Background-A myocardial bridge (MB) that partially covers the course of the left anterior descending coronary artery (LAD) sometimes causes myocardial ischemia, primarily because of hemodynamic deterioration, but without atherosclerosis. However, the mechanism of occurrence of myocardial infarction (MI) as a result of an MB in patients with spontaneously developing atherosclerosis is unclear. Methods and Results-One hundred consecutive autopsied MI hearts either with MBs [MI(ϩ)MB(ϩ) group; nϭ46] orwithout MBs (nϭ54) were obtained, as were 200 normal hearts, 100 with MBs [MI(Ϫ)MB(ϩ) group] and 100 without MBs. By microscopy on LADs that were consecutively cross-sectioned at 5-mm intervals, the extent and distribution of LAD atherosclerosis were investigated histomorphometrically in conjunction with the anatomic properties of the MB, such as its thickness, length, and location and the MB muscle index (MB thickness multiplied by MB length), according to MI and MB status. In the MI(ϩ)MB(ϩ) group, the MB showed a significantly greater thickness and greater MB muscle index (PϽ0.05) than in the MI(Ϫ)MB(ϩ) group. The intima-media ratio (intimal area/medial area) within 1.0 cm of the left coronary ostium was also greater (PϽ0.05) in the MI(ϩ)MB(ϩ) group than in the other groups. In addition, in the MI(ϩ)MB(ϩ) group, the location of the segment that exhibited the greatest intima-media ratio in the LAD proximal to the MB correlated significantly (PϽ0.001) with the location of the MB entrance, and furthermore, atherosclerosis progression in the LAD proximal to the MB was largest at 2.0 cm from the MB entrance. Conclusions-In the proximal LAD with an MB, MB muscle index is associated with a shift of coronary disease more proximally, an effect that may increase the risk of MI. (Circulation. 2009;120:376-383.)Key Words: myocardium Ⅲ myocardial infarction Ⅲ anatomy Ⅲ atherosclerosis T he coronary artery that runs through epicardial adipose tissue is often covered in part with myocardial tissue. This structure is known as a myocardial bridge (MB) 1 ; it exists almost exclusively in the left anterior descending coronary artery (LAD), 2 and it is regarded as a common anatomic variant rather than a congenital anomaly. 3 The frequency of an MB in the LAD is high, sometimes Ͼ50% by autopsy, 2 but it is Ͻ5% by angiography. 4 Because MBs have been identified angiographically indirectly through a "milking effect" phenomenon induced by systolic compression of the MB, a thin or short MB is often missed. 4 The use of other invasive imaging, such as intracoronary ultrasound and Doppler, has improved MB detection. 5,6 More recently, multidetector computed tomography (CT) has been used noninvasively to detect the MB itself directly, 7 and surprisingly, the use of multidetector CT for myocardial ischemia increases Editorial see p 357 Clinical Perspective on p 383The clinical outcome of patients with MBs has been considered benign 4 ; however, the significance of an MB to myocardial ischemia remains controversial. By multidetector CT imaging,...
Background Insulin-derived amyloidosis is a skin-related complication of insulin therapy that interferes with insulin therapy. Although toxicities of in vitro-formed insulin amyloid fibrils have been well studied, the toxicity of insulin-derived amyloidosis remains to be clarified. Case presentation A 58-year-old man with type 2 diabetes mellitus underwent a lower limb amputation due to diabetic gangrene. Several antibiotics including minocycline were administered for infection and sepsis. A hard mass at the insulin injection sites in the lower abdomen was discovered by chance four months later. Although no abnormal findings in the surface skin of the mass were observed, necrotic tissue was seen around the mass when a biopsy was performed. Histological and toxicity studies were performed for this patient and four other patients with abdominal masses at insulin injection sites. Histological and immunohistochemical studies showed that the masses had typical characteristics of amyloid deposits in all cases, whereas necrotic findings were seen adjacent to the amyloid deposit only in the case presented. Toxicity studies indicated that the amyloid tissue from the present case had significant cell toxicity compared to the control skin tissue or the amyloid tissues from the other four cases. Conclusions This report showed that toxic insulin-derived amyloidosis can occur. In addition, this report suggested that toxic insulin-derived amyloidosis may cause necrosis in the surrounding tissue. Although the toxic amyloid deposit of insulin-derived amyloidosis was found in only one patient, no structural differences between toxic and non-toxic deposits were seen on histological and immunohistochemical studies. Electronic supplementary material The online version of this article (10.1186/s12902-019-0385-0) contains supplementary material, which is available to authorized users.
Parkinsonism-dementia complex (PDC) and amyotrophic lateral sclerosis (ALS) are fatal neurological diseases. The incidence on Guam was very high between 1950 and 1965 but decreased dramatically after 1965. It is thought that drinking water containing low levels of calcium (Ca) and magnesium (Mg), and high levels of aluminum and of a plant excitatory neurotoxin are involved in the pathogenesis of these diseases. The present experiment was performed in rats that were exposed to low Ca and/or Mg intake over two generations, thus simulating the conditions of human life on Guam, where several generations live continuously in the same environment. Significant loss of dopaminergic neurons was identified exclusively in the substantia nigra in 1-year-old rats that had been exposed continuously to low Mg intake (one-fifth of the normal level) over generations. The present study suggests that low Mg intake over generations may be involved in the pathogenesis of substantia nigra degeneration in humans.
LN metastasis is regulated not only by the characteristics of cancer cells but also by microenvironmental factors of lymphatics and neutrophils, especially at the invasive front.
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