No abstract available.
Intussusception*

BACKGROUND: The basal ganglia plays a major role in regulating motor, cognitive and emotional functions. In addition, it has been proposed that the functions of the basal ganglia is also related to control of sensory discrimination and sensorimotor integration. One possible way to test this hypothesis would be to investigate sensory functions in patients with various diseases affecting basal ganglia functions. Since idiopathic Parkinson's disease (IPD) is caused by selective impairment of basal ganglia functions, it could be a good model for this purpose. METHODS: We measured the grating resolution threshold (GRT) using the JVP (Johnson-Van Boven-Phillips) dome in 52 patients with IPD and 25 age-matched healthy controls. Statistical analysis employed unpaired t-test, paired t-test and simple regression analysis. P-values less than 0.05 were considered as significant. RESULTS: Patients showed significantly higher GRT than controls (3.07 +/- 0.74 vs 2.03 +/- 0.80; p<0.05). In patients, the mean GRT was not different between symptomatically dominant and non-dominant hands (3.10 +/- 0.95 vs 2.93 +/- 0.82). In the patients with hemiparkinsonism, GRT was also significantly higher in asymptomatic hands compared with controls (3.00 +/- 0.71 vs 2.03 +/- 0.80; p<0.05). The severity of sensory dysfunction in patients was not correlated with symptom duration or to symptom severity, measured by the modified Columbia rating scale (MCRS). CONCLUSIONS: The present results demonstrate that spatial discrimination is impaired in IPD, suggesting the basal ganglia plays a role in sensory regulation.
Basal Ganglia ; Discrimination (Psychology)* ; Dopamine ; Hand ; Humans ; Parkinson Disease* ; Regression Analysis ; Sensation

PURPOSE: To determine (1) the relationship between the cortical defects seen on 99 mTc-DMSA renal scans and age, and (2) the presence and degree of vesicoureteral reflux, and then to depict the risk factors for cortical defects in children with acute urinary tract infection (UTI). Furthermore, to assess the diagnostic value of VCUG in predicting a defect on 99 mTc-DMSA renal scans. MATERIALS AND METHODS: We studied 134 kidneys in 67 children aged 15 days-10 years (M:F=39:28) in whom symptomatic UTI was present. In all these children, both DMSA renal scans and voiding cystourethrography (VCUG) were performed. Scanning took place within 7 days of diagnosis and VCUG was performed after one month of diagnosis. Scintigraphic findings were graded according to the extent and number of cortical defects. We evaluated the relationships between the cortical defects seen on DMSA scans and age, and the grade of vesicoureteral reflux. The diagnostic value of VCUG in predicting cortical defects was analysed. Results: The prevalence of cortical defects was greater in patients older than two years (38/54, 70%) than in those aged less than two (38/80, 48%). The frequency of cortical defects was related to vesicoureteral reflux (p<0.05) and grade of reflux (p<0.05). As this latter increased, the extent of cortical defects also increased (p<0.05), and DMSA scans revealed the presence of these in 76 of the 134 kidneys (57%) with acute UTI. In 30 of these 76 (39.5%), VCUG demonstrated the presence of vesicoureteral reflex. On the other hand, vesi-coureteral reflex was found in 36 of the 134 kidneys (27%), and in 30 of these 36 (83%), cortical defects were noted. The sensitivity of VCUG in predicting cortical defect was 39.5%, while specificity was 89.7%. The positive predictive value for defects was 83.3%, and the negative predictive value was 53.1%. The relative risk of cortical defect in the presence of vesicoureteral reflux was 1.78. CONCLUSION: Renal cortical defects are significantly related to age and grade of vesicoureteral reflux. Risk factors for developing cortical defects were older age (> or =2yrs) at the time of acute UTI, and high grade of vesicoureteral reflux. The specificity of VCUG in predicting cortical defects is relatively high but the sensitivitiy is low, and a significant proportion of cortical defects therefore occurred in the absence of vesicoureteral reflux.
Child* ; Diagnosis ; Hand ; Humans ; Kidney ; Prevalence ; Radionuclide Imaging* ; Reflex ; Risk Factors* ; Sensitivity and Specificity ; Succimer* ; Urinary Tract Infections* ; Urinary Tract* ; Vesico-Ureteral Reflux

