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OBJECTIVES Our goal was to evaluate the combined effects of balloon pulmonary angioplasty (BPA) followed by pulmonary endarterectomy (PEA) to treat high-surgical-risk patients with chronic thromboembolic pulmonary hypertension (CTEPH). METHODS This study included 58 patients with CTEPH who had pulmonary vascular resistance of ≥1000 dyn·s/cm5, mean pulmonary arterial pressure (mPAP) of ≥45 mmHg or mPAP of 38–44 mmHg with comorbidities. Of these, 21 patients underwent the combined therapy of BPA followed by PEA (BPA group) and 37 underwent direct PEA (non-BPA group). Preoperative and postoperative results were compared between the 2 groups. An early postoperative composite event comprised the postoperative use of extracorporeal membrane oxygenation or intra-aortic balloon pump, in-hospital death, rescue BPA, prolonged ventilation, tracheostomy, prolonged stay in the intensive care unit, deep sternal wound infection and cerebral infarction. RESULTS Before the first intervention (before BPA or direct PEA), patients in the BPA group had a higher mPAP than those in the non-BPA group. After undergoing BPA before PEA, the BPA group demonstrated significantly decreased mPAP and pulmonary vascular resistance (43 vs 52 mmHg, P CONCLUSIONS Compared with direct PEA, the combination therapy of BPA followed by PEA can be a feasible and effective risk-reduction strategy for high-surgical-risk patients with CTEPH.

Indocyanine green (ICG) videoangiography is rarely used during the surgical treatment of thoracic outlet syndrome (TOS).To evaluate subclavian artery (SA) flow dynamics using the analytical ICG videoangiography during TOS surgeries.We examined patients with neurogenic TOS who received surgical treatment and whose SA blood flow at the interscalene space was evaluated using ICG videoangiography equipped with an analytical function (FLOW800). Anterior scalenectomy with or without middle scalenectomy and first rib resection were conducted for decompression of the brachial plexus. ICG videoangiography was performed before and after decompression of the brachial plexus. After acquisition of grayscale and color-coded maps, a region of interest was placed in the SA to obtain time-intensity diagrams. Maximum intensity (MI), rise time (RT), and blood flow index (BFi) were calculated from the diagram, in arbitrary intensity (AI) units. We compared values before and after decompression. Comparisons of the three parameters before and after decompression were assessed statistically using the paired t-tests and Wilcoxon signed-rank test.We evaluated nine procedures in consecutively presenting patients. The observed mean values of MI, RT, and BFi before decompression were 174.1 ± 61.5 AI, 5.2 ± 1.1 s, and 35.2 ± 13.5 AI/s, respectively, and the observed mean values of MI, RT, and BFi after decompression were 299.3 ± 167.4 AI, 6.6 ± 0.8 s, and 44.6 ± 28.3 AI/s, respectively. These parameters showed higher values after decompression than before decompression, and the increase in MI and RT was statistically significant (P.05).ICG videoangiography allows semiquantitative evaluation of hemodynamic changes during TOS surgery. A marked decrease in the velocity of SA flow was observed after decompression.

This article re-examines Japan’s entry into international society, focusing on leading Japanese diplomats. It has been believed that Meiji leaders’ interpretation of international society and diplomacy was characterized by power-political and zero-sum thinking, and they took a realistic approach in an imperialistic system. However, the present article demonstrates that Japanese diplomacy in and after the 1890s was basically guided by interest-oriented and non–zero-sum thinking which was closely tied to the international order. Leading Japanese diplomats, who learned from their experiences in diplomacy with Western countries, understood the significance of norms as well as the importance of military power, and pursued Japan’s national interests within the rules and norms of international society. These findings offer a new image of the principles of modern Japanese diplomacy, the mechanisms of Japanese imperial expansion, and the process of the spread of norms in international society.

