous recombinant tissue plasminogen activator (rt-PA) and heparin for treatment of acute myocardial infarction (MI). Our purpose was to delineate the clinical and radiologic features of the ICHs, as well as to determine their potential risk factors and mechanisms. RESULTS: Among 1,700 patients with an acute MI treated with an investigational two-chain rt-PA, duteplase (Burroughs Wellcome Co., Research Triangle Park, NC), nine (0.53%) developed symptomatic ICH. Neurologic symptoms occurred between 7 and 96 hours after onset of rt-PA therapy. All patients received heparin concomitantly for prevention of coronary reocclusion. The activated partial thromboplastin times (aPTTs) in five of eight (63%) patients at onset of ICH were excessively prolonged (greater than two times control); hypofibrinogenemia occurred in only one of five (20%) patients tested; and thrombocytopenia was present in only one of the nine (11%) patients. Fibrin degradation products (FDPs) were elevated in all five patients tested. Minor hemorrhage (not requiring transfusion) outside the central nervous system occurred in five of the nine patients with ICH. The ICHs were often of lobar location and of moderate to large size. They occurred at multiple sites in three patients, and were fatal in four instances (44%). CONCLUSIONS: The incidence of ICH in this series was low, and consistent with figures reported from studies with alteplase in patients with acute MI. The mechanisms of these hemorrhages remain unclear; while hypofibrinogenemia was not a uniform finding, exessive prolongation of the aPTT and elevated FDPs may have contributed to the occurrence of ICH in some patients. Still unidentified local cerebrovascular factors may play an additional role in causing ICH. In order to further clarify the mechanisms of ICH in the setting of thrombolytic therapy, prospective data collection on probable risk factors for ICH in patients with acute MI treated with rt-PA will be required.

Unreinforced masonry buildings are particularly vulnerable to brittle failures during seismic events due to the poor in-plane shear capacity of masonry walls. The use of strengthening solutions with polymeric matrices is not often recommended for masonry buildings, due to breathability issues, and the adoption of inorganic matrices is sometimes considered preferable. In this paper, the use of inorganic composite materials for improving the in-plane shear capacity of tuff masonry walls is investigated. The experimental data from 83 diagonal compression tests carried out at the University of Naples Federico II in recent years have been collected and the main results are herein discussed to outline the main features of different strengthening techniques with inorganic composite materials such as Reinforced Plaster (RP), Composite Reinforced Mortar (CRM) and Fabric Reinforced Cementitious Matrix (FRCM).

We explored the optoelectronic and vibrational properties of a new class of halogen-terminated carbon atomic wires in the form of polyynes using UV–vis, infrared absorption, Raman spectroscopy, X-ray single-crystal diffraction, and DFT calculations. These polyynes terminate on one side with a cyanophenyl group and on the other side, with a halogen atom X (X = Cl, Br, I). We focus on the effect of different halogen terminations and increasing lengths (i.e., 4, 6, and 8 sp-carbon atoms) on the π-electron conjugation and the electronic structure of these systems. The variation in the sp-carbon chain length is more effective in tuning these features than changing the halogen end group, which instead leads to a variety of solid-state architectures. Shifts between the vibrational frequencies of samples in crystalline powders and in solution reflect intermolecular interactions. In particular, the presence of head-to-tail dimers in the crystals is responsible for the modulation of the charge density associated with the π-electron system, and this phenomenon is particularly important when strong I··· N halogen bonds occur.

'For the management of atrial fibrillation, oral alternatives to warfarin have arrived,' wrote Dr. Gregory J. del Zoppo and Misha Eliasziw, Ph.D., in an editorial accompanying the study. In addition [...]

Alteplase is effective for treatment of acute ischaemic stroke but debate continues about its use after longer times since stroke onset, in older patients, and among patients who have had the least or most severe strokes. We assessed the role of these factors in affecting good stroke outcome in patients given alteplase.

