Cardiovascular diseases (CVDs) are among the top three causes of mortality and disability in the world so that one-third of total mortality rate in the world is due to CVDs. Along with increase in life expectancy, an increase in prevalence of chronic diseases has taken place so that death rate due to heart diseases crossed 25% line in the late 20th century and this figure is expected to be at 35-60% range by 2025. In addition, along with changes in life style, non-communicable diseases have become the main case of mortality. Although the risk of communicable diseases is more urgent taking into account their contagious nature, the side effects of chronic diseases including CVDs are more resilient, expensive, and debilitating. Studies have shown that CVDs are among the top and most common causes of death in Iran. The most common type of CVD is myocardial infraction, which is the outcome of coronary vessels occlusion and ischemia of myocardium. Myocardial infraction is a major cause of mortality among heart patients. One myocardial infraction happens in the USA every 20s and every minute one dies due to myocardial infraction. It is one of the main reasons for hospitalization of heart patients, which is usually assumed as a threatening situation for the patient and the family.

Necrosis and apoptosis are two separate pathways of cell death in myocardium cells. In fact, there is a correlation between ischemia (I) and reperfusion (R) and biological and morphological specifications of cardiocytes under necrosis and apoptosis are very similar. Necrosis is usually referred to as random or pathologic cell death that is coincident with severe cell inflammation and split, cytoplasm protein coagulation and denaturation, breakdown and destruction of cell internal organelles and severe inflammatory response. On the contrary, apoptosis is a programmed and genetically controlled cell death. The main morphological features of apoptosis are cellular leakage, chromatin condensation, formation of cytoplasm blebbing and apoptotic objects that happen without losing integrity of cell membrane and inflammatory response. Although necrosis and apoptosis mechanisms are different, there are common features between them in pathological conditions [1-5]. Several studies have shown that ischemia-reperfusion induces apoptosis of myocardia cells in vivo; still, there is an ongoing debate if apoptosis starts with I or R.

Anthracosis is the pneumoconiosis caused by exposure to coal dust. The term “anthracotic” refers to coal particles and other black pigments of which carbon is the main element. Coal particles, mostly in the coalmine workers and to a less extent in city dweller, are found in the background of vocational and air pollution diseases as sediment at mucosa and submucosa; and under bronchoscopy, they appear as black lesions with normal or deformed bronchus with high fragility. In addition to coalmine workers, the disease is found among workers in the industries related to coal. In fact, occupational exposure to carbon, silicon dioxide, and quartz at work are the known causes of pulmonary anthracosis; although, there are cases without any pertinent occupation history as well. In other words, anthracosis is an outcome of aggregation of carbon in the lungs after long and frequent exposure to air pollution and inhaling smock and coal dust. In addition to the lungs, there are reports of anthracosis in the liver, spleen, and esophagus; the latter case should be considered as a serious disease as it demonstrates malignant melanoma. In some cases, an anthracosis case is misdiagnosed as tuberculosis, lung carcinoma, or pneumonia . Cytology studies on pulmonary tissues have shown that inter-bronchus anthracosis and lymphadenopathy mediastinum are concurrent with the early adenocarcinoma. Thereby, there is a probably significant relationship between anthracosis and lung carcinoma. Lung carcinoma is the most common type of cancer in men and more than 80% of the patients die during the first five years after diagnosis. CDH1 gene encodes E-Cadherin protein and it is a tumor suppressor gene with a key role in preserving cellular adhesion and stable connections in normal tissues through expression of Cadherin1 protein. In addition, the gene keeps epithelium cells in their normal layer and arrangement.