Serum Amyloid Alpha Research Articles

BDMARD can prevent the progression of AA amyloidosis to end-stage renal disease

IntroductionAA amyloidosis (AA) can be the consequence of any chronic inflammatory disease. AA is associated with chronic inflammatory diseases (cid+AA), autoinflammatory syndromes (auto+AA) or AA of unknown origin or idiopathic...

The role of gamma globulin, complement component 1q, factor B, properdin, body temperature, C-reactive protein and serum amyloid alpha to the activity and the function of the human complement system and its pathways

The complement system plays a crucial role in orchestrating the activation and regulation of inflammation within the human immune system. Three distinct activation pathways—classical, lectin, and alternative—converge to form the common lytic pathway, culminating in the formation of the membrane-attacking complex that disrupts the structure of pathogens. Dysregulated complement system activity can lead to tissue damage, autoimmune diseases, or immune deficiencies.In this study, the antimicrobial activity of human serum was investigated by using a bioluminescent microbe probe, Escherichia coli (pEGFPluxABCDEamp). This probe has previously been used to determine the antimicrobial activity of complement system and the polymorphonuclear neutrophils. In this study, blocking antibodies against key serum activators and components, including IgG, complement component 1q, factor B, and properdin, were utilized. The influence of body temperature and acute phase proteins, such as C reactive protein (CRP) and serum amyloid alpha (SAA), on the complement system was also examined.The study reveals the critical factors influencing complement system activity and pathway function. Alongside crucial factors like C1q and IgG, alternative pathway components factor B and properdin played pivotal roles. Results indicated that the alternative pathway accounted for approximately one third of the overall serum antimicrobial activity, and blocking this pathway disrupted the entire complement system. Contrary to expectations, elevated body temperature during inflammation did not enhance the antimicrobial activity of human serum.CRP demonstrated complement activation properties, but at higher physiological concentrations, it exhibited antagonistic tendencies, dampening the response. On the other hand, SAA enhanced the serum's activity.Overall, this study sheds a light on the critical factors affecting both complement system activity and pathway functionality, emphasizing the importance of a balanced immune response.

Serum amyloid alpha 1-2 are not required for liver inflammation in the 4T1 murine breast cancer model.

Cancers induce the production of acute phase proteins such as serum amyloid alpha (SAA) in the liver and cause inflammation in various host organs. Despite the well-known coincidence of acute phase response and inflammation, the direct roles of SAA proteins in inflammation in the cancer context remains incompletely characterized, particularly in vivo. Here, we investigate the in vivo significance of SAA proteins in liver inflammation in the 4T1 murine breast cancer model. 4T1 cancers elevate the expression of SAA1 and SAA2, the two major murine acute phase proteins in the liver. The elevation of Saa1-2 correlates with the up-regulation of immune cell-related genes including neutrophil markers. To examine this correlation in detail, we generate mice that lack Saa1-2 and investigate immune-cell phenotypes. RNA-seq experiments reveal that deletion of Saa1-2 does not strongly affect 4T1-induced activation of immune cell-related genes in the liver. Flow cytometry experiments demonstrate the dispensable roles of SAA1-2 in cancer-dependent neutrophil infiltration to the liver. Consistently, 4T1-induced gene expression changes in bone marrow do not require Saa1-2. This study clarifies the negligible contribution of SAA1-2 proteins in liver inflammation in the 4T1 breast cancer model.

