Kawasaki disease is an acute vasculitis of infancy and early childhood characterized by high fever, rash, mucositis, lymphadenopathy and coronary artery damage. The failure to indentify a causative organism using convetional culture and serological techniques, and the lack of response to antibiotics indicate that the disorder is probably not due to any known bacterial or viral pathogens. During the acute phase of the disease, the alterations of T and B cell functions, changes of cytokine and immunoglobulin levels have been reported. This study was performed to investigate the changes of immunoglobulins levels in patients with Kawasaki disease. IgG, IgA, IgM and IgG subclasses were measured using immunoprecipitation and EIA in the sera of patients with Kawasaki disease. The results were as follows: 1) Acute phase reactants such as CRP and ESR were significantly increased in Kawasaki patients compared to those in control patients(p<0.01). 2) Serum IgG levels in Kawasaki disease were markedly increased than those in control patients, while serum IgA and IgM levels showed no significant changes (P: No Significance). 3) IgG1 and IgG4 were predominantly increased increased in the sera of Kawasaki patients, while IgG2 and IgG3 were not significantly increased (P: No Significance). With these results, unidentified infectious organism with abnormal immune response could be suggested as an etiologic factor of Kawasaki disease.
Acute-Phase Proteins ; Anti-Bacterial Agents ; Child* ; Coronary Vessels ; Exanthema ; Fever ; Humans ; Immunoglobulin A ; Immunoglobulin G* ; Immunoglobulin M ; Immunoglobulins ; Immunoprecipitation ; Lymphatic Diseases ; Mucocutaneous Lymph Node Syndrome* ; Mucositis ; Vasculitis

No abstract available.
Thrombosis*

No abstract available.
Pneumothorax* ; Thoracotomy*

No abstract available.
Thyroid Gland* ; Thyroid Nodule*

Nodular glomerulosclerosis was first described by Kimmelstiel and Wilson in 1936. Diabetic retinopathy and nephropath y are manifestation of the microangiopathy associated with diabetes. The severity of diabetic nephropathy and the occurrence of retinopathy correlate with the duration of clinical diabetes. However, there have been few reports of patients presents presenting with the classic lesions of diabetic microangiopathy in the absence of a known history of diabetes. These reports raise questions regarding the relationship and significance of carbohydrate intolerance to these pathologic abnormalities. A 34-year-old male patient clinically characterized by massive proteinuria and hypertension without evidence of systemic disease is reported. Renal biopsy showed the nodular glomerulosclerosis (Kimmelstiel-Wilson lesion) characteristic of diabetes. Direct opthalmoscopy and fluorescein angiography demonstrated a picture of advanced proliferative diabetic retinopathy. The patient had no history of diabetes mellitus and upon testing had normal glucose values in response to an oral glucose tolerance test. It is concluded that the nodular glomerulosclerosis lesions and proliferative retinopathy, thought to be specific for diabetes mellitus, may present in the absence of either overt clinical diabetes or impaired glucose tolerance.
Adult ; Biopsy ; Diabetes Mellitus* ; Diabetic Angiopathies ; Diabetic Nephropathies ; Diabetic Retinopathy ; Fluorescein Angiography ; Glucose ; Glucose Tolerance Test ; Humans ; Hypertension ; Male ; Proteinuria

No abstract available.
Blood Volume* ; Hypotension* ; Nitric Oxide* ; Plasma* ; Renal Dialysis*

Cockayne syndrome is a rare autosomal recessive disorder of childhood characterized by cachectic dwarfism with senile-like appearance, mental retardation, photosensitive dermatitis, loss of adipose tissue, pigmentary degeneration of retina, microcephaly, deafness, skeletal and neurologic abnormalities. We describe here an 18 year old boy with Cockayne syndrome who had, in addition to the typical features of the disorder, fasting hyperinsulinemia and growth hormone deficiency.
Adolescent ; C-Peptide/blood ; Cockayne Syndrome/*complications/pathology ; Growth Disorders/*complications/pathology ; Growth Hormone/*deficiency ; Humans ; Hyperinsulinism/*complications/pathology ; Insulin/blood ; Male ; Optic Atrophy/pathology ; Retinal Degeneration/pathology

Purpose: As the survival of head and neck cancer (HNC) improves, survivors increasingly confront non-cancer–related deaths. This nationwide population-based study aimed to investigate non-cancer–related deaths in HNC survivors. Materials and Methods: Data from the Korean Central Cancer Registry were obtained to characterize causes of death, mortality patterns, and survival in patients with HNC between 2006 and 2016 (n=40,890). Non-cancer-related mortality relative to the general population was evaluated using standardized mortality ratios (SMRs). The 5- and 10-year cause-specific competing risks probabilities of death (cumulative incidence function, CIF) and subdistribution hazards ratios (sHR) from the Fine-Gray models were estimated. Results: Comorbidity-related mortality was frequent in older patients, whereas suicide was predominant in younger patients. The risk of suicide was greater in patients with HNC than in the general population (SMR, 3.1; 95% confidence interval [CI], 2.7 to 3.5). The probability of HNC deaths reached a plateau at 5 years (5-year CIF, 33.9%; 10-year CIF, 39.5%), whereas the probability of non-HNC deaths showed a long-term linear increase (5-year, CIF 5.6%; 10-year CIF, 11.9%). Patients who were male (sHR, 1.56; 95% CI, 1.41 to 1.72), diagnosed with early-stage HNC (localized vs. distant: sHR, 1.86; 95% CI, 1.58 to 2.21) and older age (65-74 vs. 0-44: sHR, 6.20; 95% CI, 4.92 to 7.82; ≥ 75 vs. 0-44: sHR, 9.81; 95% CI, 7.76 to 12.39) had an increased risk of non-cancer mortality. Conclusion Non-HNC–related deaths continue increasing. HNC survivors are at increased risk of suicide in the younger and comorbidity-related death in the older. Better population-specific surveillance awareness and survivorship plans for HNC survivors are warranted.

