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Open access

Natalija Marinković, Daria Pašalić, Goran Ferenčak, Branka Gršković and Ana Rukavina

Dioxins and Human Toxicity

The term dioxins usually refers to polychlorinated dibenzo-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). As 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) has the highest toxic potential, the toxic potentials of other PCDDs and PCDFs are defined in comparison with it. Human exposure to dioxins can be environmental (background), occupational, or accidental pollution. In the human body, dioxins are in part metabolised and eliminated, and the rest is stored in body fat. People vary in their capacity to eliminate TCDD, but it is also dose-dependent; the elimination rate is much faster at higher than lower levels. The liver microsomal P4501A1 enzyme oxygenates lipophilic chemicals such as dioxins. It is encoded by the CYP1A1 gene. Cytosolic aryl hydrocarbon receptor (AhR) mediates their carcinogenic action. It binds to dioxin, translocates to nucleus and together with hydrocarbon nuclear translocator (ARNT) and xenobiotic responsive element (XRE) increases the expression of CYP1A1.

Dioxins are classified as known human carcinogens, but they also cause noncancerous effects like atherosclerosis, hypertension, and diabetes. Long-term exposures to dioxins cause disruption of the nervous, immune, reproductive, and endocrine system. Short-term exposure to high levels impairs the liver function and causes chloracne. The most sensitive population to dioxin exposure are the foetuses and infants.

A large number of health effects have been documented in the scientific literature, and they all place dioxins among the most toxic chemicals known to man.

Open access

Razvan Gheorghita Mares, Goran Marinkovic, Ovidiu Simion Cotoi and Alexandru Schiopu

Abstract

Acute myocardial infarction (AMI) is a disease associated with high morbidity and mortality. Currently there are no available treatments specifically targeting the post-ischemic myocardial processes that lead to heart failure and recurrent coronary events. The innate immune system plays a central role in the two consecutive phases that follow an acute ischemic event: the inflammatory phase and the reparatory phase. The inflamatory phase involves a massive infiltration of neutrophils and inflammatory Ly6Chi monocytes into the injured myocardium. The reparatory phase is orchestrated by reparatory Ly6Clo macrophages that clear necrotic and apoptotic cells through efferocytosis, secrete anti-inflammatory mediators and stimulate fibrosis and repair. Important recent studies provided proof that Ly6Chi monocytes that enter the myocardium in the inflammatory phase upregulate the orphan nuclear receptor Nr4a1 and switch phenotype to Ly6CloNr4a1hi reparatory macrophages. Additionally, neutrophils have been shown to promote cardiac recovery by upregulating expression of the efferocytosis receptor MerTK on reparatory macrophages. A finely tuned balance between the inflammatory and the reparatory phases is thus essential for limiting myocardial damage and promoting efficient recovery. Treatment strategies targeting only the inflammatory phase have so far failed to improve prognosis in AMI patients. A detailed understanding of the interplay between the two phases of the innate immune response is paramount for designing efficient therapies able to improve post- AMI prognosis. In the current review, we summarize the state-of-the-art of the field and discuss previous therapeutic attempts and currently ongoing clinical trials targeting innate immune mechanisms in AMI patients.

Open access

Goran Kondov, Zoran Spirovski, Irena Kondova-Topuzovska, Anita Kokareva, Risto Colanceski, M. Srceva, Borislav Kondov, I Dzikovski, N. Toleska-Dimitrovska and Sanja Petrusevska-Marinkovic

Abstract

Pleural infection is a frequent clinical condition. Prompt treatment has been shown to reduce morbidity, mortality and duration of hospital stay. Unfortunately, advanced stages of empyema need to use extensive surgery - decortications or thoracoplasty. Early recognition of the parapneumonic effusion and the adequate treatment with thoracentesis or pleural drainage, which is minimally invasive, is possible not to prograde the process and not to become empyema.

Aim: To analyze the results of the surgical treatment in patients with empyema treated at Clinic for thoracic surgery.

Material and methods: In the retrospective study we analyzed 234 patients with empyema which were treated at the Clinic for Thoracic Surgery in 5 year period (2011-2015). The mean age of the patients was 51.94 years. They were treated with pleural drainage, decortications or thoracoplasty.

Results: With pleural drainage were treated 165/234 (70.51%) patients, of which successfully were finished 124/165 (75.15%), but 41/165 (24.85%) were indicated after the decortications. A total of 108/234 (46.15%) were treated with decortications from which, primary decortications were indicated in 67/234 (28.63%) patients. 5/234 (2.14%) patients were treated with thoracoplasty – 3 of the patients with decortications and 2 with primary indicated thoracoplasty according to the local findings, long term untreated empyema and bad general condition. The Mean hospitalization was 17.4 days, of which 13.4 days after surgery. In the group with primary drainage it was detected a lethal outcome in 7/124 (5.64%) patients, 5/105 (4.76%) in the group with decortications and 2/5 (40%) in the group with thoracoplasty.

Conclusion: Early detection of the parapneumonic effusion and the adequate treatment will prevent the appearance of empyema. If the empyema is detected it is necessary as early as possible to start the treatment with minimally invasive pleural drainage. In earlier stages it is possible to use less invasive decortications, using VATS than the open thoracotomy decortication which is more extensive surgical intervention.