Safety and Efficacy of Coil Embolization for Endoleak Prevention as an Adjunct to Endovascular Repair of Abdominal Aortic Aneurysm or Subsequently for the Repair of Endoleak.

Objective: This study assessed the real-world safety and efficacy of coil embolization during endovascular aneurysm repair (EVAR) of abdominal aortic aneurysms (AAA) for prophylactic endoleak prevention or as a reintervention for endoleak repair, using the Cerenovus family of coils (Cerenovus, Irvine, CA, USA).

Methods: This was a multicenter, retrospective cohort study of consecutive patients who underwent embolization of branching arteries during EVAR of an AAA or as a reintervention for endoleak repair, using Cerenovus coils between January 2017 and December 2021 in Japan. The primary outcome was 30-day reintervention-free survival, defined as cardiovascular mortality or any complication requiring reintervention within 30 days post procedure.

Successful factors for improving aortic remodeling with thoracic endovascular repair and bare stent extension.

Objective: Proximal ExTension to Induce COmplete ATtachment (PETTICOAT), which uses downstream bare metal stents for structural support, demonstrates potential, yet its adoption is limited by variable outcomes. This study elucidates the potential of PETTICOAT in aortic dissection, emphasizing the determinants that guide patient selection.

Methods: A retrospective analysis of 60 patients who underwent full PETTICOAT for aortic dissections was conducted.

Full PETTICOAT in acute type B aortic dissection with patent false lumen may offer positive remodeling for the distal aorta.

Objective: The provisional extension to induce complete attachment (PETTICOAT) technique is a unique thoracic endovascular aortic repair (TEVAR) for aortic dissection, which consists of proximal descending aortic endografting plus distal bare-metal stenting. This study aimed to investigate the efficacy of the PETTICOAT technique in patients with acute-sub-acute complicated type B aortic dissections. In particular, we compared the remodeling effect of full PETTICOAT covering down to the abdominal aorta with that of simple entry closure.

A plausible involvement of plasmalemmal voltage-dependent anion channel 1 in the neurotoxicity of 15-deoxy-Δ -prostaglandin J.

Introduction: 15-deoxy-Δ -prostaglandin J (15d-PGJ ) causes neuronal apoptosis independently of its nuclear receptor, peroxysome-proliferator activated receptor γ. Its membrane receptor, chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2), did not also mediate the neurotoxicity of 15d-PGJ . In the present study, we ascertained whether membrane targets beside CRTH2 were involved in the neurotoxicity of 15d-PGJ .

Energy redistribution and spatiotemporal evolution of correlations after a sudden quench of the Bose-Hubbard model.

An optical lattice quantum simulator is an ideal experimental platform to investigate nonequilibrium dynamics of a quantum many-body system, which is, in general, hard to simulate with classical computers. Here, we use our quantum simulator of the Bose-Hubbard model to study dynamics far from equilibrium after a quantum quench. We successfully confirm the energy conservation law in the one- and three-dimensional systems and extract the propagation velocity of the single-particle correlation in the one- and two-dimensional systems.

Outflow of N-butyl-2-cyanoacrylate into the Pancreatic Duct: Transcatheter Arterial Embolization for Hemosuccus Pancreaticus.

A 54-year-old Japanese woman, hospitalized for recurrent chronic alcoholic pancreatitis, manifested bloody stools. An esophagogastroduodenoscopy revealed active bleeding from the papilla of Vater. Contrast-enhanced computed tomography (CECT) revealed a pseudoaneurysm in the pancreatic pseudocyst (hemosuccus pancreaticus).

The Anti-Neuron-Specific Enolase Antibody Induced Neuronal Cell Death in a Novel Fashion.

Suppression of ubiquitin proteasome pathway (UPP) and stimulation of caspase-3 are involved in neurodegeneration. Can UPP activators and caspase-3 inhibitors ameliorate neurodegeneration? Here, we found a novel neuronal cell death accompanied with UPP activation and caspase-3 inhibition. Recently, plasmalemmal neuron-specific enolase (NSE) has been identified as one of membrane targets of 15-deoxy-Δ-prostaglandin J (15d-PGJ).

15-Deoxy-Δ-prostaglandin J Inhibits Cell Migration on Renal Cell Carcinoma via Down-Regulation of Focal Adhesion Kinase Signaling.

Renal cell carcinoma (RCC) is one of the chemoresistant cancers. There is a pressing need to establish therapeutic approaches to prevent RCC proliferation and metastasis. The electrophilic 15-deoxy-Δ-prostaglandin J (15d-PGJ) is an endogenous anti-cancerous agent.

4,4-Diisothiocyanatostilbene Disulfonic Acid Enhanced 15-Deoxy-Δ-prostaglandin J-Induced Neuronal Apoptosis.

4,4-Diisothiocyanatostilbene disulfonic acid (DIDS), an antagonist of anion channel including voltage-dependent anion channel (VDAC), acts as both neurotoxicant and neuroprotectant, resulting in the controversy. VDAC contributes to neuronal apoptosis and is a candidate target protein of 15-deoxy-Δ-prostaglandin J (15d-PGJ). Caspase-3 is activated during neuronal apoptosis caused by 15d-PGJ.

15-deoxy-Δ-prostaglandin J enhances anticancer activities independently of VHL status in renal cell carcinomas.

Renal cell carcinoma (RCC) is relatively resistant to chemotherapy and radiotherapy. Clear cell RCC (ccRCC) accounts for the majority of RCC, which have mutations or epigenetic silencing of the () gene. VHL-positive Caki-2 cells are killed by an endogenous anticancer substance, 15-deoxy-Δ-prostaglandin J (15d-PGJ).

Transcatheter arterial embolization for initial hemostasis in a hemodynamically unstable patient with mesenteric hemorrhage: A case report.