PURPOSE: To investigate the influence of 2 phases of short interval intracortical inhibition (SICI) on the cortical silent period (SP). MATERIALS AND METHODS: Single- and paired-pulse transcranial magnetic stimulations (TMSs) at 1 and 2.5ms interstimulus intervals (ISIs) were applied to the left motor cortex in 12 healthy subjects while their right hand muscles were moderately activated. Conditioning stimulation intensity was 90% of the active motor threshold (AMT). Test stimulation intensities were 120, 140, 160, 180, 200, 220, 240, 260% of the AMT and at 100% of the maximal stimulator output, the order of which was arranged randomly. The rectified electromyography area of motor evoked potential (MEP) and duration of the SP were measured off-line using a computerized program. RESULTS: At high-test stimulation intensities, MEP areas were saturated in both single- and paired-pulse stimulations, except that saturated MEPs were smaller for the paired-pulse TMS at 1ms ISI than for the other conditions. As the test stimulation intensity increased, SP was progressively prolonged in both single- and paired-pulse stimulations but was shorter in paired-pulse than single-pulse TMS. Overall, the ratio of SP duration/MEP area was comparable between single- and paired-pulse TMS except for the paired-pulse TMS at 1 ms ISI with a test stimulation intensity at 140-180% of the AMT, in which the ratio was significantly higher than in the single pulse TMS. CONCLUSION: These results suggest that 2 phases of SICI modulate MEP saturation and SP duration differently and provide additional evidence supporting the view that 2 phases of SICI are mediated by different inhibitory mechanisms.
Adult ; Evoked Potentials, Motor/*physiology ; Female ; Humans ; Male ; Motor Cortex/*physiology ; Transcranial Magnetic Stimulation

This study was performed to investigate the in vitro proliferation and migration of rabbit auricular chondrocytes into the various sized pore of PLLA and PLGA scaffolds. The chondrocytes were harvested, expanded, and seeded onto PLGA(50 : 50, 75 : 25, 85 : 15) and PLLA scaffold having either small(50 - 100 micrometer) or large(300 - 350 micrometer) pores. On the 4th and 8th week after culture, histologic observation and quantitative DNA assay were done. We noted that the largest amount of DNA was found in the 85 : 15 PLGA sponges than others, and in the 4th and 8th week, some amount of DNA was detected in the lower portion of 85 : 15 PLGA sponge only, and DNA amounts were increased during the culture period in the 85 : 15 PLGA, significantly. We also found that the numbers of cells were low in middle portion of scaffolds, and in large pore-sized group of 85 : 15 PLGA, there were many cells in the lower portion of the scaffolds more than that of small pore group. In conclusion, the pore size of the scaffold for chondrocyte culture is important for cell migration and proliferation, and PLGA, especially 85 : 15 PLGA with 300- 350 micrometer sized pore is the more suitable biomatrix for proliferation and migration of the chondrocytes.
Cell Movement ; Chondrocytes* ; DNA ; Porifera

