Browsing by Subject "INJURY"

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  • Tanttula, Kimmo; Haikonen, Kari; Vuola, Jyrki (2018)
    To analyse the epidemiology of burns in Finland, a comprehensive study was conducted among all hospitalized burn patients between 1980 and 2010. All patients with burn injury as the main diagnosis, 36305 cases in total, treated in the public and private sectors, were included. Patient data were obtained from the Finnish Hospital Discharge Register (FHDR). The incidence of hospitalized injuries declined from over 30 to 17 per 100000 persons. Men were at higher risk than women in all age groups. Children aged under ten years were overrepresented throughout the period and the highest incidence was found among one year old boys. The median total length of stay shortened from seven days in 1980-1995 to five days in 1996-2010. The annual number of hospitalized patients is recently under 1000 cases (17/100000). The male predominance (70%) did not change but the age group with the most injuries shifted from 20-39 years to 40-59 years. Injuries were most common during the summer months. This study of all hospitalized burn injuries of one entire country shows similar tendency of diminishing numbers and rising age of burn victims as in other western countries. The FHDR is a reliable source of data in epidemiological studies but precise recording of E- and N-codes in the registry would enable the accurate analysis of types and extent of injury. (C) 2017 Elsevier Ltd and ISBI. All rights reserved.
  • Kirss, Jaan; Pinta, Tarja; Rautio, Tero; Varpe, Pirita; Kairaluoma, Matti; Hyöty, Marja; Hurme, Saija; Böckelman, Camilla; Kairaluoma, Valtteri; Salmenkylä, Sinikka; Victorzon, Mikael (2018)
    PurposeThe aim of this multicentre study was to analyse the effects of patent sphincter lesions and previous sphincter repair on the results of sacral neuromodulation (SNM) treatment on patients with faecal incontinence (FI).MethodsPatients examined by endoanal ultrasound (EAUS) with FI as the indication for SNM treatment were included in the study. Data was collected from all the centres providing SNM treatment in Finland and analysed for differences in treatment outcomes.ResultsA total of 237 patients treated for incontinence with SNM had been examined by EAUS. Of these patients, 33 had a history of previous delayed sphincter repair. A patent sphincter lesion was detected by EAUS in 128 patients. The EAUS finding did not influence the SNM test phase outcome (p=0.129) or the final treatment outcome (p=0.233). Patient's history of prior sphincter repair did not have a significant effect on the SNM test (p=0.425) or final treatment outcome (p=0.442).ConclusionsResults of our study indicate that a sphincter lesion or previous sphincter repair has no significant effect on the outcome of SNM treatment. Our data suggests that delayed sphincter repair prior to SNM treatment initiation for FI is not necessary.
  • Repo, Jussi P.; Häkkinen, Arja H.; Porkka, Tuukka; Häkkinen, Keijo; Kautiainen, Hannu; Kyrölä, Kati; Neva, Marko H. (2019)
    Purpose: Interleukin 6 (IL-6) and the acute phase C-reactive protein (CRP) blood concentrations after lumbar spine fusion may be affected by age. The purpose of this prospective observational study was to assess postoperative serum levels of pro-inflammatory IL-6 and CRP after instrumented lumbar spine fusion surgery. We hypothesized that older patients would have increased levels of IL-6 and CRP after surgery. Methods: IL-6 and high-sensitive CRP biochemical marker levels were measured before instrumented spinal fusion, and postoperatively at 1 and 3 days, 6 weeks, and 3 months. The 49 patients in this sample were divided into two groups: age 60 years (n = 26). Results: Acute changes in IL-6 high-sensitivity and CRP from preoperative levels to postoperative day (POD) 1 increased with age. Mean (95% CI) difference between the age-groups in changes of IL-6 at PODs 1 and 3 was 45 pg/ml (10-83, p = 0.014) and 20 pg/ml (5-36, p = 0.021), respectively. Mean (95% CI) difference between groups in changes of CRP at PODs 1 and 3 was 9.6 mg/l (-3.5 to 22.7, p = 0.47) and 24.8 mg/l (-17 to 67, p = 0.33), respectively. Both groups had decreased IL-6 and CRP levels at 6 weeks after surgery compared to the preoperative level. Conclusions: Elevation of IL-6 and CRP is stronger in patients over 60 years old after instrumented lumbar spinal fusion. The CRP and IL-6 are sensitive markers for acute postoperative inflammation. Even high acute CRP values do not necessarily indicate postoperative infection.
