Survival of patients with cardiomyopathies

Cardiomyopathies are a heterogeneous group of diseases. The main pathogenetic mechanism is myocardial damage due to genetic mutations. Cardiomyopathies are one of the leading causes of heart failure, sudden cardiac death, and life-threatening arrhythmias. Certain factors associated with poor prognosis determined the prognosis in this group of patients. Survival in different types of cardiomyopathies depends on the time of diagnosis and initial treatment. The types of cardiomyopathies discussed in this review are hypertrophic cardiomyopathy, dilative cardiomyopathy, restrictive cardiomyopathy, left ventricle non-compaction, and arrhythmogenic right ventricular cardiomyopathy.

NEUROPSYCHIC POLYMORPHISM OF JUVENILE SYSTEMIC LUPUS ERYTHEMATOSUS

Damage to the nervous system (neurolupus) is one of the most common clinical manifestations of systemic lupus erythematosus (SLE) in childhood, and is also considered as an unfavorable prognostic criterion for the course of this disease. Neurolupus is characterized by a wide range of clinical manifestations in both children and adult patients, which is due in most cases to a common pathogenetic mechanism - the formation of systemic microvasculitis. The non-specificity and variability of neuropsychiatric symptoms, which may appear already at the onset of the disease, significantly complicate the early diagnosis of SLE and necessitate a close acquaintance of the pediatrician with neurolupus polymorphism in children.

Safety of Multiple Vaccinations and Durability of Vaccine-Induced Antibodies in an Italian Military Cohort 5 Years after Immunization

We previously examined the safety and immunogenicity of multiple vaccines administered to a military cohort, divided into two groups, the first composed of students at military schools, thus operating inside the national borders for at least 3 years, and the other formed of soldiers periodically engaged in a 9-month-long mission abroad (Lebanon). In the current study, we analyzed 112 individuals of this cohort, 50 pertaining to the first group and 62 to the second group, in order to examine the possible late appearance of side effects and to calculate the half-life of the induced antibodies. Moreover, the possible involvement of B-cell polyclonal activation as a pathogenetic mechanism for long term antibody persistence has even been explored. No late side effects, as far as autoimmunity and/or lymphoproliferation appearance, have been noticed. The long duration of the vaccine induced anti-HAV antibodies has been confirmed, whereas the antibodies induced by tetravalent meningococcal polysaccharide vaccine have been found to persist above the threshold for putative protection for a longer time, and anti-tetanus, diphtheria, and polio 1 and 3 for a shorter time than previously estimated. No signs of polyclonal B-cell activation have been found, as a possible mechanism to understand the long antibody persistence.

Is the Adenosine Test Obsolete in the Clinical Assessment of Syncope of Unknown Origin?

Syncope is a common clinical condition affecting 50% of the general population; however, its exact pathophysiology and underlying mechanisms remain elusive. The adenosine test (ADT) has been proposed as a complementary diagnostic test in the work-up of syncope of unknown origin aiming to further elucidate the underlying pathogenetic mechanism of spontaneous syncope. Although ADT has not been endorsed by the recent European Society of Cardiology guidelines on syncope management, the use of a quick, safe and non-invasive test which can contribute to an accurate diagnosis and rationalised therapy, may deserve further consideration. This review summarises the evidence on the role of ADT in the investigation and management of syncope of unknown origin and highlights future perspectives in this area. The authors also analyse the current challenges and research targets on adenosine plasma levels and its receptors due to the involvement of the adenosine pathway in the ADT response.

Low striatal T3 is implicated in inattention and memory impairment in an ADHD mouse model overexpressing thyroid hormone-responsive protein

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder, potentially with a biological basis; however, its exact cause remains unknown. Thyroid hormone (TH) abnormalities are more prevalent in patients with ADHD than in the general population, indicating a shared pathogenetic mechanism for these conditions. Previously, we identified that overexpression of thyroid hormone-responsive protein (THRSP), a gene highly responsive to TH status, induced inattention in male mice. Herein, we sought to explore whether TH function in THRSP-overexpressing (THRSP OE) mice influences ADHD-like (inattention) behavior. We now confirm that THRSP overexpression in male mice reproduces behavioral features of ADHD, including sustained inattention and memory impairment, accompanied by excessive theta waves that were found normal in both the THRSP-knockout and hetero groups. Physiological characterization revealed low striatal T3 levels in the THRSP OE mice due to reduced striatal T3-specific monocarboxylate transporter 8 (MCT8), indicating brain-specific hypothyroidism in this transgenic mouse strain. TH replacement for seven days rescued inattention and memory impairment and the normalization of theta waves. This study further supports the involvement of the upregulated THRSP gene in ADHD pathology and indicates that THRSP OE mice can serve as an animal model for the predominantly inattentive subtype of ADHD.

