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Several inflammation scores have shown association with survival outcomes for patients with neuroendocrine tumours (NET) treated with peptide receptor radionuclide therapy (PRRT). However, whether these scores add value to established prognostic factors remains unknown. In this retrospective, cohort study of 557 NET patients undergoing PRRT in a tertiary referral centre from 2005 to 2015, we examined inflammatory markers and scores previously associated with cancer outcomes, using Cox proportional hazard models and Akaike's information criterion. Lower albumin (hazard ratio [95% confidence interval], .91 [.87-.95] per unit), as well as higher C-reactive protein (CRP; 1.02 [1.01-1.02]), Glasgow Prognostic Score (GPS; 1 vs. 0: 1.67 [1.14-2.44], 2 vs. 0 3.60 [2.24-5.79]), CRP/albumin ratio (1.84 [1.43-2.37]) and platelet count (Plt) x CRP, but not white blood cell, neutrophil and thrombocyte counts or derived neutrophil to lymphocyte ratio (dNLR), were associated with shorter median overall survival (OS) in an adjusted analysis. The addition of parameters based on albumin and CRP, but not dNLR, to a base model including age, chromogranin A, the cell proliferation marker Ki-67, performance status, tumour site and previous treatments improved the predictive accuracy of the base model. In an exploratory analysis of patients with available erythrocyte sedimentation rate (ESR) and CRP, ESR emerged as the most powerful predictor. When added to a prognostic model for OS in NET patients treated with PRRT, most inflammation scores further improved the model. Albumin was the single marker adding most value to the set of established prognostic markers, whereas dNLR did not seem to improve the model's prognostic ability.

Background: Handgrip strength (HGS) is a surrogate marker of whole body strength that has been observed to correlate inversely with the metabolic syndrome (MetS). In this study, we examined whether HGS in young, healthy individuals, was associated with surrogate endpoints of the MetS. A secondary goal was to examine whether absolute HGS (absHGS) or relative HGS (relHGS) was a stronger predictor of MetS. Method: 834 subjects (577 women), aged 18–26, were recruited. Surrogate endpoints for MetS were waist circumference, HDL, fasting glucose, fasting insulin, triglycerides, and systolic and diastolic blood pressure (BP). We also examined the association between HGS and body fat percentage, HOMA-IR, CRP, orosomucoid and apolipoprotein A-1 and apolipoprotein B. The associations were examined using multivariable linear regression. Results: AbsHGS and relHGS were each associated with several surrogate endpoints of the metabolic syndrome, with RelHGS being statistically significantly associated with a greater number of the variables – all except fasting glucose and diastolic BP. Conclusion: RelHGS correlates with components of the MetS even in young, healthy populations. It is a better predictor of MetS components than absHGS. As a cheap and easy to use biomarker, relHGS holds merit as a screening tool for metabolic dysfunction even in preclinical contexts.

Several inflammation scores have shown association with survival outcomes for patients with neuroendocrine tumours (NET) treated with peptide receptor radionuclide therapy (PRRT). However, whether these scores add value to established prognostic factors remains unknown. In this retrospective, cohort study of 557 NET patients undergoing PRRT in a tertiary referral centre from 2005 to 2015, we examined inflammatory markers and scores previously associated with cancer outcomes, using Cox proportional hazard models and Akaike's information criterion. Lower albumin (hazard ratio [95% confidence interval], .91 [.87-.95] per unit), as well as higher C-reactive protein (CRP; 1.02 [1.01-1.02]), Glasgow Prognostic Score (GPS; 1 vs. 0: 1.67 [1.14-2.44], 2 vs. 0 3.60 [2.24-5.79]), CRP/albumin ratio (1.84 [1.43-2.37]) and platelet count (Plt) x CRP, but not white blood cell, neutrophil and thrombocyte counts or derived neutrophil to lymphocyte ratio (dNLR), were associated with shorter median overall survival (OS) in an adjusted analysis. The addition of parameters based on albumin and CRP, but not dNLR, to a base model including age, chromogranin A, the cell proliferation marker Ki-67, performance status, tumour site and previous treatments improved the predictive accuracy of the base model. In an exploratory analysis of patients with available erythrocyte sedimentation rate (ESR) and CRP, ESR emerged as the most powerful predictor. When added to a prognostic model for OS in NET patients treated with PRRT, most inflammation scores further improved the model. Albumin was the single marker adding most value to the set of established prognostic markers, whereas dNLR did not seem to improve the model's prognostic ability.

Several inflammation scores have shown association with survival outcomes for patients with neuroendocrine tumours (NET) treated with peptide receptor radionuclide therapy (PRRT). However, whether these scores add value to established prognostic factors remains unknown. In this retrospective, cohort study of 557 NET patients undergoing PRRT in a tertiary referral centre from 2005 to 2015, we examined inflammatory markers and scores previously associated with cancer outcomes, using Cox proportional hazard models and Akaike's information criterion. Lower albumin (hazard ratio [95% confidence interval], .91 [.87-.95] per unit), as well as higher C-reactive protein (CRP; 1.02 [1.01-1.02]), Glasgow Prognostic Score (GPS; 1 vs. 0: 1.67 [1.14-2.44], 2 vs. 0 3.60 [2.24-5.79]), CRP/albumin ratio (1.84 [1.43-2.37]) and platelet count (Plt) x CRP, but not white blood cell, neutrophil and thrombocyte counts or derived neutrophil to lymphocyte ratio (dNLR), were associated with shorter median overall survival (OS) in an adjusted analysis. The addition of parameters based on albumin and CRP, but not dNLR, to a base model including age, chromogranin A, the cell proliferation marker Ki-67, performance status, tumour site and previous treatments improved the predictive accuracy of the base model. In an exploratory analysis of patients with available erythrocyte sedimentation rate (ESR) and CRP, ESR emerged as the most powerful predictor. When added to a prognostic model for OS in NET patients treated with PRRT, most inflammation scores further improved the model. Albumin was the single marker adding most value to the set of established prognostic markers, whereas dNLR did not seem to improve the model's prognostic ability.

Background: Handgrip strength (HGS) is a surrogate marker of whole body strength that has been observed to correlate inversely with the metabolic syndrome (MetS). In this study, we examined whether HGS in young, healthy individuals, was associated with surrogate endpoints of the MetS. A secondary goal was to examine whether absolute HGS (absHGS) or relative HGS (relHGS) was a stronger predictor of MetS. Method: 834 subjects (577 women), aged 18–26, were recruited. Surrogate endpoints for MetS were waist circumference, HDL, fasting glucose, fasting insulin, triglycerides, and systolic and diastolic blood pressure (BP). We also examined the association between HGS and body fat percentage, HOMA-IR, CRP, orosomucoid and apolipoprotein A-1 and apolipoprotein B. The associations were examined using multivariable linear regression. Results: AbsHGS and relHGS were each associated with several surrogate endpoints of the metabolic syndrome, with RelHGS being statistically significantly associated with a greater number of the variables – all except fasting glucose and diastolic BP. Conclusion: RelHGS correlates with components of the MetS even in young, healthy populations. It is a better predictor of MetS components than absHGS. As a cheap and easy to use biomarker, relHGS holds merit as a screening tool for metabolic dysfunction even in preclinical contexts.

Several inflammation scores have shown association with survival outcomes for patients with neuroendocrine tumours (NET) treated with peptide receptor radionuclide therapy (PRRT). However, whether these scores add value to established prognostic factors remains unknown. In this retrospective, cohort study of 557 NET patients undergoing PRRT in a tertiary referral centre from 2005 to 2015, we examined inflammatory markers and scores previously associated with cancer outcomes, using Cox proportional hazard models and Akaike's information criterion. Lower albumin (hazard ratio [95% confidence interval], .91 [.87-.95] per unit), as well as higher C-reactive protein (CRP; 1.02 [1.01-1.02]), Glasgow Prognostic Score (GPS; 1 vs. 0: 1.67 [1.14-2.44], 2 vs. 0 3.60 [2.24-5.79]), CRP/albumin ratio (1.84 [1.43-2.37]) and platelet count (Plt) x CRP, but not white blood cell, neutrophil and thrombocyte counts or derived neutrophil to lymphocyte ratio (dNLR), were associated with shorter median overall survival (OS) in an adjusted analysis. The addition of parameters based on albumin and CRP, but not dNLR, to a base model including age, chromogranin A, the cell proliferation marker Ki-67, performance status, tumour site and previous treatments improved the predictive accuracy of the base model. In an exploratory analysis of patients with available erythrocyte sedimentation rate (ESR) and CRP, ESR emerged as the most powerful predictor. When added to a prognostic model for OS in NET patients treated with PRRT, most inflammation scores further improved the model. Albumin was the single marker adding most value to the set of established prognostic markers, whereas dNLR did not seem to improve the model's prognostic ability.

