Endovascular Embolization of Intracranial Aneurysms Using Bare Platinum Axium™ Detachable Coils: Immediate and Short-Term Follow-up Results from a Multicenter Registry

PurposeAxium™ coils were developed to improve the durability of coil-embolized cerebral aneurysms by increasing packing density. The purpose of this prospective multicenter registry was to evaluate the safety and durability of Axium™ coils.Materials and MethodsOne hundred twenty-six patients with 135 aneurysms of ≤ 15 mm in size underwent coil embolization using bare platinum coils, with Axium™ coils constituting over 50% of the total coil length. Immediate and short-term follow-up results were prospectively registered and retrospectively evaluated.ResultsOf the 135 aneurysms (83 unruptured and 52 ruptured), immediate post-embolization angiography revealed complete occlusion in 80 aneurysms (59.3%), neck remnants in 47 (34.8%), and incomplete occlusion in 8 (5.9%). The mean packing density was 42.8% (range, 9.5 - 90%) with Axium™ coil length constituting a mean of 87.9% of total coil length. The rate of procedure-related complications was 16.3%. Procedure-related permanent morbidity and mortality rates were 3.2% and 0.8%, respectively. Follow-up catheter or MR angiography, which was available in 101 aneurysms at 6 - 15 months (mean, 7.7 months), revealed stable or improved occlusion in 95 aneurysms and worsening in 6 aneurysms (5.9%). Lower packing density (< 30%) remained the only predictor for anatomical worsening on multivariable logistic regression analysis (P < 0.05).ConclusionIn this registry, Axium™ coils showed a relatively low rate of anatomical worsening on short-term follow-up imaging with an acceptable periprocedural safety profile compared to reports of other platinum coils. These results may warrant further study of long-term durability with Axium™ coils in larger populations

Interplay of Hydrogen Sulfide and Nitric Oxide on the Pacemaker Activity of Interstitial Cells of Cajal from Mouse Small Intestine

We studied whether nitric oxide (NO) and hydrogen sulfide (H2S) have an interaction on the pacemaker activities of interstitial cells of Cajal (ICC) from the mouse small intestine. The actions of NO and H2S on pacemaker activities were investigated by using the whole-cell patch-clamp technique and intracellular Ca2+ analysis at 30℃ in cultured mouse ICC. Exogenously applied (±)-S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, or sodium hydrogen sulfide (NaHS), a donor of H2S, showed no influence on pacemaker activity (potentials and currents) in ICC at low concentrations (10 µM SNAP and 100 µM NaHS), but SNAP or NaHS completely inhibited pacemaker amplitude and pacemaker frequency with increases in the resting currents in the outward direction at high concentrations (SNAP 100 µM and NaHS 1 mM). Co-treatment with 10 µM SNAP plus 100 µM NaHS also inhibited pacemaker amplitude and pacemaker frequency with increases in the resting currents in the outward direction. ODQ, a guanylate cyclase inhibitor, or glibenclamide, an ATP-sensitive K+ channel inhibitor, blocked the SNAP+NaHS-induced inhibition of pacemaker currents in ICC. Also, we found that SNAP+NaHS inhibited the spontaneous intracellular Ca2+ ([Ca2+]i) oscillations in cultured ICC. In conclusion, this study describes the enhanced inhibitory effects of NO plus H2S on ICC in the mouse small intestine. NO+H2S inhibited the pacemaker activity of ICC by modulating intracellular Ca2+. These results may be evidence of a physiological interaction of NO and H2S in ICC for modulating gastrointestinal motility

Hemo-metabolic impairment in patients with ST-segment elevation myocardial infarction: Data from the INTERSTELLAR registry

Background: Not only hemo-dynamic (HD) factors but also hemo-metabolic (HM) risk factors reflecting multi-organ injuries are considered as important prognostic factors in ST-segment elevation myocardial infarction (STEMI). However, studies regarding HM risk factors in STEMI patients are currently limited. Method: Under analysis were 1,524 patients with STEMI who underwent primary percutaneous coronary intervention in the INTERSTELLAR registry. Patients were divided into HM (≥ 2 risk factors) and non-HM impairment groups. The primary outcome was in-hospital all-cause mortality, and the secondary outcome was 1-year all-cause mortality. Results: Of 1,524 patients, 214 (14.0%) and 1,310 (86.0%) patients were in the HM and non-HM impairment groups, respectively. Patients with HM impairment had a higher incidence of in-hospital mortality than those without (24.3% vs. 2.7%, p &lt; 0.001). After adjusting for confounders, HM impairment was independently associated with in-hospital mortality (inverse probability of treatment weighting [IPTW]-adjusted odds ratio: 1.81, 95% confidence interval: 1.08–3.14). In the third door-to-balloon (DTB) time tertile (≥ 82 min), HM impairment was strongly associated with in-hospital mortality. In the first DTB time tertile ( &lt; 62 min), indicating relatively rapid revascularization, HM impairment was consistently associated with increased in-hospital mortality. Conclusions: Hemo-metabolic impairment is significantly associated with increased risk of in-hospital and 1-year mortality in patients with STEMI. It remains a significant prognostic factor, regardless of DTB time

