PURPOSE: The purpose of this study was to explore ways to define the concept of health inequality. METHODS: The concept analysis process by Walker and Avant was used to clarify the meaning of health inequality. RESULTS: Defining attributes of health inequality included differences in health status between individuals or groups, infringement of fundamental rights to health, unfair use of medical services, and social discrimination. The antecedents of health inequality included differences in demographic characteristics (age, gender, education, occupation, residential location), limitations in accessibility to health care, and social exclusion. Consequences of health inequality were increased costs for medical care, decreased health-related quality of life, and lack of ability to cope with health problems resulting in crisis situations, increases in morbidity and mortality, and shortening of life span. The concept was clarified through presentation of model, borderline, related, and contrary cases. CONCLUSION: Results of this study can be used to guide the direction of future studies through concept analysis in which conceptual attributes in the context of health inequality are examined. Also, based on the result of this study, development of standardized tools to measure health inequality is recommended as well as development of educational programs to reduce health inequalities.
Delivery of Health Care ; Education ; Human Rights ; Mortality ; Occupations ; Quality of Life ; Social Discrimination ; Socioeconomic Factors*

Recently, thanks to the development of the molecular genetics which had made us understand the nature of some genetic disorders, the concept of the classification has changed. Charcoal-Marie-Tooth disease (CMT) is the most conspicuous disease. The disease is inherited as an autosomal dominant trait. CMT is classified into two major forms: demyelinating CMT type 1 and axonal CMT type 2. CMT type 1 loci are known to map to chromosome 17 (CMT IA), chromosome 1 (CMT IB), X chromosome (CMT IX), and unknown autosome (CMT IC). And CMT type 2 loci are divided into chromosome 1 (CMT 2A) and chromosome 3 (CMT 2B). The most prevalent form is CMT IA caused by a duplication in a region of chromosome 17p11.2-12. Peripheral myelin protein-22 (PMP-22) gene In that region is known to being responsible for the disease. In Korea, although several families of CMT were reported, there is no report on the subtype of CMT type 1 confirmed by genetic analysis. We report a family of CMT IA confirmed by molecular genetic analysis using D17s122 markers.
Axons ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 3 ; Classification ; Humans ; Korea ; Molecular Biology* ; Myelin Sheath ; X Chromosome

Recently, thanks to the development of the molecular genetics which had made us understand the nature of some genetic disorders, the concept of the classification has changed. Charcoal-Marie-Tooth disease (CMT) is the most conspicuous disease. The disease is inherited as an autosomal dominant trait. CMT is classified into two major forms: demyelinating CMT type 1 and axonal CMT type 2. CMT type 1 loci are known to map to chromosome 17 (CMT IA), chromosome 1 (CMT IB), X chromosome (CMT IX), and unknown autosome (CMT IC). And CMT type 2 loci are divided into chromosome 1 (CMT 2A) and chromosome 3 (CMT 2B). The most prevalent form is CMT IA caused by a duplication in a region of chromosome 17p11.2-12. Peripheral myelin protein-22 (PMP-22) gene In that region is known to being responsible for the disease. In Korea, although several families of CMT were reported, there is no report on the subtype of CMT type 1 confirmed by genetic analysis. We report a family of CMT IA confirmed by molecular genetic analysis using D17s122 markers.
Axons ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 3 ; Classification ; Humans ; Korea ; Molecular Biology* ; Myelin Sheath ; X Chromosome

PURPOSE: The purpose of this study was to provide a basis for non-humidified low flow oxygen by nasal cannula and to provide a guide for consistent care in nursing practice. METHODS: A methodological study on the development of guidelines with experts' opinions on collected items, framing PICO questions, evaluating and synthesizing texts which were searched with the key words (low flow oxygen, nasal cannula, humidification of oxygen, guideline) from web search engines. RESULTS: Of the 45 researched texts on the web, 9 texts relevant to the theme were synthesized and evaluated. All patients with humidified or non-humidified oxygen therapy reported that they had no discomfort. CONCLUSION: The results indicate that there are no tangible grounds for patients' perceived differences between the humidified and non-humidified oxygen under 4L/min supplied by nasal cannula. with oxygen. Therefore, non-humidification oxygen therapy is strongly advised when suppling under 4L/min oxygen by nasal cannula (recommended grade A).
Catheters ; Humans ; Oxygen

Colorectal polyps of mesenchymal origin are a rare group of colorectal disorders. A "mucosal Schwann-cell hamartoma," which is one type of polypoid lesion that originates from the mesenchyme, is a newly-proposed disease entity to be distinguished from the neurofibromas found in type-1 neurofibromatosis. This lesion is composed of pure Schwann-cell proliferation in the lamina propria and shows diffuse immunoreactivity for the S-100 protein. We report a case of a polypoid lesion of the colon with the features of this recently-proposed disease entity.
Colon ; Hamartoma ; Mesoderm ; Mucous Membrane ; Neurofibroma ; Neurofibromatoses ; Neuroma ; Polyps ; S100 Proteins ; Schwann Cells ; SNARE Proteins

