In modern clinical practice, digital pathology has an essential role, being a technological necessity for the activity in the pathological anatomy laboratories. The development of information technology has majorly facilitated the management of digital images and their sharing for clinical use; the methods to analyze digital histopathological images, based on artificial intelligence techniques and specific models, quantify the required information with significantly higher consistency and precision compared to that provided by optical microscopy. In parallel, the unprecedented advances in machine learning facilitate, through the synergy of artificial intelligence and digital pathology, the possibility of diagnosis based on image analysis, previously limited only to certain specialties. Therefore, the integration of digital images into the study of pathology, combined with advanced algorithms and computer-assisted diagnostic techniques, extends the boundaries of the pathologist’s vision beyond the microscopic image and allows the specialist to use and integrate his knowledge and experience adequately. We conducted a search in PubMed on the topic of digital pathology and its applications, to quantify the current state of knowledge. We found that computer-aided image analysis has a superior potential to identify, extract and quantify features in more detail compared to the human pathologist’s evaluating possibilities; it performs tasks that exceed its manual capacity, and can produce new diagnostic algorithms and prediction models applicable in translational research that are able to identify new characteristics of diseases based on changes at the cellular and molecular level.

Cardiovascular disease is the leading cause of mortality and morbidity throughout the world, accounting for 16.7 million deaths each year. The underlying pathological process for the majority of cardiovascular diseases is atherosclerosis, a slowly progressing, multifocal, chronic, immune-inflammatory disease that involves the intima of large and medium-sized arteries. The process of atherosclerosis begins in childhood as fatty streaks—an accumulation of lipids, inflammatory cells, and smooth muscle cells in the arterial wall. Over time, a more complex lesion develops into an atheroma and characteristic fibrous plaques. Atherosclerosis alone is rarely fatal; it is the further changes that render fibrous plaques vulnerable to rupture; plaque rupture represents the most common cause of coronary thrombosis. The prevalence of atherosclerosis is increasing worldwide and more than 50% of people with circulatory disease die of it, mostly in modern societies. Epidemiological studies have revealed several environmental and genetic risk factors that are associated with the early formation of a pathogenic foundation for atherosclerosis, such as dyslipidemia, hypertension, diabetes mellitus, obesity, and smoking. The purpose of this review is to bring together the current information concerning the origin and progression of atherosclerosis in childhood as well as the identification of known risk factors for atherosclerotic cardiovascular disease in children.

Studies in recent years have shown increased interest in developing new methods of evaluation, but also in limiting post infarction ventricular remodeling, hoping to improve ventricular function and the further evolution of the patient. This is the point where biomarkers have proven effective in early detection of remodeling phenomena. There are six main processes that promote the remodeling and each of them has specific biomarkers that can be used in predicting the evolution (myocardial necrosis, neurohormonal activation, inflammatory reaction, hypertrophy and fibrosis, apoptosis, mixed processes). Some of the biomarkers such as creatine kinase–myocardial band (CK-MB), troponin, and N-terminal-pro type B natriuretic peptide (NT-proBNP) were so convincing that they immediately found their place in the post infarction patient evaluation protocol. Others that are related to more complex processes such as inflammatory biomarkers, atheroma plaque destabilization biomarkers, and microRNA are still being studied, but the results so far are promising. This article aims to review the markers used so far, but also the existing data on new markers that could be considered, taking into consideration the most important studies that have been conducted so far.

Cystic fibrosis (CF) is a monogenic autosomal recessive disease caused by cystic fibrosis transmembrane conductance regulator (CFTR) gene mutations. CF is characterized by a high phenotypic variability present even in patients with the same genotype. This is due to the intervention of modifier genes that interact with both the CFTR gene and environmental factors. The purpose of this review is to highlight the role of non-CFTR genetic factors (modifier genes) that contribute to phenotypic variability in CF. We analyzed literature data starting with candidate gene studies and continuing with extensive studies, such as genome-wide association studies (GWAS) and whole exome sequencing (WES). The results of both types of studies revealed that the number of modifier genes in CF patients is impressive. Their identification offers a new perspective on the pathophysiological mechanisms of the disease, paving the way for the understanding of other genetic disorders. In conclusion, in the future, genetic analysis, such as GWAS and WES, should be performed routinely. A challenge for future research is to integrate their results in the process of developing new classes of drugs, with a goal to improve the prognosis, increase life expectancy, and enhance quality of life among CF patients.

Atrial fibrillation, the most frequent arrhythmia in clinical practice and chronic coronary syndrome, is one of the forms of coronary ischemia to have a strong dual relationship. Atrial fibrillation may accelerate atherosclerosis and may increase oxygen consumption in the myocardium, creating a mismatch between supply and demand, thus promoting the development or worsening of coronary ischemia. Chronic coronary syndrome alters the structure and function of gap junction proteins, affecting the conduction of action potential and leading to ischemic necrosis of cardiomyocytes and their replacement with fibrous tissue, in this way sustaining the focal ectopic activity in atrial myocardium. They have many risk factors in common, such as hypertension, obesity, type 2 diabetes mellitus, and dyslipidemia. It is vital for the prognosis of patients to break this vicious circle by controlling risk factors, drug therapies, of which antithrombotic therapy may sometimes be challenging in terms of prothrombotic and bleeding risk, and interventional therapies (revascularization and catheter ablation).

Background and Objectives. Uterine fibroids are relatively common in reproductive-age women and are directly linked to pregnancy. There are many debates about performing a myomectomy at the same time as a caesarian section (CS) in such cases due to the risk of a hemorrhage. Our study aims to investigate fibroid features and their evolution in pregnancy, complications of a myomectomy during CS and maternal and fetal obstetric outcomes of pregnancies with fibroids. Materials and methods. We realize a prospective study that includes 57 patients with fibroids in pregnancy diagnosed in January 2017–June 2019. We analyze the number, the location and the growth of fibroids during pregnancy and the maternal and fetal outcome. We appreciate the bleeding in patients with a myomectomy and without a myomectomy during CS, using hemoglobin values before and after birth. Results. Most of the patients present single fibroids that are 30–160 mm in size, located on the anterior uterine wall. Vaginal delivery is used in 7% of women, whereas 85.96% deliver by CS. In addition, 68% of fibroids are diagnosed in the first trimester. In most cases, the fibroid has maximum growth in the second trimester of pregnancy. The myomectomy rate for fibroids during CS is 24.48. Hemoglobin values showed no statistically significant difference between the two groups with and without myomectomy. The operating time is double for the group with a myomectomy associated with a CS. The results of the obstetric outcomes are abortion in 7% of all patients, whereas premature delivery and births at term are 9.43% and 90.57%, respectively. Conclusions. The decision of performing a myomectomy during pregnancy can be a challenge and must be performed for selected cases. This procedure may have several benefits, such as avoiding another operation to remove fibroids.