BACKGROUND: The C-reactive protein/albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, yet less is known about if CAR is superior to C-reactive protein (CRP) in the general population. METHODS: Prospective study design on the UK Biobank, where serum samples of CRP and Albumin were used. Cox regression analyses were conducted to assess all-cause and cardiovascular mortality, myocardial infarction, ischemic stroke, and heart failure over a follow-up period of approximately 12.5 years. The Cox model was adjusted for established cardiovascular disease (CVD) risk factors, including age, sex, smoking habits, physical activity level, BMI level, systolic blood pressure, LDL-cholesterol, statin treatment, diabetes, and previous CVD, with hazard ratios (HRs) and corresponding 95% confidence intervals (CIs). Analyses were also stratified by sex, CRP level (< 10 and ≥ 10 mg/ml) and age (< 60 and ≥ 60 years). RESULTS: In total, 411,506 individuals (186,043 men and 225,463 women) were included. In comparisons between HRs for all adverse outcomes, the results were similar or identical for CAR and CRP. For example, both CAR and CRP, adjusted HRs for all-cause mortality were 1.13 (95% CI 1.12-1.14). Regarding CVD mortality, the adjusted HR for CAR was 1.14 (95% CI 1.12-1.15), while for CRP, it was 1.13 (95% CI 1.11-1.15). CONCLUSIONS: Within this study CAR was not superior to CRP in predictive ability of mortality or CVD disorders. CLINICAL TRIAL REGISTRATION NUMBER: Not applicable (cohort study).

Background: High fat diet causes oxidation of accumulated fat cells which leads to Atherosclerosis. The inflammatory marker C-reactive protein has recently been identified as an independent predictor of future coronary heart disease. The inflammatory marker C-reactive protein has recently been identified as an independent predictor of future coronary heart disease. Present study evaluated the cardioprotective role of Ajwa seed paste on lipid profile and C-reactive protein (CRP) level in rabbits. Methodology: 7 months old rabbits (n=15) for 30 days were kept in animal house school under standard laboratory conditions. Rabbits were divided into three groups (n=5). Group1 served as control group fed basal diet, group 2 fed high fat diet, group 3 fed high fat diet supplemented with 6gm ajwa seed paste. Feed consumption ratio was determined in all groups on daily basis. Results: Feed consumption ratio showed significant (P>0.05) decrease in group 2and 3 fed high fat diet. In this study, lipid profile (cholesterol, triglyceride, LDL and VLDL) values were increased in group 2 compared to control group. It was found that significant (P>0.05) decrease in the level of bad cholesterol (LDL, VLDL) in group 3 (fed ajwa seed supplemented diet).HDL value showed significant (P>0.05) increase in group 3. HDL is good cholesterol and increased the level of HDL protect against the stroke and heart attack. and increase the level of good cholesterol (HDL).HDL takes the cholesterol from the body and back to liver where liver removes the bad cholesterol. The value of CRP is higher in group 2 due to the consumption of HFD and CRP level in group 3 showed significant (P>0.05) reduction. Conclusion: It is concluded from present study that ajwa seed paste is beneficial for heart health.

Background: High fat diet causes oxidation of accumulated fat cells which leads to Atherosclerosis. The inflammatory marker C-reactive protein has recently been identified as an independent predictor of future coronary heart disease. The inflammatory marker C-reactive protein has recently been identified as an independent predictor of future coronary heart disease. Present study evaluated the cardioprotective role of Ajwa seed paste on lipid profile and C-reactive protein (CRP) level in rabbits. Methodology: 7 months old rabbits (n=15) for 30 days were kept in animal house school under standard laboratory conditions. Rabbits were divided into three groups (n=5). Group1 served as control group fed basal diet, group 2 fed high fat diet, group 3 fed high fat diet supplemented with 6gm ajwa seed paste. Feed consumption ratio was determined in all groups on daily basis. Results: Feed consumption ratio showed significant (P>0.05) decrease in group 2and 3 fed high fat diet. In this study, lipid profile (cholesterol, triglyceride, LDL and VLDL) values were increased in group 2 compared to control group. It was found that significant (P>0.05) decrease in the level of bad cholesterol (LDL, VLDL) in group 3 (fed ajwa seed supplemented diet).HDL value showed significant (P>0.05) increase in group 3. HDL is good cholesterol and increased the level of HDL protect against the stroke and heart attack. and increase the level of good cholesterol (HDL).HDL takes the cholesterol from the body and back to liver where liver removes the bad cholesterol. The value of CRP is higher in group 2 due to the consumption of HFD and CRP level in group 3 showed significant (P>0.05) reduction. Conclusion: It is concluded from present study that ajwa seed paste is beneficial for heart health.

BACKGROUND: The C-reactive protein/albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, yet less is known about if CAR is superior to C-reactive protein (CRP) in the general population. METHODS: Prospective study design on the UK Biobank, where serum samples of CRP and Albumin were used. Cox regression analyses were conducted to assess all-cause and cardiovascular mortality, myocardial infarction, ischemic stroke, and heart failure over a follow-up period of approximately 12.5 years. The Cox model was adjusted for established cardiovascular disease (CVD) risk factors, including age, sex, smoking habits, physical activity level, BMI level, systolic blood pressure, LDL-cholesterol, statin treatment, diabetes, and previous CVD, with hazard ratios (HRs) and corresponding 95% confidence intervals (CIs). Analyses were also stratified by sex, CRP level (< 10 and ≥ 10 mg/ml) and age (< 60 and ≥ 60 years). RESULTS: In total, 411,506 individuals (186,043 men and 225,463 women) were included. In comparisons between HRs for all adverse outcomes, the results were similar or identical for CAR and CRP. For example, both CAR and CRP, adjusted HRs for all-cause mortality were 1.13 (95% CI 1.12-1.14). Regarding CVD mortality, the adjusted HR for CAR was 1.14 (95% CI 1.12-1.15), while for CRP, it was 1.13 (95% CI 1.11-1.15). CONCLUSIONS: Within this study CAR was not superior to CRP in predictive ability of mortality or CVD disorders. CLINICAL TRIAL REGISTRATION NUMBER: Not applicable (cohort study).

Background/Objective: Systemic inflammation is common in chronic obstructive pulmonary disease (COPD), and evidence suggests that inflammatory biomarkers can predict acute exacerbations (AECOPDs). The aim of this study was to analyse whether C-reactive protein (CRP), fibrinogen, white blood cell count (WBC), or the blood cell indices PLR (platelet-to-lymphocyte ratio), SII (systemic immune inflammation index), SIRI (systemic inflammation response index), and AISI (aggregate index of systemic inflammation) can predict future AECOPDs. Methods: In the Tools Identifying Exacerbations (TIE) cohort study, participants with spirometry-confirmed COPD were recruited from primary and secondary care in three Swedish regions and assessed during a stable phase of COPD. AECOPD frequency during the three-year follow-up was reviewed in medical records. Associations were analysed via ordinal logistic regressions. Results: Of the 571 participants, 46% had >= 1 AECOPD during follow-up, and the mean +/- SD AECOPD frequency was 0.63 +/- 1.2/year. In unadjusted analyses, high levels of CRP (odds ratio 1.86, 95% CI 1.29-2.67), fibrinogen (2.09, 1.38-3.16), WBCs (2.18, 1.52-3.13), SII (1.52, 1.05-2.19), SIRI (1.76, 1.23-2.52), and AISI (1.99, 1.38-2.87) were associated with a higher AECOPD frequency. After adjustment for AECOPD history, age, sex, smoking, body mass index, COPD Assessment Test score, lung function, and inhaled corticosteroid use, associations remained for high levels of CRP (adjusted odds ratio of 1.64; 95% CI of 1.08-2.49), fibrinogen (1.55; 1.07-2.24), and WBC (1.65; 1.10-2.47). Conclusions: CRP, fibrinogen, and WBC, assessed during stable-phase COPD, enhanced AECOPD prediction, whereas PLR, SII, SIRI, and AISI did not.

