To investigate the infection status of pigs with Cryptosporidium parvum, 589 fecal samples were collected from pigs raised at farm in Chungcheongbuk-do and Chungcheongnam-do. Of the 589 pig fecal samples, 62 (10.5%) were positive for C. parvum. The area showing the highest positive rate was Dangjin-gun, Chungcheongnam-do (14.0%), and the lowest (0%) Salmi-myon, Chungcheongbuk-do. The positive rate of C. parvum in Judok-eup increased from 12.7% in the winter to 22.1% in the summer. The results of this study suggest that the pigs may be a source of human C. parvum infection.
Animal Husbandry ; Animals ; Cryptosporidiosis/epidemiology/parasitology/*veterinary ; Cryptosporidium parvum/*isolation & purification ; Feces/parasitology ; Korea/epidemiology ; Parasite Egg Count ; Swine ; Swine Diseases/*epidemiology/*parasitology

The reservoir hosts of Thelazia callipaeda were examined. The eyes of the 76 dogs raised at farm, 78 military dogs (shepherds), 96 cattle, and 105 pigs were investigated for the presence of eyeworm. Among them, six worms of T. callipaeda were collected from two dogs raised at farm (2.7%), and 188 worms from 26 shepherds (33.5%). No worms were recovered from the cattle or pigs. These results suggest that the dogs, especially the military dogs are serving as a reservoir host of T. callipaeda. in Korea.
Animals ; Cattle ; Disease Reservoirs/*veterinary ; Dog Diseases/epidemiology/*parasitology ; Dogs ; Eye/parasitology ; Female ; *Host-Parasite Interactions ; Korea/epidemiology ; Male ; Prevalence ; Spirurida Infections/epidemiology/parasitology/*veterinary ; Swine ; Thelazioidea/*isolation & purification

Pneumocystis carinii causes serious pulmonary infection in immunosuppressed patients. This study was undertaken to observe the cytoskeletal proteins of P. carinii by immuno-electron microscopy. P. carinii infection was experimentally induced by immunosuppression of Sprague-Dawley rats for seven weeks, and their lungs were used for the observations of this study. The gold particles localized actin, tropomyosin, and tubulin. The actin was irregularly scattered in the cytoplasm of the trophic forms but was much more concentrated in the inner space of the cell wall of the cystic forms called the inner electron-lucent layer. No significant amount of tropomyosin was observed in either trophic forms or cystic forms. The tubulin was distributed along the peripheral cytoplasm and filopodia of both the trophic and cystic forms rather than in the inner side of the cytoplasm. Particularly, in the cystic forms, the amount of tubulin was increased and located mainly in the inner electron-lucent layer of the cell wall where the actin was concentrated as well. The results of this study showed that the cell wall of P. carinii cystic forms is a structure whose inner side is rich in actin and tubulin. The location of the actin and tubulin in P. carinii suggests that the main role of these proteins is an involvement in the protection of cystic forms from the outside environment by maintaining rigidity of the cystic forms.
Actins/analysis ; Animals ; Cytoskeletal Proteins/*analysis ; Fungal Proteins/*analysis ; Histocytochemistry ; Microscopy, Immunoelectron ; Pneumocystis/*chemistry/cytology ; Rats ; Rats, Wistar ; Support, Non-U.S. Gov't ; Tropomyosin/analysis ; Tubulin/analysis

Acute intermittent porphyria (AIP) is a rare disorder characterized biochemically by the increased excretion of porphyrins and porphyrin precursors, including delta-aminolevulinic acid (ALA) and porphobilinogen (PBG). AIP has variable clinical manifestations, such as acute abdominal pain, vomiting, nausea, constipation, peripheral neuropathy, seizures, tachycardia, and hypertension. A 16-year-old girl presented with recurrent abdominal pain, vomiting, hypertension, seizures, hypercholesterolemia, and red urine. AIP was confirmed by clinical features and increased 24-hour urine ALA and PBG. AIP should be considered in the differential diagnosis of patients who have abdominal pain, hypertension, and seizures when the results of all other tests are normal.
Abdominal Pain ; Adolescent ; Aminolevulinic Acid ; Constipation ; Diagnosis, Differential ; Humans ; Hypercholesterolemia ; Hypertension ; Nausea ; Peripheral Nervous System Diseases ; Porphobilinogen ; Porphyria, Acute Intermittent ; Porphyrins ; Seizures ; Tachycardia ; Vomiting