The correlation of TNF alpha levels with acute phase proteins in acute Toxoplasma gondii infection in mice

Acute Toxoplasma gondii infections can influence the liver as well as other organs. Many cytokines and proteins play a role in the acute response against infection. Tumor necrosis factor alpha (TNF alpha) is a cytokine that plays a key function in stimulating hepatocytes to produce acute phase proteins. In this study, we investigated TNF alpha levels associated with the levels of macroglobulin, haptoglobin, hemopexin, C-reactive protein (CRP), albumin, serum amyloid alpha protein (SAA), and clusterin, which are acute phase proteins, in serum of mice with T. gondii infection. In the experiment, a total of 24 mice were used; 6 mice constituted the control group and 18 mice were infected with the RH strain. On the 2nd, 4th, and 6th days following the infection, 6 animals were euthanized, and their serums were collected. Compared to the control group, we observed a statistically significant decrease in albumin concentration in the group with T. gondii infection on the 6th day. Also, this group displayed a statistically significant, gradual increase in clusterin levels on the 2nd and 6th days, C-reactive protein levels on the 4th day, haptoglobin levels on the 2nd and 4th days, hemopexin levels on the 2nd day, serum amyloid A levels on the 2nd, 4th, and 6th days, and TNF-α levels on the 2nd, 4th, and 6th days (p < 0.05). TNF-α was strongly positively correlated with CRP, SAA, and clusterin, moderately positively correlated with hemopexin, and strongly negatively correlated with albumin. The increase in CRP, SAA, clusterin, and hemopexin levels on the 2nd day after infection, in parallel with the increase in TNF-α levels, indicates that these proteins can be considered as major acute phase proteins in acute T. gondii infection in mice. The data obtained here may be helpful for the diagnosis of T. gondii infection and for monitoring treatments.

Inflammatory Proteins and Clinical Response to Psychological Therapy in Patients with Depression: An Exploratory Study.

In people with depression, immune dysfunctions have been linked with treatment non-response, but examinations of psychological therapy outcomes, particularly longitudinal biomarker studies, are rare. This study investigated relationships between inflammation, depressive subtypes and clinical outcomes to psychological therapy. Adults with depression (n = 96) were assessed before and after a course of naturalistically-delivered psychological therapy. In total, 32 serum inflammatory proteins were examined alongside therapy outcomes and depressive subtypes (somatic/cognitive symptom subtype, and bipolar/unipolar depression). Overall, 49% of participants responded to treatment. High levels of tumour necrosis factor (TNFα), interleukin-6 (IL-6) and soluble intracellular adhesion molecule-1 (sICAM1), and low interferon-γ (IFNγ), preceded a poorer response to therapy. After therapy, non-responders had elevated c-reactive protein (CRP), thymus and activation-regulated chemokine (TARC) and macrophage chemoattractant protein-4 (MCP4), and attenuated IFNy. Non-somatic depressive symptoms were universally not associated with proteins, while somatic-depressive symptom severity was positively correlated with several pro-inflammatory markers. In the somatic subgroup only, IL-6 and serum amyloid alpha (SAA) decreased between pre- and post-therapy timepoints. Regardless of treatment response, IL-7, IL-8, IL-15 and IL-17 increased over time. These results suggest that inflammation is associated with somatic symptoms of depression and non-response to psychological therapy. Future work may enhance the prospective prediction of treatment-response by examining larger samples of individuals undertaking standardised treatment programmes.

Tryptophan Metabolites Are Associated With Symptoms and Nigral Pathology in Parkinson's Disease.

BackgroundThe objective of this study was to determine whether neurotoxic kynurenine metabolites, induced by inflammation, in plasma and cerebrospinal fluid (CSF) are associated with symptom severity and nigral pathology in Parkinson's disease (PD).MethodsClinical and MRI data were obtained from 97 PD and 89 controls. We used ultra‐performance liquid chromatography to quantify kynurenine metabolites and high‐sensitivity multiplex assays to quantify inflammation in plasma and CSF. We evaluated group‐wise differences as well as associations between the biomarkers, motor and nonmotor symptoms, and nigral R2* (MRI metric reflecting iron content).ResultsPD subjects had >100% higher 3‐hydroxykynurenine and 14% lower 3‐hydroxyanthranilic acid in plasma. The 3‐HK in plasma was closely associated with both symptom severity and disease duration. PD subjects also had 23% lower kynurenic acid in the CSF. Higher CSF levels of the excitotoxin quinolinic acid were associated with more severe symptoms, whereas lower levels of the neuroprotective kynurenic acid were linked to olfactory deficits. An elevated quinolinic acid/picolinic acid ratio in the CSF correlated with higher R2* values in the substantia nigra in the entire cohort. Plasma C‐reactive protein and serum amyloid alpha were associated with signs of increased kynurenine pathway activity in the CSF of PD patients, but not in controls.ConclusionsIn PD, the kynurenine pathway metabolite levels are altered in both the periphery and the central nervous system, and these changes are associated with symptom severity. Replication studies are warranted in other cohorts, and these can also explore if kynurenine metabolites might be PD biomarkers and/or are involved in PD pathogenesis. © 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

