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At least 37 records · Page 2Linked to original sources
PubMed2026

Characterizing the impact of plasma protein levels on human brain structure and disorders leveraging integrative multi-omics analysis.

With recent advances in high-throughput proteomic technologies, population-scale plasma proteomics datasets, often linked to extensive genetic and phenotypic information, have become increasingly accessible. Yet the relationships between circulating protein levels, brain imaging phenotypes, and risk for neurological and psychiatric disorders remain largely unexplored. Proteome-wide association studies offer a promising approach for elucidating biological mechanisms that connect genetic variation to complex brain-related traits and diseases. In this study, we integrated protein quantitative trait loci (pQTLs) from the two largest plasma proteomic resources (the UK Biobank Pharma Proteomics Project [UKB-PPP] and Ferkingstad et al. [deCODE]) with genome-wide association studies of brain imaging-derived phenotypes in UK Biobank using Mendelian randomization and colocalization analyses. We identified 120 cis and 20 trans associations between plasma proteins and imaging phenotypes and validated these findings using brain tissue-derived proteomic and transcriptomic datasets. Multivariable Mendelian randomization revealed eleven plasma proteins (coding genes APOE, ARL3, MICB, NSF, RHOC, RSPO3, ENPP2, BTN2A1, EIF2AK3, MRVI1, and OPLAH) with significant direct effects on the risk of Alzheimer's disease, Parkinson's disease, multiple sclerosis, bipolar disorder, and schizophrenia. Single-cell expression and pathway enrichment analyses further revealed cell-type-specific effects and distinct biological processes underlying these protein-disease associations. Together, these findings demonstrate robust links between plasma protein variation and brain structure, delineate protein-disease pathways, and highlight the cellular and molecular mechanisms that contribute to neurobiological diversity and pathology.

Journal Article↗
PubMed2026

Large-Scale Plasma Proteomics Identifies Early Molecular Deviations and Improves Risk Prediction for Heart Failure Among Individuals With Obesity.

AIMS: Heart failure (HF) is a major global public health challenge, with obesity being one of its key risk factors. Although several HF risk prediction models have been developed in the general population, few are specifically tailored to individuals with obesity. This underscores the urgent need for precise biomarkers to improve individual risk stratification and enable personalized prevention strategies. We aimed to develop and validate a plasma proteomics-based protein risk score (PRS) to predict incident HF among individuals with obesity. MATERIALS AND METHODS: We analysed 9831 participants with obesity (BMI ≥ 30 kg/m2) from the UK Biobank with baseline measurements of 2911 circulating proteins and up to 16 years of follow-up. Multivariable Cox regression identified proteins associated with incident HF after comprehensive covariate adjustment. A PRS was constructed using LASSO regression and evaluated in a held-out test set. Protein trajectories before HF onset were reconstructed using LOESS modelling. To enhance clinical feasibility, a minimal protein panel was identified using LightGBM with forward feature selection. RESULTS: A total of 727 participants developed HF during follow-up. Multivariable cox analyses identified 578 proteins significantly associated with HF. LASSO regression further selected 81 proteins to build the PRS, which showed a strong association with HF risk in both training (HR 3.57; 95% CI 3.19-4.00) and test cohorts (HR 2.45; 95% CI 2.20-2.74). Adding the PRS improved prediction beyond age and sex (ΔC = 0.091) and beyond the Pooled Cohort Equations to Prevent Heart Failure (PCP-HF) model (ΔC = 0.052), with consistent gains in NRI and IDI. Proteomic deviations were detectable up to 16 years before diagnosis. A four-protein panel (GDF15, NT-proBNP, TNFRSF10B, CTHRC1) achieved robust discrimination (AUC 0.789), outperforming NT-proBNP alone (AUC 0.695) and complementing the PCP-HF model (combined AUC 0.803). DISCUSSION: Large-scale plasma proteomics substantially improves HF risk prediction in individuals with obesity and reveals long-standing molecular alterations preceding clinical onset. A simplified four-protein panel maintains robust predictive accuracy and provides a practical approach for the early detection and targeted prevention of obesity-related HF.

Humans↗
PubMed1977

[Alteration of platelet function during intensive replacement therapy in haemophilia A (author's transl)].

