Crystal structures of the Lpt[B.sub.2]FG ABC transporter and of the LptB ATPase dimer bound to ATP have been solved and provide some insights into how ATP hydrolysis drives LPS through the Lpt system [128, 132, 134].
Comparison of the ATP-bound LptB dimer and the nucleotide-free LptB dimer of the Lpt[B.sub.2]FG ABC transporter suggests that ATP binding to the transporter will cause the LptB subunits to rotate ~15[degrees] [128, 134].
LptF is shown in red, while LptG is shown in yellow, and LptB subunits are shown in cyan and blue.
For MPTB and LPTB, single-species RDs were generally null or slightly elevated in early weeks, and null afterward with some negative risks at the latest weeks.
RDs for VPTB, MPTB, and LPTB were generally elevated across all weeks of gestation in single- and multi-species models.
RDs for EC exposure and VPTB, MPTB, and LPTB were higher than would be expected on an additive scale for women of black race/ethnicity and women who smoked during pregnancy (Figure 5).
Associations for EC and LPTB diverged between single- and multi-species models, with negative RDs in single-species models and positive RDs in multi-species models.
(A) ExPTB: birth at 20-27 weeks, (B) VPTB: birth at 28-31 weeks, (C) MPTB: birth at 32-34 weeks, and (D) LPTB: birth at 35-36 weeks of gestation.
For LPTB (Figure 1D), associations were negative with the earliest weeks of exposure, with some positive though fluctuating RDs through week 20.
LPTB RDs are positive for exposures with lags 0-3 and lags 4-5.
For example, with exposure during week 15 of gestation, NNHs for [PM.sub.2.5] and LPTB correspond to 5,587, meaning that for every 1-[micro]g/[m.sup.3] increase in ambient [PM.sub.2.5] concentrations for 5,587 pregnant women, 1 LPTB occurs (assuming associations are causal).
Risk of birth at (4) 20-27 weeks of gestation (ExPTB), (B) 28-31 weeks of gestation (VPTB), (C) 32-34 weeks of gestation (MPTB), and (D) 35-36 weeks of gestation (LPTB).