SEARCH · Search PubMed

Results for “Biologic pathways”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources

PubMed2005

Iron and the athlete.

Iron is an important mineral necessary for many biologic pathways. Different levels of deficiency can occur in the athlete, resulting in symptoms that range from none to severe fatigue. Iron deficiency without anemia may adversely affect athletic performance. Causes of iron deficiency include poor intake, menstrual losses, gastrointestinal and genitourinary losses due to exercise-induced ischemia or organ movement, foot strike hemolysis, thermohemolysis, and sweat losses. A higher incidence of deficiency occurs in female athletes compared with males.

Adolescent↗

PubMed2004

Does ambient temperature affect foodborne disease?

BACKGROUND: Foodborne illness is a significant public health issue in most countries, including Australia. We examined the association between temperature and salmonellosis notifications, and compared these associations for 5 Australian cities. METHODS: Log-linear models describing monthly salmonellosis notifications in terms of calendar time and monthly average temperatures were fitted over the period 1991 to 2001 for each city. We used a negative binomial chance model to accommodate overdispersion in the counts. RESULTS: The long-term trend showed an increase in salmonellosis notifications in each of the 5 cities. There was a positive association between monthly salmonellosis notifications and mean monthly temperature of the previous month in every city. Seasonal patterns in salmonellosis notifications were fully explained by changes in temperature. DISCUSSION: The strength of the association, the consistency across 5 cities, and a plausible biologic pathway suggest that higher ambient temperatures are a cause of higher salmonellosis notifications. The lag of 1 month suggests that temperature might be more influential earlier in the production process rather than at the food preparation stage. This knowledge can help to guide policy on food preparation and distribution. It also suggests a basis for an early warning system for increased risk from salmonellosis, and raises yet another possible health problem with global warming.

Australia↗

PubMed2006

A study of TH01 and IGF2-INS-TH haplotypes in relation to smoking initiation in three independent surveys.

OBJECTIVES: Recent studies suggest an association between a microsatellite locus (TH01) located in intron 1 of the tyrosine hydroxylase gene (TH) and nicotine dependence. We aimed here to study whether both TH01 and haplotypes of the wider IGF2-INS-TH region influence initiation of regular smoking in current smokers. METHODS: A total of 3637 individuals from three independent studies (two of adults and one of adolescents) were analysed in relation to the age of first regular smoking (AFRS). Haplotypes and genotypes were obtained for the polymorphisms TH01, IGF2 ApaI, INS HphI and DRD4 VNTR (48 bp)n. Association between IGF2-INS-TH haplotypes and AFRS was tested by a regression model. A genotype-based genetic model assuming additivity was followed in order to estimate the effect of individual loci. RESULTS: Overall, no significant associations were found after correcting for multiple tests. However, an IGF2-INS-TH haplotype (*5) was found to be nominally associated with AFRS at younger ages in adult smokers. Analyses of individual loci points to TH01 as a possible candidate influencing initiation of regular smoking. An AFRS-lowering trend nominally associated with allele 9 in a dosage-dependent manner was identified in both adult cohorts. TH01 did not show association or trend with age of initiation (first puff) either in adolescents or in the adolescents smoking regularly at age 18. CONCLUSION: This study adds to the genetic evaluation of the associations of TH01 with smoking predisposition. Differences between historical and prospective surveys, different biological pathways and possible functional roles of this microsatellite in smoking initiation are discussed.

Genetic Predisposition to Disease↗

PubMed2005

Genetic influences on smoking: a brief review.

Smoking is a complex behavior influenced by environ-mental and genetic factors. A number of twin studies demonstrate genetic influences on multiple aspects of smoking including initiation, dependence, continuation, amount consumed, and cessation. It is likely that this genetic risk involves a complex interaction between multiple genes in different biologic pathways. These may include genes involved in the general aspect of dependence (eg, genes within the dopaminergic system) and those more specific to nicotine dependence (eg, genes encoding nicotinic acetylcholine receptors and nicotine-metabolizing enzymes). Genome-wide linkage analyses and gene association studies provide approaches for identifying these genes. This review provides a brief highlight of data from some of the candidate gene association studies and discusses some of the discrepancies found in the literature. In addition, the authors have reviewed some recent studies examining how genetic variations in drug-metabolizing enzymes and drug targets can influence the response to treatment with drugs such as bupropion and nicotine.These latter studies provide the potential for maximizing treatment efficacy by individualizing the type, dosage, and duration of the treatment based on an individual's genotype/phenotype. Significant advances have been made in understanding the genetic contribution to smoking behaviors. These and future studies will provide potential directions for novel prevention and treatment strategies.