This report describes two patients with haemophilia A who developed a transient thrombocytopathy with haemorrhagic diathesis during post-operative high-dose replacement therapy with antihaemophilic globulin. At the time of the bleeding the factor VIII-activity was in the normal range in both patients. The fibrinogen level, however, was elevated to 1700 mg-% and the factor VIII-associated antigen rose to more than 6-fold. At no time of replacement therapy with antihaemophilic globulin could either fibrinogen split products or fragments of the factor VIII-protein be detected by the usual methods. In view of the results of the thrombocyte aggregation experiments the authors postulate a disturbance of platelet function at the level of the membrane surface due to an overload of increased amounts of circulating proteins. Both the possible interference of dialysable factor VIII-components and the role of immunpathologic phenomena are discussed.

Adult↗
PubMed2026

GWAS Meta-analysis Identifies Novel Associated Loci and Points to Causal Tissues in Central Serous Chorioretinopathy.

OBJECTIVE: To define CSC genetic architecture and identify implicated ocular tissues, cell types, genes, and circulating proteins. DATA SOURCES: Genome-wide data were assembled from FinnGen, All of Us, Mass General Brigham Biobank, Million Veteran Program, and a Dutch chronic CSC cohort. Serum protein quantitative trait loci, human single-cell ocular atlases, and UK Biobank macular optical coherence tomography (OCT) imaging were used for downstream analyses. STUDY SELECTION: Five European-ancestry cohorts with genome-wide data and cohort-specific CSC case-control definitions were included, comprising 2,584 cases and 1,044,455 controls. Variants present in at least 2 cohorts were meta-analyzed. DATA EXTRACTION AND SYNTHESIS: Cohort-level GWASs were adjusted for age, age squared, sex, genotyping array or batch, and 10 genetic principal components, then combined using fixed-effects inverse-variance meta-analysis. Post-GWAS analyses included gene prioritization, colocalization, Mendelian randomization, single-cell disease-relevance scoring, and testing of a CSC genetic risk score in UK Biobank OCT images. MAIN OUTCOMES AND MEASURES: Genome-wide significant CSC loci, effector genes and proteins, tissue and cell-type enrichment, and CSC-relevant OCT abnormalities. RESULTS: Across 11,068,938 variants, 10 loci reached genome-wide significance (P < 5 &#xd7; 10-8), including 3 novel loci near TGFB1, LINC00551, and LOC105375630 and 7 replicated loci near CFH, CD46, NOTCH4, PREX1, PTPRB, GATA5, and TNFRSF10A. Integrative analyses prioritized 10 candidate effector genes. Colocalization and Mendelian randomization implicated circulating TNFRSF10A, TGFB1, and CASP10 levels. Single-cell analyses localized genetic risk to sclera (P = 2.0 &#xd7; 10-4) and vascular endothelial cells (P = 4.0 &#xd7; 10-4), with fibroblast enrichment. In UK Biobank, OCT abnormalities were more frequent in the top vs bottom 1% of CSC genetic risk (18 of 109 [16.5%] vs 8 of 134 [6.0%]; odds ratio, 4.05; 95% CI, 1.65-10.87; P = .002). CONCLUSIONS AND RELEVANCE: In this GWAS meta-analysis, CSC susceptibility localized predominantly to scleral and vascular biology rather than primary retinal pigment epithelial dysfunction. These findings support CSC as a sclerovascular disorder and nominate complement regulation, endothelial signaling, and extracellular matrix pathways for future study.

Journal Article↗
PubMed2026

Plasma Proteomic Profiling Identifies Candidate Biomarkers for Pancreatic Ductal Adenocarcinoma.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy that is often diagnosed after curative treatment is no longer feasible. Existing biomarkers, particularly CA19-9, have limited sensitivity and specificity. Plasma proteins that capture tumor-associated biological alterations may therefore provide useful signals for earlier detection. METHODS: Plasma samples from 99 patients with PDAC and 30 healthy controls were analyzed using data-independent acquisition (DIA) proteomics. Differentially expressed proteins were identified using predefined statistical thresholds and further examined by functional enrichment analysis. Selected candidate biomarkers were validated by ELISA in an independent subset. RESULTS: Among 565 quantified plasma proteins, 52 were differentially expressed between PDAC and controls. These proteins were enriched in extracellular processes, cholesterol metabolism, complement and coagulation cascades, and pancreatic secretion pathways. ELISA validation confirmed higher plasma levels of Cathepsin S, CTRB2, MARCO, PIGR, PRDX6, REG1A, Trypsin-2, and PEP-FAP in patients with PDAC compared with healthy controls. ROC analyses showed moderate-to-good discriminatory performance for several candidates, and the MARCO&#x2009;+&#x2009;PEP-FAP model improved classification compared with either marker alone. CONCLUSION: These findings reveal circulating proteins linked to key PDAC-related biological processes and identify eight candidates for further evaluation in multi-protein diagnostic panels. Larger validation studies incorporating clinically relevant disease control groups are warranted to determine their diagnostic specificity and clinical utility.