PURPOSE: Tumor necrosis factor-alpha (TNF-alpha) polymorphism has been suggested to play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) in obese adults, and known to be a mediator of insulin resistance. In this study, we evaluated the role of TNF-alpha promoter polymorphisms and insulin resistance in the development of NAFLD in obese children. METHODS: A total of 111 obese children (M:F=74:37; mean age, 11.1+/-2.0 yrs) were included. The children were divided into 3 groups: controls (group I, n=61), children with simple steatosis (group II, n=17), and children with non-alcoholic steatohepatitis (group III, n=33). Serum TNF-alpha levels, homeostasis model assessment of insulin resistance (HOMA-IR), and TNF-alpha -308 and -238 polymorphisms were evaluated. RESULTS: There were no differences in TNF-alpha polymorphism at the -308 or the -238 loci between group I and group II + III (p=0.134 and p=0.133). The medians of HOMA-IR were significantly different between group I and group II + III (p=0.001), with significant difference between group II and group III (p=0.007). No difference was observed in the HOMA-IR among the genotypes at the -308 locus (p=0.061) or the -238 locus (p=0.207) in obese children. CONCLUSION: TNF-alpha promoter polymorphisms at the -308 and -238 loci were not significantly associated with the development of NAFLD in children; nevertheless, insulin resistance remains a likely essential factor in the pathogenesis of NAFLD in obese children, especially in the progression to NASH.
Adult ; Child ; Fatty Liver ; Genotype ; Homeostasis ; Humans ; Insulin ; Insulin Resistance ; Obesity ; Tumor Necrosis Factor-alpha

This study was performed to analyze 6 day-term variations in bacterial communities contaminating the floor of two dry saunas that were operated at 64degrees C (low temp) and 76degrees C (high temp). Bacteria were sampled daily from the saunas for 6 days from Monday to Saturday. Genomic DNA was isolated directly from bacteria-collected cotton swabs. The diversity of the bacterial communities collected from the saunas was analyzed using thermal gradient gel electrophoresis (TGGE). The total numbers of DNA bands separated by TGGE for bacteria collected from the low temp and high temp sauna were 20 and 18, respectively, during the 6 days. Seven of 20 bacteria in the low temp sauna and eight of 18 bacteria in the high temp sauna were detected more than three times over the 6 experimental days. Twelve of the 26 bacterial genera contaminating the saunas were cross detected. Bacteria belonging to the genera Moraxella and Acinetobacter were selectively detected in the low temp sauna, whereas those belonging to Aquaspirillum, Chromobacterium, Aquabacterium, Gulbenkiania, Pelomonas, and Aquitalea were selectively detected in the high temp sauna. Three species of bacteria contaminating both the low and high temp saunas were thermophile or thermoduric. The results indicate that the sauna-contaminating bacteria may have been transferred from outside the saunas by user traffic but did not inhabit the saunas.
Acinetobacter ; Bacteria ; Chromobacterium ; DNA ; Electrophoresis ; Floors and Floorcoverings ; Moraxella ; Steam Bath