Background: High fat diet causes oxidation of accumulated fat cells which leads to Atherosclerosis. The inflammatory marker C-reactive protein has recently been identified as an independent predictor of future coronary heart disease. The inflammatory marker C-reactive protein has recently been identified as an independent predictor of future coronary heart disease. Present study evaluated the cardioprotective role of Ajwa seed paste on lipid profile and C-reactive protein (CRP) level in rabbits. Methodology: 7 months old rabbits (n=15) for 30 days were kept in animal house school under standard laboratory conditions. Rabbits were divided into three groups (n=5). Group1 served as control group fed basal diet, group 2 fed high fat diet, group 3 fed high fat diet supplemented with 6gm ajwa seed paste. Feed consumption ratio was determined in all groups on daily basis. Results: Feed consumption ratio showed significant (P>0.05) decrease in group 2and 3 fed high fat diet. In this study, lipid profile (cholesterol, triglyceride, LDL and VLDL) values were increased in group 2 compared to control group. It was found that significant (P>0.05) decrease in the level of bad cholesterol (LDL, VLDL) in group 3 (fed ajwa seed supplemented diet).HDL value showed significant (P>0.05) increase in group 3. HDL is good cholesterol and increased the level of HDL protect against the stroke and heart attack. and increase the level of good cholesterol (HDL).HDL takes the cholesterol from the body and back to liver where liver removes the bad cholesterol. The value of CRP is higher in group 2 due to the consumption of HFD and CRP level in group 3 showed significant (P>0.05) reduction. Conclusion: It is concluded from present study that ajwa seed paste is beneficial for heart health.

BACKGROUND: The C-reactive protein/albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, yet less is known about if CAR is superior to C-reactive protein (CRP) in the general population. METHODS: Prospective study design on the UK Biobank, where serum samples of CRP and Albumin were used. Cox regression analyses were conducted to assess all-cause and cardiovascular mortality, myocardial infarction, ischemic stroke, and heart failure over a follow-up period of approximately 12.5 years. The Cox model was adjusted for established cardiovascular disease (CVD) risk factors, including age, sex, smoking habits, physical activity level, BMI level, systolic blood pressure, LDL-cholesterol, statin treatment, diabetes, and previous CVD, with hazard ratios (HRs) and corresponding 95% confidence intervals (CIs). Analyses were also stratified by sex, CRP level (< 10 and ≥ 10 mg/ml) and age (< 60 and ≥ 60 years). RESULTS: In total, 411,506 individuals (186,043 men and 225,463 women) were included. In comparisons between HRs for all adverse outcomes, the results were similar or identical for CAR and CRP. For example, both CAR and CRP, adjusted HRs for all-cause mortality were 1.13 (95% CI 1.12-1.14). Regarding CVD mortality, the adjusted HR for CAR was 1.14 (95% CI 1.12-1.15), while for CRP, it was 1.13 (95% CI 1.11-1.15). CONCLUSIONS: Within this study CAR was not superior to CRP in predictive ability of mortality or CVD disorders. CLINICAL TRIAL REGISTRATION NUMBER: Not applicable (cohort study).

Background/Objective: Systemic inflammation is common in chronic obstructive pulmonary disease (COPD), and evidence suggests that inflammatory biomarkers can predict acute exacerbations (AECOPDs). The aim of this study was to analyse whether C-reactive protein (CRP), fibrinogen, white blood cell count (WBC), or the blood cell indices PLR (platelet-to-lymphocyte ratio), SII (systemic immune inflammation index), SIRI (systemic inflammation response index), and AISI (aggregate index of systemic inflammation) can predict future AECOPDs. Methods: In the Tools Identifying Exacerbations (TIE) cohort study, participants with spirometry-confirmed COPD were recruited from primary and secondary care in three Swedish regions and assessed during a stable phase of COPD. AECOPD frequency during the three-year follow-up was reviewed in medical records. Associations were analysed via ordinal logistic regressions. Results: Of the 571 participants, 46% had >= 1 AECOPD during follow-up, and the mean +/- SD AECOPD frequency was 0.63 +/- 1.2/year. In unadjusted analyses, high levels of CRP (odds ratio 1.86, 95% CI 1.29-2.67), fibrinogen (2.09, 1.38-3.16), WBCs (2.18, 1.52-3.13), SII (1.52, 1.05-2.19), SIRI (1.76, 1.23-2.52), and AISI (1.99, 1.38-2.87) were associated with a higher AECOPD frequency. After adjustment for AECOPD history, age, sex, smoking, body mass index, COPD Assessment Test score, lung function, and inhaled corticosteroid use, associations remained for high levels of CRP (adjusted odds ratio of 1.64; 95% CI of 1.08-2.49), fibrinogen (1.55; 1.07-2.24), and WBC (1.65; 1.10-2.47). Conclusions: CRP, fibrinogen, and WBC, assessed during stable-phase COPD, enhanced AECOPD prediction, whereas PLR, SII, SIRI, and AISI did not.

BACKGROUND: The C-reactive protein/albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, yet less is known about if CAR is superior to C-reactive protein (CRP) in the general population. METHODS: Prospective study design on the UK Biobank, where serum samples of CRP and Albumin were used. Cox regression analyses were conducted to assess all-cause and cardiovascular mortality, myocardial infarction, ischemic stroke, and heart failure over a follow-up period of approximately 12.5 years. The Cox model was adjusted for established cardiovascular disease (CVD) risk factors, including age, sex, smoking habits, physical activity level, BMI level, systolic blood pressure, LDL-cholesterol, statin treatment, diabetes, and previous CVD, with hazard ratios (HRs) and corresponding 95% confidence intervals (CIs). Analyses were also stratified by sex, CRP level (< 10 and ≥ 10 mg/ml) and age (< 60 and ≥ 60 years). RESULTS: In total, 411,506 individuals (186,043 men and 225,463 women) were included. In comparisons between HRs for all adverse outcomes, the results were similar or identical for CAR and CRP. For example, both CAR and CRP, adjusted HRs for all-cause mortality were 1.13 (95% CI 1.12-1.14). Regarding CVD mortality, the adjusted HR for CAR was 1.14 (95% CI 1.12-1.15), while for CRP, it was 1.13 (95% CI 1.11-1.15). CONCLUSIONS: Within this study CAR was not superior to CRP in predictive ability of mortality or CVD disorders. CLINICAL TRIAL REGISTRATION NUMBER: Not applicable (cohort study).

BACKGROUND: The C-reactive protein/albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, yet less is known about if CAR is superior to C-reactive protein (CRP) in the general population. METHODS: Prospective study design on the UK Biobank, where serum samples of CRP and Albumin were used. Cox regression analyses were conducted to assess all-cause and cardiovascular mortality, myocardial infarction, ischemic stroke, and heart failure over a follow-up period of approximately 12.5 years. The Cox model was adjusted for established cardiovascular disease (CVD) risk factors, including age, sex, smoking habits, physical activity level, BMI level, systolic blood pressure, LDL-cholesterol, statin treatment, diabetes, and previous CVD, with hazard ratios (HRs) and corresponding 95% confidence intervals (CIs). Analyses were also stratified by sex, CRP level (< 10 and ≥ 10 mg/ml) and age (< 60 and ≥ 60 years). RESULTS: In total, 411,506 individuals (186,043 men and 225,463 women) were included. In comparisons between HRs for all adverse outcomes, the results were similar or identical for CAR and CRP. For example, both CAR and CRP, adjusted HRs for all-cause mortality were 1.13 (95% CI 1.12-1.14). Regarding CVD mortality, the adjusted HR for CAR was 1.14 (95% CI 1.12-1.15), while for CRP, it was 1.13 (95% CI 1.11-1.15). CONCLUSIONS: Within this study CAR was not superior to CRP in predictive ability of mortality or CVD disorders. CLINICAL TRIAL REGISTRATION NUMBER: Not applicable (cohort study).

Background/Objective: Systemic inflammation is common in chronic obstructive pulmonary disease (COPD), and evidence suggests that inflammatory biomarkers can predict acute exacerbations (AECOPDs). The aim of this study was to analyse whether C-reactive protein (CRP), fibrinogen, white blood cell count (WBC), or the blood cell indices PLR (platelet-to-lymphocyte ratio), SII (systemic immune inflammation index), SIRI (systemic inflammation response index), and AISI (aggregate index of systemic inflammation) can predict future AECOPDs. Methods: In the Tools Identifying Exacerbations (TIE) cohort study, participants with spirometry-confirmed COPD were recruited from primary and secondary care in three Swedish regions and assessed during a stable phase of COPD. AECOPD frequency during the three-year follow-up was reviewed in medical records. Associations were analysed via ordinal logistic regressions. Results: Of the 571 participants, 46% had >= 1 AECOPD during follow-up, and the mean +/- SD AECOPD frequency was 0.63 +/- 1.2/year. In unadjusted analyses, high levels of CRP (odds ratio 1.86, 95% CI 1.29-2.67), fibrinogen (2.09, 1.38-3.16), WBCs (2.18, 1.52-3.13), SII (1.52, 1.05-2.19), SIRI (1.76, 1.23-2.52), and AISI (1.99, 1.38-2.87) were associated with a higher AECOPD frequency. After adjustment for AECOPD history, age, sex, smoking, body mass index, COPD Assessment Test score, lung function, and inhaled corticosteroid use, associations remained for high levels of CRP (adjusted odds ratio of 1.64; 95% CI of 1.08-2.49), fibrinogen (1.55; 1.07-2.24), and WBC (1.65; 1.10-2.47). Conclusions: CRP, fibrinogen, and WBC, assessed during stable-phase COPD, enhanced AECOPD prediction, whereas PLR, SII, SIRI, and AISI did not.