Humans↗
PubMed2026

Systemic Proteomic Alterations and Predictive Biomarkers of Paroxetine Response in Refractory Rosacea: A Secondary Analysis of a Randomized Clinical Trial.

IMPORTANCE: Rosacea is a chronic inflammatory cutaneous disorder characterized by persistent erythema and vascular dysregulation. While paroxetine has shown clinical efficacy in reducing these symptoms, the systemic molecular mechanisms underlying its therapeutic response remain poorly characterized. OBJECTIVE: To investigate systemic proteomic alterations and identify potential predictive biomarkers in patients with refractory erythematous rosacea following paroxetine treatment. DESIGN, SETTING, AND PARTICIPANTS: This prospective plasma proteomic analysis was nested within a multicenter, randomized, double-blind, placebo-controlled clinical trial (Prospective Rosacea Refractory Erythema Randomized Clinical Trial [PRRERCT]). Participants included patients aged 18 to 65 years with refractory rosacea (Clinician's Erythema Assessment [CEA] score &#x2265;3). Plasma samples were collected at baseline and after 12 weeks of treatment. The data for this study were analyzed between September 2025 and November 2025. INTERVENTIONS: Participants received oral paroxetine, 25 mg per day, for a 12-week treatment period. MAIN OUTCOMES AND MEASURES: Systemic protein expression profiles were analyzed using data-independent acquisition liquid chromatography-tandem mass spectrometry. Clinical response was evaluated using CEA and the Flushing Assessment Tool. Correlations between proteomic changes and clinical improvements were assessed, and predictive biomarkers were identified using receiver operating characteristic curve analysis. RESULTS: Among 24 participants (mean [SD] age, 35 [11] years; 24 [100%] female), paroxetine treatment significantly reduced mean (SD) CEA scores from 3.1 (0.3) to 2.3 (0.7) and Flushing Assessment Tool scores from 3.1 (0.6) to 2.0 (0.9) (P&#x2009;<&#x2009;.001). Exploratory proteomic analysis revealed 497 candidate differentially expressed proteins after treatment. Downregulated proteins showed preliminary enrichment in pathways related to immune response activation, insulin receptor signaling, and neuronal remodeling. A subset of 98 reversed-response proteins was observed, primarily linked to synaptic vesicle cycles and vascular smooth muscle contraction. Proteomic alterations were associated with clinical improvement (65 proteins for erythema; 73 for flushing). Candidate biomarkers, notably OLFML3 (area under the receiver operating characteristic curve [AUC], 0.87 [95% CI, 0.70-1.00]) and IGFBP2 (AUC, 0.80 [95% CI 0.55-1.00]), demonstrated high predictive value for clinical response. CONCLUSIONS AND RELEVANCE: In this secondary analysis of a randomized clinical trial, paroxetine treatment was associated with modulation of systemic neuro-vascular-immune networks in patients with rosacea. These exploratory findings provide preliminary mechanistic clues regarding the possible disease-modifying potential of paroxetine and point to circulating protein signatures that may facilitate personalized therapeutic strategies for rosacea management. TRIAL REGISTRATION: Chinese Clinical Trial Registry Identifier: ChiCTR2000031479.

Humans↗
PubMed2025

Genome-Wide Aggregated Trans Effects Analysis Identifies Genes Encoding Immune Checkpoints as Core Genes for Rheumatoid Arthritis.

OBJECTIVE: The sparse effector "omnigenic" hypothesis postulates that the polygenic effects of common single nucleotide polymorphisms (SNPs) on a typical complex trait are mediated by trans effects that coalesce on expression of a relatively sparse set of core genes. The objective of this study was to identify core genes for rheumatoid arthritis by testing for association of rheumatoid arthritis with genome-wide aggregated trans effects (GATE) scores for expression of each gene as transcript in whole blood or as circulating protein levels. METHODS: GATE scores were calculated for 5,400 cases and 453,705 non-cases of primary rheumatoid arthritis in UK Biobank participants of European ancestry. RESULTS: Testing for association with GATE scores identified 16 putative core genes for rheumatoid arthritis outside the HLA region, of which six-TP53BP1, PDCD1, TNFRSF14, LAIR1, LILRA4, and IDO1-were supported by Mendelian randomization analysis based on the marginal likelihood of the causal effect parameter. Five of these 16 genes were validated by a reported association of rheumatoid arthritis with SNPs within 200 kb of the transcription site, eight by association of the measured protein level with rheumatoid arthritis in UK Biobank, 10 by experimental perturbation in mouse models of inflammatory arthritis, and two-CTLA4 and PDCD1-by evidence that drugs targeting the gene cause or ameliorate inflammatory arthritis in humans. Fourteen of these 16 genes are in pathways affecting immunity or inflammation, and six-CD5, CTLA4, TIGIT, LAIR1, TNFRSF14, and PDCD1-encode receptors that have been characterized as immune checkpoints exploited by cancer cells to escape the immune response. CONCLUSION: These results highlight the key role of immune checkpoints in rheumatoid arthritis and identify possible therapeutic targets.

