Effects on muscle strength, maximal jump height, flexibility and postural sway after soccer and Zumba exercise among female hospital employees: A 9-month randomized controlled trial

This 9-month randomised controlled workplace physical activity trial investigated the effects of soccer and Zumba exercise, respectively, on muscle strength, maximal jump height, sit-and-reach flexibility and postural sway among female workers. A total of 107 female hospital employees aged 25–63 were cluster-randomised to a soccer group, a Zumba group or a control group. Training was conducted outside working hours as two to three 1-h weekly sessions the first 3 months and once a week the last 6 months. Tests were conducted at baseline, after 3 and 9 months. The soccer group improved maximal neck extension strength both after 3 (1.2 kg; P < 0.05) and 9 months (1.7 kg; P < 0.01) compared to the control group. The Zumba group improved maximal trunk extension strength (3.1 kg; P = 0.04) after 3 months, with improvements in postural sway velocity moment (−9.2 mm2/s; P < 0.05) and lower limb lean mass (0.4 kg; P < 0.05) after 9 months. No significant intervention effects were revealed in vertical jump height or sit-and-reach flexibility. The present study indicates that workplace-initiated soccer and Zumba exercise may be beneficial for improvement of the neck and trunk strength, which may have preventive effects with regard to future perceived muscle pain in the respective body regions. Furthermore, the Zumba group revealed positive effects on lower limb lean mass and postural sway compared to the control group

Granulocyte and monocyte CD11b expression during plasma separation is dependent on complement factor 5 (C5) – an ex vivo study with blood from a C5-deficient individual

This is the pre-peer reviewed version of the following article: Hardersen, R., Enebakk, T., Christiansen, D., Bergseth, G., Brekke, L.-O., Mollnes, T.E., ... Hovland, A.W. (2018). Granulocyte and monocyte CD11b expression during plasma separation is dependent on complement factor 5 (C5) ? an ex vivo study with blood from a C5-deficient individual. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 126(4), 342-352, which has been published in final form at https://doi.org/10.1111/apm.12821. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.The aim of the study was to investigate the role of complement factor 5 (C5) in reactions elicited by plasma separation using blood from a C5‐deficient (C5D) individual, comparing it to C5‐deficient blood reconstituted with C5 (C5DR) and blood from healthy donors. Blood was circulated through an ex vivo plasma separation model. Leukocyte CD11b expression and leukocyte–platelet conjugates were measured by flow cytometry during a 30‐min period. Other markers were assessed during a 240‐min period. Granulocyte and monocyte CD11b expression did not increase in C5D blood during plasma separation. In C5DR samples granulocytes CD11b expression, measured by mean fluorescence intensity (MFI), increased from 10481 ± 6022 (SD) to 62703 ± 4936, and monocytes CD11b expression changed from 13837 ± 7047 to 40063 ± 713. Granulocyte–platelet conjugates showed a 2.5‐fold increase in the C5DR sample compared to the C5D sample. Monocyte–platelet conjugates increased independently of C5. In the C5D samples, platelet count decreased from 210 × 109/L (201–219) (median and range) to 51 × 109/L (50–51), and C3bc increased from 14 CAU/mL (21–7) to 198 CAU/mL (127–269), whereas TCC formation was blocked during plasma separation. In conclusion, up‐regulation of granulocyte and monocyte CD11b during plasma separation was C5‐dependent. The results also indicate C5 dependency in granulocyte–platelet conjugates formation

Blood transcriptome analysis of septic patients reveals a long non-coding Alu-RNA in the complement C5a receptor 1 gene

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Complement C3b contributes to Escherichia coli-induced platelet aggregation in human whole blood

We found that compstatin, which inhibits the cleavage of complement component C3 to its components C3a and C3b, reduced the E. coli-induced platelet aggregation by 42%-76% (p = 0.0417). This C3-dependent aggregation was not C3a-mediated as neither inhibition of C3a using a blocking antibody or a C3a receptor antagonist, nor the addition of purified C3a had any effects. In contrast, a C3b-blocking antibody significantly reduced the E. coli-induced platelet aggregation by 67% (p = 0.0133). We could not detect opsonized C3b on platelets, indicating that the effect of C3 was not dependent on C3b-fragment deposition on platelets. Indeed, inhibition of glycoprotein IIb/IIIa (GPIIb/IIIa) and complement receptor 1 (CR1) showed that these receptors were involved in platelet aggregation. Furthermore, aggregation was more pronounced in hirudin whole blood than in hirudin platelet-rich plasma, indicating that E. coli-induced platelet aggregation involved other blood cells. In conclusion, the E. coli-induced platelet aggregation in human whole blood is partly C3b-dependent, and GPIIb/IIIa and CR1 are also involved in this process

Complement C3b contributes to Escherichia coli-induced platelet aggregation in human whole blood

IntroductionPlatelets have essential functions as first responders in the immune response to pathogens. Activation and aggregation of platelets in bacterial infections can lead to life-threatening conditions such as arterial thromboembolism or sepsis-associated coagulopathy.MethodsIn this study, we investigated the role of complement in Escherichia coli (E. coli)-induced platelet aggregation in human whole blood, using Multiplate® aggregometry, flow cytometry, and confocal microscopy.Results and DiscussionWe found that compstatin, which inhibits the cleavage of complement component C3 to its components C3a and C3b, reduced the E. coli-induced platelet aggregation by 42%-76% (p = 0.0417). This C3-dependent aggregation was not C3a-mediated as neither inhibition of C3a using a blocking antibody or a C3a receptor antagonist, nor the addition of purified C3a had any effects. In contrast, a C3b-blocking antibody significantly reduced the E. coli-induced platelet aggregation by 67% (p = 0.0133). We could not detect opsonized C3b on platelets, indicating that the effect of C3 was not dependent on C3b-fragment deposition on platelets. Indeed, inhibition of glycoprotein IIb/IIIa (GPIIb/IIIa) and complement receptor 1 (CR1) showed that these receptors were involved in platelet aggregation. Furthermore, aggregation was more pronounced in hirudin whole blood than in hirudin platelet-rich plasma, indicating that E. coli-induced platelet aggregation involved other blood cells. In conclusion, the E. coli-induced platelet aggregation in human whole blood is partly C3b-dependent, and GPIIb/IIIa and CR1 are also involved in this process

