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This study aimed to investigate the implications of antinuclear antibodies (ANAs) in juvenile idiopathic arthritis (JIA), the association with uveitis and the favorable evolution of the disease.

Introduction. Heart failure (HF) is characterized by neuroendocrine activation. The cardiac natriuretic hormones, including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), together with their related pro-peptides (proANP and proBNP) represent a group of peptide hormones produced by the heart. A normal NT-proBNP level has a high negative predictive value for heart failure. The use of NT-proBNP testing is helpful in diagnosing acute HF in the emergency care setting, allowing an early and optimal treatment. The purpose of this study is to assess the prognostic value of NT-proBNP in heart failure in children younger than 3 years old and to establish whether it correlates with the NYHA/Ross functional class and left ventricle systolic function.

Background and Aims. Two-dimensional (2D) and Doppler echocardiography are the main methods for the non-invasive evaluation of ventricular function in children. Our study monitored the evaluation of systolic and diastolic function in pediatric patients, using classical echocardiographic parameters and pulsed tissue Doppler parameters, as well as the correlation between these.

Obiective. Scopul acestui studiu a fost de a examina efectele polimorfismelor (SNPs) genei PON1 la nivelul regiunii promotor (-909 şi -832) şi a primului exon (+575, 20352A>G, rezultând substituirea Q192R) asupra activităţilor paraoxonazei-1 (PON1) într-un grup format din 53 de pacienţi cu boală coronariană (CHD) dovedită angiografic şi 17 subiecţi fără CHD. Metode şi rezultate. Activităţile PON1 din ser, respectiv arilesteraza (AR-ase) şi paraoxonaza NaCl-stimulată (ssPO-ase), au fost evaluate cu metode spectrofotometrice manuale, folosind acetat de fenil, respectiv paraoxon ca substrat. Markerii biochimici uzuali au fost analizaţi prin metode enzimatice, pe analizorul Roche/Hitachi 912, folosind kituri comerciale. Genotipurile PON1 au fost determinate folosind PCR, iar pentru secvenţierea ampliconilor s-a utilizat kitul BigDye® Terminator v3.1 şi analizorul ABI PRISMTM 310. Severitatea stenozei coronariane s-a evaluat şi clasificat folosind scorul Gensini. Nu s-au observat diferenţe semnificative statistic între grupurile cu şi fără CHD în ceea ce priveste activităţile PON1 şi polimorfismele -909G>C, -832G>A şi +575A>G. Dar, luând în considerare toţi subiecţii investigaţi, am constatat că SNPs -909G>C şi +575A>G au avut efecte semnificative statistic asupra AR-ase, respectiv PO-ase. Folosind modelul regresiei multiple am constatat că diabetul, LDL-colesterolul şi numărul de alele mutante au fost determinanţi semnificativi, independenţi, ai scorului Gensini. O corelaţie pozitivă semnificativă a fost observată numai între scorul Gensini şi numărul de alele mutante. Concluzii. Nu există diferenţe între subiecţi cu si fără CHD în ceea ce priveşte genotipurile şi fenotipurile PON1, dar creşterea numărului de alele PON1 mutante este un factor important în determinarea severităţii leziunilor coronariene

Adenilat kinaza este o enzimă ubiquitară prezentă atât la procariote cât şi la eucariote. în această lucrare am testat acţiunea inhibitorie a şase 5-ariliden-tiazolidin-4-on-2-tione faţă de adenilat kinaza din Strepto- coccus pneumoniae (A\Ksp) prin metoda colorimetrică cu 2,4-dinitrofenilhidrazonă. Efectul inhibitor al compuşilor de sinteză a fost testat faţă de enzima recombinantă supra-exprimată în E. coli. Compusul C10H6BrNOS2 cu atomul de brom în poziţia -orto a fost cel mai eficace inhibitor, valoarea I50 (concentraţia de inhibitor care determină inhibarea activităţii cu 50%) a fost 0.067mM.

Abstract Background Bullous pemphigoid is a subepidermal blistering disorder associated with tissue-bound and circulating autoantibodies directed mainly to the hemidesmosomal component collagen XVII. While recapitulating the main immunopathological features of the human disease, frank skin blistering does not develop in the absence of skin rubbing in experimental pemphigoid models that have been established in neonatal mice. Moreover, due to their experimental design they only allow for short-term disease observation. In the present study we aimed to establish a model that reproduces the frank skin blistering seen in patients and allows for longer observation times. Methods Rabbit and sheep antibodies specific to several fragments of collagen XVII were generated and the purified antibodies were passively transferred into adult mice. Results Collagen XVII-specific IgG bound to the basal membrane of the skin and mucous membranes activating murine complement in vivo. Mice injected with collagen XVII-specific antibodies, in contrast to mice receiving control antibodies, developed frank skin blistering disease, reproducing human bullous pemphigoid at the clinical, histological and immunopathological levels. Titres of circulating IgG in the serum of mice correlated with the extent of the clinical disease. Mice receiving sheep antibodies specific to murine collagen XVII showed an early onset and a more active disease when compared to litter mates receiving specific rabbit antibodies. Conclusion This novel animal model for bullous pemphigoid should facilitate further investigations of the pathogenesis of bullous pemphigoid and the development of innovative therapies for this disease.

