Biomedical subjects

Shinji Nakahara

Publications and source records attributed to Shinji Nakahara.

21 records · Page 2Linked to original sources

PubMed2002

Mechanism of destructive pathologic changes in the spinal cord under chronic mechanical compression.

STUDY DESIGN: A histologic and histochemical study was performed both in the autopsy of a human patient with cervical spinal cord compression caused by ossification of the posterior longitudinal ligament and in a tiptoe-walking Yoshimura mouse model of progressive cervical cord compression. OBJECTIVES: To clarify the mechanism of destructive pathologic changes in the spinal cord under chronic mechanical compression. SUMMARY OF BACKGROUND DATA: Under chronic compression, the spinal cord exhibits destructive changes considered to be causes of profound and irreversible motor paresis. Recently, some investigators have found that apoptosis in acute spinal cord injury induces both secondary degeneration at the site of injury and chronic demyelination of tracts away from the site of injury. However, the mechanism responsible for these destructive spinal cord changes under chronic compression remains unclear. METHODS: The spinal cord was examined histologically, and an attempt was made to detect apoptotic cells using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling in both the autopsy of a human patient and tiptoe-walking mice exhibiting spinal cord compression. RESULTS: Apoptotic cells were observed in the chronically compressed spinal cord in both the autopsy of a human patient and model mice. In tiptoe-walking mice exhibiting spinal cord compression, descending degeneration in the anterior and lateral columns and ascending degeneration in the posterior column were observed. The distribution of oligodendrocytes with positive results from terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling was similar to that for degeneration of the long tracts. CONCLUSIONS: Spinal cord cell apoptosis may produce destructive changes in the spinal cord under chronic compression, with a resulting irreversible neurologic deficit.

Aged↗

PubMed2002

Changes in nitric oxide and expression of nitric oxide synthase in spinal cord after acute traumatic injury in rats.

The aim of this study was to observe the time course of NO production and NOS expression in the spinal cord following acute traumatic injury. Rat spinal cord was injured by extradural static weight-compression, which resulted in an incomplete transverse spinal cord lesion with paralysis of the lower extremities. Using this model, measurement of NO by microdialysis and Griess reaction and histological and immunohistochemical examinations using polyclonal antibodies to nNOS and iNOS were performed from immediately to 14 days after injury. In injured cord, the amount of NO markedly increased immediately after injury and gradually decreased between 1 and 12 h after injury. A second wave of increase in NO level was observed at 24 h and 3 days after injury. Histologically, hematomas and necrotic changes were observed after injury and demyelination of nerve fibers increased with time in the compressed segment. Immunohistochemically, the number of cells with expression of nNOS was increased immediately to 12 h after injury. Expression of iNOS was observed from 12 h to 3 days after injury. These findings suggested that the initial maximal increase of NO production might be caused mainly by nNOS and that the second wave of increase in NO might be due mainly to iNOS.

Animals↗

PubMedDate not supplied

Availability of childcare support and nutritional status of children of non-working and working mothers in urban Nepal.

In many developing countries, poor women have multiple roles, and often their time constraints are so severe that their participation in income-generating activities results in reduced childcare time, which in turn affects child health. Previous studies have tended to investigate how childcare support influences nutrition of children with working mothers' based on comparisons with non-working mothers. However, non-working mothers are not a homogeneous group, and we therefore need to distinguish between those who need not work and those who wish to but cannot, for example, due to a lack of substitute caregivers. We examined the association between availability of childcare support and the nutritional status of children of both non-working and working mothers in poor areas of Pokhara, a sub-metropolitan city in Nepal. We recruited 150 children of age 10-24 months from the waiting lists of 17 daycare centers and measured their weights and heights. Those with height-for-age and weight-for-age Z scores of less than -2 were defined as stunted and underweight, respectively. To collect information on childcare practices and socioeconomic characteristics, mothers were interviewed using a pre-tested structured questionnaire. Unavailability of adult childcare support was associated with increased risk of malnutrition among children of both non-working and working mothers. Peer childcare was not significantly associated with child malnutrition among children of non-working mothers, but it was associated with an increased risk of malnutrition among children of working mothers. Although further longitudinal research is required, we suggest that childcare support from adult substitute caregivers is essential for children of non-working mothers with limited resources.

Adult↗