PURPOSE: To report a case of endogenous endophthalmitis due to Aeromonas hydrophila in a patient with distal common bile duct carcinoma and biliary sepsis. METHODS: A 72-year-old woman with distal common bile duct carcinoma, obstructive jaundice, diabetes mellitus, and hypertension had a 1-day history of blurred vision, redness, and eye discharges in the right eye. An ophthalmic examination showed no light perception vision, increased intraocular pressure, severe corneal edema, severe anterior chamber reaction, exudative membranes on the anterior lens surface, and severe vitreal reaction. There was no ocular history of trauma, infection, or surgery in either eye. RESULTS: Under the impression of endogenous bacterial endophthalmitis, immediate intraocular cultures and intravitreal antibiotic injections were performed, but the anterior chamber reaction, and the ultrasonogram findings were deteriorated. Evisceration was undertakened because of extrusion of the intraocular contents, and Aeromonas hydrophila was isolated by intraocular culture. CONCLUSIONS: Endogenous endophthalmitis due to Aeromonas hydrophila is rare, but has a rapid clinical course and a poor prognosis, despite of prompt diagnosis and management.
Vitreous Body ; Ultrasonography ; Treatment Failure ; Tomography, X-Ray Computed ; Injections ; *Immunocompromised Host ; Humans ; *Gram-Negative Bacterial Infections/drug therapy ; Female ; Eye Evisceration ; Endophthalmitis/diagnosis/*microbiology/pathology ; Anti-Bacterial Agents/administration & dosage/therapeutic use ; Aged ; *Aeromonas hydrophila

Naegleria fowleri, a brain-eating amoeba, thrives in lakes and rivers with aquatic vegetation and causes primary amoebic meningoencephalitis (PAM) in humans. Most recently, it has become such a serious problem that N. fowleri was detected in tap water in Houston, USA. Several pathogenic factors are considered very important to destroy target cells in the brain. In particular, the food-cup where N. fowleri antigen-1 (Nfa1) is located, is strongly expressed in pseudopodia involved in the movement of N. fowleri, and is involved in phagocytosis by attaching to target cells. In this article, we reviewed the role of the Nfa1 protein and its associated pathogenicity. The nfa1 gene was cloned by cDNA library immunoscreening using infection serum and immune serum. Nfa1 protein is mainly distributed in pseudopodia important to movement and vacuoles. Moreover, heat shock protein 70, cathepsin-like proteare and Nf-actin are also associated with pseudopodia in which Nfa1 is localized. Interestingly, the amount of the nfa1 gene changed as N. fowleri trophozoites transformed into cysts. Polyclonal antiserum against Nfa1 showed a protective effect against cytotoxicity of approximately 19.7%. Nfa1-specific IgA antibodies prevent N. fowleri trophozoites from adhering to the nasal mucosa, delaying invasion. The nfa1-vaccinated mice showed significantly higher levels of Nfa1-specific antibody. The duration of anti-Nfa1 IgG in the vaccinated mice lasted 12 weeks, strongly suggesting that nfa1 is a significant pathogenic gene and that Nfa1 is a pathogenic protein. Several factors related to pseudopodia and locomotion have been linked to Nfa1. A clearer function of N. fowleri targeting nfa1 with other genes might enable target-based inhibition of N. fowleri pathogenicity.

Naegleria fowleri, a brain-eating amoeba, thrives in lakes and rivers with aquatic vegetation and causes primary amoebic meningoencephalitis (PAM) in humans. Most recently, it has become such a serious problem that N. fowleri was detected in tap water in Houston, USA. Several pathogenic factors are considered very important to destroy target cells in the brain. In particular, the food-cup where N. fowleri antigen-1 (Nfa1) is located, is strongly expressed in pseudopodia involved in the movement of N. fowleri, and is involved in phagocytosis by attaching to target cells. In this article, we reviewed the role of the Nfa1 protein and its associated pathogenicity. The nfa1 gene was cloned by cDNA library immunoscreening using infection serum and immune serum. Nfa1 protein is mainly distributed in pseudopodia important to movement and vacuoles. Moreover, heat shock protein 70, cathepsin-like proteare and Nf-actin are also associated with pseudopodia in which Nfa1 is localized. Interestingly, the amount of the nfa1 gene changed as N. fowleri trophozoites transformed into cysts. Polyclonal antiserum against Nfa1 showed a protective effect against cytotoxicity of approximately 19.7%. Nfa1-specific IgA antibodies prevent N. fowleri trophozoites from adhering to the nasal mucosa, delaying invasion. The nfa1-vaccinated mice showed significantly higher levels of Nfa1-specific antibody. The duration of anti-Nfa1 IgG in the vaccinated mice lasted 12 weeks, strongly suggesting that nfa1 is a significant pathogenic gene and that Nfa1 is a pathogenic protein. Several factors related to pseudopodia and locomotion have been linked to Nfa1. A clearer function of N. fowleri targeting nfa1 with other genes might enable target-based inhibition of N. fowleri pathogenicity.

