Estimation of the Adenoma Detection Rate From the Polyp Detection Rate by Using a Conversion Factor in a Predominantly Hispanic Population.

BACKGROUND: Calculating the adenoma detection rate (ADR) is a complex process in contrast to the polyp detection rate (PDR) that can be easily calculated. The average adenoma to polyp detection rate quotient (APDRQ) was proposed as a conversion factor to estimate the ADR for individual endoscopists from the endoscopist's PDR. However, this conversion factor was not validated in different practice settings. GOAL: To validate the use of the proposed conversion factor in a practice setting with a predominantly Hispanic population. STUDY: We conducted a retrospective, cross-sectional study (December 2007 to November 2012) of screening colonoscopies at a university practice setting with an 86.9% Hispanic population. The actual ADR and PDR were calculated for all endoscopists. The weighted average of ADR to PDR ratio for each endoscopist was used to obtain APDRQ. The APDRQ was used as a conversion multiplier to estimate each endoscopist's ADR using the single endoscopist's PDR. RESULTS: A total of 2148 screening colonoscopies were included. The average PDR for the whole group was 36.9% (range, 11% to 49%). The actual ADR was estimated as 25.5% (range, 11% to 37%). The average APDRQ for our group was 0.68. The estimated ADR was 25.48% (range, 8% to 33%). There was a high correlation between actual ADR and the estimated ADR (Pearson correlation=0.92). CONCLUSIONS: In a practice setting with a predominantly Hispanic population, a conversion factor can be used to estimate ADR from PDR providing a high degree of correlation with the actual ADR.

Quantifying school officials' exposure to bacterial pathogens at graduation ceremonies using repeated observational measures.

The purpose of this study was to estimate the risk of acquiring pathogenic bacteria as a result of shaking hands at graduation ceremonies. School officials participating in graduation ceremonies at elementary, secondary, and postsecondary schools were recruited. Specimens were collected before and immediately following graduation. Cultures identified any pathogenic bacteria in each specimen. Subjects shook a total of 5,209 hands. Staphylococcus aureus was separately detected on one pregraduation right hand, one postgraduation right hand, and one postgraduation left hand. Nonpathogenic bacteria were collected in 93% of specimens. Pregraduation and postgraduation specimens were of different strains. We measured a risk of one new bacterial acquisition in a sample exposed to 5,209 handshakes yielding an overall estimate of 0.019 pathogens acquired per handshake. We conclude that a single handshake at a graduation offers only a small risk of bacterial pathogen acquisition.

Inhibition of the soluble epoxide hydrolase promotes albuminuria in mice with progressive renal disease.

Epoxyeicotrienoic acids (EETs) are cytochrome P450-dependent anti-hypertensive and anti-inflammatory derivatives of arachidonic acid, which are highly abundant in the kidney and considered reno-protective. EETs are degraded by the enzyme soluble epoxide hydrolase (sEH) and sEH inhibitors are considered treatment for chronic renal failure (CRF). We determined whether sEH inhibition attenuates the progression of CRF in the 5/6-nephrectomy model (5/6-Nx) in mice. 5/6-Nx mice were treated with a placebo, an ACE-inhibitor (Ramipril, 40 mg/kg), the sEH-inhibitor cAUCB or the CYP-inhibitor fenbendazole for 8 weeks. 5/6-Nx induced hypertension, albuminuria, glomerulosclerosis and tubulo-interstitial damage and these effects were attenuated by Ramipril. In contrast, cAUCB failed to lower the blood pressure and albuminuria was more severe as compared to placebo. Plasma EET-levels were doubled in 5/6 Nx-mice as compared to sham mice receiving placebo. Renal sEH expression was attenuated in 5/6-Nx mice but cAUCB in these animals still further increased the EET-level. cAUCB also increased 5-HETE and 15-HETE, which derive from peroxidation or lipoxygenases. Similar to cAUCB, CYP450 inhibition increased HETEs and promoted albuminuria. Thus, sEH-inhibition failed to elicit protective effects in the 5/6-Nx model and showed a tendency to aggravate the disease. These effects might be consequence of a shift of arachidonic acid metabolism into the lipoxygenase pathway.

CHWs get credit: a 10-year history of the first college-credit certificate for community health workers in the United States.

Community health workers have become increasingly important in the U.S. health care system, playing a significant role in basic health promotion and care coordination; however, their status and visibility have not kept pace with their wider use. A major impediment has been the absence of systematic preparation-the field needs standardized education in programs that emphasize the actual skills and knowledge used by community health workers, programs that attract and retain nontraditional students from underserved communities and that foster professional advancement. This article chronicles the 10-year history of the first college credit-bearing community health worker certificate program in the country to address this need. Systematic research resulted in a program centered on the core competencies universally practiced by community health workers regardless of their topical focus. The certificate program combines performance-based methods with popular education into an innovative pedagogical approach that teaches skills, while solidifying, contextualizing, and enhancing crucial experiential knowledge. Program outcomes validate the approach.

Tyrphostins protect neuronal cells from oxidative stress.

Tyrphostins are a family of tyrosine kinase inhibitors originally synthesized as potential anticarcinogenic compounds. Because tyrphostins have chemical structures similar to those of the phenolic antioxidants, we decided to test the protective efficacy of tyrphostins against oxidative stress-induced nerve cell death (oxytosis). Many commercially available tyrphostins, at concentrations ranging from 0.5 to 200 microm, protect both HT-22 hippocampal cells and rat primary neurons from oxytosis brought about by treatment with glutamate, as well as by treatment with homocysteic acid and buthionine sulfoximine. The tyrphostins protect nerve cells by three distinct mechanisms. Some tyrphostins, such as A25, act as antioxidants and eliminate the reactive oxygen species that accumulate as a result of glutamate treatment. These tyrphostins also protect cells from hydrogen peroxide and act as antioxidants in an in vitro assay. In contrast, tyrphostins A9 and AG126 act as mitochondrial uncouplers, collapsing the mitochondrial membrane potential and thereby reducing the generation of reactive oxygen species from mitochondria during glutamate toxicity. Finally, the third group of tyrphostins does not appear to be effective as antioxidants but rather protects cells by increasing the basal level of cellular glutathione. Therefore, the effects of tyrphostins on cells are not limited to their ability to inhibit tyrosine kinases.