To attempt a rigorous definition of the structure of the accessory spleen (AS) in the Chinese hamster, we examined twenty-one animals, and found AS in 5 animals (23.8%), which were over 7-month-old. The AS had no connection with the main spleen and was seen as a dark red oval organ (0.7 mm x 1.5 mm), which was embedded in the adipose tissue near the tail of the pancreas. It was demarcated from the adipose tissue and some pancreatic tissue. The organ was encapsulated by thin collagenous connective tissue and smooth muscle fibers, and contained lymphatic nodules, reticular fibers, nodular central arterioles, macrophages and megakaryocytes. Notably the incidence of AS appeared to increase with age in the Chinese hamsters.
Adipose Tissue/anatomy & histology ; Age Factors ; Animals ; Connective Tissue/anatomy & histology ; Cricetinae ; Cricetulus/*anatomy & histology ; Erythrocytes/cytology ; Lymphocytes/cytology ; Muscle, Smooth/anatomy & histology ; Pancreas ; Spleen/*anatomy & histology/cytology

Intracranial pial arteriovenous fistulas (AVFs) are uncommon, high-flow connection between an artery and a vein without an intervening nidus, vascular lesions treated using endovascular approach with a variety of embolic materials. To our knowledge, hyperperfusion syndrome as a result of embolization of pial AVFs has not been reported before. We report our experience in the treatment of high-flow pial AVF using detachable coils and hyperperfusion syndrome after coil embolization.
Arteries ; Arteriovenous Fistula* ; Embolization, Therapeutic* ; Veins

Increasing evidence implicates changes in [Ca²⁺]i and oxidative stress as causative factors in amyloid beta (Aβ)-induced neuronal cell death. Cyanidin-3-glucoside (C3G), a component of anthocyanin, has been reported to protect against glutamate-induced neuronal cell death by inhibiting Ca²⁺ and Zn²⁺ signaling. The present study aimed to determine whether C3G exerts a protective effect against Aβ₂₅₋₃₅-induced neuronal cell death in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using MTT assay for cell survival, and caspase-3 assay and digital imaging methods for Ca²⁺, Zn²⁺, MMP and ROS. Treatment with Aβ25–35 (20 µM) for 48 h induced neuronal cell death in cultured rat pure hippocampal neurons. Treatment with C3G for 48 h significantly increased cell survival. Pretreatment with C3G for 30 min significantly inhibited Aβ₂₅₋₃₅-induced [Zn²⁺]i increases as well as [Ca²⁺]i increases in the cultured rat hippocampal neurons. C3G also significantly inhibited Aβ₂₅₋₃₅-induced mitochondrial depolarization. C3G also blocked the Aβ₂₅₋₃₅-induced formation of ROS. In addition, C3G significantly inhibited the Aβ₂₅₋₃₅-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid β-induced neuronal cell death by reducing multiple apoptotic signals.
Amyloid* ; Animals ; Anthocyanins ; Caspase 3 ; Cell Death* ; Cell Survival ; Membrane Potential, Mitochondrial ; Neurons* ; Neuroprotection ; Oxidative Stress ; Rats* ; Rats, Sprague-Dawley

