Biomedical subjects

Kevin R Flaherty

Publications and source records attributed to Kevin R Flaherty.

22 records · Page 2Linked to original sources

PubMed2003

The solitary pulmonary nodule.

More than 150,00 patients a year present to their physicians with the diagnostic dilemma of a solitary pulmonary nodule (SPN) found either on chest radiography or chest CT. A thoughtful and timely workup of this finding is essential if lung cancer is to be recognized early and the chance for cure optimized. Based on the literature to date, recommendations are made for appropriate imaging modalities and diagnostic testing, as well as indications for obtaining preoperative tissue diagnosis for the patient with an SPN.

Biopsy, Needle↗

PubMed2003

Macrophage migration inhibitory factor and CXC chemokine expression in non-small cell lung cancer: role in angiogenesis and prognosis.

PURPOSE: The purpose of this study was to determine whether expression of migration inhibitory factor (MIF) is increased in non-small cell lung cancer, and whether it correlates with angiogenesis and/or prognosis. EXPERIMENTAL DESIGN: We measured vessel density, and levels of MIF, angiogenic CXC chemokines, and vascular-endothelial growth factor (VEGF; by ELISA) in tumor and normal lung tissue from 87 patients after resection of lung cancer. We compared vessel density with levels of MIF, VEGF, or angiogenic CXC chemokines in the corresponding tumor homogenate. Disease-free survival was analyzed in a Cox proportional hazards model. RESULTS: Levels of MIF in lung cancer demonstrated a bimodal distribution, with some having "normal" values (relative to normal lung tissue) and a second cluster with markedly high values. The increased levels of MIF in lung cancer were statistically significant in both paired and unpaired comparisons (P < 0.05). The strongest correlation of vessel density was with the sum of angiogenic CXC chemokines. MIF correlated very strongly with levels of angiogenic CXC chemokines. Tumors in the high MIF group had a strong correlation between MIF level and vessel density. Risk of recurrence was associated with high levels of glutamic acid-leucine-arginine amino acid motif CXC chemokines, MIF, and/or VEGF in a Cox proportional hazards model. CONCLUSIONS: MIF expression in non-small cell lung cancer occurs in a bimodal distribution, and is closely associated with tumor levels of angiogenic CXC chemokines and with vessel density. High levels of tumor-associated CXC chemokines, MIF, or VEGF are associated with risk of recurrence after resection of lung cancer.

Carcinoma, Non-Small-Cell Lung↗

PubMed2002

Informal caregiving for chronic lung disease among older Americans.

STUDY OBJECTIVE: To obtain nationally representative estimates of the additional time, and related cost, of unpaid family caregiving (informal caregiving) associated with chronic lung disease among older Americans. DESIGN: Multivariable regression models using data from the 1993 Asset and Health Dynamics Study, a nationally representative survey of people > or = 70 years old (n = 7,443). PARTICIPANTS: National population-based sample of the community-dwelling elderly. MEASUREMENTS: Weekly hours of informal caregiving, and imputed cost of caregiver time, for community-dwelling elderly who reported the following: (1) no lung disease, (2) lung disease without associated activity limitations, or (3) lung disease with associated activity limitations. RESULTS: After adjusting for sociodemographic variables, potential caregiver network, and comorbid conditions, individuals with chronic lung disease and associated activity limitations (n = 403) received an additional 5.1 h/wk of informal care when compared to those with no lung disease (n = 6,593; p < 0.001). The associated additional yearly cost of informal care per case was $2,200 USD. This represents a national annual cost of informal caregiving for chronic lung disease of > $2 billion USD. CONCLUSIONS: The quantity and associated economic cost of informal caregiving for elderly individuals with chronic lung disease are substantial. These costs to families and society must be accounted for if the full societal costs of chronic lung disease are to be calculated. Pulmonary physicians caring for elderly individuals with chronic lung disease should be mindful of the importance of informal care for the well-being of their patients, as well as the potential for significant burden on those (often elderly) individuals providing the care.

Aged↗

PubMedDate not supplied

A plasminogen activator inhibitor-1 promoter polymorphism and idiopathic interstitial pneumonia.

The normal fibrinolytic activity within the alveolar space is suppressed in fibrotic lung diseases in part because of increased levels of plasminogen activator inhibitor-1 (PAI-1). Studies with animals have shown that inhibition of the plasminogen system by PAI-1 increases the generation of pulmonary fibrosis. To determine if a similar relationship occurs in human fibrotic lung diseases, we took advantage of a polymorphism (4G/5G) that occurs in the promoter region of the human PAI-1 gene and influences the expression of PAI-1. We hypothesized that the 4G/4G genotype, because of its association with higher levels of PAI-1, would occur in patients with idiopathic interstitial pneumonia more frequently than in a control population. PAI-1 promoter genotype was determined in 88 well-characterized patients with idiopathic interstitial pneumonia consisting of 62 patients with usual interstitial pneumonia and 26 with nonspecific interstitial pneumonia. DNA was extracted from paraffin-embedded biopsy tissue and the genotype identified by polymerase chain reaction and restriction endonuclease digestion. We found that the distribution of PAI-1 genotypes in the idiopathic interstitial pneumonia population was similar to that of a large control population. However, subgroup analysis showed that patients with nonspecific interstitial pneumonia were more likely than the control population to have the promoter genotype (4G/4G) that is associated with higher levels of PAI-1. A similar pattern in PAI-1 polymorphism was not seen in the usual interstitial pneumonia subgroup. The results of this study support the conclusion that PAl-1 expression influences the development of nonspecific interstitial pneumonia in a similar manner to what occurs in animal models of pulmonary fibrosis. Patients with usual interstitial pneumonia did not show the same relationship with PAl-1 genotype.

Female↗