Effect of chlorine dioxide in reduction of harmful microbes on fermented hot pepper paste.

In this study, the in vitro effects of chlorine dioxide (ClO2) in growth reduction against Candia glaebosa, Zygosaccharomyces bisporus, Saccharomycopsis capsularis and Pichia pastoris involving in deterioration of fermented hot pepper paste were studied to assess the applicability of chlorine dioxide to preparation of fermented hot pepper paste, and the concentration of ClO2 required for destruction of harmful microorganisms through the fumigation of fermented hot pepper paste was evaluated. ClO2 was treated by using ClO2 generator for 15 min. C. glaebosa, Z. bisporus and S. capsularis were reduced by ClO2 concentration dependent and not detected by ClO2 over 10 ppmV, whereas the P. pastoris was significantly perished by the treatment of ClO2 over 30 ppmV. We suggest that the ClO2 fumigation in stages of the preparation, disintegration, and fermentation of the paste made of fermented hot pepper might be useful for control of harmful microbes therein.

Insulin resistance and carotid atherosclerosis in patients with type 2 diabetes.

OBJECTIVE: Insulin resistance may provide a crucial link between type 2 diabetes and cardiovascular disease. However, it is still unclear whether insulin resistance itself or hyperinsulinemia is independently associated with subclinical atherosclerosis. We hypothesized that insulin resistance, but not hyperinsulinemia, would be associated with carotid atherosclerosis in patients with type 2 diabetes. METHODS: We examined 2471 patients with type 2 diabetes, consecutively enrolled in Huh Diabetes Center. Insulin sensitivity was directly assessed by a rate constant for plasma glucose disappearance (Kitt) using short insulin tolerance test. Fasting insulin levels were used as a marker of hyperinsulinemia. Both carotid arteries were examined by B-mode ultrasound. Carotid atherosclerosis was defined by having a clearly isolated focal plaque or mean carotid intima-media thickness (IMT) >or=1.1mm. RESULTS: In multiple regression models, insulin sensitivity index (Kitt) but not hyperinsulinemia was significantly associated with carotid IMT adjusting for known risk factors such as age, sex, BMI, smoking, systolic pressure, HDL and LDL cholesterol. One standard deviation decrease in Kitt was associated with 0.046 mm increase in carotid IMT (p=0.015). Furthermore, odds ratio for carotid atherosclerosis was 1.43 (95% CI: 1.10, 1.86) in type 2 diabetic patients with insulin resistance (lowest quartile of insulin sensitivity) adjusting for known risk factors. The results were consistent in all subgroups stratified by sex, age, smoking and hypertension. CONCLUSION: Insulin resistance measured by short insulin tolerance test, but not hyperinsulinemia, is independently associated with carotid atherosclerosis in patients with type 2 diabetes.

Echogenic carotid artery plaques are associated with vertebral fractures in postmenopausal women with low bone mass.

Although low bone mass has been associated with atherosclerosis even after adjustment for age, little is known about the association between vertebral fractures and calcified atherosclerotic plaques. Our objective was to investigate whether osteoporotic vertebral fractures are independently related to the prevalence of atherosclerotic carotid plaques in postmenopausal women with low bone mass. We enrolled 195 postmenopausal women with osteopenia or osteoporosis. Bone mineral density and the presence of vertebral fractures were assessed. Intima media thickness and atherosclerotic plaques of the carotid artery were assessed using ultrasonography. Of the 195 subjects in the study, 84 had no plaques and 111 had at least one. The percentage of women with vertebral fractures was significantly higher in subjects with echogenic carotid plaques than in those without (27% vs. 11%, respectively; P < 0.05). However, there was no difference in the prevalence of vertebral fractures between women with echolucent plaques and those without (10.9% vs. 10.7%, respectively; P = nonsignificant). By logistic regression analysis with multivariate adjustment, age (P < 0.01), dyslipidemia (P < 0.05), and the presence of vertebral fracture (P < 0.05) were independent risk factors for echogenic carotid plaques. Osteoporotic vertebral fractures are associated with an increased risk of echogenic atherosclerotic plaques in postmenopausal women with low bone mass. It appears that the high association of echogenic atherosclerotic plaques and vertebral fractures could partially explain why osteoporotic vertebral fractures are linked to increased mortality.

HoxD10 gene delivery using adenovirus/adeno-associate hybrid virus inhibits the proliferation and tumorigenicity of GH4 pituitary lactotrope tumor cells.

Prolactinoma is one of the most common types of pituitary adenoma. It has been reported that a variety of growth factors and cytokines regulating cell growth and angiogenesis play an important role in the growth of prolactinoma. HoxD10 has been shown to impair endothelial cell migration, block angiogenesis, and maintain a differentiated phenotype of cells. We investigated whether HoxD10 gene delivery could inhibit the growth of prolactinoma. Rat GH4 lactotrope tumor cells were infected with adenovirus/adeno-associated virus (Ad/AAV) hybrid vectors carrying the mouse HoxD10 gene (Hyb-HoxD10) or the beta-galactosidase gene (Hyb-Gal). Hyb-HoxD10 expression inhibited GH4 cell proliferation in vitro. The expression of FGF-2 and cyclin D2 was inhibited in GH4 cells infected with Hyb-HoxD10. GH4 cells transduced with Hyb-HoxD10 did not form tumors in nude mice. These results indicate that the delivery of HoxD10 could potentially inhibit the growth of PRL-secreting tumors. This approach may be a useful tool for targeted therapy of prolactinoma and other neoplasms.