Naegleria fowleri, a brain-eating amoeba, thrives in lakes and rivers with aquatic vegetation and causes primary amoebic meningoencephalitis (PAM) in humans. Most recently, it has become such a serious problem that N. fowleri was detected in tap water in Houston, USA. Several pathogenic factors are considered very important to destroy target cells in the brain. In particular, the food-cup where N. fowleri antigen-1 (Nfa1) is located, is strongly expressed in pseudopodia involved in the movement of N. fowleri, and is involved in phagocytosis by attaching to target cells. In this article, we reviewed the role of the Nfa1 protein and its associated pathogenicity. The nfa1 gene was cloned by cDNA library immunoscreening using infection serum and immune serum. Nfa1 protein is mainly distributed in pseudopodia important to movement and vacuoles. Moreover, heat shock protein 70, cathepsin-like proteare and Nf-actin are also associated with pseudopodia in which Nfa1 is localized. Interestingly, the amount of the nfa1 gene changed as N. fowleri trophozoites transformed into cysts. Polyclonal antiserum against Nfa1 showed a protective effect against cytotoxicity of approximately 19.7%. Nfa1-specific IgA antibodies prevent N. fowleri trophozoites from adhering to the nasal mucosa, delaying invasion. The nfa1-vaccinated mice showed significantly higher levels of Nfa1-specific antibody. The duration of anti-Nfa1 IgG in the vaccinated mice lasted 12 weeks, strongly suggesting that nfa1 is a significant pathogenic gene and that Nfa1 is a pathogenic protein. Several factors related to pseudopodia and locomotion have been linked to Nfa1. A clearer function of N. fowleri targeting nfa1 with other genes might enable target-based inhibition of N. fowleri pathogenicity.

Naegleria fowleri, a brain-eating amoeba, thrives in lakes and rivers with aquatic vegetation and causes primary amoebic meningoencephalitis (PAM) in humans. Most recently, it has become such a serious problem that N. fowleri was detected in tap water in Houston, USA. Several pathogenic factors are considered very important to destroy target cells in the brain. In particular, the food-cup where N. fowleri antigen-1 (Nfa1) is located, is strongly expressed in pseudopodia involved in the movement of N. fowleri, and is involved in phagocytosis by attaching to target cells. In this article, we reviewed the role of the Nfa1 protein and its associated pathogenicity. The nfa1 gene was cloned by cDNA library immunoscreening using infection serum and immune serum. Nfa1 protein is mainly distributed in pseudopodia important to movement and vacuoles. Moreover, heat shock protein 70, cathepsin-like proteare and Nf-actin are also associated with pseudopodia in which Nfa1 is localized. Interestingly, the amount of the nfa1 gene changed as N. fowleri trophozoites transformed into cysts. Polyclonal antiserum against Nfa1 showed a protective effect against cytotoxicity of approximately 19.7%. Nfa1-specific IgA antibodies prevent N. fowleri trophozoites from adhering to the nasal mucosa, delaying invasion. The nfa1-vaccinated mice showed significantly higher levels of Nfa1-specific antibody. The duration of anti-Nfa1 IgG in the vaccinated mice lasted 12 weeks, strongly suggesting that nfa1 is a significant pathogenic gene and that Nfa1 is a pathogenic protein. Several factors related to pseudopodia and locomotion have been linked to Nfa1. A clearer function of N. fowleri targeting nfa1 with other genes might enable target-based inhibition of N. fowleri pathogenicity.