SAT-LB99 Inflammation May Mediate Coronary Artery Disease in Women With Hypothalamic Hypoestrogenemia: Findings From the NHLBI-Sponsored Women’s Ischemia Syndrome Evaluation (WISE)

Background: Among premenopausal women presenting with ischemia, hypothalamic hypoestrogenemia (HHE) has been associated with angiographic coronary artery disease (CAD). Further, serum amyloid-alpha (SAA), a marker of systemic inflammation strongly predicts future adverse cardiovascular events. We sought to relate inflammatory markers to HHE and understand if inflammation mediates relations between HHE and CAD. Methods: We assessed premenopausal women not on exogenous hormones undergoing coronary angiography for suspected ischemia. HHE was defined as estradiol<50 pg/ml, luteinizing hormone<10 IU/l and follicle stimulating hormone<10 IU/l. Serum inflammatory markers, reproductive hormones, and angiographic CAD were measured. Results: Overall, 40 (31%) of the 127 women had HHE with similar age and body mass index compared to no HHE (p=0.48 and p=0.77, respectively). Women with HHE had lower estradiol compared to no HHE (30.4+11.7 vs 112.5+62.4 pg/ml, p<0.0001). There were no significant differences between high sensitivity C-reactive protein (hsCRP) (0.86 ± 1.45 vs 0.65 ± 1.17, p=0.5211) and interleukin 6 (IL-6) (4.95 ± 6.06 vs 3.90 ± 3.90, p=0.2358). However, HHE women had significantly higher SAA compared to no HHE (4.44+13.5 vs 0.94+2.37, p=0.0495). Conclusion: Among premenopausal women undergoing coronary angiography for suspected myocardial ischemia, SAA levels were significantly elevated in women with HHE, suggesting that inflammation may serve as a mediator between HHE and CAD. Further investigation relative to inflammation as a treatment target in this cohort may be warranted.

Serum Amyloid Alpha Is Downregulated in Peripheral Tissues of Parkinson’s Disease Patients

We report the changed levels of serum amyloid alpha, an immunologically active protein, in Parkinson’s disease (PD) patients’ peripheral tissues. We have previously shown that Saa-1 and -2 (serum amyloid alpha-1,-2, genes) were among the top downregulated genes in PD patients’ skin, using whole-genome RNA sequencing. In the current study, we characterized the gene and protein expression profiles of skin and blood samples from patients with confirmed PD diagnosis and age/sex matched controls. qRT-PCR analysis of PD skin demonstrated downregulation of Saa-1 and -2 genes in PD patients. However, the lowered amount of protein could not be visualized using immunohistochemistry, due to low quantity of SAA (Serum Amyloid Alpha, protein) in skin. Saa-1 and -2 expression levels in whole blood were below detection threshold based on RNA sequencing, however significantly lowered protein levels of SAA1/2 in PD patients’ serum were shown with ELISA, implying that SAA is secreted into the blood. These results show that SAA is differentially expressed in the peripheral tissues of PD patients.

Single and combined effects of inflammatory markers on 10year diabetes incidence: The mediating role of adiposity-Results from the ATTICA cohort study.