While there is a discordance between fractional flow reserve (FFR) and non-hyperemic pressure ratios (NHPRs) in some cases, the mechanisms underlying these discordances have not yet been fully clarified. We examined whether vascular damage as assessed by measurement of the brachial-ankle pulse wave velocity (baPWV), a marker of arterial stiffness, or ankle brachial pressure index (ABI), a marker of atherosclerotic arterial stenosis, might be associated with their discordances.FFR and NHPRs were measured in 283 consecutive patients (69 ± 10 years old). Based on previously established cut-off values of the two markers (i.e. +/- = FFR ≤/0.80 or =NHPRs ≤/0.89), the study participants were divided into four groups (the + and - signs denoting "predictive of significant stenosis" and "not predictive of significant stenosis," respectively): the FFR+/NHPRs+ group (n = 124), FFR-/NHPRs+ group (n = 16), FFR+/NHPRs- group(n = 65), and FFR-/NHPRs- group (n = 78). The baPWV and ABI were also measured in all the participants, and values of2000 cm/s and ≥1.00 of the baPWV and ABI, respectively, were considered as representing relatively less advanced atherosclerotic systemic vascular damage.The prevalence of subjects with ABI ≥1.00 was higher in the FFR+/NHPRs- group than in the FFR-/NHPRs- group (p 0.05). When the study subjects were divided into 2 groups, namely, the FFR+/NHPRs- group and the combined group, the prevalence of ABI ≥1.00 and that of baPWV2000 cm/s were higher in the FFR+/NHPRs- group as compared with those in the combined group (p 0.05). The results of binary logistic regression analysis demonstrated that ABI ≥1.00 was associated with a significant odds ratio (2.34, p 0.05) for the FFR+/NHPRs- discordance.The FFR+/NHPRs- discordance appears to be observed in patients with relatively less advanced atherosclerotic systemic vascular damage. Thus, ABI ≥1.00 may be a marker of the presence of the FFR+/NHPRs- discordance.

Background Pulmonary endarterectomy (PEA) is the standard treatment for chronic thromboembolic pulmonary hypertension (CTEPH), although some patients may experience residual pulmonary hypertension (PH). It is unclear whether balloon pulmonary angioplasty (BPA) is effective for residual PH after PEA. This study aimed to compare the BPA outcomes between patients with residual PH after PEA and those with inoperable CTEPH. Methods This retrospective study compared BPA for residual PH after PEA (25 patients, 101 BPA sessions) and BPA alone for inoperable CTEPH (21 patients, 89 BPA sessions). All patients underwent right heart catheterisation and functional and laboratory tests before PEA or before and after BPA. Results There was no difference in the number of BPA sessions per patient (4.0 ± 1.9 vs. 4.2 ± 1.9, p = 0.671). No significant differences were observed with respect to the mean pulmonary artery pressure (23.6 ± 9.1 vs. 21.9 ± 5.7 mmHg, p = 0.44), pulmonary vascular resistance (3.7 ± 0.5 vs. 2.8 ± 1.2 Wood units, p = 0.14), 6-min walking distance (392.1 ± 117.7 vs. 452.4 ± 90.1 m, p = 0.096), and World Health Organization functional class (I/II/III/IV: 14/11/0/0 vs. 9/12/0/0, p = 0.375). Severe haemoptysis requiring embolisation was more common in the PH after PEA group (16.0% vs. 5.4%, p = 0.018). However, no patients required mechanical ventilation or extracorporeal membrane oxygenation, and there were no procedural deaths. Conclusion Although BPA might be effective for residual PH after PEA, it was associated with a high rate of haemoptysis.

Various types of electromagnetic shielding structures for specific frequency band have been reported in recent years. A gasket-free electromagnetic shielding structure using folded quarter-wavelength substrate integrated waveguide (FQ-SIW) resonators for 2.4-GHz band is one of them. In the structure, SIW resonators of different resonant frequencies in 2.4-GHz band are cascaded and positioned on inner walls of a gap. The structure is almost free of deterioration since contact-type gaskets are not used. In this paper, a gasket-free electromagnetic shielding structure for 2.4-GHz and 5-GHz bands using cascaded dual-behavior (DB) SIW resonators is proposed and evaluated. A DB-SIW resonator consists of two FQ-SIW resonators sharing one coupling slot and has two almost-independent resonant frequencies in the two bands. The design results showed attenuation characteristics at the two bands, and the configuration was miniaturized by 4% compared with conventional cascaded FQ-SIW resonators. Shielding effectiveness (SE) was also evaluated, and the measured results showed more than 20-dB improvement of SE near the two bands, though frequency shifts were observed.

