Publications

Parasitic infections, although common in tropical and subtropical regions, are prevalent worldwide because of changing immigration patterns and in international travel. The burden of worm infection is enormous and the intensity of infection is usually high among the poor and in immunocompromised individuals. Pulmonary eosinophilia occurs in almost all metazoan infections. In the Western world, the most common infections are caused by Strongyloides, Ascaris, Toxocara, and Ancylostoma species. Most of the nematodes multiply within the human host and cause pulmonary eosinophilia during larval migration through the lungs. Despite larval migration through the lungs, there is usually no permanent lung damage. The result is an increased number of eosinophils in the airways or lung parenchyma with or without peripheral eosinophilia. Löffler's syndrome, visceral larva migrans, and tropical pulmonary eosinophilia are the most common infections that cause pulmonary eosinophilia. The most serious parasitic eosinophilic lung disease is tropical pulmonary eosinophilia, a disorder caused by the filarial worms Wuchereria bancrofti and Brugia malayi, in which cases have typically been reported to masquerade acute or refractory bronchial asthma. Increasing awareness, newer diagnostic techniques, preventative measures, and antiparasitic drugs are important in reducing the worldwide morbidity and mortality from parasitic helminths and protozoa. This review focuses on common and some uncommon causes of pulmonary parasitic eosinophilia and their manifestations, diagnosis, and management.

OBJECTIVE

To estimate costs of routine care for female urinary incontinence, health-related quality of life, and willingness to pay for incontinence improvement.

METHODS

In a cross-sectional study at 5 U.S. sites, 293 incontinent women quantified supplies, laundry, and dry cleaning specifically for incontinence. Costs were calculated by multiplying resources used by national resource costs and presented in 2005 United States dollars (2005). Health-related quality of life was estimated with the Health Utilities Index. Participants estimated willingness to pay for 25-100% improvement in incontinence. Potential predictors of these outcomes were examined using multivariable linear regression.

RESULTS

Mean age was 56 +/- 11 years; participants were racially diverse and had a broad range of incontinence severity. Nearly 90% reported incontinence-related costs. Median weekly cost (25%, 75% interquartile range) increased from 0.37 dollars (0, 4 dollars) for slight to 10.98 dollars (4, 21 dollars) for very severe incontinence. Costs increased with incontinence severity (P < .001). Costs were 2.4-fold higher for African American compared with white women (P < .001) and 65% higher for women with urge compared with those having stress incontinence (P < .001). More frequent incontinence was associated with lower Health Utilities Index score (mean 0.90 +/- 0.11 for weekly and 0.81 +/- 0.21 for daily incontinence; P = .02). Women were willing to pay a mean of 70 dollars +/- 64 dollars per month for complete resolution of incontinence, and willingness to pay increased with income and greater expected benefit.

CONCLUSION

Women with severe urinary incontinence pay 900 dollars annually for incontinence routine care, and incontinence is associated with a significant decrement in health-related quality of life. Effective incontinence treatment may decrease costs and improve quality of life.

LEVEL OF EVIDENCE

III.

The proximal region of the NK gene complex encodes the NKR-P1 family of killer cell lectin-like receptors which in mice bind members of the genetically linked C-type lectin-related family, while the distal region encodes Ly49 receptors for polymorphic MHC class I molecules. Although certain members of the NKR-P1 family are expressed by all NK cells, we have identified a novel inhibitory rat NKR-P1 molecule termed NKR-P1C that is selectively expressed by a Ly49-negative NK subset with unique functional characteristics. NKR-P1C(+) NK cells efficiently lyse certain tumor target cells, secrete cytokines upon stimulation, and functionally recognize a nonpolymorphic ligand on Con A-activated lymphoblasts. However, they specifically fail to kill MHC-mismatched lymphoblast target cells. The NKR-P1C(+) NK cell subset also appears earlier during development and shows a tissue distribution distinct from its complementary Ly49s3(+) subset, which expresses a wide range of Ly49 receptors. These data suggest the existence of two major, functionally distinct populations of rat NK cells possessing very different killer cell lectin-like receptor repertoires.

BACKGROUND

Excessive vascular oxidant stress has been implicated in cardiac transplant-associated arteriosclerosis (TxAA). In a recent placebo-controlled study of 40 cardiac transplant recipients, vitamin C 500 mg twice a day and vitamin E 400 IU twice a day for 1 year retarded the progression of TxAA, as assessed by intravascular ultrasound (IVUS). Endothelial dysfunction is a key feature of TxAA and reflects oxidant stress. We hypothesized that coronary endothelial dysfunction portends greater TxAA progression and a larger therapeutic response to anti-oxidant vitamins.

METHODS

In this pre-specified analysis, the 40 cardiac transplant recipients were categorized according to normal or abnormal coronary endothelial vasomotor function at baseline, as assessed by acetylcholine (10(-8) to 10(-6) mol/liter). The effect of anti-oxidant vitamins within these two groups of patients was assessed by the change in intimal index over 1 year using IVUS.

RESULTS

With placebo (n = 21), the increase in intimal index was greater in the presence vs absence of endothelial dysfunction (11 +/- 3% vs 5 +/- 1%, p < 0.05). Among patients with endothelial dysfunction (n = 21), the intimal index increased 11 +/- 3% with placebo, but decreased -1 +/- 2% with vitamins (p = 0.002). Among patients with normal endothelial function (n = 14), the intimal index increased 5 +/- 1% with placebo and 1 +/- 1% with vitamins (p < 0.05).

CONCLUSIONS

Endothelial dysfunction indicates rapid TxAA progression, even in the statin era. Although anti-oxidant vitamins reduce disease progression in patients with normal or abnormal endothelial function, the magnitude of benefit is larger in patients with endothelial dysfunction.