BACKGROUND: The C-reactive protein/albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, yet less is known about if CAR is superior to C-reactive protein (CRP) in the general population. METHODS: Prospective study design on the UK Biobank, where serum samples of CRP and Albumin were used. Cox regression analyses were conducted to assess all-cause and cardiovascular mortality, myocardial infarction, ischemic stroke, and heart failure over a follow-up period of approximately 12.5 years. The Cox model was adjusted for established cardiovascular disease (CVD) risk factors, including age, sex, smoking habits, physical activity level, BMI level, systolic blood pressure, LDL-cholesterol, statin treatment, diabetes, and previous CVD, with hazard ratios (HRs) and corresponding 95% confidence intervals (CIs). Analyses were also stratified by sex, CRP level (< 10 and ≥ 10 mg/ml) and age (< 60 and ≥ 60 years). RESULTS: In total, 411,506 individuals (186,043 men and 225,463 women) were included. In comparisons between HRs for all adverse outcomes, the results were similar or identical for CAR and CRP. For example, both CAR and CRP, adjusted HRs for all-cause mortality were 1.13 (95% CI 1.12-1.14). Regarding CVD mortality, the adjusted HR for CAR was 1.14 (95% CI 1.12-1.15), while for CRP, it was 1.13 (95% CI 1.11-1.15). CONCLUSIONS: Within this study CAR was not superior to CRP in predictive ability of mortality or CVD disorders. CLINICAL TRIAL REGISTRATION NUMBER: Not applicable (cohort study).

Background/Objective: Systemic inflammation is common in chronic obstructive pulmonary disease (COPD), and evidence suggests that inflammatory biomarkers can predict acute exacerbations (AECOPDs). The aim of this study was to analyse whether C-reactive protein (CRP), fibrinogen, white blood cell count (WBC), or the blood cell indices PLR (platelet-to-lymphocyte ratio), SII (systemic immune inflammation index), SIRI (systemic inflammation response index), and AISI (aggregate index of systemic inflammation) can predict future AECOPDs. Methods: In the Tools Identifying Exacerbations (TIE) cohort study, participants with spirometry-confirmed COPD were recruited from primary and secondary care in three Swedish regions and assessed during a stable phase of COPD. AECOPD frequency during the three-year follow-up was reviewed in medical records. Associations were analysed via ordinal logistic regressions. Results: Of the 571 participants, 46% had >= 1 AECOPD during follow-up, and the mean +/- SD AECOPD frequency was 0.63 +/- 1.2/year. In unadjusted analyses, high levels of CRP (odds ratio 1.86, 95% CI 1.29-2.67), fibrinogen (2.09, 1.38-3.16), WBCs (2.18, 1.52-3.13), SII (1.52, 1.05-2.19), SIRI (1.76, 1.23-2.52), and AISI (1.99, 1.38-2.87) were associated with a higher AECOPD frequency. After adjustment for AECOPD history, age, sex, smoking, body mass index, COPD Assessment Test score, lung function, and inhaled corticosteroid use, associations remained for high levels of CRP (adjusted odds ratio of 1.64; 95% CI of 1.08-2.49), fibrinogen (1.55; 1.07-2.24), and WBC (1.65; 1.10-2.47). Conclusions: CRP, fibrinogen, and WBC, assessed during stable-phase COPD, enhanced AECOPD prediction, whereas PLR, SII, SIRI, and AISI did not.

BACKGROUND: The C-reactive protein/albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, yet less is known about if CAR is superior to C-reactive protein (CRP) in the general population. METHODS: Prospective study design on the UK Biobank, where serum samples of CRP and Albumin were used. Cox regression analyses were conducted to assess all-cause and cardiovascular mortality, myocardial infarction, ischemic stroke, and heart failure over a follow-up period of approximately 12.5 years. The Cox model was adjusted for established cardiovascular disease (CVD) risk factors, including age, sex, smoking habits, physical activity level, BMI level, systolic blood pressure, LDL-cholesterol, statin treatment, diabetes, and previous CVD, with hazard ratios (HRs) and corresponding 95% confidence intervals (CIs). Analyses were also stratified by sex, CRP level (< 10 and ≥ 10 mg/ml) and age (< 60 and ≥ 60 years). RESULTS: In total, 411,506 individuals (186,043 men and 225,463 women) were included. In comparisons between HRs for all adverse outcomes, the results were similar or identical for CAR and CRP. For example, both CAR and CRP, adjusted HRs for all-cause mortality were 1.13 (95% CI 1.12-1.14). Regarding CVD mortality, the adjusted HR for CAR was 1.14 (95% CI 1.12-1.15), while for CRP, it was 1.13 (95% CI 1.11-1.15). CONCLUSIONS: Within this study CAR was not superior to CRP in predictive ability of mortality or CVD disorders. CLINICAL TRIAL REGISTRATION NUMBER: Not applicable (cohort study).

Background/Objective: Systemic inflammation is common in chronic obstructive pulmonary disease (COPD), and evidence suggests that inflammatory biomarkers can predict acute exacerbations (AECOPDs). The aim of this study was to analyse whether C-reactive protein (CRP), fibrinogen, white blood cell count (WBC), or the blood cell indices PLR (platelet-to-lymphocyte ratio), SII (systemic immune inflammation index), SIRI (systemic inflammation response index), and AISI (aggregate index of systemic inflammation) can predict future AECOPDs. Methods: In the Tools Identifying Exacerbations (TIE) cohort study, participants with spirometry-confirmed COPD were recruited from primary and secondary care in three Swedish regions and assessed during a stable phase of COPD. AECOPD frequency during the three-year follow-up was reviewed in medical records. Associations were analysed via ordinal logistic regressions. Results: Of the 571 participants, 46% had >= 1 AECOPD during follow-up, and the mean +/- SD AECOPD frequency was 0.63 +/- 1.2/year. In unadjusted analyses, high levels of CRP (odds ratio 1.86, 95% CI 1.29-2.67), fibrinogen (2.09, 1.38-3.16), WBCs (2.18, 1.52-3.13), SII (1.52, 1.05-2.19), SIRI (1.76, 1.23-2.52), and AISI (1.99, 1.38-2.87) were associated with a higher AECOPD frequency. After adjustment for AECOPD history, age, sex, smoking, body mass index, COPD Assessment Test score, lung function, and inhaled corticosteroid use, associations remained for high levels of CRP (adjusted odds ratio of 1.64; 95% CI of 1.08-2.49), fibrinogen (1.55; 1.07-2.24), and WBC (1.65; 1.10-2.47). Conclusions: CRP, fibrinogen, and WBC, assessed during stable-phase COPD, enhanced AECOPD prediction, whereas PLR, SII, SIRI, and AISI did not.

BACKGROUND: The C-reactive protein/albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, yet less is known about if CAR is superior to C-reactive protein (CRP) in the general population. METHODS: Prospective study design on the UK Biobank, where serum samples of CRP and Albumin were used. Cox regression analyses were conducted to assess all-cause and cardiovascular mortality, myocardial infarction, ischemic stroke, and heart failure over a follow-up period of approximately 12.5 years. The Cox model was adjusted for established cardiovascular disease (CVD) risk factors, including age, sex, smoking habits, physical activity level, BMI level, systolic blood pressure, LDL-cholesterol, statin treatment, diabetes, and previous CVD, with hazard ratios (HRs) and corresponding 95% confidence intervals (CIs). Analyses were also stratified by sex, CRP level (< 10 and ≥ 10 mg/ml) and age (< 60 and ≥ 60 years). RESULTS: In total, 411,506 individuals (186,043 men and 225,463 women) were included. In comparisons between HRs for all adverse outcomes, the results were similar or identical for CAR and CRP. For example, both CAR and CRP, adjusted HRs for all-cause mortality were 1.13 (95% CI 1.12-1.14). Regarding CVD mortality, the adjusted HR for CAR was 1.14 (95% CI 1.12-1.15), while for CRP, it was 1.13 (95% CI 1.11-1.15). CONCLUSIONS: Within this study CAR was not superior to CRP in predictive ability of mortality or CVD disorders. CLINICAL TRIAL REGISTRATION NUMBER: Not applicable (cohort study).