PURPOSE: This study was conducted to evaluate the role of adiponectin, leptin, and tumor necrosis factor-alpha (TNF-alpha) in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) in obese children, and to elucidatethe relationship between these adipokines and insulin resistance. METHODS: A total of 61 obese children (M : F=42 : 19, mean age 11.2+/-1.3 years) admitted to our facility between March 2004 and June 2005 were included in this study. Patients were divided into three groups based on their NAFLD status obese children without fatty liver (N=23); obese children with simple steatosis (N=20); and obese children with non-alcoholic steatohepatitis (NASH) (N=18). The serum levels of adiponectin, leptin, and TNF-alpha were measured, and insulin resistance determined by homeostasis model assessment (HOMA-IR) was calculated to estimate insulin resistance. In addition, the VSR (visceral-subcutaneous fat ratio) was estimated using abdominal computed tomography. RESULTS: There was no difference in serum TNF-alpha and leptin levels observed between the 3 groups (22.13+/-6.37 vs. 21.35+/-6.95 vs. 25.17+/-9.30; p=0.342 & 20.29+/-8.57 vs. 16.42+/-6.85 vs. 20.10+/-7.86; p=0.330). However, the serum adiponectin level was significantly lower in children with non-alcoholic steatohepatitis (NASH) than in the other two groups (6.08+/-1.38 in children without steatosis vs. 5.69+/-0.79 in simple steatosis vs. 4.93+/-1.75 in NASH; p=0.026). In addition, the VSR was significantly increased in the NASH group (0.31+/-0.08 vs. 0.32+/-0.11 vs. 0.47+/-0.14; p=0.001), and HOMA-IR revealed a significant difference among the three groups (4.77+/-3.67 vs. 6.89+/-7.05 vs. 10.42+/-6.73; p=0.000). However, there was no significant correlation observed between the adiponectin levels and the HOMA-IR or the VSR (r=-0.117; p=0.450 & r=-0.106; p=0.499). CONCLUSION: Insulin resistance may affect the development of hepatic steatosis and steatohepatitis in children, and the results of this study suggest that, of several adipokines evaluated, adiponectin is important in the progression of steatosis to steatohepatitis in obese children.
Adipokines* ; Adiponectin ; Adipose Tissue* ; Body Fat Distribution* ; Child* ; Fatty Liver* ; Homeostasis ; Humans ; Insulin Resistance* ; Insulin* ; Leptin ; Obesity ; Tumor Necrosis Factor-alpha

PURPOSE: This study was conducted to evaluate the role of adiponectin, leptin, and tumor necrosis factor-alpha (TNF-alpha) in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) in obese children, and to elucidatethe relationship between these adipokines and insulin resistance. METHODS: A total of 61 obese children (M : F=42 : 19, mean age 11.2+/-1.3 years) admitted to our facility between March 2004 and June 2005 were included in this study. Patients were divided into three groups based on their NAFLD status obese children without fatty liver (N=23); obese children with simple steatosis (N=20); and obese children with non-alcoholic steatohepatitis (NASH) (N=18). The serum levels of adiponectin, leptin, and TNF-alpha were measured, and insulin resistance determined by homeostasis model assessment (HOMA-IR) was calculated to estimate insulin resistance. In addition, the VSR (visceral-subcutaneous fat ratio) was estimated using abdominal computed tomography. RESULTS: There was no difference in serum TNF-alpha and leptin levels observed between the 3 groups (22.13+/-6.37 vs. 21.35+/-6.95 vs. 25.17+/-9.30; p=0.342 & 20.29+/-8.57 vs. 16.42+/-6.85 vs. 20.10+/-7.86; p=0.330). However, the serum adiponectin level was significantly lower in children with non-alcoholic steatohepatitis (NASH) than in the other two groups (6.08+/-1.38 in children without steatosis vs. 5.69+/-0.79 in simple steatosis vs. 4.93+/-1.75 in NASH; p=0.026). In addition, the VSR was significantly increased in the NASH group (0.31+/-0.08 vs. 0.32+/-0.11 vs. 0.47+/-0.14; p=0.001), and HOMA-IR revealed a significant difference among the three groups (4.77+/-3.67 vs. 6.89+/-7.05 vs. 10.42+/-6.73; p=0.000). However, there was no significant correlation observed between the adiponectin levels and the HOMA-IR or the VSR (r=-0.117; p=0.450 & r=-0.106; p=0.499). CONCLUSION: Insulin resistance may affect the development of hepatic steatosis and steatohepatitis in children, and the results of this study suggest that, of several adipokines evaluated, adiponectin is important in the progression of steatosis to steatohepatitis in obese children.
Adipokines* ; Adiponectin ; Adipose Tissue* ; Body Fat Distribution* ; Child* ; Fatty Liver* ; Homeostasis ; Humans ; Insulin Resistance* ; Insulin* ; Leptin ; Obesity ; Tumor Necrosis Factor-alpha

