Systemic sclerosis is a multisystemic disorder of unknown etiology characterized by fibrosis of skin, blood vessel, and visceral organ. A 38-week pregnant, 29 year-old woman with systemic sclerosis and migraine was scheduled for cesarean section under lumbar epidural anesthesia because of dyspnea, decreased diffusion lung capacity and Raynaud's phenomenon. She suffered from sudden onset of severe headache, repetitive nausea, vomiting, and hypertension during cesarean section under the epidural anesthesia. The above symptoms did not respond to beta-blocker, vasodilator during the operation period. In the recovery room, the headache and vomiting were relieved by intravenous injection of ketorolac and metoclopramide. She experienced single tonic-clonic generalized seizure and intermittent migraine after operation in the ward, and discharged 7 days after operation.
Adult ; Anesthesia, Epidural ; Blood Vessels ; Cesarean Section* ; Diffusion ; Dyspnea ; Female ; Fibrosis ; Headache ; Humans ; Hypertension ; Injections, Intravenous ; Ketorolac ; Lung Volume Measurements ; Metoclopramide ; Migraine Disorders ; Nausea ; Pregnancy ; Recovery Room ; Scleroderma, Systemic* ; Seizures ; Skin ; Vomiting

Purpose: Several polymorphic sites have been reported in the tumor necrosis factor alpha (TNF-alpha) promoter. Comparative studies on TNF-alpha production with promoter genotype have reported variable results, particularly in the 308 promoter region. Therefore, genetic polymorphism of TNF-alpha promoter region ( 308) was investigated to determine if it was associated with bladder tumor. MATERIALS AND METHODS: The DNA from 113 and 109 respective blood samples of bladder tumor patients and controls was analyzed by a PCR-based restriction fragment length polymorphism (RFLP) method to characterize the genetic polymorphism of the 308 region of the TNF-alpha promoter. TNF-alpha expression was also checked by measuring the mRNA and protein content using a quantitative-competitive PCR and ELISA method, respectively. RESULTS: The difference in the genetic variations of TNF-alpha promoter did not exist between the bladder tumor patients and the control group (p=0.259). The tumor grade was significantly related to the GA genotype (p=0.04). The mRNA levels of TNF-alpha in the GA genotype were significantly higher than those in the GG genotype in bladder tumors (p=0.022). The TNF-alpha serum levels in the GA genotype were significantly higher than those in the GG genotype regardless of whether there was a bladder tumor. In addition, the TNF-alpha serum levels in bladder tumor patients were significantly higher than the controls in either the GG or GA type (GG type, p=0.001; GA type, p=0.009). CONCLUSIONS: The GA genotype of the TNF-alpha promoter region ( 308) had a significant impact on TNF-alpha production and is related to a higher-grade tumor compared to the GG genotype. The TNF-alpha serum levels in the bladder tumor patients were significantly higher than in the controls. This suggests that TNF-alpha might be involved in the tumorigenesis of the bladder.
Carcinogenesis ; DNA ; Enzyme-Linked Immunosorbent Assay ; Genetic Variation ; Genotype* ; Humans ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Promoter Regions, Genetic ; RNA, Messenger ; Tumor Necrosis Factor-alpha* ; Urinary Bladder Neoplasms* ; Urinary Bladder*

On page 173, the incorrect image which was not submitted by the author was mistakenly printed for Fig. 5 by a system error of the editing company.

Left ventricular pseudoaneurysm, in which a ventricular free wall rupture is locally contained by adherent pericardium, is a rare complication of myocardial infarction. Compared w'th a true left ventricular aneunsm, a pseudoaneurysm has a greater propensity to sudden rupture, with catastrophic sequelae. Pseudoaneurysm may be surgically curable, a prompt and accurate diagnosis is thus essential. Transthoracic echocardiography has been the procedure of choice in the diagnosis of pseu- doaneurysm. Transesophageal echocardiography can provide more accurate information than transthoracic echocardiography for the evaluation of ventricular pseudoaneurysm located in posterior and inferior wall. We experienced a case of pseudoaneurysm of left ventricle in a 75-year-old female who presented with dyspnea. A large pseudoaneurysm of left ventricle vith narrow neck was de- tected by transesophageal echocardiography.
Aged ; Aneurysm, False* ; Diagnosis ; Dyspnea ; Echocardiography ; Echocardiography, Transesophageal* ; Female ; Heart Rupture ; Heart Ventricles ; Humans ; Myocardial Infarction ; Neck ; Pericardium ; Rupture

