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Articles by A Johnson
Total Records ( 3 ) for A Johnson
  M. M Saba , J Akella , J Gammie , R Poston , A Johnson , R. E Hood , T. M Dickfeld and S. R. Shorofsky
  Aims

Reference values exist for endocardial but not for epicardial (EPI) substrate mapping in cases of cardiomyopathy-associated ventricular tachycardia. We sought to establish such values for EPI electrogram voltage, including areas with overlying fat.

Methods and results

Ten patients (six males) undergoing cardiac surgery were studied. After opening the pericardium, the distal bipole of an electrophysiology catheter was placed tangential to the EPI surface to obtain an electrogram recording. The bipole was tangentially rotated 90° and the higher of the two amplitudes (mV) was taken as the local amplitude. Recordings were taken from normal left and right ventricular myocardium (n = 26 data points each), over thick (≥0.5 cm) fat at both ventricular bases (n = 16) and thin (<0.5 cm) fat at the mid-ventricular level (n = 32). A total of 100 recordings (mean 10/patient) were analysed. Four patients underwent valvular surgery, three bypass surgery, and three combined procedures. Mean age was 61.7 ± 10.4 years and mean left ventricular ejection fraction was 46 ± 12%. Electrogram amplitude was inversely related to EPI fat thickness. Over thick fat, 31% of recordings were <0.5 mV.

Conclusion

Human EPI electrogram amplitude varies by ventricular chamber and significantly by EPI fat thickness. A cut-off of 0.5 mV to define ‘scar’ will include normal areas with thick overlying fat. EPI substrate maps should include data on EPI fat thickness for higher specificity.

  D Baris , M. R Karagas , C Verrill , A Johnson , A. S Andrew , C. J Marsit , M Schwenn , J. S Colt , S Cherala , C Samanic , R Waddell , K. P Cantor , A Schned , N Rothman , J Lubin , J. F Fraumeni , R. N Hoover , K. T Kelsey and D. T. Silverman
  Background

Cigarette smoking is a well-established risk factor for bladder cancer. The effects of smoking duration, intensity (cigarettes per day), and total exposure (pack-years); smoking cessation; exposure to environmental tobacco smoke; and changes in the composition of tobacco and cigarette design over time on risk of bladder cancer are unclear.

Methods

We examined bladder cancer risk in relation to smoking practices based on interview data from a large, population-based case–control study conducted in Maine, New Hampshire, and Vermont from 2001 to 2004 (N = 1170 urothelial carcinoma case patients and 1413 control subjects). We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression. To examine changes in smoking-induced bladder cancer risk over time, we compared odds ratios from New Hampshire residents in this study (305 case patients and 335 control subjects) with those from two case–control studies conducted in New Hampshire in 1994–1998 and in 1998–2001 (843 case patients and 1183 control subjects).

Results

Regular and current cigarette smokers had higher risks of bladder cancer than never-smokers (for regular smokers, OR = 3.0, 95% CI = 2.4 to 3.6; for current smokers, OR = 5.2, 95% CI = 4.0 to 6.6). In New Hampshire, there was a statistically significant increasing trend in smoking-related bladder cancer risk over three consecutive periods (1994–1998, 1998–2001, and 2002–2004) among former smokers (OR = 1.4, 95% CI = 1.0 to 2.0; OR = 2.0, 95% CI = 1.4 to 2.9; and OR = 2.6, 95% CI = 1.7 to 4.0, respectively) and current smokers (OR = 2.9, 95% CI = 2.0 to 4.2; OR = 4.2, 95% CI = 2.8 to 6.3; OR = 5.5, 95% CI = 3.5 to 8.9, respectively) (P for homogeneity of trends over time periods = .04). We also observed that within categories of intensity, odds ratios increased approximately linearly with increasing pack-years smoked, but the slope of the increasing trend declined with increasing intensity.

Conclusions

Smoking-related risks of bladder cancer appear to have increased in New Hampshire since the mid-1990s. Based on our modeling of pack-years and intensity, smoking fewer cigarettes over a long time appears more harmful than smoking more cigarettes over a shorter time, for equal total pack-years of cigarettes smoked.

  S. E Dunn , R Bhat , D. S Straus , R. A Sobel , R Axtell , A Johnson , K Nguyen , L Mukundan , M Moshkova , J. C Dugas , A Chawla and L. Steinman
 

Peroxisome proliferator–activated receptors (PPARs; PPAR-, PPAR-, and PPAR-) comprise a family of nuclear receptors that sense fatty acid levels and translate this information into altered gene transcription. Previously, it was reported that treatment of mice with a synthetic ligand activator of PPAR-, GW0742, ameliorates experimental autoimmune encephalomyelitis (EAE), indicating a possible role for this nuclear receptor in the control of central nervous system (CNS) autoimmune inflammation. We show that mice deficient in PPAR- (PPAR-–/–) develop a severe inflammatory response during EAE characterized by a striking accumulation of IFN-+IL-17A and IFN-+IL-17A+ CD4+ cells in the spinal cord. The preferential expansion of these T helper subsets in the CNS of PPAR-–/– mice occurred as a result of a constellation of immune system aberrations that included higher CD4+ cell proliferation, cytokine production, and T-bet expression and enhanced expression of IL-12 family cytokines by myeloid cells. We also show that the effect of PPAR- in inhibiting the production of IFN- and IL-12 family cytokines is ligand dependent and is observed in both mouse and human immune cells. Collectively, these findings suggest that PPAR- serves as an important molecular brake for the control of autoimmune inflammation.

 
 
 
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