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Objectives Experimental studies indicate a role for galectin-1 and galectin-3 in metabolic disease, but clinical evidence from larger populations is limited. Methods We measured circulating levels of galectin-1 and galectin-3 in the Prospective investigation of Obesity, Energy and Metabolism (POEM) study, participants ( n  = 502, all aged 50 years) and characterized the individual association profiles with metabolic markers, including clinical measures, metabolomics, adipose tissue distribution (Imiomics) and proteomics. Results Galectin-1 and galectin-3 were associated with fatty acids, lipoproteins and triglycerides including lipid measurements in the metabolomics analysis adjusted for body mass index (BMI). Galectin-1 was associated with several measurements of adiposity, insulin secretion and insulin sensitivity, while galectin-3 was associated with triglyceride-glucose index (TyG) and fasting insulin levels. Both galectins were associated with inflammatory pathways and fatty acid binding protein (FABP)4 and -5-regulated triglyceride metabolic pathways. Galectin-1 was also associated with several proteins related to adipose tissue differentiation. Conclusions The association profiles for galectin-1 and galectin-3 indicate overlapping metabolic effects in humans, while the distinctly different associations seen with fat mass, fat distribution, and adipose tissue differentiation markers may suggest a functional role of galectin-1 in obesity.

The inflammatory bowel diseases (IBD), which include mainly Crohn's disease (CD) and ulcerative colitis (UC), are common chronic inflammatory conditions of the digestive system. The diagnosis of IBD relies on the use of a combination of factors including symptoms, endoscopy and levels of serum proteins such as C-reactive protein (CRP) or faecal calprotectin. Currently there is no single reliable biomarker to determine IBD. Galectins are a family of galactoside-binding proteins that are commonly altered in the circulation of disease conditions such as cancer and inflammation. This study investigated serum galectin levels as possible biomarkers in determining IBD and IBD disease activity. Levels of galectins-1, -2, -3, -4, -7 and -8 were analysed in 208 samples from ambulant IBD patients (97 CD, 71 UC) patients and 40 from healthy people. Disease activity was assessed using Harvey-Bradshaw Index for CD and simple clinical colitis activity index for UC. The relationship of each galectin in determining IBD and IBD disease activity were analysed and compared with current IBD biomarker CRP. It was found that serum level of galectin-1 and -3, but not galectins-2, -4, -7 and -8, were significantly higher in IBD patients than in healthy people. At cut-off of 4.1ng/ml, galectin-1 differentiated IBD from healthy controls with 71% sensitivity and 87% specificity. At cut-off of 38.5ng/ml, galectin-3 separated IBD from healthy controls with 53% sensitivity and 87% specificity. None of the galectins however were able to distinguish active disease from remission in UC or CD. Thus, levels of galectins-1 and -3 are significantly elevated in both UC and CD patients compared to healthy people. Although the increased galectin levels are not able to separate active and inactive UC and CD, they may have the potential to be developed as useful biomarkers for IBD diagnosis either alone or in combination with other biomarkers.

The aim of this study was to assess the expression patterns of serum galectin-1 (Gal-1), galectin-3 (Gal-3), galectin-9 (Gal-9), and galectin-3 binding protein (Gal-3BP) and their associations with stroke outcome in large artery atherosclerotic (LAA) stroke. The serum levels of Gal-1, Gal-3, Gal-9, and Gal-3BP were measured by ELISA in 130 patients with LAA stroke and 130 age- and sex-matched controls. Serum samples were collected from the patients on day 1, day 6, and in the 4th week after ischaemic stroke (IS). An unfavourable outcome was defined as a modified Rankin Scale score of >2 on day 90 after IS. Our results indicated that the Gal-3 and Gal-9 levels were higher in patients with LAA stroke than in controls. A higher Gal-3 level was independently associated with an unfavourable outcome both on day 1 and day 6 after IS. In addition, Gal-9 and Gal-1 levels were upregulated on day 6 and in the 4th week after IS, respectively. For Gal-3BP, no difference was detected between patients and controls and no predictive value was found in patients. In conclusion, these findings suggest that the serum levels of Gal-1, Gal-3, and Gal-9 may be associated with LAA stroke.