Investigation of the efficiency of the joint transfer impulse load using finite element analysis

Load transfer efficiency (LTE) is the measure of the integrity of the joint to share the load to adjacent bars. It is being evaluated in the field by imposing impact load through heavy/falling weight deflector (H/FWD) and measuring the pavements response. These test are being analyzed statically assuming that if the same magnitude of peak load is applied on the pavement, it will result to the peak response gathered by deflection sensors. It has been proven by numerous research that the use of static analysis for the dynamic testing results to overestimation/underestimation. This study investigates the behavior of the joint based on impulse loading conducted in the field and gives a better understanding by simulating the same load using finite element analysis in Abaqus. Findings from the field are presented and the difference between the static and dynamic analysis using finite element analysis (Abaqus, 2017) were compared

Synthesis of Hollow Conductive Polypyrrole Balls by the Functionalized Polystyrene as Template

We report the preparation of hollow spherical polypyrrole balls (HSPBs) by two different approaches. In the first approach, core-shell conductive balls, CSCBs, were prepared with poly(styrene) as core and polypyrrole (PPy) as shell by in situ polymerization of pyrrole in the presence of polystyrene (PS) latex particles. In the other approach, CSCBs were obtained by in situ copolymerization of pyrrole in the presence of PS(F) with hydrophilic groups like anhydride, boronic acid, carboxylic acid, or sulfonic acid, and then HSPBs were obtained by the removal of PS or PS(F) core from CSCBs. TEM images reveal the spherical morphology for HSPBs prepared from PS(F). The conductivity of CSCBs and HSPBs was in the range of 0.20–0.90 S/cm2

Action of imipramine on activated ATP-sensitive K(+) channels in interstitial cells of Cajal from murine small intestine

Tricyclic antidepressants have been widely used for the treatment of depression and as a therapeutic agent for the altered gastrointestinal (GI) motility of irritable bowel syndrome (IBS). The aim of this study was to clarify whether antidepressants directly modulate pacemaker currents in cultured interstitial cells of Cajal (ICC). We used the whole-cell patch-clamp techniques at 30 degrees C in cultured ICC from the mouse small intestine. Treatment of pinacidil, an ATP-sensitive K(+) channel opener, in the ICC using the current clamping mode, produced hyperpolarization of the membrane potential and decreased the amplitude of the pacemaker potentials. With the voltage clamp mode, we observed a decrease in the frequency and amplitude of pacemaker currents and increases in the resting outward currents. These effects of pinacidil on pacemaker potentials and currents were completely suppressed by glibenclamide, an ATP-sensitive K(+) channel blocker. Also, with the current clamp mode, imipramine blocked the affect of pinacidil on the pacemaker potentials. Observations of the voltage clamp mode with imipramine, desipramine and amitryptyline suppressed the action of pinacidil in the ICC. Next, we examined whether protein kinase C (PKC) and the G protein are involved in the action of imipramine on pinacidil induced pacemaker current inhibition. We used chelerythrine, a potent PKC inhibitor and GDPbetaS, a nonhydrolyzable guanosine 5-diphosphate (GDP) analogue that permanently inactivates GTP-binding proteins. We found that pretreatment with chelerythrine and intracellular application of GDPbetaS had no influence on the blocking action of imipramine on inhibited pacemaker currents by pinacidil. We conclude that imipramine inhibited the activated ATP-sensitive K(+) channels in ICC. This action does not appear to be mediated through the G protein and protein kinase C. Furthermore, this study may suggest another possible mechanism for tricyclic antidepressants related modulation of GI motility

Involvement of Thromboxane A2 in the Modulation of Pacemaker Activity of Interstitial Cells of Cajal of Mouse Intestine

Although many studies show that thromboxane A2 (TXA2) has the action of gastrointestinal (GI) motility using GI muscle cells and tissue, there are no reports on the effects of TXA2 on interstitial cells of Cajal (ICC) that function as pacemaker cells in GI tract. So, we studied the modulation of pacemaker activities by TXA2 in ICC with whole cell patch-clamp technique. Externally applied TXA2 (5µM) produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode. The tonic inward currents by TXA2 were inhibited by intracellular application of GDP-β-S. The pretreatment of ICC with Ca2+ free solution and thapsigargin, a Ca2+-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker currents and suppressed the TXA2-induced tonic inward currents. However, chelerythrine or calphostin C, protein kinase C inhibitors, did not block the TXA2-induced effects on pacemaker currents. These results suggest that TXA2 can regulate intestinal motility through the modulation of ICC pacemaker activities. This modulation of pacemaker activities by TXA2 may occur by the activation of G protein and PKC independent pathway via extra and intracellular Ca2+ modulation