Background: Handgrip strength (HGS) is a surrogate marker of whole body strength that has been observed to correlate inversely with the metabolic syndrome (MetS). In this study, we examined whether HGS in young, healthy individuals, was associated with surrogate endpoints of the MetS. A secondary goal was to examine whether absolute HGS (absHGS) or relative HGS (relHGS) was a stronger predictor of MetS. Method: 834 subjects (577 women), aged 18–26, were recruited. Surrogate endpoints for MetS were waist circumference, HDL, fasting glucose, fasting insulin, triglycerides, and systolic and diastolic blood pressure (BP). We also examined the association between HGS and body fat percentage, HOMA-IR, CRP, orosomucoid and apolipoprotein A-1 and apolipoprotein B. The associations were examined using multivariable linear regression. Results: AbsHGS and relHGS were each associated with several surrogate endpoints of the metabolic syndrome, with RelHGS being statistically significantly associated with a greater number of the variables – all except fasting glucose and diastolic BP. Conclusion: RelHGS correlates with components of the MetS even in young, healthy populations. It is a better predictor of MetS components than absHGS. As a cheap and easy to use biomarker, relHGS holds merit as a screening tool for metabolic dysfunction even in preclinical contexts.

BACKGROUND: Handgrip strength (HGS) is a surrogate marker of whole body strength that has been observed correlate inversely with the metabolic syndrome (MetS). In this study, we examined whether HGS in young, healthy individuals, was associated with surrogate endpoints of the MetS. A secondary goal was to examine whether absolute HGS (absHGS) or relative HGS (relHGS) was a stronger predictor of MetS. METHOD: 834 subjects (577 women), aged 18-26, were recruited. Surrogate endpoints for MetS were waist circumference, HDL, fasting glucose, fasting insulin, triglycerides, and systolic and diastolic blood pressure (BP). We also examined the association between HGS and body fat percentage, HOMA-IR, CRP, orosomucoid and apolipoprotein A-1 and apolipoprotein B. The associations were examined using linear regression. RESULTS: AbsHGS and relHGS were each associated with several surrogate endpoints of the metabolic syndrome, with RelHGS being statistically significantly associated with a greater number of the variables - all except fasting glucose and diastolic BP. CONCLUSION: RelHGS correlates with components of the MetS even in young, healthy populations. It is a better predictor of MetS components than absHGS. As a cheap and easy to use biomarker, relHGS holds merit as a screening tool for metabolic dysfunction even in preclinical contexts.

Background: Handgrip strength (HGS) is a surrogate marker of whole body strength that has been observed to correlate inversely with the metabolic syndrome (MetS). In this study, we examined whether HGS in young, healthy individuals, was associated with surrogate endpoints of the MetS. A secondary goal was to examine whether absolute HGS (absHGS) or relative HGS (relHGS) was a stronger predictor of MetS. Method: 834 subjects (577 women), aged 18–26, were recruited. Surrogate endpoints for MetS were waist circumference, HDL, fasting glucose, fasting insulin, triglycerides, and systolic and diastolic blood pressure (BP). We also examined the association between HGS and body fat percentage, HOMA-IR, CRP, orosomucoid and apolipoprotein A-1 and apolipoprotein B. The associations were examined using multivariable linear regression. Results: AbsHGS and relHGS were each associated with several surrogate endpoints of the metabolic syndrome, with RelHGS being statistically significantly associated with a greater number of the variables – all except fasting glucose and diastolic BP. Conclusion: RelHGS correlates with components of the MetS even in young, healthy populations. It is a better predictor of MetS components than absHGS. As a cheap and easy to use biomarker, relHGS holds merit as a screening tool for metabolic dysfunction even in preclinical contexts.

Background: Handgrip strength (HGS) is a surrogate marker of whole body strength that has been observed to correlate inversely with the metabolic syndrome (MetS). In this study, we examined whether HGS in young, healthy individuals, was associated with surrogate endpoints of the MetS. A secondary goal was to examine whether absolute HGS (absHGS) or relative HGS (relHGS) was a stronger predictor of MetS. Method: 834 subjects (577 women), aged 18–26, were recruited. Surrogate endpoints for MetS were waist circumference, HDL, fasting glucose, fasting insulin, triglycerides, and systolic and diastolic blood pressure (BP). We also examined the association between HGS and body fat percentage, HOMA-IR, CRP, orosomucoid and apolipoprotein A-1 and apolipoprotein B. The associations were examined using multivariable linear regression. Results: AbsHGS and relHGS were each associated with several surrogate endpoints of the metabolic syndrome, with RelHGS being statistically significantly associated with a greater number of the variables – all except fasting glucose and diastolic BP. Conclusion: RelHGS correlates with components of the MetS even in young, healthy populations. It is a better predictor of MetS components than absHGS. As a cheap and easy to use biomarker, relHGS holds merit as a screening tool for metabolic dysfunction even in preclinical contexts.

Background: Soluble P-selectin (sP-selectin) and high-sensitivity C-reactive protein (hsCRP) have previously been associated with hypertension, but the relation with out-of-office blood pressure (BP) and coronary artery calcification score is unknown. We aimed to examine the relationship between sP-selectin, hsCRP and home BP, as well as coronary artery calcification score and carotid artery plaques. Methods: In the Swedish CArdioPulmonary bioImage Study (SCAPIS), 5057 randomly selected participants were evaluated with office and home BP using the semi-automatic Omron M10-IT device. For this cross-sectional study, participants with sP-selectin <4 standard deviations above mean and hsCRP <5 mg/l, representing low-grade inflammation, were included. Using generalized linear models, these inflammatory markers were evaluated in relation to BP classifications, as well as coronary artery calcification score and carotid artery plaques. Results: Of participants, 4548 were included in the analyses. The median age was 57.2 (53.4–61.2) years, and 775 (17.0%) reported taking medication for hypertension. Participants in the highest quartile of sP-selectin [odds ratio (OR) 1.67, 95% confidence interval (CI) 1.40–1.98, P < 0.001] and hsCRP [OR 2.25, (95% CI 1.89–2.60), P < 0.001] were more likely to have sustained hypertension. Participants in the highest quartile of hsCRP were also more likely to have masked hypertension, OR (95% CI) 2.31 (1.72–3.10), P < 0.001 and carotid artery plaques, OR (95% CI) 1.21 (1.05–1.38), P = 0.007. Conclusion: Increased sP-selectin and hsCRP were independently associated with sustained hypertension. These findings indicate an association between hypertension and platelet activity, as expressed by sP-selectin.

Wildtype Escherichia coli cells cannot grow on L-1,2-propanediol, as the fucAO operon within the fucose (fuc) regulon is thought to be silent in the absence of L-fucose. Little information is available concerning the transcriptional regulation of this operon. Here, we first confirm that fucAO operon expression is highly inducible by fucose and is primarily attributable to the upstream operon promoter, while the fucO promoter within the 3'-end of fucA is weak and uninducible. Using 5'RACE, we identify the actual transcriptional start site (TSS) of the main fucAO operon promoter, refuting the originally proposed TSS. Several lines of evidence are provided showing that the fucAO locus is within a transcriptionally repressed region on the chromosome. Operon activation is dependent on FucR and Crp but not SrsR. Two Crp-cAMP binding sites previously found in the regulatory region are validated, where the upstream site plays a more critical role than the downstream site in operon activation. Furthermore, two FucR binding sites are identified, where the downstream site near the first Crp site is more important than the upstream site. Operon transcription relies on Crp-cAMP to a greater degree than on FucR. Our data strongly suggest that FucR mainly functions to facilitate the binding of Crp to its upstream site, which in turn activates the fucAO promoter by efficiently recruiting RNA polymerase.

