OBJECTIVES: A different sequence change, in the mitochondrial tRNA gene, has been proposed as a candidate mutation in the sensorineurnal hearing loss. The purpose of current study is to identify the association between the noise-induced sensorineurnal hearing loss and the A to G mutation at nucleotide 3243 of mitochondrial DNA. METHODS: Subjects were established by history and chart review, and audiological and clinical data were obtained. Blood was sampled from 101 controls, 50 noise-induced hearing loss, and 12 sensorineural deafness. The DNA of these individuals was extracted, and mitochondrial genome was analyzed by polymerase chain reaction. Subsequently, the coding sequence of mitochondrial genome was sequenced, and compared to the normal sequence, and all sequence variations were analyzed by restriction endonuclease ApaI. RESULTS: Mitochondrial DNA mutation (3243A->G) was not detected by polymerase chain reaction (PCR) in any patients with noise-induced hearing loss, sensorineural hearing loss, and normal control without hearing loss in Koreans. The DNA sequencing of PCR products did not revealed an A to G substitution at nucleotide 3243 of mitochondrial DNA. CONCLUSIONS: The noise-induced sensorineural hearing loss was not associated with mitochondrial DNA mutation (3243A->G)
Clinical Coding ; Deafness ; DNA ; DNA Restriction Enzymes ; DNA, Mitochondrial* ; Genome, Mitochondrial ; Hearing Loss ; Hearing Loss, Noise-Induced ; Hearing Loss, Sensorineural* ; Humans ; Polymerase Chain Reaction ; RNA, Transfer ; Sequence Analysis, DNA

No abstract available.
Histiocytoma*

Adenosquamous cell carcinoma (Ad-SCC) of the colon is rare. The pathogenesis of Ad-SCC is unclear, however, several hypotheses have been suggested. The clinical presentation and gross findings of Ad-SCC of the colon are similar to those of adenocarcinoma of the colon, but Ad-SCC has a more aggressive clinical course and a poorer prognosis. We report on two cases of Ad-SCC of the colon with obstruction; a collision-type Ad-SCC that has not only obstruction but also numerous hepatic metastases, and a composite-type Ad-SCC treated with left hemicolectomy followed by an adjuvant chemotherapy.
Adenocarcinoma ; Carcinoma, Adenosquamous ; Chemotherapy, Adjuvant ; Colon ; Colonic Neoplasms ; Neoplasm Metastasis ; Prognosis

No abstract available.
Digoxigenin* ; DNA* ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

Various cancer types have been associated with cancer-related cerebral infarction. In this study, we describe the first case of cancer-related cerebral infarction in which the underlying disease was primary bone marrow lymphoma (PBML). A 79-year-old man presented with abruptly developed bilateral lower extremity weakness and confusion. Diffusion-weighted imaging on admission showed multiple cortical and subcortical embolic infarction lesions in multiple vascular territories. Diagnostic evaluations to determine the embolic source revealed no abnormalities. Laboratory testing demonstrated elevated D-dimer (2.59 μg/mL) but no other prothrombotic abnormalities. In suspicion of cancer-related stroke, we performed chest CT, abdomen CT, and FDG-PET to detect the hidden malignancy. Findings revealed no evidence of cancer; however, they did reveal signs of anemia (hemoglobin 9.0 g/dL). Bone marrow aspiration biopsy showed large atypical B cell involvement suggestive of high-grade B cell lymphoma. The patient was diagnosed with primary bone marrow diffuse large B-cell lymphoma initially presenting with ischemic stroke. Our case suggests that primary bone marrow cancer may be a candidate for the differential diagnosis of hidden malignancy in patients with suspected cancer-related stroke. Bone marrow biopsy may be essential for establishing an appropriate differential diagnosis in patients with abnormal hematologic findings.

The effects of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) on movement and tyrosine hydroxylase (TH)-immunoreactive (ir) neuronal changes in young (5~6 weeks) and aged (10~12 months) C57BL/6 mice were studied. Locomotor activity was measured during 180 minutes after a single injection of 30 mg/kg of MPTP. For immunohistochemistry both young and aged mice were injected four repeated dosages of 10 mg/kg of MPTP 12 hours apart. We counted the numbers of TH-ir cell bodies using immunohistochemical technique in substantia nigra (SN), ventral tegmental area (VTA) and locus ceruleus (LC) 7 days after the last injection of MPTP. There was a marked decrease of locomotor activity in MPTP-treated young and aged mice, and a delay in recovery of locomotor activity in MPTP-treated aged mice. In young mice, there was a decrease in the number of TH-ir cell bodies in the SN of young mice, but not in VTA or LC. In aged mice, there was a significant decrease in the number of TH-ir cell bodies in VTA as well as SN. It was concluded that aged mice were more sensitive to MPTP than young mice, and MPTP-treated aged mice a more useful animal model for studing the characteristics of Parkinson's disease.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine* ; Aging* ; Animals ; Immunohistochemistry ; Locus Coeruleus ; Mice* ; Models, Animal ; Motor Activity ; Neurons* ; Parkinson Disease ; Substantia Nigra ; Tyrosine 3-Monooxygenase ; Ventral Tegmental Area

Adult ; Angiolymphoid Hyperplasia with Eosinophilia ; Biopsy ; Endothelial Cells ; Eosinophils ; Humans ; Lymphocytes ; Mouth ; Plasma Cells

Lead is a major environmental and occupational neurotoxicant. It has been shown that long-term exposure to a low level of lead impairs the development of brain. For example, it was reported that lead exposure during the childhood causes a learning difficulty and a memory deficit of children. Neurotoxic agents including the lead are believed to cause neuronal death in developing brain by two mechanisms: apoptosis and necrosis. However, the exact mechanism of neuronal death caused by lead exposure is still not known explicitly. In this study, we conducted a study to clarify a mechanism of hippocampal neuronal cell death caused by lead acetate. Hippocampal neurons were cultured for 14-16 days and treated with lead acetate of 1. 10, 100 1 microM concentrations for 12 hours. With the MTT(methyl tetrazolium test) kit, the viability of neuronal cells was measured. Next, in order to examine apoptosis caused by lead acetate, TUNEL (TdT-mediated d-UTP Nick End Labelling) assay was performed. It has been shown that lead acetate reduced the viability of neuronal cells in a dose dependent manner, especially at the concentration of 100 ~M lead acetate. TUNEL immunostain showed brownish signals in the nucleus of apoptotic cells. The proportions of apoptotic cells in the lead?acetate treated group were more higher than those in the controls and increased as lead acetate concentration increased. From above results, it may be concluded that lead in the hippocampal neuronal cells reduced cell viability and one of mechanisms in neuronal cell death by lead appears to be apoptosis.
Apoptosis* ; Brain ; Cell Death ; Cell Survival ; Child ; Hippocampus ; Humans ; In Situ Nick-End Labeling ; Learning ; Memory Disorders ; Necrosis ; Neurons*

No abstract available.
Blast Crisis* ; Leukemia*

No abstract available.
Blast Crisis* ; Leukemia*