Antidepressive Agents, Second-Generation↗

PubMed2005

Nuclear beta-catenin expression is rare and its potential association with short survival in colorectal signet-ring cell carcinoma.

Colorectal signet-ring cell carcinoma (SRCC) is a rare cancer and the prognosis is usually very poor. The biologic pathways involved in its oncogenesis are unknown. beta-catenin, a key target in the Wnt-signaling pathway, is recognized to play an important role in the carcinogenesis in conventional colorectal carcinoma. This study explores the involvement of Wnt-signaling molecules beta-catenin and cyclin D1, cell cycle regulators cyclin D3, proliferative index Ki-67, apoptotic index, and angiogenic indicator CD31 in 20 colorectal SRCC paraffin-embedded specimens. Results showed that there were 2 specimens with nuclear beta-catenin and higher expression of cyclin D1 than the remaining 18 specimens. Surprisingly, those 2 patients had a much shorter survival of 6 months than the remaining 15 patients, who had around 24 months. Moreover, all colorectal SRCC specimens had an overexpression of cyclin D1, cyclin D3, and Ki-67, as well as much more angiogenesis and apoptosis than adjacent normal epithelial tissues. The authors make the preliminary comment that nuclear beta-catenin is a rare phenomenon in colorectal SRCC, but the involvement of it may indicate a worse prognosis with shorter survival than colorectal SRCC without nuclear beta-catenin expression. Besides, overexpression of cyclin D1, cyclin D3, Ki-67, and increased angiogenesis and apoptosis may play a vital role in promoting colorectal SRCC development.

Apoptosis↗

PubMed2006

Intraductal papillary mucinous neoplasm (IPMN) of the pancreas: its histopathologic difference between 2 major types.

Intraductal papillary mucinous neoplasm (IPMN) is a unique pancreatic neoplasm developing in the ductal system. Two major histologic subtypes have been reported, that is the gastric type and the intestinal type. However, their histopathologic features, especially those of the gastric type, have not been fully described. To evaluate the features of these two types and refine their differences, we analyzed 80 IPMNs including 50 cases of the gastric type and 30 cases of the intestinal type with mucin immunohistochemistry. By defining a main duct-type lesion as predominantly involving the main pancreatic duct with or without branch ducts, and a branch duct-type lesion as exclusively centered on branch ducts or consisting of a collection of small cystic lesions, gastric-type IPMNs were mostly branch duct-type lesions (98%), whereas the intestinal-type IPMNs were usually main duct type (73%). The histologic grade of the intestinal type was generally higher than that of the gastric type. The intestinal type was also characterized by frequent intraluminal nodular growth, and severe atrophy and fibrosis of the surrounding parenchyma with mucous lake formation. In contrast, pyloric glandlike structures at the base of the papillae and pancreatic intraepithelial neoplasia (PanIN)-like complexes were more frequently observed in the gastric type. A significant difference was observed between the gastric type and the intestinal type with regard to all the above features (P<0.05). Seven cases (23%) of the intestinal type were associated with an invasive adenocarcinoma (6 mucinous and 1 ductal), versus only 1 case (2%) of the gastric type (invasive ductal carcinoma). All cases of both gastric and intestinal types expressed MUC5AC; however, high immunolabeling scores for MUC2 were mostly observed in the intestinal type (P<0.05). In conclusion, gastric and intestinal types of IPMNs have distinct histopathologic features and mucin profiles, suggesting that they may follow different biologic pathways.

Adenocarcinoma, Mucinous↗

PubMedDate not supplied

Socioeconomic status and stress-related biological responses over the working day.

