This study examined the knowledge and consumption patterns of fermented foods among undergraduate students, comparing those enrolled in Food and Nutrition programs with students from other academic disciplines.
A cross-sectional survey of 328 Canadian university students gathered demographic data and assessed familiarity, understanding, and intake of fermented food products.
While 78% of students reported familiarity with fermented foods, only 23% could accurately define fermentation. Students in Food and Nutrition programs demonstrated stronger knowledge, correctly answering 67% of related questions versus 62% in other disciplines (p = 0.07; 90% CI). Consumption rates were high overall, with 96% of participants reporting they consumed fermented foods. Significant differences were found between groups in specific categories: fermented fruits and vegetables (p = 0.02), soybeans (p = 0.002), grains (p = 0.02), and meat products (p = 0.017). Regarding frequency, 36% of students consumed a variety of fermented foods weekly, while 30% reported monthly consumption.
Cultural background, taste preference, and educational focus also appear to influence dietary behaviors. Enrollment in a Food and Nutrition program was linked to both higher knowledge and increased intake. To the best of our knowledge, this is the first Canadian study to explore differences in fermented food knowledge and consumption across academic disciplines. These results support the potential of education-based strategies to promote healthier dietary patterns and warrant further research across more diverse populations.
This study examined the knowledge and consumption patterns of fermented foods among undergraduate students, comparing those enrolled in Food and Nutrition programs with students from other academic disciplines.
A cross-sectional survey of 328 Canadian university students gathered demographic data and assessed familiarity, understanding, and intake of fermented food products.
While 78% of students reported familiarity with fermented foods, only 23% could accurately define fermentation. Students in Food and Nutrition programs demonstrated stronger knowledge, correctly answering 67% of related questions versus 62% in other disciplines (p = 0.07; 90% CI). Consumption rates were high overall, with 96% of participants reporting they consumed fermented foods. Significant differences were found between groups in specific categories: fermented fruits and vegetables (p = 0.02), soybeans (p = 0.002), grains (p = 0.02), and meat products (p = 0.017). Regarding frequency, 36% of students consumed a variety of fermented foods weekly, while 30% reported monthly consumption.
Cultural background, taste preference, and educational focus also appear to influence dietary behaviors. Enrollment in a Food and Nutrition program was linked to both higher knowledge and increased intake. To the best of our knowledge, this is the first Canadian study to explore differences in fermented food knowledge and consumption across academic disciplines. These results support the potential of education-based strategies to promote healthier dietary patterns and warrant further research across more diverse populations.
Liquid biopsy (LB) is a complex of procedures aimed at the detection of tumor-derived fragments (nucleic acids, proteins, cells, etc.) persisting in the blood or other body fluids. It can be utilized for early cancer diagnosis, analysis of biomarkers of tumor drug sensitivity and prognosis, monitoring of minimal residual disease (MRD), etc. Circulating tumor DNA (ctDNA) is an accessible and reliable LB analyte as it may contain tumor-specific mutations and is amenable to efficient detection by next-generation sequencing (NGS) or droplet digital PCR (ddPCR). High level of ctDNA is typically associated with increased tumor burden and poor prognosis, whereas treatment-related ctDNA clearance increases the probability of a favorable disease outcome. Major efforts have been invested in enhancing the analytical performance of ctDNA detection. Stimulation of apoptosis of tumor cells by irradiation of cancer lumps has been shown to result in a transient but modest increase in ctDNA concentration. There are several sophisticated modifications of ultra-deep NGS protocols, which discriminate between “true” low-copy mutation-specific signals and sequencing artifacts. Slowing physiological ctDNA decay by interfering with liver macrophages and circulating nucleases has shown promise in animal experiments. Reproducibility of ctDNA-based LB assays remains insufficient for samples with ultra-low content of ctDNA; hence, interlaboratory harmonization of ctDNA testing procedures is of paramount importance.
Liquid biopsy (LB) is a complex of procedures aimed at the detection of tumor-derived fragments (nucleic acids, proteins, cells, etc.) persisting in the blood or other body fluids. It can be utilized for early cancer diagnosis, analysis of biomarkers of tumor drug sensitivity and prognosis, monitoring of minimal residual disease (MRD), etc. Circulating tumor DNA (ctDNA) is an accessible and reliable LB analyte as it may contain tumor-specific mutations and is amenable to efficient detection by next-generation sequencing (NGS) or droplet digital PCR (ddPCR). High level of ctDNA is typically associated with increased tumor burden and poor prognosis, whereas treatment-related ctDNA clearance increases the probability of a favorable disease outcome. Major efforts have been invested in enhancing the analytical performance of ctDNA detection. Stimulation of apoptosis of tumor cells by irradiation of cancer lumps has been shown to result in a transient but modest increase in ctDNA concentration. There are several sophisticated modifications of ultra-deep NGS protocols, which discriminate between “true” low-copy mutation-specific signals and sequencing artifacts. Slowing physiological ctDNA decay by interfering with liver macrophages and circulating nucleases has shown promise in animal experiments. Reproducibility of ctDNA-based LB assays remains insufficient for samples with ultra-low content of ctDNA; hence, interlaboratory harmonization of ctDNA testing procedures is of paramount importance.
Our cells and, therefore, our organism, need energy to function at their best, which is mainly produced by mitochondria. These intracellular organelles generate energy from food macromolecules across the Krebs cycle by oxidative phosphorylation. Energy is developed by converting adenosine triphosphate (ATP) to adenosine diphosphate (ADP). It is essential, for adequate mitochondrial energy production in the form of ATP, to have the right number of well-functioning mitochondria and the right amount of oxygen (O2) available. Unfortunately, the aging process and the chronic diseases that arise over the years are associated with a reduction in the number of mitochondria and their insufficient functioning. Among the chronic diseases related to significant damage of the arteries with a reduction in the supply of O2, there is atherosclerosis, where the process of atherothrombosis occurs. To keep our organs well-functioning despite aging, we must therefore protect our mitochondria and arteries. This can be achieved by intervening early in prevention with a lifestyle correction and diet integration with effective natural substances or, in some cases, with drugs. Among the many natural substances that have good scientific support, we have chosen four that have demonstrated benefits in the absence of side effects and that we know best: quercetin and pyrroloquinoline quinone to stimulate mitochondrial biogenesis and mitophagy, while L-arginine and nattokinase to protect the arteries from atherothrombosis.
Our cells and, therefore, our organism, need energy to function at their best, which is mainly produced by mitochondria. These intracellular organelles generate energy from food macromolecules across the Krebs cycle by oxidative phosphorylation. Energy is developed by converting adenosine triphosphate (ATP) to adenosine diphosphate (ADP). It is essential, for adequate mitochondrial energy production in the form of ATP, to have the right number of well-functioning mitochondria and the right amount of oxygen (O2) available. Unfortunately, the aging process and the chronic diseases that arise over the years are associated with a reduction in the number of mitochondria and their insufficient functioning. Among the chronic diseases related to significant damage of the arteries with a reduction in the supply of O2, there is atherosclerosis, where the process of atherothrombosis occurs. To keep our organs well-functioning despite aging, we must therefore protect our mitochondria and arteries. This can be achieved by intervening early in prevention with a lifestyle correction and diet integration with effective natural substances or, in some cases, with drugs. Among the many natural substances that have good scientific support, we have chosen four that have demonstrated benefits in the absence of side effects and that we know best: quercetin and pyrroloquinoline quinone to stimulate mitochondrial biogenesis and mitophagy, while L-arginine and nattokinase to protect the arteries from atherothrombosis.
