Recent studies have shown an increased abundance of Sphingomonas paucimobilis, an aerobic, Gram-negative bacterium with a distinctive cell envelope rich in glycosphingolipids, within the gut microbiome of individuals with Alzheimer Disease (AD). However, the fact that S. paucimobilis is a well-known pathogen associated with nosocomial infections presents a significant challenge in investigating whether its presence in the gut microbiome is detrimental or beneficial, particularly in the context of AD. This study examines the impact of S. paucimobilis-derived extracellular vesicles (Spa-EV) on Aβ-induced pathology in cellular and animal models of AD. Microarray analysis reveals that Spa-EV treatment modulates Aβ42-induced alterations in gene expression in both HT22 neuronal cells and BV2 microglia cells. Among the genes significantly affected by SpaEV, notable examples include Bdnf, Nt3/4, and Trkb, which are key players of neurotrophic signaling; Pgc1α, an upstream regulator of mitochondrial biogenesis; Mecp2 and Sirt1, epigenetic factors that regulate numerous gene expressions; and Il1β, Tnfα, and Nfκb-p65, which are associated with neuroinflammation. Remarkably, Spa-EV effectively reverses Aβ42-induced alteration in the expression of these genes through the upregulation of Mecp2. Furthermore, administration of Spa-EV in Tg-APP/PS1 mice restores the reduced expression of neurotrophic factors, Pgc1α, MeCP2, and Sirt1, while suppressing the increased expression of proinflammatory genes in the brain. Our results indicate that Spa-EV has the potential to reverse Aβ-induced dysregulation of gene expression in neuronal and microglial cells. These alterations encompass those essential for neurotrophic signaling and neuronal plasticity, mitochondrial function, and the regulation of inflammatory processes.

Recent studies have shown an increased abundance of Sphingomonas paucimobilis, an aerobic, Gram-negative bacterium with a distinctive cell envelope rich in glycosphingolipids, within the gut microbiome of individuals with Alzheimer Disease (AD). However, the fact that S. paucimobilis is a well-known pathogen associated with nosocomial infections presents a significant challenge in investigating whether its presence in the gut microbiome is detrimental or beneficial, particularly in the context of AD. This study examines the impact of S. paucimobilis-derived extracellular vesicles (Spa-EV) on Aβ-induced pathology in cellular and animal models of AD. Microarray analysis reveals that Spa-EV treatment modulates Aβ42-induced alterations in gene expression in both HT22 neuronal cells and BV2 microglia cells. Among the genes significantly affected by SpaEV, notable examples include Bdnf, Nt3/4, and Trkb, which are key players of neurotrophic signaling; Pgc1α, an upstream regulator of mitochondrial biogenesis; Mecp2 and Sirt1, epigenetic factors that regulate numerous gene expressions; and Il1β, Tnfα, and Nfκb-p65, which are associated with neuroinflammation. Remarkably, Spa-EV effectively reverses Aβ42-induced alteration in the expression of these genes through the upregulation of Mecp2. Furthermore, administration of Spa-EV in Tg-APP/PS1 mice restores the reduced expression of neurotrophic factors, Pgc1α, MeCP2, and Sirt1, while suppressing the increased expression of proinflammatory genes in the brain. Our results indicate that Spa-EV has the potential to reverse Aβ-induced dysregulation of gene expression in neuronal and microglial cells. These alterations encompass those essential for neurotrophic signaling and neuronal plasticity, mitochondrial function, and the regulation of inflammatory processes.

