Background/Aims: N-acetylcysteine (NAC) affects signaling pathways involved in apoptosis, angiogenesis, cell growth and arrest, redox-regulated gene expression, and the inflammatory response. However, it is not known how the signal mechanism for tight junctional protein claudin (CLDN) 18 is regulated in asthma patients. Methods: To investigate the effects of NAC on CLDN18 expression in a mouse model of asthma, and to assess plasma levels of CLDN18 in asthma patients. A murine model of asthma induced by ovalbumin (OVA) was established using wild-type BALB/c female mice, and the levels of CLDNs, phosphorylated-pyruvate dehydrogenase kinase 1 (p-PDK1), and protein kinase B (Akt) pathway proteins following NAC treatment were examined by Western blotting and immunohistochemistry. In addition, the plasma levels of CLDN18 were evaluated in asthmatic patients and control subjects. Results: NAC diminished OVA-induced airway hyper-responsiveness and inflammation.Levels of CLDN18 protein were higher in lung tissue from OVA mice than tissue from control mice, and were increased by treatment with NAC or dexamethasone. Treatment with NAC or dexamethasone decreased the OVA-induced increase in interleukin-1α protein levels. Although treatment with NAC increased OVA-induced p-PDK1 protein levels, it decreased phosphorylated Akt (pAkt)/Akt levels. Soluble CLDN18 levels were lower in patients with asthma than in controls and were correlated with the percentage of neutrophils, forced expiratory volume in 1 second (FEV1)/forced vital capacity % (FVC%) and FEV1%. Conclusions CLDN18 plays a role in the pathogenesis of asthma and NAC diminishes airway inflammation and responsiveness by modulating CLDN18 expression.

The third-stage larvae (L3) of the parasitic nematode, Anisakis simplex, have been implicated in the induction of hyperimmune allergic reactions in orally infected humans. In this work, we have conducted a review of an investigation into immune reactions occurring in animals experimentally infected with A. simplex L3. The patterns of serum antibody productions in the experimental animals against excretory-secretory products (ESP) of A. simplex L3 contributed to our current knowledge regarding specific humoral immune reactions in humans. In our review, we were able to determine that L3 infection of experimental animals may constitute a good model system for further exploration of immune mechanisms and allergy in anisakiasis of humans.
Rats ; Mice ; Larva/immunology ; Immunoglobulin E/blood ; Hypersensitivity/*etiology/immunology ; Humans ; Enzyme-Linked Immunosorbent Assay ; Disease Models, Animal ; Antigens, Helminth/immunology ; Anisakis/growth & development/*immunology ; Anisakiasis/immunology ; Animals

Clopidogrel is an antiplatelet agent prescribed widely to prevent stent thrombosis after coronary or peripheral vascular interventions and for stroke prophylaxis. The side effects of this drug include gastrointestinal symptoms, such as nausea, abdominal pain, vomiting, and bleeding. Thrombotic thrombocytopenia purpura (TTP) is a rare complication of this drug. Here, we report a case of clopidogrel-associated TTP in a patient with cerebral infarction. To our knowledge, it is first reported case of clopidogrel-associated TTP in Korea.
Abdominal Pain ; Cerebral Infarction* ; Hemorrhage ; Humans ; Korea ; Nausea ; Purpura ; Purpura, Thrombotic Thrombocytopenic* ; Stents ; Stroke ; Thrombocytopenia ; Thrombosis ; Vomiting

Clopidogrel is an antiplatelet agent prescribed widely to prevent stent thrombosis after coronary or peripheral vascular interventions and for stroke prophylaxis. The side effects of this drug include gastrointestinal symptoms, such as nausea, abdominal pain, vomiting, and bleeding. Thrombotic thrombocytopenia purpura (TTP) is a rare complication of this drug. Here, we report a case of clopidogrel-associated TTP in a patient with cerebral infarction. To our knowledge, it is first reported case of clopidogrel-associated TTP in Korea.
Abdominal Pain ; Cerebral Infarction* ; Hemorrhage ; Humans ; Korea ; Nausea ; Purpura ; Purpura, Thrombotic Thrombocytopenic* ; Stents ; Stroke ; Thrombocytopenia ; Thrombosis ; Vomiting