Objective Risk control of thromboembolic complications (TECs) during stent-assisted coil embolization (SACE) for unruptured intracranial aneurysms (UIAs) is crucial for satisfactory treatment outcomes. We retrospectively evaluated the data from our cohort of SACE for UIAs to analyze the role of anatomical, clinical, and stent type-related factors to determine the optimal preoperative values of light transmission aggregometry (LTA) for TEC prevention. Methods From July 2015 to May 2018, we retrospectively analyzed the data from 132 patients with SACE-treated UIAs at our hospital. Data regarding the aneurysm location, maximum diameter, stent type used, preoperative LTA value, and ischemic and hemorrhagic complications were collected. Aspirin 100 mg and clopidogrel 75 mg were started 7 days before surgery, with a “boost” dose (an additional 75 mg of clopidogrel for an LTA value >60%) added after August 2016 to address clopidogrel resistance. After multivariate analysis, we developed our original combined parameter termed the thromboembolic predictor (TEP). Receiver operating characteristic (ROC) analysis for TEP and each significant variable was performed. Results TECs were confirmed in 5 of the 132 patients (3.8%) and hemorrhagic complications in 9 of the 132 patients (6.8%). From the multivariate analysis results, the LTA value and maximum diameter were chosen as significant variables and included in the TEP. ROC analysis of the LTA value revealed a sensitivity and specificity of 0.866 and 0.600, respectively (area under the curve, 0.747), with a cutoff of 62%. TEP permitted the establishment of an optimal LTA value according to the aneurysm maximum diameter to predict for TECs. The complication rate for the Neuroform EZ, Enterprise, Neuroform Atlas, and LVIS stents was 2.9%, 10.5%, 1.4%, and 14.3%, respectively. Conclusions The preoperative LTA value contributes to the prediction of TECs after SACE for UIAs. The TEP (relating the LTA cutoff to aneurysm size) allows for improved antiplatelet therapy adjustment before SACE to reduce TECs.

Early detection of hemorrhagic transformation (HT) in patients with large vessel occlusion (LVO) after endovascular treatment is important for postoperative patient management. We investigated the diagnostic performance of intraoperative cone beam computed tomography (CBCT) with reference standard magnetic resonance imaging (MRI) for detecting HT.Consecutive patients with LVO treated by endovascular treatment who underwent intraoperative CBCT and postoperative MRI were included. Two observers evaluated all images for the presence of HT. Sensitivity and specificity for detecting HT were calculated with MRI as reference standard. The observers classified HT according to the European Cooperative Acute Stroke Study (ECASS). Inter-method and inter-rater agreement for the detection of HT and for the ECASS classification were assessed using kappa or weighted Brennan-Prediger (wBP) statistics.Images of 106 procedures (94 for anterior circulation) were analyzed. The sensitivity and specificity for detecting HT on CBCT were 0.77 and 0.83, respectively, for all procedures and 0.83 and 0.8, respectively, for anterior circulation. The inter-method agreement for HT detection (κ = 0.63 overall, κ = 0.69 anterior circulation) and ECASS classification (wBP = 0.67 overall, wBP = 0.77 anterior circulation) were substantial. The inter-rater agreement for HT detection (κ = 0.87 overall, κ = 0.85 anterior circulation) and for ECASS classification (wBP = 0.95 overall, wBP = 0.92 anterior circulation) were almost perfect.The diagnostic performance of CBCT for the detection of HT in stroke patients treated for LVO was acceptable with excellent inter-rater agreement. Intraoperative CBCT may be useful to trigger early interventions if HT is detected, although detailed classifications of HT may be difficult.