This article addresses the current understanding of the bidirectional relationship between iron metabolism and the gut microbiota. Both iron deficiency and iron overload in the gut can negatively affect the composition and function of the intestinal microbiota. Conversely, beneficial members of the colonic microbiota play a key role in enhancing systemic iron absorption. Particular attention is given to the potential use of microbiota-modulating agents for the correction of colonic dysbiosis as part of a comprehensive therapeutic approach to iron deficiency/overload conditions. Therefore, these interventions, by supporting microbiota restoration and reduction of intestinal inflammation, may also offer novel therapeutic avenues for disorders of iron metabolism.
This article addresses the current understanding of the bidirectional relationship between iron metabolism and the gut microbiota. Both iron deficiency and iron overload in the gut can negatively affect the composition and function of the intestinal microbiota. Conversely, beneficial members of the colonic microbiota play a key role in enhancing systemic iron absorption. Particular attention is given to the potential use of microbiota-modulating agents for the correction of colonic dysbiosis as part of a comprehensive therapeutic approach to iron deficiency/overload conditions. Therefore, these interventions, by supporting microbiota restoration and reduction of intestinal inflammation, may also offer novel therapeutic avenues for disorders of iron metabolism.
Heavy metal contamination of food is a critical global health issue due to its toxic, bioaccumulative, and often carcinogenic effects. This study presents a comprehensive bibliometric analysis of research published between 2000 and 2024 on health risk assessments associated with heavy metal exposure through the consumption of cereal products. Data were extracted from the Web of Science database and analyzed using VOSviewer software to visualize trends in terms of authors, institutional and international collaboration, and areas of thematic interest. The findings reveal a growing scientific interest in this field, with a peak in publication volume in 2020. China emerged as the main contributor, accounting for almost half of all publications, followed by Iran, Spain, and Brazil. The Chinese Academy of Sciences and Shahid Beheshti University of Medical Sciences were among the most active institutions. Journals such as Environmental Science and Pollution Research and Science of the Total Environment were identified as key publication platforms. The collaborative analysis highlights China and the USA as major centres of international collaboration, with peripheral but active contributions from countries such as England, Bangladesh, and Malaysia. Most studies focused on exposure pathways and assessed both carcinogenic and non-carcinogenic health risks, frequently reporting values above safe thresholds. These findings highlight the urgent need for national long-term monitoring programmes and the development of country-specific strategies to reduce exposure to heavy metals in food, thereby enhancing public health protection and regulatory compliance.
Heavy metal contamination of food is a critical global health issue due to its toxic, bioaccumulative, and often carcinogenic effects. This study presents a comprehensive bibliometric analysis of research published between 2000 and 2024 on health risk assessments associated with heavy metal exposure through the consumption of cereal products. Data were extracted from the Web of Science database and analyzed using VOSviewer software to visualize trends in terms of authors, institutional and international collaboration, and areas of thematic interest. The findings reveal a growing scientific interest in this field, with a peak in publication volume in 2020. China emerged as the main contributor, accounting for almost half of all publications, followed by Iran, Spain, and Brazil. The Chinese Academy of Sciences and Shahid Beheshti University of Medical Sciences were among the most active institutions. Journals such as Environmental Science and Pollution Research and Science of the Total Environment were identified as key publication platforms. The collaborative analysis highlights China and the USA as major centres of international collaboration, with peripheral but active contributions from countries such as England, Bangladesh, and Malaysia. Most studies focused on exposure pathways and assessed both carcinogenic and non-carcinogenic health risks, frequently reporting values above safe thresholds. These findings highlight the urgent need for national long-term monitoring programmes and the development of country-specific strategies to reduce exposure to heavy metals in food, thereby enhancing public health protection and regulatory compliance.
Autoimmune cytopenias are disorders driven by immune-mediated destruction of hematopoietic cells. Recent studies have linked these conditions to inborn errors of immunity (IEI), particularly in patients with recurrent and/or chronic forms. Common variable immunodeficiency (CVID) is the most common IEI in humans, and autoimmune cytopenias represent the most prevalent autoimmune manifestations of the disease. TNFRSF13B/TACI alterations are the most common genetic defects in CVID patients. The aim of this study was to investigate both the incidence of hypogammaglobulinemia—including immunoglobulin subclass deficiencies—in patients with autoimmune cytopenias, as well as possible correlations with common TNFRSF13B/TACI defects in selective patients.
A cohort of 123 patients (110 adults and 13 children, male/female: 58/65, median age at diagnosis: 50.0 years, range: 1.5–87.0) with autoimmune cytopenias [113 with autoimmune thrombocytopenia (AIT), 8 with autoimmune hemolytic anemia (AHA), and 2 with Evans syndrome] were enrolled in the study. The main immunoglobulin types (IgG, IgM, and IgA) were measured in all patients, while serum for the estimation of IgG subclass levels was available in 84 patients. Genetic analysis of TNFRSF13B/TACI was performed by PCR and Sanger sequencing.
Although no deficiency of main immunoglobulin types was detected in any patient, 8 of 84 patients (9.5%) displayed selective IgG4 deficiency (sIgG4D). Among them, three suffered from acute/newly diagnosed AIT, three from chronic AIT, and two from AHA. Interestingly, two patients with sIgG4D exhibited a family history of IEI. Furthermore, one patient (12.5%) carried a pathogenic missense mutation (c.542C>A, p.A181E, rs72553883) in a heterozygous state, while the remaining patients carried only common polymorphisms.
IgG4 could be considered a useful biomarker in patients with autoimmune cytopenias, while further studies may elucidate its precise role in disease pathogenesis and prognosis.
Autoimmune cytopenias are disorders driven by immune-mediated destruction of hematopoietic cells. Recent studies have linked these conditions to inborn errors of immunity (IEI), particularly in patients with recurrent and/or chronic forms. Common variable immunodeficiency (CVID) is the most common IEI in humans, and autoimmune cytopenias represent the most prevalent autoimmune manifestations of the disease. TNFRSF13B/TACI alterations are the most common genetic defects in CVID patients. The aim of this study was to investigate both the incidence of hypogammaglobulinemia—including immunoglobulin subclass deficiencies—in patients with autoimmune cytopenias, as well as possible correlations with common TNFRSF13B/TACI defects in selective patients.
A cohort of 123 patients (110 adults and 13 children, male/female: 58/65, median age at diagnosis: 50.0 years, range: 1.5–87.0) with autoimmune cytopenias [113 with autoimmune thrombocytopenia (AIT), 8 with autoimmune hemolytic anemia (AHA), and 2 with Evans syndrome] were enrolled in the study. The main immunoglobulin types (IgG, IgM, and IgA) were measured in all patients, while serum for the estimation of IgG subclass levels was available in 84 patients. Genetic analysis of TNFRSF13B/TACI was performed by PCR and Sanger sequencing.