Thrombotic thrombocytopenic purpura (TTP) is a rare blood disorder with a mortality rate of over 90% without prompt treatment. It is caused by congenital, idiopathic, or secondary diseases; idiopathic TTP is mainly associated with deficiency of ADAMTS13, a von Willebrand factor cleaving protease or ADAMTS13 inhibitors. The long-term survival rate of TTP has improved since the introduction of therapeutic plasma exchange (TPE), and the therapeutic aims have also been established. However, deciding on the end-point and appropriate treatment method requires careful assessment of clinical conditions of patients. The present study reports a case of a 33-year-old male patient with reduced ADAMTS13 activity and ADAMTS13 inhibitor, who developed symptoms after an early termination of TPE with improved symptoms, which finally improved with retreatment and additionally corticosteroid. We report our case with relevant literature review on TPE in TTP with this case.
Adult ; Humans ; Male ; Methods ; Mortality ; Plasma Exchange* ; Plasma* ; Plasmapheresis ; Purpura, Thrombotic Thrombocytopenic* ; Retreatment ; Survival Rate ; von Willebrand Factor

PURPOSE: To investigate the clinical characteristics of late-onset epilepsy combined with autism spectrum disorder (ASD), and the relationship between certain types of electroencephalography (EEG) abnormalities in ASD and associated neuropsychological problems. METHODS: Thirty patients diagnosed with ASD in early childhood and later developed clinical seizures were reviewed retrospectively. First, the clinical characteristics, language and behavioral regression, and EEG findings of these late-onset epilepsy patients with ASD were investigated. The patients were then classified into 2 groups according to the severity of the EEG abnormalities in the background rhythm and paroxysmal discharges. In the severe group, EEG showed persistent asymmetry, slow and disorganized background rhythms, and continuous sharp and slow waves during slow sleep (CSWS). RESULTS: Between the two groups, there was no statistically significant difference in mean age (P=0.259), age of epilepsy diagnosis (P=0.237), associated family history (P=0.074), and positive abnormal magnetic resonance image (MRI) findings (P=0.084). The severe EEG group tended to have more neuropsychological problems (P=0.074). The severe group statistically showed more electrographic seizures in EEG (P=0.000). Rett syndrome was correlated with more severe EEG abnormalities (P=0.002). Although formal cognitive function tests were not performed, the parents reported an improvement in neuropsychological function on the follow up checkup according to a parent's questionnaire. CONCLUSION: Although some ASD patients with late-onset epilepsy showed severe EEG abnormalities, including CSWS, they generally showed an improvement in EEG and clinical symptoms in the long-term follow up. In addition, severe EEG abnormalities tended to be related to the neuropsychological function.
Autistic Disorder ; Child ; Autism Spectrum Disorder ; Electroencephalography ; Epilepsy ; Follow-Up Studies ; Humans ; Magnetic Resonance Spectroscopy ; Parents ; Retrospective Studies ; Rett Syndrome ; Seizures

BACKGROUND: Rat mast cells were regarded as a good model for mast cell function in immune response. METHODS: Rat bone marrow mast cells (BMMC) were prepared both by recombinant rat IL-3 (rrIL-3) and by recombinant mouse stem cell factor (rmSCF), and investigated for both proliferation and differentiation in time course. Rat BMMC was induced by culture of rat bone marrow cells (BMCs) in the presence of both rrIL-3 (5 ng/ml) and rmSCF (5 ng/ml). Culture media were changed 2 times per week with the cell number condition of 5x10(4)/ml in 6 well plate. Proliferation was analyzed by cell number and cell counting kit-8 (CCK-8) and differentiation was by rat mast cell protease (RMCP) II and histamine. RESULTS: Cell proliferation rates reached a maximum at 8 or 11 days of culture and decreased thereafter. However, both RMCP II production and histamine synthesis peaked after 11 days of culture. By real time RT-PCR, the level of histidine decarboxylase mRNA was more than 500 times higher on culture day 11 than on culture day 5. By transmission electron microscopy, the cells were heterogeneous in size and contained cytoplasmic granules. Using gated flow cytometry, we showed that cultured BMCs expressed high levels of FcepsilonRI and the mast cell antigen, ganglioside, on culture day 11. CONCLUSION: These results indicate that rat BMMCs were generated by culturing BMCs in the presence of rrIL-3 and rmSCF and that the BMMCs have the characteristics of mucosal mast cells.
Animals ; Bone Marrow ; Bone Marrow Cells ; Cell Count ; Cell Proliferation ; Culture Media ; Cytoplasmic Granules ; Flow Cytometry ; Histamine ; Histidine Decarboxylase ; Interleukin-3 ; Kinetics ; Mast Cells ; Mice ; Microscopy, Electron, Transmission ; Phenotype ; Rats ; RNA, Messenger ; Stem Cell Factor