  • Gailus, Bjoern; Naundorf, Hannah; Welzel, Lisa; Johne, Marie; Roemermann, Kerstin; Kaila, Kai; Loescher, Wolfgang (2021)
    Objective: Birth asphyxia is a major cause of hypoxic-ischemic encephalopathy (HIE) in neonates and often associated with mortality, neonatal seizures, brain damage, and later life motor, cognitive, and behavioral impairments and epilepsy. Preclinical studies on rodent models are needed to develop more effective therapies for preventing HIE and its consequences. Thus far, the most popular rodent models have used either exposure of intact animals to hypoxia-only, or a combination of hypoxia and carotid occlusion, for the induction of neonatal seizures and adverse outcomes. However, such models lack systemic hypercapnia, which is a fundamental constituent of birth asphyxia with major effects on neuronal excitability. Here, we use a recently developed noninvasive rat model of birth asphyxia with subsequent neonatal seizures to study later life adverse outcome. Methods: Intermittent asphyxia was induced for 30 min by exposing male and female postnatal day 11 rat pups to three 7 + 3-min cycles of 9% and 5% O-2 at constant 20% CO2. All pups exhibited convulsive seizures after asphyxia. A set of behavioral tests were performed systematically over 14 months following asphyxia, that is, a large part of the rat's life span. Video-electroencephalographic (EEG) monitoring was used to determine whether asphyxia led to the development of epilepsy. Finally, structural brain alterations were examined. Results: The animals showed impaired spatial learning and memory and increased anxiety when tested at an age of 3-14 months. Video-EEG at similar to 10 months showed an abundance of spontaneous seizures, which was paralleled by neurodegeneration in the hippocampus and thalamus, and by aberrant mossy fiber sprouting. Significance: The present model of birth asphyxia recapitulates several of the later life consequences associated with human HIE. This model thus allows evaluation of the efficacy of novel therapies designed to prevent HIE and seizures following asphyxia, and of how such therapies might alleviate long-term adverse consequences.
  • Barreto, Goncalo; Senturk, B.; Colombo, L.; Brück, O.; Neidenbach, P.; Salzmann, G.; Zenobi-Wong, M.; Rottmar, M. (2020)
    Objective: Lumican (LUM) is a major extracellular matrix glycoprotein in adult articular cartilage and its expression is known to be upregulated upon cartilage degeneration. LUM is associated with the pathogen-associated molecular pattern (PAMP) activation of the TLR4 signalling cascade, with TLR4 being highly associated with inflammation in rheumatic diseases. However, the main role of the LUM structural molecule in osteoarthritis (OA) remains elusive. The aim of this study was, therefore, to understand the role of LUM during TLR4-mediated activation in OA. Methods: After measuring LUM levels in synovial fluid (SF) of OA patients and lipopolysaccharide (LPS)-induced TLR4 activation, the role of LUM in the expression of pro-inflammatory molecules and cartilage degradation was assessed in vitro and ex vivo in a cartilage explant model. Primary macrophage activation and polarization were studied upon LUM co-stimulation with LPS. Results: We demonstrate that LUM is not only significantly upregulated in SF from OA patients compared to healthy controls, but also that LUM increases lipopolysaccharide (LPS)-induced TLR4 activation. Furthermore, we show that a pathophysiological level of LUM augments the LPS-induced TLR4 activation and expression of downstream pro-inflammatory molecules, resulting in extensive cartilage degradation. LUM co-stimulation with LPS also provided a pro-inflammatory stimulus, upregulating primary macrophage activation and polarization towards the M1-like phenotype. Conclusions: These findings strongly support the role of LUM as a mediator of PAMP-induced TLR4 activation of inflammation, cartilage degradation, and macrophage polarization in the OA joint and potentially other rheumatic diseases. (C) 2019 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
  • Hästbacka, Johanna; Freden, Filip; Hult, Maarit; Bergquist, Maria; Wilkman, Erika; Vuola, Jyrki; Sorsa, Timo; Tervahartiala, Taina; Huss, Fredrik (2015)
    Introduction Matrix metalloproteinases (MMPs) -8 and -9 are released from neutrophils in acute inflammation and may contribute to permeability changes in burn injury. In retrospective studies on sepsis, levels of MMP-8, MMP-9, and tissue inhibitor of metalloproteinase-1 (TIMP-1) differed from those of healthy controls, and TIMP-1 showed an association with outcome. Our objective was to investigate the relationship between these proteins and disease severity and outcome in burn patients. Methods In this prospective, observational, two-center study, we collected plasma samples from admission to day 21 post-burn, and burn blister fluid samples on admission. We compared MMP-8, -9, and TIMP-1 levels between TBSA20% (N = 30) injured patients and healthy controls, and between 90-day survivors and non-survivors. MMP-8, -9, and TIMP-1 levels at 24-48 hours from injury, their maximal levels, and their time-adjusted means were compared between groups. Correlations with clinical parameters and the extent of burn were analyzed. MMP-8, -9, and TIMP-1 levels in burn blister fluids were also studied. Results Plasma MMP-8 and -9 were higher in patients than in healthy controls (P20% groups. MMP-8 and -9 were not associated with clinical severity or outcome measures. TIMP-1 differed significantly between patients and controls (P20% groups (P
  • Suominen, Janne S.; Lampela, Hanna; Heikkila, Paivi; Lohi, Jouko; Jalanko, Hannu; Pakarinen, Mikko P. (2014)
  • Hukkinen, M; Mutanen, A; Nissinen, M; Merras-Salmio, L; Gylling, H; Pakarinen, M. P (2017)
    Background: Parenteral plant sterols (PSs) are considered hepatotoxic; however, liver PSs and their associations with liver injury in patients with intestinal failure (IF) have not been reported. Materials and Methods: We analyzed liver and serum PS (avenasterol, campesterol, sitosterol, and stigmasterol) concentrations and ratios to cholesterol and their associations with biochemical and histologic liver damage in children with IF during (n = 7) parenteral nutrition (PN) and after weaning off it (n = 9), including vegetable oil-based lipid emulsions. Results: Liver avenasterol, sitosterol, and total PS concentrations and cholesterol ratios were 2.4-fold to 5.6-fold higher in PN-dependent patients (P <.05). Parenteral PS delivery reflected liver avenasterol and sitosterol ratios to cholesterol (r = 0.83-0.89, P = .02-.04), while serum and liver total PS levels were positively interrelated (r = 0.98, P <.01). Any liver histopathology was equally common while portal inflammation more frequent (57 vs 0%, P = .02) in PN-dependent patients. All liver PS fractions correlated positively with histologic portal inflammation (r = 0.53-0.66, P <.05), and their total concentration was significantly (P = .01) higher among patients with versus without portal inflammation. In PN-dependent patients, liver fibrosis and any histopathology correlated with liver campesterol and stigmasterol levels (r = 0.79-0.87, P .03). Conclusion: Among children with IF, parenteral PSs accumulate in the liver, reflect their increased serum levels, and relate with biochemical liver injury, portal inflammation, and liver fibrosis, thus supporting their role in promoting liver damage.
