Chronic inflammation and platelet hyperactivity are central contributors to the pathogenesis of cardiovascular diseases (CVD), including atherosclerosis and thrombosis. Sideritis scardica (Greek mountain tea), a medicinal herb endemic to the Balkans, is rich in polyphenols, flavonoids, carotenoids, and polar lipids—compounds known for their anti-inflammatory and vascular-protective properties.

This study investigated the potential of S. scardica extracts to modulate key molecular processes associated with cardiovascular inflammation and thrombotic risk. Phytochemical profiling via liquid chromatography–mass spectrometry (LC-MS) and Fourier transform infrared (FTIR) spectroscopy revealed a high content of bioactive secondary metabolites. Antioxidant activity was confirmed through DPPH, FRAP, and ABTS assays, indicating strong free radical scavenging capacity. Crucially, anti-inflammatory and antithrombotic activities were evaluated using ex vivo human platelet aggregation assays. The extracts significantly inhibited platelet-activating factor (PAF) while mildly inhibited ADP-induced platelet aggregation —two major pathways implicated in vascular inflammation and thrombus formation.

These findings suggest that S. scardica extracts may offer a novel, natural therapeutic approach for mitigating inflammatory and thrombotic mechanisms in CVD. Given their favorable safety profile and bioactivity, these phytochemicals warrant further exploration in preclinical and clinical models as adjuncts in cardiovascular disease prevention and management.

Background: Despite the increasing attention that sarcopenia has received in the field of oncology, particularly in relation to treatment tolerance and functional decline, most existing reviews have either focused on general cancer populations or included mixed age groups without specifically addressing older adults. Furthermore, considerable heterogeneity exists across studies regarding the diagnostic methods for sarcopenia, cancer types, and reported outcomes. To date, no systematic review has exclusively examined the association between sarcopenia and mortality in older adults with cancer using validated sarcopenia criteria. Given that individuals aged ≥65 represent the majority of cancer patients and are more vulnerable to adverse outcomes, there is a clear need to synthesize evidence specifically for this population. This systematic review aimed to synthesize current evidence of the association between sarcopenia and mortality in elderly cancer patients.

Methods:
We systematically searched PubMed, Web of Science, and Scopus up to October 29, 2024. The inclusion criteria encompassed observational studies reporting mortality outcomes in adults with cancer, with a mean age above 65 years and sarcopenia assessed using validated tools. Reviews, case reports, and studies lacking sufficient methodological quality were excluded. Two reviewers independently screened records and assessed methodological quality using the Joanna Briggs Institute checklist.

Results:
Nineteen studies comprising 6,555 participants were included. Most studies used CT at the L3 level to assess muscle mass, with sarcopenia prevalence ranging from 15.6% to 65.1%. Across studies, sarcopenia was consistently associated with increased overall or cancer-specific mortality. Reported hazard ratios ranged from 1.51 to 4.5, with the highest risk observed in patients with head and neck cancer. Quality assessment rated 15 studies as high-quality and 4 as moderate-quality.

Limitations:
The limitations of this review included heterogeneity in cancer types, diagnostic criteria, and follow-up periods, which may affect comparability across studies.

Introduction: The diagnosis of secondary bacterial meningitis in intensive care units and surgical departments is usually complicated by frequent false-negative cerebrospinal fluid (CSF) culture results because of previous antibacterial therapy or false-positive CSF culture results because of sample contamination. Some nonspecific clinical and laboratory criteria of CSF content can be used, but they do not provide 100% sensitivity and selectivity. The search for new diagnostic approaches is a relevant direction.

Objectives: The aim of this study was to construct various multivariate models based on biomarkers and metabolites in the cerebrospinal fluid for the diagnosis of secondary bacterial meningitis in patients with acute or chronical critical illness.

Methods: Patients with acute (n = 17, CSF samples = 19) or chronical critical illness (n = 35, CSF samples = 77) were divided into CSF sample groups without (n = 63, group I) and with secondary bacterial meningitis (n=33, group II). CSF samples were analyzed by UPLC-MS/MS to determine aromatic metabolites, and by electrochemiluminescence to determine interleukin-6 (IL-6), NSE, and S100 protein.

