Multipotent neural stem cells (NSCs) are operationally defined by their ability to self-renew, to differentiate into cells of all glial and neuronal lineages throughout the neuraxis, and to populate developing or degenerating CNS regions. Thus their use as a graft material can be considered analogous to hematopoietic stem cell-mediated reconstitution and gene transfer. The recognition that NSCs propagated in culture could be reimplanted into mammalian brain, where they might integrate appropriately throughout the mammalian CNS and stably express foreign genes, has unveiled a new role for neural transplantation and gene therapy and a possible strategy for addressing the CNS manifestations of diseases that heretofore has been refractory to intervention. We have tracked the response of host and transplanted NSCs to brain or spinal cord injury and explored the therapeutic potential of NSCs injected into the animal CNS subjected to focal hypoxic-ische-mic (HI) brain or spinal cord injury. Such cells integrated appropriately into the degenerating CNS, showed robust engraftment and foreign gene expression within the region of CNS injury, and appeared to have migrated preferentially to the site of injury, experienced limited proliferation, and differentiated into neural cells lost to injury, trying to repopulate the damaged CNS area. The transplantation of exogenous NSCs may, in fact, augment a natural self-repair process in which the damaged CNS "attempts" to mobilize its own pool of stem cells. Providing additional NSCs and trophic factors may optimize this response. Therefore, NSCs may provide a novel approach to reconstituting CNS damaged by HI brain or spinal cord injury. Preliminary data in animal models of hypoxic-ischemic brain injury or contusive spinal cord injury lend support to these hypotheses.
Animals ; Brain ; Brain Injuries ; Gene Expression ; Genetic Therapy ; Models, Animal ; Neural Stem Cells* ; Neurons ; Spinal Cord Injuries ; Stem Cells ; Transplants

No abstract available.
Anemia, Aplastic*

No abstract available.
Vietnam*

No abstract available.
Korea* ; Pharmacology*

Diagnosis of mycobacterial infection is dependent upon the isolation and identification of causative agents. The procedures involved are time consuming and technically demanding. To improve the laborious identification process mycobacterial systematics supported by gene analysis is feasible, being particularly useful for slowly growing or uncultivable mycobacteria. To complement genetic analysis for the differentiation and identification of mycobacterial species, an alternative marker gene, rpoB encoding the B subunit of RNA polymerase, was investigated. rpoB DNAs (342 bp) were amplified from 52 reference strains of mycobacteria including Mycobacterium tuberculosis H37Rv (ATCC 27294) and clinical isolates by the PCR. The nucleotide sequences were directly determined (306 bp) and aligned using the multiple alignment algorithm in the MegAlign package (DNASTAR) and MEGA program. A phylogenetic tree was constructed with a neighborhood joining method. Comparative sequence analysis of rpoB DNA provided the basis for species differentiation. By being grouped into species-specific clusters with low sequence divergence among strains belonging to same species, all the clinical isolates could be easily identified. Furthermore RFLP analysis enabled rapid identification of clinical isolates.
Base Sequence ; Classification ; Complement System Proteins ; Diagnosis ; DNA ; DNA-Directed RNA Polymerases ; Mycobacterium tuberculosis ; Polymerase Chain Reaction* ; Polymorphism, Restriction Fragment Length* ; Residence Characteristics ; Sequence Analysis*

No abstract available.
Chimerism* ; Stem Cell Transplantation* ; Stem Cells*

No abstract available.

No abstract available.
Antigens, Surface* ; Humans ; Urinalysis*

In order to study the change of laboratory parameters of lead poisoning, 8 persons who had not been treated previously for lead poisoning (Group 1) and 6 persons who had been inadequately treated for few months for chronic lead poisoning at local clinic (Group 2) were examined. They had occupational exposure to lead for 3 to 18 years (mean, 7.6). In group 1 blood lead, urine lead, urine coproporphyrin and delta-aminolevulinic acid levels before our treatment exceeded the critical levels of lead poisoning. In group 2 urine lead level exceeded but blood lead, urine coproporphyrin and delta-aminolevulinic acid levels were within normal limits. All of them were treated with D-penicillamine for 4 months as inpatients at Industiral Accident Hospital. The dose of D-penicillamine was the same in all patients; 600 mg per day p.o. and the chelating agent was administer every other week. For laboratory analysis, 24 hour urine and 10 gm of whole blood were collected every 1 month on last day of non-administration period. The results were as follows: 1. It was found that urine lead level was decreased below the critical level of lead poisoning after 4 month's treatment with D-penicillamine and blood lead level was decreased more progressively below the critical level after 1 month treatment. 2. Urine coproporphyrin and delta-aminolevulinic acid levels were decreased progressively to normal range after 1 month treatment. 3. Two months after treatment, blood lead, urine lead, urine coproporphyrin and delta-adminolevulinic acid levels showed some increasing trends. 4. Urine lead level should be checked in a person who had been inadequately treated with chelating agents because blood lead, coproporphyrin and delta-adminolevulinic acid might be in normal range.
Aminolevulinic Acid ; Chelating Agents ; Humans ; Inpatients ; Lead Poisoning* ; Occupational Exposure ; Penicillamine ; Reference Values

No abstract available.
Antigens, Surface* ; Humans ; Urinalysis*