The role of inflammation in diabetes development is not fully elucidated. The aim of this work was to investigate the independent effect of individual inflammatory markers and combinations of them on diabetes incidence and the potential mediating role of obesity. In 2001 to 2002, a random sample of 1514 men (18-87years old) and 1528 women (18-89years old) was selected to participate in the ATTICA study, where Athens is a major metropolis. Interleukin-6 (IL-6), C-reactive protein (CRP), tumour necrosis factor-alpha, serum amyloid alpha, fibrinogen, and homocysteine were measured. Covariates included various clinical, demographic, and lifestyle characteristics, assessed with standard procedures. In 2012, the 10year follow-up was performed. Diabetes diagnosis was defined according to American Diabetes Association criteria among n=1485 participants. One hundred ninety-one incident cases of diabetes were documented, yielding an incidence of 12.9% (13.4% in men and 12.4% in women). After adjustments, only elevated IL-6 increased by 2.2 times the 10year diabetes risk (third vs first tertile, 95% CI: 1.13, 4.28). After investigating combinations of inflammatory markers, combined elevated levels of CRP and IL-6 or CRP and fibrinogen (both markers ≥75th percentile vs <75th percentile) increased the risk by 1.93 times (95% CI: 1.20, 3.08) and 2.37 times (95% CI: 1.37, 4.16), respectively. Body mass index was found to significantly mediate the aggravating effect of inflammation. The reported results underline the significant role of individual IL-6 or combinations of CRP-IL-6 and CRP-fibrinogen in diabetes prediction. Adiposity seems to be primarily responsible for an increase in inflammatory markers, leading through this mechanism to insulin resistance and increasing diabetes risk.

Inflammatory biomarkers CRP, MCP-1, serum amyloid alpha and interleukin-18 in patients with HTN and dyslipidemia: impact of diabetes mellitus on metabolic syndrome and the effect of statin therapy

The objective of this study was to determine the relationship of HTN (HTN) and the inflammatory markers C-reactive protein (CRP), monocyte chemoattractant protein-1 (MCP-1), amyloid alpha (AA) and interleukin-18 (IL-18) in persons with HTN, considering concomitant diabetes mellitus (DM) or metabolic syndrome (MS). This was a multicenter twelve-week, single-step titration, open-label study of individuals with dyslipidemia, assigned according to their initial risk assessment, to atorvastatin starting doses of 10, 20, 40 or 80 mg. In subjects with HTN (N=677) versus no HTN (N=581), there were significantly (P<0.02) higher levels of CRP, IL-18, MCP-1 and AA but not for IL-18 when combined with DM or MS, and AA or CRP when combined with MS. Systolic blood pressure significantly (P<0.02) correlated with CRP, MCP-1 and AA but not IL-18. The greatest increase in CRP was with HTN plus DM. Statin therapy produced significant dose-dependent reductions in CRP but not with similar changes in other inflammatory markers. In summary, these data suggest a complex relationship between inflammation and HTN with dyslipidemia. Although HTN is associated with an increase in these inflammatory markers, the associated conditions DM or MS lead to different patterns of increases-MCP-1 being the most consistently increased with HTN, the greatest CRP increase was with HTN and DM, and no relationship was found with IL-18 and HTN in the presence of DM or MS. In addition, there are different responses to statins depending on the nature of the inflammatory marker.

Serum amyloid alpha in parapneumonic effusions.

Study objectives. To assess serum amyloid alpha (SAA) pleural fluid levels in parapneumonic effusion (PPE) and to investigate SAA diagnostic performance in PPE diagnosis and outcome. Methods. We studied prospectively 57 consecutive patients with PPE (empyema (EMP), complicated (CPE), and uncomplicated parapneumonic effusion (UPE)). SAA, CRP, TNF-α, IL-1β, and IL-6 levels were evaluated in serum and pleural fluid at baseline. Patients were followed for 6-months to detect pleural thickening/loculations. Results. Pleural SAA levels (mg/dL) median(IQR) were significantly higher in CPE compared to UPE (P < 0.04); CRP levels were higher in EMP and CPE compared to UPE (P < 0.01). There was no significant difference between IL-1β, IL-6, TNF-α level in different PPE forms. No significant association between SAA levels and 6-month outcome was found. At 6-months, patients with no evidence of loculations/thickening had significantly higher pleural fluid pH, glucose levels (P = 0.03), lower LDH (P = 0.005), IL-1β levels (P = 0.001) compared to patients who presented pleural loculations/thickening. Conclusions. SAA is increased in complicated PPE, and it might be useful as a biomarker for UPE and CPE diagnosis. SAA levels did not demonstrate considerable diagnostic performance in identifying patients who develop pleural thickening/loculations after a PPE.