Cardiac surgery-associated acute kidney injury

This literature review is devoted to one of the topical multidisciplinary problems of modern clinical practice the development of acute kidney injury after cardiac surgery. The prevalence of this pathology varies on average from 5 to 43 %, while the frequency of early hospital mortality increases significantly in the population of such patients compared with patients without cardiac surgery-associated renal damage. It is assumed that the work of the artificial circulatory system contributes to the development of such complications, but as shown by many studies, the etiology of such kidney damage is multifactorial and cannot be explained by only one pathogenetic mechanism. The article highlights the current understanding of the etiology, pathogenesis and risk factors of acute kidney injury after cardiovascular interventions, describes new markers of early detection of renal dysfunction, and describes some prognostic aspects of the disease. Early identification and stratification of risk groups will allow for a timely preventive strategy, which will significantly improve early and long-term postoperative outcomes in such patients.

MUCOSAL ABNORMALITIES AS AN ETIOPATHOGENETIC FACTOR IN THE DEVELOPMENT OF GINGIVAL RECESSION

Subject. A review of the literature devoted to the current problem of dentistry - mucogingival anomalies (small vestibule of the mouth, short frenulum of the lips, tongue, muco-alveolar cords) is presented. Purpose of the study — study the materials of publications devoted to mucogingival anomalies as etiopathogenetic factors in the development of gingival recession. Methodology. In detail, in the light of modern ideas described mucogingival anomalies (shallow vestibule of the mouth, short frenulum of the lips, tongue, mucous-alveolar cords) and their effect on the development of gum recession. Results. It has been established that a large role in the occurrence and development of gingival recession is played by the ratio of the size of the attached and free gums, which is normally equal to 5: 1, and in pathology — 1: 1. The pathogenetic mechanism of the negative impact of mucogingival abnormalities is associated with the absence, first of all, of a sufficient width of the attached gums with a shallow vestibule of the mouth, which is a factor of constant chronic trauma to the gums with, leading to disturbances in microcirculation and tissue metabolism, resulting in resorption of bone structures, etermined radiographically. In the mechanism of gum recession, a significant role is also played by the pulling mucous-alveolar cords, shortened and massive frenum of the lips and tongue. The main signs of arising ischemic disorders are anemization and mobility of the marginal gums when the lower or upper lip, cheeks, and tongue are abducted. To prevent severe destructive lesions, it is necessary to timely identify and eliminate, with the help of vestibulo- or frenuloplasty operations, conditions conducive to functional chronic traumatization of the periodontal tissues. Conclusions. The results of the review indicate that knowledge of the anatomical and topographic parameters of the vestibule and oral mucosa is necessary to prevent the development of gingival recession, prescribe timely and adequate treatment, predict and prevent complications. However, it should be recognized that this problem, in our opinion, continues to remain relevant to this day due to the lack of an integrated approach to the prevention, diagnosis and treatment of gum recession.

Adenosine and Inflammation: Here, There and Everywhere

Adenosine is a ubiquitous endogenous modulator with the main function of maintaining cellular and tissue homeostasis in pathological and stress conditions. It exerts its effect through the interaction with four G protein-coupled receptor (GPCR) subtypes referred as A1, A2A, A2B, and A3 adenosine receptors (ARs), each of which has a unique pharmacological profile and tissue distribution. Adenosine is a potent modulator of inflammation, and for this reason the adenosinergic system represents an excellent pharmacological target for the myriad of diseases in which inflammation represents a cause, a pathogenetic mechanism, a consequence, a manifestation, or a protective factor. The omnipresence of ARs in every cell of the immune system as well as in almost all cells in the body represents both an opportunity and an obstacle to the clinical use of AR ligands. This review offers an overview of the cardinal role of adenosine in the modulation of inflammation, showing how the stimulation or blocking of its receptors or agents capable of regulating its extracellular concentration can represent promising therapeutic strategies for the treatment of chronic inflammatory pathologies, neurodegenerative diseases, and cancer.