Lectin-like oxidized low-density lipoprotein (ox-LDL) causes vascular senescence and atherosclerosis. It has been reported that ox-LDL scavenger receptor-1 (LOX-1) is associated with the angiotensin II type 1 receptor (AT1R). While mitochondria play a crucial role in the development of vascular senescence and atherosclerosis, they also undergo quality control through mitochondrial dynamics and autophagy. The aim of this study was to investigate (1) whether LOX-1 associates with AT1R, (2) if this regulates mitochondrial quality control, and (3) whether AT1R inhibition using Candesartan might ameliorate ox-LDL-induced vascular senescence. We performed in vitro and in vivo experiments using vascular smooth muscle cells (VSMCs), and C57BL/6 and apolipoprotein E-deficient (ApoE KO) mice. Administration of oxidized low-density lipoprotein (ox-LDL) to VSMCs induced mitochondrial dysfunction and cellular senescence accompanied by excessive mitochondrial fission, due to the activation of fission factor Drp1, which was derived from the activation of the Raf/MEK/ERK pathway. Administration of either Drp1 inhibitor, mdivi-1, or AT1R blocker candesartan attenuated these alterations. Electron microscopy and immunohistochemistry of the co-localization of LAMP2 with TOMM20 signal showed that AT1R inhibition also increased mitochondrial autophagy, but this was not affected by Atg7 deficiency. Conversely, AT1R inhibition increased the co-localization of LAMP2 with Rab9 signal. Moreover, AT1R inhibition-induced mitochondrial autophagy was abolished by Rab9 deficiency, suggesting that AT1R signaling modulated mitochondrial autophagy derived from Rab9-dependent alternative autophagy. Inhibition of the Raf/MEK/ERK pathway also decreased the excessive mitochondrial fission, and Rab9-dependent mitochondrial autophagy, suggesting that AT1R signaling followed the Raf/MEK/ERK axis modulated both mitochondrial dynamics and autophagy. The degree of mitochondrial dysfunction, reactive oxygen species production, vascular senescence, atherosclerosis, and the number of fragmented mitochondria accompanied by Drp1 activation were all higher in ApoE KO mice than in C57BL/6 mice. These detrimental alterations were successfully restored, and mitochondrial autophagy was upregulated with the administration of candesartan to ApoE KO mice. The association of LOX-1 with AT1R was found to play a crucial role in regulating mitochondrial quality control, as cellular/vascular senescence is induced by ox-LDL, and AT1R inhibition improves the adverse effects of ox-LDL.

Cerebral small vessel disease (CSVD) is not only a cause of vascular dementia (VD) but also a contributing factor to Alzheimer's disease (AD). The essential pathological feature of CSVD is the disruption of blood-brain barrier (BBB). Dysfunction of BBB due to degeneration of both endothelial cells and pericytes in capillaries leads to neuronal damage and progressive brain atrophy. Moreover, deterioration of amyloid-β (Aβ) clearance due to the failure of the transvascular BBB transport system results in accumulation of Aβ in the brain. Intravenous infusion of mesenchymal stem cells (MSCs) elicits functional recovery in experimental models including stroke and spinal cord injury. One effect of MSCs is to restore disrupted BBB through remodeling of microvasculature. Using spontaneously hypertensive rats (stroke-prone) with impaired cognitive function as a CSVD model, we have shown that infused MSCs has a therapeutic effect for cognitive function. Restoration of BBB function via remodeling of microvasculature and inhibition of Aβ accumulation could inhibit progressive brain atrophy and lead to restore cognitive dysfunction. Gene expression analysis indicated that infused MSCs activates both transforming growth factor-β and angiopoietin 1 signaling pathways and promotes the remodeling of microvasculature. Thus, infused MSCs may represent a novel therapy for both VD and AD.

Introduction: Angiotensin II (Ang II) causes vascular senescence by damaging mitochondria that undergo quality control by mitochondrial dynamics and mitophagy. We examined whether and how AngII type I receptor (AT1R) signal regulates mitochondrial dynamics and mitophagy in the etiology of vascular senescence. Methods: We used vascular smooth muscle cells (VSMC) and C57BL6 (WT), apolipoprotein E deficient (ApoE KO) and the double knockout of ApoE and AT1R mice. Results: Administration of Ang II to VSMC forced mitochondria to fission and induced cellular senescence and mitochondrial dysfunction, which were restored by inhibition of fission by use of Mdivi-1. Treatment of ox-LDL also induced cellular senescence accompanied by excessive mitochondrial fission through phosphorylation of Drp1 at Ser616 and mitochondrial dysfunction. These alterations were ameliorated by inhibition of AT1R signal, suggesting that AT1R signal inhibition may contribute anti-cellular senescence by modification of mitochondrial dynamics. AT1R signal inhibition also induced mitophagy assessed by electron microscopy and immunohistochemistry of LAMP2 and TOMM20. AT1R inhibition-induced mitophagy was not affected by Atg7 Knockdown, whereas it was diminished by Rab9 knockdown. Immunohistochemistry showed TOMM20 dots were co-localized to LAMP2 and Rab9 but not LC3. These results suggest that AT1R signal induces mitophagy derived from Rab9-dependent alternative autophagy. Treatment of ox-LDL activated Ras, Raf and MEK, and AT1R inhibition inactivated them. Inhibition of Ras/Raf/MEK decreased excessive mitochondrial fission and induced mitophagy, suggesting that AT1R signal followed by Ras/Raf/MEK pathway modulates both mitochondrial dynamics and mitophagy. The degree of arterial senescence and atherosclerosis, Drp1 expression in mitochondrial fraction and oxidative stress in artery were higher and the number of mitophagy, fused mitochondria and its function were lower in ApoE KO than those of WT mice. AT1R KO to ApoE KO attenuated these adverse effects of ApoE KO. Conclusions: Inhibition of AT1R signal contributes vascular senescence through modification of mitochondrial dynamics and mitophagy by inactivation of Ras/Raf/MEK pathway.

