ABSTRACT
PURPOSE: Increasingly, autoidentification technology is being utilized in healthcare settings to make delivery of care cheaper, more efficient, and safer. However, the risk of electromagnetic interference (EMI) when using these autoidentification systems is not entirely clear. Thus, we sough to evaluate the likelihood of electromagnetic interference (EMI) in high technology healthcare areas with a low frequency, magnetic-field based wireless autoidentification protocol. METHODS: Thirty-two devices were tested for EMI with an autoidentification technology whose maximal magnetic field output ranged from 8 to 800mgauss between November 2008 and March 2009. Testing was performed at Mayo Clinic (Rochester, MN) and Holy Cross Hospital (Miami, FL). All tests were started from 4 feet away and devices were approached in 1 foot increments with the signal antenna. EMI was characterized as light, significant, hazardous, or none per established testing standards. Significant to hazardous EMI was considered to potentially cause significant problems with clinical management of patients. RESULTS: Of 32 devices, light to hazardous EMI was seen in 8 (25%). Hazardous EMI was seen in 2 12-lead ECG machines, significant EMI in fluoroscopy, echocardiograms, and 1 of 5 cardiac monitors, and light EMI in a defibrillator and cardiac monitor. Average magnetic field strengths experienced by the devices were similar at each distance regardless of the presence of EMI. No EMI was recorded with any device at distances greater than 4 feet, with no loss of signal fidelity at distances up to 17 feet. CONCLUSION: A low frequency, magnetic field based wireless autoidentification technology induced distance dependent EMI in healthcare settings, making implementation potentially safe at antenna distances greater than 4 feet from clinical equipment. However, implementation requires rigorous in vivo testing to ensure the antenna is located a safe distance away.
Subject(s)
Electronics/instrumentation , Equipment Failure , Magnetics/instrumentation , Patient Identification Systems , Electromagnetic Fields , Equipment Design , Equipment Failure AnalysisABSTRACT
Terahertz time-domain spectroscopy (THZ-TDS) has been used to measure the absorption spectra in the range 7-100 cm(-1) (0.2-3 THz) of single crystal pentaerythritol tetranitrate (PETN). Absorption was measured in transmission mode as a function of incident polarization with the incident and transmitted wave vectors oriented along the crystallographic directions [100], <10(a/c)(2)>, and <110>. Samples were rotated with respect to the incident polarization while absorption was measured at both 300 and 20 K. Comparatively minor differences were observed among the three orientations. Two broad absorptions at 72 and >90 cm(-1), and several weaker absorptions at 36, 55, 80, and 82 cm(-1), have been observed at cryogenic temperatures.
ABSTRACT
Evidence that a gene or genes on chromosome 22 is involved in susceptibility to schizophrenia comes from two sources: the increased incidence of schizophrenia in individuals with 22q11 deletion syndrome (22q11DS) and genetic linkage studies. In mice, hemizygous deletion of either Tbx1 or Gnb1l can cause deficits in pre-pulse inhibition, a sensory motor gating defect which is associated with schizophrenia. We tested the hypothesis that variation at this locus confers risk of schizophrenia and related disorders in a series of case-control association studies. First, we found evidence for a male-specific genotypic association (P = 0.00017) TBX1/GNB1L in 662 schizophrenia cases and 1416 controls from the UK. Moreover, we replicated this finding in two independent case-control samples (additional 746 cases and 1330 controls) (meta analysis P = 1.8 x 10(-5)) and also observed significant evidence for genotypic association in an independent sample of 480 schizophrenia parent-proband trios from Bulgaria with markers at this locus, which was again strongest in the male probands (P = 0.004). Genotyping the most significant SNPs in a sample of 83 subjects with 22q11DS with and without psychosis again revealed a significant allelic association with psychosis in males with 22q11DS (P = 0.01). Finally, using allele specific expression analysis, we have shown that the markers associated with psychosis are also correlated with alterations in GNB1L expression, raising the hypothesis that the risk to develop psychosis at this locus could be mediated in a dose sensitive manner via gene expression. However, other explanations are possible, and further analyses will be required to clarify the correct functional mechanism.
