This study was performed to observe the present status of intestinal parasitic infections in a remote island, Yondo, located in southern part of Jeonranam-do(province), Korea. In February and May 1988, total 1,011 individual stool samples were collected and examined for intestinal helminths and protozoa using formalin-ether centrifugal sedimentation technique. The results are summarized as follows: Of 1,011 ingabitants examined, 398(39.4%) were positive for intestinal parasites. Helminth positives were 372(36.8%), and protozoan cyst positives were 56(5.5%). Ten species of parasites were found. Trichuris trichiura revealed the highest infection rate of 27.5%, Ascaris lumbricoides 17.4%, Taenia sp. 5.8%, Entamoeba coli 3.3%, Giardia lamblia 1.5%, Endolimax nana 0.8%, Hymenolepis nana 0.4%, hookworm 0.2%, Trichostrongylus orientalis 0.2%, and Entamoeba histolytica 0.2%, respectively. The female group showed higher positive rate (44.0%) than males (34.7%). Also, higher positive rates were observed among adults as compared with the group younger than 10 years old. Average value of E.P.G. was 1,876(range 200-17,800) in A. lumbricoides positives, and 327(range 200-1,600) in T. trichiura positive cases. In helminth egg positive cases, single infection was 63.4%, double infection 34.7%, and triple infection 1.9%, respectively. Among protozoan cyst positives, single infection was 94.6%, and double infection was 5.4%. The present study revealed that the prevalence of intestinal parasites among inhabitants in Yondo island is still so high that special control measures should be performed.
parasitology-helminth-trematoda ; cestoda-nematoda-protozoa ; epidemiology ; Ascaris lumbricoides ; Taenia sp. ; Entamoeba coli ; Giardia lamblia ; Endolimax nana ; hookworm ; Trichostrongylus orientalis ; Entamoeba histolytica

With 4-Channel Nicolet-CA 1000 clinical averager, somatosensory evoked potentials(SSEP) and brainstem auditory evoked potentials(BAEP) were studied in 40 patients with intracerebral hematoma and 40 patients with cerebral infarction. SSEP was more sensitive response in putamen(20/23) or thalamic(6/7) hemorrhage and infarction of middle cerebral artery territory(13/28). in contrast BAEP was high percentage in abnormality in brainstem or cerebellar lesion. Cortical wave(N18) was usually not traceable in large size of hematoma or having midline shift in brain CT scan. There was close correlation between the severity of motor weakness and abnormality of SSEP. The best neurological outcome was found in the patients of P24 wave formation. In our results, SSEP and BAEP seemed to be very useful for evaluation of stroke patients.
Brain ; Brain Stem ; Cerebral Infarction ; Evoked Potentials* ; Hematoma ; Hemorrhage ; Humans ; Infarction ; Middle Cerebral Artery ; Stroke ; Tomography, X-Ray Computed

PURPOSE: Medullary sponge kidney (MSK) is a rare congenital disease characterized by diffuse ectasia or dilatation of precalyceal collecting tubules. MSK incidence and prevalence in the general population is uncertain and only a few patients are reported especially in the pediatric age. There has been increasing reports of patients with MSK who have other malformative disorders. Also several case reports concerning about etiological association of some genes. METHODS: Collaborative study through nation-wide survey was done to investigate the incidence and etiological association of some genes such as GDNF gene, ATP6V1B1, ATP6V0A4 gene in developing MSK in Korean children. RESULTS: Four cases of MSK who have various other malformative disorders were collected. There are no mutations of GDNF gene, ATP6V1B1, ATP6V0A4 gene in all patients. CONCLUSION: MSK is one of the very rare diseases in pediatric age. The etiological association of GDNF gene , ATP6V1B1, ATP6V0A4 gene in developing MSK in Korean children is not proved.
Child ; Dilatation ; Dilatation, Pathologic ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Incidence ; Medullary Sponge Kidney ; Prevalence ; Rare Diseases

PURPOSE: To determine whether there is a discrepancy between the medical professions perception of what patients should know and that of the patients themselves, we studied patients need to be informed about different aspects of epilepsy and compared findings with medical personnels perceptions of the issue. METHODS: Our study population consisted of 39 patients with epilepsy from the inpatient epilepsy unit, and 51patients from the outpatients clinic of the S. University Hospital between July and November 1997. However, the patients who declined to participate or who were not able to understand the directions and content of the questionnaire were excluded. The medical personnel participated in this study were 56 residents or nurses who were working in either Neurology or Neuro surgery Units. The questionnaire consisted of 6 categories with a total of 79 questions. The responses were indicated on a 5point Likert scale with 5 indicating the highest need . The data were analyzed with descriptive statistics, students t-tests, and chi-square. RESULTS: Of the 90 patients and 56 medical personnel studied, the need for lifestyle information such as smoking, drinking, sleep, driving, employment, and marriage was significantly higher from medical personnel than that of the patients(p=0.00). Regarding medical knowledge about epilepsy, the patients group had higher scores in the need for information on the structure of the brain (p=0.00), whereas medical personnel had higher scores on the symptoms of epilepsy. There was no correlation between the length of epilepsy and the need for information on every item on the questionnaire. The patients had higher rank regarding diet, although it was not significantly different from the medical personnel. Regarding antiepileptic drugs and what to do when there is an attack, medical personnel scored higher. The items on which the patients group scored higher than 4.5 were the possibility of inheritance, the factors that might reduce the number of attacks, the period of usage of AED, and the food they have to avoid or the food they have to take to reduce seizure attacks. CONCLUSIONS: Our study indicates that the patients group requires higher educational need in the structure of the brain, diet, and surgical treatment, but less in lifestyles and what to do when there is an attack. The educational program for the patients with epilepsy should emphasize medical knowledge with regard to brain anatomy, what to eat and what to avoid, and details of surgical treatment.
Anticonvulsants ; Brain ; Diet ; Drinking ; Employment ; Epilepsy* ; Humans ; Inpatients ; Life Style ; Marriage ; Neurology ; Outpatients ; Surveys and Questionnaires ; Seizures ; Smoke ; Smoking ; Wills

