Cellular and Systemic Interactions of Orientia tsutsugamushi with Mammalian Host

Scrub typhus is an acute febrile illness caused by Orientia tsutsugamushi infection and one of main causes of febrile illness in the Asia-Pacific region. It has been estimated that one billion people are at risk and one million new cases arise each year in the endemic region. Despite of aggressive attempts to develop a prophylactic vaccine against scrub typhus during last several decades, all approaches have failed to generate long lasting immunity. In addition, little is known about the immunological pathogenesis of scrub typhus. In this review, we summarized recent findings of cellular and systemic interaction of O. tsutsugamushi with mammalian host, especially focusing on the molecular basis of intracellular invasion and immunological changes observed during the bacterial infection.

The Effect of RGP Lens and Reverse Geometry Lens on Corneal Epithelial Proliferation Rate in Rabbit

PURPOSE: To investigate proliferation rate of the corneal epithelium with rigid gas permeable lens(RGP) or reverse geometry lens(RGL) wearing. METHODS: Twenty-four rabbits were fitted with either a RGP or RGL on right eye, with left eye serving as a control. They were sacrificed at 1, 3, 7, and 14 days after lens fitting. after immunohistochemistry using 5-bromo-2-deotyuridine, BrdU-labeled cells were counted in 10-medium power fields (X200) in each sample using light microscope by 1.0 mm intervals between superior limbus and the center. RESULTS: The number of BrdU-labeled cells was highest in peripheral cornea, and lowest in limbus(p<0.05). The BrdU-labeled cells of limbus increased by 127% but labeled-cells of the center decreased by 24% in RGP group after 1-day fitting. Increase of the labeled cells was observed in the mid-peripheral and central cornea by 12% and 121% each but the decrease of labelled cells was found at the limbus by 16% in RGL fitting group at 1 day. After 14days, Both RGP and RGL group showed decrease of BrdU-labeled cells in limbus by 8% each, and in the center by 32% and 63%, respectively. CONCLUSIONS: Normal rabbit cornea was characterized by different epithelial proliferation rates according to location. However these pattern was significantly altered with both RGL and RGP fitting group. The change was greater in RGL group than in RGP group. This suggested wearing the RGL might be less physiologic than RGP fitting.

The variation of pancreatic beta-cell specific glucokinase gene promoter at the position of -30 bp in Koreans with gestational diabetes mellitus / 대한내과학회지

Glucokinase is expressed only in both liver and pancreatic beta cells and has a key role in the regulation of glucose metabolism in these tissues. A number of gene defects associated with glucokinase gene and the cause of non-insulin-dependent diabetes mellitus are known, and the defects along the -30bp promoter site in particular are thought to be related to diabetes and glucose intolerance. To research on gene study related to diabetes, we looked into the relationship between the variation at -30bp of pancreatic beta cell specific glucokinase gene promoter and gestational diabetes mellitus(GDM) in Korea. METHODS: Forty patients with GDM and 62 normal controls were studied. Genomic DNA was extracted from peripheral leukocyte of patients with GDM and normal controls. The nucleotide variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter was analyzed by PCR-SSCP methods. The sequences of amplified DNA were confirmed with direct sequencing method. The clinical features and the response of insulin secretion to oral glucose were analyzed between patients with GDM according to genotypes. RESULTS: Allelic frequency of position -30 bp of pancreatic beta cell specific glucokinase gene promoter did not differ between patients with GDM and normal subjects. However the frequency of G/A and A/A genotypes seemed to show a higher tendency in patients with GDM compare to the normal subjects. Clinical features, insulin response to oral glucose did not differ according to the type of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter. CONCLUSION: These data suggested that the variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter in patients with GDM are unlikely to be one of the possibilities of the genetic factors in the development of GDM. Therefore more sophisticated studies will be needed to elucidate the role of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter in the insulin secretion to oral glucose.