Severe low back pain (LBP) is an occasional complaint in patients with neuromuscular disorders (NMDs). Accurate diagnosis and treatment are required to manage LBP; however, the precise pathophysiology differs for each patient. This study aimed to evaluate the efficacy of lumbar facet joint denervation (FJD) and adjunctive modalities in the treatment of LBP in patients with NMD-associated kyphoscoliosis. A total of 16 patients (22 sites) with NMD (bilateral, n = 6; unilateral, n = 10) and LBP treated with lumbar FJD were evaluated. The patients were divided into two groups: those treated with FJD alone (group 1) and those treated with multimodal treatment, including FJD along with radiofrequency ablation for sacroiliac joint pain, piriform muscle block, botulinum toxin injection into the paraspinal muscles, spinal cord stimulation, or any of their combinations (group 2). All patients were followed up for 48 weeks postoperatively. The two groups were compared with respect to the duration required for improvements in LBP by more than 50% (numerical rating scale ≤ 5). There was no significant difference between the groups regarding the age, duration since the onset of Parkinson’s syndrome, and radiographic analysis. The effective period of improved pain was greater in group 2 than in group 1 (30.7 vs. 8.4 weeks, P < 0.01). Multimodal treatment including FJD is safe and relatively effective in patients with NMD-associated kyphoscoliosis. Hence, it is a potential substitute for conventional spinal fixation surgery, which has a higher risk of complications.

In orbit satellite, it is major source of unit malfunction that spacecraft material discharging. The two major reason of malfunction are, 1: Low voltage threshold material/process for creeping discharge, and 2: Weak unit for noise. If the switching unit is affected by noise, critical failure occurs due to the hot-switching. In addition, it is susceptible to noise by using the newest components/COTS.In the through of previous satellite development, we decided that satellite manufacturer selected discharge hardened material, but not enough to evaluate knowledge for effects of noise propagation caused by material discharge. There are two possible propagation paths for the discharge noise: space propagation and panel propagation.Well known as that some unit cannot find problems with existing test methods. The major perspective of current standard test method (from MIL/ESA) are space propagation for coupling of cable. It is not enough to evaporate the influence of panel propagation. The test method that is currently the world's standard is focused on applying noise to cables by spatial propagation. It is not sufficient as a method for evaluating the noise that propagates through the panel and the effects other than the cable.In this paper, we propose the test method to evaluate the effect on the unit for noise propagation on the structure panel, based on our test results performed by the gun generator.First of all, we got Dielectric Surface Breakdowns Voltage of some materials by ELECTRON-BEAM RESISTIVITY TEST that are basic characteristics. After that, the unit was mounted on a satellite model panel (modeling the satellite structure: it is Al honeycomb core/Al skin), and the noise injection test was performed. Measured the threshold at which the device malfunctioned.A simple evaluation model (using Al metal panel) and a satellite model panel were compared, and the same evaluation result as the satellite model panel result was obtained.Therefore, we propose a simple test method using an Al flat panel and a noise source as an evaluation method for the noise propagating through the satellite structure panel.We also introduce our activity to implement our findings into EMC technical standards not only Japanese standard document, but also international standard such as ISO.