Two endocrine active pituitary microadenomas were treated by transsphenoidal microsurgery and evaluated endocrinologically by radioimmunoassay of hormones. They showed significant rise of serum human growth hormone(HGH) after thyrotrophine releasing hormone(TRH) administration and no suppression by oral glucose tolerance test(GTT) before operation. Pathologic findings are acidophilic adenomas.
Adenoma, Acidophil ; Glucose Tolerance Test ; Humans ; Microsurgery ; Radioimmunoassay ; Thyrotropin

BACKGROUND: The efficacy of dialysis on the autonomic and peripheral nerve function has been a subject of considerable debate. In addition, no longitudinal study on the course of uremic neuropathy in end-stage renal disease (ESRD) during dialysis has been reported. We carried out a prospective study to investigate the effect of dialysis on the autonomic and peripheral nerve function during the first 12 months of dialysis. METHODS: Twenty-five patients with ESRD (14 on HD and 11 on CAPD; 11 diabetic and 14 non- diabetic) were enrolled. Autonomic nerve function test and median nerve conduction velocity study were done at the initiation of dialysis and then repeated after 12 months of dialysis. RESULTS: At the initiation of dialysis, sympathetic nerve function and parasympathetic nerve function were abnormal in all HD and CAPD patients. After 12 months of dialysis, no significant changes occurred in autonomic function test. There was no significant difference in autonomic function test between HD and CAPD patients. There was no significant difference in median nerve conduction velocity between HD and CAPD patients after 12 months of dialysis. At the initiation of dialysis, 6 of 11 diabetic and 4 of 14 non-diabetic patients had abnormal median nerve conduction velocity. After 12 months of dialysis, normalization of median nerve conduction velocity occurred only in 3 non-diabetic patients. There was a singinficant difference in median nerve conduction velocity between diabetic and non-diabetic patients after 12 months of dialysis. CONCLUSION: We conclude that dialysis does not significantly alter the autonomic nerve function during the first 12 months of dialysis, but may improve the peripheral nerve function in non-diabetic uremic patients.
Autonomic Pathways ; Dialysis* ; Humans ; Kidney Failure, Chronic* ; Longitudinal Studies ; Median Nerve ; Peripheral Nerves* ; Peritoneal Dialysis, Continuous Ambulatory ; Prospective Studies

Aberrant expression of BORIS/CTCFL (Brother of the Regulator of Imprinted Sites/CTCF-like protein) is reported in different malignancies. In this study, we characterized the entire promoter region of BORIS/CTCFL, including the CpG islands, to assess the relationship between BORIS expression and lung cancer. To simplify the construction of luciferase reporter cassettes with various-sized portions of the upstream region, genomic copies of BORIS were isolated using TAR cloning technology. We analyzed three promoter blocks: the GATA/CCAAT box, the CpG islands and the minisatellite region BORIS-MS2. Polymorphic minisatellite sequences were isolated from genomic DNA prepared from the blood of controls and cases. Of the three promoter blocks, the GATA/CCAAT box was determined to be a critical element of the core promoter, while the CpG islands and the BORIS-MS2 minisatellite region were found to act as regulators. Interestingly, the polymorphic minisatellite region BORIS-MS2 was identified as a negative regulator that repressed the expression levels of luciferase reporter cassettes less effectively in cancer cells compared with normal cells. We also examined the association between the size of BORIS-MS2 and lung cancer in a case–control study with 590 controls and 206 lung cancer cases. Rare alleles of BORIS-MS2 were associated with a statistically significantly increased risk of lung cancer (odds ratio, 2.04; 95% confidence interval, 1.02–4.08; and P=0.039). To conclude, our data provide information on the organization of the BORIS promoter region and gene regulation in normal and cancer cells. In addition, we propose that specific alleles of the BORIS-MS2 region could be used to identify the risk for lung cancer.
Alleles ; Clone Cells ; Cloning, Organism ; CpG Islands ; DNA ; Gene Expression* ; Luciferases ; Lung Neoplasms* ; Lung* ; Minisatellite Repeats* ; Promoter Regions, Genetic