Two-protein signature of novel serological markers apolipoprotein-A2 and serum amyloid alpha predicts prognosis in patients with metastatic renal cell cancer and improves the currently used prognostic survival models

BackgroundIn metastatic renal cell cancer (mRCC), the Memorial Sloan-Kettering Cancer Center (MSKCC) risk model is widely used for clinical trial design and patient management. To improve prognostication, we applied proteomics to identify novel serological proteins associated with overall survival (OS). Patients and methodsSera from 114 mRCC patients were screened by surface-enhanced laser desorption ionization time-of-flight mass spectrometry (SELDI-TOF MS). Identified proteins were related to OS. Three proteins were subsequently validated with enzyme-linked immunosorbent assays and immunoturbidimetry. Prognostic models were statistically bootstrapped to correct for overestimation. ResultsSELDI-TOF MS detected 10 proteins associated with OS. Of these, apolipoprotein A2 (ApoA2), serum amyloid alpha (SAA) and transthyretin were validated for their association with OS (P = 5.5 × 10-9, P = 1.1 × 10-7 and P = 0.0004, respectively). Combining ApoA2 and SAA yielded a prognostic two-protein signature [Akaike's Information Criteria (AIC) = 732, P = 5.2 × 10-7]. Including previously identified prognostic factors, multivariable Cox regression analysis revealed ApoA2, SAA, lactate dehydrogenase, performance status and number of metastasis sites as independent factors for survival. Using these five factors, categorization of patients into three risk groups generated a novel protein-based model predicting patient prognosis (AIC = 713, P = 4.3 × 10-11) more robustly than the MSKCC model (AIC = 729, P = 1.3 × 10-7). Applying this protein-based model instead of the MSKCC model would have changed the risk group in 38% of the patients. ConclusionsProteomics and subsequent validation yielded two novel prognostic markers and survival models which improved prediction of OS in mRCC patients over commonly used risk models. Implementation of these models has the potential to improve current risk stratification, although prospective validation will still be necessary.

Green tea minimally affects biomarkers of inflammation in obese subjects with metabolic syndrome

Objective Green tea ( Camellia sinensis) has shown to exert cardioprotective benefits in observational studies. The objective of this clinical trial was to assess the effects of green tea on features of metabolic syndrome and inflammation in obese subjects. Methods We conducted a randomized controlled trial in obese subjects with metabolic syndrome. Thirty-five subjects [(mean ± SE) age 42.5 ± 1.7 y, body mass index 36.1 ± 1.3 kg/m 2] completed the 8-wk study and were randomly assigned to receive green tea (4 cups/d), green tea extract (2 capsules and 4 cups water/d), or no treatment (4 cups water/d). Both the beverage and extract groups had similar dosing of epigallocatechin-3-gallate, the active green tea polyphenol. Fasting blood samples were collected at screening, 4 and 8 wk of the study. Results Green tea beverage or extract supplementation did not significantly alter features of metabolic syndrome or biomarkers of inflammation including adiponectin, C-reactive protein, interleukin-6, interleukin-1β, soluble vascular cell adhesion molecule-1, soluble intercellular adhesion molecule-1, leptin, or leptin:adiponectin ratio. However, both green tea beverage and extracts significantly reduced plasma serum amyloid alpha versus no treatment ( P < 0.005). Conclusion This study suggests that the daily consumption of green tea beverage or extracts for 8 wk was well tolerated but did not affect the features of metabolic syndrome. However, green tea significantly reduced plasma serum amyloid alpha, an independent cardiovascular disease risk factor, in obese subjects with metabolic syndrome.

