Estimating health literacy in family medicine clinics in metropolitan Detroit: a MetroNet study.

OBJECTIVE: Assessing health literacy during the clinical encounter is difficult. Many established instruments are lengthy and not practical for use in a busy practice setting. Our objective was to compare the performance of 3 health literacy screening questions against the Short Test of Functional Health Literacy for Adults (S-TOFHLA) in an urban, ethnically diverse primary care practice-based research network. METHODS: A convenience sample of patients in clinics in the Detroit area were recruited to complete a questionnaire that included the S-TOFHLA and 3 items similar to the Chew screening questions. Area under the receiver operating characteristic (AUROC) curves compared the test characteristics of the screening questions to the S-TOFHLA. RESULTS: The participation rate was 92% (N = 599). Most participants were women (65%) and African American (51%); 51.8% had a household annual income of <$20,000. Almost all (96.7%) had an adequate score on the S-TOFHLA. The screening question with the largest AUROC (0.83; 95% CI, 0.70-0.95) was "How often do you have someone help you read instructions, pamphlets or other written materials from your doctor or pharmacy?"; the AUROC for all 3 questions was 0.90 (95% CI, 0.85-0.95). CONCLUSIONS: Self-administration of the 3 screening questions demonstrated high performance compared with the 36-item S-TOFHLA interview instrument. These screening questions should help providers identify patients who may need extra support to follow health prescriptions.

VACM-1/cul5 expression in vascular tissue in vivo is induced by water deprivation and its expression in vitro regulates aquaporin-1 concentrations.

VACM-1, a cul5 gene product, when overexpressed in vitro, has an antiproliferative effect. In vivo, VACM-1/cul5 is present in tissues involved in the regulation of water balance. Neither proteins targeted for VACM-1/cul5-specific degradation nor factors that may regulate its expression in those tissues have been studied. To identify genes that may be misregulated by VACM-1 cDNA, we performed microarray analysis. Our results indicate that in cos-1 cells transfected with VACM-1 cDNA, mRNA levels for several genes, including AQP1, were decreased when compared to the control group. Our results also indicate that in cos-1 cells transfected with VACM-1 cDNA, endogenous AQP1 protein was decreased about 6-fold when compared to the controls. To test the hypothesis that VACM-1/cul5 may be regulated by conditions that compromise water homeostasis in vivo, we determined if 24 h of water deprivation affects VACM-1/cul5 levels or the effect of VACM-1/cul5 on AQP1. VACM-1 mRNA and protein levels were significantly higher in rat mesenteric arteries, skeletal muscle and the heart ventricle but not in the heart atrium from 24-h water-deprived rats when compared to the controls. Interestingly, 24 h of water deprivation increased modification of VACM-1 by an ubiquitin-like protein, Nedd8, essential for cullin-dependent E3 ligase activity. Although water deprivation did not significantly change AQP1 levels in the mesenteric arteries, AQP1 protein concentrations were inversely correlated with the ratio of the VACM-1 to Nedd8-modified VACM-1. These results suggest that VACM-1/cul5 may regulate endothelial AQP1 concentration both in vivo and in vitro.

Truncated form of VACM-1/cul-5 with an extended 3' untranslated region stimulates cell growth via a MAPK-dependent pathway.

We have sequenced a 4.9kb clone (KLB22) which shares 99% sequence homology with the rabbit vasopressin-activated calcium mobilizing (VACM-1) protein. The 5' terminus sequence of KLB22 cDNA (nucleotides 1-1961) is continuous and overlapping with nucleotides 1226-3186 of the VACM-1 cDNA sequence. The 3'UTR of KLB22 cDNA extends beyond the 3'UTR of VACM-1 by 2999nt. KLB22 cDNA encodes a 497 amino acid protein, which putatively begins at Met 284 of the 780 amino acid VACM-1 protein. The in vitro translation of KLB22 cDNA yields a 59kDa protein. When expressed in cos-1 cells, the truncated VACM-1 protein localizes to the nucleus. KLB22 cDNA transfected cells show increased growth rates and increased levels of phosphorylated MAPK when compared to the vector or to VACM-1 cDNA transfected cells. Finally, in vivo, KLB22 protein expression is tissue specific and can be detected in kidney and in heart atrium. These results suggest that truncated VACM-1 cDNA (KLB22) increases cell proliferation through a MAPK pathway.