We present an all-solution processed multilayered structure completely obtained via spin-coating, which can be used to study and optimize the phenomenon of metal-enhanced fluorescence. Indeed, the electromagnetic interactions occurring between fluorescent probes and localized surface plasmons typical of metal nanoparticles (NPs), which influence the fluorescence quantum yield, are strongly dependent on the nanoparticle/molecule distance. The platform proposed here offers unique advantages in terms of processability, allowing a fine-tuning of such a distance in a single deposition step. Fluorescence versus fluorophore/AuNP spacing curves are shown for two organic systems, namely, a perylene-based dye dispersed in a polymer matrix and a polyconjugated polymer (poly(3-hexylthiophene)), interacting with a nanostructured gold thin film. In both cases, optimal distances and enhancement factors have been measured.

Recombinant tissue plasminogen activator (rt-PA, alteplase) improved functional outcome in patients treated soon after acute ischaemic stroke in randomised trials, but licensing is restrictive and use varies widely. The IST-3 trial adds substantial new data. We therefore assessed all the evidence from randomised trials for rt-PA in acute ischaemic stroke in an updated systematic review and meta-analysis.

Multiple approaches are being studied to enhance the rate of thrombolysis for acute ischemic stroke. Treatment of myocardial infarction with a combination of a reduced-dose fibrinolytic agent and a glycoprotein (GP) IIb/IIIa receptor antagonist has been shown to improve the rate of recanalization versus fibrinolysis alone. The combined approach to lysis utilizing eptifibatide and recombinant tissue-type plasminogen activator (rt-PA) (CLEAR) stroke trial assessed the safety of treating acute ischemic stroke patients within 3 hours of symptom onset with this combination.

Our goal is to provide an overview of the current evidence about components of the evaluation and treatment of adults with acute ischemic stroke. The intended audience is physicians and other emergency healthcare providers who treat patients within the first 48 hours after stroke. In addition, information for healthcare policy makers is included.

The integrity of the cerebral microvasculature depends on the interaction between its component cells and the extracellular matrix, as well as reorganized cell–cell interactions. In the central nervous system, matrix adhesion receptors are expressed in the microvasculature and by neurons and their supporting glial cells. Cells within cerebral microvessels express both the integrin and dystroglycan families of matrix adhesion receptors. However, the functional significance of these receptors is only now being explored. Endothelial cells and astrocytes within cerebral capillaries co-operate to generate and maintain the basal lamina and the unique barrier functions of the endothelium. Integrins and the dystroglycan complex are found on the matrix-proximate faces of both endothelial cells and astrocyte end-feet. Pericytes rest against the basal lamina. In the extravascular compartment, select integrins are expressed on neurons, microglial cells and oligodendroglia. Significant alterations in both cellular adhesion receptors and their matrix ligands occur during focal cerebral ischaemia, which support their functional significance in the normal state. We propose that matrix adhesion receptors are essential for the maintenance of the integrity of the blood–brain permeability barrier and that modulation of these receptors contributes to alterations in the barrier during brain injury.

This workshop examined the opportunities for translational research directed at immune and inflammatory mechanisms. This summary presents the background data in 3 general areas: (1) inflammation and hemostasis in cerebrovascular and cardiovascular disease, (2) immune interactions in the central nervous system and heart, and (3) translation of immune modulation in the brain and heart, all of which supported a consensus derivation of the opportunities for future research in these areas. The summary concludes with 11 recommendations.

Women have poorer outcomes from stroke than men. Women also have risk factors that are unique, including pregnancy and hormone therapy. Hormone therapy for postmenopausal replacement increased the risk of ischemic stroke according to results of the Women’s Health Initiative clinical trials. Based on the current understanding of the mechanisms of action of estrogen, the reasons for this increased risk are uncertain. One method to better understand the reasons for this increased risk is to re-evaluate estrogen’s role in the neurovascular unit, simplistically comprised of the neurons, glia, and endothelial cells, as well as the processes of inflammation, and hemostasis/thrombosis. Besides the role of estrogen there are many gaps of knowledge about issues specific to women and stroke.