Recent studies have shown an increased abundance of Sphingomonas paucimobilis, an aerobic, Gram-negative bacterium with a distinctive cell envelope rich in glycosphingolipids, within the gut microbiome of individuals with Alzheimer Disease (AD). However, the fact that S. paucimobilis is a well-known pathogen associated with nosocomial infections presents a significant challenge in investigating whether its presence in the gut microbiome is detrimental or beneficial, particularly in the context of AD. This study examines the impact of S. paucimobilis-derived extracellular vesicles (Spa-EV) on Aβ-induced pathology in cellular and animal models of AD. Microarray analysis reveals that Spa-EV treatment modulates Aβ42-induced alterations in gene expression in both HT22 neuronal cells and BV2 microglia cells. Among the genes significantly affected by SpaEV, notable examples include Bdnf, Nt3/4, and Trkb, which are key players of neurotrophic signaling; Pgc1α, an upstream regulator of mitochondrial biogenesis; Mecp2 and Sirt1, epigenetic factors that regulate numerous gene expressions; and Il1β, Tnfα, and Nfκb-p65, which are associated with neuroinflammation. Remarkably, Spa-EV effectively reverses Aβ42-induced alteration in the expression of these genes through the upregulation of Mecp2. Furthermore, administration of Spa-EV in Tg-APP/PS1 mice restores the reduced expression of neurotrophic factors, Pgc1α, MeCP2, and Sirt1, while suppressing the increased expression of proinflammatory genes in the brain. Our results indicate that Spa-EV has the potential to reverse Aβ-induced dysregulation of gene expression in neuronal and microglial cells. These alterations encompass those essential for neurotrophic signaling and neuronal plasticity, mitochondrial function, and the regulation of inflammatory processes.

Recent studies have shown an increased abundance of Sphingomonas paucimobilis, an aerobic, Gram-negative bacterium with a distinctive cell envelope rich in glycosphingolipids, within the gut microbiome of individuals with Alzheimer Disease (AD). However, the fact that S. paucimobilis is a well-known pathogen associated with nosocomial infections presents a significant challenge in investigating whether its presence in the gut microbiome is detrimental or beneficial, particularly in the context of AD. This study examines the impact of S. paucimobilis-derived extracellular vesicles (Spa-EV) on Aβ-induced pathology in cellular and animal models of AD. Microarray analysis reveals that Spa-EV treatment modulates Aβ42-induced alterations in gene expression in both HT22 neuronal cells and BV2 microglia cells. Among the genes significantly affected by SpaEV, notable examples include Bdnf, Nt3/4, and Trkb, which are key players of neurotrophic signaling; Pgc1α, an upstream regulator of mitochondrial biogenesis; Mecp2 and Sirt1, epigenetic factors that regulate numerous gene expressions; and Il1β, Tnfα, and Nfκb-p65, which are associated with neuroinflammation. Remarkably, Spa-EV effectively reverses Aβ42-induced alteration in the expression of these genes through the upregulation of Mecp2. Furthermore, administration of Spa-EV in Tg-APP/PS1 mice restores the reduced expression of neurotrophic factors, Pgc1α, MeCP2, and Sirt1, while suppressing the increased expression of proinflammatory genes in the brain. Our results indicate that Spa-EV has the potential to reverse Aβ-induced dysregulation of gene expression in neuronal and microglial cells. These alterations encompass those essential for neurotrophic signaling and neuronal plasticity, mitochondrial function, and the regulation of inflammatory processes.

