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Proton magnetic resonance spectroscopy (1H-MRS) has shown inconsistent alterations in the brain metabolites of individuals with chronic pain. We used 3T 1H-MRS to investigate the brain metabolites in the anterior cingulate cortex and thalamus of 22 patients with chronic mild pain and no gait disturbance and 22 healthy controls. The chronic-pain group included patients with chronic low back pain and/or osteoarthritis but none suffering from hypersensitivity. There were no significant between group-differences in glutamate, glutamate plus glutamine (Glx), N-acetylaspartate, glycerophosphorylcholine (GPC), glutamine, creatine plus phosphocreatine, or myo-inositol in the anterior cingulate cortex, but the patients showed a significant decrease in GPC, but not other metabolites, in the thalamus compared to the controls. The GPC values in the patients' thalamus were significantly correlated with pain components on the Short-Form McGill Pain Questionnaire (SF-MPQ-2) and affective empathy components on the Questionnaire of Cognitive and Affective Empathy (QCAE). The GPC in the patients' anterior cingulate cortex showed significant correlations with cognitive empathy components on the QCAE. Myo-inositol in the controls' anterior cingulate cortex and Glx in the patients' thalamus each showed significant relationships with peripheral responsivity on the QCAE. These significances were not significant after Bonferroni corrections. These preliminary findings indicate important roles of GPC, myo-inositol, and Glx in the brain of patients with chronic mild pain. [ABSTRACT FROM AUTHOR]

Recent studies have indicated the involvement of neutrophil-mediated inflammatory responses in the process leading to intracranial aneurysm (IA) rupture. Receptors mediating neutrophil recruitment could thus be therapeutic targets of unruptured IAs. In this study, complement C5a receptor 1 (C5AR1) was picked up as a candidate that may cause neutrophil-dependent inflammation in IA lesions from comprehensive gene expression profile data acquired from rat and human samples. The induction of C5AR1 in IA lesions was confirmed by immunohistochemistry; the up-regulations of C5AR1/C5ar1 stemmed from infiltrated neutrophils, which physiologically express C5AR1/C5ar1, and adventitial fibroblasts that induce C5AR1/C5ar1 in human/rat IA lesions. In in vitro experiments using NIH/3T3, a mouse fibroblast-like cell line, induction of C5ar1 was demonstrated by starvation or pharmacological inhibition of mTOR signaling by Torin1. Immunohistochemistry and an experiment in a cell-free system using recombinant C5 protein and recombinant Plasmin indicated that the ligand of C5AR1, C5a, could be produced through the enzymatic digestion by Plasmin in IA lesions. In conclusion, we have identified a potential contribution of the C5a–C5AR1 axis to neutrophil infiltration as well as inflammatory responses in inflammatory cells and fibroblasts of IA lesions. This cascade may become a therapeutic target to prevent the rupture of IAs. [ABSTRACT FROM AUTHOR]

Proton magnetic resonance spectroscopy (1H-MRS) has shown inconsistent alterations in brain metabolites of adults with autism spectrum disorder (ASD). We investigated brain metabolites in the medial prefrontal cortex and amygdala of 24 drug-naive adults with ASD and no intellectual disability and 24 non-ASD control subjects, using 3 T 1H-MRS. Adults with ASD showed no significant differences from control in glutamate, glutamate plus glutamine, N-acetylaspartate, glycerophosphorylcholine plus phosphorylcholine, creatine plus phosphocreatine, or myo-inositol in either region. However, ASD subjects did show significant correlations of localized brain metabolites with autistic traits, empathy deficits, and personality traits using the Autism-Spectrum Quotient, Questionnaire of Cognitive and Affective Empathy, Interpersonal Reactivity Index, and NEO Personality Inventory-Revised. These findings should be taken as preliminary or exploratory. [ABSTRACT FROM AUTHOR]