Menopause leads to decreased estradiol levels affecting tissue health and causing local inflammation in the genital organs and urinary tract. The rise of blood C-reactive protein (CRP) levels in menopausal women may indicate systemic inflammation associated with estradiol decline. The aim of this study was to determine the relationship between serum estradiol and CRP levels on genitourinary syndrome in menopausal women. A cross-sectional study was conducted among menopausal women who had not experienced menstruation for at least 12 consecutive months at Prof. dr. Chairuddin P. Lubis Hospital, Medan, Indonesia, in 2023. Estradiol and CRP levels were measured using enzyme-linked immunosorbent assay (ELISA) and the presence of genitourinary syndrome was assessed using the Menopause-Specific Quality of Life (MENQOL) questionnaire. The mean levels of estradiol and CRP were compared to menopausal women with and without genitourinary syndrome with the Mann-Whitney test. To assess the correlation between estradiol and CRP levels, and between their levels with the presence of genitourinary symptoms, the Spearman correlation test was used. The genitourinary syndrome was reported in 25% of the total included menopausal women. Our data indicated that the mean estradiol levels were not significantly different between menopausal women with and without genitourinary syndrome (9.13±2.47 pg/mL vs 18.96±31.23 pg/mL, p=0.881). The mean serum CRP level of menopausal women with genitourinary syndrome (9.72±6.30 mg/L) was higher than that of women without the syndrome (2.09±1.26 mg/L) with p<0.001. In addition, serum CRP level, not estradiol, was correlated with the symptom score of genitourinary syndrome. This study highlights that to identify and manage genitourinary syndrome, monitoring of CRP levels is essential in menopausal women.

Metabolomics has gained much attention due to its potential to reveal molecular disease mechanisms and present viable biomarkers. This work uses a panel of untargeted serum metabolomes from 602 children from the COPSAC2010 mother–child cohort. The annotated part of the metabolome consists of 517 chemical compounds curated using automated procedures. We created a filtering method for the quantified metabolites using predicted quantitative structure–bioactivity relationships for the Tox21 database on nuclear receptors and stress response in cell lines. The metabolites measured in the children’s serums are predicted to affect specific targeted models, known for their significance in inflammation, immune function, and health outcomes. The targets from Tox21 have been used as targets with quantitative structure–activity relationships (QSARs). They were trained for ~7000 structures, saved as models, and then applied to the annotated metabolites to predict their potential bioactivities. The models were selected based on strict accuracy criteria surpassing random effects. After application, 52 metabolites showed potential bioactivity based on structural similarity with known active compounds from the Tox21 set. The filtered compounds were subsequently used and weighted by their bioactive potential to show an association with early childhood hs-CRP levels at six months in a linear model supporting a physiological adverse effect on systemic low-grade inflammation. Keywords: metabolomics; QSAR; inflammation; cortisol; cortisone; vitamin A; CRP, Metabolomics has gained much attention due to its potential to reveal molecular disease mechanisms and present viable biomarkers. This work uses a panel of untargeted serum metabolomes from 602 children from the COPSAC2010 mother–child cohort. The annotated part of the metabolome consists of 517 chemical compounds curated using automated procedures. We created a filtering method for the quantified metabolites using predicted quantitative structure–bioactivity relationships for the Tox21 database on nuclear receptors and stress response in cell lines. The metabolites measured in the children’s serums are predicted to affect specific targeted models, known for their significance in inflammation, immune function, and health outcomes. The targets from Tox21 have been used as targets with quantitative structure–activity relationships (QSARs). They were trained for ~7000 structures, saved as models, and then applied to the annotated metabolites to predict their potential bioactivities. The models were selected based on strict accuracy criteria surpassing random effects. After application, 52 metabolites showed potential bioactivity based on structural similarity with known active compounds from the Tox21 set. The filtered compounds were subsequently used and weighted by their bioactive potential to show an association with early childhood hs-CRP levels at six months in a linear model supporting a physiological adverse effect on systemic low-grade inflammation.

Metabolomics has gained much attention due to its potential to reveal molecular disease mechanisms and present viable biomarkers. This work uses a panel of untargeted serum metabolomes from 602 children from the COPSAC2010 mother–child cohort. The annotated part of the metabolome consists of 517 chemical compounds curated using automated procedures. We created a filtering method for the quantified metabolites using predicted quantitative structure–bioactivity relationships for the Tox21 database on nuclear receptors and stress response in cell lines. The metabolites measured in the children’s serums are predicted to affect specific targeted models, known for their significance in inflammation, immune function, and health outcomes. The targets from Tox21 have been used as targets with quantitative structure–activity relationships (QSARs). They were trained for ~7000 structures, saved as models, and then applied to the annotated metabolites to predict their potential bioactivities. The models were selected based on strict accuracy criteria surpassing random effects. After application, 52 metabolites showed potential bioactivity based on structural similarity with known active compounds from the Tox21 set. The filtered compounds were subsequently used and weighted by their bioactive potential to show an association with early childhood hs-CRP levels at six months in a linear model supporting a physiological adverse effect on systemic low-grade inflammation. Keywords: metabolomics; QSAR; inflammation; cortisol; cortisone; vitamin A; CRP, Metabolomics has gained much attention due to its potential to reveal molecular disease mechanisms and present viable biomarkers. This work uses a panel of untargeted serum metabolomes from 602 children from the COPSAC2010 mother–child cohort. The annotated part of the metabolome consists of 517 chemical compounds curated using automated procedures. We created a filtering method for the quantified metabolites using predicted quantitative structure–bioactivity relationships for the Tox21 database on nuclear receptors and stress response in cell lines. The metabolites measured in the children’s serums are predicted to affect specific targeted models, known for their significance in inflammation, immune function, and health outcomes. The targets from Tox21 have been used as targets with quantitative structure–activity relationships (QSARs). They were trained for ~7000 structures, saved as models, and then applied to the annotated metabolites to predict their potential bioactivities. The models were selected based on strict accuracy criteria surpassing random effects. After application, 52 metabolites showed potential bioactivity based on structural similarity with known active compounds from the Tox21 set. The filtered compounds were subsequently used and weighted by their bioactive potential to show an association with early childhood hs-CRP levels at six months in a linear model supporting a physiological adverse effect on systemic low-grade inflammation.

Several inflammation scores have shown association with survival outcomes for patients with neuroendocrine tumours (NET) treated with peptide receptor radionuclide therapy (PRRT). However, whether these scores add value to established prognostic factors remains unknown. In this retrospective, cohort study of 557 NET patients undergoing PRRT in a tertiary referral centre from 2005 to 2015, we examined inflammatory markers and scores previously associated with cancer outcomes, using Cox proportional hazard models and Akaike's information criterion. Lower albumin (hazard ratio [95% confidence interval], .91 [.87-.95] per unit), as well as higher C-reactive protein (CRP; 1.02 [1.01-1.02]), Glasgow Prognostic Score (GPS; 1 vs. 0: 1.67 [1.14-2.44], 2 vs. 0 3.60 [2.24-5.79]), CRP/albumin ratio (1.84 [1.43-2.37]) and platelet count (Plt) x CRP, but not white blood cell, neutrophil and thrombocyte counts or derived neutrophil to lymphocyte ratio (dNLR), were associated with shorter median overall survival (OS) in an adjusted analysis. The addition of parameters based on albumin and CRP, but not dNLR, to a base model including age, chromogranin A, the cell proliferation marker Ki-67, performance status, tumour site and previous treatments improved the predictive accuracy of the base model. In an exploratory analysis of patients with available erythrocyte sedimentation rate (ESR) and CRP, ESR emerged as the most powerful predictor. When added to a prognostic model for OS in NET patients treated with PRRT, most inflammation scores further improved the model. Albumin was the single marker adding most value to the set of established prognostic markers, whereas dNLR did not seem to improve the model's prognostic ability.

The inherent stochasticity of metabolism raises a critical question for understanding homeostasis: are cellular processes regulated in response to internal fluctuations? Here, we show that, in E. coli cells under constant external conditions, catabolic enzyme expression continuously responds to metabolic fluctuations. The underlying regulatory feedback is enabled by the cyclic AMP (cAMP) and cAMP receptor protein (CRP) system, which controls catabolic enzyme expression based on metabolite concentrations. Using single-cell microscopy, genetic constructs in which this feedback is disabled, and mathematical modeling, we show how fluctuations circulate through the metabolic and genetic network at sub-cell-cycle timescales. Modeling identifies four noise propagation modes, including one specific to CRP regulation. Together, these modes correctly predict noise circulation at perturbed cAMP levels. The cAMP-CRP system may thus have evolved to control internal metabolic fluctuations in addition to external growth conditions. We conjecture that second messengers may more broadly function to achieve cellular homeostasis.

Evolutionary algorithms have been successfully applied to attack Physically Unclonable Functions (PUFs). CMA-ES is recognized as the most powerful option for a type of attack called the reliability attack. In this paper, we take a step back and systematically evaluate several metaheuristics for the challenge-response pair-based attack on strong PUFs. Our results confirm that CMA-ES has the best performance, but we note several other algorithms with similar performance while having smaller computational costs.

This paper presents a study on the interplay between obstructive sleep apnea and metabolic syndrome.