PURPOSE: Henoch-Schonlein purpura (HSP) is a systemic vasculitis involving the skin, joints, gastrointestinal tract, and kidney. Although the pathogenesis of HSP is still unclear, tumor necrosis factor (TNF-alpha) is regarded as an important cytokine contributing to the disease. The goal of this study was to determine the role of TNF-alpha in the pathogenesis of HSP, and to evaluate the TNF-alpha polymorphism for genetic susceptibility to HSP. METHODS: From March 2004 to November 2005, 40 children with HSP and 32 healthy controls were included. Serum TNF-alpha levels were measured using the ELISA method during the acute and convalescent phase of HSP. The genotypic and allelic frequencies of the TNF-alpha gene polymorphisms at positions -308 and -238 were evaluated in patients and controls. RESULTS: Serum TNF-alpha levels were 23.17+/-11.31 pg/mL in the acute phase of children with HSP and 10.56+/-5.59 pg/mL in the convalescent phase (p=0.000). There was no significant correlation between the serum TNF-alpha levels and the clinical scores of HSP (r=0.310, p=0.070). The genotypic frequency of the TNF-alpha - 308 polymorphism in children with HSP was not significantly different compared to healthy controls (GG 80%, GA 20% vs. GG 93.8%, GA 6.2%; p=0.094). The genotypic frequency of the TNF-alpha -238 polymorphism in children with HSP was not significantly different (GG 97.5%, GA 2.5% vs. GG 93.8%, GA 6.3%; p=0.429). CONCLUSION: TNF-alpha is assumed to be the main cytokine associated with the pathogenesis of HSP during the acute phase. However, the presence of TNF-alpha gene polymorphisms at positions -308 and -238 did not distinguish children with HSP from normal controls.
Child* ; Enzyme-Linked Immunosorbent Assay ; Gastrointestinal Tract ; Genetic Predisposition to Disease ; Humans ; Joints ; Kidney ; Purpura, Schoenlein-Henoch* ; Skin ; Systemic Vasculitis ; Tumor Necrosis Factor-alpha*

PURPOSE: The resistance of H. pylori to clarithromycin is one of the major causes of eradication failure. In H. pylori, clarithromycin resistance is due to point mutation in 23S rRNA. The aims of this study were to investigate the mutation of 23S rRNA and to examine the association of cagA, vacA genotype and clarithromycin resistant genes. METHODS: H. pylori DNA was extracted from antral biopsy specimens from 27 children with H. pylori infection. Specific polymerase chain reaction (PCR) assays were used for cagA and vacA. Mutations associated with clarithromycin resistance were detected by using PCR restriction fragment length polymorphism (RFLP) analysis of 23S rRNA gene. RESULTS: A2143G mutation was detected in one case and A2144G in 4, indicating 18.5% were clarithromycin resistant. Among the total of 27, cagA was present in 25 (93%), vacA s1a/m1 in 6 (22%), s1a/m2 in 3 (11%), s1c/m1 in 16 (59%), and s1c/m2 in 1 (4%). All of the 5 clarithromycin resistant strains were cagA (+), among which 2 were s1a/m1 and 2 were s1c/m1. There was no relation between genotypes and clarithromycin resistant genes. CONCLUSION: Detection of H. pylori resistance to clarithromycin using PCR RFLP from biopsy specimens might be useful for the selection of antibiotics. Clarithromycin resistant genes are not associated with genotypes of cagA and vacA.
Anti-Bacterial Agents ; Biopsy ; Child* ; Clarithromycin* ; DNA ; Genes, rRNA ; Genotype ; Helicobacter pylori* ; Helicobacter* ; Humans ; Point Mutation ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length