BACKGROUND: Soman, a potent irreversible acetylcholinesterase (AChE) inhibitor, induces delayed neuronal injury by reactive oxygen species (ROS). Midazolam is used in patients with pathologic effects of oxidative stresses such as infection, hemodynamic instability and hypoxia. We investigated whether midazolam protects the Central Nervous System (CNS) from soman intoxication. The present study was performed to determine whether midazolam protects B35 cells from ROS stress for the purpose of exploring an application of midazolam to soman intoxication. METHODS: Glucose oxidase (GOX) induced ROS stress was used in a B35 neuroblastoma cell model of ROS induced neuronal injury. To investigate the effect of midazolam on cell viability, LDH assays and fluorescence activated cell sorting (FACS) analysis was performed. Western blotting was used for evaluating whether Akt-phosphorylation is involved in cell-protective effects of midazolam. RESULTS: GOX derived ROS injury decreased cell viability about 1.6-2 times compared to control; midazolam treatment (5 and 10 microg/ml) dose-dependently increased cell viability during ROS injury. On western blots, Akt-phosphorylation was induced during pretreatment with midazolam; it was diminished during co-treatment with LY-294002, an inhibitor of Akt-phosphorylation. FACS analysis confirmed that the cell protective effect of midazolam is mediated by an anti-apoptotic effect. GOX-induced apoptosis was inhibited by midazolam and the finding was diminished by LY-294002. CONCLUSIONS: Midazolam protects neuronal cells from GOX-induced ROS injury; this effect is mediated by an anti-apoptotic effect through Akt-phosphorylation. This shows that midazolam may be useful in soman intoxication.
Acetylcholinesterase ; Anoxia ; Apoptosis ; Blotting, Western ; Cell Survival ; Central Nervous System ; Chromones ; Flow Cytometry ; Glucose Oxidase ; Hemodynamics ; Humans ; Midazolam ; Morpholines ; Neuroblastoma ; Neurons ; Oxidative Stress ; Reactive Oxygen Species ; Soman

Ultrafiltration failure has been known as a major cause of dropout from long-term peritoneal dialysis and is often related to peritoneal hyperpermeability. This can be explained in part by progressive peritoneal fibrosis. The present experiment has been undertaken to evaluate the effects of peritoneal rest on peritoneal transport and morphology in rat model of peritoneal dialysis. Twenty-four male rats(Sprague-Dawley, 250-300g) were used and divided into three groups : group 1 (control, n=6) without dialysis, group 2(n=9) sacrificed immediately after 3 weeks of dialysis, and group 3 (n=9) sacrificed after 4 weeks of peritoneal rest after 3 weeks of dialysis. Peritoneal dialysis was performed twice a day with 25mL of 3.86% dextrose solution for 3 weeks. Peritonitis was induced by supplementing lipopolysaccharide(5 microgram/mL) in the dialysis fluid on days 8, 10 and 12 of peritoneal dialysis. Peritoneal equilibration tests were performed before dialysis and repeated on the 4th and 8th week of dialysis. Morphometric analysis of the peritoneal membrane and immunohistochemistry for collagen type I and type III were done in tissue specimens obtained at the time of sacrifice. The D/Do ratio for glucose at two hours in groups 2 and 3 at the beginning of week 4 were significantly lower than baseline value, indicating increase in the peritoneal penneability to glucose after 3 weeks of dialysis. D/Do in group 3 at the beginning of week 8, after 4 weeks of peritoneal rest, was significantly higher than at week 4. The drained dialysate volumes in groups 2 and 3 at week 4 were significantly lower than at baseline; however, The drained dialysate volume in group 3 at week 8 was significantly greater than at week 4. The thickness of the parietal peritoneal membraoe in group 2 and 3 were significantly greater than in group 1. Severity of the thickness of the parietal peritoneal membrane in group 3 was not much than that of group 2(group 1, 11.4+/-7.6; group 2, 37.5+/-18.4; group 3, 21.4+/-12.1 micromiter). Histologically, the thickened peritoneum in group 2 showed a monolayer of mesothelial cells and under-lying multilayer of curled collagen bundles. Mononuciear cells and fibroblasts were embedded in these collagen layers and capillary proliferation was present. Immunohistochemistry for collagen type I and Z demonstrated that the distribution of collagen type llI was richer than that of collagen l in group 2 at fibrotic area of submesothelial region. These findings were decreased in group 3. Ultrastructural examination of the peritoneum showed thicker fibrotic zone and the activated fibroblasts in group 2 compared to group 1 and 3. Meso-thelial cells were plump and the number of mesothelial microvilli was decreased in group 2. Nucleus was enlarged and irregular. Intracytoplasmic orga-nelles were also richer than those of group I or 3. In conclusion, peritoneal rest improves ultrafiltration in rats by decreasing the hyperpermeability of glucose and also reduces the degree of peritoneal fibrosis. These data suggest that dialysis-induced changes in peritoneal transport and morphology are reversible under the condition of peritoneal rest in this experimental model.
Animals ; Capillaries ; Collagen ; Collagen Type I ; Dialysis ; Fibroblasts ; Glucose ; Humans ; Immunohistochemistry ; Male ; Membranes ; Microvilli ; Models, Animal ; Models, Theoretical ; Patient Dropouts ; Peritoneal Dialysis ; Peritoneal Dialysis, Continuous Ambulatory* ; Peritoneal Fibrosis* ; Peritoneum ; Peritonitis ; Rabeprazole ; Rats* ; Ultrafiltration