OBJECTIVES: The influence of low socioeconomic status on cardiovascular disease may be mediated in part by sustained activation of stress-related autonomic and neuroendocrine processes. We hypothesized that low socioeconomic status would be associated with heightened ambulatory blood pressure and cortisol output over the working day. METHODS: One hundred eight men and 94 women from the Whitehall II epidemiological cohort participated. Blood pressure and heart rate were monitored every 20 minutes over a working day and evening, and salivary cortisol was sampled on waking up and at 2-hour intervals. Measures were also taken under resting laboratory conditions. Socioeconomic status was indexed by grade of employment. RESULTS: Resting blood pressure, heart rate, and cortisol did not differ by grade. Ambulatory systolic pressure was greater in the morning in the lower (128.9 +/- 15.7 mm Hg) than the intermediate (122.6 +/- 12.5 mm Hg) and higher grades (123.3 +/- 12.7 mm Hg) after adjustment for age, sex, smoking, and alcohol intake (p =.019). Heart rate was also raised in the morning in the lower grade participants. Differences in morning systolic pressure and heart rate were independent of concurrent physical activity. Cortisol concentration was greater in lower than higher grade men (9.54 +/- 4.1 vs. 7.38 +/- 2.8 nmol/liter, p =.008) but was more elevated in higher than lower grade women (7.84 +/- 2.5 vs. 6.35 +/- 1.9 nmol/liter, p =.014). Differences remained significant after adjustment for age, time of awakening, smoking, and alcohol intake. CONCLUSIONS: Socioeconomic differences in blood pressure and cortisol may reflect stress-related activation of biological pathways that contribute to variations in disease risk.

Alcohol Drinking↗

PubMedDate not supplied

Psychological stress and antibody response to influenza vaccination: when is the critical period for stress, and how does it get inside the body?

OBJECTIVES: This study attempted to determine whether stress of moderate intensity could modulate the antibody response to an influenza vaccination in healthy young adults, identify critical periods during which stress could influence antibody response, and delineate behavioral and biological pathways that might explain relations between stress and antibody. METHODS: A cohort of 83 healthy young adults underwent 13 days of ambulatory monitoring before, during, and after vaccination. Four times daily, subjects reported the extent to which they felt stressed and overwhelmed and collected a saliva sample that was later used to measure cortisol. A battery of health practices (cigarette smoking, alcohol use, physical activity, sleep hygiene) was assessed daily. Antibody titers to the vaccine components were measured at baseline and at 1-month and 4-month follow-up assessments. RESULTS AND CONCLUSIONS: To the extent that they reported higher levels of stress across the monitoring period, subjects exhibited poorer antibody responses to the New Caledonia strain of the vaccine. Stress ratings on the 2 days before the vaccine and the day it was given were not associated with antibody response. However, the 10 days afterward appeared to be a window of opportunity during which stress could shape the long-term antibody response to varying degrees. With respect to potential mediating pathways, little evidence emerged in favor of cortisol secretion, alcohol consumption, physical activity, or cigarette smoking. However, analyses were consistent with a pattern in which feelings of stress and loss of sleep become locked into a feed-forward circuit that ultimately diminishes the humoral immune response. These findings may shed light on the mechanisms through which stress increase vulnerability to infectious disease.

Adolescent↗

PubMedDate not supplied

Depression, alterations in platelet function, and ischemic heart disease.

Platelets, the smallest corpuscular component of human blood, are central to various crucial biologic pathways in the human body. Diminished platelet function is thought to contribute to the increased risk of ischemic heart disease in patients with major depressive disorder, and to the increased morbidity and diminished survival of depressed patients after an index myocardial infarction. We reviewed both recent studies that evaluated platelet function in various patient groups and recent information regarding the potential beneficial effects of selective serotonin reuptake inhibitors on platelet reactivity.

Blood Platelet Disorders↗

PubMed2026

The causal relationship between multiple cardiovascular diseases and glioblastoma: A Mendelian randomization study.

Observational studies suggest an association between glioblastoma (GBM) and cardiovascular diseases (CVDs), but a causal relationship remains unestablished. This study aimed to investigate the causal link between multiple CVDs and GBM risk. The inverse variance weighted method indicated that all 18 CVDs had significant causal associations with GBM (P < .05). Genetically predicted CVDs were uniformly associated with a lower risk of GBM (odds ratio < 1), identifying them as potential protective factors. Sensitivity analyses confirmed the absence of significant heterogeneity or horizontal pleiotropy, and the MR-Steiger test validated the correct causal direction. This Mendelian randomization (MR) study provides evidence that a range of CVDs are causally associated with a decreased risk of developing GBM. These findings suggest shared biological pathways and offer new insights for understanding GBM etiology. We conducted a 2-sample MR analysis using publicly available genome-wide association study data. GBM was the outcome, and 18 cardiovascular-related traits (including coronary artery disease, myocardial infarction, and venous thromboembolism) were exposures. Instrumental variables were single-nucleotide polymorphisms significantly associated with exposures (P < 5 × 10-8). The primary analysis used the inverse variance weighted method, supplemented with MR-Egger, weighted median, and weighted mode methods. Sensitivity analyses, including Cochran Q test, MR-Egger intercept test, leave-one-out analysis, and MR-Steiger directionality test, were performed to ensure robustness.

