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Introduction: Artificial Intelligence (AI) has emerged as a seminal force in healthcare, fundamentally transforming various aspects of medical practice and patient care. This review explores the transformative impact of AI on the treatment of cardiovascular diseases (CVDs). State of Knowledge: AI has revolutionized diagnostic accuracy, treatment precision, and patient management in the realm of cardiovascular care. It enhances diagnostic processes, enabling the early detection of CVDs through advanced imaging analysis and interpretation. Additionally, AI facilitates precision in risk stratification, identifying high-risk patient cohorts with heightened accuracy and informing personalized treatment strategies. Furthermore, AI optimizes drug selection and dosage regimens through pharmacogenomics, maximizing therapeutic efficacy while minimizing adverse drug reactions. Moreover, AI improves precision and safety during interventional procedures, guiding clinicians in real-time decision-making and enhancing procedural outcomes. Conclusions: AI is poised to revolutionize cardiovascular care, fostering innovation and improving patient outcomes.

Introduction and purpose: Chronic inflammation in the oral cavity poses significant risks to both the heart and the circulatory system. A growing number of studies indicate a correlation between periodontal health and the likelihood of developing cardiovascular conditions, including myocardial infarction, coronary artery disease, hypertension, and stroke. This review aims to summarize recent reports, define current state of knowledge, and propose optimal treatment and prevention strategies. State of knowledge: Risk factors such as obesity, smoking, and genetic predisposition contribute to the development of both PD and cardiovascular diseases (CVDs). Inflammation serves as a common factor linking the two conditions, with periodontal pathogens directly affecting cardiovascular health. Epigenetic mechanisms, particularly in response to environmental stimuli, further exacerbate the relationship between PD and CVDs. Additionally, the oral microbiome plays a crucial role, with periodontal pathogens infiltrating systemic circulation and triggering immune-inflammatory responses that promote cardiovascular damage. Conclusions: People with periodontitis have a higher risk of CVDs, especially when other risk factors such as smoking and obesity are present. Periodontal treatment has been demonstrated to enhance cardiovascular health parameters. Implementing preventive strategy, addressing both periodontitis and cardiovascular risk factors, could potentially decrease morbidity and mortality associated with cardiovascular disease.

Introduction: Parkinson's disease (PD) is one of the most common neurodegenerative diseases that mainly affects older people over 60 years of age. Since life expectancy is increasing not only in Europe but also around the world, the number of people suffering from PD will gradually increase. State of knowledge: One of the newest techniques used to study the mechanisms of diseases of the nervous system, which allows monitoring the activity of neurons by modifying their functions, is optogenetics. This method involves controlling neuronal activity using light. The sensitivity of cells to light is achieved by introducing into the body the genes of ion channels from algae or bacteria, which are incorporated into the cell membrane and then become excited when exposed to light. Depending on the gene used, the activity of a nerve cell can be intensified or inhibited. An important advantage of the method is the possibility of using it in vivo and recording the results in real time. Summary: This publication aims to present the basics of optogenetics and is a review of works related to its use in the study of PD pathomechanism. For this purpose, the PubMed and Google Scholar databases were verified using the following words: "Parkinson optogenetic", "optogenetic stimulation", "channelrhodopsin".

Chronic pain is a debilitating condition that affects millions of patients worldwide, contributing to a high disease burden and millions of dollars in lost wages, missed workdays, and healthcare costs. Opioids, NSAIDs, acetaminophen, gabapentinoids, muscle relaxants, anticonvulsants, and antidepressants are the most used medications for chronic pain and carry significant side effects, including gastric bleeding, hepatotoxicity, stroke, kidney damage, constipation, dizziness, and arrhythmias. Opioids in particular carry the risk of long-term dependence, drug tolerance, and overdose. In 2022, 81,806 people died from opioid overdose in the United States alone. Alternative treatments for chronic pain are critically needed, and nanotechnology has emerged as a promising means of achieving effective long-term analgesia while avoiding the adverse side effects associated with conventional pharmacological agents. Nanotechnology-based treatments include liposomes, Poly Lactic-co-Glycolic Acid (PLGA) and other polymeric nanoparticles, and carbon-based polymers, which can help mitigate those adverse side effects. These nanomaterials can serve as drug delivery systems that facilitate controlled release and drug stability via the encapsulation of free molecules and protein-based drugs, leading to longer-lasting analgesia and minimizing side effects. In this review, we examine the role of nanotechnology in addressing concerns associated with conventional chronic pain treatments and discuss the ongoing efforts to develop novel, nanotechnology-based treatments for chronic pain such as nanocapacitor patches, gene therapy, the use of both viral and non-viral vectors, CRISPR, and scavengers.