Although no deficiency of main immunoglobulin types was detected in any patient, 8 of 84 patients (9.5%) displayed selective IgG4 deficiency (sIgG4D). Among them, three suffered from acute/newly diagnosed AIT, three from chronic AIT, and two from AHA. Interestingly, two patients with sIgG4D exhibited a family history of IEI. Furthermore, one patient (12.5%) carried a pathogenic missense mutation (c.542C>A, p.A181E, rs72553883) in a heterozygous state, while the remaining patients carried only common polymorphisms.
IgG4 could be considered a useful biomarker in patients with autoimmune cytopenias, while further studies may elucidate its precise role in disease pathogenesis and prognosis.
Treatment resistant depression (TRD) is frequently encountered in clinical practice. The lack of response of the condition to conventional medications and augmentation strategies has spawned the search for novel treatment approaches. Psychedelic medications used in conjunction with intensive psychotherapy, so-called psychedelic-assisted psychotherapy (PAP), have been evaluated in a limited number of studies as an alternative tactic. This psychedelic renaissance has seen psilocybin, a naturally occurring, potentially hallucinogenic substance occurring in some species of mushrooms, used as one exemplar. The definition of “treatment resistance” varies between different authorities, but there is general agreement that a minimum standard is failure to respond to at least two pharmacological agents from different classes used at a therapeutic dose for an adequate length of time. In the studies to date, more stringent definitions have mostly been applied. Each of the clinical evaluations finds that the addition of a single dose of psilocybin to the psychotherapeutic regimen produces a rapid and clinically significant decline in depressive symptomatology, which is mostly retained in follow-up evaluations out to 12 weeks or longer. Psilocybin was well tolerated with mostly mild to moderate side effects of elevated blood pressure, fatigue, lack of concentration, headache, lethargy, vertigo, feeling of physical or emotional weakness, decreased appetite, nausea, feeling dull, and being easily exhausted, which were transient. Hallucinogen persisting perception disorder (HPPD) has occasionally been reported, while there were few reports of suicidal ideation and behaviour. Psilocybin appears to offer the promise of rapid alleviation of resistant depressive symptoms, but further controlled evaluations are necessary before the drug can be given routinely.
Treatment resistant depression (TRD) is frequently encountered in clinical practice. The lack of response of the condition to conventional medications and augmentation strategies has spawned the search for novel treatment approaches. Psychedelic medications used in conjunction with intensive psychotherapy, so-called psychedelic-assisted psychotherapy (PAP), have been evaluated in a limited number of studies as an alternative tactic. This psychedelic renaissance has seen psilocybin, a naturally occurring, potentially hallucinogenic substance occurring in some species of mushrooms, used as one exemplar. The definition of “treatment resistance” varies between different authorities, but there is general agreement that a minimum standard is failure to respond to at least two pharmacological agents from different classes used at a therapeutic dose for an adequate length of time. In the studies to date, more stringent definitions have mostly been applied. Each of the clinical evaluations finds that the addition of a single dose of psilocybin to the psychotherapeutic regimen produces a rapid and clinically significant decline in depressive symptomatology, which is mostly retained in follow-up evaluations out to 12 weeks or longer. Psilocybin was well tolerated with mostly mild to moderate side effects of elevated blood pressure, fatigue, lack of concentration, headache, lethargy, vertigo, feeling of physical or emotional weakness, decreased appetite, nausea, feeling dull, and being easily exhausted, which were transient. Hallucinogen persisting perception disorder (HPPD) has occasionally been reported, while there were few reports of suicidal ideation and behaviour. Psilocybin appears to offer the promise of rapid alleviation of resistant depressive symptoms, but further controlled evaluations are necessary before the drug can be given routinely.
Emerging evidence suggests that genetic variations in taste receptor genes may influence dietary behaviors, energy homeostasis, and metabolic risk, contributing to type 2 diabetes mellitus (T2DM) pathogenesis. The objective of this study is to evaluate the association between single nucleotide polymorphisms (SNPs) in taste receptor genes and T2DM.
This systematic review followed the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) 2020 guidelines and was registered with the International Prospective Register of Systematic Reviews (PROSPERO; CRD42022351880). A comprehensive literature search was conducted across PubMed, ScienceDirect, Cochrane Library, and Google Scholar through June 2025. Original studies examining SNPs in taste receptor genes among individuals with T2DM were included. Quality assessment was performed independently by using the Newcastle-Ottawa scale.
Sixteen studies involving diverse populations met the inclusion criteria. Significant associations with T2DM were observed for SNPs in type 2 taste receptor gene family R member 3 (TAS2R3; rs11763979), TAS2R4 (rs2233998), TAS2R7, TAS2R9, TAS2R38, TAS2R50, cluster determinant 36 (CD36; rs1761667, rs3211956, rs7755), carbonic anhydrase VI gene (CA6; rs2274327), transient receptor potential vanilloid-1 (TRPV1; rs161364, rs8065080), transient receptor potential cation channel subfamily M gene member 5 (TRPM5; rs4929982), and TRPM8 (rs12472151). These polymorphisms may alter taste perception and gut hormone responses [e.g., glucagon-like peptide 1 (GLP-1)], affecting dietary intake, satiety, insulin secretion, and glucose regulation.
The findings suggest that genetic variations in taste receptor genes may contribute to T2DM through behavioral and metabolic mechanisms. Incorporating gustatory phenotyping with genotypic profiling could enable personalized dietary strategies and inform novel therapeutic approaches targeting taste-mediated gut signaling. Further large-scale, multi-ethnic, and mechanistic studies are warranted to confirm these associations and elucidate their clinical implications.
Emerging evidence suggests that genetic variations in taste receptor genes may influence dietary behaviors, energy homeostasis, and metabolic risk, contributing to type 2 diabetes mellitus (T2DM) pathogenesis. The objective of this study is to evaluate the association between single nucleotide polymorphisms (SNPs) in taste receptor genes and T2DM.
This systematic review followed the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) 2020 guidelines and was registered with the International Prospective Register of Systematic Reviews (PROSPERO; CRD42022351880). A comprehensive literature search was conducted across PubMed, ScienceDirect, Cochrane Library, and Google Scholar through June 2025. Original studies examining SNPs in taste receptor genes among individuals with T2DM were included. Quality assessment was performed independently by using the Newcastle-Ottawa scale.
Sixteen studies involving diverse populations met the inclusion criteria. Significant associations with T2DM were observed for SNPs in type 2 taste receptor gene family R member 3 (TAS2R3; rs11763979), TAS2R4 (rs2233998), TAS2R7, TAS2R9, TAS2R38, TAS2R50, cluster determinant 36 (CD36; rs1761667, rs3211956, rs7755), carbonic anhydrase VI gene (CA6; rs2274327), transient receptor potential vanilloid-1 (TRPV1; rs161364, rs8065080), transient receptor potential cation channel subfamily M gene member 5 (TRPM5; rs4929982), and TRPM8 (rs12472151). These polymorphisms may alter taste perception and gut hormone responses [e.g., glucagon-like peptide 1 (GLP-1)], affecting dietary intake, satiety, insulin secretion, and glucose regulation.