Subarachnoid hemorrhage being the rupture of intracranial aneurysm (IA) as a major cause has quite poor prognosis, despite the modern technical advances. Thereby, the mechanisms underlying the rupture of lesions should be clarified. Recently, we and others have clarified the formation of vasa vasorum in IA lesions presumably for inflammatory cells to infiltrate in lesions as the potential histopathological alternation leading to rupture. In the present study, we clarified the origin of vasa vasorum as arteries located at the brain surface using 3D-immunohistochemistry with tissue transparency. Using Hypoxyprobe, we then found the presence of hypoxic microenvironment mainly at the adventitia of intracranial arteries where IA is formed. In addition, the production of vascular endothelial growth factor (VEGF) from cultured macrophages in such a hypoxic condition was identified. Furthermore, we found the accumulation of VEGF both in rupture-prone IA lesions induced in a rat model and human unruptured IA lesions. Finally, the VEGF-dependent induction of neovessels from arteries on brain surface was confirmed. The findings from the present study have revealed the potential role of hypoxic microenvironment and hypoxia-induced VEGF production as a machinery triggering rupture of IAs via providing root for inflammatory cells in lesions to exacerbate inflammation. [ABSTRACT FROM AUTHOR]

The role of the bifurcation angle in progression of saccular intracranial aneurysms (sIAs) has been undetermined. We, therefore, assessed the association of bifurcation angles with aneurysm progression using a bifurcation-type aneurysm model in rats and anterior communicating artery aneurysms in a multicenter case–control study. Aneurysm progression was defined as growth by ≥ 1 mm or rupture during observation, and controls as progression-free for 30 days in rats and ≥ 36 months in humans. In the rat model, baseline bifurcation angles were significantly wider in progressive aneurysms than in stable ones. In the case–control study, 27 and 65 patients were enrolled in the progression and control groups. Inter-observer agreement for the presence or absence of the growth was excellent (κ coefficient, 0.82; 95% CI, 0.61–1.0). Multivariate logistic regression analysis showed that wider baseline bifurcation angles were significantly associated with subsequent progressions. The odds ratio for the progression of the second (145°–179°) or third (180°–274°) tertiles compared to the first tertile (46°–143°) were 5.5 (95% CI, 1.3–35). Besides, the bifurcation angle was positively correlated with the size of aneurysms (Spearman's rho, 0.39; P = 0.00014). The present study suggests the usefulness of the bifurcation angle for predicting the progression of sIAs. [ABSTRACT FROM AUTHOR]

Reported empathy deficits in autism spectrum disorder (ASD) could be attributable to other ASD-related features. We evaluated 28 ASD adults with no intellectual disability and 24 age-matched non-ASD control subjects using the Autism-Spectrum Quotient (AQ), Questionnaire of Cognitive and Affective Empathy (QCAE), Interpersonal Reactivity Index (IRI), and NEO Personality Inventory-Revised (NEO). Compared to the controls, ASD participants showed lower scores for perspective taking, online simulation, cognitive empathy, and peripheral responsivity on the QCAE, and lower scores for perspective taking and empathic concern on the IRI. Within the ASD group, the AQ scores showed significant relationships with perspective taking, online simulation and cognitive empathy on the QCAE, and perspective taking on the IRI. The ASD group also showed higher scores for neuroticism and lower scores for extraversion on the NEO compared to the controls. However, there were no relationships between AQ scores and NEO factors within the ASD group. Multiple regression analysis with stepwise linear regression demonstrated that perspective taking score on the QCAE and extraversion score on the NEO were good predictor variables to autistic traits on the AQ. These findings help us to understand empathy and personality traits in ASD adults with no intellectual disability. [ABSTRACT FROM AUTHOR]

Purpose: We developed a new technique, sutureless mesh fixation, using 2-octyl cyanoacrylate (Dermabond, a surgical tissue adhesive) for incisional hernia repair. The objective of this article is to introduce the new technique and to examine whether the technique provides sufficient resistance to abdominal pressure. Methods: We conducted two tests using a porcine model, a traction experiment and artificial pneumoperitoneum test. In the traction experiment, the adherence properties of Dermabond with mesh and peritoneum were examined using a tissue fragment from a pig. In the artificial pneumoperitoneum test, which used an incisional hernia porcine model, mesh was implanted on the peritoneum in the abdominal cavity with Dermabond. It was then determined whether sutureless mesh fixation could bear artificial abdominal air pressure. Results: In the traction experiment, Dermabond, which bonded the mesh to the peritoneum, tolerated pressure up to 2.45 × 10 mmHg. In the artificial pneumoperitoneum test, the mesh was strongly fastened to the peritoneum by means of only Dermabond, and there was little air circulation even without closing the wound over the mesh. Conclusions: Sutureless mesh fixation with Dermabond is technically feasible and promises to provide sufficient resistance to abdominal pressure. [ABSTRACT FROM AUTHOR]