Results: Median values of CSF parameters (leukocytes, relative content of neutrophils, protein, IL-6, S100, 4-hydroxyphenyllactic, phenyllactic, indole-3-lactic acids) were statistically higher in group II compared to group I (p-value < 0.001), with CSF glucose higher in group I compared to group II (p-value < 0.001).

ROC-analysis of univariate models based on these CSF parameters did not reveal any model with 100% sensitivity and selectivity, while ROC-analysis of various multivariate models based on CSF biomarkers and metabolites demonstrated excellent prognostic ability for CSF sample stratification into two groups: the best model was constructed using Catboost [https://doi.org/10.48550/arXiv.1706.09516] with AUC-ROC=1.00 with 100% sensitivity and selectivity.

Conclusion: Multivariate models based on various CSF biomarkers and metabolites demonstrated better characteristics compared to univariate prognostic models for CSF sample stratification into groups with or without secondary bacterial meningitis.

Background
Glucocorticoids (GCs) are widely used in the treatment of hematological malignancies as well as in the systemic therapy of autoimmune and inflammatory diseases. The therapeutic effects of GCs are realized via glucocorticoid receptor (GR) activation by DNA-independent transrepression (TR), while their side effects are associated with transactivation (TA). Side effects could be reduced by developing selective glucocorticoid receptor agonists (SEGRAs), acting via the activation of TR. Recently, we synthesized a novel compound, 2-(hexylamino)-1-(4-nitrophenyl)ethanol (13S-G2), which was a derivative of synephrine, and its biological activity was studied in leukemia and lymphoma cells in vitro.
Methodology
The effect of 13S-G2 on the viability of chronic myeloid leukemia (CML) K562 cells and B-cell lymphoma Granta-519 cells was evaluated using the MTT assay. TA induction was assessed by quantitative PCR (qPCR) of GR-dependent genes (GILZ, FKBP51, REDD1/DDIT4). TR induction was studied using a luciferase reporter assay (with NF-κB reporter construct) and qPCR analysis of key TR marker genes (COX2, IL-1α, IL-6, CCNE1). The affinity of 13S-G2 was assessed in silico by molecular docking (Molegro Virtual Docker), and in vitro via a radioligand binding assay.
Results
Compound 13S-G2 showed cytotoxicity with IC50 values of 184±95 μM in K562 and 26.8±1.2 μM in Granta-519. In silico, we demonstrated that 13S-G2 occupied a sterically advantageous location at the GR binding site formed by the amino acid residues Arg611, Asn564, and Gln642. In a radioligand binding assay (IC50), the radiolabeled Dexamethasone displacement in K562 cells by 13S-G2 was 0.69 μM. The inhibitory effect of 13S-G2 on luciferase activity was 55% in K562 and 15% in Granta-519. Compound 13S-G2 suppressed the expression of TR marker genes, in most cases by 1.5-2.0 fold. The absence of TA induction was proved for 13S-G2.
Conclusions
The novel SEGRA 13S-G2 demonstrates promising transrepression-driven anti-cancer activity in hematological malignancies with the absence of TA induction and low potential for side effect development.

Introduction: Dementia is a neurodegenerative disorder characterized by progressive cognitive decline and increasing care needs. Occupational Therapy (OT) is recommended by the Italian guidelines for Mild Cognitive Impairment and dementia as an effective intervention to support functional abilities and to manage non-cognitive symptoms through structured, person-centered approaches. In this context, the Cognitive Disorders and Dementia Center of Modena (Italy) provides home-based OT aiming to enhance engagement in meaningful daily activities and actively involve caregivers in the therapeutic process. While this intervention is increasingly recognized as beneficial in dementia care, its specific impact on caregivers’ experiences within home settings remains unclear.

Methods: This qualitative, exploratory study involved semi-structured interviews with five caregivers of individuals with dementia who had completed a successful cycle of home-based OT. The interview guide was developed using a structured qualitative framework. Collected data were analyzed thematically and organized into key categories to identify common and unique experiences among caregivers, with particular attention to perceived success factors.