Background: Creatine, a naturally occurring compound plays a crucial role in cellular energy metabolism, particularly in tissues with high energy demands like muscles and the brain. Beyond its well-established role in physical performance enhancement, recent research has revealed its potential benefits for cognitive functions and mood regulation. This review paper aims to comprehensively analyze the existing literature on creatine supplementation's effects on cognitive functions and mood. State of Knowledge: Findings suggest that creatine supplementation enhances memory, attention, and executive functions, especially under conditions of stress or sleep deprivation. Moreover, it exhibits mood-stabilizing effects, potentially offering relief for symptoms of depression and fatigue. Creatine's ability to augment brain energy metabolism, alongside its neuroprotective properties, underlies its cognitive and mood-enhancing effects. While generally safe, caution is advised, particularly in populations with kidney diseases or those using medications affecting kidney function. Summary: Creatine emerges as a promising adjunct therapy for enhancing cognitive functions and promoting emotional well-being beyond its traditional role in physical performance.The review underscores the need for further research to elucidate the precise mechanisms of creatine's effects and explore its synergistic potential with other cognitive-enhancing supplements.

Introduction: Neurodegenerative diseases pose a significant diagnostic challenge due to the increasing elderly population and the rising prevalence of these conditions. State of Knowledge: Differential diagnosis among these diseases is particularly challenging; thus, numerous clinical trials have been conducted to identify markers that could facilitate accurate disease diagnosis. Among various diagnostic approaches, imaging techniques play a crucial role, especially magnetic resonance imaging (MRI), which includes advanced modalities such as proton magnetic resonance spectroscopy (¹H-MRS). ¹H-MRS offers a non-invasive assessment of neurometabolite profiles, providing critical information that aids in precise diagnosis. Conclusions: With ongoing clinical trials, the importance of ¹H-MRS in diagnosing neurodegenerative diseases continues to grow. This paper reviews the results of recent and relevant clinical trials examining changes in ¹H-MRS in the most prevalent neurodegenerative diseases.

Introduction: Children with chronic kidney disease (CKD) require a specialized diet to manage their condition and support healthy growth and development. A proper diet for children with CKD aims to control the intake of certain nutrients, such as protein, lipid, calcium, phosphorus, potassium, sodium, and vitamin D, while ensuring they receive adequate nutrition for growth and development. Aim of the study: This article discusses the epidemiology, causes and pathomechanism of CKD in children. It also presents existing clinical trials and dietary recommendations from societies such as Kidney Disease: Improving Global Outcomes (KDIGO) 2024, Kidney Disease Outcomes Quality Initiative (KDOQI) and Pediatric Renal Nutrition Taskforce (PRNT) and identifies potential sources of selected macronutrients and micronutrients in children's diets. Materials and methods: Comprehensive literature searches were performed across the main electronic databases of PubMed, Google Scholar, KDIGO2024, KDQQI and PRNT recommendations for studies published in the English language about dietary recommendations for children with CKD. Results: The approach to nutrition for children with CKD is still evolving, and specific macronutrient and micronutrient ratios should be established based on the clinical condition, the child's age, and body weight. Care should be taken to ensure that the child's diet is varied, and a healthy eating style should be promoted.

Intruduction and purpose: Patients with severe asthma account for approximately 3% to 10% of all asthma patients. They have higher hospital utilization rates and treatment costs than patients with non-severe asthma. Previously, treatment options for these patients were limited due to unacceptable side effects. However, the advent of biologic therapies has provided promising targeted therapy for these patients. State of knowledge: Biologic therapies target inflammatory modulators that play a key role in the pathogenesis of asthma, particularly in patients with high T2 cells. These therapies have shown promising results in reducing asthma symptoms, improving lung function, decreasing the use of oral corticosteroids, and enhancing patients' quality of life. Conclusions: This article reviews the mechanism of action, efficacy, and indications of currently approved biologic drugs available in Poland, as well as potential therapeutic targets for the future.