BACKGROUND: Charcot-Marie-Tooth disease type 1A (CMT1A) is an autosomal dominant inherited demyelinating peripheral neuropathy characterized by progressive distal muscular atrophy and marked slowing of nerve conduction velocities. A 1.5 Mb DNA duplication within chromosome 17p11.2-p12 has been reported. This disease appears to be caused by an altered copy number of the PMP-22 gene within the critical region. METHODS: DNA analysis was carried out for 158 persons from 40 unrelated families. PCR was done by D17S122 and D17S261. The DNA of the patients was ana-lyzed to detect three alleles for the presence of duplication. RESULTS: CMT1A duplication was found in 7 families (64%) of the patients with CMT1 by D17S122, but not by D17S261. CONCLUSIONS: We have found seven families of Charcot-Marie-Tooth disease type 1A with chromosome 17p11.2-p12 duplication by D17S122. We recommend the screening test by D17S122 for the detection of CMT1A in Korean because genetic analysis done by D17S261 was not informative.
Alleles ; Charcot-Marie-Tooth Disease* ; DNA ; Humans ; Mass Screening ; Molecular Biology* ; Muscular Atrophy ; Neural Conduction ; Peripheral Nervous System Diseases ; Polymerase Chain Reaction

BACKGROUND: Charcot-Marie-Tooth disease type 1A (CMT1A) is an autosomal dominant inherited demyelinating peripheral neuropathy characterized by progressive distal muscular atrophy and marked slowing of nerve conduction velocities. A 1.5 Mb DNA duplication within chromosome 17p11.2-p12 has been reported. This disease appears to be caused by an altered copy number of the PMP-22 gene within the critical region. METHODS: DNA analysis was carried out for 158 persons from 40 unrelated families. PCR was done by D17S122 and D17S261. The DNA of the patients was ana-lyzed to detect three alleles for the presence of duplication. RESULTS: CMT1A duplication was found in 7 families (64%) of the patients with CMT1 by D17S122, but not by D17S261. CONCLUSIONS: We have found seven families of Charcot-Marie-Tooth disease type 1A with chromosome 17p11.2-p12 duplication by D17S122. We recommend the screening test by D17S122 for the detection of CMT1A in Korean because genetic analysis done by D17S261 was not informative.
Alleles ; Charcot-Marie-Tooth Disease* ; DNA ; Humans ; Mass Screening ; Molecular Biology* ; Muscular Atrophy ; Neural Conduction ; Peripheral Nervous System Diseases ; Polymerase Chain Reaction

The purposes of this study are to establish standard model in which endothelial cell proliferations are induced by DMH stimulation in vitro, and to analyze the gene expressions of proliferative HUVECs using DNA chip technique which could evaluate the mechanisms of angiogenesis, and the development of vascular tumors. To perform the MTT assay in 96-well microplates, 104 cells were seeded in each well which were cultured in medium. On the third day, the cells were treated with 5 different concentrations of diluted DMH from 10 to 10-3 ng/ml. Five DMH-treated groups were compared with the control group which was not treated with DMH. The optical densities in each group were measured at the time of 0, 6, 12, 24, 36, 48, and 72 hours after DMH treatment. The same experiment was repeated 9 times. Statistically significant cell proliferations were observed in 1 and 10-1ng/ml group. The RNAs were isolated from HUVECs of control group and 1ng/ml DMH-treated group, and they were used to analyze the gene expressions using DNA chip technique. One hundred and seventy-seven genes(142 of up-retulated genes and 35 down-regulated genes) were identified, and several genes were associated with VEGF and FGF production. Also DMH could affect expression of genes that involve oncogenesis. Further study should be performed to evaluate the processes of angiogenesis and morphogenesis of vascular tumors, which could be utilized in the development of new therapeutic approaches.
Carcinogenesis ; Dimenhydrinate ; Dimethylhydrazines ; Endothelial Cells ; Gene Expression Profiling* ; Gene Expression* ; Human Umbilical Vein Endothelial Cells* ; Humans* ; Morphogenesis ; Oligonucleotide Array Sequence Analysis ; RNA ; Umbilical Veins ; Vascular Endothelial Growth Factor A

A case of diffuse cerebrospinal gliomatosis with extensive leptomeningeal spread is presented. The patient, an 18-year-old girl, was admitted due to progressive weakness and paresthesia of both legs, following rapid neuropsychiatric deterioration. An initial magnetic resonance imaging (MRI) study of the T-spine showed diffuse high signal intensities from T9 to T12 spinal cords on a T2 sagittal image and diffuse cord bulging at T1WI. This suggested an inflammatory lesion such as tuberculosis or fungal meningoencephalitis. A limited autopsy was performed. A microscopic examination revealed multifocal GFAP-positive astrocytic proliferations that were low grade astrocytoma in the cerebral leptomeninges, parietal, occipital and temporal lobes and anaplastic astrocytoma in the spinal cord and spinal leptomeninges. The high proliferative indices of the spinal lesion and aneuploidy correspond to a diagnosis of malignant astrocytoma and a rapid fatal clinical course.
Adolescence ; Brain/pathology ; Case Report ; Cell Division ; Diagnosis, Differential ; Female ; Human ; Magnetic Resonance Imaging ; Meninges/pathology* ; Neoplasms, Neuroepithelial/pathology* ; Neoplasms, Neuroepithelial/diagnosis ; Spinal Cord/pathology

Hypoglycemic hemiplegia is an under-recognized manifestation of hypoglycemia and mimics cerebrovascular dis-ease, especially in elderly patients. We report a 70-year-old diabetic woman with hypoglycemic hemiplegia, whose dif-fusion- and perfusion- weighted images showed large cortical high signal intensities and hypoperfusion of the right hemisphere during the period of hypoglycemia. We suggest that the regional cerebral blood redistribution and selective vulnerability in hypoglycemia are responsible for the laterality of neurological deficits observed during hypoglycemic episodes.
Aged ; Female ; Hemiplegia* ; Humans ; Hypoglycemia ; Magnetic Resonance Imaging*