The variation of pancreatic beta-cell specific glucokinase gene promoter at the position of -30 bp in Koreans with gestational diabetes mellitus / 대한내과학회지

Glucokinase is expressed only in both liver and pancreatic beta cells and has a key role in the regulation of glucose metabolism in these tissues. A number of gene defects associated with glucokinase gene and the cause of non-insulin-dependent diabetes mellitus are known, and the defects along the -30bp promoter site in particular are thought to be related to diabetes and glucose intolerance. To research on gene study related to diabetes, we looked into the relationship between the variation at -30bp of pancreatic beta cell specific glucokinase gene promoter and gestational diabetes mellitus(GDM) in Korea. METHODS: Forty patients with GDM and 62 normal controls were studied. Genomic DNA was extracted from peripheral leukocyte of patients with GDM and normal controls. The nucleotide variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter was analyzed by PCR-SSCP methods. The sequences of amplified DNA were confirmed with direct sequencing method. The clinical features and the response of insulin secretion to oral glucose were analyzed between patients with GDM according to genotypes. RESULTS: Allelic frequency of position -30 bp of pancreatic beta cell specific glucokinase gene promoter did not differ between patients with GDM and normal subjects. However the frequency of G/A and A/A genotypes seemed to show a higher tendency in patients with GDM compare to the normal subjects. Clinical features, insulin response to oral glucose did not differ according to the type of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter. CONCLUSION: These data suggested that the variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter in patients with GDM are unlikely to be one of the possibilities of the genetic factors in the development of GDM. Therefore more sophisticated studies will be needed to elucidate the role of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter in the insulin secretion to oral glucose.

The beta-adrenergic Receptor Concentration and Plasma Catecholamine in Congestive Heart Failure

To identify the role of the myocardial beta-adrenergic pathway in congestive heart failure, we examined beta-adrenergic receptor density and C-AMP by receptor assay with mononuclrear cell and polymorphonuclear cell in 7 cases of normal control and 7 cases of congestive heart failure. The results were as follows: 1)The mean serum concerntrations of norepinephrine(566.00+/-48.12 pg/ml)and epinephrine(353.14+/-44.24 pg/ml) in congestive heart failure group were significantly higher than those(218.12+/-17.08 pg/ml, 187.23+/-24.62 pg/ml)in normal contral group(P<0.05 for each comparison). 2) In normal control group, the receptor concentration of mononuclear cell was 35.51+/-19.19 fmol/mg and that of polymorphonuclrear cell was 35.53+/-15.05 fmol/mg. The affinity constant of mononuclear cell was(2.47+/-0.42)x10(9)/m and that of polymorphonuclear cell was(2.24+/-0.58)x10(9)/m. 3) In congestive heart failure group, the receptor concentration of mononuclear cell(29.31+/-5.41 fmol/mg) was significantly lower than that in normal control group(p<0.05). And the affinity constant(3.57+/-1.02)x10(9)/m) was significantly higher than that in normal control group(p<0.05). 4) In congestive heart failue group, the receptor concentration of polymorphonuclear cell(33.15+/-10.46 fmol/mg) was not significantly different from that in normal control group. And the affinity constant(2.66+/-0.43)x109/m) was not significantly different from that in normal control group. 5) In congestive heart failure group, the C-AMP concentrations of mononuclear cell(basal 119.9+/-17.2 pmol/min/mg, isoproterenol stimulation 137.2+/-23.2 pmol/min/mg) were significantly lower than those(basal 205.2+/-21.1 pmol/min/mg, isoproterenol stimulation 267.5+/-34.3 pmol/min/mg) in normal control group(p<0.05 for each comparison). 6) In congestive heart failure group, the C-AMP concentrations of polymorphonuclear cell(basal 115.2+/-34.3 pmol/min/mg, isoproterenol stimulation 142.5+/-20.5 pmol/min/mg) were significantly lower thatn those(basal 186.3+/-24.2 pmol/min/mg, isoproterenol stimulation 233.4+/-32.2 pmol/min/mg) in normal control group(P<0.05 for each comparison). In conclusion, a decrease in beta-adrenergic density in congestive heart failure leads to subsensitivity of the beta-adrenergic pathway and decreased beta-agonist-stimulated contraction. However, other factors may be important in adenylate cyclase activation, and so further research is needed.