The integrity of cerebral microvessels requires the close apposition of the endothelium to the astrocyte endfeet. Integrins α1β1and α6β4are cellular matrix receptors that may contribute to cerebral microvascular integrity. It has been hypothesized that focal ischemia alters integrin expression in a characteristic time-dependent manner consistent with neuron injury. The effects of middle cerebral artery occlusion (MCAO) and various periods of reperfusion on microvasclar integrin α1β1and α6β4expression were examined in the basal ganglia of 17 primates. Integrin subunits α1and β1colocalized with the endothelial cell antigen CD31 in nonischemic microvessels and with glial fibrillary acidic protein on astrocyte fibers. Rapid, simultaneous, and significant disappearance of both integrin α1and β1subunits and integrin α6β4occurred by 2 hours MCAO, which was greatest in the region of neuron injury (ischemic core, Ic), and progressively less in the peripheral (Ip) and nonischemic regions (N). Transcription of subunit β1mRNA on microvessels increased significantly in the Ic/Ip border and in multiple circular subregions within Ic. Microvascular integrin α1β1and integrin α6β4expression are rapidly and coordinately lost in Ic after MCAO. With loss of integrin α1β1, multiple regions of microvascular β1mRNA up-regulation within Ic suggest that microvessel responses to focal ischemia are dynamic, and that multiple cores, not a single core, are generated. These changes imply that microvascular integrity is modified in a heterogeneous, but ordered pattern.

Abstract.: An excitation function of the ground-state γ0-ray capture transition in 12C (α,γ)16O at θγ = 90� was obtained in far geometry using six Ge detectors, where the study of the reaction was initiated in inverse kinematics involving a windowless gas target. The detectors observed predominantly the E1 capture amplitude. The data at E = 1.32 to 2.99 MeV lead to an extrapolated astrophysical S factor S E1(E 0) = 90�15 keV b at E 0 = 0.3 MeV (for the case of constructive interference between the two lowest E1 sources), in good agreement with previous works. However, a novel Monte Carlo approach in the data extrapolation reveals systematic differences between the various data sets such that a combined analysis of all available data sets could produce a biased estimate of the S E1(E 0) value. As a consequence, the case of destructive interference between the two lowest E1 sources with S E1(E 0) = 8�3 keV b cannot be ruled out rigorously.

It has been shown recently that matrix metalloproteinases (MMPs) are elevated after cerebral ischemia. In the current study, we investigated the pathophysiologic role for MMP-9 (gelatinase B, EC.3.4.24.35) in a mouse model of permanent focal cerebral ischemia, using a combination of genetic and pharmacologic approaches, Zymography and Western blot analysis demonstrated that MMP-9 protein levels were rapidly up-regulated in brain after ischemic onset. Reverse transcription polymerase chain reaction showed increased transcription of MMP-9. There were no differences in systemic hemodynamic parameters and gross cerebrovascular anatomy between wild type mice and mutant mice with a targeted knockout of the MMP-9 gene. After induction of focal ischemia, similar reductions in cerebral blood flow were obtained. In the MMP-9 knockout mice, ischemic lesion volumes were significantly reduced compared with wild type littermates in male and female mice. In normal wild type mice, the broad spectrum MMP inhibitor BB-94 (batimastat) also significantly reduced ischemic lesion size, However, BB-94 had no detectable protective effect when administered to MMP-9 knockout mice subjected to focal cerebral ischemia. These data demonstrate that MMP-9 plays a deleterious role in the development of brain injury after focal ischemia.