Introduction and Purpose: In last years gene modification technologies such as CRISPR/Cas9 has had a revolutionary impact on the treatment of inherited diseases. Technologies developed from bacterial defense mechanisms, has become a basic tools in scientific research and medical therapies. In our article we provided an overview of applications of gene modifications technologies, directly focusing on CRISPR/Cas9, in genetic disease treatment. State of Knowledge: New applications of CRISPR/Cas9 are still being explored. Treating inherited diseases such as cystic fibrosis, Duchenne muscular dystrophy, thalassemia, hemophilia, Huntington's disease, Crigler-Najjar syndrome, sickle cell anemia, Marfan syndrome, and phenylketonuria, is feasible with this novel technique. A comparative analysis with other gene editing methods highlights CRISPR/Cas9's efficacy, ease of use, and multiplexing capabilities. Summary: CRISPR/Cas9 is a groundbreaking technology with broad applications in genetic research and therapy. Its ease of use, cost-effectiveness, and ability to target multiple genes simultaneously position it as a preferred method. However, there are some challenges associated with precision issues and ethical considerations in human embryo gene editing. As CRISPR/Cas9 continues to evolve, responsible application and ethical considerations are important for maximizing its potential in treatment of genetic diseases.

Dermatan sulfate (DS) is a glycosaminoglycan characterized by having a variable structure and wide distribution in animal tissues. We previously demonstrated that some structural variants of DS were able to rapidly induce moderate necroptosis in luminal breast cancer cells when used at a high concentration. We have now investigated the mechanisms underlying the DS-mediated activation of the necroptotic executor MLKL using immunofluorescence, Western blotting and pharmacological inhibition. The two main processes, by which DS influences the phosphorylation of MLKL, are the activation of NFκB, which demonstrates a suppressive impact, and the induction of oxidative stress, which has a stimulatory effect. Moreover, the triggering of the redox imbalance by DS occurs via the modulatory influence of this glycosaminoglycan on the rearrangement of the actin cytoskeleton, requiring alterations in the activity of small Rho GTP-ase Rac1. All of these processes that were elicited by DS in luminal breast cancer cells showed a dependence on the structure of this glycan and the type of cancer cells. Furthermore, our results suggest that a major mechanism that is involved in the stimulation of necroptosis in luminal breast cancer cells by high doses of DS is mediated via the effect of this glycan on the activity of adhesion molecules.

Introduction and purpose: Gaucher's Disease (GD), a rare genetic disorder, is a difficult challenge in genetic and metabolic disorders. The aim of this review is to provide an exploration of GD, spanning its pathophysiology to the latest advancements in diagnostic and therapeutic innovations. In this review we aimed to underscore the challenges it presents and the ongoing efforts to overcome them. State of knowledge: GD, characterized by the accumulation of glucocerebroside, involves molecular, cellular, and systemic dysfunctions. At the molecular level, mutations in the GBA gene give rise to diverse manifestations, influencing disease severity. Cellular disruptions lead to lysosomal dysfunction, altered calcium homeostasis, and chronic inflammation, impacting various organ systems. Diagnostic approaches involve biomarkers, genetic testing, and imaging studies, each playing a crucial role in confirming the disease type and assessing its grade. Summary: Management and treatment strategies for GD have evolved, with enzyme replacement therapy and substrate reduction therapy serving as the basics. However, challenges persist, including limited efficacy in treating neurological symptoms and the high cost of treatments. The review highlights ongoing research and future perspectives in GD therapy.

Background: The symbiotic relationship between the gut microbiota and cardiovascular health has become a main point in contemporary research, offering valuable insights into the pathogenesis of cardiovascular diseases (CVDs). This review aims to comprehensively examine the bidirectional communication between gut microbial communities and the cardiovascular system, explaining the intricate mechanisms that connect gut dysbiosis to the initiation and progression of CVDs. Material and Methods: A systematic literature review was conducted to compile and analyze relevant studies investigating the impact of the gut microbiota on cardiovascular health. Emphasis was placed on explaining the molecular and physiological mechanisms underlying the interaction between gut microbes and cardiovascular function. Results: Our review confirmed evidence linking gut microbiota-derived metabolites, such as short-chain fatty acids, trimethylamine N-oxide and lipopolysaccharides to vascular function and inflammation. Additionally, we explored the modulation of host metabolism and immune responses by gut microbes, providing insights into their roles in atherosclerosis and hypertension. The review highlight the influence of diet and lifestyle on shaping the gut microbiome and, consequently, cardiovascular outcomes. Conclusions: Gut microbiota plays a crucial role in cardiovascular health and is involved in the start and development of various heart diseases. The identified molecular and physiological mechanisms highlight the need for complete understanding of the gut-cardiovascular axis. Moreover, the review emphasizes the potential of microbiota-targeted interventions, including probiotics and fecal microbiota transplantation, as innovative strategies for preventing and managing CVDs.