Results: The caregivers reported a high perceived value of home-based OT. Key success factors included the acquisition of practical strategies for managing daily routines, a holistic and individualized approach to care, improved awareness of and access to local support services, and a diminished perception of disease-related burden. These aspects contributed to strengthening the caregivers’ abilities to support autonomy and communication in their relatives with dementia. Additionally, the caregivers expressed a greater sense of involvement, reassurance, and emotional well-being. Some participants also highlighted the need for continued support and follow-up, especially in the face of disease progression.

Conclusions: These results align with the current literature and suggest that the identified success factors can help shape more effective home-based OT programs. Further research is needed to expand these findings and explore the long-term outcomes across different settings and populations.

The International Classification of Diseases first recorded obesity in 1948. The misconception that obesity is merely a lifestyle decision that can be reversible through the exercise of willpower has persisted in public discourse and in the medical community. However, obesity is recognized by the World Health Organization (WHO) as a chronic disease characterized by “an abnormal or excessive accumulation of fat that is a health hazard.” In the context of patient care, there is an important and simple logical inconsistency: the therapeutic field is still based on the Body Mass Index (BMI). This indicator only measures weight and height, without considering body fat, muscle mass, or metabolic status, leading to imprecise diagnoses. The consideration of obesity as a disease based on BMI alone impedes progress in social recognition and understanding of the disease, leading to unintended iatrogenesis and hindering research. Hence, it is indispensable to evaluate body composition and metabolic status, as well as to differentiate between clinical and preclinical obesity, in order to target and treat more equitably. The purpose of this systematic review is to address the latest progress in the ambiguity surrounding the diagnosis of obesity based on BMI, and how it impacts individuals.

Small Intestinal Bacterial Overgrowth (SIBO) is gaining increasing recognition in gastroenterology, yet its diagnosis and management remain inconsistent across clinical settings. Despite its high prevalence in symptomatic patients, standard diagnostic thresholds (≥10³ vs. ≥10⁵ CFU/mL) and breath testing remain controversial.

This review aims to integrate current clinical and microbiome research to propose a novel microbiota-based framework for understanding and managing SIBO. Specifically, we highlight the Proteobacteria/Firmicutes ratio, particularly values >0.39, as a promising biomarker correlated with symptoms such as bloating and fecal urgency. This approach provides a unifying lens through which diagnostic variability may be reduced and microbial imbalance more precisely addressed. Additionally, we examine emerging evidence on the role of dietary patterns in reshaping the gut microbiota, proposing targeted nutritional interventions to reduce recurrence rates.

While this review draws from existing literature, it offers a novel synthesis that links microbial composition with diagnostic and therapeutic strategies. The recent introduction of ICD-10 code K82.11 further emphasizes the need for standardized frameworks in epidemiological tracking. Our findings support a shift from symptom-driven to microbiota-informed care models, with the potential to enhance clinical decision-making and long-term patient outcomes.

BACKGROUND: Rosmarinic acid (RA) is a polyphenol found in various plants, especially in the Lamiaceae family, such as rosemary, sage, lemon balm, and basil, and especially in peppermint. Mitochondria have cell-type-specific phenotypes, perform dozens of interconnected functions, and undergo dynamic and often reversible physiological recalibrations. One of the main current goals is to enhance mitochondrial function through various strategies, including nutritional ones.
METHODOLOGY: Mouse muscle cells (C2C12) were differentiated and treated with RA. Mitochondrial genes were measured by RT-qPCR, and proteins by Western blotting. Mitochondrial respiration was measured using Seahorse XF and Oroboros O2k. Mitochondrial biogenesis was analyzed by citrate synthase activity, and finally, the antioxidant role was observed by hydrogen peroxide production, catalase activity, and malondialdehyde (MDA) levels using HPLC.
RESULTS: Mitochondrial genes were overexpressed compared to the control group using AR. Both basal and maximal respiration, including ATP production, were higher with AR exposure. There was increased activity of the citrate synthase enzyme and proteins such as PGC-1α and TFAM related to mitochondrial biogenesis. There was increased catalase activity, lower hydrogen peroxide levels, and lower MDA levels.
CONCLUSIONS: AR at nutritionally relevant doses (100 nM) increases mitochondrial function, both in respiration and mitochondrial biogenesis, and acts as an antioxidant in differentiated mouse muscle cells.

