Quarterly communicable disease review April to June 1998. From the PHLS Communicable Disease Surveillance Centre.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Hawker.
Explore the source record for details and available documents.
OBJECTIVES: To describe the epidemiology of tuberculosis (TB) in Birmingham, UK, by ethnic group and to assess the implications of the findings for future trends in TB in the UK. METHODS: Retrospective review of records of all patients notified with TB in Birmingham during 1989-1994. RESULTS: The decline in TB notifications in Birmingham halted and then reversed in 1987-1992. Trends in overall notifications were mainly influenced by trends in cases of Asian origin. Crude notification rates in 1989-1994 are 17 times higher in Asian than Caucasian residents (p < 0.01). Rates in African Caribbean residents are also statistically significantly higher than in Caucasians (p < 0.01) but significantly lower than in Asians. Crude rates for Asian people born abroad are 4.1 times higher than for Asians born in the UK (p < 0.01) but only 3.8% of Asian patients had been resident in the UK for less than 1 year. The group accounting for the highest number of cases were female Asians aged 20-29, followed by male Asians of the same age. Age-specific rates show that incidence increases with age in both Asian and white groups, with a small peak in 20-29-year-old Asians. TB is uncommon in all Caucasian age-groups under 50 years of age (less than 1 per 10,000) but is relatively common in all Asian age-groups over 15 years of age (over 10 per 10,000). CONCLUSIONS: The different epidemiology of TB in the Caucasian and Asian populations in the UK suggests that from about the second decade of the next century, TB in the UK will almost be entirely a problem of ethnic minorities and that even if new infection was eliminated now in Asian people, cases due to reactivation would continue to occur until the third quarter of the next century.
Explore the source record for details and available documents.
The FK506-binding protein, FKBP12, is a putative target of type I receptors for transforming growth factor-beta (TbetaR-I). As the FK506 motif that competes with TbetaR-I for FKBP12 resembles an invariant Leu-Pro dipeptide in TbetaR-I, we replaced Leu193 and Pro194 with Ala, along with mutations across the Gly/Ser box. L193A, P194A, and L193A/P194A do not alter TbetaR-I function; T204D partially activates, independent of ligand; L193A/P194A/T204D was an even more potent constitutive mutation. Association with FKBP12 in a yeast two-hybrid assay was disrupted by P194A, L193A/P194A, and L193A/P194A/T204D, but not L193A or T204D alone. Thus, FKBP12 recognition is dispensable for TGFbeta signaling.
Explore the source record for details and available documents.
Noscapine, a non-narcotic, centrally-acting anti-tussive drug induces polyploidy in Chinese hamster CHL cells; further studies were carried out to investigate whether similar effects could be induced in other rodent cells (Chinese hamster V79) and in human lymphocytes. In both cases, large increases in the frequency of polyploid cells were induced at test concentrations ranging from 15 to 120 micrograms/ml after 24 and 48 h continuous treatment in the absence of S9 mix. In addition, spindle damage was observed in V79 cells and human skin fibroblasts after 24 h treatment with test concentrations of 30 and 60 micrograms/ml. Furthermore, after treatment of human skin fibroblasts there was a marked increase in the proportion of cells containing chromosomes which had become dislocated from the spindle. Treatment of the mouse/human hybrid cell line R3-5 induced a significant increase in the number of 6-thioguanine resistant colonies and it was confirmed cytogenetically that these colonies had arisen due to loss of human chromosome 2. From these experiments it can be concluded that noscapine induces polyploidy in both rodent and human somatic cells, and that this could arise through a direct effect upon spindle structure and/or function. The aneugenic properties of noscapine are less certain and further work is required in this area. Exposure to the drug through its therapeutic use (15mg up to four times daily) could exceed, at least locally within the gastrointestinal (GI) tract, the concentration range shown to be active in these in vitro studies. An immediate topical hazard might exist within the buccal cavity and GI tract, but further confirmation of these in vitro results are required using suitable in vivo systems before definite conclusions can be made regarding any potential hazard associated with the administration of this drug.
Explore the source record for details and available documents.