Causality↗

PubMed2026

HIV immunological nonresponders show low SKAP1 concentration and DNA hypermethylation in the SKAP1 promotor region.

OBJECTIVE: The aim of this study was to improve understanding of biological pathways underlying inadequate CD4 + T-cell restoration after initiating antiretroviral treatment as these so called Immunological nonresponders are at increased risk for morbidity and mortality while treatment options are lacking. DESIGN: We compared baseline multiomics data from 88 Immunological nonresponders and 1467 immunological responders that participated in the 2000HIV study, separated into a discovery and validation cohort. METHODS: We measured expression levels of 2367 plasma proteins, comparing the immunological responders and nonresponders. As this highlighted low Src kinase-associated phosphoprotein 1 (SKAP1) levels in Immunological nonresponders, we measured intracellular SKAP1 levels in CD4 + T-cells, investigated DNA methylation and assessed single-nucleotide polymorphisms (SNPs). We also explored whether HIV or CMV infection may influence SKAP1 expression. RESULTS: SKAP1 plasma levels were significantly lower in Immunological nonresponders in both cohorts. SKAP1 plasma concentrations reflected intracellular levels in CD4 + T-cells. DNA methylation analysis showed significant hypermethylation at the SKAP1 promotor region. Three SNPs close to the SKAP1 gene were associated with poor Immunological response. Preliminary data suggest that HIV or CMV may influence SKAP1 levels. CONCLUSION: Our data show decreased SKAP1 concentrations in immunological nonresponders, potentially driven by hypermethylation of the SKAP1 promoter. Downregulation of SKAP1, which is known to play a role in T cell proliferation and migration, may therefore contribute to the poor restoration of CD4 + cell count after ART.

Humans↗

PubMed2026

Two Genomes, one Outcome: Stratifying Donor and Recipient Polygenic Risk Score to Improve Kidney Allograft Longevity.

Kidney transplantation outcomes arise from complex interactions among donor organ quality, recipient susceptibility, and immunologic compatibility, yet conventional clinical risk models explain only a modest fraction of outcome variability. Polygenic risk scores (PRS) offer a promising framework to enhance transplant risk assessment by integrating genome-wide genetic information from both donor and recipient into biologically informed models. This narrative review examines the mechanistic basis for PRS application in kidney transplantation and variant clustering approaches that link polygenic signals to specific biological pathways underlying alloimmunity, fibrosis, and metabolic dysfunction. We compare current PRS construction methodologies, highlighting their respective strengths and limitations in transplant cohorts. Transplant PRS are distinguished from single-genome disease models by their capacity to capture dual-genome interactions, simultaneously quantifying inherited donor organ liability and recipient genetic susceptibility within an integrated framework. This dual-genome architecture requires novel risk stratification paradigms in which combined donor-recipient polygenic profiles inform pretransplant decision-making in ways that neither genome alone can achieve. However, current PRS contribute only incremental variance beyond established clinical predictors, and critical limitations persist, including European ancestry bias, small cohort sizes, incomplete replication, and undefined clinical actionability thresholds. We critically evaluate these implementation barriers and outline future directions for integrating dual-genome PRS with clinical, molecular, and environmental data. The longer-term goal is to advance precision kidney transplantation through applications such as donor selection, immunosuppression tailoring, and individualized posttransplant surveillance. Realizing this potential will require validation in adequately powered, ancestry diverse, prospective transplant cohorts.

Journal Article↗

PubMed2003

Genetics of early-onset Alzheimer dementia.