INTRODUCTIONS

Prebiotic supplementation represents a promising method to influence gut microbial composition and achieve better metabolic results since it supports metabolic health through gut–microbiota functions. Some researches have evaluated the changes that prebiotic intake makes on gut microbiota diversity, metabolic health characteristics, and short-chain fatty acid (SCFA) formation in normal-functioning adults.

METHODS

We performed a placebo-controlled double-blind randomized study involving 120 participants, 20–45 years old, but only 50 completed it. The participants received either 15 g/day of inulin and fructo-oligosaccharides in the prebiotic group or a placebo for twelve weeks. We measured gut microbiota diversity through the Shannon and Simpson indices and detected metabolic markers, including fasting glucose, insulin, HOMA-IR, lipid profiles, inflammatory markers, and SCFA levels, at baseline and weeks 6 and 12.

RESULTS

The participants in the prebiotic group showed significant improvements in gut microbiota diversity (Shannon index: 5.12 ± 0.89 to 5.78 ± 0.95, p < 0.001), alongside increased SCFAs (acetate: 65.12 ± 8.45 to 70.23 ± 9.45 µg/mL, p < 0.001) and fasting glucose (89.5 ± 8.2 to 87.6 ± 7.5 mg/dL, p = 0.045), while insulin (8.12 ± 3.45 to 7.65 ± 3.01 µIU/mL, p = 0.023), HOMA-IR scores (1.82 ± 0.91 to 1.72 ± 0.83, p = 0.031), and CRP (3.45 ± 1.23 to 3.12 ± 1.08 mg/L, p = 0.015) reached lower significant levels. The analysis showed a direct relationship between reduced microbial diversity and higher metabolic markers (Shannon diversity index showed a negative correlation with fasting glucose at r = -0.32 and p = 0.002).

CONCLUSIONS

These preliminary data from our research show that prebiotics can be a nutritional approach to more effective metabolism and make up part of personalized strategies to prevent and cure several diseases (e.g., obesity, diabetes, cardiovascular conditions) linked to gut dysbiosis and metabolic imbalance.

Due to the lack of data on antimicrobial resistance patterns in Russian Helicobacter pylori clinical isolates, we aimed, for the first time, to comprehensively investigate resistance determinants in H. pylori isolates to metronidazole (MTZ) and levofloxacin (LVX) and to evaluate the correlation between genotypic and phenotypic antimicrobial susceptibility testing (AST). A retrospective analysis of 43 H. pylori clinical isolates from adult patients (2014-2022) was performed. Phenotypic AST was performed via the disk diffusion method. Total DNA was extracted using the QIAamp DNA Mini Kit. WGS of 43 H. pylori isolates was performed on the DNBSEQ-G50 sequencer. The phenotypic AST results revealed that 31 isolates were susceptible to LVX (LVX-S) and 11 were susceptible to MTZ (MTZ-S), while 12 were resistant to LVX (LVX-R) and 32 were resistant to MTZ (MTZ-R). To identify associations between phenotypic and genotypic resistance, a comprehensive analysis of nucleotide substitutions was performed in the following genes: gyrA, gyrB, rdxA, frxA, fdxB, and fur. Of all mutations identified in gyrA and gyrB, only D91G/N/Y in gyrA was associated with phenotypic resistance to LVX, being present in 4 of 12 (33.3%) LVX-R isolates (p<0.05). The combined mutation D91G/N/Y+N87K+A88P in gyrA was detected in 7 of 12 (58.3%) LVX-R isolates (p<0.001). No mutations in rdxA were associated with resistance to MTZ; however, 7 of 32 (21.9%) MTZ-R isolates had point mutations leading to a frameshift or premature termination of protein synthesis. Similarly, no mutations in frxA, fur, or fdxB were associated with resistance to MTZ. Based on the first results of whole-genome sequencing of Russian H. pylori clinical isolates, mutation D91G/N/Y was associated with phenotypic levofloxacin resistance. Despite the low frequency of point mutations N87K and A88P in gyrA gene, detection of the combined mutations D91G/N/Y+N87K+A88P may serve as a predictor of phenotypic resistance to levofloxacin in clinical isolates.