Galectins are innate immune system regulators associated with disease progression in cancer. This paper aims to investigate the correlation between mutated cancer-critical genes and galectin levels in breast cancer patients to determine whether galectins and genetic profiles can be used as biomarkers for disease and potential therapy targets. Prisma Health Cancer Institute’s Biorepository provided seventy-one breast cancer samples, including all four stages spanning the major molecular subtypes and histologies. Hotspot mutation statuses of cancer-critical genes were determined using multiplex PCR in tumor samples from the same patients by Precision Genetics and the University of South Carolina Functional Genomics Core Facility. The galectin-1, -3, and -9 levels in patients’ sera were analyzed using Enzyme-linked Immunosorbent Assay (ELISA). An analysis was performed using JMP software to compare mean and median serum galectin levels between samples with and without specific cancer-critical genes, including pooled t-test, Wilcoxon Rank Sum Test, ANOVA, and Steel Dwass Test (α=0.05). Our analysis indicates that KIT mutations correlate with elevated serum levels of galectin-9 in patients with breast cancer. In patients with Luminal A subtype, FLT3 mutation correlates with lower serum galectin-1 and -9 levels and TP53 mutations correlate with higher serum galectin-3 levels. Patients with invasive ductal carcinoma had significantly higher serum galectin-3 levels than patients with ductal carcinoma in situ. Patients with both TP53 and PIK3CA mutations exhibit elevated serum galectin-3 levels, while patients with one or neither mutation show no significant difference in serum galectin-3 levels. In addition, metastatic breast cancer samples were more likely to have a KIT or PIK3CA mutation compared to primary breast cancer samples. The relationship between genetic mutations and galectin levels has the potential to identify appropriate candidates for combined therapy, targeting genetic mutations and galectins. Further understanding of the effect of genetic mutations and galectin levels on cancer progression and metastasis could aid in the search for biomarkers for breast cancer diagnosis, disease progression, and prognosis.

Background: Circulating concentrations of the cytokines interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and chemokines monocyte chemotatic protein 1 (MCP-1)/CCL2 and growth-regulator oncogene α (GRO α )/chemokine C-X-C motif ligand 1 are commonly increased in cancer patients and they are increasingly recognised as important promoters, via divergent mechanisms, of cancer progression and metastasis. Methods: The effect of galectins-2, -4 and -8, whose circulating levels are highly increased in cancer patients, on endothelial secretion of cytokines was assessed in vitro by cytokine array and in mice. The relationship between serum levels of galectins and cytokines was analysed in colon and breast cancer patients. Results: Galectins-2, -4 and -8 at pathological concentrations induce secretion of G-CSF, IL-6, MCP-1 and GRO α from the blood vascular endothelial cells in vitro and in mice. Multiple regression analysis indicates that increased circulation of these galectins accounts for 41∼83% of the variance of these cytokines in the sera of colon and breast cancer patients. The galectin-induced secretion of these cytokines/chemokines is shown to enhance the expression of endothelial cell surface adhesion molecules, causing increased cancer-endothelial adhesion and increased endothelial tubule formation. Conclusion: The increased circulation of galectins -2, -4 and -8 in cancer patients contributes substantially to the increased circulation of G-CSF, IL-6 and MCP-1 by interaction with the blood vascular endothelium. These cytokines and chemokines in turn enhance endothelial cell activities in angiogenesis and metastasis.

Galectin-1 and -9 (Gal1/9) are essential mediators of immune-inflammatory responses, which makes these proteins potential biomarkers for immune-mediated diseases (IMIDs), such as rheumatoid arthritis (RA), psoriasis (PS), psoriatic arthritis (PsA), inflammatory bowel disease, and systemic lupus erythematosus (SLE). Our aim was to evaluate plasma Gal1/9 differences between IMID patients and healthy donors (HD). We analyzed 980 plasma samples divided into two analytical cohorts (600 discovery group and 380 validation group). Generalized linear models estimated Gal1/9 levels, adjusting for sex, age, storage time, and plate variability. In the overall IMID group, plasma Gal1 levels were comparable to those of HD, while Gal9 levels were significantly elevated. Levels varied across individual diseases: SLE patients consistently showed the highest Gal1/9 levels compared to both HD and other IMIDs, and RA patients had elevated Gal9 levels versus HD. Both Gal1 and Gal9 plasma levels correlated positively with higher disease activity, and Gal1 was higher in patients with longer disease duration. After adjustment for these confounders, SLE and RA patients maintained the highest Gal9 levels compared to HD. Our study demonstrates that Gal1 and Gal9 are differentially expressed across IMIDs, with particularly elevated levels in SLE, and both galectins are associated with disease activity.