Objective: To assess whether local anesthetic infiltration could minimize the carotid baroreceptor reflex (CBR) which has an incidence after carotid artery stenting (CAS) that varies from 29% to 51%. Methods: This retrospective single-center study included 51 patients (mean age, 70.47 years) who underwent CAS for carotid stenosis. The groups included patients who underwent CAS for asymptomatic ischemic stroke (n=41) or symptomatic disease (n=10). Preprocedural percutaneous lidocaine injections (PPLIs) were administered to 70.6% and 5.9% of patients who underwent elective CAS and emergency CAS, respectively. Results: Among patients who received PPLIs, the mean degree of stenosis was 80.5% (95% confidence interval [CI]: ±10.74, 51–98%). The mean distance from the common carotid artery bifurcation to the most stenotic lesion (CSD) was 8.3 mm (95% CI: ±0.97, 6.3–10.2 mm); the mean angle between the internal carotid artery and common carotid artery (CCA) trunk (IAG) was 65.6° (95% CI: ±2.39, 61–70°). Among patients who did not receive PPLIs, the mean degree of stenosis was 84.0% (95% CI: ±8.96, 70–99%). The mean CSD was 5.9 mm (95% CI: ±1.83, 1.9–9.9 mm); the mean IAG was 60.4° (95% CI: ±4.41, 51–70°). The procedure time was longer in the PPLI group than in the no PPLI group (28.19 [n=39] vs. 18.88 [n=12] days) (P=0.057); the length of intensive care unit stay was shorter in the PPLI group (20.01 [n=36] vs. 28.10 [n=5] days) (P=0.132). Conclusions Targeted PPLI administration to the carotid bulb decreased aberrant heart rates and blood pressure changes induced by carotid stent deployment and balloon inflation. As CBR sensitivity increases with decreasing distance to the stenotic lesion from the CCA bifurcation, PPLIs may help stabilize patients during procedures for stenotic lesions closer to the CCA.

Progressive epidural hematoma is a form of acute epidural hematoma that graduallyexpands from a small initial hematoma; in cases that are clinically aggravated dueto the presence of a mental illness or neurological condition, patients should be surgicallytreated for evacuation of the hematoma, but poorer outcomes are expected ifthe patient has several medical co-morbidities for surgery. We experienced two casesof progressive epidural hematoma which were successfully managed by endovasculartreatment: an 85-year-old male with medical co-morbidities and a 51-year-oldfemale with a poor-grade subarachnoid hemorrhage resulting from the rupture of adissecting aneurysm of the vertebral artery. In both cases, a middle meningeal arteryembolization was performed and contrast leakage was observed and controlled usingcerebral angiography, halting the progression of their epidural hematomas. Thus,endovascular embolization of a middle meningeal artery may play a useful role in salvagetherapy in certain complicated situations that limit treatment of the hematomaby surgical evacuation.

Striatal-enriched protein tyrosine phosphatase (STEP) is abundantly expressed in the striatum, which strongly expresses dopamine and opioid receptors and mediates the effects of many drugs of abuse. However, little is known about the role of STEP in opioid receptor function. In the present study, we generated STEP-targeted mice carrying a nonsense mutation (C230X) in the kinase interaction domain of STEP by screening the N-ethyl-N-nitrosourea (ENU)-driven mutant mouse genomic DNA library and subsequent in vitro fertilization. It was confirmed that the C230X nonsense mutation completely abolished functional STEP protein expression in the brain. STEP(C230X−/−) mice showed attenuated acute morphine-induced psychomotor activity and withdrawal symptoms, whereas morphine-induced analgesia, tolerance and reward behaviors were unaffected. STEP(C230X−/−) mice displayed reduced hyperlocomotion in response to intrastriatal injection of the μ-opioid receptor agonist DAMGO, but the behavioral responses to δ- and κ-opioid receptor agonists remained intact. These results suggest that STEP has a key role in the regulation of psychomotor action and physical dependency to morphine. These data suggest that STEP inhibition may be a critical target for the treatment of withdrawal symptoms associated with morphine.
Analgesia* ; Animals ; Brain ; Codon, Nonsense ; Dopamine ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)- ; Ethylnitrosourea ; Fertilization in Vitro ; Gene Library ; Mass Screening ; Mice ; Morphine* ; Phosphotransferases ; Protein Tyrosine Phosphatases ; Receptors, Opioid ; Reward* ; Street Drugs ; Substance Withdrawal Syndrome*