Refractory esophageal ulcerations occur rarely after cardiovascular surgery, occasionally leading to perforation. There is little consensus on their optimal management. Herein, we present a case of refractory esophageal ulceration after cardiovascular surgery. A 62-year-old woman with Marfan's syndrome was referred to our hospital with cardiac failure due to aortic regurgitation. She underwent root replacement by the modified Bentall method. Refractory esophageal ulceration developed 3 months later and persisted for 3 months despite conservative therapy. With the patient's informed consent, Kirschner bypass surgery was performed. A jejunostomy using a 20 Fr. Nelaton catheter was made in the Roux-en-Y loop of the jejunum for postoperative endoscopy. The postoperative course was uneventful and transjejunostomal endoscopy revealed excellent healing of the ulceration. Esophageal bypass surgery and transjejunostomal endoscopy were very effective in this patient with refractory esophageal ulceration. [ABSTRACT FROM AUTHOR]

Non-occlusive mesenteric ischemia (NOMI), leading to intestinal gangrene without a demonstrable occlusion in the mesenteric artery, is a rare condition with extremely high mortality. We report a case of NOMI diagnosed preoperatively by computed tomography and treated successfully with surgery, assisted by indocyanine green (ICG) fluorescence in the HyperEye Medical System (HEMS), a new device that can simultaneously detect color and near-infrared rays under room light. This allowed for precise intraoperative evaluation of the mesenteric and bowel circulation. Although the necrotic bowel wall of the distal ileum and the segmental ischemia of the jejunum were visible, the jejunum was finally preserved because perfusion of ICG fluorescence was confirmed. The patient, an 84-year-old man, had an uneventful postoperative course and is alive without critical illness 8 months after surgery. We report this case to demonstrate the potential effectiveness of HEMS during surgery for NOMI. [ABSTRACT FROM AUTHOR]

The HyperEye Medical System is a newly developed device that allows for the visualization of the fluorescent image of indocyanine green enhanced by near-infrared light among the surrounding vivid color images. We recently applied this system to confirm the blood flow of an esophageal substitute, and for sentinel node navigation during esophagectomy. Five consecutive patients with thoracic esophageal cancer who underwent a subtotal esophagectomy between June 2010 and May 2011 were enrolled in the study. The esophageal substitute used for reconstruction was the stomach and ileocecum in four and one cases, respectively. In all cases with a reconstructive stomach, fine arterial blood flow and venous perfusion were observed. The blood flow of the reconstructive colon was poor before microvascular anastomosis, however, it dramatically increased after anastomosis. Concerning the sentinel node navigation, the fluorescence of lymph nodes, lymphatic vessels, and the tumor site were detected. The postoperative courses of all cases were uneventful, with no mortalities or anastomotic leakage occurring. [ABSTRACT FROM AUTHOR]

Introduction: Some authors pointed out that there were more than a few patients with inadvertent C2–C3 union after C1–C2 posterior fusion, although few detailed studies of C2–C3 union have been reported. The purpose of this study was to clarify whether C2–C3 union accelerated adjacent C3–C4 disc degeneration after C1–C2 posterior fusion and to investigate the related factors for C2–C3 union. Methods: Sixteen patients with rheumatoid arthritis (RA group) (4 males, 12 females, mean age 60 years, mean follow-up period 4 years and 3 months) and fifteen patients without RA (non-RA group) (11 males, 4 females, mean 52 years, mean follow-up period 3 years and 10 months) who underwent C1–C2 posterior fusion were radiologically assessed. The C2–C3 union was defined as trabecular bone formation at C2–C3 interlamina in lateral radiograph. C3–C4 disc height was measured to evaluate the disc degeneration. Results: C2–C3 union rate was 56% and 60% in RA group and non-RA group, respectively. In RA group, postoperative C3–C4 disc height was lower (Student’s t-test, P = 0.029) and the decrease rate of C3–C4 disc height was higher (Student’s t-test, P = 0.015) in patients with C2–C3 union than in patients without C2–C3 union. In non-RA group, the age at operation was older (Student’s t-test, P = 0.0007), and the C1–C2 fusion angle (Student’s t-test, P = 0.012) was smaller in patients with C2–C3 union than in patients without C2–C3 union. Conclusions: C2–C3 union after C1–C2 posterior fusion occurred in more than half of both groups. Inadvertent C2–C3 union should be considered a radiological complication and a potential risk factor due to acceleration of C3–C4 disc degeneration in RA. [ABSTRACT FROM AUTHOR]