The findings suggest that genetic variations in taste receptor genes may contribute to T2DM through behavioral and metabolic mechanisms. Incorporating gustatory phenotyping with genotypic profiling could enable personalized dietary strategies and inform novel therapeutic approaches targeting taste-mediated gut signaling. Further large-scale, multi-ethnic, and mechanistic studies are warranted to confirm these associations and elucidate their clinical implications.
Celiac disease is an immune-mediated disorder with significant metabolic implications. Several factors have been proposed to explain the association between celiac disease in patients following a gluten-free diet and metabolic disorders, including metabolic syndrome. Growing evidence suggests a pivotal role of gut microbiome dysbiosis in the onset of celiac disease and its associated metabolic disturbances. The present narrative review examines (i) the connections between celiac disease and metabolism-related comorbidities, including metabolic syndrome and metabolic dysfunction-associated steatotic liver disease; (ii) the role of the gut microbiome in celiac disease, including the outcomes of gut microbiome dysbiosis in celiac children and adults; and (iii) the potential of microbial therapeutic strategies within the context of personalized medicine for patients with celiac disease and comorbid metabolic conditions. A synthesis of existing studies highlights several protective factors and interventions for future celiac disease prevention research. Adopting plant-based, health-promoting dietary patterns such as the Mediterranean or vegetarian diet within the first two years of life reduces celiac disease risk. These fiber- and phytochemical-rich diets support beneficial gut microbiota growth and short-chain fatty acid production, which maintain intestinal barrier integrity by enhancing mucus and tight junction proteins. Short-chain fatty acids also modulate immunity by inducing Tregs that secrete IL-10, suppressing pro-inflammatory Th1 responses and autoantibody production. Precision probiotics offer diverse therapeutic benefits in celiac disease by reducing inflammation, restoring beneficial microbes, and degrading immunogenic gliadin peptides. Postbiotics complement these effects by reinforcing barrier integrity and counteracting gliadin-induced inflammation. Thus, integrating clinical models with microbial biomarkers promises to improve celiac disease diagnosis and monitoring, enabling better risk stratification, earlier detection, and personalized management of this heterogeneous disease.
Celiac disease is an immune-mediated disorder with significant metabolic implications. Several factors have been proposed to explain the association between celiac disease in patients following a gluten-free diet and metabolic disorders, including metabolic syndrome. Growing evidence suggests a pivotal role of gut microbiome dysbiosis in the onset of celiac disease and its associated metabolic disturbances. The present narrative review examines (i) the connections between celiac disease and metabolism-related comorbidities, including metabolic syndrome and metabolic dysfunction-associated steatotic liver disease; (ii) the role of the gut microbiome in celiac disease, including the outcomes of gut microbiome dysbiosis in celiac children and adults; and (iii) the potential of microbial therapeutic strategies within the context of personalized medicine for patients with celiac disease and comorbid metabolic conditions. A synthesis of existing studies highlights several protective factors and interventions for future celiac disease prevention research. Adopting plant-based, health-promoting dietary patterns such as the Mediterranean or vegetarian diet within the first two years of life reduces celiac disease risk. These fiber- and phytochemical-rich diets support beneficial gut microbiota growth and short-chain fatty acid production, which maintain intestinal barrier integrity by enhancing mucus and tight junction proteins. Short-chain fatty acids also modulate immunity by inducing Tregs that secrete IL-10, suppressing pro-inflammatory Th1 responses and autoantibody production. Precision probiotics offer diverse therapeutic benefits in celiac disease by reducing inflammation, restoring beneficial microbes, and degrading immunogenic gliadin peptides. Postbiotics complement these effects by reinforcing barrier integrity and counteracting gliadin-induced inflammation. Thus, integrating clinical models with microbial biomarkers promises to improve celiac disease diagnosis and monitoring, enabling better risk stratification, earlier detection, and personalized management of this heterogeneous disease.
Fibromyalgia syndrome (FMS) is a chronic condition characterized by widespread musculoskeletal pain, fatigue, cognitive impairments, and sleep disturbances. Although traditionally considered psychogenic, recent research supports a multifactorial etiology involving central nervous system (CNS) dysregulation and significant immune involvement. This narrative review synthesizes current evidence regarding the role of immune mechanisms in FMS, with comparative insights into chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) and irritable bowel syndrome (IBS)—previously grouped under functional somatic syndromes (FSS). In FMS, immune dysregulation is evidenced by elevated levels of pro-inflammatory cytokines (e.g., IL-6, IL-8, TNF-α) and decreased anti-inflammatory mediators such as IL-10, contributing to symptomatology including pain amplification and fatigue. Neuroinflammation, as indicated by microglial activation in pain-processing CNS regions, further supports the role of immune signaling in central sensitization. Other contributing factors include oxidative stress, mitochondrial dysfunction, and immune cell alterations, particularly involving regulatory T cells and natural killer (NK) cells. Compared to FMS, CFS/ME exhibits greater systemic immune activation and more severe mitochondrial impairment, correlating with profound fatigue and cognitive decline. IBS, on the other hand, shows immune activation localized to the gastrointestinal tract, emphasizing the gut-brain axis. These findings highlight both shared and syndrome-specific immune features. To better reflect their systemic and immunological complexity, this review refers to these conditions collectively as chronic multisystem immune-related disorders (CMIRDs). The evidence supports the development of biomarker-based diagnostics and personalized immunomodulatory therapies. A multidisciplinary approach that integrates immunology and neurology is essential to improve outcomes for patients with FMS and related disorders.
Fibromyalgia syndrome (FMS) is a chronic condition characterized by widespread musculoskeletal pain, fatigue, cognitive impairments, and sleep disturbances. Although traditionally considered psychogenic, recent research supports a multifactorial etiology involving central nervous system (CNS) dysregulation and significant immune involvement. This narrative review synthesizes current evidence regarding the role of immune mechanisms in FMS, with comparative insights into chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) and irritable bowel syndrome (IBS)—previously grouped under functional somatic syndromes (FSS). In FMS, immune dysregulation is evidenced by elevated levels of pro-inflammatory cytokines (e.g., IL-6, IL-8, TNF-α) and decreased anti-inflammatory mediators such as IL-10, contributing to symptomatology including pain amplification and fatigue. Neuroinflammation, as indicated by microglial activation in pain-processing CNS regions, further supports the role of immune signaling in central sensitization. Other contributing factors include oxidative stress, mitochondrial dysfunction, and immune cell alterations, particularly involving regulatory T cells and natural killer (NK) cells. Compared to FMS, CFS/ME exhibits greater systemic immune activation and more severe mitochondrial impairment, correlating with profound fatigue and cognitive decline. IBS, on the other hand, shows immune activation localized to the gastrointestinal tract, emphasizing the gut-brain axis. These findings highlight both shared and syndrome-specific immune features. To better reflect their systemic and immunological complexity, this review refers to these conditions collectively as chronic multisystem immune-related disorders (CMIRDs). The evidence supports the development of biomarker-based diagnostics and personalized immunomodulatory therapies. A multidisciplinary approach that integrates immunology and neurology is essential to improve outcomes for patients with FMS and related disorders.