Humans↗
PubMed1977

Split unresponsiveness to the trinitrophenyl determinant. I. Manoeuvers which suppress either humoral or cell-mediated immune responses.

2,4,6-Trinitrobenzene sulfonic acid (TNBS) injected intravenously (i.v.) makes mice fully tolerant to the trinitrophenyl (TNP) determinant. Administration of in vitro TNP-labeled syngeneic erythrocytes or thymocytes renders mice unable to develop contact sensitivity to picryl chloride, while the humoral anti-TNP responses seem to be unaffected. The reverse was found after pretreatment of mice with TNP-labeled isologous IgG (MGG) since only anti-TNP antibody responses, but not contact sensitivity to picryl chloride, were significantly reduced. TNP-coupled macrophages given to animals suppressed both the cell-mediated and humoral responses, and this might be due to the presence on their surface of TNP-labeled cytophilic antibody. TNBS administered i.v. binds to circulating proteins and formed blood elements. Thus the split unresponsiveness affecting either humoral or cell-mediated compartments after the injection of TNP-MGG or of haptenated cells respectively, is presumably due to dissecting events which in vivo after the injection of TNBS, occur simultaneously. These results may be interpreted to indicate that split unresponsive states to TNP determinants are mediated two independent mechanisms which require different tolerogen presentations to be triggered.

Animals↗
PubMed2026

Tissue origins of the plasma proteomic response to glucose ingestion in humans.

AIMS/HYPOTHESIS: Circulating proteins act as important hormonal signals of nutrient intake. We aimed to systematically characterise the time-resolved proteomic response to glucose ingestion in humans, and to assess its robustness following prolonged complete caloric restriction. METHODS: We conducted oral glucose tolerance tests (OGTTs) in 11 healthy volunteers before and after 7 days of complete caloric restriction and measured the response of >2900 targets through high-resolution plasma protein profiling. RESULTS: We identified a signature of 44 proteins that changed significantly following glucose ingestion, which was reproducible after 7 days without food, and was strongly (20-fold) enriched for 'stomach-specific' proteins. We report that annexin A10 (ANXA10) shows the most significant post-glucose change observed, similar to the trajectories of secreted hormones. We present observational human evidence from multiple sources suggesting that ANXA10 is secreted upon sensing an increase in gastric pH, with the stomach as the major contributing tissue. Despite a profound metabolic shift after 7 days of complete caloric restriction, characterised by delayed insulin secretion and postprandial hyperglycaemia, only four proteins showed robust evidence for a differential trajectory during both OGTTs. This included plasma levels of tryptophanyl-tRNA synthetase&#xa0;1 (WARS), for which we found a genetic association with glucose homeostasis and coronary artery disease. CONCLUSIONS/INTERPRETATION: Our exploratory study identifies the proteomic response to glucose ingestion and demonstrates its reproducibility despite major shifts in glucose homeostasis. We characterise the gastrointestinal origin of these changes, and hypothesise a hitherto under-recognised role for sensing of changes in gastric pH on the plasma proteome.

Humans↗
PubMed2026

Pathogenesis of psoriasis and psoriatic arthritis: Insights from animal models and single-cell and spatial transcriptomic analyses of skin, synovium and entheses.