Essential fatty acid (EFA) is known to be required for the body to function normally and healthily. However, the effect of EFA on glucose uptake in skeletal muscle has not yet been fully investigated. In this study, we examined the effect of two EFAs, linoleic acid (LA) and alpha-linolenic acid (ALA), on glucose uptake of C2C12 skeletal muscle cells and investigated the mechanism underlying the stimulatory effect of polyunsaturated EFAs in comparison with monounsaturated oleic acid (OA). In palmitic acid (PA)-induced insulin resistant cells, the co-treatment of EFAs and OA with PA almost restored the PA-induced decrease in the basal and insulin-stimulated 2-NBDG (fluorescent D-glucose analogue) uptake, respectively. Two EFAs and OA significantly protected PA-induced suppression of insulin signaling, respectively, which was confirmed by the increased levels of Akt phosphorylation and serine/threonine kinases (PKCtheta and JNK) dephosphorylation in the western blot analysis. In PA-untreated, control cells, the treatment of 500 microM EFA significantly stimulated 2-NBDG uptake, whereas OA did not. Phosphorylation of AMP-activated protein kinase (AMPK) and one of its downstream molecules, acetyl-CoA carboxylase (ACC) was markedly induced by EFA, but not OA. In addition, EFA-stimulated 2-NBDG uptake was significantly inhibited by the pre-treatment of a specific AMPK inhibitor, adenine 9-beta-D-arabinofuranoside (araA). These data suggest that the restoration of suppressed insulin signaling at PA-induced insulin resistant condition and AMPK activation are involved at least in the stimulatory effect of EFA on glucose uptake in C2C12 skeletal muscle cells.
Acetyl-CoA Carboxylase ; Adenine ; alpha-Linolenic Acid ; AMP-Activated Protein Kinases* ; Blotting, Western ; Fatty Acids, Essential* ; Glucose* ; Insulin ; Linoleic Acid ; Muscle, Skeletal* ; Oleic Acid ; Palmitic Acid ; Phosphorylation ; Phosphotransferases

BACKGROUND/AIMS: Renal aging-related changes are characterized by oxidative stress. SIRT1 regulates cellular conditions by activating Nrf2. The present study investigated the processes of renal changes by antioxidant enzymes and the relationship between SIRT1 and Nrf2. METHODS: We used male 2-, 12-, and 24-month-old C57BL/6 mice. We measured renal function, histological changes, oxidative stress, and expression of SIRT1–Nrf2 signaling in the kidneys. RESULTS: 24-month-old mice exhibited increased albuminuria and serum creatinine. Creatinine clearance was decreased in 24-month-old mice compared with 12-month-old mice. There were increases in mesangial volume and tubulointerstitial fibrosis in 24-month-old mice. Moreover, oxidative stress marker, 3-Nitrotyrosine, expression and apoptosis were increased in 24-month-old mice. The 24 h urinary 8-isoprostane and 8-hydroxy-deoxyguanosine excretion increased with aging. The levels of expression of SIRT1 and nuclear Nrf2 were decreased in 24-month-old mice. The antioxidant enzymes HO-1 and NQO-1 were down-regulated in 24-month-old mice. Another antioxidant enzyme, SOD2, was decreased in 24-month-old mice. CONCLUSIONS: Our results demonstrated that SIRT1 was down-regulated with aging, and this may be related to changes in the expression of target molecules including Nrf2. As a result, oxidative stress was induced. The pharmacological targeting of these signaling molecules may reduce the pathological changes associated with aging in the kidney.
Aging ; Albuminuria ; Animals ; Apoptosis ; Child, Preschool ; Creatinine ; Fibrosis ; Humans ; Infant ; Kidney* ; Male ; Mice ; NF-E2-Related Factor 2 ; Oxidative Stress ; Sirtuin 1