Identification of a 17-protein signature in the serum of lung cancer patients

Early detection of lung cancer may potentially help to improve the outcome of this fatal disease. Currently, no satisfactory laboratory tests are available to screen for this type of cancer. The aim of this study was to improve diagnostic procedures for lung cancer through the discovery of serum biomarkers using SELDI-TOF MS (surface-enhanced laser desorption/ionization time-of-flight mass spectrometry). Mass spectrometric profiling was applied to the serum of a total of 139 lung cancer patients and 158 healthy individuals for developing a prognostic signature. For validation, two separate groups were employed, comprising of 126 and 50 individuals, respectively. Informative regions of mass spectra were identified by forming protein mass clusters and identifying predictive clusters in a logistic regression model. A total of 17 differential predictive protein mass clusters were identified in patients with metastatic lung cancer disease compared to healthy individuals. These clusters provide for a robust risk prediction model. The sensitivity and specificity of this model was estimated to be 87.3 and 81.9%, respectively, for the first validation set, and 96.0 and 66.7%, respectively, for a second validation set of patients with early disease (stages I and II). A differential 11.5/11.7 kDa double-peak could be identified as serum amyloid alpha (SAA) by peptide mapping. Our data suggest that the SELDI-TOF MS technology in combination with a careful statistical analysis appears to be a useful experimental platform which delivers a rapid insight into the proteome of body fluids and may guide to identify novel biomarkers for lung cancer disease.

Use of serum proteins identified by proteomics to predict prognosis in patients with metastatic renal cell cancer (mRCC) and comparison to the currently used MSKCC survival model

11078 Background: In mRCC the Memorial Sloan-Kettering Cancer Center (MSKCC) risk model (Motzer et al.,JCO2002) is widely used for clinical trial design and patient management. To improve this model, we searched for serum proteins associated with overall survival (OS) using proteomics and determined their potential contribution to the composition of better prognostic models. Methods: Sera from 125 mRCC patients, mostly interferon-treated, collected between 2001–2006 in three Dutch Cancer Centers, were screened by SELDI-TOF mass spectrometry (MS). Identified proteins were analyzed for their association with OS by Cox regression analysis and Kaplan-Meier curves. Three proteins were subsequently validated with conventional ELISAs and immunoturbidimetry. Computed Cox PH regression models were individually compared with the Akaike's Information Criteria (AIC). The final model was statistically bootstrapped to strengthen its validity. Results: SELDI-TOF MS successfully detected eleven prognostic proteins associated with OS. The strongest prognostic proteins, apolipoprotein A-II (ApoA2), serum amyloid alpha (SAA), and transthyretin were validated by alternative methods and confirmed for their association with OS (p=7.4×10-9, p=3.2×10-8 and p=0.0002, respectively). Stepwise multivariable Cox regression analysis provided an optimal combination of prognostic factors; ApoA2, SAA, LDH, performance status and number of metastasis sites. Subsequent categorization of patients into three risk groups generated a novel survival model that robustly predicts patient prognosis (AIC=684 and p=5.8×10-15) with increased accuracy compared to the MSKCC model (AIC=719, p=2.0×10-7). Bootstrapping our model resulted in an optimism correction of 0.04 (R2=0.45). Initiating systemic therapy according to novel proposed model instead of the MSKCC model would result in a change of treatment in 14% of the patients. Conclusions: Using proteomics, serum proteins associated with OS in mRCC patients can be identified. Incorporating some of these factors together with traditional risk factors yields a prognostic model outperforming the MSKCC risk model thereby further improving patients’ management. No significant financial relationships to disclose.