Neuropeptide S (NPS), which is a peptide that is involved in the regulation of the stress response, seems to be relevant to the mechanism of action of antidepressants that have anxiolytic properties. However, to date, there have been no reports regarding the effect of long-term treatment with escitalopram or venlafaxine on the NPS system under stress conditions. This study aimed to investigate the effects of the above-mentioned antidepressants on the NPS system in adult male Wistar rats that were exposed to neonatal maternal separation (MS). Animals were exposed to MS for 360 min. on postnatal days (PNDs) 2–15. MS causes long-lasting behavioral, endocrine and neurochemical consequences that mimic anxiety- and depression-related features. MS and non-stressed rats were given escitalopram or venlafaxine (10mg/kg) IP from PND 69 to 89. The NPS system was analyzed in the brainstem, hypothalamus, amygdala and anterior olfactory nucleus using quantitative RT-PCR and immunohistochemical methods. The NPS system was vulnerable to MS in the brainstem and amygdala. In the brainstem, escitalopram down-regulated NPS and NPS mRNA in the MS rats and induced a tendency to reduce the number of NPS-positive cells in the peri-locus coeruleus. In the MS rats, venlafaxine insignificantly decreased the NPSR mRNA levels in the amygdala and a number of NPSR cells in the basolateral amygdala, and increased the NPS mRNA levels in the hypothalamus. Our data show that the studied antidepressants affect the NPS system differently and preliminarily suggest that the NPS system might partially mediate the pharmacological effects that are induced by these drugs.

Background: Creatine, a naturally occurring compound plays a crucial role in cellular energy metabolism, particularly in tissues with high energy demands like muscles and the brain. Beyond its well-established role in physical performance enhancement, recent research has revealed its potential benefits for cognitive functions and mood regulation. This review paper aims to comprehensively analyze the existing literature on creatine supplementation's effects on cognitive functions and mood. State of Knowledge: Findings suggest that creatine supplementation enhances memory, attention, and executive functions, especially under conditions of stress or sleep deprivation. Moreover, it exhibits mood-stabilizing effects, potentially offering relief for symptoms of depression and fatigue. Creatine's ability to augment brain energy metabolism, alongside its neuroprotective properties, underlies its cognitive and mood-enhancing effects. While generally safe, caution is advised, particularly in populations with kidney diseases or those using medications affecting kidney function. Summary: Creatine emerges as a promising adjunct therapy for enhancing cognitive functions and promoting emotional well-being beyond its traditional role in physical performance. The review underscores the need for further research to elucidate the precise mechanisms of creatine's effects and explore its synergistic potential with other cognitive-enhancing supplements. [ABSTRACT FROM AUTHOR]

Introduction: Neurodegenerative diseases pose a significant diagnostic challenge due to the increasing elderly population and the rising prevalence of these conditions. State of Knowledge: Differential diagnosis among these diseases is particularly challenging; thus, numerous clinical trials have been conducted to identify markers that could facilitate accurate disease diagnosis. Among various diagnostic approaches, imaging techniques play a crucial role, especially magnetic resonance imaging (MRI), which includes advanced modalities such as proton magnetic resonance spectroscopy (¹H-MRS). ¹H-MRS offers a noninvasive assessment of neurometabolite profiles, providing critical information that aids in precise diagnosis. Conclusions: With ongoing clinical trials, the importance of ¹H-MRS in diagnosing neurodegenerative diseases continues to grow. This paper reviews the results of recent and relevant clinical trials examining changes in ¹H-MRS in the most prevalent neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Introduction: Children with chronic kidney disease (CKD) require a specialized diet to manage their condition and support healthy growth and development. A proper diet for children with CKD aims to control the intake of certain nutrients, such as protein, lipid, calcium, phosphorus, potassium, sodium, and vitamin D, while ensuring they receive adequate nutrition for growth and development. Aim of the study: This article discusses the epidemiology, causes and pathomechanism of CKD in children. It also presents existing clinical trials and dietary recommendations from societies such as Kidney Disease: Improving Global Outcomes (KDIGO) 2024, Kidney Disease Outcomes Quality Initiative (KDOQI) and Pediatric Renal Nutrition Taskforce (PRNT) and identifies potential sources of selected macronutrients and micronutrients in children's diets. Materials and methods: Comprehensive literature searches were performed across the main electronic databases of PubMed, Google Scholar, KDIGO2024, KDQQI and PRNT recommendations for studies published in the English language about dietary recommendations for children with CKD. Results: The approach to nutrition for children with CKD is still evolving, and specific macronutrient and micronutrient ratios should be established based on the clinical condition, the child's age, and body weight. Care should be taken to ensure that the child's diet is varied, and a healthy eating style should be promoted. [ABSTRACT FROM AUTHOR]