Gastrointestinal cancers (GIC), encompassing colonic, rectal, and gastric malignancies, rank among the most prevalent cancer types globally, contributing significantly to cancer-related mortality. In the scientific literature, various syndromes associated with colorectal and gastric cancers have been elucidated, highlighting the intricate interplay between genetic factors and disease manifestation. The primary objective of this study was to conduct a genetic exploration aimed at elucidating these associations and identifying shared genetic determinants across these cancer types. Notably, considerable research has focused on the KRAS gene mutations, polymorphisms in nucleic acids, the Wnt signaling pathway, and the role of chemokine ligands in tumorigenesis. While investigations into natural plant extracts as potential therapeutic agents are still in their nascent stages, they represent a promising avenue for future research. Ongoing studies are essential to uncover suitable biomarkers that could facilitate the identification and understanding of the genetic links between these GIC. This exploration not only seeks to enhance our comprehension of the underlying genetic architecture but also aims to inform the development of targeted therapies and preventive strategies. [ABSTRACT FROM AUTHOR]

Gastric cancer (GC) remains a significant public health concern because of its lethality, underscoring the need for deeper insights into its molecular mechanisms. Recent studies have increasingly highlighted the role of epigenetic modifications as critical players in cancer progression. Despite their importance, research specifically addressing epigenetic factors in GC is relatively scarce. This paper seeks to bridge that gap by examining recent literature that elucidates the epigenetic landscape associated with GC. The investigation of long noncoding RNAs (lncRNAs) has revealed their substantial involvement in gene dysregulation and epigenetic alterations within GC tumors. Notably, lncRNAs such as LINC00853 and LINC01266 have been identified as significant contributors to the epigenetic modulation of gene expression. Furthermore, the overexpression of KAT5 and GPX4 has been shown to mitigate the antiproliferative effects resulting from the depletion of circRHOT1, suggesting a complex interplay between these molecules in GC pathophysiology. Another pivotal aspect of epigenetic regulation in GC involves modifications in N6-methyladenosine (m6A), which play crucial roles in mRNA maturation processes such as splicing, export, degradation, and translation. m6A modifications are known for their influence on various cancer-related pathways, thus presenting a potential avenue for targeted interventions. Our findings indicate that the most pronounced instances of epigenetic dysregulation in GC can be traced back to the effects of long lncRNAs and alterations in m6A modification patterns. This underscores the urgent need for comprehensive investigations into these epigenetic factors, as a deeper understanding could lead to enhanced diagnostic markers and innovative therapeutic strategies. The integration of genetic and epigenetic considerations is essential for advancing the field of GC research. This synthesis of recent findings concerning epigenetic regulation offers valuable insights that could inform future studies and therapeutic developments. There is a critical need for ongoing research to elucidate the complexities of epigenetic modifications in GC, ultimately improving patient outcomes through tailored interventions. [ABSTRACT FROM AUTHOR]

Researchers have performed numerous studies on immunotherapy because of the high death rate associated with gastric cancer (GC). GC immunotherapy research has made tremendous progress, and we wanted to provide an update on this topic. On the basis of this update, we suggest performing a new medical evaluation before initiating immunotherapy in patients with GC to increase the success rate of immunotherapies. We propose that before patients start GC immunotherapy, they should be evaluated and given a score of one to two points for the following factors: immunopathological features, molecular and genomic features, potential consequences for bacterial pathogens, potential immunotherapeutic resistance and hyperprogressive illness, and the potential to use biomarkers to gauge their prognosis and immunotherapy responses to optimize immunotherapy following surgery. The proposed scoring system could also help in the diagnosis of GC. With all the advances in genetics, immunology, and microbiology, the diagnosis of GC could be improved, not changed. Currently, patients diagnosed with GC undergo surgical resection as the only permanent solution. Patients who meet the maximum score from the presented proposal could be eligible immediately after diagnosis for immunotherapy. Therefore, immunotherapy could be a first-line option for clinicians. [ABSTRACT FROM AUTHOR]

Simple Summary: The normal calcification process is essential for bone formation, but calcification found elsewhere can result in cardiovascular and joint complications. Ectopic calcification, influenced by factors such as hormonal imbalance and oxidative stress, can impact soft tissues and becomes more prevalent with age and chronic illness. The stiffening of soft tissues due to calcification is a complex process influenced by cell type, interactions, the extracellular matrix, and mechanical forces. Understanding these mechanisms is vital for developing treatments for calcification-related complications. This review explores the similarities between vascular and cartilage calcifications, offering insights into both normal and pathological aspects. Physiological calcification occurs in bones and epiphyseal cartilage as they grow, whereas ectopic calcification occurs in blood vessels, cartilage, and soft tissues. Although it was formerly thought to be a passive and degenerative process associated with aging, ectopic calcification has been identified as an active cell-mediated process resembling osteogenesis, and an increasing number of studies have provided evidence for this paradigm shift. A significant association between vascular calcification and cardiovascular risk has been demonstrated by various studies, which have shown that arterial calcification has predictive value for future coronary events. With respect to cartilaginous calcification, calcium phosphate or hydroxyapatite crystals can form asymptomatic deposits in joints or periarticular tissues, contributing to the pathophysiology of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, tendinitis, and bursitis. The risk factors and sequence of events that initiate ectopic calcification, as well as the mechanisms that prevent the development of this pathology, are still topics of debate. Consequently, in this review, we focus on the nexus of the mechanisms underlying vascular and cartilaginous calcifications, trying to circumscribe the similarities and disparities between them to provide more clarity in this regard. [ABSTRACT FROM AUTHOR]