Zusammenfassung: Die Bedeutung hämorrhagischer Transformationen, entweder als klinisch stumme hämorrhagische Infarkte oder als klinisch auffällige bis lebensbedrohliche parenchymatöse Blutungen, ist entscheidend für die Beurteilung des Risiko-Nutzen-Verhältnisses der Thrombolyse, aber auch anderer gerinnungshemmender Therapien, wie der Antikoagulation, beim Hirninfarkt. Insbesondere kann die Thrombolyse das Risiko schwerer Blutungskomplikationen verglichen mit unbehandelten Hirninfarktpatienten bis zu 10fach erhöhen. Verschiedene Konzepte der Entwicklung intrazerebraler Blutungen und hämorrhagischer Transformationen werden vorgestellt. Die Rolle der zerebralen Mikrogefäßstrombahn wird betont. Es konnte in experimentellen Untersuchungen der fokalen zerebralen Ischämie ein signifikanter Verlust von Basalmembranbestandteilen der zerebralen Mikrogefäße nachgewiesen werden. Dieser Verlust von Basalmembranstrukturen, der zu einer deutlichen Integritätsminderung der Gefäßwand führte, war auch signifikant mit der Entwicklung petechialer Blutungen in der Umgebung zerstörter Gefäße verbunden. Mechanismen für die mikrovaskuläre Schädigung können die Plasmin-vermittelte Laminindegradation, die Aktivierung von Matrixmetalloproteinasen, sowie die Transmigration von Leukozyten durch die Gefäßwand sein. Eine mögliche Verbesserung der mikrovaskulären Integrität mit nachfolgender Reduktion der Blutungsrate ist theoretisch über verschiedene Wege möglich: 1. Durch eine Verbesserung der Definition des individuellen Zeitfensters zur Behandlung, z.B. durch neue Kernspintechniken 2. durch den biochemischen Nachweis der Basalmembranschädigung, insbesondere um Patienten mit starken Basalmembranschädigungen von einer Intervention auszuschließen, und 3. durch pharmakologische Behandlungsmöglichkeiten zum Schutz der Basalmembran während der Thrombolyse.

The effect of 50 to 200 mM NaCl on two lines (CP with solid stem and CV with hollow stem) of ×Haynaldoticum sardoum was studied. NaCl significantly reduced root and shoot fresh and dry masses, root length and less markedly shoot length of CP and CV plants. The sodium accumulated in the leaves in relation to the concentration of NaCl and length of the treatment; CP leaves contained twice as much sodium as CV leaves. The leaf chlorophyll a/b ratio was not affected by NaCl. NaCl decreased the leaf water and osmotic potentials. The pressure potential increased due to the increased concentration of dissolved solutes in the leaf, particularly sodium. The proteinase and exopeptidase activities increased during NaCl treatment.

Both vascular endothelial growth factor (VEGF) and integrin αvβ3play roles in angiogenesis. In noncerebral vascular systems, VEGF can induce endothelial integrin αvβ3expression. However, it is unknown whether VEGF, like integrin αvβ3, appears in the initial response of microvessels to focal brain ischemia. Their coordinate expression in microvessels of the basal ganglia after middle cerebral artery occlusion (MCAO) in the nonhuman primate model was examined quantitatively. Cells incorporating deoxyuridine triphosphate (dUTP+) by the polymerase I reaction at 1 hour (n = 3), 2 hours (n = 3), and 7 days (n = 4) after MCAO defined the ischemic core (Ic) and peripheral regions. Both VEGF and integrin αvβ3were expressed by activated noncapillary (7.5- to 30.0-μm diameter) microvessels in the Ic region at 1 and 2 hours after MCAO. At 7 days after MCAO, the number of VEGF+, integrin αvβ3+, or proliferating cell nuclear antigen-positive microvessels had decreased within the Ic region. The expressions of VEGF, integrin αvβ3, and proliferating cell nuclear antigen were highly correlated on the same microvessels using hierarchical log-linear statistical models. Also, VEGF and subunit αvmessenger ribonucleic acids were coexpressed on selected microvessels. Here, noncapillary microvessels are activated specifically early during a focal cerebral ischemic insult and rapidly express VEGF and integrin αvβ3together.

Microvascular integrity is lost during focal cerebral ischemia. The degradation of the basal lamina and extracellular matrix are, in part, responsible for the loss of vascular integrity. Matrix metalloproteinases (MMPs) may play a primary role in basal lamina degradation. By using a sensitive modification of gelatin zymography, the authors investigated the activity of MMP-2 and MMP-9 in frozen 10-µm sections of ischemic and nonischemic basal ganglia and plasma samples of 27 non-human primates after middle cerebral artery occlusion/reperfusion (MCAO/R) for various periods. The gelatinolytic activities were compared with parallel cell dUTP incorporation in the ischemic zones of adjacent sections. In the brain, the integrated density of MMP-2 increased significantly by 1 hour after MCAO and was persistently elevated thereafter. Matrix metalloproteinase-2 expression was highly correlated with the extent of neuron injury and the number of injured neurons (r = 0.9763, SE = 0.004, 2P< 0.0008). Matrix metalloproteinase-9 expression only was significantly increased in subjects with hemorrhagic transformation. In plasma, only MMP-9 increased transiently at 2 hours of MCAO. These findings highlight the early potential role of MMP-2 in the degradation of basal lamina leading to neuronal injury, and an association of MMP-9 with hemorrhagic transformation after focal cerebral ischemia.

