Alteration of Akt, p-Akt, ERK, and p-ERK Proteins Expression in the Kidney of Hypokalemic Rat / 체질인류학회지

Hypokalemia causes metabolic alkalosis and morphological changes of the kidney. K⁺ balance is regulated not only by ion channels or pump gene, but also by various genes including NF-E2-related factor 2 (Nrf2). Previous study suggested the possibility that Akt and ERK kinase may be involved in Nrf2 transcriptional gene activation. In present study, we investigate the alterations of Akt, p-Akt, ERK, p-ERK protein in both normal kidney and K⁺-deficient diet kidney using Western blot analysis, and immunohistochemisrty. Our western blot data showed that the expression of Akt and p-Akt was increased gradually in K⁺-depleted diet (from 1W-3W) compared to normal group. The expression of ERK and p-ERK was markedly increased in K⁺-depleted diet 2W in comparison with normal group. Based on our immunostaining results, Akt protein immunoreactivity was prominently increased in outer medullary collecting duct, especially in K⁺-depleted diet 2 weeks. The localization of p-Akt proteins in K⁺-depleted groups was not different from normal group, but the immunoreactivity was significantly increased in distal convoluted tubule, macula densa and outer medullary thick ascending limb in K⁺-depleted diet 1 and 2 weeks groups. ERK protein immunoreactivity was prominently increased in outer medullary collecting duct, especially in K⁺-depleted diet 2 and 3 weeks. The localization of p-ERK proteins in K⁺-depleted groups was not different from normal group, but the immunoreactivity was prominently increased in the nucleus of outer medullary collecting duct especially in K⁺-depleted diet 2 weeks. Taken together, we suggest that the expression of p-Akt was gradually increased in K⁺-depleted groups of kidney, but the expression of p-ERK was markedly increased in K⁺-depleted diet 2 week group. Hence, the promotion of AKT and ERK phosphorylation in hypokalemic condition may be involved in the regulation of ion channels, ion transporters and subsequent intracellular signal transduction.

Placental apoptosis in preeclampsia / 대한산부인과학회잡지

OBJECTIVE: Our purpose was to investigate the incidence of placental apoptosis in pregnancies complicated by preeclampsia. METHODS: Placental samples were obtained from 15 uncomplicated third-trimester pregnancies and from 17 pregnancies complicated by preeclampsia. TUNEL (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling) staining and electron microscopy were performed on all placental samples and identified apoptosis within the cells of the placenta. TUNEL positive stained cells were counted at each photograph(five sections were photoragphed at 1,500 magnifications for each sample). We focused on only the syncytiotrophoblast nuclei of the placenta. The number of apoptotic syncytiotrophoblast nuclei identified was expressed as a percentage of total number of syncytiotrophoblast nuclei counted. RESULTS: Quantification of apoptosis (mean+/-SD) was as follows: normal third trimester (n=15) 0.57+/- 0.47% of cells and preeclampsia third trimester (n=17) 1.41+/-0.67% of cells. The incidence of apoptosis was significantly increased in placentas from pregnancies with preeclampsia compared with normal placentas (p< 0.01). CONCLUSION: These results suggest that placental apoptosis may play a role in the pathophysiologic mechanisms of preeclampsia.

p53 Mutation and Epidermal Growth Factor Receptor Overexpression in Glioblastoma

Recent molecular studies indicate two different genetic pathways leading to the development of glioblastoma; final progression of astrocytoma and de novo formation. To define the mutual relationships of cytogenetic changes in the pathogenesis of glioblastoma, molecular histopathologic alterations of p53 and epidermal growth factor receptor (EGFR) were evaluated by single stranded conformational polymorphion, reverse transcriptase-polymerase chain reaction and immunohistochemical stains in 15 primary and 21 secondary glioblastomas. Mutations in p53 gene and positive immunoreactivity to p53 protein (DO1) were more prevalent in secondary glioblastomas than in primary glioblastomas. A correlation between p53 mutations and p53 immunopositivities in glioblastomas was observed in 83.3% of the cases. All cases with positive p53 immunoreactivities showed p53 mutations; however, 13.9% of glioblastomas with p53 immuno-positivities lacked the relevant mutations. EGFR amplifications were detected in 73.3% of primary glioblastomas and 9.5% of secondary glioblastomas (p<0.001). The concurrence of p53 mutation and EGFR amplification was revealed in only 2 out of 15 primary glioblastomas and none among the secondary glioblastomas. Immunoreactivities for EGFR were noted in 66.7% of primary glioblastomas and in 9.5% of secondary glioblastomas (p<0.001). A correlation between EGFR amplification and EGFR immunopositivity in glioblastomas was observed in 91.7% of the cases. These data indicate that EGFR amplification and p53 mutations are two independent genetic events in the development of glioblastomas.

Variations in the Korean Metacarpal Bones / 체질인류학회지

Six hundred fifty-one metacarpal bones of Koreans were studied for variations in articular and non-articular surface and the number, position and direction of the diaphyseal nutrient foramina. The facets for articulation of the metacarpal bone with one another showed very frequent variations from the standard text-book description. The number and the sites of entry of the diaphyseal nutrient foramina also showed considerable variations. These findings show no apparent racial difference in variations of metacarpal bones between a Korean and an Indian.