Alzheimer's dementia (AD) is the most common degenerative disorder of the central nervous system. Although the onset of dementia is above 65 years of age in the majority of the patients (late-onset AD, LOAD), a small subgroup of patients develops AD before 65 years of age (early-onset AD, EOAD). To date 3 genes responsible for EOAD have been identified: the amyloid precursor protein gene (APP), presenilin 1 (PSEN1) and presenilin 2 (PSEN2). PSEN1 is the most frequently mutated EOAD gene with a mutation frequency of 18 to 50% in autosomal dominant EOAD. In addition, the epsilon4 allele of the gene encoding apolipoprotein E (APOE) was identified as a risk factor for both LOAD and EOAD. Many studies reported other susceptibility genes, but the APOEepsilon4 alelle has been the only risk factor that was consistently replicated in all AD populations. Extensive cell biology research in the past ten years led to the hypothesis that the 4 EOAD genes lead to AD through a common biological pathway resulting in abnormal APP processing by subtle different mechanisms. Now, transgenic mice are produced to study the influence of EOAD mutations in vivo, eventually leading to the development of novel therapeutic strategies.

Alzheimer Disease↗

PubMed2023

Beyond antibiotic resistance: the whiB7 transcription factor coordinates an adaptive response to alanine starvation in mycobacteria.

Pathogenic mycobacteria are a significant cause of morbidity and mortality worldwide. These bacteria are highly intrinsically drug resistant, making infections challenging to treat. The conserved whiB7 stress response is a key contributor to mycobacterial intrinsic drug resistance. Although we have a comprehensive structural and biochemical understanding of WhiB7, the complex set of signals that activate whiB7 expression remain less clear. It is believed that whiB7 expression is triggered by translational stalling in an upstream open reading frame (uORF) within the whiB7 5' leader, leading to antitermination and transcription into the downstream whiB7 ORF. To define the signals that activate whiB7, we employed a genome-wide CRISPRi epistasis screen and identified a diverse set of 150 mycobacterial genes whose inhibition results in constitutive whiB7 activation. Many of these genes encode amino acid biosynthetic enzymes, tRNAs, and tRNA synthetases, consistent with the proposed mechanism for whiB7 activation by translational stalling in the uORF. We show that the ability of the whiB7 5' regulatory region to sense amino acid starvation is determined by the coding sequence of the uORF. The uORF shows considerable sequence variation among different mycobacterial species, but it is universally and specifically enriched for alanine. Providing a potential rationalization for this enrichment, we find that while deprivation of many amino acids can activate whiB7 expression, whiB7 specifically coordinates an adaptive response to alanine starvation by engaging in a feedback loop with the alanine biosynthetic enzyme, aspC. Our results provide a holistic understanding of the biological pathways that influence whiB7 activation and reveal an extended role for the whiB7 pathway in mycobacterial physiology, beyond its canonical function in antibiotic resistance. These results have important implications for the design of combination drug treatments to avoid whiB7 activation, as well as help explain the conservation of this stress response across a wide range of pathogenic and environmental mycobacteria.

Preprint↗

PubMed2025

Genome-wide association study of adolescent-onset depression.

Adolescent depression is a heritable psychiatric condition with rising global prevalence and severe long-term outcomes, yet its biological underpinnings remain poorly understood. We conducted the first genome-wide association study of adolescent-onset depression, comprising 102,428 cases (diagnosis or clinical symptom thresholds) and 286,911 controls, including diverse ancestries. Cross-ancestry meta-analysis identified 52 independent variants across 17 loci; European-only analysis found 61 variants at 29 loci, with a SNP-based heritability of 9.8%. Comparative analyses revealed two genes unique to adolescent-onset versus lifetime depression, enriched in neuronal subtypes, and two genes as potential drug repurposing targets. Polygenic scores were associated with adolescent-onset depression across ancestries, persistent depression trajectories, more severe outcomes, as well as reduced cortical volume, surface area and white matter integrity. Genetic correlation and Mendelian randomisation analyses support shared genetic liability and causal links with early puberty and modifiable health and behavioural risk factors. These findings uncover novel genetic loci and refine biological pathways underlying adolescent-onset depression, revealing age-specific mechanisms and early intervention opportunities.

Journal Article↗

PubMed2026

A pangenome framework uncovers the role of deletions in repeated evolution of cave-derived traits.