Introduction: Mucormycosis is opportunistic fungal infection characterized by extensive inflammation, necrosis and infarction of the involved tissues. It is associated with rise in levels of inflammatory markers [Erythrocyte sedimentation rate (ESR) , C-reactive protein (CRP)]. This study was done to know the role of ESR, CRP as prognostic indicators in the treatment of covid-19 associated mucormycosis (CAM). Materials and Methods: : A retrospective descriptive study was conducted between May 2021 and December 2021 at a tertiary centre. 315 patients with post-covid ROCM (Rhino-orbito-cerebral mucormycosis) were included in study. ESR and CRP were sent for all patients at the time of admission. Postoperatively the same were  repeated on post-op (POD) day 7, day 14, and day 30 during follow-up. Results: 243 (77.14%) patients were male and 72 (22.86%) were female. 6 patients with stage IV ROCM had recurrence of the disease in the postoperative period. Mean  ESR values in these patients at the time of admission, POD-7, 14, 30 were 98.17, 68.17, 44.00, 80.33 respectively. Mean CRP values in these patients at the time of admission, POD-7, 14, 30 were 58.50, 48.17, 26.33,37.83 respectively. Conclusion: Serial measurements of inflammatory markers (ESR, CRP) levels helps in the diagnosis and prognostication of  ROCM along with clinical evaluation and imaging.

This paper presents a study on the interplay between obstructive sleep apnea and metabolic syndrome.

C-reactive protein (CRP)/Albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, which we aimed to study. As method we use a prospective study design; the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS; n = 912, women 50%; mean age 70 years, baseline 2001 and 2004, median follow-up 15.0 years, end of follow-up 2019) and the Uppsala Longitudinal Study of Adult Men (ULSAM, n = 924 mean age 71 years, baseline 1991-1995, median follow-up 15.6 years, end of follow-up 2016). Serum samples were used for analyses of CRP and Albumin. Cox regression analyses were performed for cardiovascular and all-cause mortality in models adjusting for several factors (age; physical activity; Interleukin-6; cardiovascular (CVD) risk factors: smoking, BMI level, systolic blood pressure, LDL-cholesterol, and diabetes), with 95% confidence interval (CI). When adjusting for age and CVD risk factors, CAR was significantly associated with cardiovascular mortality for meta-analyzed results from PIVUS and ULSAM, HR 1.09 (95% 1.01-1.18), but neither in PIVUS (HR 1.14, 95% CI 0.99-1.31) nor in ULSAM (1.07, 95% CI 0.98-1.17). Additionally, CAR was significantly associated with all-cause mortality in ULSAM 1.31 (95% CI 1.12-1.54) but not in PIVUS HRs 1.01 (95% 0.089-1.15). The predictive value of CAR was similar to CRP alone in PIVUS and ULSAM and slightly better than albumin for the prediction of CVD-mortality in ULSAM. In conclusion, CAR was not consistently associated with cardiovascular and all-cause mortality in the two cohorts. The prognostic value of CAR for long-term CVD-mortality was similar to CRP.

C-reactive protein (CRP)/Albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, which we aimed to study. As method we use a prospective study design; the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS; n = 912, women 50%; mean age 70 years, baseline 2001 and 2004, median follow-up 15.0 years, end of follow-up 2019) and the Uppsala Longitudinal Study of Adult Men (ULSAM, n = 924 mean age 71 years, baseline 1991-1995, median follow-up 15.6 years, end of follow-up 2016). Serum samples were used for analyses of CRP and Albumin. Cox regression analyses were performed for cardiovascular and all-cause mortality in models adjusting for several factors (age; physical activity; Interleukin-6; cardiovascular (CVD) risk factors: smoking, BMI level, systolic blood pressure, LDL-cholesterol, and diabetes), with 95% confidence interval (CI). When adjusting for age and CVD risk factors, CAR was significantly associated with cardiovascular mortality for meta-analyzed results from PIVUS and ULSAM, HR 1.09 (95% 1.01-1.18), but neither in PIVUS (HR 1.14, 95% CI 0.99-1.31) nor in ULSAM (1.07, 95% CI 0.98-1.17). Additionally, CAR was significantly associated with all-cause mortality in ULSAM 1.31 (95% CI 1.12-1.54) but not in PIVUS HRs 1.01 (95% 0.089-1.15). The predictive value of CAR was similar to CRP alone in PIVUS and ULSAM and slightly better than albumin for the prediction of CVD-mortality in ULSAM. In conclusion, CAR was not consistently associated with cardiovascular and all-cause mortality in the two cohorts. The prognostic value of CAR for long-term CVD-mortality was similar to CRP.

Amyotrophic lateral sclerosis (ALS) is a clinical diagnosis used to define a neurodegenerative process that involves progressive loss of voluntary muscle function and leads to death within 2-5 years after diagnosis, in most cases because of respiratory function failure. Respiratory vital capacity (VC) measurements are reproducible and strong predictors of survival. To understand the role of the innate immune response in progressive VC loss we evaluated ALS clinical trial and biomarker results from a 6-month phase 2 study of NP001, a regulator of innate immune function. All ALS baseline values were similar between treated and controls except for those > 65 years old who were excluded from analysis. Treated patients with plasma CRP ≥ 1.13 mg/L (high CRP) showed a 64% slower rate of VC decline compared with placebo and those with plasma CRP < 1.13 mg/L (low CRP) who showed no response. High CRP patients showed no age associated loss of VC whereas low CRP patients showed an age dependent loss of VC function. Plasma levels of serum amyloid A (SAA) were similarly elevated in high CRP patients consistent with ongoing innate immune activation. Plasma TGFB1 in high CRP treated patients was 95% higher than placebo at 6-months, confirming the activation and release of this anti-inflammatory factor by the innate immune alpha 2 macroglobulin (A2M) system. This report is the first to link a biomarker confirmed regulation of the innate immune system with a therapeutic approach for controlling VC loss in ALS patients.

C-reactive protein (CRP)/Albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, which we aimed to study. As method we use a prospective study design; the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS; n = 912, women 50%; mean age 70 years, baseline 2001 and 2004, median follow-up 15.0 years, end of follow-up 2019) and the Uppsala Longitudinal Study of Adult Men (ULSAM, n = 924 mean age 71 years, baseline 1991-1995, median follow-up 15.6 years, end of follow-up 2016). Serum samples were used for analyses of CRP and Albumin. Cox regression analyses were performed for cardiovascular and all-cause mortality in models adjusting for several factors (age; physical activity; Interleukin-6; cardiovascular (CVD) risk factors: smoking, BMI level, systolic blood pressure, LDL-cholesterol, and diabetes), with 95% confidence interval (CI). When adjusting for age and CVD risk factors, CAR was significantly associated with cardiovascular mortality for meta-analyzed results from PIVUS and ULSAM, HR 1.09 (95% 1.01-1.18), but neither in PIVUS (HR 1.14, 95% CI 0.99-1.31) nor in ULSAM (1.07, 95% CI 0.98-1.17). Additionally, CAR was significantly associated with all-cause mortality in ULSAM 1.31 (95% CI 1.12-1.54) but not in PIVUS HRs 1.01 (95% 0.089-1.15). The predictive value of CAR was similar to CRP alone in PIVUS and ULSAM and slightly better than albumin for the prediction of CVD-mortality in ULSAM. In conclusion, CAR was not consistently associated with cardiovascular and all-cause mortality in the two cohorts. The prognostic value of CAR for long-term CVD-mortality was similar to CRP.

There is an increasing incidence of coronary artery disease in India. We therefore need a tool to evaluate the severity and prognosis of this acute myocardial infarction. In acute myocardial infarction, the function of plaque rupture and inflammation has already been identified. Aim: To study the organization of LDL-C/HDL-C ratio and inflammatory marker CRP in acute myocardial infarction. Methods and Material: Patients who have been diagnosed as acute myocardial infarction (ST Elevation Acute myocardial Infarction or Unstable angina/Non ST Elevation Myocardial Infarction) and admitted to ICCU of Rajiv Gandhi institute of Medical Sciences, Kadapa, AP. are the subjects. Sample consists of 100 cases of acute myocardial infarction. Case history was taken from the patients, and studied according to proforma. Conclusion: Elevated levels of CRP are independent indicators of adverse effects. When contrast with the LDL / HDL ratio, CRP is used for risk stratification and as a prognostic predictor. These findings suggest that in patients with acute myocardial infarction, raised CRP Levels is significant as compared to LDL/HDL ratio.