Flavonoids have an ability to suppress various ion channels. We determined whether one of flavonoids, cyanidin-3-glucoside, affects adenosine 5'-triphosphate (ATP)-induced calcium signaling using digital imaging methods for intracellular free Ca2+ concentration ([Ca2+]i), reactive oxygen species (ROS) and mitochondrial membrane potential in PC12 cells. Treatment with ATP (100microM) for 90 sec induced [Ca2+]i increases in PC12 cells. Pretreatment with cyanidin-3-glucoside (1micro g/ml to 100microg/ml) for 30 min inhibited the ATP-induced [Ca2+]i increases in a concentration-dependent manner (IC50=15.3microg/ml). Pretreatment with cyanidin-3-glucoside (15microg/ml) for 30 min significantly inhibited the ATP-induced [Ca2+]i responses following removal of extracellular Ca2+ or depletion of intracellular [Ca2+]i stores. Cyanidin-3-glucoside also significantly inhibited the relatively specific P2X2 receptor agonist 2-MeSATP-induced [Ca2+]i responses. Cyanidin-3-glucoside significantly inhibited the thapsigargin or ATP-induced store-operated calcium entry. Cyanidin-3-glucoside significantly inhibited the ATP-induced [Ca2+]i responses in the presence of nimodipine and omega-conotoxin. Cyanidin-3-glucoside also significantly inhibited KCl (50 mM)-induced [Ca2+]i increases. Cyanidin-3-glucoside significantly inhibited ATP-induced mitochondrial depolarization. The intracellular Ca2+ chelator BAPTA-AM or the mitochondrial Ca2+ uniporter inhibitor RU360 blocked the ATP-induced mitochondrial depolarization in the presence of cyanidin-3-glucoside. Cyanidin-3-glucoside blocked ATP-induced formation of ROS. BAPTA-AM further decreased the formation of ROS in the presence of cyanidin-3-glucoside. All these results suggest that cyanidin-3-glucoside inhibits ATP-induced calcium signaling in PC12 cells by inhibiting multiple pathways which are the influx of extracellular Ca2+ through the nimodipine and omega-conotoxin-sensitive and -insensitive pathways and the release of Ca2+ from intracellular stores. In addition, cyanidin-3-glucoside inhibits ATP-induced formation of ROS by inhibiting Ca2+-induced mitochondrial depolarization.
Adenosine ; Adenosine Triphosphate ; Animals ; Calcium ; Calcium Signaling ; Flavonoids ; Ion Channels ; Ion Transport ; Membrane Potential, Mitochondrial ; Nimodipine ; omega-Conotoxins ; PC12 Cells* ; Reactive Oxygen Species ; Receptors, Purinergic P2X2 ; Thapsigargin

BACKGROUND: The balance of the risks and the benefits of cardiac surgery in the elderly remains a major concern. We evaluated the early and mid-term clinical results of patients aged over 75 years who underwent major cardiovascular surgery. METHODS: Two hundred and fifty-one consecutive patients, who underwent cardiac surgery at Seoul National University Bundang Hospital between July 2003 and June 2011, were included in this study (mean age, 78.7+/-3.4 years; male:female=130:121). Elective surgery was performed in 112 patients, urgent in 90, and emergency in 49. RESULTS: Early mortality was 12.7% (32/251). Follow-up completion was 100%, and the mean follow-up duration was 2.8+/-2.2 years. Late mortality was 24.2% (53/219). There were 283 readmissions in a total of 109 patients after discharge. However, the reason for readmission was related more to non-cardiac factors (71.3%) than to cardiac factors. The overall survival estimates were 79.2% at the 1-year follow-up and 58.4% at the 5-year follow-up. Patients who underwent elective surgery had a lower early mortality rate (elective, 4.5%; urgent, 13.3%; emergency, 30.6%) and better overall survival rate than those that underwent urgent or emergency surgery (p <0.001). CONCLUSION: The timing of cardiac surgery was found to be an independent risk factor for early and late mortality. Thus, earlier referral and intervention may improve operative results. Further, comprehensive coordinated postoperative care is needed for other comorbid problems in aged patients.
Aged ; Cardiac Surgical Procedures ; Emergencies ; Follow-Up Studies ; Humans ; Mortality ; Postoperative Care ; Referral and Consultation ; Risk Factors ; Seoul ; Survival Rate ; Thoracic Surgery

Glycogen storage disease type IX (GSD IX) is caused by a defect in phosphorylase b kinase (PhK) that results from mutations in the PHKA2, PHKB, and PHKG2 genes. Patients usually manifest recurrent ketotic hypoglycemia with growth delay, but some may present simple hepatomegaly. Although GSD IX is one of the most common causes of GSDs, its biochemical and genetic diagnosis has been problematic due to its rarity, phenotypic overlap with other types of GSDs, and genetic heterogeneities. In our report, a 22-month-old boy with GSD IX is described. No other manifestations were evident except for hepatomegaly. His growth and development also have been proceeding normally. Diagnosed was made by histologic examination, an enzyme assay, and genetic testing with known c.3210_3212del (p.Arg1070del) mutation in PHKA2 gene.
Child* ; Diagnosis ; Enzyme Assays ; Genetic Heterogeneity ; Genetic Testing ; Glycogen Storage Disease ; Glycogen* ; Growth and Development ; Hepatomegaly* ; Humans ; Hypoglycemia ; Infant ; Male ; Phosphorylase Kinase

