Abstract. Sulfate particles play a key role in the air quality and the global climate, but the heterogeneous formation mechanism of sulfates on surfaces of atmospheric particles is not well established. Carbonates, which act as a reactive component in mineral dust due to their special chemical properties, may contribute significantly to the sulfate formation by heterogeneous processes. This paper presents a study on the oxidation of SO 2 by O 3 on CaCO 3 particles. Using Diffuse Reflectance Infrared Fourier Transform Spectroscopy (DRIFTS), the formation of sulfite and sulfate on the surface was identified, and the roles of O 3 and water in oxidation processes were determined. The results showed that in the presence of O 3 , SO 2 can be oxidized to sulfate on the surface of CaCO 3 particles. The reaction is first order in SO 2 and zero order in O 3 . The reactive uptake coefficient for SO 2 [(0.6-9.8)×10 14 molecule cm −3 ] oxidation by O 3 [(1.2-12)×10 14 molecule cm −3 ] was determined to be (1.4±0.3)×10 −7 using the BET area as the reactive area and (7.7±1.6)×10 −4 using the geometric area. A twostage mechanism that involves adsorption of SO 2 followed by O 3 oxidation is proposed and the adsorption of SO 2 on the CaCO 3 surface is the rate-determining step. The proposed mechanism can well explain the experiment results. The atmospheric implications were explored based on a box model calculation. It was found that the heterogeneous reaction might be an important pathway for sulfate formation in the atmosphere.

OBJECTIVES Early thrombosis (ET) contributes to autogenous arteriovenous fistula (AVF) failure. We studied patients undergoing AVF placement in the Hemodialysis Fistula Maturation (HFM) Study, a prospective, observational cohort study, using a nested case-control analysis to identify pre-operative and intra-operative predictors of ET. METHODS ET cases were compared to controls who were matched on gender, age, diabetes, dialysis status, and surgeon fistula volume. ET was defined as thrombosis diagnosed by physical exam or ultrasound within 18 days of AVF creation. Conditional logistic regression models were fit to identify risk factors for ET. RESULTS Thirty-two ET cases (5.3%) occurred among 602 study participants; 198 controls were matched. ET was associated with female gender (OR=2.75, CI 1.19–6.38, P=0.018), fistula location (forearm vs. upper arm) (OR=2.76, CI 1.05–7.23, P=0.039), feeding artery (radial vs. brachial) (OR=2.64, CI 1.03–6.77, P=0.043) and arterial diameter (OR=1.52, CI 1.02–2.26, P=0.039, per mm smaller). Draining vein diameter was nonlinearly associated with ET, with highest risk in 2–3 mm veins. Surprisingly, ET risk was lower in diabetics (OR=0.19, CI 0.07–0.47, P=0.0004), lower with less nitroglycerin-mediated brachial artery dilatation (NMD%) (OR=0.42, CI 0.20–1.92, P=0.029 for each 10% lower) and higher with lower carotid-femoral pulse wave velocity (OR=1.49, CI 1.02–2.20, P=0.041, for each m/sec lower). Intraoperative protamine use was associated with a higher ET risk (OR 3.26, CI 1.28-∞, P=0.038). Surgeon’s intraoperative perceptions were associated with ET: surgeons’ greater concern about maturation success (likely, marginal, unlikely) was associated with higher thrombosis risk (OR 8.09, CI 4.03-∞, p<0.0001, per category change), as were absence vs. presence of intraoperative thrill (OR 21.0, CI 5.07-∞, P=0.0002) and surgeons’ reported frustration during surgery (OR 6.85, CI 2.70-∞, P=0.0004). Reduced extent of intraoperative thrill (proximal, mid or distal third of the forearm or upper arm, based on AVF placement) was also associated with ET (OR 2.91, CI 1.31-∞, P=0.014, per diminished level). Oral antithrombotic medication use was not significantly associated with ET. CONCLUSIONS ET was found to be associated with female gender, forearm AVF, smaller arterial size, draining vein diameter of 2–3 mm, and protamine use. Paradoxically, diabetes and stiff, noncompliant feeding arteries were associated with lower frequency of ET. Absent or attenuated intraoperative thrill, and both surgeon frustration and concern about successful maturation during surgery, were strongly correlated with ET.

Background Gut microbes play a critical role in the production of trimethylamine N-oxide (TMAO), an atherogenic metabolite that impacts platelet responsiveness and thrombosis potential. Involving both microbe and host enzymatic machinery, TMAO generation utilizes a metaorganismal pathway, beginning with ingestion of trimethylamine (TMA)-containing dietary nutrients such as choline, phosphatidylcholine and carnitine, which are abundant in a Western diet. Gut microbial TMA lyases use these nutrients as substrates to produce TMA, which upon delivery to the liver via the portal circulation, is converted into TMAO by host hepatic flavin monooxygenases (FMOs). Gut microbial production of TMA is rate limiting in the metaorganismal TMAO pathway because hepatic FMO activity is typically in excess. Objectives FMO3 is the major FMO responsible for host generation of TMAO; however, a role for FMO3 in altering platelet responsiveness and thrombosis potential in vivo has not yet been explored. Methods The impact of FMO3 suppression (antisense oligonucleotide-targeting) and overexpression (as transgene) on plasma TMAO levels, platelet responsiveness and thrombosis potential was examined using a murine FeCl -induced carotid artery injury model. Cecal microbial composition was examined using 16S analyses. Results Modulation of FMO3 directly impacts systemic TMAO levels, platelet responsiveness and rate of thrombus formation in vivo. Microbial composition analyses reveal taxa whose proportions are associated with both plasma TMAO levels and in vivo thrombosis potential. Conclusions The present studies demonstrate that host hepatic FMO3, the terminal step in the metaorganismal TMAO pathway, participates in diet-dependent and gut microbiota-dependent changes in both platelet responsiveness and thrombosis potential in vivo.