Structural variants (SVs) are increasingly recognized as key contributors to adaptive evolution, yet they remain underexplored compared with single-nucleotide variation. To understand how large-scale genomic changes shape repeated evolution, we leveraged multiple levels of sequence data across the powerful evolutionary model system of the Mexican tetra fish (Astyanax mexicanus). We constructed one of the first pangenome graphs from a naturally evolving vertebrate, enabling comprehensive discovery of SVs among 120 fish from 11 populations. We discover substantial amounts of structural variation and explore the roles of genomic biases and selection in shaping the distribution of these variants. More than 2400 high-confidence cave-specific deletions are enriched in biological pathways involved in vision, metabolism, and behavior and cluster nonrandomly in quantitative trait loci linked to cavefish traits. Additionally, 67 genes harbor unique deletions between independent cavefish lineages. These reused genes show evidence of population-specific selection (99% contain selective sweeps compared with 8%-15% in genes lacking SVs), indicating that deletions likely rose in frequency through repeated positive selection rather than drift. Together, these results reveal that recurrent deletion events have repeatedly contributed to the evolution of cave-adapted phenotypes and highlight deletions as underexplored contributors of adaptive evolution in extreme environments.

Animals↗

PubMed2001

Nitric oxide induces stomatal closure and enhances the adaptive plant responses against drought stress.

Nitric oxide (NO) is a very active molecule involved in many and diverse biological pathways where it has proved to be protective against damages provoked by oxidative stress conditions. In this work, we studied the effect of two NO donors, sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine SNP-treated on the response of wheat (Triticum aestivum) to water stress conditions. After 2 and 3 h of drought, detached wheat leaves pretreated with 150 microM SNP retained up to 15% more water than those pretreated with water or NO(2)(-)/NO(3)(-). The effect of SNP treatment on water retention was also found in wheat seedlings after 7 d of drought. These results were consistent with a 20% decrease in the transpiration rate of SNP-treated detached wheat leaves for the same analyzed time. In parallel experiments, NO was also able to induce a 35%, 30%, and 65% of stomatal closure in three different species, Tradescantia sp. (monocotyledonous) and two dicotyledonous, Salpichroa organifolia and fava bean (Vicia faba), respectively. In SNP-treated leaves of Tradescantia sp., the stomatal closure was correlated with a 10% increase on RWC. Ion leakage, a cell injury index, was 25% lower in SNP-treated wheat leaves compared with control ones after the recovery period. Carboxy-PTIO (2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide), a specific NO scavenger, reverted SNP action by restoring the transpiration rate, stomatal aperture, and the ion leakage to the level found in untreated leaves. Northern-blot analysis showed that SNP-treated wheat leaves display a 2-fold accumulation of a group three late embryogenesis abundant transcript with respect to control leaves both after 2 and 4 h of drought periods. All together, these results suggest that the exogenous application of NO donors might confer an increased tolerance to severe drought stress conditions in plants.

Adaptation, Physiological↗

PubMed2026

A Comprehensive Analysis of Differential Protein Expression in the Plasma of Rheumatoid Arthritis Patients Utilizing Data-Independent Acquisition (DIA) Proteomics Technology.

BACKGROUND: Rheumatoid Arthritis (RA) is a Prevalent Autoimmune Disorder Affecting Millions of People Worldwide. A Thorough Understanding of Its Clinical and Pathological Features Is Essential to Improve Patient Outcomes. METHODS: This Study Combined Data-Independent Acquisition Proteomics and Enzyme-Linked Immunosorbent Assay (ELISA) to Identify and Validate Potential Plasma Protein Biomarkers for the Early Diagnosis of RA. RESULTS: Differential Proteomic Analysis Identified Differentially Expressed Proteins Between Patients With RA and Healthy Controls and Characterized Their Functions. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes Enrichment Analyses Were Performed to Explore Protein Functions and Associated Biological Pathways. The STRING Database and the Metascape Platform Were Used to Conduct an in-Depth Analysis of the Protein-Protein Interaction Network, Highlighting the Functional Attributes and Interconnections of Upregulated Proteins and Identifying Key Protein Complexes Involved in RA. ELISA Analysis of Plasma Samples Revealed Significantly Elevated SERPINA3 Levels in Patients With RA, Which Were Positively Correlated With Disease Activity Indicators-Including Erythrocyte Sedimentation Rate, C-Reactive Protein, and Disease Activity Score 28-But Were Not Correlated With Rheumatoid Factor or Its Subtypes. CONCLUSIONS: This Study Provides New Insights and Identifies Potential Biomarkers for the Early Diagnosis of RA.

Humans↗