The excitation function (EF) data for dissipative processes in 19F + 27Al system in the incident energy interval from 113.5 to 130 MeV are used to obtain the dependence of the charge variance and of the interaction time as a function of the incident energy. Fluctuations are observed in the EFs of both these secondary observables. Their correlation is supported by a mechanism based on stochastic exchange of nucleons.

The characteristics of the dissipative processes in the collisions of light heavy ion systems at incident energies below 10 MeV/nucleon have been studied. The correlations between different experimental observables show similar trends as those known at much heavier systems and semiempirical relationships are established starting from assumptions on the nature of the microscopic mechanisms. The charge equilibration process in light systems is also studied.

The antithrombotic plasma enzyme, activated protein C (APC), may play a role in thrombolysis. In vitro, acceleration of clot lysis by APC depends on its ability to inhibit the activation of prothrombin. The effect of APC on the assembly and dispersion of fibrin network was studied using turbidimetry, plasmin digestion of fibrin, and electron microscopy of plasma clots. The addition of APC before clotting but not after clotting accelerated clot lysis. The rate of increase in the turbidity of clotting plasma was reduced by APC. The turbidity of plasma clots containing APC was directly related to the clot lysis time. Fibrin from plasma clots that were formed in the presence of APC yielded less fibrin degradation products than fibrin from clots without added APC. Furthermore, APC reduced the diameter and relative number of fibrin fibers in plasma clots during gel assembly. We propose that APC may enhance the efficacy of thrombolysis by reducing the relative mass of fibrin within maturing thrombi.

Quantum chemical ab initio calculations have been performed on a model push–pull polyene. In these calculations the mean bond length alternation of the chain has been constrained to specific discrete values so as to yield various structures ranging from a polyenelike geometry to a zwitterionic geometry. It is shown that this purely geometric distortion of the nuclei induces relevant changes of the electronic properties such as molecular dipole moment, molecular polarizabilities, and hyperpolarizabilities. Also, simulated vibrational spectra are heavily affected by changes in geometry. By changing the molecular environment (solvent effect) the theoretically predicted molecular nonlinear optical behavior parallels the trends observed experimentally, thus showing the key role played by the bond length alternation parameter. In Appendix A the derivative relationship among hyperpolarizabilities at various orders as a function of the bond length alternation parameter is discussed.

A NaI sum-spectrometer combined with Ge-counters has been used to characterize the members of the island of high spin isomers nearN=82. On the basis of half lives, total?-decay energies and discrete?-lines, assignments of 22 isomers are given or confirmed. The isomers are localized to the region 82?N?86 andZ?68, and the excitation energies vary from 3 MeV to 12.2 MeV. An empirical relation between spin and excitation energy is presented and on this basis isomeric spin values up to (33±2)h are deduced. The isomers are thought to be due to strong alignment of 2 to 8 shell-model particles in a spherical or possibly weakly oblate potential.