Parkinson's disease is a neurodegenerative disease characterized by the progressive loss of dopaminergic neurons within the substantia nigra pars compacta. In the present study, we investigated whether β-Lapachone (β-LAP), a natural naphthoquinone compound isolated from the lapacho tree (Tabebuia avellanedae), elicits neuroprotective effects in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease mouse model. β-LAP reduced the tyrosine hydroxylase (TH)-immuno-reactive fiber loss induced by MPTP in the dorsolateral striatum, and alleviated motor dysfunction as determined by the rotarod test. In addition, β-LAP protected against MPTP-induced loss of TH positive neurons, and upregulated B-cell lymphoma 2 protein (Bcl-2) expression in the substantia nigra. Based on previous reports on the neuroprotective role of nuclear factor-E2-related factor-2 (Nrf2) in neurodegenerative diseases, we investigated whether β-LAP induces upregulation of the Nrf2-hemeoxygenae-1 (HO-1) signaling pathway molecules in MPTP-injected mouse brains. Western blot and immunohistochemical analyses indicated that β-LAP increased HO-1 expression in glial fibrillary acidic protein-positive astrocytes. Moreover, β-LAP increased the nuclear translocation and DNA binding activity of Nrf2, and the phosphorylation of upstream adenosine monophosphate-activated protein kinase (AMPK). β-LAP also increased the localization of p-AMPK and Nrf2 in astrocytes. Collectively, our data suggest that β-LAP exerts neuroprotective effect in MPTP-injected mice by upregulating the p-AMPK/Nrf2/HO-1 signaling pathways in astrocytes.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Adenosine ; Animals ; Astrocytes ; Blotting, Western ; Brain ; DNA ; Dopaminergic Neurons ; Lymphoma, B-Cell ; Mice ; Neurodegenerative Diseases ; Neurons ; Neuroprotection ; Neuroprotective Agents ; Parkinson Disease ; Pars Compacta ; Phosphorylation ; Protein Kinases ; Rotarod Performance Test ; Substantia Nigra ; Trees ; Tyrosine 3-Monooxygenase ; Up-Regulation

Microglial priming is the process of microglial proliferation and activation in response to neurodegeneration and abnormal protein accumulation. Priming makes microglia susceptible to secondary inflammatory stimuli and causes exaggerated inflammatory responses. In the present study, we established a microglial priming model in mice by administering a single injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 20 mg/kg). MPTP induced microglial activation without dopaminergic degeneration;however, subsequent treatment with a sub-toxic dose of lipopolysaccharides (LPS) induced an amplified inflammatory response and caused nigrostriatal dopaminergic degeneration. These pathological and inflammatory changes, including microglial activation and dopaminergic cell loss in the substantia nigra (SN) area were reversed by papaverine (PAP) administration. In addition, MPTP/LPS enhanced interleukin-1β (IL-1β) expression and processing via nod-like receptor protein 3 (NLRP3) inflammasome activation in the SN region of mice. However, PAP treatment suppressed inflammasome activation and subsequent IL-1β maturation. Moreover, PAP inhibited nuclear factor-κB (NF-κB) and enhanced cAMP-response element binding protein (CREB) activity in the SN of MPTP/LPS mice. These results suggest that PAP inhibits the activation of NLRP3 inflammasome by modulating NF-κB and CREB signaling pathways, which results in reduced microglial activation and neuronal cell death. Thus, PAP may be a potential candidate for the treatment of Parkinsons’s disease, which is aggravated by systemic inflammation.

Microglial priming is the process of microglial proliferation and activation in response to neurodegeneration and abnormal protein accumulation. Priming makes microglia susceptible to secondary inflammatory stimuli and causes exaggerated inflammatory responses. In the present study, we established a microglial priming model in mice by administering a single injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 20 mg/kg). MPTP induced microglial activation without dopaminergic degeneration;however, subsequent treatment with a sub-toxic dose of lipopolysaccharides (LPS) induced an amplified inflammatory response and caused nigrostriatal dopaminergic degeneration. These pathological and inflammatory changes, including microglial activation and dopaminergic cell loss in the substantia nigra (SN) area were reversed by papaverine (PAP) administration. In addition, MPTP/LPS enhanced interleukin-1β (IL-1β) expression and processing via nod-like receptor protein 3 (NLRP3) inflammasome activation in the SN region of mice. However, PAP treatment suppressed inflammasome activation and subsequent IL-1β maturation. Moreover, PAP inhibited nuclear factor-κB (NF-κB) and enhanced cAMP-response element binding protein (CREB) activity in the SN of MPTP/LPS mice. These results suggest that PAP inhibits the activation of NLRP3 inflammasome by modulating NF-κB and CREB signaling pathways, which results in reduced microglial activation and neuronal cell death. Thus, PAP may be a potential candidate for the treatment of Parkinsons’s disease, which is aggravated by systemic inflammation.