Hypertrophic cardiomyopathy (HCM) is the most prevalent heritable cardiomyopathy. HCM is considered to be caused by mutations in cardiac sarcomeric protein genes. Recent research suggests that the genetic foundation of HCM is much more complex than originally postulated. The clinical presentations of HCM are very variable. Some mutation carriers remain asymptomatic, while others develop severe HCM, terminal heart failure, or sudden cardiac death. Heterogeneity regarding both genetic mutations and the clinical course of HCM hinders the establishment of universal genotype–phenotype correlations. However, some trends have been identified. The presence of a mutation in some genes encoding sarcomeric proteins is associated with earlier HCM onset, more severe left ventricular hypertrophy, and worse clinical outcomes. There is a diversity in the mechanisms implicated in the pathogenesis of HCM. They may be classified into groups, but they are interrelated. The lack of known supplementary elements that control the progression of HCM indicates that molecular mechanisms that exist between genotype and clinical presentations may be crucial. Secondary molecular changes in pathways implicated in HCM pathogenesis, post-translational protein modifications, and epigenetic factors affect HCM phenotypes. Cardiac loading conditions, exercise, hypertension, diet, alcohol consumption, microbial infection, obstructive sleep apnea, obesity, and environmental factors are non-molecular aspects that change the HCM phenotype. Many mechanisms are implicated in the course of HCM. They are mostly interconnected and contribute to some extent to final outcomes.

The determination of genetic background in metabolic syndrome (MetS) represents one of the necessary steps to prevent the disorder, thus reducing the cost of medical treatments and helping to design targeted therapy. The study explores the association between individual alleles of the LRP1 gene and the diagnosis of MetS to find correlation between the low-density lipoprotein receptor-related (LRP1) gene polymorphism and each individual anthropometric and biochemical parameter. The study included 93 males and females, aged from 19 to 65, divided into two groups. The genotype of each person was determined from the restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) profile. Results indicated the association of the T allele form of exon 3 LRP1 gene with development and progression of MetS that further pointed out its negative impact on tested anthropometric and biochemical parameters. The presence of the T allele in patients multiplies the chance of occurrence of deviations from the reference values of body mass index (BMI), (4.24-fold) and low-density lipoprotein (LDL) (20.26-fold) compared to C allele carriers. The results showed that T allele presence multiplies the chance (4.76 fold) for the occurrence of MetS in comparison to C allele carriers. Correlation found that the T allele of the LRP1 gene with MetS determinants is not negligible, therefore, the T allele may be considered as a risk factor for MetS development.

The filamentous fungus Fusarium graminearum is a well-known cereal pathogen and F. avenaceum is a pathogen with a wide host range. Recently, both species were reported as causal agents of apple rot, raising concerns about postharvest yield losses and mycotoxin contamination. Here, we report genome assemblies of F. avenaceum KA13 and F. graminearum TaB10, both isolated from fruits with symptoms of apple rot. The final F. avenaceum KA13 genome sequence assembly of 41.7 Mb consists of 34 scaffolds, with an N₅₀ value of 2.2 Mb and 15,886 predicted genes. The total size of the final F. graminearum TaB10 assembly is 36.76 Mb, consisting of 54 scaffolds with an N₅₀ value of 1.7 Mb, and it consists of 14,132 predicted genes. These new genomes provide valuable resources to better understand plant-microbe interaction in stored apple rot disease. [ ] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY 4.0 International license .

Introduction. Cytomegalovirus is the most common cause of infections in the post-transplantation period. A reliable and timely laboratory diagnosis of cytomegalovirus infection in patients on dialysis and in the post-transplantation period is significant because of the possibility of preventing or mitigating the effects of cytomegalovirus disease. The main objective of this study was to compare serological and molecular polymerase chain reaction methods to determine the presence of cytomegalovirus in the blood of dialysis patients. Material and Methods. The study included 28 dialysis patients, potential renal transplant recipients. All patients were evaluated for the presence of cytomegalovirus in the blood by a quantitative polymerase chain reaction method as well as in the serum for the presence of anti-cytomegalovirus Immunoglobulin G and Immunoglobulin M antibodies. Results. According to the comparative enzyme-linked immunosorbent assay for detecting antibodies in dialysis patients, 96.4% were once exposed to the virus, while 7.1% showed current infection not confirmed by polymerase chain reaction test. No statistically significant association was found between the positive finding of anti-cytomegalovirus Immunoglobulin M antibodies and the findings of the polymerase chain reaction cytomegalovirus method when Chi-square (χ2) and Fisher’s correlation tests were conducted (p > 0.05). Conclusion. Due to 7.1% false positives results for the presence of anti-cytomegalovirus Immunoglobulin M antibodies in the serum of immunocompromised dialysis patients, not confirmed by polymerase chain reaction test, serological techniques are not reliable in detecting active cytomegalovirus infection causing positive finding of anti-cytomegalovirus Immunoglobulin M, so confirmation of cytomegalovirus deoxyribonucleic acid by polymerase chain reaction method is required.