Intruduction and purpose: Patients with severe asthma account for approximately 3% to 10% of all asthma patients. They have higher hospital utilization rates and treatment costs than patients with non-severe asthma. Previously, treatment options for these patients were limited due to unacceptable side effects. However, the advent of biologic therapies has provided promising targeted therapy for these patients. State of knowledge: Biologic therapies target inflammatory modulators that play a key role in the pathogenesis of asthma, particularly in patients with high T2 cells. These therapies have shown promising results in reducing asthma symptoms, improving lung function, decreasing the use of oral corticosteroids, and enhancing patients' quality of life. Conclusions: This article reviews the mechanism of action, efficacy, and indications of currently approved biologic drugs available in Poland, as well as potential therapeutic targets for the future. [ABSTRACT FROM AUTHOR]

Introduction and Purpose: In last years gene modification technologies such as CRISPR/Cas9 has had a revolutionary impact on the treatment of inherited diseases. Technologies developed from bacterial defense mechanisms, has become a basic tools in scientific research and medical therapies. In our article we provided an overview of applications of gene modifications technologies, directly focusing on CRISPR/Cas9, in genetic disease treatment. State of Knowledge: New applications of CRISPR/Cas9 are still being explored. Treating inherited diseases such as cystic fibrosis, Duchenne muscular dystrophy, thalassemia, hemophilia, Huntington's disease, Crigler-Najjar syndrome, sickle cell anemia, Marfan syndrome, and phenylketonuria, is feasible with this novel technique. A comparative analysis with other gene editing methods highlights CRISPR/Cas9's efficacy, ease of use, and multiplexing capabilities. Summary: CRISPR/Cas9 is a groundbreaking technology with broad applications in genetic research and therapy. Its ease of use, cost-effectiveness, and ability to target multiple genes simultaneously position it as a preferred method. However, there are some challenges associated with precision issues and ethical considerations in human embryo gene editing. As CRISPR/Cas9 continues to evolve, responsible application and ethical considerations are important for maximizing its potential in treatment of genetic diseases. [ABSTRACT FROM AUTHOR]

Introduction and purpose: Gaucher's Disease (GD), a rare genetic disorder, is a difficult challenge in genetic and metabolic disorders. The aim of this review is to provide an exploration of GD, spanning its pathophysiology to the latest advancements in diagnostic and therapeutic innovations. In this review we aimed to underscore the challenges it presents and the ongoing efforts to overcome them. State of knowledge: GD, characterized by the accumulation of glucocerebroside, involves molecular, cellular, and systemic dysfunctions. At the molecular level, mutations in the GBA gene give rise to diverse manifestations, influencing disease severity. Cellular disruptions lead to lysosomal dysfunction, altered calcium homeostasis, and chronic inflammation, impacting various organ systems. Diagnostic approaches involve biomarkers, genetic testing, and imaging studies, each playing a crucial role in confirming the disease type and assessing its grade. Summary: Management and treatment strategies for GD have evolved, with enzyme replacement therapy and substrate reduction therapy serving as the basics. However, challenges persist, including limited efficacy in treating neurological symptoms and the high cost of treatments. The review highlights ongoing research and future perspectives in GD therapy. [ABSTRACT FROM AUTHOR]