Consumption of Green Tea Bioactive Compounds Alters Expression of Inflammatory Cytokine mRNA

In a human study, we previously showed that consumption of capsules containing L‐theanine and a standardized amount of catechins (Green Tea Formula, GTF) for 21d resulted in fewer cold symptoms, increased γδ T cell proliferation, increased interferon‐γ secretion and reduced blood levels of serum amyloid alpha, an inflammatory biomarker. A targeted microarray analysis of PBMC cultured 24h with ethylamine (EA) identified changes in mRNA expression in subjects who consumed the GTF capsules. Quantitative RT‐PCR analysis verified higher levels of interferon‐γ and CCL3L1 mRNA expression in EA‐stimulated cells after GTF intake compared to before consumption, consistent with the idea that the immune cells were primed by GTF. Levels of CCL5 did not change, nor did levels of CD4 or IL‐7 mRNA. Consumption of GTF reduced CSF‐receptor 1 expression in non‐stimulated cells. CSF‐R1 expression is associated with survival of mature monocytes; down regulation promotes apoptosis and perhaps reduces inflammation. We conclude that this formulation based on green tea bioactive components will prime immunity without promoting inflammation. Funded in part by UF/IFAS Agriculture Experiment Station, Nature Trade Center, Inc., and Taiyo International, Inc.

α-1 Microglobulin as a New Inflammatory Marker in Newly Diagnosed Hypertensive Patients

The alpha-1 microglobulin (A1M) is considered to be a marker of renal insufficiency, suggesting disturbed tubular function. In the present study we examined the ability of urinary A1M excretion to reflect the overall inflammatory status in patients with newly diagnosed essential hypertension and normal renal function. The study population consisted of 1445 nondiabetic patients with newly diagnosed arterial hypertension and no evidence of renal insufficiency. Serum levels of C-reactive protein (CRP), serum amyloid alpha (SAA), and plasma fibrinogen, as well as urinary A1M excretion, were estimated. Multivariate analysis was performed to evaluate the associations between hypertension; A1M urinary excretion; and circulating levels of CRP, SAA, and fibrinogen. Patients with systolic hypertension had higher CRP, SAA, fibrinogen, and A1M compared with patients with isolated diastolic hypertension (P < .0001 for all). In multivariate analysis, systolic (but not diastolic) blood pressure (BP) was independently associated with A1M, CRP, and SAA (P < .0001 for all), whereas urinary A1M was also independently correlated with inflammatory markers such as CRP (P = .0001) and SAA (P = .0001). Urinary A1M is independently associated with circulating acute phase proteins in patients with newly diagnosed hypertension, whereas it is closely associated with systolic but not diastolic BP. Our findings suggest that urinary alpha-1 microglobulin may reflect the overall inflammatory status in patients with newly diagnosed essential hypertension, beyond its value as a marker of renal function.

A Standardized Green Tea Formula Lowers Serum Amyloid Alpha and Blood Pressure

A Standardized Green Tea Formula Lowers Serum Amyloid Alpha and Blood Pressure

Identifizierung von Biomarkern und therapeutischen Targets beim Nierenzellkarzinom mittels ProteinChip-Technologie

In order to understand tumour biology in its complexity, it is necessary to investigate the proteomics in addition to the DNA and RNA level. SELDI-TOF-MS represents a new technology allowing a highly sensitive high-throughput analysis to detect specific protein profiles. In renal cancer, it was possible to define specific protein patterns in serum. Several proteins have been identified, i.e. serum amyloid alpha (SAA). Analysis of tumour tissues leads to a better understanding of tumour biology and provides the basis for differential classification and evaluation of prognosis. Investigation of the proteome concerning therapy results opens up the possibility of assessing downstream effects on the one hand and identifying biomarkers for selection of patients and therapy monitoring on the other hand. This review presents the first results for renal cancer.

Serum Protein Profiling by SELDI Mass Spectrometry: Detection of Multiple Variants of Serum Amyloid Alpha in Renal Cancer Patients

Serum Protein Profiling by SELDI Mass Spectrometry: Detection of Multiple Variants of Serum Amyloid Alpha in Renal Cancer Patients