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Articles by S Lai
Total Records ( 4 ) for S Lai
  R Cianci , P Martina , F Borghesi , D di Donato , L Polidori , S Lai , G Ascoli , I de Francesco , A Zaccaria , A Gigante and B. Barbano

Endovascular procedures may play a role in renal artery stenosis (RAS) treatment in attempt to preserve renal function and improve hypertension control. We determined renal outcome and the incidence of restenosis in patients with RAS treated with renal percutaneous transluminal angioplasty and stenting (RPTAs) and medical therapy versus patients with RAS treated only with medical therapy. We performed an observational study based on 93 patients with RAS. In all, 53 patients underwent RPTAs in association with medical therapy and 40 patients were only treated pharmacologically. In patients receiving RPTAs, a better renal outcome, a decrease of restenosis rate, and systolic—diastolic blood pressure were associated with angiotensin receptor blockers (ARBs) + angiotensin-converting enzyme inhibitors (ACE-is) therapy. In patients treated with medical therapy alone, renal improvement was related to ARBs in association with BBs (β-blockers; P < .0001). This study suggests that medical therapy may exert beneficial effects in patients with RAS.

  P. V Johnston , T Sasano , K Mills , R Evers , S. T Lee , R. R Smith , A. C Lardo , S Lai , C Steenbergen , G Gerstenblith , R Lange and E. Marban

Background— Cardiosphere-derived cells (CDCs) isolated from human endomyocardial biopsies reduce infarct size and improve cardiac function in mice. Safety and efficacy testing in large animals is necessary for clinical translation.

Methods and Results— Mesenchymal stem cells, which resemble CDCs in size and thrombogenicity, have been associated with infarction after intracoronary infusion. To maximize CDC engraftment while avoiding infarction, we optimized the infusion protocol in 19 healthy pigs. A modified cocktail of CDCs in calcium-free PBS, 100 U/mL of heparin, and 250 µg/mL of nitroglycerin eliminated infusion-related infarction. Subsequent infusion experiments in 17 pigs with postinfarct left ventricular dysfunction showed CDC doses ≥107 but <2.5x107 result in new myocardial tissue formation without infarction. In a pivotal randomized study, 7 infarcted pigs received 300 000 CDCs/kg (107 total) and 7 received placebo (vehicle alone). Cardiac magnetic resonance imaging 8 weeks later showed CDC treatment decreased relative infarct size (19.2% to 14.2% of left ventricle infarcted, P=0.01), whereas placebo did not (17.7% to 15.3%, P=0.22). End-diastolic volume increased in placebo, but not in CDC-treated animals. Hemodynamically, the rate of pressure change (dP/dt) maximum and dP/dt minimum were significantly better with CDC infusion. There was no difference between groups in the ability to induce ventricular tachycardia, nor was there any tumor or ectopic tissue formation.

Conclusions— Intracoronary delivery of CDCs in a preclinical model of postinfarct left ventricular dysfunction results in formation of new cardiac tissue, reduces relative infarct size, attenuates adverse remodeling, and improves hemodynamics. The evidence of efficacy without obvious safety concerns at 8 weeks of follow-up motivates human studies in patients after myocardial infarction and in chronic ischemic cardiomyopathy.

  K. V Tarasov , S Sanna , A Scuteri , J. B Strait , M Orru , A Parsa , P. I Lin , S Lai , M. G Piras , M Masala , T Tanaka , W Post , J. R O`Connell , D Schlessinger , A Cao , R Nagaraja , B. D Mitchell , G. R Abecasis , A. R Shuldiner , M Uda , E. G Lakatta and S. S. Najjar

Background— Pulse wave velocity (PWV), a noninvasive index of central arterial stiffness, is a potent predictor of cardiovascular mortality and morbidity. Heritability and linkage studies have pointed toward a genetic component affecting PWV. We conducted a genome-wide association study to identify single-nucleotide polymorphisms (SNPs) associated with PWV.

Methods and Results— The study cohort included participants from the SardiNIA study for whom PWV measures were available. Genotyping was performed in 4221 individuals, using either the Affymetrix 500K or the Affymetrix 10K mapping array sets (with imputation of the missing genotypes). Associations with PWV were evaluated using an additive genetic model that included age, age2, and sex as covariates. The findings were tested for replication in an independent internal Sardinian cohort of 1828 individuals, using a custom chip designed to include the top 43 nonredundant SNPs associated with PWV. Of the loci that were tested for association with PWV, the nonsynonymous SNP rs3742207 in the COL4A1 gene on chromosome 13 and SNP rs1495448 in the MAGI1 gene on chromosome 3 were successfully replicated (P=7.08x10–7 and P=1.06x10–5, respectively, for the combined analyses). The association between rs3742207 and PWV was also successfully replicated (P=0.02) in an independent population, the Old-Order Amish, leading to an overall P=5.16x10–8.

Conclusions— A genome-wide association study identified a SNP in the COL4A1 gene that was significantly associated with PWV in 2 populations. Collagen type 4 is the major structural component of basement membranes, suggesting that previously unrecognized cell-matrix interactions may exert an important role in regulating arterial stiffness.

  S Sanna , F Busonero , A Maschio , P. F McArdle , G Usala , M Dei , S Lai , A Mulas , M. G Piras , L Perseu , M Masala , M Marongiu , L Crisponi , S Naitza , R Galanello , G. R Abecasis , A. R Shuldiner , D Schlessinger , A Cao and M. Uda

Bilirubin, resulting largely from the turnover of hemoglobin, is found in the plasma in two main forms: unconjugated or conjugated with glucuronic acid. Unconjugated bilirubin is transported into hepatocytes. There, it is glucuronidated by UGT1A1 and secreted into the bile canaliculi. We report a genome wide association scan in 4300 Sardinian individuals for total serum bilirubin levels. In addition to the two known loci previously involved in the regulation of bilirubin levels, UGT1A1 (P = 6.2 x 10–62) and G6PD (P = 2.5 x 10–8), we observed a strong association on chromosome 12 within the SLCO1B3 gene (P = 3.9 x 10–9). Our findings were replicated in an independent sample of 1860 Sardinians and in 832 subjects from the Old Order Amish (combined P < 5 x 10–14). We also show that SLC01B3 variants contribute to idiopathic mild unconjugated hyperbilirubinemia. Thus, SLC01B3 appears to be involved in the regulation of serum bilirubin levels in healthy individuals and in some bilirubin-related disorders that are only partially explained by other known gene variants.

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