Dermatan sulfate (DS) is a glycosaminoglycan characterized by having a variable structure and wide distribution in animal tissues. We previously demonstrated that some structural variants of DS were able to rapidly induce moderate necroptosis in luminal breast cancer cells when used at a high concentration. We have now investigated the mechanisms underlying the DS-mediated activation of the necroptotic executor MLKL using immunofluorescence, Western blotting and pharmacological inhibition. The two main processes, by which DS influences the phosphorylation of MLKL, are the activation of NFκB, which demonstrates a suppressive impact, and the induction of oxidative stress, which has a stimulatory effect. Moreover, the triggering of the redox imbalance by DS occurs via the modulatory influence of this glycosaminoglycan on the rearrangement of the actin cytoskeleton, requiring alterations in the activity of small Rho GTP-ase Rac1. All of these processes that were elicited by DS in luminal breast cancer cells showed a dependence on the structure of this glycan and the type of cancer cells. Furthermore, our results suggest that a major mechanism that is involved in the stimulation of necroptosis in luminal breast cancer cells by high doses of DS is mediated via the effect of this glycan on the activity of adhesion molecules. [ABSTRACT FROM AUTHOR]

Dermatan sulfate (DS) is widespread in the extracellular matrix (ECM) of animal tissues. This glycosaminoglycan is characterized by a variable structure, which is reflected in the heterogeneity of its sulfation pattern. The sulfate groups are responsible for the binding properties of DS, which determine an interaction profile of this glycan. However, the detailed role of DS in biological processes such as the neoplasm is still poorly understood. The aim of the study was to assess the effects of the structural variants of DS on breast cancer cells. We found that DS isoforms from normal and fibrotic fascia as well as from intestinal mucosa were able to quickly induce oxidative stress in the cytoplasm and affect the mitochondrial function in luminal breast cancer cells. Moreover, the variants caused the necroptosis of the cells most likely via the first of these mechanisms. This death was responsible for a reduction in the viability and number of breast cancer cells. However, the dynamics and intensity of all of the DS variants-triggered effects were strongly dependent on the cell type and the structure of these molecules. The most pronounced activity was demonstrated by those variants that shared structural features with the DS from the tumor niche.

Aim. Many data showed a role of inflammation and dysfunction of immune system as important factors in the risk of schizophrenia. The TNFR2 receptor is a molecule that adapts to both areas. Tumor necrosis factor receptor 2 (TNFR2) is a receptor for the TNF-α cytokine which is a strong candidate gene for schizophrenia. The serum level of TNFR2 was significantly increased in schizophrenia and associated with more severe symptoms of schizophrenia. Methods. We examined the association of the three single nucleotide polymorphisms (rs3397, rs1061622, and rs1061624) in TNFR2 gene with a predisposition to and psychopathology of paranoid schizophrenia in Caucasian population. The psychopathology was measured by a five-factor model of the PANSS scale. We also assessed a haplotype analysis with the -308G/A of TNF-α gene. Results. Our case-control study (401 patients and 657 controls) revealed that the genetic variants of rs3397, rs1061622, and rs1061624 in the TNFR2 gene are associated with a higher risk of developing schizophrenia and more severe course in men. However, the genotypes with polymorphic allele for rs3397 SNP are protective for women. The rs1061624 SNP might modulate the appearance of the disease in relatives of people with schizophrenia. The CTGG haplotype build with tested SNPs of TNFR2 and SNP -308G/A of TNF-α has an association with a risk of schizophrenia in Caucasian population depending on sex. Our finding is especially true for the paranoid subtypes of schizophrenia.

Schizophrenia is a devastating mental disorder with undetermined aetiology. Previous research has suggested that dysregulation of proinflammatory cytokines and their receptors plays a role in developing schizophrenia. We examined the association of the three single nucleotide polymorphisms (SNPs; rs4149576, rs4149577, and rs1860545) in the tumor necrosis factor receptor 1 (TNFR1) gene with the development and psychopathology of paranoid schizophrenia in the Polish Caucasian sample consisting of 388 patients and 657 control subjects. The psychopathology was assessed using a five-factor model of the Positive and Negative Syndrome Scale (PANSS). SNPs were genotyped using the TaqMan 5′-exonuclease allelic discrimination assay. The SNPs tested were not associated with a predisposition to paranoid schizophrenia in either the entire sample or after stratification according to gender. However, rs4149577 and rs1860545 SNPs were associated with the intensity of the PANSS excitement symptoms in men, which may contribute to the risk of violent behavior. Polymorphisms in the TNFR1 gene may have an impact on the symptomatology of schizophrenia in men.