Purpose: Claudins are a type of tight junction proteins in human endothelia and epithelia. Ozone brings about oxidative stress and lung inflammation in humans and experimental models. However, the impact of ozone on claudins in subjects with asthma remains poorly understood. The aim of this study was to find variations in the tight junction proteins claudin-4 and claudin-5 in subjects with asthma in relation to ambient ozone concentration. Methods: We previously recruited 50 patients with stable/exacerbated asthmatics and 25 controls. Furthermore, to examine the influence of ozone concentration, we reanalyzed 18 patients with stable or exacerbated asthma and 3 controls. The plasma claudin-4 and claudin-5 levels in response to high concentrations of ozone were compared to stable/exacerbated asthma, and controls. Results: The lung functions were significantly lower in subjects with asthma than those in controls. Blood eosinophil proportions were significantly higher in exacerbated asthmatics than in subjects with stable asthma. In high concentration period of ozone, plasma claudin-4 levels were significantly higher in subjects with exacerbated asthma (0.44 ± 0.30 ng/mL, P = 0.005) or stable asthma (0.38± 0.31 ng/mL, P= 0.009) compared to those in control subjects (0.16± 0.1 ng/mL). Plasma claudin-5 levels were lower in subjects with stable asthma (2.97 ± 1.38 ng/mL, P = 0.011) than in control subjects (6.92 ± 3.9 ng/mL), and higher in subjects with exacerbated asthma (7.49 ± 4.23 ng/mL, P < 0.001) than those with stable asthma. Conclusion These results reveal that claudins be changed in patients with asthma following ozone exposure in subjects with asthma.

Purpose: Claudins are a type of tight junction proteins in human endothelia and epithelia. Ozone brings about oxidative stress and lung inflammation in humans and experimental models. However, the impact of ozone on claudins in subjects with asthma remains poorly understood. The aim of this study was to find variations in the tight junction proteins claudin-4 and claudin-5 in subjects with asthma in relation to ambient ozone concentration. Methods: We previously recruited 50 patients with stable/exacerbated asthmatics and 25 controls. Furthermore, to examine the influence of ozone concentration, we reanalyzed 18 patients with stable or exacerbated asthma and 3 controls. The plasma claudin-4 and claudin-5 levels in response to high concentrations of ozone were compared to stable/exacerbated asthma, and controls. Results: The lung functions were significantly lower in subjects with asthma than those in controls. Blood eosinophil proportions were significantly higher in exacerbated asthmatics than in subjects with stable asthma. In high concentration period of ozone, plasma claudin-4 levels were significantly higher in subjects with exacerbated asthma (0.44 ± 0.30 ng/mL, P = 0.005) or stable asthma (0.38± 0.31 ng/mL, P= 0.009) compared to those in control subjects (0.16± 0.1 ng/mL). Plasma claudin-5 levels were lower in subjects with stable asthma (2.97 ± 1.38 ng/mL, P = 0.011) than in control subjects (6.92 ± 3.9 ng/mL), and higher in subjects with exacerbated asthma (7.49 ± 4.23 ng/mL, P < 0.001) than those with stable asthma. Conclusion These results reveal that claudins be changed in patients with asthma following ozone exposure in subjects with asthma.

Purpose: Claudins are a type of tight junction proteins in human endothelia and epithelia. Ozone brings about oxidative stress and lung inflammation in humans and experimental models. However, the impact of ozone on claudins in subjects with asthma remains poorly understood. The aim of this study was to find variations in the tight junction proteins claudin-4 and claudin-5 in subjects with asthma in relation to ambient ozone concentration. Methods: We previously recruited 50 patients with stable/exacerbated asthmatics and 25 controls. Furthermore, to examine the influence of ozone concentration, we reanalyzed 18 patients with stable or exacerbated asthma and 3 controls. The plasma claudin-4 and claudin-5 levels in response to high concentrations of ozone were compared to stable/exacerbated asthma, and controls. Results: The lung functions were significantly lower in subjects with asthma than those in controls. Blood eosinophil proportions were significantly higher in exacerbated asthmatics than in subjects with stable asthma. In high concentration period of ozone, plasma claudin-4 levels were significantly higher in subjects with exacerbated asthma (0.44 ± 0.30 ng/mL, P = 0.005) or stable asthma (0.38± 0.31 ng/mL, P= 0.009) compared to those in control subjects (0.16± 0.1 ng/mL). Plasma claudin-5 levels were lower in subjects with stable asthma (2.97 ± 1.38 ng/mL, P = 0.011) than in control subjects (6.92 ± 3.9 ng/mL), and higher in subjects with exacerbated asthma (7.49 ± 4.23 ng/mL, P < 0.001) than those with stable asthma. Conclusion These results reveal that claudins be changed in patients with asthma following ozone exposure in subjects with asthma.