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“BACKGROUND: Overcrowded emergency departments
(EDs) are used by undiagnosed tuberculosis (TB) patients. TB infection control measures are seldom prioritised, making EDs potential foci of unrecognised nosocomial transmission.
OBJECTIVE: To quantify TB infection risk among health care workers in an ED in a high TB-burden setting, Lima, Peru, and to evaluate TB infection control measures.
METHODS: Consenting ED staff were tested for TB infection at baseline and after 1 year using the Quanti-FERON(R)-TB Gold In-Tube (QFT-G). In parallel, sputum for TB culture was requested from patients spending >2 h in the ED, irrespective of presenting complaint. PF-02341066 Protein Tyrosine Kinase inhibitor Infection control measures were documented and room ventilation measured.
RESULTS: Over 1 year, there were 2246 TB patient-hours of exposure in the ED from 153 different patients. At baseline, 56% of the 70 staff recruited were QFT-G-positive; 27 of 31 baseline-negatives GW786034 consented to follow-up after 1 year, and eight (30%, all clinical staff) tested positive. Annual incidence of infection was 1730 per 100000 population. TB infection control measures were sub-optimal, with no patient screening,
no isolation rooms, inadequate ventilation and sporadic respirator use.
CONCLUSIONS: ED staff were exposed to an unexpectedly large TB burden in the workplace, resulting in a high rate of TB infection. TB infection control should be prioritised in EDs, especially in high-prevalence
settings.”
“Objective: To investigate the inhibitory effects and the regulatory mechanisms of histone deacetylase (HDAC) inhibitors on mechanical stress-induced gene expression of runt-related transcription factor (RUNX)-2 and a disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)-5 in human chondrocytes.
Methods: Human chondrocytes were seeded in stretch chambers at a concentration of 5 x 10(4) cells/chamber. Cells were pre-incubated buy PLX4032 with or without HDAC inhibitors (MS-275 or trichostatin A; TSA) for 12 h, followed by uniaxial cyclic tensile strain (CTS) (0.5 Hz, 10% elongation), which was applied for 30 min using the ST-140-10 system (STREX, Osaka, Japan). Total RNA was extracted and the expression of RUNX-2, ADAMTS-5, matrix metalloproteinase (MMP)-3, and MMP-13 at the mRNA and protein levels were examined by real-time polymerase chain reaction (PCR) and immunocytochemistry, respectively. The activation of diverse mitogen-activated protein kinase (MAPK) pathways with or without HDAC inhibitors during CTS was examined by western blotting.
Results: HDAC inhibitors (TSA: 10 nM, MS-275: 100 nM) suppressed CTS-induced expression of RUNX-2, ADAMTS-5, and MMP-3 at both the mRNA and protein levels within 1 h. CTS-induced activation of p38 MAPK (p38), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (INK) MAPKs was downregulated by both HDAC inhibitors.