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Background: The rising incidence of ductal carcinoma in situ (DCIS) since the widespread enactment of mammography screening has been well documented. Patterns in DCIS incidence among women of various ages and across different racial and ethnic groups have not been well described.Study Design: The Surveillance, Epidemiology, and End Results public-use data set was queried for all women aged 40 years and older diagnosed with DCIS between 1990 and 2014. Annual age-adjusted incidence rates were compared among white, black, Hispanic, and Asian-Pacific Islander women. Additionally, using mammography screening data obtained from the CDC, patterns in mammography screening over time and as they relate to DCIS incidence rates by race and ethnicity were evaluated.Results: We identified 200,400 women aged 40 years or older with DCIS. Between 1998 and 2014, a period that saw flux in national breast screening guidelines, DCIS incidence rates increased in blacks, Hispanics, and Asian-Pacific Islanders, but remained relatively unchanged in whites (increase in number of DCIS diagnoses per 100,000 individuals in the population per year among blacks +0.66/p < 0.01, Hispanics +3.0/p < 0.01, Asian-Pacific Islanders +0.53/p < 0.01, and whites +0.07/p = 0.21). After accounting for age, year of diagnosis, and mammography screening rates, DCIS incidence was found to be similar between white and black women (0.8 fewer diagnoses per 100,000 individuals compared with whites; p = 0.36) but lower for Hispanic women (9.7 fewer diagnoses per 100,000 individuals compared with whites; p < 0.01).Conclusions: The DCIS incidence rates are influenced substantially by breast cancer mammography screening patterns. However, differences exist by race and ethnicity and are not fully explained by screening mammography trends alone. Consideration should be given to including race and ethnicity in determining optimal breast screening guidelines. [ABSTRACT FROM AUTHOR]

Postcardiac injury syndrome (PCIS) is characterized by the appearance of pericardial, pleural, or pulmonary parenchymal inflammation following a cardiac operation. The autoimmune disorder is characterized by eosinophilia, pleuritic chest pain, pleural, and pericardial effusion. It is a troublesome complication, which may prolong hospital stay and lead to severe and life-threatening conditions. Recently, its incidence appears to be declining, owing to modern immunomodulatory drug therapies. Here we report an uncommon case of PCIS, which occurred following a pulmonary vein isolation for atrial fibrillation. The patient suffered from pulmonary parenchymal inflammation but no pleuropericarditis after the operation. We describe with detailed clinical information, laboratory, and imaging tests, treatment processes, and a favorable prognosis in the content. This case illustrates that even after initially uneventful radiofrequency catheter ablation, careful, long-term follow-up is necessary to recognize the potential development of postcardiac injury syndrome. < Learning objective: Although uncommon, physicians should keep postcardiac injury syndrome in mind following radiofrequency catheter ablation. The pattern does not always resemble the classical picture described by Dressler, but may take many forms and should be sought. Diagnosis is based on the clinical signs and symptoms and is mostly confirmed after excluding other diseases. Prognosis is usually benign, and therapeutic response to anti-inflammatory drugs and corticosteroids can aid in the diagnosis.> [ABSTRACT FROM AUTHOR]

Abstract: Homocysteine is a risk factor for atherosclerosis and hypertension and induces endothelium-dysfunction. Accumulation of cholesterol and reactive oxygen species plays a key role in the endothelium-dysfunction. This study investigated the hypothesis of an involvement of mevalonate pathway and oxidative pathway in homocysteine-induced endothelial damage. Homocysteine induced impairment of the endothelium-dependent vasorelaxation of rat aortic rings by isometric tension, while it also reduced the nitric oxide level and the nitric oxide synthase activity in human umbilical vein endothelial cells, followed by accumulation of superoxide anion and cholesterol. However, the level of asymmetric dimethylarginine remained unaffected by homocysteine. The adverse effect of homocysteine on endothelial function was found to be partially enhanced either by squalestatin-reducing cholesterol or by superoxide dismutase-reducing superoxide anion. Moreover, this effect of homocysteine could be completely ameliorated by simvastatin, very similar to that of cotreatment of squalestatin and superoxide dismutase. Respectively, mevalonolactone partly or squalene fully attenuated the effect of simvastatin or squalestatin on homocysteine-induced endothelial dysfunction. In conclusion, our results suggested that the mevalonate pathway mediates homocysteine-induced endothelium dysfunction besides the oxidative pathway. Interference in the mevalonate pathway and oxidative pathway provides effective protection of endothelial function. [Copyright &y& Elsevier]