There is increasing interest in the role of polymorphonuclear (PMN) leukocytes in the evolution of focal cerebral infarction. Surgical preparation of focal cerebral ischemia models may alter leukocyte reactivity and thereby make interpretation of leukocyte function following ischemia/reperfusion difficult. The effects of surgical preparation and of experimental ischemia/reperfusion on granulocyte function have been examined prospectively in a baboon model. Twenty-six adolescent male baboons underwent surgical preparation, of which 21 underwent middle cerebral artery occlusion/reperfusion. Four additional animals served as nonsurgical controls. Peripheral venous blood specimens were taken for performing assays of leukocyte function at defined intervals before and after both the surgical preparation (i.e., the overall procedure for implantation of the middle cerebral artery occlusion device) and occlusion/reperfusion. A stress-related elevation in total leukocyte number was attributed mainly to an increase in the number of circulating PMN leukocytes. Values rose from 13.9 ± 4.9 × 103to 27.8 ± 5.8 × 103/μl, (±SD; n= 21) for total leukocyte number, with p< 0.001, and from 4.3 ± 2.1 × 103to 15.9 ± 4.7 × 103/μl (n= 21) for PMN leukocytes, with p< 0.001. Surgical preparation had no effect (p≥ 0.4) on the ability of PMN leukocytes, isolated 24 h after the implantation procedure, to display polarization, O2– production, or β-glucuronidase release when stimulated with human C5a. A moderate decrease in the chemotactic response to C5a resolved within the 7-day postsurgery (preocclusion) period. Three-hour middle cerebral artery occlusion and 1-h reperfusion resulted in a significant reduction in C5a-induced polarization. The preocclusion value of 82 ± 9.7 (n= 7) was compared with the occlusion/reperfusion value at 58.8 ± 13.7 (n= 6; p< 0.05). A moderate decrease was observed in C5a-induced O2– and β-glucuronidase release, as well as a decrease in the chemotactic response. In the nonhuman primate model, the reversible alterations (i.e., chemotaxis) in granulocyte function that were noted following surgical preparation resolved within 7 days. In contrast, middle cerebral artery occlusion/reperfusion was associated with a more dramatic and significant reduction in multiple granulocyte functions elicited by the endogenous mediator C5a as observed 1 h postreperfusion.

Smoking and elevated leukocyte counts are risk factors for cardiovascular disease. Experimental studies suggest that leukocyte activation may be a requirement for certain cardiovascular complications. Clinical studies have demonstrated activated leukocytes in the peripheral blood of stroke victims. Accordingly, neutrophil activation in unseparated whole blood of smokers as well as naive neutrophils of non-smokers exposed to plasma of smokers was investigated. Both spontaneous superoxide formation as determined by nitroblue tetrazolium reduction, as well as pseudopod formation, are significantly elevated in autologous neutrophils of smokers. The surface expression of CD18 and L-selectin on autologous circulating neutrophils of smokers is not significantly different from non-smoker controls. In contrast, incubation of naive neutrophils with smoker plasma leads to significantly higher levels of superoxide formation, pseudopod formation, and L-selectin shedding, compared with non-smoker plasma, suggesting that the plasma of smokers contains a transferable factor which causes leukocyte activation. The results indicate that analysis of blood samples from large peripheral veins may not accurately reflect leukocyte activation in the circulation since activated leukocytes have a higher probability to be trapped in the microcirculation.

The reaction232Th(?,f) is studied using bremsstrahlung?-beams in the (5.45–6.85) MeV end point energy range. Fragments angular distributions are measured and yield components with opposite parities are separated. The unfolded cross sections have resonant behaviour which indicates the existence of low damped vibrational states. Furthermore, a near degeneracy forKp=0+ andKp= 0- resonances at ~5.5 MeV and ~6 MeV is observed. Data are analysed in terms of a double humped barrier configuration within the doorway state model for fission. For each component maxima with almost equal heights and a shallow intermediate minimum are determined. Moreover almost equal potential barriers withK=0 and opposite parities are found. This is a signature for mass-asymmetric shapes and seems a clear indication for a threehumped barrier configuration with a low inner maximum and a third mass asymmetric shallow minimum due to the fragmentation of the normal mass-asymmetric second maximum.

Deep subthreshold photofission data of238U are analysed. Spectroscopic properties of highly deformed states from experiments in the literature are introduced into a model calculation based on the doorway state formalism which is extended to fission at energies as low as the isomeric level. It is shown that starting from the results of a detailed analysis of the photofission measurements near the top of the fission barrier it is possible to describe the process in the energy range covered by the intermediate well in the double-humped deformation potential. In particular, the so-called “shelf effect” in the low energy photofission is reproduced in terms of delayed isomeric fission through a few undamped vibrational states localised in the pairing gap region above the isomer.