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Kidney*

Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor. Although it is well known to have various physiological roles in cancer, its inhibitory effect on inflammation remains poorly understood. In the present study, a human PTEN gene was fused with PEP-1 peptide in a bacterial expression vector to produce a genetic in-frame PEP-1-PTEN fusion protein. The expressed and purified PEP-1-PTEN fusion protein were transduced efficiently into macrophage Raw 264.7 cells in a time- and dose- dependent manner when added exogenously in culture media. Once inside the cells, the transduced PEP-1-PTEN protein was stable for 24 h. Transduced PEP-1-PTEN fusion protein inhibited the LPS-induced cyclooxygenase 2 (COX-2) and iNOS expression levels in a dose-dependent manner. Furthermore, transduced PEP-1-PTEN fusion protein inhibited the activation of NF-kappa B induced by LPS. These results suggest that the PEP-1-PTEN fusion protein can be used in protein therapy for inflammatory disorders.
Animals ; Cell Line ; Cyclooxygenase 2/*metabolism ; Cysteamine/*analogs & derivatives ; Enzyme Activation ; Humans ; Lipopolysaccharides/*pharmacology ; Macrophages/*metabolism ; Mice ; NF-kappa B/metabolism ; Nitric Oxide/*biosynthesis ; Nitric Oxide Synthase Type II/metabolism ; PTEN Phosphohydrolase/*genetics ; Peptides/*genetics ; Recombinant Fusion Proteins/*biosynthesis/genetics ; Signal Transduction

Chlorogenic acid (CGA) possesses various biological activities such as anti-oxidant, anti-inflammatory, and anti-diabetic activities. In the present study, we examined the effect of CGA on the transduction efficiency of PEP-1-ribosomal protein S3 (PEP-1-rpS3) into cells and brain tissues, and its neuroprotective potential against ischemia/reperfusion. We found that, in the presence of CGA, the transduction efficiency of PEP-1-rpS3 into astrocytes and the CA1 region of the hippocampus was enhanced, compared to its transduction in the absence of CGA. Also, cell viability data demonstrated that the sample treated with CGA + PEP-1-rpS3 exhibited improved cell viability against hydrogen peroxide (H2O2)-induced toxicity more significantly than the sample treated with PEP-1-rpS3 alone. Also, in a gerbil ischemia model, data demonstrated that following the ischemic insult, the group treated with PEP-1-rpS3 + CGA showed markedly enhanced protection of neuron cells in CA1 region of hippocampus, compared to those treated with CGA or PEP-1-rpS3 alone. Taken together, these results suggest that CGA may improve the transduction efficiency of protein transduction domain (PTD) fusion proteins into target cells or tissues, thereby enhancing their therapeutic potential against various diseases.
Astrocytes ; Brain ; Cell Survival ; Chlorogenic Acid ; Gerbillinae ; Hippocampus ; Hydrogen Peroxide ; Ischemia ; Neurons ; Neuroprotective Agents ; Proteins

Primary venous thrombosis caused by deficiency or qualitative abnormality of antithrombin III, protein C and protein S is usually inherited as an autosomal dominant trait. Usually, deep vein thrombosis or pulmonary thromboembolism is developed by such abnormalities, however, mesenteric vein thrombosis is rarely reported. A 27-year-old man with previous history of deep vein thrombosis underwent segmental resection of jejunum due to mesenteric vein thrombosis complicated by necrosis of jejunum. Postoperative investigation disclosed combined deficiency of antithrombin III and protein C. His son also showed deficiency of antithrombin III. Postoperatively, he is on life-long warfarin therapy without experiencing recurrence of venous thrombosis.
Adult ; Antithrombin III* ; Humans ; Jejunum ; Mesenteric Veins ; Necrosis ; Protein C* ; Protein S ; Pulmonary Embolism ; Recurrence ; Thrombosis ; Venous Thrombosis* ; Warfarin