ORCID Profile
0000-0002-5113-299X
Current Organisations
National Autonomous University of Mexico
,
National Institute of Public Health
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Publisher: Oxford University Press (OUP)
Date: 30-04-2018
Publisher: American Diabetes Association
Date: 04-1997
Abstract: Intake of carbohydrates that provide a large glycemic response has been hypothesized to increase the risk of NIDDM, whereas dietary fiber is suspected to reduce incidence. These hypotheses have not been evaluated prospectively. We examined the relationship between diet and risk of NIDDM in a cohort of 42,759 men without NIDDM or cardiovascular disease, who were 40–75 years of age in 1986. Diet was assessed at baseline by a validated semiquantitative food frequency questionnaire. During 6-years of follow-up, 523 incident cases of NIDDM were documented. The dietary glycemic index (an indicator of carbohydrate's ability to raise blood glucose levels) was positively associated with risk of NIDDM after adjustment for age, BMI, smoking, physical activity, family history of diabetes, alcohol consumption, cereal fiber, and total energy intake. Comparing the highest and lowest quintiles, the relative risk (RR) of NIDDM was 1.37 (95% CI, 1.02–1.83, P trend = 0.03). Cereal fiber was inversely associated with risk of NIDDM (RR = 0.70 95% CI, 0.51–0.96, P trend = 0.007 for & 8.1 g/day vs. & 3.2 g/day). The combination of a high glycemic load and a low cereal fiber intake further increased the risk of NIDDM (RR = 2.17, 95% CI, 1.04–4.54) when compared with a low glycemic load and high cereal fiber intake. These findings support the hypothesis that diets with a high glycemic load and a low cereal fiber content increase risk of NIDDM in men. Further, they suggest that grains should be consumed in a minimally refined form to reduce the incidence of NIDDM.
Publisher: Wiley
Date: 09-09-2016
DOI: 10.1002/IJC.30391
Publisher: Elsevier BV
Date: 10-2016
Publisher: Elsevier BV
Date: 12-2014
Publisher: American Society for Microbiology
Date: 02-2015
DOI: 10.1128/CVI.00457-14
Abstract: The efficacy of the human papillomavirus type 16 (HPV-16)/HPV-18 AS04-adjuvanted vaccine against cervical infections with HPV in the Pa pilloma Tri al against C ancer i n Young A dults (PATRICIA) was evaluated using a combination of the broad-spectrum L1-based SPF 10 PCR-DNA enzyme immunoassay (DEIA)/line probe assay (LiPA 25 ) system with type-specific PCRs for HPV-16 and -18. Broad-spectrum PCR assays may underestimate the presence of HPV genotypes present at relatively low concentrations in multiple infections, due to competition between genotypes. Therefore, s les were retrospectively reanalyzed using a testing algorithm incorporating the SPF 10 PCR-DEIA/LiPA 25 plus a novel E6-based multiplex type-specific PCR and reverse hybridization assay (MPTS12 RHA), which permits detection of a panel of nine oncogenic HPV genotypes (types 16, 18, 31, 33, 35, 45, 52, 58, and 59). For the vaccine against HPV types 16 and 18, there was no major impact on estimates of vaccine efficacy (VE) for incident or 6-month or 12-month persistent infections when the MPTS12 RHA was included in the testing algorithm versus estimates with the protocol-specified algorithm. However, the alternative testing algorithm showed greater sensitivity than the protocol-specified algorithm for detection of some nonvaccine oncogenic HPV types. More cases were gained in the control group than in the vaccine group, leading to higher point estimates of VE for 6-month and 12-month persistent infections for the nonvaccine oncogenic types included in the MPTS12 RHA assay (types 31, 33, 35, 45, 52, 58, and 59). This post hoc analysis indicates that the per-protocol testing algorithm used in PATRICIA underestimated the VE against some nonvaccine oncogenic HPV types and that the choice of the HPV DNA testing methodology is important for the evaluation of VE in clinical trials. (This study has been registered at ClinicalTrials.gov under registration no. NCT00122681.)
No related grants have been discovered for Jorge Salmerón.