Surgical treatment of mesenteric injuries is necessary to control hemorrhage, manage bowel injuries, and evaluate bowel perfusion. It has recently been suggested that some patients can be managed with transcatheter arterial embolization (TAE) for initial hemostasis. We present a hemodynamically unstable patient who was initially managed by TAE for traumatic mesenteric hemorrhage.

Pathophysiological Roles of Intracellular Proteases in Neuronal Development and Neurological Diseases.

Proteases are classified into six distinct classes (cysteine, serine, threonine, aspartic, glutamic, and metalloproteases) on the basis of catalytic mechanism. The cellular control of protein quality senses misfolded or damaged proteins principally by selective ubiquitin-proteasome pathway and non-selective autophagy-lysosome pathway. The two pathways do not only maintain cell homeostasis physiologically, but also mediate necrosis and apoptosis pathologically.

Necrotizing enterocolitis associated with in a Japanese man.

Case: Necrotizing enterocolitis (NEC) caused by is common in neonates; however, a case of NEC in adults has not been previously reported. An 84-year-old Japanese man developed -related NEC during hospitalization for treatment of stab wounds to the left side of the neck and lower abdomen, without organ damage, and concomitant pneumonia.

Outcome: The patient developed acute onset of emesis accompanied by shock during his admission; partial resection of the small intestine was carried out due to necrosis.

Synergistic effects of 15-deoxy Δ-prostaglandin J on the anti-tumor activity of doxorubicin in renal cell carcinoma.

An endogenous anticancer agent, 15-deoxy -Δ-prostaglandin J (15d-PGJ) induces apoptosis in the chemoresistant renal cell carcinoma (RCC). Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear receptor for 15d-PGJ, and mediates the cytotoxicity of 15d-PGJ in many cancerous cells. However, 15d-PGJ induces apoptosis independently of PPARγ in human RCC cell line such as Caki-2.

Anti-heat Shock 70 kDa Protein Antibody Induced Neuronal Cell Death.

Heat shock protein 70 (Hsp70) is not only a molecular chaperone in cytosol, but also presents in synaptic plasma membranes. To detect plasmalemmal Hsp70 (pl-Hsp70), neurons were immunostained with anti-Hsp70 antibody without permeabilization and fixation. Dotted immunofluorescent signals at neuronal cell bodies and neurites indicated the localization of Hsp70 on the neuronal cell surface.

Physiological and Pathological Roles of 15-Deoxy-Δ-Prostaglandin J in the Central Nervous System and Neurological Diseases.

Prostaglandins (PGs) are divided into conventional PGs, e.g., PGD, and cyclopentenone-type PGs, e.

15-Deoxy-Δ-prostaglandin J induced neurotoxicity via suppressing phosphoinositide 3-kinase.

15-Deoxy-Δ-prostaglandin J (15d-PGJ) induces neuronal cell death via apoptosis independently of its receptors. 15d-PGJ inhibits growth factor-induced cell proliferation of primary astrocytes via down-regulating phosphoinositide 3-kinase (PI3K)-Akt pathway. Although 15d-PGJ-reduced cell viability is accompanied with attenuation of the PI3K signaling in neuroblastoma, it has not been sufficiently clarified how 15d-PGJ induces cell death in primary neurons.

Localization of 14-3-3δ/ξ on the neuronal cell surface.

14-3-3 proteins are intracellularly expressed as ubiquitous adaptor proteins. Here, we found localization of 14-3-3δ/ξ on the neuronal cell surface. 14-3-3δ/ξ was identified as a membrane target for 15-deoxy-Δ(12,14)-prostaglandin J2 (15d-PGJ2).

Pathophysiological Roles of Cyclooxygenases and Prostaglandins in the Central Nervous System.

Cyclooxygenases (COXs) oxidize arachidonic acid to prostaglandin (PG) G2 and H2 followed by PG synthases that generates PGs and thromboxane (TX) A2. COXs are divided into COX-1 and COX-2. In the central nervous system, COX-1 is constitutively expressed in neurons, astrocytes, and microglial cells.

Hydrogen peroxide mediated the neurotoxicity of an antibody against plasmalemmal neuronspecific enolase in primary cortical neurons.

Neuron-specific enolase (NSE) is not only a glycolytic enzyme in the cytosol, but also localized in the synaptic plasma membrane. The plasmalemmal NSE is one of autoantigen targets in post-streptococcal autoimmune central nervous system disease. Although anti-neuronal antibodies in patients bind to a restricted group of NSE in cerebral cortex, it has not yet been clarified how the anti-NSE antibody have negative impacts on cortical neurons.

Treatment of etoposide combined with 15-deoxy-Δ-prostaglandin J exerted synergistic antitumor effects against renal cell carcinoma via peroxisome proliferator-activated receptor-γ-independent pathways.

Renal cell carcinoma (RCC) is characterized by diverse clinical manifestations, few early warning signs and a resistance to radiotherapy and chemotherapy. Although several clinical trials have investigated potential effective therapeutic strategies for RCC, the chemoresistance of RCC has not yet been overcome. An endogenous ligand for the peroxisome proliferator-activated receptor-γ (PPARγ), 15-deoxy-Δ-prostaglandin J (15d-PGJ), was shown to induce apoptosis in RCC.

The role of secretory phospholipase A₂ in the central nervous system and neurological diseases.

Secretory phospholipase A2 (sPLA2s) are small secreted proteins (14-18 kDa) and require submillimolar levels of Ca(2+) for liberating arachidonic acid from cell membrane lipids. In addition to the enzymatic function, sPLA2 can exert various biological responses by binding to specific receptors. Physiologically, sPLA2s play important roles on the neurotransmission in the central nervous system and the neuritogenesis in the peripheral nervous system.