Introduction: Metabolic stress including oxidized low density lipoprotein (ox-LDL) cause mitochondrial dysfunction and evoke vascular senescence and atherosclerosis. Mitochondria are highly dynamic organelles that undergo quality control by mitochondrial dynamics and mitophagy. This study aims to clarify whether and how mitochondrial dynamics and mitophagy are involved in the etiology of vascular senescence and arteriosclerosis. Methods: VSMC were stimulated by ox-LDL. We also conducted in vivo experiment using C57BL6 (WT), apolipoprotein E (ApoE) deficient and the double knockout of ApoE mice and Angiotensin II Type1 Receptor (AT1R). Results: Treatment of ox-LDL forced mitochondria to fission through activation of Drp1, induced mitochondrial dysfunction and oxidative stress, and developed cellular senescence. Inhibition of either Drp1, AT1R, MAPK retarded them, suggesting that mitochondrial fission plays key roles to develop premature cellular senescence and is modulated by AT1R/MAPK signal.Administration of ox-LDL decreased the number of mitophagy assessed by electron microscopy and immunohistochemistry of LAMP2 and TOMM20. AT1R signal inhibition increased mitophagy which was not affected by Atg7 knockdown, whereas it was decreased by either Rab9 or Ulk1 knockdown. Immunohistochemistry showed Rab9 dots were co-localized to TOMM20 and LAMP2, whereas LC3 dots were not, suggesting that AT1R signal induces mitophagy through Rab9-dependent alternative autophagy. The degree of vascular senescence was higher, the number of fused mitochondria and mitochondrial function were lower and mitochondrial oxidative stress was higher in ApoE KO than those in WT. DKO attenuated these adverse effect of ApoE KO. Conclusion: AT1R regulates vascular senescence and arteriosclerosis via induction of mitochondrial fission and inhibition of mitophagy.

Background Carpal tunnel syndrome is a common peripheral nerve compression disorder. However, there is no established opinion regarding the predictors of symptom improvement after surgery. This study aimed to identify the predictors of surgical outcomes of severe carpal tunnel syndrome patients. Methods In the patients who underwent a carpal tunnel syndrome surgery, we selected the patients who had a preoperative Bland’s classification of grade 5 or 6, and assessed for the changes in Bland’s classification grade before and after surgery. Those who showed improvement from preoperative grades 5–6 to postoperative grades 1–4 comprised the improvement group. In contrast, those who did not show improvement and had postoperative grades 5 or 6 comprised the non-improvement group. In a nerve conduction study, amplitudes of the compound muscle action potential and sensory nerve action potential of the palms were assessed between the improvement and non-improvement groups. Results Among the 60 hands of 46 patients who had a preoperative Bland’s classification of grade 5 or 6, 49 hands of 37 patients comprised the improvement group, and 11 hands of 9 patients comprised the non-improvement group. The amplitudes of the compound muscle action potential and sensory nerve action potential of the palms before surgery were significantly higher in the improvement group. The degree of improvement in Bland’s classification grade was correlated with the degree of clinical symptom improvement. Conclusions Amplitudes of compound muscle action potential and sensory nerve action potential before surgery induced by palmar stimulation can predict improvements in nerve conduction study scores and clinical findings after surgical treatment.

Background: Control of risks of thromboembolic complications (TEC) during stent assisted coil embolization (SACE) for unruptured intracranial aneurysm (UIA) is crucial for outcome. We evaluated retrospectively our cohort of SACE for UIA, analyzing the role of anatomical, clinical and stent type related factors to determine optimal presurgical values of light transmission aggregometry (LTA) for TEC prevention. Methods: From July 2015 to May 2018 we retrospectively analyzed 132 SACE treated UIA patients at our hospital. Aneurysm location and maximum diameter, preoperative LTA-value, ischemic and hemorrhagic complications, preoperative and discharge Modified Rankin scale (mRS) were collected. Aspirin 100 mg and clopidogrel 75 mg were started 7 days before operation, with “boost” therapy (additional 75mg clopidogrel in LTA-value >60) added after August 2016, addressing clopidogrel resistance. After multivariate analysis we developed our original combined parameter called TEC predictor (TEP). Receiver operating characteristic (ROC) analysis for TEP and each significant variable were performed. Results: TEC were confirmed in five (3.8%, 5/132) and hemorrhagic - in nine patients (6.8%, 9/132), with mRS deterioration post-operatively in five patients (5/132, 3.8%). By multivariate analysis, LTA-value and maximum diameter were chosen as significant variables, and included in TEP. ROC analysis of LTA-value showed sensitivity and specificity of 0.866 and 0.600 respectively (AUC=0.747) with cut-off point of 62. TEP permitted establishing optimal LTA-value according to the aneurysm maximum diameter to predict TEC. Neuroform-EZ, Enterprise, Neuroform-Atlas, and LVIS stents complications were 2.9%, 10.5%, 1.4%, and 14.3%, respectively. Conclusions: Preoperative LTA-value contributes to predicting TEC after SACE of UIA. TEP (relating LTA cutoff value to aneurysm size) provides improved antiplatelet therapy adjustment prior to SACE for TEC reduction.