White blood cells (WBCs) play vital roles in host defense. Recently, increasing interest has been directed toward the question of whether WBCs, particularly polymorphonuclear leukocytes, could also act as mediators of secondary brain damage in the setting of focal and global cerebral ischemia with and without reperfusion. Considerable insight into the importance of WBC-mediated tissue injury has been gained from studies employing antileukocyte interventions in experimental cerebral ischemia. The purpose of this article is to survey the different approaches taken to interfere with WBC inflammatory function. Emphasis is laid on a discussion of the efficacy of these interventions, their effects and side effects on cerebral and systemic parameters, and the power of evidence they provide for identification of WBCs as important factors in cerebral ischemia. The role of WBCs has been investigated in a great variety of global and focal cerebral ischemia models with and without reperfusion, leading to spmetimes contradictory results. In the light of currently available data, it seems likely that WBCs contribute to secondary brain damage in the scenario of experimental transient focal cerebral ischemia, if the insult is not too severe.

Hemorrhagic transformation after cerebral ischemia is a well known clinical concern. The frequency of intact basal lamina (BL), identified by laminin antigen, in hemorrhagic and nonhemorrhagic zones after middle cerebral artery occlusion (MCA:O) and 3-h MCA:O with reperfusion in adolescent male baboons was assessed. Parenchymal hemoglobin was not detected prior to 24-h reperfusion. A significant decrease in the density of laminin (BL) in hemorrhagic zones (6.2 ± 2.4) compared with nonhemorrhagic ischemic zones (10.5 ± 2.4) (p < 0.05) and nonischemic basal ganglia (17.0 ± 2.7) (p < 0.01) was observed. Time-dependent changes in BL integrity appear linked to the extravasation of blood components.

PMNs are believed to play an important role in eschemia and C5a uptake is an important functional indicator for G protein-coupled receptor trafficking. The ability of PMNs to internalize 125I-labeled C5a in vitro is an index of the functional state of these cells. We evaluated the effects of model preparation and focal cerebral ischemia by middle cerebral artery occlusion and reperfusion (MCA:O/R) on internalization of C5a by PMNs isolated from baboons (Papio anubis/ cynocephalus). Similar assays were performed on PMNs isolated before and after exposing the animals undergoing MCA:O/R to an anti-inflammatory 21-aminosteroid, tirilazad mesylate (U74006F). Surgical implantation of the MCA occlusion device had no measurable effect on uptake of C5a to the cytosol by the PMN. In contrast, MCA:O/R appeared to decrease uptake of C5a. Both in vivo and in vitro administration of tirilazad, to otherwise untreated animals and to isolated cells, respectively, reduced baseline values of C5a uptake in the PMNs. Cytosolic uptake of C5a was also reduced in PMNs isolated from subjects that had undergone MCA:O/R and tirilazad treatment. These results suggest that focal cerebral ischemia, with or without exposure to tirilazad mesylate, may inhibit internalization of C5a by the PMN receptors. The effects of stroke on the ability of C5a to gain entry into the PMN may result from receptor down-regulation or “desentization” of the cell, possibly due to activation of complement and generation of C5a which occupied the receptors. Alternatively, the effect of tirilazad presumably results from the ability of this drug to enter the membrane lipid layer and reduce fluidity.

The compact heavy ion spectrometer MACISTE is going to be realized at the Laboratorio Nazionale del Sud-Catania (LNS). It should allow to resolve the single mass unit up to A/spl ap/70 and the single charge up to Z/spl ap/45 when operating on ions around 50 MeV/amu. Coupling this device with other multidetectors already installed at LNS will give access to a large series of experiments concerning the projectile-like and the-quasi-fusion physics at intermediate energy.

This article discusses mechanisms of intracerebral hemorrhage, clinical attributes of intracerebral hemorrhage, intracerebral hemorrhage in the setting of altered hemostasis, and antithrombotic agents.

Linear and helical graphene nanoribbons (L-PyGNRand H-PyGNR) bearing electron-rich pyrrole units have been synthesized by using the photochemical cyclodehydrochlorination (CDHC) reaction. The pyrrole units in the polymer backbone make the polymer electron-rich with moderate bandgap values and relatively high HOMO energy levels. The planarization of the pyrrole unit through cyclization yields a bandgap value almost 0.5 eV lower than that measured for polypyrrole. Conductivity values in the thin film up to 0.12 S/cm were measured for the chemically oxidized L-PyGNR(four-point method). Both GNRs showed excellent fluorescence sensing properties for TNT in solution with KSVvalues up to 6.4 × 106M–1.