Dental and Periodontal Health in Acute Intermittent Porphyria

In the inherited metabolic disorder acute intermittent porphyria (AIP), high sugar intake prevents porphyric attacks due to the glucose effect and the following high insulin levels that may lower AIP disease activity. Insulin resistance is a known risk factor for periodontitis and sugar changes diabetogenic hormones and affects dental health. We hypothesized differences in homeostasis model assessment (HOMA) scores for insulin resistance in AIP cases vs. controls and in those with periodontitis. Our aim was to systematically study dental health in AIP as poor dental health was previously only described in case reports. Further, we aimed to examine if poor dental health and kidney failure might worsen AIP as chronic inflammation and kidney failure might increase disease activity. In 47 AIP cases and 47 matched controls, X-rays and physical examination of clinical attachment loss (CAL), probing pocket depth (PPD), and decayed missing filled teeth (DMFT) were performed. Dietary intake was evaluated through a diet logbook. Plasma cytokines and diabetogenic hormones were measured using multiplex technology and urine porphobilinogen and kidney and liver function by routine methods. An excel spreadsheet from the University of Oxford was used to estimate HOMA scores; beta cell function, HOMA%B (%B), insulin sensitivity, HOMA%S (%S), and insulin resistance HOMA-IR (IR), based on glucose and plasma (P) C-peptide. The Wilcoxon matched-pairs signed rank test, the Mann–Whitney U-test, and Spearman’s nonparametric correlation were used. Insulin (p = 0.007) and C-peptide (p = 0.006) were higher in the AIP cases with periodontitis versus those without. In AIP patients, the liver fibrosis index 4 correlated with DMFT (p < 0.001) and CAL ≥4 mm (p = 0.006); the estimated glomerular filtration rate correlated with DMFT (p < 0.001) and CAL ≥4 mm (p = 0.02). CAL ≥4 mm was correlated with chemokine ligand 11 and interleukin (IL)-13 (p = 0.04 for both), and PPD >5 mm was correlated with plasminogen activator inhibitor-1 (p = 0.003) and complement component 3 (p = 0.02). In conclusion, dental health in AIP cases was correlated with insulin resistance, inflammatory markers, and biomarkers of kidney and liver function, demonstrating that organ damage in the kidney and liver are associated with poorer dental health

The NADPARK study: A randomized phase I trial of nicotinamide riboside supplementation in Parkinson’s disease

We conducted a double-blinded phase I clinical trial to establish whether nicotinamide adenine dinucleotide (NAD) replenishment therapy, via oral intake of nicotinamide riboside (NR), is safe, augments cerebral NAD levels, and impacts cerebral metabolism in Parkinson’s disease (PD). Thirty newly diagnosed, treatment-naive patients received 1,000 mg NR or placebo for 30 days. NR treatment was well tolerated and led to a significant, but variable, increase in cerebral NAD levels—measured by 31phosphorous magnetic resonance spectroscopy—and related metabolites in the cerebrospinal fluid. NR recipients showing increased brain NAD levels exhibited altered cerebral metabolism, measured by 18fluoro-deoxyglucose positron emission tomography, and this was associated with mild clinical improvement. NR augmented the NAD metabolome and induced transcriptional upregulation of processes related to mitochondrial, lysosomal, and proteasomal function in blood cells and/or skeletal muscle. Furthermore, NR decreased the levels of inflammatory cytokines in serum and cerebrospinal fluid. Our findings nominate NR as a potential neuroprotective therapy for PD, warranting further investigation in larger trials.publishedVersio

Establishing IMMULITE® 2000 cut-off values for serum allergen-specific immunoglobulin and exploring their relationship to exhaled nitric oxide

Aim: Paediatric cut-off values for serum allergen-specific IgE (sIgE) using the Siemens IMMULITE 2000 system to diagnose allergic rhinoconjunctivitis have not been established. We aimed to determine cut-off levels for sIgE for 10 common inhalant allergens and to study the relationship between sIgE, total IgE and fractional exhaled nitric oxide (FENO). Methods: We enrolled 243 schoolchildren, including 164 with allergic rhinoconjunctivitis. Parental interviews, skin prick tests, sIgE, total IgE, FENO measurements, spirometry and exercise tests were performed. Results: Cut-off values with the best combined sensitivity and specificity were above the detection limit of the assay for seven of the ten allergens (0.23–1.1 kU/L). The overall accuracy of the IMMULITE in detecting allergic rhinoconjunctivitis was good. sIgE was superior to total IgE and FENO in predicting allergic rhinoconjunctivitis to timothy, birch, mugwort, cat, dog and house dust mite. FENO was elevated in children with allergic rhinoconjunctivitis, irrespective of asthma. Conclusion: Cut-off values for sIgE were dependent on the allergic phenotype and were above the IMMULITE detection limit for seven of ten inhalant allergens. Consequently, using the detection limit for sIgE as the decision point would result in over-diagnosing allergic rhinoconjunctivitis. When measuring elevated FENO in children, allergic rhinoconjunctivitis should be suspected