Psoriasis (PsO) and psoriatic arthritis (PsA) are immune-mediated diseases characterized by chronic systemic inflammation, including inflammation of the skin and joints. Recent advances in animal models, single-cell transcriptomics, spatial transcriptomics, and proteomics have greatly enhanced our understanding of disease pathogenesis. Mouse models exhibit key features of skin and joint inflammation, facilitating analysis of molecular pathways, and identification of therapeutic targets. Single-cell and spatial transcriptomic analyses have revealed cell-type-specific contributions to inflammation, highlighting interactions between keratinocytes, T cells, fibroblasts, and dendritic cells that drive psoriatic pathology. In psoriatic synovium, type 17 tissue-resident memory T cells, monocytes, and fibroblasts contribute to local inflammation and joint damage, whereas the roles of B cells and plasma cells are less clear. Proteomic and metabolomic profiling in patients with PsA has identified circulating protein signatures and metabolites associated with disease progression, sex-specific differences, and response to therapy. The integration of these multiomic approaches provides a detailed map of immune-stromal-epithelial crosstalk across skin, synovium, and entheses, uncovering mechanisms that were previously inaccessible. These insights have implications for predicting disease progression, identifying novel therapeutic targets, and optimizing treatment strategies. Collectively, advances in animal models and multiomic profiling are reshaping our understanding of PsO and PsA, providing a framework for future research, disease monitoring, and therapeutic development.

Animals↗
PubMed2026

Genomic and proteogenomic insights into Spontaneous Coronary Artery Dissection (SCAD): A systematic review of emerging multi-omic evidence.

BACKGROUND: Spontaneous coronary artery dissection (SCAD) is a major cause of myocardial infarction in young women without traditional cardiovascular risk factors (Hayes et al., 2018; Adlam et al., 2018 [1, 2]). Despite growing awareness, its biological underpinnings remain incompletely understood, and clinical management is largely based on observational evidence rather than mechanistic insight (Saw et al., 2014; Lettieri et al., 2015; Steg et al., 2024 [3-5]). OBJECTIVES: To systematically integrate genomic, epitranscriptomic, proteomic, and metabolomic data in order to characterize the multi-omic architecture of SCAD and identify potential biomarkers and therapeutic targets. METHODS: A systematic review was conducted in accordance with the PRISMA 2020 statement (Arbelo et al., 2023 [6]). PubMed/MEDLINE was searched for original studies investigating genomic and multi-omic features of SCAD. Data were extracted on study design, patient characteristics, identified variants, circulating biomarkers, and implicated biological pathways. Functional enrichment analysis was performed using the DAVID bioinformatics resource (Page et al., 2021 [7]). RESULTS: A total of 16 studies were included. Genome-wide association studies consistently identified susceptibility loci related to arterial structure and extracellular matrix integrity, including ADAMTSL4, PHACTR1/EDN1, LRP1, and FBN1 (Huang et al., 2009; Saw et al., 2020; Turley et al., 2020 [8-10]). Rare variant analyses further supported the role of genes involved in extracellular matrix remodeling and vascular smooth muscle cell function, including COL3A1, COL4A1/2, SMAD3, and TLN1 (Adlam et al., 2023; Turley et al., 2021, 2019; Carss et al., 2020; Zekavat et al., 2022; Wang et al., 2022 [11-16]), while ancestry-specific signals such as TSR1 variants were observed in distinct populations (Turley et al., 2023 [17]). Proteogenomic approaches linked genetic susceptibility loci to circulating proteins involved in matrix remodeling and inflammation, including cathepsin B and ECM1 (Maioli et al., 2010 [18]). Epitranscriptomic analyses identified differential microRNA expression profiles associated with vascular injury and repair pathways (Sun et al., 2019 [19]). CONCLUSIONS: SCAD is characterized by a complex, multi-layered biological architecture involving genetic susceptibility, extracellular matrix dysregulation, and vascular signaling pathways. Integration of multi-omic data provides novel insights into disease mechanisms and highlights potential biomarkers and targets for precision medicine approaches in SCAD.

Animals↗
PubMed2025

Identification of plasma proteomic markers underlying polygenic risk of type 2 diabetes and related comorbidities.

Genomics can provide insight into the etiology of type 2 diabetes and its comorbidities, but assigning functionality to non-coding variants remains challenging. Polygenic scores, which aggregate variant effects, can uncover mechanisms when paired with molecular data. Here, we test polygenic scores for type 2 diabetes and cardiometabolic comorbidities for associations with 2,922 circulating proteins in the UK Biobank. The genome-wide type 2 diabetes polygenic score associates with 617 proteins, of which 75% also associate with another cardiometabolic score. Partitioned type 2 diabetes scores, which capture distinct disease biology, associate with 342 proteins (20% unique). In this work, we identify key pathways (e.g., complement cascade), potential therapeutic targets (e.g., FAM3D in type 2 diabetes), and biomarkers of diabetic comorbidities (e.g., EFEMP1 and IGFBP2) through causal inference, pathway enrichment, and Cox regression of clinical trial outcomes. Our results are available via an interactive portal ( https://public.cgr.astrazeneca.com/t2d-pgs/v1/ ).