Systemic administration of mesenchymal stem cells (MSCs) following cerebral infarction exerts functional improvements. Previous research has suggested potential therapeutic mechanisms that promote neuroprotection and synaptogenesis. These include secretion of neurotrophic factors, remodeling of neural circuits, restoration of the blood brain barrier, reduction of inflammatory infiltration and demyelination, and elevation of trophic factors. In addition to these mechanisms, we hypothesized that restored interhemispheric bilateral motor cortex connectivity might be an additional mechanism of functional recovery. In the present study, we have shown, with both MRI diffusion tensor imaging (DTI) and neuroanatomical tracing techniques using an adeno-associated virus (AAV) expressing GFP, that there was anatomical restoration of cortical interhemispheric connections through the corpus callosum after intravenous infusion of MSCs in a rat middle cerebral artery occlusion (MCAO) stroke model. Moreover, the degree of connectivity was greater in the MSC-treated group than in the vehicle-infused group. In accordance, both the thickness of corpus callosum and synaptic puncta in the contralateral (non-infarcted) motor cortex connected to the corpus callosum were greater in the MSC-treated group than in the vehicle group. Together, these results suggest that distinct preservation of interhemispheric cortical connections through corpus callosum was promoted by intravenous infusion of MSCs. This anatomical preservation of the motor cortex in the contralateral hemisphere may contribute to functional improvements following MSC therapy for cerebral stroke.

Background Surgical treatment of vertebral artery (VA)-thrombosed giant aneurysms requires achieving both obliteration of the parent artery to prevent bleeding and dome thrombectomy to relieve the brain stem from mass effect. To secure both proximal and distal control of complex VA aneurysms, the contralateral approach to the aneurysm might be a useful alternative, as previously described. We successfully treated a case of VA-thrombosed giant aneurysm in a new, original way by combining craniotomy (ipsilateral and contralateral) and the endovascular technique. Case Description A 48-year-old man presented with a thrombosed giant aneurysm of the right VA compressing the brain stem. Treatment consisted of endovascular proximal ligation of the VA followed by 2-staged craniotomy for complete trapping of the aneurysm and intra-aneurysmal thrombectomy. The VA distal to the aneurysm was obliterated via contralateral craniotomy as only that provided adequate working space. Finally, intra-aneurysmal partial thrombectomy was performed through an ipsilateral craniotomy, which also made possible the obliteration of the eventually dangerous remaining vasa vasorum and additional proximal ligation of the VA. Conclusions Based on pathologic and surgical anatomical characteristics, a combination of an endovascular procedure with 2-staged craniotomy for complete trapping, thrombectomy, and vasa vasorum obliteration could be considered a feasible way to treat VA-thrombosed giant aneurysms located ventral to the brain stem and have their distal neck portions/patent vessel beyond the midline toward the contralateral side.

The ability to coat porous media is critical for forming composite functional thin films. A major technical concern for accurately predicting this process is that the flow of the coating bead and the penetration process must be considered. These phenomena strongly influence each other. Therefore, both the flow into porous media and the coating-bead flow should be simultaneously treated. In this study, the target is a high-productivity coating system based on a roll-to-roll process using a slot die. Slot-die coating is a premetered, precision coating method. We investigated the coating of porous media to estimate the practical operability window and the penetration depth using two-dimensional numerical analysis. For this purpose, both the coating-bead pressure and the capillary pressure were considered as driving forces of penetration. Moreover, the curvature of the backup roll opposite the slot die was also taken into account to achieve an accurate estimation. We demonstrate that the penetration depth and operability window for defect-free coatings can be well estimated and that the results are consistent with experimental results.