Soya (Glycine max L.) is a legume rich in nutrients (proteins, lipids, carbohydrates, and minerals) but also in anti-nutrients such as oxalate, which hampers the bioavailability of nutrients. The various processes used to treat it reduce the anti-nutrient content while affecting the protein content to a greater or lesser extent. This study aimed to evaluate the impact of a soaking period followed by cooking on the reduction of oxalates and enhancement of protein availability in soya flour.
To achieve this, the response surface methodology with the centred composite design was used to reduce the oxalate content and increase the protein content of cooked soya flour. The factors chosen were soaking time (5–24 h), cooking time (15–50 min), and cooking temperature (70–100°C). The soya flours obtained were characterised for protein and oxalate content using standard methods. The optimal samples were also characterised.
The results obtained showed that cooking and soaking times, followed by the quadratic effect of soaking time, significantly (p < 0.05) increase the protein content and decrease the oxalate content. In terms of optimal conditions, a soaking time of 25.44 h, a cooking temperature of 101.05°C, and a cooking time of 61.93 min reduced the oxalate content by 87.43% and also increased the protein content from 35.98 g/100 g DM to 49.16 g/100 g DM. Optimal conditions of the different treatments also increase lipids, reducing sugar, and the main minerals like Ca, P, Mg, and Fe.
The application of such conditions would help to combat protein deficiencies.
Soya (Glycine max L.) is a legume rich in nutrients (proteins, lipids, carbohydrates, and minerals) but also in anti-nutrients such as oxalate, which hampers the bioavailability of nutrients. The various processes used to treat it reduce the anti-nutrient content while affecting the protein content to a greater or lesser extent. This study aimed to evaluate the impact of a soaking period followed by cooking on the reduction of oxalates and enhancement of protein availability in soya flour.
To achieve this, the response surface methodology with the centred composite design was used to reduce the oxalate content and increase the protein content of cooked soya flour. The factors chosen were soaking time (5–24 h), cooking time (15–50 min), and cooking temperature (70–100°C). The soya flours obtained were characterised for protein and oxalate content using standard methods. The optimal samples were also characterised.
The results obtained showed that cooking and soaking times, followed by the quadratic effect of soaking time, significantly (p < 0.05) increase the protein content and decrease the oxalate content. In terms of optimal conditions, a soaking time of 25.44 h, a cooking temperature of 101.05°C, and a cooking time of 61.93 min reduced the oxalate content by 87.43% and also increased the protein content from 35.98 g/100 g DM to 49.16 g/100 g DM. Optimal conditions of the different treatments also increase lipids, reducing sugar, and the main minerals like Ca, P, Mg, and Fe.
The application of such conditions would help to combat protein deficiencies.
Despite being a fruit rich in resistant starch, acorns remain undervalued. Resistant starch is known to improve food acceptability when compared to traditional insoluble fibers, and recent research suggests the usage of acorn starch as an additive in fermented yogurt and milk products. Furthermore, non-thermal technologies such as high hydrostatic pressure and pulsed electric field can produce clean-labelled starches. Milk puddings are widely consumed all over the world and are usually produced using representative amounts of starch, making them an enticing food matrix for incorporating acorn starches. Hence, the effects of replacing commercial corn starch with acorn starch extracted by high hydrostatic pressure and pulsed electric field on the nutritional composition, functional and sensorial properties, and shelf-life of puddings were studied.
Extraction of starch from Quercus robur acorns was performed using high hydrostatic pressure or pulsed electric field. Extracted starch was used in chocolate puddings, replacing commercial corn starch. Shelf-life storage and microbiological analysis were conducted over 28 days, along with texture, color, pH, and nutritional composition assessments. Rheological properties, scanning electron microscopy, in vitro digestion, and soluble sugar, fatty acid, and salt content analyses were performed. Sensorial analysis was conducted with 71 volunteer panelists to evaluate the acceptability, preference, and similarity of puddings.
Replacing the commercial corn starch with acorn starch improves the rheological properties of puddings and has no negative impact on the nutritional composition, internal structure, or in vitro digestibility. Sensory analysis revealed that panelists preferred the acorn starch puddings over the control. After 28 days of storage at 4°C, there was a greater stabilization of the color parameters and an improvement in textural parameters of puddings without compromising microbial safety.
This study demonstrates the potential usage of starch from acorns in food applications, a fruit that is so undervalued.
Despite being a fruit rich in resistant starch, acorns remain undervalued. Resistant starch is known to improve food acceptability when compared to traditional insoluble fibers, and recent research suggests the usage of acorn starch as an additive in fermented yogurt and milk products. Furthermore, non-thermal technologies such as high hydrostatic pressure and pulsed electric field can produce clean-labelled starches. Milk puddings are widely consumed all over the world and are usually produced using representative amounts of starch, making them an enticing food matrix for incorporating acorn starches. Hence, the effects of replacing commercial corn starch with acorn starch extracted by high hydrostatic pressure and pulsed electric field on the nutritional composition, functional and sensorial properties, and shelf-life of puddings were studied.
Extraction of starch from Quercus robur acorns was performed using high hydrostatic pressure or pulsed electric field. Extracted starch was used in chocolate puddings, replacing commercial corn starch. Shelf-life storage and microbiological analysis were conducted over 28 days, along with texture, color, pH, and nutritional composition assessments. Rheological properties, scanning electron microscopy, in vitro digestion, and soluble sugar, fatty acid, and salt content analyses were performed. Sensorial analysis was conducted with 71 volunteer panelists to evaluate the acceptability, preference, and similarity of puddings.
Replacing the commercial corn starch with acorn starch improves the rheological properties of puddings and has no negative impact on the nutritional composition, internal structure, or in vitro digestibility. Sensory analysis revealed that panelists preferred the acorn starch puddings over the control. After 28 days of storage at 4°C, there was a greater stabilization of the color parameters and an improvement in textural parameters of puddings without compromising microbial safety.
This study demonstrates the potential usage of starch from acorns in food applications, a fruit that is so undervalued.
Plants possess tremendous medicinal properties which have been supposed to be promising candidates for biomedical applications, especially in the field of nanobiotechnology. To analyze one such view, the current study was adopted to synthesize gold nanoparticles (Au*nps) by employing the extract of Murraya koenigii (EMk) for the evaluation of phenolics, antioxidant, antimicrobial, hemolytic, and biocompatible activities.
The synthesis process was carried out in a single step by mixing EMk and gold salt (Au salt) solution and monitored using UV/Visible spectroscopy. The process was optimized via variation in environmental variables. Characterization techniques such as Fourier transform infrared (FTIR) spectroscopy, transmission electron microscopy (TEM), scanning electron microscopy (SEM), X-ray diffractometer (XRD), and energy dispersive X-rays (EDX) were employed. In vitro biological activities (total phenolic, antioxidant, antimicrobial, and hemolytic) using different concentrations of Au*nps along with EMk were assessed. An in vivo histopathology study on Wistar rats was analyzed.
The band of Au*nps was observed at 540 nm, which showed successful synthesis. The FTIR spectra of Au*nps indicated the role of different functional groups (alkane, aromatic ester, thiol, nitro, and aldehyde) of EMk during synthesis. The TEM analysis illustrated a 50 nm size of Au*nps; SEM showed the presence of some aggregates; EDX represented elemental nature, and XRD proved the crystalline nature of these Au*nps. The Au*nps possessed significant phenolic content and displayed prominent antioxidant activities by quenching free radicals. Similarly, momentous inhibitory action was observed against microbial strains of Escherichia coli and Bacillus subtilis. The hemolytic study showed the least to non-toxic effect of these nanoparticles on red blood cells (RBCs) even at enhanced concentration. Histopathology study showed fair compatibility without inducing any apparent pathological lesions on the liver tissues of Wistar rats.
Plausibly, all the above investigations strongly emphasized the use of medicinal plant-based Au*nps for biological applications.
Plants possess tremendous medicinal properties which have been supposed to be promising candidates for biomedical applications, especially in the field of nanobiotechnology. To analyze one such view, the current study was adopted to synthesize gold nanoparticles (Au*nps) by employing the extract of Murraya koenigii (EMk) for the evaluation of phenolics, antioxidant, antimicrobial, hemolytic, and biocompatible activities.
The synthesis process was carried out in a single step by mixing EMk and gold salt (Au salt) solution and monitored using UV/Visible spectroscopy. The process was optimized via variation in environmental variables. Characterization techniques such as Fourier transform infrared (FTIR) spectroscopy, transmission electron microscopy (TEM), scanning electron microscopy (SEM), X-ray diffractometer (XRD), and energy dispersive X-rays (EDX) were employed. In vitro biological activities (total phenolic, antioxidant, antimicrobial, and hemolytic) using different concentrations of Au*nps along with EMk were assessed. An in vivo histopathology study on Wistar rats was analyzed.
The band of Au*nps was observed at 540 nm, which showed successful synthesis. The FTIR spectra of Au*nps indicated the role of different functional groups (alkane, aromatic ester, thiol, nitro, and aldehyde) of EMk during synthesis. The TEM analysis illustrated a 50 nm size of Au*nps; SEM showed the presence of some aggregates; EDX represented elemental nature, and XRD proved the crystalline nature of these Au*nps. The Au*nps possessed significant phenolic content and displayed prominent antioxidant activities by quenching free radicals. Similarly, momentous inhibitory action was observed against microbial strains of Escherichia coli and Bacillus subtilis. The hemolytic study showed the least to non-toxic effect of these nanoparticles on red blood cells (RBCs) even at enhanced concentration. Histopathology study showed fair compatibility without inducing any apparent pathological lesions on the liver tissues of Wistar rats.
Plausibly, all the above investigations strongly emphasized the use of medicinal plant-based Au*nps for biological applications.
Down syndrome (DS), caused by trisomy 21, is strongly associated with an increased risk of early-onset Alzheimer’s disease (AD). This work explores the cellular, genetic, epigenetic, and neuropsychological mechanisms that underlie the accelerated development of AD in individuals with DS. We review key contributors such as amyloid-β accumulation, mitochondrial dysfunction, oxidative stress, tau pathology, neuroinflammation, and chromosomal and epigenetic instability in the neuropathology of AD in DS. Particular attention is given to genes, microRNAs, and chromatin remodeling factors encoded by human chromosome 21 (Hsa21) that regulate these pathological processes. We also highlight the roles of non-coding RNAs and altered DNA methylation patterns in modulating gene expression and neuronal vulnerability. Additionally, the writing evaluates current pharmacological and non-pharmacological interventions and addresses the critical need for inclusive, person-centered health services. Integrating molecular biology with clinical perspectives, the review emphasizes the importance of early diagnosis and coordinated care strategies for individuals with DS at risk for AD.
Down syndrome (DS), caused by trisomy 21, is strongly associated with an increased risk of early-onset Alzheimer’s disease (AD). This work explores the cellular, genetic, epigenetic, and neuropsychological mechanisms that underlie the accelerated development of AD in individuals with DS. We review key contributors such as amyloid-β accumulation, mitochondrial dysfunction, oxidative stress, tau pathology, neuroinflammation, and chromosomal and epigenetic instability in the neuropathology of AD in DS. Particular attention is given to genes, microRNAs, and chromatin remodeling factors encoded by human chromosome 21 (Hsa21) that regulate these pathological processes. We also highlight the roles of non-coding RNAs and altered DNA methylation patterns in modulating gene expression and neuronal vulnerability. Additionally, the writing evaluates current pharmacological and non-pharmacological interventions and addresses the critical need for inclusive, person-centered health services. Integrating molecular biology with clinical perspectives, the review emphasizes the importance of early diagnosis and coordinated care strategies for individuals with DS at risk for AD.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease worldwide. Its prevalence is increasing due to its close relationship with obesity, insulin resistance, and other metabolic disorders. In this context, the gut-liver axis has been identified as a fundamental regulator in the progression of MASLD, integrating metabolic, immunological, and inflammatory signals that influence hepatic homeostasis. This article reviews the interconnection between the intestine and the liver in the onset and progression of MASLD, highlighting the roles of cholesterol and its metabolism, intestinal barrier permeability, microbiota, and hepatic signaling pathways. We analyze how intestinal dysbiosis and alterations in the enterohepatic circulation of bile acids affect cholesterol absorption and metabolism. Furthermore, we address the influence of endotoxin translocation, activation of the innate immune system, and the interaction of key transcription factors on disease progression from steatosis to advanced fibrosis and hepatocellular carcinoma (HCC). Finally, therapeutic strategies, including pharmacological, dietary, and immunomodulation-based approaches, are discussed to regulate cholesterol metabolism, modulate the intestinal microbiota, and restore gut-liver axis homeostasis. Integrating this knowledge could open new perspectives for treating and preventing MASLD, addressing the disease from a broader and multidisciplinary viewpoint.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease worldwide. Its prevalence is increasing due to its close relationship with obesity, insulin resistance, and other metabolic disorders. In this context, the gut-liver axis has been identified as a fundamental regulator in the progression of MASLD, integrating metabolic, immunological, and inflammatory signals that influence hepatic homeostasis. This article reviews the interconnection between the intestine and the liver in the onset and progression of MASLD, highlighting the roles of cholesterol and its metabolism, intestinal barrier permeability, microbiota, and hepatic signaling pathways. We analyze how intestinal dysbiosis and alterations in the enterohepatic circulation of bile acids affect cholesterol absorption and metabolism. Furthermore, we address the influence of endotoxin translocation, activation of the innate immune system, and the interaction of key transcription factors on disease progression from steatosis to advanced fibrosis and hepatocellular carcinoma (HCC). Finally, therapeutic strategies, including pharmacological, dietary, and immunomodulation-based approaches, are discussed to regulate cholesterol metabolism, modulate the intestinal microbiota, and restore gut-liver axis homeostasis. Integrating this knowledge could open new perspectives for treating and preventing MASLD, addressing the disease from a broader and multidisciplinary viewpoint.