Background: Anti-PD-(L)1 agents have revolutionized the treatment paradigms of non-small cell lung cancer (NSCLC), while predictive biomarkers are limited. It has been previously shown that systemic inflammation, indicated by elevated C-reactive protein (CRP) level, is associated with a poor prognosis in anti-PD-(L)1 treated. The aim of the study was to analyze the prognostic and predictive value of CRP in addition to traditional prognostic and predictive markers and tumor PD-L1 score. Methods: We identified all NSCLC patients (n = 329) who had undergone PD-L1 tumor proportion score (TPS) analysis at Oulu University Hospital 2015–22. CRP levels, treatment history, immune checkpoint inhibitor (ICI) therapy details, and survival were collected. The patients were categorized based on CRP levels (≤10 vs. >10) and PD-L1 TPS scores (<50 vs. ≥50). Results: In the whole cohort (n = 329), CRP level of ≤10 mg/L was associated with improved survival in univariate (HR 0.30, Cl 95% 0.22–0.41) and multivariate analyzes (HR 0.44, CI 95% 0.28–0.68). With ICI treated (n = 70), both CRP of ≤10 and PD-L1 TPS of ≥50 were associated with improved progression-free survival (PFS) in univariate (HR 0.51, CI 95% 0.27–0.96; HR 0.54, CI 95% 0.28–1.02) and multivariate (HR 0.48, CI 95% 0.26–0.90; HR 0.50, CI 95% 0.26–0.95) analyzes. The combination (PD-L1 TPS ≥50 and CRP >10) carried a high negative predictive value with a median PFS of 4.11 months (CI 95% 0.00–9.63), which was similar to patients with low PD-L1 (4.11 months, CI 95% 2.61–5.60). Conclusions: Adding plasma CRP levels to PD-L1 TPS significantly increased the predictive value of sole PD-L1. Furthermore, patients with high CRP beard little benefit from anti-PD-(L)1 therapies independent of PD-L1 score. The study highlights the combined evaluation of plasma CRP and PD-L1 TPS as a negative predictive marker for ICI therapies.

Evolutionary algorithms have been successfully applied to attack Physically Unclonable Functions (PUFs). CMA-ES is recognized as the most powerful option for a type of attack called the reliability attack. In this paper, we take a step back and systematically evaluate several metaheuristics for the challenge-response pair-based attack on strong PUFs. Our results confirm that CMA-ES has the best performance, but we note several other algorithms with similar performance while having smaller computational costs., Green Open Access added to TU Delft Institutional Repository ‘You share, we take care!’ – Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public., Cyber Security

The inherent stochasticity of metabolism raises a critical question for understanding homeostasis: are cellular processes regulated in response to internal fluctuations? Here, we show that, in E. coli cells under constant external conditions, catabolic enzyme expression continuously responds to metabolic fluctuations. The underlying regulatory feedback is enabled by the cyclic AMP (cAMP) and cAMP receptor protein (CRP) system, which controls catabolic enzyme expression based on metabolite concentrations. Using single-cell microscopy, genetic constructs in which this feedback is disabled, and mathematical modeling, we show how fluctuations circulate through the metabolic and genetic network at sub-cell-cycle timescales. Modeling identifies four noise propagation modes, including one specific to CRP regulation. Together, these modes correctly predict noise circulation at perturbed cAMP levels. The cAMP-CRP system may thus have evolved to control internal metabolic fluctuations in addition to external growth conditions. We conjecture that second messengers may more broadly function to achieve cellular homeostasis., BN/Sander Tans Lab

Background: In individuals with schizophrenia, inflammation is associated with depression, somatic comorbidity and reduced quality of life. Physical exercise is known to reduce inflammation in other populations, but we have only limited knowledge in the field of schizophrenia. We assessed inflammatory markers in plasma samples from individuals with schizophrenia participating in an exercise intervention randomized controlled trial. We hypothesized that (i) physical exercise would reduce levels of inflammatory markers and (ii) elevated inflammatory status at baseline would be associated with improvement in cardiorespiratory fitness (CRF) following intervention. Method: Eighty-two individuals with schizophrenia were randomized to a 12-week intervention of either high-intensity interval training (HIIT, n = 43) or active video gaming (AVG, n = 39). Participants were assessed at baseline, post intervention and four months later. The associations between exercise and the inflammatory markers soluble urokinase plasminogen activator receptor, c-reactive protein, tumor necrosis factor (TNF), soluble TNF receptor 1 and interleukin 6 (IL-6) were estimated using linear mixed effect models for repeated measures. For estimating associations between baseline inflammation and change in CRF, we used linear regression models. Results: Our main findings were (i) TNF and IL-6 increased during the intervention period for both groups. Other inflammatory markers did not change during the exercise intervention period; (ii) baseline inflammatory status did not influence change in CRF during intervention, except for a positive association between baseline IL-6 levels and improvements of CRF to post intervention for both groups. Conclusion: In our study, HIIT and AVG for 12-weeks had no reducing effect on inflammatory markers. Patients with high baseline IL-6 levels had a positive change in CRF during intervention. In order to increase our knowledge regarding association between inflammato

Background and methods: Inflammation is a hallmark of cancer and its progression. Plasma levels of C-reactive protein (CRP), interleukin-6 (IL-6) and YKL-40 reflect inflammation, and are elevated in patients with cancer. This study investigated whether plasma CRP, IL-6 and YKL-40 had diagnostic value in 753 patients referred with nonspecific signs and symptoms of cancer to a diagnostic outpatient clinic. Results: In total, 111 patients were diagnosed with cancer within 3 months and 30 after 3 months. CRP, IL-6 and YKL-40 were elevated in 44%, 60% and 45% of the cancer patients, and in 15%, 33% and 25% of the patients without cancer. Elevated levels of all three markers were associated with risk of cancer within 3 months: CRP (odds ratio (OR) 4.41, 95% confidence interval (CI) 2.86–6.81), IL-6 (OR = 2.89, 1.91–4.37) and YKL-40 (OR = 2.42, 1.59–3.66). Multivariate explorative analyses showed that increasing values were associated with the risk of getting a cancer diagnosis (continuous scale: CRP (OR = 1.28, 1.12–1.47), carcinoembryonic antigen (CEA) (OR = 1.61, 1.41–1.98), CA19-9 (OR = 1.15, 1.03–1.29), age (OR = 1.29, 1.02–1.63); dichotomized values: CRP (OR = 2.54, 1.39–4.66), CEA (OR = 4.22, 2.13–8.34), age (OR = 1.42, 1.13–1.80)). CRP had the highest diagnostic value (area under the curve = 0.69). Combined high CRP, IL-6 and YKL-40 was associated with short overall survival (HR = 3.8, 95% CI 2.5–5.9, p < 0.001). Conclusion: In conclusion, plasma CRP, IL-6 and YKL-40 alone or combined cannot be used to identify patients with cancer, but high levels were associated with poor prognosis. CRP may be useful to indicate whether further diagnostic evaluation is needed when patients present with nonspecific signs and symptoms of cancer.

C-reactive protein (CRP)/Albumin ratio (CAR) seems to mirror disease severity and prognosis in several acute disorders particularly in elderly patients, which we aimed to study. As method we use a prospective study design; the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS; n = 912, women 50%; mean age 70 years, baseline 2001 and 2004, median follow-up 15.0 years, end of follow-up 2019) and the Uppsala Longitudinal Study of Adult Men (ULSAM, n = 924 mean age 71 years, baseline 1991-1995, median follow-up 15.6 years, end of follow-up 2016). Serum samples were used for analyses of CRP and Albumin. Cox regression analyses were performed for cardiovascular and all-cause mortality in models adjusting for several factors (age; physical activity; Interleukin-6; cardiovascular (CVD) risk factors: smoking, BMI level, systolic blood pressure, LDL-cholesterol, and diabetes), with 95% confidence interval (CI). When adjusting for age and CVD risk factors, CAR was significantly associated with cardiovascular mortality for meta-analyzed results from PIVUS and ULSAM, HR 1.09 (95% 1.01-1.18), but neither in PIVUS (HR 1.14, 95% CI 0.99-1.31) nor in ULSAM (1.07, 95% CI 0.98-1.17). Additionally, CAR was significantly associated with all-cause mortality in ULSAM 1.31 (95% CI 1.12-1.54) but not in PIVUS HRs 1.01 (95% 0.089-1.15). The predictive value of CAR was similar to CRP alone in PIVUS and ULSAM and slightly better than albumin for the prediction of CVD-mortality in ULSAM. In conclusion, CAR was not consistently associated with cardiovascular and all-cause mortality in the two cohorts. The prognostic value of CAR for long-term CVD-mortality was similar to CRP.