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Articles by L Hou
Total Records ( 2 ) for L Hou
  A Baccarelli , I Martinelli , V Pegoraro , S Melly , P Grillo , A Zanobetti , L Hou , P. A Bertazzi , P. M Mannucci and J. Schwartz
 

Background— Particulate air pollution has been consistently linked to increased risk of arterial cardiovascular disease. Few data on air pollution exposure and risk of venous thrombosis are available. We investigated whether living near major traffic roads increases the risk of deep vein thrombosis (DVT), using distance from roads as a proxy for traffic exposure.

Methods and Results— From 1995 through 2005, we examined 663 patients with DVT of the lower limbs and 859 age-matched controls from cities with population >15 000 inhabitants in Lombardia Region, Italy. We assessed distance from residential addresses to the nearest major traffic road using geographic information system methodology. The risk of DVT was estimated from logistic regression models adjusting for multiple clinical and environmental covariates. The risk of DVT was increased (odds ratio=1.33; 95% confidence interval, 1.03 to 1.71; P=0.03 in age-adjusted models; odds ratio=1.47; 95% confidence interval, 1.10 to 1.96; P=0.008 in models adjusted for multiple covariates) for subjects living near a major traffic road (index distance of 3 meters, 10th centile of the distance distribution) compared with those living farther away (reference distance of 245 meters, 90th centile). The increase in DVT risk was approximately linear over the observed distance range (from 718 to 0 meters) and was not modified after adjusting for background levels of particulate matter (odds ratio=1.47; 95% confidence interval, 1.11 to 1.96; P=0.008 for 10th versus 90th distance centile in models adjusting for area levels of particulate matter <10 µm in aerodynamic diameter in the year before diagnosis).

Conclusions— Living near major traffic roads is associated with increased risk of DVT.

  L Hou , M Deo , P Furspan , S. V Pandit , S Mironov , D. S Auerbach , Q Gong , Z Zhou , O Berenfeld and J. Jalife
  Rationale:

The rapid delayed rectifier potassium current, IKr, which flows through the human ether-a-go-go-related (hERG) channel, is a major determinant of the shape and duration of the human cardiac action potential (APD). However, it is unknown whether the time dependency of IKr enables it to control APD, conduction velocity (CV), and wavelength (WL) at the exceedingly high activation frequencies that are relevant to cardiac reentry and fibrillation.

Objective:

To test the hypothesis that upregulation of hERG increases functional reentry frequency and contributes to its stability.

Methods and Results:

Using optical mapping, we investigated the effects of IKr upregulation on reentry frequency, APD, CV, and WL in neonatal rat ventricular myocyte (NRVM) monolayers infected with GFP (control), hERG (IKr), or dominant negative mutant hERG G628S. Reentry frequency was higher in the IKr-infected monolayers (21.12±0.8 Hz; n=43 versus 9.21±0.58 Hz; n=16; P<0.001) but slightly reduced in G628S-infected monolayers. APD80 in the IKr-infected monolayers was shorter (>50%) than control during pacing at 1 to 5 Hz. CV was similar in both groups at low frequency pacing. In contrast, during high-frequency reentry, the CV measured at varying distances from the center of rotation was significantly faster in IKr-infected monolayers than controls. Simulations using a modified NRVM model predicted that rotor acceleration was attributable, in part, to a transient hyperpolarization immediately following the AP. The transient hyperpolarization was confirmed experimentally.

Conclusions:

hERG overexpression dramatically accelerates reentry frequency in NRVM monolayers. Both APD and WL shortening, together with transient hyperpolarization, underlies the increased rotor frequency and stability.

 
 
 
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