Phenolic compounds affect intracellular free Ca2+ concentration ([Ca2+]i) signaling. The study examined whether the simple phenolic compound octyl gallate affects ATP-induced Ca2+ signaling in PC12 cells using fura-2-based digital Ca2+ imaging and whole-cell patch clamping. Treatment with ATP (100 micrometer) for 90 s induced increases in [Ca2+]i in PC12 cells. Pretreatment with octyl gallate (100 nM to 20 micrometer) for 10 min inhibited the ATP-induced [Ca2+]i response in a concentration-dependent manner (IC50=2.84 micrometer). Treatment with octyl gallate (3 micrometer) for 10 min significantly inhibited the ATP-induced response following the removal of extracellular Ca2+ with nominally Ca2+-free HEPES HBSS or depletion of intracellular Ca2+ stores with thapsigargin (1 micrometer). Treatment for 10 min with the L-type Ca2+ channel antagonist nimodipine (1 micrometer) significantly inhibited the ATP-induced [Ca2+]i increase, and treatment with octyl gallate further inhibited the ATP-induced response. Treatment with octyl gallate significantly inhibited the [Ca2+]i increase induced by 50 mM KCl. Pretreatment with protein kinase C inhibitors staurosporin (100 nM) and GF109203X (300 nM), or the tyrosine kinase inhibitor genistein (50 micrometer) did not significantly affect the inhibitory effects of octyl gallate on the ATP-induced response. Treatment with octyl gallate markedly inhibited the ATP-induced currents. Therefore, we conclude that octyl gallate inhibits ATP-induced [Ca2+]i increase in PC12 cells by inhibiting both non-selective P2X receptor-mediated influx of Ca2+ from extracellular space and P2Y receptor-induced release of Ca2+ from intracellular stores in protein kinase-independent manner. In addition, octyl gallate inhibits the ATP-induced Ca2+ responses by inhibiting the secondary activation of voltage-gated Ca2+ channels.
Adenosine Triphosphate ; Animals ; Calcium ; Constriction ; Extracellular Space ; Gallic Acid ; Genistein ; HEPES ; Indoles ; Maleimides ; Nimodipine ; PC12 Cells ; Phenol ; Protein Kinase C ; Protein-Tyrosine Kinases ; Thapsigargin

Objective: To assess the feasibility of quantitatively assessing pancreatic steatosis using magnetic resonance imaging (MRI) and its correlation with obesity and metabolic risk factors in pediatric patients. Materials and Methods: Pediatric patients (≤ 18 years) who underwent liver fat quantification MRI between January 2016 and June 2019 were retrospectively included and divided into the obesity and control groups. Pancreatic proton density fat fraction (P-PDFF) was measured as the average value for three circular regions of interest (ROIs) drawn in the pancreatic head, body, and tail. Age, weight, laboratory results, and mean liver MRI values including liver PDFF (L-PDFF), stiffness on MR elastography, and T2* values were assessed for their correlation with P-PDFF using linear regression analysis. The associations between P-PDFF and metabolic risk factors, including obesity, hypertension, diabetes mellitus (DM), and dyslipidemia, were assessed using logistic regression analysis. Results: A total of 172 patients (male:female = 125:47; mean ± standard deviation [SD], 13.2 ± 3.1 years) were included. The mean P-PDFF was significantly higher in the obesity group than in the control group (mean ± SD, 4.2 ± 2.5% vs. 3.4 ± 2.4%; p = 0.037). L-PDFF and liver stiffness values showed no significant correlation with P-PDFF (p = 0.235 and p = 0.567, respectively). P-PDFF was significantly associated with obesity (odds ratio 1.146, 95% confidence interval 1.006–1.307, p = 0.041), but there was no significant association with hypertension, DM, and dyslipidemia. Conclusion MRI can be used to quantitatively measure pancreatic steatosis in children. P-PDFF is significantly associated with obesity in pediatric patients.