Humans↗
PubMed1976

Acclimatization in a hot, humid environment: body fluid adjustments.

Four trained men worked 4 h/day at 40-50% of their maximum aerobic capacity first for 3 days at 25 degrees C db, 18 degrees C wb and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. Between days 1 and 2 of heat exposure mean total circulating protein (TCP) and plasma volume (PV) increased 11.6% and 9%, respectively. Preexposure TCP and PV increased until day 6 of heat exposure. Of the protein fractions beta-globulins underwent the largest relative increase. During work movement of protein into and out of the vascular compartment was similar in control and acclimatizing subjects but the latter generally maintained a greater amount of protein and fluid within the vascular volume. There was no evidence of salt and water retention. The increase in vascualr volume was ascribed to transfer of interstitial protein and water to the vascular volume. Regression coefficients indicated significant correlations for changes in plasma volume versus heart rate, stroke volume, and cardiac output during acclimatization. It was concluded that the most critical event in heat acclimatization is the expansion of the plasma volume.

Acclimatization↗
PubMed2026

Disentangling adiposity-related and non-adiposity-related genetic pathways for type 2 diabetes.

OBJECTIVE: To identify circulating proteins associated with type 2 diabetes (T2D) risk through pathways not fully explained by body mass index (BMI), and to assess therapeutic actionability. RESEARCH DESIGN AND METHODS: We applied GWAS-by-subtraction within a genomic structural equation model to European ancestry summary statistics for T2D (74,124 cases, 824,006 controls) and BMI (n = 681,275), partitioning T2D liability into BMI-related and BMI-subtracted components. We then performed proteome-wide Mendelian randomization (MR) using cis-protein quantitative trait loci from four plasma proteomics cohorts: ARIC, deCODE, Fenland, and the UK Biobank Pharma Proteomics Project. Prioritized proteins passed sensitivity analyses with alternative MR methods and were supported by colocalization evidence. Tissue-resolution regulatory support was assessed using cis-eQTL colocalization across GTEx and pancreatic islet, subcutaneous adipose, and whole-blood resources. Actionability was evaluated using the druggable genome and Open Targets. RESULTS: GWAS-by-subtraction attenuated the genetic correlation between BMI and BMI-subtracted T2D from 0.54 (SE 0.02) to 0.35 (SE 0.02). Proteome-wide MR prioritized 29 proteins for BMI-subtracted T2D. Thirteen showed eQTL colocalization in at least one tissue, implicating liver and intermediary metabolism (GCDH, NOTCH2), pancreatic islet biology (CTRB2, MANBA), adipose and Wnt signaling (RSPO3, GALNT3), and whole blood regulatory signals (PAM, SNUPN). Sixteen proteins were classified within druggable-genome Tiers 1-3, and five had existing Open Targets compounds. CONCLUSIONS: Integrating GWAS-by-subtraction, proteome-wide MR, and colocalization nominated 29 proteins associated with T2D liability not fully explained by BMI. These findings highlight genetically supported targets for follow-up studies of T2D therapies that complement weight-centered approaches.

Journal Article↗
PubMed1977

[Correction of volemic disorders in stenosing gastric and duodenal ulcers in the process of treatment].

While analysing the circulating blood volume (CBV), plasma volume (PV), globular volume (GV) and the amount of circulating protein (ACP) in 109 cases of stenosing gastric and duodenal ulcer, the authors have found that the most of patients (89.9%) develop concomitant hypovolemia, the severity of which depends on the severity of the disease itself and on the degree of the interstitial protein metabolic disorders. Gastric resection aggravated volemic disturbances or caused the new ones. The authors elaborated some recommendations helping to combat volemic disturbances.

Adolescent↗
PubMed1979

The radioimmunoassay of placental protein 5 and circulating levels in maternal blood in the third trimester of normal pregnancy.

A radioimmunoassay has been developed for placental protein 5 (PP5), a product of the human placenta. Circulating concentrations of PP5 were measured in the third trimester of normal pregnancy in 400 women. Concentrations of PP5 showed a skewed distribution and rose progressively to reach a plateau in the last four weeks of pregnancy. The development of this assay will permit studies on the potential clinical application of maternal PP5 levels during normal and abnormal pregnancy.

Cross Reactions↗