Translational research : the journal of laboratory and clinical medicine
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Asbestos causes asbestosis (pulmonary fibrosis caused by asbestos inhalation) and malignancies (bronchogenic carcinoma and mesothelioma) by mechanisms that are not fully elucidated. Despite a dramatic reduction in asbestos use worldwide, asbestos-induced lung diseases remain a substantial health concern primarily because of the vast amounts of fibers that have been mined, processed, and used during the 20th century combined with the long latency period of up to 40 years between exposure and disease presentation. This review summarizes the important new epidemiologic and pathogenic information that has emerged over the past several years. ⋯ Furthermore, recent evidence underscores crucial roles for specific cellular signaling pathways that regulate the production of cytokines and growth factors. An evolving role for epithelial-mesenchymal transition (EMT) is also reviewed. The translational significance of these studies is evident in providing the molecular basis for developing novel therapeutic strategies for asbestos-related lung diseases and, importantly, other pulmonary diseases, such as interstitial pulmonary fibrosis and lung cancer.
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The well-accepted biopsychosocial model proposes that the experience of pain and responses to it result from a complex interaction of biological, psychological, and social factors. However, the separation of these constructs is substantially artificial, and we presume that psychological processes have biological effects, that biological processes affect an individual's psychosocial environment, and so on. Considerable research has demonstrated that pain-coping strategies influence perceived pain intensity and physical functioning, and individual differences in styles of pain coping even shape the persistence of long-term pain complaints in some populations. ⋯ Although catastrophic thinking regarding pain-related symptoms is often classified under the "psychologic" category within the broader biopsychosocial model, we propose that catastrophizing exerts biologic effects that may account for some of its negative consequences. In general, the cognitive and affective processes captured within the construct of catastrophizing may exert effects on the neuromuscular, cardiovascular, immune, and neuroendocrine systems, and on the activity in the pain neuromatrix within the brain. The interface between pain-related neurobiology and processes such as pain-related catastrophizing represents an important avenue for future pain research.
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Comparative Study
Differences in subclinical cardiovascular disease between African American and Caucasian women with systemic lupus erythematosus.
Racial differences exist in disease rates and mortality in both cardiovascular disease (CVD) and systemic lupus erythematosus (SLE). The objective of this cross-sectional study was to compare the frequency and risk factors for subclinical CVD in African American (AA) and Caucasian women with SLE and no prior CVD events. Traditional CVD risk factors and SLE-related factors were assessed in 309 SLE women. ⋯ All factors contributed to the result, but no individual risk factor fully accounted for the association between race and plaque. In conclusion, the presence of carotid plaque was higher in AA compared with Caucasian women with SLE, in contrast to studies of non-SLE subjects, in which AA have similar or less plaque than Caucasians. A combination of SLE-related and traditional CVD risk factors explained the racial difference in plaque burden.
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Our specific aims were to determine whether low serum 25 (OH) vitamin D (D2 + D3) (<32 ng/mL) was associated with myalgia in statin-treated patients and whether the myalgia could be reversed by vitamin D supplementation while continuing statins. After excluding subjects who took corticosteroids or supplemental vitamin D, serum 25 (OH) D was measured in 621 statin-treated patients, which consisted of 128 patients with myalgia at entry and 493 asymptomatic patients. The 128 myalgic patients had lower mean +/- standard deviation (SD) serum vitamin D than the 493 asymptomatic patients (28.6 +/- 13.2 vs 34.2 +/- 13.8 ng/mL, P < 0.0001), but they did not differ (p > 0.05) by age, body mass index (BMI), type 2 diabetes, or creatine kinase levels. ⋯ Serum 25 (OH) D was low in 82 of 128 (64%) patients with myalgia versus 214 of 493 (43%) asymptomatic patients (chi(2) = 17.4, P < 0.0001). Of the 82 vitamin-D-deficient, myalgic patients, while continuing statins, 38 were given vitamin D (50,000 units/week for 12 weeks), with a resultant increase in serum vitamin D from 20.4 +/- 7.3 to 48.2 +/- 17.9 ng/mL (P < 0.0001) and resolution of myalgia in 35 (92%). We speculate that symptomatic myalgia in statin-treated patients with concurrent vitamin D deficiency may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle.