Introduction and aim:Down syndrome is the most common chromosomal disorder characterized by a wide spectrum of clinical symptoms such as immune system dysregulation and co-occurring metabolic disorders, including an increased risk of cardiovascular disease. Therefore, the aim of this study was to evaluate the immunometabolic interactions in children adolescents and adults with Down syndrome (DS) and to compare selected inflammatory and metabolic parameters with those observed in their siblings. Materials and methods:The study included n= 63 individuals who were divided into two groups: group with DS n=42 (mean age: 14.2 ± 6.6) and control group (CG) n=21 (mean age: 15.6 ± 6.9). In addition, patients in both groups were also divided according to age ≤ 18 years and >18 years of age. Carbohydrate-lipid and immunological profiles were analyzed using spectrophotometric and immunoenzymatic methods. Statistical analysis was performed using R studio software. Results:In the DS group ≤ 18 years significantly higher obesity rates, i.e., Ponderal Mass Index (TMI), were observed (p=0.04), which was also associated with statistically significantly higher level of non-HDL (p=0.02) and apoB (p=0.04). Among lipid parameters, apolipoprotein A demonstrated relatively high diagnostic utility (AUC = 0.818, sens%=60.0, spec%=95.2). Significantly lower cytokine levels were observed in the DS group for IL-10 (p=0.006), IL-13 (p<0.01), and IL-22 (p=0.002). The highest diagnostic utility among the assessed cytokines was demonstrated for IL-5 (AUC = 0.814, sens%=71.10, spec%=88.1). Conclusion:The analyses conducted indicate significant differences between the studied groups of patients with Down syndrome and the control group. The presence of an additional copy of 21 the chromosome leads to changes in the immune system, influences the heterogeneous cytokine profile, and consequently may increase the development of metabolic disorders.

In the study, the polyphenol profile, volatile compounds, antioxidant, anti-inflammatory, antidiabetic, antiageing, and anticancer properties of tea methanolic extracts were analysed. Five types of tea were investigated: green, black, red, blue (oolong), and white. The highest phenolics content (30.68 g/100 g) was found in green tea, while the lowest (23.38 g/100 g)was observed in oolong tea. Using the GC-MS Arrow-HS method, 117 volatile compounds were identified based on MS spectra and retention indices. White tea demonstrated the highest antioxidant activity, while green tea exhibited the strongest inhibition of COX-1 and COX-2 enzymes (up to 77 %). Oolong and white teas showed the most potent alpha-amylase inhibition (up to 96.9 %). White and blue teas displayed the strongest anticancer activity, with significant cytotoxic effects on lung cancer cells. The dual role of tea polyphenols in oxidative stress and anticancer therapy is highlighted by ROS regulation in cancer cells.

Background/Objectives: Metformin (Met) is a potent antidiabetic drug that also exhibits anticancer, antioxidant, and organ-protective properties. Luteolin (Lut), a naturally occurring flavonoid found in many plant species, possesses anticancer, antioxidant, and anti-inflammatory effects. Since both compounds affect cellular metabolism and oxidative balance, the analysis of metabolites produced in living cells provides insight into biochemical alterations occurring in cancer cells and enables monitoring of treatment response. Methods: In this study, Met (1–20 mM) and Lut (1–100 µM) were tested in vitro, both individually and in combination, to evaluate their effects on cell viability, free radical levels, and metabolite profile alterations in cancer and normal cell lines (MDA-MB-231, SW620, and V79). Cell viability was assessed using the MTT assay at two time points (24 h and 48 h), while reactive oxygen species (ROS) levels were measured after hydrogen peroxide stimulation (100 µM H2O2) using the DCF-DA assay. Metabolomic changes induced by Met and Lut were analyzed by 1H NMR spectroscopy. Results: The analysis showed that Lut reduced the viability of MDA-MB-231 cells at both time points, whereas Met decreased viability only after prolonged incubation. Met did not inhibit the proliferation of SW620 colorectal cancer cells, while Lut reduced viability at higher concentrations (100 µM after 24 h, and 50–100 µM after 48 h). Conclusions: The combination of metformin and luteolin demonstrated additive effects in reducing cell viability and oxidative stress compared with single-compound treatments. Normal V79 fibroblasts responded to both Met and Lut, individually and in combination. Both compounds exhibited moderate antioxidant properties in cells exposed to 100 µM H2O2. Lut (25 µM) reduced free radical levels in MDA-MB-231 cells, whereas Met (2.5 mM) did so in SW620 cells. The combination of both compounds increased ROS levels in SW620 cells subjected to oxidative stress. Overall, co-treatment with metformin and luteolin altered metabolic pathways and induced changes in intra- and extracellular metabolite levels across all tested cell lines. The observed additive effects suggest that the combined use of metformin and luteolin may enhance anticancer and antioxidant responses, warranting further in vivo studies to confirm these interactions.

Lung cancer is the leading cause of cancer mortality worldwide, with a poor prognosis driven by late diagnosis, systemic toxicity of existing therapies, and rapid development of multidrug resistance (MDR) to agents such as paclitaxel and cisplatin. MDR arises through multiple mechanisms, including overexpression of efflux transporters, alterations in apoptotic pathways, and tumour microenvironment-mediated resistance. The application of nanotechnology offers a potential solution to the aforementioned challenges by facilitating the enhancement of drug solubility, stability, bioavailability, and tumour-specific delivery. Additionally, it facilitates the co-loading of agents, thereby enabling the attainment of synergistic effects. Halloysite nanotubes (HNTs) are naturally occurring aluminosilicate nanocarriers with unique dual-surface chemistry, allowing hydrophobic drug encapsulation in the positively charged lumen and functionalisation of the negatively charged outer surface with targeting ligands or MDR modulators. This architecture supports dual-delivery strategies, enabling simultaneous administration of phytocannabinoids and chemotherapeutics or efflux pump inhibitors to enhance intracellular retention and cytotoxicity in resistant tumour cells. HNTs offer additional advantages over conventional nanocarriers, including mechanical and chemical stability and low production cost. Phytocannabinoids such as cannabidiol (CBD) and cannabigerol (CBG) show multitarget anticancer activity in lung cancer models, including apoptosis induction, proliferation inhibition, and oxidative stress modulation. However, poor solubility, instability, and extensive first-pass metabolism have limited their clinical use. Encapsulation in HNTs can overcome these barriers, protect against degradation, and enable controlled, tumour-targeted release. This review examined the therapeutic potential of HNT-based phytocannabinoid delivery systems in the treatment of lung cancer, with an emphasis on improving therapeutic selectivity, which represents a promising direction for more effective and patient-friendly treatments for lung cancer.

Oxidative stress (OS), arising from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, plays a pivotal role in cellular dysfunction and the pathogenesis of numerous diseases. This study evaluates the impact of oxidative stress induced by hydrogen peroxide on the metabolomic profiles of the human embryonic kidney (HEK-293) and African green monkey kidney (COS-7) cell lines. Viability (MTT) and free radical accumulation (DCF-DA) assays confirmed a dose-dependent cytotoxic effect of hydrogen peroxide, with COS-7 cells exhibiting greater resistance and producing lower levels of intracellular ROS compared to HEK-293. Metabolomic profiling was conducted using nuclear magnetic resonance spectroscopy (1H NMR) to identify and quantify metabolic changes. Exposure to a free radical inducer significantly altered both intracellular and extracellular metabolites compared to control H2O2-free samples. The analysis revealed common changes in intracellular metabolites between the two lines, including glutamate, NAD+, glutathione, ATP/ADP, AMP, and pyruvate — key molecule for mitochondrial function, as well as extracellular metabolites such as glutamate, glutamine, acetate, lactate, and pyruvate. Metabolomic differences observed in COS-7 cells suggest a potentially greater capacity for metabolic adaptation to oxidative stress. These included elevated levels of branched-chain amino acids (BCAA), supporting energy production, and increased formate production, which may aid purine synthesis and cellular resilience. These findings highlight the distinct metabolic adaptations of COS-7 cells to oxidative stress in comparison to the HEK-293 cell line. They also provide insights into the direct cellular responses to altered redox potential, offering possible therapeutic strategies aimed at targeting metabolic pathways to mitigate oxidative stress.

This article presents framework guidelines for the care of adolescent transgender (T) and non-binary (NB) individuals experiencing gender dysphoria (GD) and/or gender incongruence (GI). Developed by a multidisciplinary expert panel, these guidelines aim to address the complex medical, psychological, and social needs of this diverse population. The document emphasises the importance of individualised, affirmative care that respects the autonomy, identity, and rights of adolescents. It outlines best practices for psychiatric, psychological, and sexological assessment; criteria and protocols for gender-affirming hormonal interventions (GAHI) and puberty suppression; and ethical considerations for medical decision-making. The guidelines advocate for comprehensive support systems, including family involvement and multidisciplinary team collaboration, while addressing co-occurring mental health conditions and neurodiversity. The article also highlights global perspectives on gender-affirming care, comparing practices and policies across countries to provide a contextualised approach that aligns with international standards while addressing local legal and healthcare frameworks. The proposed care model is designed to enhance the mental and physical well-being of adolescents, reduce stigma, and improve their overall quality of life. This work serves as a vital resource for healthcare professionals, policymakers, and advocates seeking to advance equitable, effective, and compassionate care for gender-diverse youths.

Background: Colorectal cancer is one of the leading and most lethal neoplasms. Standard chemotherapy is ineffective, especially in metastatic cancer, and does not target cancer stem cells. A promising approach to improve cancer treatment is the combination therapy of standard cytostatic drugs with natural compounds. Several plant-derived compounds have been proven to possess anticancer properties, including the induction of apoptosis and inhibition of cancer invasion. This study was focused on investigating in vitro the combination of camptothecin (CPT) with celastrol (CEL) or resveratrol (RSV) as a potential strategy to target metastatic (LOVO) and stem-like (LOVO/DX) colon cancer cells. Methods: The genotoxic effects that drive cancer cells into death-inducing pathways and the ability to inhibit the migratory properties of cancer cells were evaluated. The γH2AX+ assay and Fast-Halo Assay (FHA) were used to evaluate genotoxic effects, the annexin-V apoptosis assay to rate the level of apoptosis, and the scratch test to assess antimigratory capacity. Results: The results showed that both combinations CPT-CEL and CPT-RSV improve general genotoxicity of CPT alone on metastatic cells and CSCs. However, the assessment of specific double-stranded breaks (DSBs) indicated a better efficacy of the CPT-CEL combination on LOVO cells and CPT-RSV in LOVO/DX cells. Interestingly, the combinations CPT-CEL and CPT-RSV did not improve the pro-apoptotic effect of CPT alone, with both LOVO and LOVO/DX cells suggesting activation of different cell death mechanisms. Furthermore, it was found that the combinations of CPT-CEL and CPT-RSV improve the inhibitory effect of camptothecin on cell migration. Conclusions: These findings suggest the potential utility of combining camptothecin with celastrol or resveratrol in the treatment of colon cancer, including more aggressive forms of the disease. So far, no studies evaluating the effects of combinations of these compounds have been published in the available medical databases.

Phytocannabinoids, compounds found in Cannabis sativa L., are used in oncology and palliative care to reduce the adverse reactions of standard therapies. Cancer patients use formulations of Cannabis sativa L. to manage the anxiety, pain, and nausea associated with cancer treatment, and there is growing evidence that some of them may exhibit anticancer properties. In this study, we tested the anticancer potential of selected cannabinoids CBD (cannabidiol) and its quinone derivative CBD-HQ (cannabidiol hydroquinone), CBG (cannabigerol) and its acid derivative CBG-A (cannabigerolic acid), as well as a combination of CBD+CBG on the colon cancer cell line SW-620. The MTT assay was used to determine the cannabinoids’ ability to induce colon cancer cell death. All cannabinoids were cytotoxic at the lowest concentration (3 μg/mL). The half maximal inhibitory concentration (IC50) ranged from 3.90 to 8.24 μg/mL, depending on the substance. Cytotoxicity was confirmed in a 3D spheroidal cell culture with calcein and propidium iodide staining. The amount of intracellular reactive oxygen species (ROS) was examined using a DCF-DA assay. CBG showed the lowest antioxidant activity of all the cannabinoids tested. The level of intracellular ROS decreased only by 0.7–18%. However, CBG-A induced the strongest reduction in ROS level by 31–39%. Our results suggest that cannabinoids represent an interesting research direction with great implementation potential. These preliminary results represent the beginning of research into the potential of these substances for anticancer treatment and underscore the potential for further research.

Background: This study investigates the impact of environmental pollution on the quality and viability of dental stem cells (DSCs) from impacted third molars. By comparing DSCs from patients in industrial areas with high air pollution and those from non-industrial regions, the research assesses the adverse effects of heavy metals on stem cell proliferation. Methods: Impacted lower third molars were collected from 28 patients-10 from industrial and 18 from non-industrial areas. Patients were divided into two age groups: 18-27 years and 28-38 years old. Dental pulp was extracted under sterile conditions, and DSCs were isolated and cultured. Heavy metal concentrations in dental tissues were measured using atomic absorption/emission spectrometry. Results: The study found significantly higher concentrations of copper and lead in the dental tissues of patients in industrial areas. Cell viability was lower in samples from these areas, with a statistically significant difference in average doubling time and the number of cells obtained after the first passage. There was no significant impact of gender on heavy metal content, except for higher iron levels in men. Conclusions: Exposure to industrial pollutants negatively affects the viability and proliferation of DSCs, but there are no differences in differentiation in the osteogenic medium regarding cell mineralization. These studies highlight the importance of environmental factors for oral health, suggesting that residents of polluted areas may face greater difficulties in dental and regenerative treatments. Further research is needed to develop strategies to mitigate the effects and improve clinical outcomes for affected populations.

INTRODUCTION:Down syndrome (DS), a common genetic disorder, leads to various physical, cognitive, and developmental challenges. The supplementary copy of chromosome 21 introduces an abundance of genes, which potentially can influence metabolic irregularities. The aim of the study is to conduct a comprehensive comparative assessment of oxidative stress indicators (TAS, TOS, OSI), BMI, fasting glucose, and insulin levels, HOMA-IR among children and adolescents with DS in contrast to their non-DS siblings.MATERIAL AND METHODS:and the control group (CG) comprised 20 individuals, siblings of SG (mean age 15.92 years). Anthropometric measurements were conducted. TAS, TOS, fasting glucose, and insulin were assessed. BMI, BMI SDS, OSI and HOMA-IR were calculated.RESULTS:SG vs. CG: BMI - overweight (29,19% vs. 15%), obese (19,05% vs. 5%); TAS (1.92 mmol/l vs. 1.79 mmol/l (p = 0.0015)); TOS (51.52 mmol/l vs. 33.05 mmol/l (p = 0.014)); OSI (2475.02 vs. 1949,75 (p = 0.038)); no significant differences in fasting glucose, insulin and HOMA-IR. Statistically significant correlations in SG: TOS and BMI, BMI SDS, HOMA-IR; OSI and BMI, BMI SDS, HOMA-IR; HOMA-IR and BMI SDS; fasting insulin and BMI PC; in CG: TAS and BMI; fasting glucose and fasting insulin.CONCLUSIONS:The research results indicate differences in metabolic processes between the group of individuals with DS compared to the CG, despite shared environmental conditions. The presence of an additional copy of chromosome 21 may contribute to the occurrence of metabolic disorders. These findings emphasize the need for further research that will lead to a better understanding of these relationships and contribute to the development of effective therapeutic strategies.

Background:MicroRNAs are endogenous, small noncoding RNA molecules that play a pivotal role in the regulation of gene expression. MicroRNAs are involved in many biological processes such as proliferation, cell differentiation, neovascularization, and apoptosis. Studies on microRNA expression may contribute to a better understanding of the pathomechanism of chronic inflammatory demyelinating polyneuropathy (CIDP) and consequently enable the development of new therapeutic measures using antisense miRNAs (antagomirs). In this study, we evaluated the level of miR-31-5p in the serum of patients with CIDP and its correlation with the miR-31-5p level and clinical presentation and electrophysiological and biochemical parameters.Methods:The study group consisted of 48 patients, mean age 61.60 ± 11.76, who fulfilled the diagnostic criteria of a typical variant of CIDP. The expression of miR-31-5p in patient serum probes was investigated by droplet digital PCR. The results were correlated with neurophysiological findings and the patient's clinical and biochemical parameters.Results:The mean copy number of miRNA-31 in 100 μl serum was 1288.64 ± 2001.02 in the CIDP group of patients, while in the control group, it was 3743.09 ± 4026.90. There was a significant positive correlation (0.426) between IgIV treatment duration and miR-31-5p expression. Patients without IgIV treatment showed significantly lower levels of miR-31 compared to the treated group (259.44 ± 304.02 vs. 1559.48 ± 2168.45; p = 0.002). The group of patients with body weight > 80 kg showed statistically significantly lower levels of miRNA-31-5p than the patients with lower body weight (934.37 ± 1739.66 vs. 1784.62 ± 2271.62, respectively; p = 0.014). Similarly, the patients with elevated cerebrospinal fluid (CSF) protein levels had significantly higher miRNA-31-5p expression than those with normal protein levels (1393.93 ± 1932.27 vs. 987.38 ± 2364.10, respectively; p = 0.044).Conclusion:The results may support the hypothesis that miR-31-5p is strongly involved in the autoimmune process in CIDP. The positive correlation between higher miR-31-5p levels and duration of IVIg treatment may be an additional factor explaining the efficacy of prolonged IVIg therapy in CIDP.

In this study, the SiO2-CaO (SC) and SiO2-CaO-P2O5 (SCP) glass powders doped with 0.3 mol% of Tm3+ and 4 mol% of Yb3+ ions were prepared by the sol-gel method. The samples were immersed for four weeks in a simulated physiological environment (Dulbecco's phosphate-buffered saline, DPBS) to investigate the bioactivity of the glasses. Their structure, morphology, and spectroscopic properties were investigated in the function of immersion time. X-ray diffractograms and infrared spectra showed that after incubation in DPBS, the hy-droxyapatite starts to build up after 1-3 days. The energy dispersive X-ray spectroscopy analysis indicated the dynamics of ion exchange resulting from the biomineralization process in the glasses. Moreover, the upcon-version emission spectra of Tm3+ were measured for all samples under 980 nm excitation wavelength in reso-nance with the 2F7/2 & RARR; 2F5/2 absorption of Yb3+. It was observed that the upconversion luminescence continuously decreased and the decay times shorten slightly after the immersion in the buffer. In vitro cyto-toxicity assays revealed that the SC glass was biocompatible for all tested cell lines (human chondrocytes, os-teoblasts, and fibrosarcoma). However, the SCP powder showed an inhibitory effect on human chondrocyte and fibrosarcoma cells in small concentrations and fibrosarcoma cells in high concentrations.

Introduction Atherosclerosis, a precursor to cardiovascular disease (CVD), is deeply intertwined with lipid metabolism. The metabolic process in the Down syndrome (DS) population remain less explored. Aim of the study: This study examines the lipid profiles of DS in comparison to their siblings (CG), aiming to uncover potential atherosclerotic and CVD risks. Material and methods The study included 42 people with DS (mean age 14.17 years) and the CG – 20 individuals (mean age 15.92 years). Anthropometric measurements: BMI, BMI SDS, and TMI were calculated. Lipid profile (LP) and metabolomics were determined. Results LP: DS display significantly reduced HDL (DS vs. CG: 47±10 vs. 59 ±12 mg/dl; p = 0.0001) and elevated LDL (104 ±25 vs. 90 ±22 mg/dl; p = 0.0331). Triglycerides, APO A1, and APO B/APO A1 ratio corroborate with the elevated risk of CVD in DS. Despite no marked differences in: TCH and APO B, the DS group demonstrated a concerning BMI trend. Of 31 identified metabolites, 12 showed statistical significance (acetate, choline, creatinine, formate, glutamine, histidine, lysine, proline, pyroglutamate, threonine, tyrosine, and xanthine). However, only 8 metabolites passed the FDR validation (acetate, creatinine, formate, glutamine, lysine, proline, pyroglutamate, xanthine). Conclusions Down syndrome individuals show distinct cardiovascular risks, with decreased HDL and increased LDL levels. Combined with metabolomic disparities and higher BMI and TMI, this suggests an increased atherosclerosis risk compared to controls.

Colorectal cancers are one of the leading cancers worldwide and are known for their high potential for metastasis and resistance to therapy. The aim of this study was to investigate the effect of various combination therapies of irinotecan with melatonin, wogonin, and celastrol on drug-sensitive colon cancer cells (LOVO cell line) and doxorubicin-resistant colon cancer stem-like cells (LOVO/DX cell subline). Melatonin is a hormone synthesized in the pineal gland and is responsible for circadian rhythm. Wogonin and celastrol are natural compounds previously used in traditional Chinese medicine. Selected substances have immunomodulatory properties and anti-cancer potential. First, MTT and flow cytometric annexin-V apoptosis assays were performed to determine the cytotoxic effect and the induction of apoptosis. Then, the potential to inhibit cell migration was evaluated using a scratch test, and spheroid growth was measured. The results showed important cytotoxic effects of the drug combinations on both LOVO and LOVO/DX cells. All tested substances caused an increase in the percentage of apoptotic cells in the LOVO cell line and necrotic cells in the LOVO/DX cell subline. The strongest effect on the induction of cancer cell death was observed for the combination of irinotecan with celastrol (1.25 µM) or wogonin (50 µM) and for the combination of melatonin (2000 µM) with celastrol (1.25 µM) or wogonin (50 µM). Statistically significant improvements in the effect of combined therapy were found for the irinotecan (20 µM) and celastrol (1.25 µM) combination and irinotecan (20 µM) with wogonin (25 µM) in LOVO/DX cells. Minor additive effects of combined therapy were observed in LOVO cells. Inhibition of cell migration was seen in LOVO cells for all tested compounds, while only irinotecan (20 µM) and celastrol (1.25 µM) were able to inhibit LOVO/DX cell migration. Compared with single-drug therapy, a statistically significant inhibitory effect on cell migration was found for combinations of melatonin (2000 µM) with wogonin (25 µM) in LOVO/DX cells and irinotecan (5 µM) or melatonin (2000 µM) with wogonin (25 µM) in LOVO cells. Our research shows that adding melatonin, wogonin, or celastrol to standard irinotecan therapy may potentiate the anti-cancer effects of irinotecan alone in colon cancer treatment. Celastrol seems to have the greatest supporting therapy effect, especially for the treatment of aggressive types of colon cancer, by targeting cancer stem-like cells.

The goal of this study was to the assess anti-cancer and antioxidant properties of the Ganoderma lucidum fruiting body, and to identify bioactive compounds found in their extracts. Significant antiproliferative activity was observed against MCF-7, MCF-7/DX, LOVO, LOVO/DX, MDA-MB 231, SW 620, and NHDF cell lines. With IC50 values of 25.38 µg/mL and 47.90 µg/mL, respectively, the extract was most effective against MDA-MB 231 and SW 620 cell lines. The bioactive compounds were identified using an ACQUITY UPLC-PDA-MS system. The extracts contained 13 triterpenoids and 28 polyphenols from the flavonols, phenolic acids, flavones, flavan-3-ols, and stilbenes families. Ganoderic acid derivative was found to be the most abundant triterpenoid (162.4 mg/g DW), followed by ganoderic acid B (145.6 mg/g DW). Resveratrol was the most abundant phenolic in the extract (5155.7 mg/100 g DM). The findings could explain why G. lucidum extracts are used in folk medicine.

CD38 is a myeloid antigen present both on the cell membrane and in the intracellular compartment of the cell. Its occurrence is often enhanced in cancer cells, thus making it a potential target in anticancer therapy. Daratumumab and isatuximab already received FDA approval, and novel agents such as MOR202, TAK079 and TNB-738 undergo clinical trials. Also, novel therapeutics such as SAR442085 aim to outrank the older antibodies against CD38. Multiple myeloma and immunoglobulin light-chain amyloidosis may be effectively treated with anti-CD38 immunotherapy. Its role in other hematological malignancies is also important concerning both diagnostic process and potential treatment in the future. Aside from the hematological malignancies, CD38 remains a potential target in gastrointestinal, neurological and pulmonary system disorders. Due to the strong interaction of CD38 with TCR and CD16 on T cells, it may also serve as the biomarker in transplant rejection in renal transplant patients. Besides, CD38 finds its role outside oncology in systemic lupus erythematosus and collagen-induced arthritis. CD38 plays an important role in viral infections, including AIDS and COVID-19. Most of the undergoing clinical trials focus on the use of anti-CD38 antibodies in the therapy of multiple myeloma, CD19- B-cell malignancies, and NK cell lymphomas. This review focuses on targeting CD38 in cancer and non-cancerous diseases using antibodies, cell-based therapies and CD38 inhibitors. We also provide a summary of current clinical trials targeting CD38.

Down Syndrome (DS) is a chromosomal abnormality associated with a spectrum of cognitive and physical disabilities. Children with DS are exposed to both lower and excess body weight and follow distinct growth-curve patterns that deviate significantly from those of children without chromosomal defects. Anthropometric parameters are assessed in the pediatric population with the use of growth charts. The study is based on data from 411 children and adults with DS from Poland. Detailed information concerning children and online survey results were also analyzed. Centiles and standard deviation scores (SDS) of obtained anthropometric parameters were aligned with the data using the LMS method. The study aims to identify which type of growth chart (standard vs specialized) is a leading tool for earlier detection of developmental disorders in DS. The results obtained in the two types of growth charts differed. The advantage of the specialized growth charts over the standard ones cannot be unequivocally determined. Only the combination of both tools allows to detect the development disorders early in the broadest possible way.

People with Down syndrome (PWDS) are more at risk for developing obesity, oxidative stress disorders, metabolic disorders, and lipid and carbohydrate profile disorders than the general population. The presence of an additional copy of genes on chromosome 21 (i.e., the superoxide dismutase 1 gene (SOD1) and gene coding for the cystathionine β-synthase (CBS) enzyme) raises the risk for cardiovascular disease (CVD). As a result of disorders in metabolic processes and biochemical pathways, theoretically protective factors (low homocysteine level, high SOD1 level) do not fulfil their original functions. Overexpression of the CBS gene leads to the accumulation of homocysteine—a CVD risk factor. An excessive amount of protective SOD1, in the case of a lack of compensatory increase in the activity of catalase and peroxidase, leads to intensifying free radical processes. The occurrence of metabolic disorders and the amplified effect of oxidative stress carries higher risk of exposure of people with DS to CVD. At present, classic predispositions are known, but it is necessary to identify early risk factors in order to be able to employ CVD and obesity prophylaxis. Detailed determination of the metabolic and lipid profile may provide insight into the molecular mechanisms underlying CVD.