Psoriasis is a complex inflammatory disease related to cardiometabolic disorders (CMDs). Galectin-4 (gal-4) is involved in biological processes such as lipid raft stabilization, intestinal inflammation and tumorigenesis. Charcot-Leyden crystals (CLCs), inter alia, Charcot-Leyden crystal/galectin-10 (CLC/gal-10), are involved in eosinophil-derived diseases. To date, neither of these galectins has been investigated in the context of psoriasis. The study aimed to evaluate serum galectin-4 and -10 levels in psoriatic patients and explore potential relationships with disease activity, metabolic or inflammatory indices. Blood samples were collected from 60 patients with plaque-type psoriasis and 30 healthy volunteers and evaluated using an Enzyme-Linked Immunosorbent Assay (ELISA). Morphological and biochemical indices were measured using routine laboratory techniques. Plasma gal-4 and gal-10 concentrations were significantly higher in patients with psoriasis than in the control group (p < 0.05). Galectins did not correlate with the Psoriasis Area Severity Index (PASI) nor age (p > 0.5); however, gal-4 showed a significant positive correlation with Body Mass Index (BMI), psoriasis duration (p = 0.03), and transaminase activity. Both proteins were the highest in obese psoriatics (p < 0.05). The results indicate that galectin-4 and galectin-10 may be involved in the pathophysiological mechanisms underlying CMDs in psoriatics. These galectins represent promising candidates for biomarkers of metabolically driven inflammation, with galectin-4, in particular, emerging as a potential indicator of hepatic dysfunction in psoriatic patients.

Endometriosis, a benign, chronic gynecological disorder characterized by the presence of endometrial-like tissue outside the uterine cavity, affects 15% of women of reproductive age. Galectins, a family of beta-galactoside-binding proteins, regulate inflammation and autoimmunity and are widely expressed in reproductive tissues. This study aimed to assess Galectin-3 (Gal-3) levels in the serum of patients with endometriosis compared to asymptomatic controls and investigate serum Gal-3 level changes over a one-year follow-up period of patients with endometriosis. To determine the levels of soluble Gal-3 in the serum of women with endometriosis or gynecological tumors as well as healthy controls, a human Gal-3-specific ELISA was used. Our findings revealed significantly elevated serum Gal-3 levels in patients with endometriosis compared with healthy controls. Furthermore, Gal-3 concentrations were markedly higher in patients with malignant gynecological transformation of the endometrium than in patients with or without endometriosis. During the one-year follow-up, patients with endometriosis exhibited a progressive increase in serum Gal-3 levels. These findings highlight the potential of Gal-3 as a biomarker for endometriosis and related gynecological conditions. However, further prospective studies with larger, more representative patient cohorts are needed to validate its clinical value.

Background Parkinson's disease (PD) is a prevalent neurodegenerative disorder with poor prognosis. Observational studies have demonstrated a significant correlation between serum galectin‐3 and PD, suggesting a potential role of galectin‐3 as a biomarker for PD. However, it is still unclear whether galectin‐3 contributes to the risk of the disease. Methods A two‐sample Mendelian randomization (MR) approach was used in this study. Genetic instruments for serum galectin‐3 level were selected from a genome‐wide association study (GWAS), including 30,931 European individuals. Summary‐level statistics for PD were derived from another published GWAS, including 33,674 cases and 449,056 controls. Primary analysis was conducted using the inverse‐variance weighting (IVW) method. Weighted median, MR‐Egger, simple mode, weighted mode, and MR‐pleiotropy residual sum and outlier (MR‐PRESSO) methods were used as complementary analyses. To detect heterogeneity, Cochran's Q statistic and leave‐one‐out analysis were used. For testing potential horizontal pleiotropy, the MR‐Egger intercept test and MR‐PRESSO global test were conducted. Results MR analysis using IVW model (OR 1.112, 95% CI 1.025–1.206, p = 0.010), weighted median (OR 1.135, 95% CI 1.037–1.242, p = 0.006), weighted mode (OR 1.142, 95% CI 1.038–1.257, p = 0.030), and MR‐PRESSO (OR 1.112, 95% CI 1.046–1.182, p = 0.012) presented a consistent result, indicating that increased serum galectin‐3 was associated with a higher risk of PD. No heterogeneity or horizontal pleiotropy was detected in the analyses. Conclusions The study shows a suggestive association between galectin‐3 and PD. Increasing serum galectin‐3 was associated with an increase in PD risk. Galectin‐3 may play an important role in the causal pathway to PD. A suggestive association between genetic susceptibility to serum galectin‐3 and risk of Parkinson's disease (PD) was demonstrated. Galectin‐3 may play an important role in the causal pathway to PD.

Galectin-3 and Suppression of tumorigenicity-2 (ST2) are known markers of cardiac fibrosis. We investigated the prognostic value of fibrotic markers for the development of diastolic dysfunction and long-term outcome in patients suffering an ST-elevated myocardial infarction (STEMI). We analyzed 236 patients from the GIPS-III cohort with available echocardiographic studies and plasma measurements at hospitalization and after 4 months follow-up. Adjusted logistic mixed effects modelling revealed no association between the occurrence of diastolic dysfunction over time with abnormal plasma levels of galectin-3 and ST2. We observed no differences regarding survival outcome at follow-up of 5 years between patients with normal versus abnormal values in both galectin-3 ( P  = 0.75), and ST2 ( P  = 0.85). In conclusion, galectin-3 and sST2 were not associated with the development of diastolic dysfunction in non-diabetic patients that presented with a STEMI.