Compression of the airway is relatively common in pediatric patients, although it is often an unrecognized complication of congenital cardiac and aortic arch anomalies. Aortopexy has been established as a surgical treatment for tracheobronchial obstruction associated with vascular anomaly, aortic arch anomaly, esophageal atresia, and tracheoesophageal fistula. The tissue-to-tissue arch repair technique could result in severe airway complication such as compression of the left main bronchus which was not a problem before the correction. We report three cases of corrective open heart surgery monitored by intraoperative bronchoscopy performed during prebypass, and performed immediately before weaning from bypass, to evaluate tracheobronchial obstruction caused by congenital, complex cardiac anomalies in the operating room.
Airway Obstruction* ; Aorta, Thoracic ; Aortic Coarctation ; Bronchi ; Bronchoscopy* ; Esophageal Atresia ; Humans ; Operating Rooms ; Thoracic Surgery ; Tracheoesophageal Fistula ; Weaning

OBJECTIVE: The optimal threshold of the infusion volume of cement has been a continuous subject in percutaneous vertebroplasty (PVP). This study verifies a causal relationship between the cement volume and the clinical outcome, and suggests the parameters of the appropriate volume of cement in PVP. METHODS: This is a retrospective study. One hundred nine patients, who underwent PVP between 2012 and 2015, were included in the study. Various factors such as patients' fracture levels, fracture types, fracture body volumes, fracture rates, bone mineral densities, and infused cement volumes were analyzed. Cement infusion ratios were calculated, using total amount of infused cement and fractured body volume. Follow up was done after one-week, one-month and three-months, postoperatively. Changes in the middle body height and the cement leakage levels were monitored and clinical outcomes were evaluated using a visual analogue scale. RESULTS: Among the variables, the infusion ratio (r=-0.320, p=0.003, Pearson's correlation) was the only index that showed a significant cause and effect relationship with favorable clinical outcome, except the group with a T-score of higher than -2.5, and the group with a upper thoracic vertebral level. The patients with a cement infusion ratio of 27.8% or more of the fractured body volume had favorable results. CONCLUSION: This study showed that high cement infusion ratio revealed favorable outcome in the vertebroplasty of the osteoporotic compression fractures. Infusion ratio of more than 27.8% to osteoporotic compressed vertebrae is optimal for rapid recovery after PVP.
Body Height ; Bone Cements ; Bone Density ; Follow-Up Studies* ; Fractures, Compression ; Humans ; Multivariate Analysis* ; Retrospective Studies ; Spine ; Vertebroplasty*

BACKGROUND: The aim of this study is to evaluate the status and adverse events of anesthesiologist-administered sedation and general anesthesia, outside of the operating room. METHODS: Patients undergoing sedation and general anesthesia, outside of the operating room, were retrospectively reviewed, during the study period from March to October of 2011. The patient's characteristics, primary diagnosis for the procedure, procedures performed outside of the operating room, adverse events associated with sedation and anesthesia, sedatives/anesthetic agents, and anesthetic time, were all assessed. RESULTS: A total of 429 patient's submitted data on 44 sedation/401 general anesthesia were encountered, during the study period. The range of age varied from 2 months to 83 yrs. Most common primary diagnosis for the procedure, during sedation or general anesthesia, was vascular or neurologic problem, respectively. The most frequently used sedatives or analgesics were propofol alone, during sedation (45%) and propofol with remifentanil, during general anesthesia (60%), respectively. Adverse events occurred in 32%, during sedation and 29%, during general anesthesia. Bradycardia occurred in 16% of sedation and hypotension occurred in 15% of general anesthesia. CONCLUSIONS: Our data suggest that the sedation/general anesthesia for procedures, outside of the operating room, have been performed in a complex situation, various location, and wide age groups. Adequate monitoring, sufficient anesthesia support, including skilled staff and emergency equipments, and appropriate drug for each procedure are needed for the patient's safety.
Analgesics ; Anesthesia ; Anesthesia, General ; Bradycardia ; Emergencies ; Humans ; Hypnotics and Sedatives ; Hypotension ; Operating Rooms ; Piperidines ; Propofol ; Retrospective Studies