PURPOSE: Unexpected requests for non-cardiac surgery requiring discontinuation of dual antiplatelet therapy (DAPT) frequently occur in daily clinical practice. The objectives of this study were to evaluate prevalence, timing and clinical outcomes of such unexpected requests for non-cardiac surgery or other invasive procedures during the first year after drug-eluting stents (DESs) implantation. MATERIALS AND METHODS: We prospectively investigated the prevalence, timing and clinical outcomes of unexpected requests for non-cardiac surgery or other procedures during the first year after DESs implantation in 2117 patients. RESULTS: The prevalence of requested non-cardiac surgery or invasive procedures was 14.6% in 310 requests and 12.3% in 261 patients. Among 310 requests, those were proposed in 11.3% <1 month, 30.0% between 1 and 3 months, 36.8% between 4 and 6 months and 21.9% between 7 and 12 months post-DES implantation. The rates of actual discontinuation of DAPT and non-cardiac surgery or procedure finally performed were 35.8% (111 of 310 requests) and 53.2% (165 of 310 requests), respectively. On multivariate regression analysis, the most significant determinants for actual discontinuation of DAPT were Endeavor zotarolimus-eluting stent implantation with 3-month DAPT (OR=5.54, 95% CI 2.95-10.44, p<0.001) and timing of request (OR=2.84, 95% CI 1.97-4.11, p<0.001). There were no patients with any death, myocardial infarction, or stent thrombosis related with actual discontinuation of DAPT. CONCLUSION: Those unexpected requests with premature discontinuation of DAPT were relatively common and continuously proposed during the first year following DES implantation. No death, myocardial infarction or stent thrombosis occurred in patients with actual discontinuation of DAPT.
Coronary Artery Disease ; Drug-Eluting Stents* ; Humans ; Methods* ; Myocardial Infarction ; Prevalence ; Prospective Studies* ; Regression Analysis ; Stents ; Thrombosis

Fluoxetine, a widely used anti-depressant compound, has several additional effects, including blockade of voltage-gated ion channels. We examined whether fluoxetine affects ATP-induced calcium signaling in PC12 cells by using fura-2-based digital calcium imaging and assay for [3H]-inositol phosphates (IPs). Treatment with ATP (100microM) for 2 min induced [Ca2+]i increases. The ATP-induced [Ca2+]i increases were significantly decreased by removal of extracellular Ca2+ and treatment with the inhibitor of endoplasmic reticulum Ca2+ ATPase thapsigargin (1microM). Treatment with fluoxetine for 5 min blocked the ATP-induced [Ca2+]i increase concentration-dependently. Treatment with fluoxetine (30microM) for 5 min blocked the ATP-induced [Ca2+]i increase following removal of extracellular Ca2+ and depletion of intracellular Ca2+ stores. While treatment with the L-type Ca2+ channel antagonist nimodipine for 10 min inhibited the ATP-induced [Ca2+]i increases significantly, treatment with fluoxetine alone blocked the ATP-induced responses. Treatment with fluoxetine also inhibited the 50 mM K+-induced [Ca2+]i increases completely. However, treatment with fluoxetine did not inhibit the ATP-induced [3H]-IPs formation. Collectively, we conclude that fluoxetine inhibits ATP-induced [Ca2+]i increases in PC12 cells by inhibiting both an influx of extracellular Ca2+ and a release of Ca2+ from intracellular stores without affecting IPs formation.
Adenosine Triphosphate ; Animals ; Calcium Signaling* ; Calcium* ; Calcium-Transporting ATPases ; Endoplasmic Reticulum ; Fluoxetine* ; Inositol Phosphates ; Ion Channels ; Nimodipine ; PC12 Cells* ; Phosphates ; Thapsigargin