Expression and role of estrogen receptor alpha and beta in medullary thyroid carcinoma: different roles in cancer growth and apoptosis.

Medullary thyroid carcinoma (MTC) originates from parafollicular C cells. Estrogen receptor beta(ERbeta) expressionwas detected in normal parafollicular C cells and MTC tumor tissue, but ERalpha expression in MTC tumors still remains undetermined. The appearance and loss of ERalpha or ERbeta expression has been known to play a role in the development and progression of many human cancers. We performed immunohistochemical studies of ERalpha, ERbeta, and Ki67, a mitotic index, in 11 human MTC tissue samples. ERalpha was detected in 10 cases (91%), and ERbeta expression was observed in 8 cases (72.7%). A majority (8/10) of ERalpha-positive tumors showing ERbeta Ki67 expression was detected in three cases (27.3%). Neither clinical parameters nor tumor node metastasis (TNM) tumor staging was correlated with the positivity for ERs or Ki67. To investigate the biological role of each ER, we used ER-negative MTC TT cells and adenoviral vectors carrying ERalpha (Ad-ERalpha), ERbeta (Ad-ERbeta), estrogen response element (ERE)-Luc (Ad-ERE-Luc), and activator protein 1 (AP1)-Luc (Ad-AP1-Luc). Estrogen stimulated and anti-estrogen, ICI 182 780, suppressed ERE reporter activity in TT cells expressing ERalpha or ERbeta, suggesting that both ERs use the same classical ERE-mediated pathway. Ad-ERalpha infection stimulated TT cell growth; in contrast, Ad-ERbeta infection suppressed their growth. Apoptosis was detected in Ad-ERbeta-infected TT cells. Estrogen and anti-estrogen suppressed AP1 activity in Ad-ERalpha-infected cells, whereas upon Ad-ERbeta infection estrogen further stimulated AP1 activity which in turn is suppressed by anti-estrogen, suggesting that each ER acts differently through a non-ERE-mediated pathway. Our results suggest that ERalpha and ERbeta may play different roles in MTC tumor growth and progression.

The adaptation and relationship of FGF-23 to changes in mineral metabolism in Graves' disease.

OBJECTIVE: The aim of this study was to observe the changes in bone and mineral metabolism and to confirm the regulation of fibroblast growth factor-23 (FGF-23) in untreated Graves' disease. PATIENTS AND MEASUREMENTS: The study comprised 39 patients, with or without Graves' disease. The Graves' disease group was made up of 21 newly diagnosed patients, enrolled before starting treatment. Their disease was determined by biochemical and radiological means. The control group was composed of 18 people who were proven to be euthyroid without any diseases affecting bone and mineral metabolism. FGF-23, calcium, phosphate, PTH, 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)2D] levels and bone turnover markers were compared between these groups. RESULTS: Serum calcium and phosphate, plasma FGF-23 and free T4 were significantly higher in the Graves' disease group than in the healthy control group (P < 0.05). The bone turnover markers serum osteocalcin and C-terminal cross-linked telopeptide of type 1 collagen (s-CTx) were also significantly elevated in the Graves' disease group, and had a positive correlation with free T4 levels. However, there was no significant decrease in PTH and 1,25(OH)2D in the Graves' disease group. Plasma levels of FGF-23 exhibited a positive correlation with serum phosphate levels and with free T4 levels (P < 0.05). CONCLUSIONS: These findings suggest that FGF-23 is physiologically related to serum phosphate homeostasis, as indicated indirectly by the changes in bone and mineral metabolism, in untreated Graves' disease.

The H723R mutation in the PDS/SLC26A4 gene is associated with typical Pendred syndrome in Korean patients.

Inherited as an autosomal recessive trait, Pendred syndrome is a disease that shows congenital sensorineural hearing loss and goiter, with a positive finding in the perchlorate discharge test. Pendred syndrome results from various mutations in the PDS/SLC26A4 gene that cause production of an abnormal pendrin protein. More than 90 mutations in the PDS/SLC26A4 gene have been reported throughout the world. A recent study of 26 Korean patients with a relatively high frequency (65%) of a mutated PDS/SLC26A4 gene exhibited nonsyndromic deafness and an enlarged vestibular aqueduct. We report two patients with characteristics of typical Pendred syndrome, a 26-yr-old female and a 61-yr-old male, who were both homozygous for a previously reported missense mutation, H723R (Histidine 723Arginine) in the PDS/SLC26A4 gene.