The science of manipulating matter at almost atomic scales to create new structures and devices that function at nanoscale dimensions is known as nanotechnology, which is essential to many sciences, such as medicine and environment. This field of study has been reported to investigate better alternatives for the advancement of medicine; one such alternative is the use of plants, which contain substantial amounts of essential phytochemicals. This study aims to utilize such a plant species, Canna indica (C. indica) leaves, known as traditional medicinal plants or commonly grown plants, to synthesize silver nanoparticles (AgNPs) and evaluate their potential in green medicine.
The synthesis was carried out using five varieties of leaf water extracts: Pink red, Yellow, Pink, Yellow red, and Red, under different conditions, to which scanning electron microscopy was performed. The antioxidant capacity was evaluated by total flavonoid content, total phenolic content, total antioxidant capacity, and 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay. The antibacterial activity of AgNPs and water extracts was evaluated against Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli). Finally, the cytotoxicity of AgNP is evaluated using the brine shrimp lethality assay.
The optimum condition for AgNP synthesis was determined to be room temperature, and Pink_AgNPs were observed as spherical with a size of 27–48 nm in scanning electron microscopy. The antioxidant assays concluded that AgNPs show significantly higher antioxidant capacity and exhibit higher scavenging activity. This study’s findings showed the efficiency of AgNPs against both strains, and higher efficiency against S. aureus. It was observed that with 240 ppm of AgNPs, 100% viability is obtained.
These novel findings emphasize the significance of C. indica AgNPs, their promise in the medical field, and their application in manufacturing green medicine for environmentally friendly healthcare.
The science of manipulating matter at almost atomic scales to create new structures and devices that function at nanoscale dimensions is known as nanotechnology, which is essential to many sciences, such as medicine and environment. This field of study has been reported to investigate better alternatives for the advancement of medicine; one such alternative is the use of plants, which contain substantial amounts of essential phytochemicals. This study aims to utilize such a plant species, Canna indica (C. indica) leaves, known as traditional medicinal plants or commonly grown plants, to synthesize silver nanoparticles (AgNPs) and evaluate their potential in green medicine.
The synthesis was carried out using five varieties of leaf water extracts: Pink red, Yellow, Pink, Yellow red, and Red, under different conditions, to which scanning electron microscopy was performed. The antioxidant capacity was evaluated by total flavonoid content, total phenolic content, total antioxidant capacity, and 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay. The antibacterial activity of AgNPs and water extracts was evaluated against Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli). Finally, the cytotoxicity of AgNP is evaluated using the brine shrimp lethality assay.
The optimum condition for AgNP synthesis was determined to be room temperature, and Pink_AgNPs were observed as spherical with a size of 27–48 nm in scanning electron microscopy. The antioxidant assays concluded that AgNPs show significantly higher antioxidant capacity and exhibit higher scavenging activity. This study’s findings showed the efficiency of AgNPs against both strains, and higher efficiency against S. aureus. It was observed that with 240 ppm of AgNPs, 100% viability is obtained.
These novel findings emphasize the significance of C. indica AgNPs, their promise in the medical field, and their application in manufacturing green medicine for environmentally friendly healthcare.
Cancer remains one of the leading causes of morbidity and mortality globally, driven by genetic alterations, uncontrolled cell proliferation, and metabolic reprogramming. The tumor microenvironment (TME) is a highly dynamic and heterogeneous system composed of tumor cells, immune cells, stromal cells, and extracellular matrix (ECM) components, which influence cancer progression. Tumor-associated macrophages (TAMs), especially those polarized into the M2 phenotype, play a critical role in modulating this environment. M2 macrophages promote tumor progression through mechanisms such as immune suppression, angiogenesis, and metastasis. This polarization is heavily influenced by the altered metabolic landscape of tumors, where the Warburg effect leads to excessive lactate production, which in turn drives M2 polarization through G protein-coupled receptor 132 (GPR132). M2 macrophages secrete cytokines like IL-10, transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF), which contribute to immune escape, tumor growth, and metastasis. The metabolic shifts within TAMs, especially the transition from oxidative phosphorylation to glycolysis, further support the pro-tumoral functions of these cells. This review explores the intricate relationship between M2 macrophage polarization bias, tumor metabolism, and the resulting impact on cancer progression, highlighting the potential of targeting these pathways for therapeutic strategies. The findings suggest that M2 macrophage polarization could serve as a key prognostic factor for cancer outcomes and provide a basis for future research into therapeutic interventions that target macrophage polarization and the tumor metabolic milieu.
Cancer remains one of the leading causes of morbidity and mortality globally, driven by genetic alterations, uncontrolled cell proliferation, and metabolic reprogramming. The tumor microenvironment (TME) is a highly dynamic and heterogeneous system composed of tumor cells, immune cells, stromal cells, and extracellular matrix (ECM) components, which influence cancer progression. Tumor-associated macrophages (TAMs), especially those polarized into the M2 phenotype, play a critical role in modulating this environment. M2 macrophages promote tumor progression through mechanisms such as immune suppression, angiogenesis, and metastasis. This polarization is heavily influenced by the altered metabolic landscape of tumors, where the Warburg effect leads to excessive lactate production, which in turn drives M2 polarization through G protein-coupled receptor 132 (GPR132). M2 macrophages secrete cytokines like IL-10, transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF), which contribute to immune escape, tumor growth, and metastasis. The metabolic shifts within TAMs, especially the transition from oxidative phosphorylation to glycolysis, further support the pro-tumoral functions of these cells. This review explores the intricate relationship between M2 macrophage polarization bias, tumor metabolism, and the resulting impact on cancer progression, highlighting the potential of targeting these pathways for therapeutic strategies. The findings suggest that M2 macrophage polarization could serve as a key prognostic factor for cancer outcomes and provide a basis for future research into therapeutic interventions that target macrophage polarization and the tumor metabolic milieu.
Hypersensitivity reactions (HSRs) to paclitaxel, particularly those mediated by the solubilizer Cremophor® EL, are common, occurring in approximately 10% of patients despite premedication. Nab-paclitaxel, a newer formulation using human serum albumin as the vehicle, is generally considered a safer alternative due to a lower rate of HSRs. We present the case of a 44-year-old woman with breast cancer who developed severe HSRs following multiple doses of paclitaxel and carboplatin. Despite standard premedication, she experienced fever, erythematous skin eruptions, arthralgias, and systemic symptoms following her fourth and fifth cycles of treatment. Subsequent administration of nab-paclitaxel also elicited a similar severe reaction. Skin testing revealed a positive reaction to paclitaxel, but not to carboplatin, suggesting sensitization to paclitaxel. In the context of the similar reaction to nab-paclitaxel, this suggests sensitization to the taxane moiety itself rather than to the solubilizer. The combination of features consistent with both type IV hypersensitivity and cytokine release syndrome further complicates the presentation as well. To our knowledge, this is the first reported case of cross-reactivity between paclitaxel and nab-paclitaxel, challenging the assumption that nab-paclitaxel is always a safe alternative. This emphasizes the need for vigilance and thorough evaluation in patients experiencing atypical chemotherapy reactions, as cytokine release reactions may play a role even in the absence of immunotherapy. It also raises the concern that alternative formulations like nab-paclitaxel may not always be safe in patients with atypical or severe reactions, as they could possibly be sensitized to the taxane moiety itself.