Simple Summary: The incidence of gastric cancer (GC) is increasing. Many people receive an advanced diagnosis of GC. Furthermore, a large number of patients are surgically inoperable and are unresponsive to preoperative chemotherapy. Patients with GC do not currently have an immunotherapy option. Our study's objective was to provide insight into extracellular vesicles (EVs) and GC. EVs in GC can be studied, as this article explains. EVs screening, which is available for all patients, is an option for combatting GC. Extracellular vesicles, or EVs, are membrane-bound nanocompartments produced by tumor cells. EVs carry proteins and nucleic acids from host cells to target cells, where they can transfer lipids, proteomes, and genetic material to change the function of target cells. EVs serve as reservoirs for mobile cellular signals. The collection of EVs using less invasive processes has piqued the interest of many researchers. Exosomes carry substances that can suppress the immune system. If the results of exosome screening are negative, immunotherapy will be beneficial for GC patients. In this study, we provide an update on EVs and GC based on ongoing review papers and clinical trials. [ABSTRACT FROM AUTHOR]

Many studies on gastric cancer treatment have identified predictors of immunotherapy benefits. This article provides an update on the major developments in research related to predictive factors of immunotherapy for gastric cancer. We used the search term "predictive factors, immunotherapy, gastric cancer" to find the most current publications in the PubMed database related to predictive factors of immunotherapy in gastric cancer. Programmed cell death, genetic, and immunological factors are the main study topics of immunotherapy's predictive factors in gastric cancer. Other preventive factors for immunotherapy in gastric cancer were also found, including clinical factors, tumor microenvironment factors, imaging factors, and extracellular factors. Since there is currently no effective treatment for gastric cancer, we strongly propose that these studies be prioritized. [ABSTRACT FROM AUTHOR]

Malocclusion, characterized by its diverse phenotypic expression, significantly impacts patients’ quality of life. Over recent years, extensive attention has been directed towards the genetic basis of this condition, particularly focusing on various polymorphisms of the MATN1 gene. Among these, the rs1065755 polymorphism has emerged as particularly relevant, associated with an elevated risk of mandibular prognathism. In this study, employing DNA sequencing, we investigated the extent of association between the rs1065755 SNP and malocclusion risk within the Romanian population. Our approach concentrated on assessing continuous phenotypic variation through four cephalometric measurements, aiming for a comprehensive understanding beyond categorical phenotypes. The findings shed light on the relationship between the MATN1 rs1065755 SNP and the investigated dentofacial disorder, revealing a positive association between TT homozygous individuals and Class II skeletal malocclusion. However, further investigations employing larger sample sizes are necessary to validate these findings conclusively. [ABSTRACT FROM AUTHOR]

Kawasaki disease (KD) is a medium vessel systemic vasculitis that predominantly occurs in children below five years of age. It is an acute febrile condition in which coronary artery aneurysms and myocarditis are the most common cardiovascular complications. It is most often characterized by hypercytokinemia. The etiopathogenesis of KD is not fully understood. The present review synthesizes the recent advances in the pathophysiology and treatment options of KD. According to different studies, the genetic, infections and autoimmunity factors play a major role in pathogenesis. Several susceptibility genes (e.g. caspase 3) and cytokines (e.g. IL-2, IL-4, IL-6, IL-10, IFN-γ and TNF-α) have been identified in KD. Patients with high cytokine levels are predisposed to KD shock syndrome. The importance of respiratory viruses in the pathogenesis of the disease is unclear. Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may induce in children and adults an abnormal systemic inflammatory response. This syndrome shares characteristics with KD. It has been called by many terms like MIS-C (Multisystem Inflammatory Syndrome in Children), PIMS-TS (pediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2), hyperinflammatory shock syndrome, cytokine storm (cytokine release syndrome) or simply, Kawasaki-like syndrome. The cytokine’s role in the development of KD or Kawasaki-like syndrome being triggered by COVID-19 is controversial. The presences of the antiendothelial cell autoantibodies (AECAs) together with the newly developed hypothesis of immunothrombosis are considered potential pathogenic mechanisms for KD. In consequence, the diagnosis and treatment of KD and Kawasaki-like syndrome, one of the most common causes of acquired heart disease in developed countries, are challenging without a clearly defined protocol. [ABSTRACT FROM AUTHOR]