Publications

BACKGROUND

Few studies have examined whether patients with language barriers receive worse hospital care in terms of quality or efficiency.

OBJECTIVE

: To examine whether patients' primary language influences hospital outcomes.

DESIGN AND SETTING

Observational cohort of urban university hospital general medical admissions between July 1, 2001 to June 30, 2003.

PATIENTS

Eighteen years old or older whose hospital data included information on their primary language, specifically English, Russian, Spanish or Chinese.

MEASUREMENTS

Hospital costs, length of stay (LOS), and odds for 30-day readmission or 30-day mortality.

RESULTS

Of 7023 admitted patients, 84% spoke English, 8% spoke Chinese, 4% Russian and 4% Spanish. In multivariable models, non-English and English speakers had statistically similar total cost, LOS, and odds for mortality. However, non-English speakers had higher adjusted odds of readmission (odds ratio [OR], 1.3; 95% confidence interval [CI], 1.0-1.7). Higher odds for readmission persisted for Chinese and Spanish speakers when compared to all English speakers (OR, 1.7; 95% CI, 1.2-2.3 and OR, 1.5; 95% CI, 1.0-2.3 respectively).

CONCLUSIONS

After accounting for socioeconomic variables and comorbidities, non-English speaking Latino and Chinese patients have higher risk for readmission. Whether language barriers produce differences in readmission or are a marker for less access to post-hospital care remains unclear. Journal of Hospital Medicine 2010;5:276-282. (c) 2010 Society of Hospital Medicine.

The beneficial effects of high-density lipoprotein (HDL) on atherosclerosis have largely been attributed to its major protein, apolipoprotein A-I (apoA-I). Used as a therapeutic intervention, apoA-I is a large protein that requires venous administration, and is both difficult and expensive to manufacture. Because of these problems with apoA-I, the generation of smaller, easier to manufacture apoA-I mimetic peptides has become a target for pharmacologic development in the therapeutic management of human atherosclerosis. A potent apoA-I mimetic peptide, 4F, was found to have significant activity in various inflammatory states in both mice and monkeys. The anti-inflammatory and antiatherogenic effects of 4F include increased pre-beta HDL formation, increased cholesterol efflux, the conversion of pro-inflammatory HDL to anti-inflammatory HDL, and reduced lipoprotein oxidation. In addition, improved arterial vasoreactivity is another important function of 4F. In a rat model of diabetes, D-4F increased arterial concentrations of heme oxygenase-1 (HO-1) and superoxide dismutase, decreased superoxide levels, reduced levels of circulating endothelial cells, decreased endothelial cell fragmentation, and restored arterial vasoreactivity to normal. In a mouse model of systemic sclerosis, D-4F functioned to improve vasodilation and angiogenic potential, while reducing myocardial inflammation and oxidative stress. With respect to mouse models of heart transplant-associated atherosclerosis, D-4F induced HO-1. In addition, D-4F was shown to improve cognitive performance in low-density lipoprotein-receptor null mice with Western diet-induced cognitive decline. D-4F also reduced the kidney content of oxidized phospholipids in a mouse model of hyperlipidemia-induced renal inflammation. In early human studies in patients with significant cardiovascular risk, a single dose of oral D-4F was found to safely improve the anti-inflammatory index of HDL. L-4F is also being studied in clinical trials as a potential treatment modality for obesity and the metabolic syndrome.

SUMMARY

In response to acute infections or vaccines, naive antigen-specific CD8(+) T cells proliferate and differentiate into effector cytotoxic lymphocytes that acquire the ability to kill infected cells. While the majority of differentiated effector cells die after pathogen clearance, a small number evade terminal differentiation, downregulate active effector functions, and survive as long-lived, self-renewing memory T cells. Our understanding of how effector CD8(+) T cells adopt these different cell fates has grown greatly in recent years. In this review, we discuss the transcriptional regulators that are known to support general effector differentiation, terminal effector differentiation, and memory cell formation. We propose that the diversity of activated CD8(+) T-cell differentiation states is achieved via gradients of activity or expression of transcriptional regulators that are regulated by the level of inflammation and antigenic signaling the T cells experience during infection.

A prospective cohort design was used to measure the association between daily cotrimoxazole-prophylaxis and infection with Plasmodium falciparum containing mutations associated with antifolate resistance among persons infected with human immunodeficiency virus (HIV) in Tororo and Busia District, in eastern Uganda. Of 149 cases of P. falciparum parasitemia diagnosed, 147 (99%) (smears from participants taking prophylaxis = 91 and smears from those not taking cotrimoxazole prophylaxis = 56) were successfully assessed for mutations in the dihydrofolate reductase (dhfr) and dihydropteroate synthase (dhps) mutations associated with antifolate resistance. Prevalences of the dhfr pure triple mutant (74% and 70%; P = 0.71), the dhps pure double mutant (95% and 88%; P = 0.21), and the dhfr/dhps pure quintuple mutant (73% and 64%; P = 0.36), were not significantly different between those taking and those not taking cotrimoxazole-prophylaxis, respectively. The overall prevalence of the pure quintuple mutant in this study was 69%, which is among the highest in Africa. Although resistance rates of P. falciparum to antifolate drugs are high, cotrimoxazole-prophylaxis in HIV-infected persons was not associated with a higher prevalence of mutations associated with antifolate resistance.