Introduction: Metabolic stress, such as oxidized low density lipoprotein (ox-LDL) and advanced glycation end products (AGE) cause mitochondrial dysfunction and evoke vascular senescence and atherosclerosis. Mitochondria are highly dynamic organelles that constantly change their morphology to fusion or fission. This study aims to clarify whether mitochondrial dynamics is involved in the etiology of vascular senescence. Methods: We used C57BL6 (WT), apolipoprotein E deficient (ApoE KO) and db/db mice. We also conducted in vitro experiments using VSMC and HUVEC. Results: The degree of arterial senescence, arterial protein level of Drp1 in mitochondrial fraction and mitochondrial oxidative stress were higher and the number of fused mitochondria and mitochondrial function were lower in either ApoE KO or db/db mice than those of WT mice. Treatment with Drp1-specific inhibitor, mdivi-1, to these mice reduced excessive mitochondrial fission, oxidative stress and attenuated vascular senescence. Administration of either ox-LDL or AGE to cells also induced excessive mitochondrial fission though phosphorylation of Drp1 at Ser616, mitochondrial dysfunction, reactive oxygen species production and cellular senescence. Treatment with mdivi-1 to these cells restored imbalance of mitochondrial dynamics and these detrimental alterations. These results suggest that metabolic stress-induced mitochondrial dysfunction and cellular senescence were derived from Drp1-dependent mitochondrial fission. Treatment with angiotensin II type1 receptor (AT1R) blocker (ARB) to either Apo E KO mice or db/db in in vivo experiments and administration of ARB to cells with ox-LDL or AGE stimulation in in vitro experiments inactivated Drp1 and improved imbalance of mitochondrial dynamics, mitochondrial dysfunction and cellular senescence, suggesting that AT1R signal is involved in regulating metabolic stress-induced mitochondrial fission. Finally, inhibition of Rho kinase ROCK1 successfully attenuated Drp1-mediated mitochondrial fission and cellular senescence derived from metabolic stress. Conclusion: Metabolic stress causes cellular and vascular senescence through AT1R signal/Rho kinase-mediated mitochondrial fission.

Introduction: Metabolic stress including oxidized low density lipoprotein (ox-LDL) and angiotensin II (AngII) cause mitochondrial dysfunction and vascular senescence. Mitochondria are highly dynamic organelles that constantly change their morphology to fusion or fission. This study aims to clarify how mitochondrial dynamics are involved in the etiology of vascular senescence. Methods: VSMC and HUVEC were stimulated by either ox-LDL or AngII. We also conducted in vivo experiment using C57BL6 (WT), apolipoprotein E (ApoE) deficient and the double knockout of ApoE and AT1R (DKO) mice. Results: Either ox-LDL or AngII induced excessive mitochondrial fission though phosphorylation of Drp1 at Ser616, mitochondrial dysfunction assessed by JC1, reactive oxygen species production measured with Mito-Sox Red and Amplex assay and cellular senescence analyzed by senescence associated beta galactosidase staining and immunoblot of p53 and p21 in cells. Administration of mdivi-1, a specific inhibitor of Drp1, restored imbalance of mitochondrial dynamics and these detrimental alterations. Treatment with angiotensin II type1 receptor (AT1R) inhibitor also inactivated Drp1 and improved imbalance of mitochondrial dynamics, mitochondrial dysfunction and cellular senescence. These results suggest that ox-LDL- or AngII-induced mitochondrial dysfunction and cellular senescence were derived from Drp1-dependent mitochondrial fission. Administration of AT1R inhibitor to HUVEC or SMC with ox-LDL prevented cells against excessive mitochondrial fission, its dysfunction and cellular senescence. The degree of vascular senescence was higher, the number of fused mitochondria and mitochondrial function were lower and mitochondrial oxidative stress were higher in either C57BL6 with AngII infusion or ApoE KO mice than those of control or WT mice, respectively. Treatment with mdivi-1 to these mice reduced mitochondrial fission, oxidative stress and attenuated vascular senescence. The number of fused mitochondria and its function were higher and the degree of vascular senescence were lower in DKO than those in ApoE KO mice. Conclusion: Either ox-LDL or AngIIcauses cellular and vascular senescence through AT1R signal-mediated mitochondrial fission.