Hypersensitivity reactions (HSRs) to paclitaxel, particularly those mediated by the solubilizer Cremophor® EL, are common, occurring in approximately 10% of patients despite premedication. Nab-paclitaxel, a newer formulation using human serum albumin as the vehicle, is generally considered a safer alternative due to a lower rate of HSRs. We present the case of a 44-year-old woman with breast cancer who developed severe HSRs following multiple doses of paclitaxel and carboplatin. Despite standard premedication, she experienced fever, erythematous skin eruptions, arthralgias, and systemic symptoms following her fourth and fifth cycles of treatment. Subsequent administration of nab-paclitaxel also elicited a similar severe reaction. Skin testing revealed a positive reaction to paclitaxel, but not to carboplatin, suggesting sensitization to paclitaxel. In the context of the similar reaction to nab-paclitaxel, this suggests sensitization to the taxane moiety itself rather than to the solubilizer. The combination of features consistent with both type IV hypersensitivity and cytokine release syndrome further complicates the presentation as well. To our knowledge, this is the first reported case of cross-reactivity between paclitaxel and nab-paclitaxel, challenging the assumption that nab-paclitaxel is always a safe alternative. This emphasizes the need for vigilance and thorough evaluation in patients experiencing atypical chemotherapy reactions, as cytokine release reactions may play a role even in the absence of immunotherapy. It also raises the concern that alternative formulations like nab-paclitaxel may not always be safe in patients with atypical or severe reactions, as they could possibly be sensitized to the taxane moiety itself.
This study attempts to offer a viable and sustainable solution related to the tomato value chain, which plays an active role in human diets but deteriorates very fast due to its short shelf life.
Fresh lemons (Citrus limon) and tomatoes (Solanum lycopersicum L.) were purchased from the local market. Previously, varying percentages of lemon juice (0%, 1%, 3%, 5%, and 10%) were added to clear jars containing peeled and pasted tomatoes, which were then sterilized. The physicochemical, antioxidant, nutritional, and microbiological characteristics of appertized tomato samples were assessed through the use of standardized techniques.
The addition of lemon juice significantly (P ˂ 0.05) reduced the total phenolic content of appertized tomatoes, while increasing the titratable acidity (P ˂ 0.05) and decreasing the hydrogen potential (pH) content (P ˂ 0.05). However, the addition of 10 g of lemon juice recorded the high flavonoid content (0.01 mg CE/g) and carotenoid content (16.52 mg/100 g) of samples. In terms of nutritional value, adding lemon juice to appertized tomatoes considerably reduced (P ˂ 0.05) their protein content while increasing their carbohydrate content. Regarding the mineral composition, the addition of lemon juice considerably (P ˂ 0.05) raised the amounts of calcium (Ca), phosphorus (P), and magnesium (Mg) in the appertized tomato samples. The results of this investigation fall within the ranges of the daily allowances that are advised. Pathogens including Salmonella, Clostridium, and Escherichia coli are inhibited, and yeasts and molds are destroyed, ensuring the product’s microbiological quality [476.57 to 0 colony-forming unit (CFU)].
Lemon juice helps to preserve consumer health and improve the preservation of appertized tomatoes.
This study attempts to offer a viable and sustainable solution related to the tomato value chain, which plays an active role in human diets but deteriorates very fast due to its short shelf life.
Fresh lemons (Citrus limon) and tomatoes (Solanum lycopersicum L.) were purchased from the local market. Previously, varying percentages of lemon juice (0%, 1%, 3%, 5%, and 10%) were added to clear jars containing peeled and pasted tomatoes, which were then sterilized. The physicochemical, antioxidant, nutritional, and microbiological characteristics of appertized tomato samples were assessed through the use of standardized techniques.
The addition of lemon juice significantly (P ˂ 0.05) reduced the total phenolic content of appertized tomatoes, while increasing the titratable acidity (P ˂ 0.05) and decreasing the hydrogen potential (pH) content (P ˂ 0.05). However, the addition of 10 g of lemon juice recorded the high flavonoid content (0.01 mg CE/g) and carotenoid content (16.52 mg/100 g) of samples. In terms of nutritional value, adding lemon juice to appertized tomatoes considerably reduced (P ˂ 0.05) their protein content while increasing their carbohydrate content. Regarding the mineral composition, the addition of lemon juice considerably (P ˂ 0.05) raised the amounts of calcium (Ca), phosphorus (P), and magnesium (Mg) in the appertized tomato samples. The results of this investigation fall within the ranges of the daily allowances that are advised. Pathogens including Salmonella, Clostridium, and Escherichia coli are inhibited, and yeasts and molds are destroyed, ensuring the product’s microbiological quality [476.57 to 0 colony-forming unit (CFU)].
Lemon juice helps to preserve consumer health and improve the preservation of appertized tomatoes.
Scientific evidence seems to indicate that, in males, intense and prolonged endurance sport can favor the onset of atrial fibrillation. A plausible explanation may be the impact that intense endurance sports produce on the three vertices of Coumel’s triangle. However, genetics is probably also involved in translating this impact into an arrhythmic phenotype. On a management level, the first task of the cardiologist is to exclude the presence of structural heart disease, channelopathy, endocrine and/or electrolyte disorders, and substance use. As for the treatment of arrhythmia, the “CARE” paradigm proposed by the latest ESC guidelines should probably be accompanied by detraining, although this suggestion is often rejected by the athlete. Anticoagulant therapy, where indicated, must take into account the risk of trauma that the sport entails, even if the particular pharmacodynamics/pharmacokinetics of DOACs should allow training/competition to take place when the anticoagulant effect of the previous administration has completely or almost completely worn off.
Scientific evidence seems to indicate that, in males, intense and prolonged endurance sport can favor the onset of atrial fibrillation. A plausible explanation may be the impact that intense endurance sports produce on the three vertices of Coumel’s triangle. However, genetics is probably also involved in translating this impact into an arrhythmic phenotype. On a management level, the first task of the cardiologist is to exclude the presence of structural heart disease, channelopathy, endocrine and/or electrolyte disorders, and substance use. As for the treatment of arrhythmia, the “CARE” paradigm proposed by the latest ESC guidelines should probably be accompanied by detraining, although this suggestion is often rejected by the athlete. Anticoagulant therapy, where indicated, must take into account the risk of trauma that the sport entails, even if the particular pharmacodynamics/pharmacokinetics of DOACs should allow training/competition to take place when the anticoagulant effect of the previous administration has completely or almost completely worn off.