The mechanism(s) of cystic fibrosis transmembrane conductance regulator (CFTR) trafficking from the endoplasmic reticulum (ER) through the Golgi apparatus, the step impaired in individuals afflicted with the prevalent CFTR-⌬F508 mutation leading to cystic fibrosis, is largely unknown. Recent morphological observations suggested that CFTR is largely absent from the Golgi in situ (Bannykh, S. I., Bannykh, G. I., Fish, K. N., Moyer, B. D., Riordan, J. R., and Balch, W. E. (2000) Traffic 1, 852-870), raising the possibility of a novel trafficking pathway through the early secretory pathway. We now report that export of CFTR from the ER is regulated by the conventional coat protein complex II (COPII) in all cell types tested. Remarkably, in a cell type-specific manner, processing of CFTR from the core-glycosylated (band B) ER form to the complex-glycosylated (band C) isoform followed a non-conventional pathway that was insensitive to dominant negative Arf1, Rab1a/Rab2 GTPases, or the SNAp REceptor (SNARE) component syntaxin 5, all of which block the conventional trafficking pathway from the ER to the Golgi. Moreover, CFTR transport through the non-conventional pathway was potently blocked by overexpression of the late endosomal target-SNARE syntaxin 13, suggesting that recycling through a late Golgi/endosomal system was a prerequisite for CFTR maturation. We conclude that CFTR transport in the early secretory pathway can involve a novel pathway between the ER and late Golgi/endosomal compartments that may influence developmental expression of CFTR on the cell surface in polarized epithelial cells.
BACKGROUND AND PURPOSE:Placement of a covered stent to control carotid blowout (CB) in malignant tumors of the head and neck has been reported to be an effective treatment. However, it is not uncommon to encounter recurrent hemorrhage. The purpose of this study was to evaluate the follow-up results of patients treated with covered stents.
We studied the seroprevalence of HBsAg, anti-HBs and anti-HBc and the vaccination histories among health care workers (HCWs) at a large suburban referral hospital in Korea. The purpose of this study was to determine the immune status of HCWs against hepatitis B virus and we also wanted to prepare a practical guideline to protect HCWs from occupational exposure. During December, 2003, 571 HCWs (56 physicians, 289 nurses, 113 technicians and 113 aid-nurses) aged between 21 and 74 yr were included in the surveillance. The positive rates of HBsAg and anti-HBs were 2.4% (14/571) and 76.9% (439/571), respectively. The positive rate of anti-HBs was lower in the physician group, and this was associated with the male gender and older age. Of the 439 anti-HBs positive cases, 320 cases (73.1%) were anti-HBc negative and this was significantly associated with a past history of HBV vaccination. The distribution of the anti-HBs levels was not associated with age (except for HCWs in their sixties), gender or occupation. Our study revealed that the seroprevalence rates of HBsAg and anti-HBs in HCWs in Korea were not different from those of the general population. Based on this surveillance, we can make reasonable decisions in case of occupational exposure to hepatitis B virus.
The prevalence of toxigenic Clostridium difficile in Korea has been reported to be approximately 60–80 %. Although the prevalence of the tcdA−tcdB+ C. difficile strain was less then 5 % prior to the year 2000, it has become an emerging nosocomial pathogen in Korea. Therefore, we have attempted to determine the multicentre nationwide prevalence of tcdA+tcdB+
and tcdA−tcdB+ C. difficile for epidemiological purposes. C. difficile strains (n=724, 30 from 2000, 80 from 2001, 74 from 2002, 76 from 2003, 179 from 2004, 285 from 2005) were obtained retrospectively from January 2000 to December 2005 from in-patients at 6 hospitals, all of whom were suspected of having C. difficile-associated disease (CDAD), colitis or pseudomembranous colitis. The numbers of participating hospitals varied yearly (1 in 2000, 2 in 2001–2003, 3 in 2004, 5 in 2005). The hospitals were located in Seoul (n=4), Kyunggi Province (n=1) and Busan (n=1), Korea. PCR assays for tcdA and tcdB genes were conducted using 724 unduplicated C. difficile isolates. The mean prevalence of tcdA+tcdB+
and tcdA−tcdB+ C. difficile strains over the 6 years was 51.8 % (38.4–59.3 %) and 25.8 %(10–56.0 %), respectively. The mean prevalence of tcdA−tcdB+ C. difficile strains was less than 7 % until 2002, but began to increase in 2003 (13.2 %) and achieved a peak in 2004 (50.3 %). In 2005, the mean prevalence of tcdA+tcdB+
and tcdA−tcdB+ C. difficile strains was 47.7 % (30.9–60.3 %) and 27.0 % (17.6–54.8 %), respectively. This nationwide epidemiological study showed that tcdA−tcdB+ C. difficile strains have already spread extensively throughout Korea, and our results provide basic data regarding the controversies currently surrounding the toxigenicity of tcdA−tcdB+
C. difficile. The use of enzyme immunoassays capable of detecting both TcdA and TcdB is strongly recommended for the diagnosis of CDAD in microbiology laboratories, in order to control the spread of the tcdA−tcdB+
strains of C. difficile.
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