-S-V-S-A-N-N-V-T-N-N-N-E-T.This sequence is identical from S-152 to T-164 predicted from the nucleotide sequence. So, it seems that the mature hemolysin in V. mimicus is processed upon deleting the first 151 amino acids, and the molecular mass is 65,972 Da. Analyzing the deduced amino-acid sequence, we also found a potential signal sequence of 24 amino acids at the amino terminal. Our results suggest that, like V. cholerae hemolysin, two-step processing also exists in V. mimicus hemolysin.

Methods and Materials:Newly diagnosed patients (Յ90 days prior to REVEAL enrollment) aged Ն19 yrs were divided by reported presyncope/ syncope history: initial pre-diagnosis symptoms only (IS), first PAH-clinic visit only (FV), both IS and FV, or neither IS nor FV. Means (SD) or frequencies (%) describe characteristics at enrollment by presyncope/syncope history. Kaplan-Meier methodology estimated up to three-year survival from enrollment. Results: Patients with presyncope/syncope history at IS and FV (nϭ70) were younger, had a poorer functional class, higher mPAP and mRAP and lower cardiac index compared with patients who did not have presyncope/ syncope history (Table). Three-year survival appears worse for the IS group despite being younger and having better exercise capacity. Conclusions: PAH patients with presyncope/syncope history appear to have more severe disease. It is important to validate the effect and prognosis of reported syncope in PAH as evidence-based PAH treatment guidelines are further defined.Purpose: Pulmonary arterial hypertension (PAH) results from the imbalance of various vasoactive mediators responsible for the vasoconstriction and proliferation of pulmonary arterial (PA) endothelial and smooth-muscle cells. Targeting these neurohormonal mediators has become the mainstay of PAH therapy. In PAH rat models, the administration of relaxin, a potent vasodilatory and anti-fibrotic hormone, significantly attenuated PA remodeling and improved several hemodynamic parameters. To date, no study has measured the levels of relaxin in PAH. Additionally, while recently studied in heart failure, no study has evaluated relaxin levels in diastolic heart failure-induced pulmonary hypertension (DHF-P). As an initial step in evaluating the role of relaxin in the treatment of both PAH and DHF-P, we measured serum relaxin levels in patients with PAH and DHF-P as compared to normal controls. Methods and Materials: We measured serum relaxin levels in patients with PAH (mean PAP Ͼ25 mmHg, with PCWP Ͻ 15 mmHg) and DHF-P (mean PAP Ͼ25 mmHg with gradient PA-diastolic PCWP Յ 5 mmHg) as measured by right-heart catheterization and compared these results to normal controls. Results: Seventeen and 16 patients comprised the PAH and DHF-P groups, respectively. Serum relaxin levels were significantly elevated in the PAH group compared to the DHF-P and control groups (169.4 Ϯ 63.4, 64.0 Ϯ 18.0 and 39.2 Ϯ 22.1, respectively; p ϭ 0.002).Conclusions: This is the first study to measure serum relaxin levels in patients with PAH, and compare them to levels in patients with DHF-P.Relaxin was found to be significantly elevated in PAH as compared to DHF-P and controls, suggesting its role as a compensatory mediator in PAH and highlighting its possible role as a future therapy for PAH.