  • Ollila, A.; Vikatmaa, Leena; Virolainen, J.; Vikatmaa, Pirkka; Leppaniemi, A.; Albäck, Anders; Salmenperä, Markku; Pettilä, Ville (2017)
    Background and Aims: Perioperative myocardial infarction is an underdiagnosed complication causing morbidity, mortality, and considerable costs. However, evidence of preventive and therapeutic options is scarce. We investigated the incidence and outcome of perioperative myocardial infarction in non-cardiac surgery patients in order to define a target population for future interventional trials. Material and Methods: We conducted a prospective single-center study on non-cardiac surgery patients aged 50years or older. High-sensitivity troponin T and electrocardiograph were obtained five times perioperatively. Perioperative myocardial infarction diagnosis required a significant troponin T release and an ischemic sign or symptom. Perioperative risk calculator was used for risk assessment. Results: Of 385 patients with systematic ischemia screening, 27 patients (7.0%) had perioperative myocardial infarction. The incidence was highest in vascular surgery19 of 172 patients (11.0%). The 90-day mortality was 29.6% in patients with perioperative myocardial infarction and 5.6% in non-perioperative myocardial infarction patients (p Conclusion: Perioperative myocardial infarction is a common complication associated with a 90-day mortality of 30%. The ability of the perioperative risk calculator to predict perioperative myocardial infarction was fair supporting its routine use.
  • Kolosowska, Natalia; Keuters, Meike H.; Wojciechowski, Sara; Keksa-Goldsteine, Velta; Laine, Mika; Malm, Tarja; Goldsteins, Gundars; Koistinaho, Jari; Dhungana, Hiramani (2019)
    Neuroinflammation is strongly induced by cerebral ischemia. The early phase after the onset of ischemic stroke is characterized by acute neuronal injury, microglial activation, and subsequent infiltration of blood-derived inflammatory cells, including macrophages. Therefore, modulation of the microglial/macrophage responses has increasingly gained interest as a potential therapeutic approach for the ischemic stroke. In our study, we investigated the effects of peripherally administered interleukin 13 (IL-13) in a mouse model of permanent middle cerebral artery occlusion (pMCAo). Systemic administration of IL-13 immediately after the ischemic insult significantly reduced the lesion volume, alleviated the infiltration of CD45(+) leukocytes, and promoted the microglia/macrophage alternative activation within the ischemic region, as determined by arginase 1 (Arg1) immunoreactivity at 3 days post-ischemia (dpi). Moreover, IL-13 enhanced the expression of M2a alternative activation markers Arg1 and Ym1 in the peri-ischemic (PI) area, as well as increased plasma IL-6 and IL-10 levels at 3 dpi. Furthermore, IL-13 treatment ameliorated gait disturbances at day 7 and 14 and sensorimotor deficits at day 14 post-ischemia, as analyzed by the CatWalk gait analysis system and adhesive removal test, respectively. Finally, IL-13 treatment decreased neuronal cell death in a coculture model of neuroinflammation with RAW 264.7 macrophages. Taken together, delivery of IL-13 enhances microglial/macrophage anti-inflammatory responses in vivo and in vitro, decreases ischemia-induced brain cell death, and improves sensory and motor functions in the pMCAo mouse model of cerebral ischemia.
  • Loppi, Sanna; Korhonen, Paula; Bouvy-Liivrand, Maria; Caligola, Simone; Turunen, Tiia A.; Turunen, Mikko P.; de Sande, Ana Hernandez; Kolosowska, Natalia; Scoyni, Flavia; Rosell, Anna; Garcia-Berrocoso, Teresa; Lemarchant, Sighild; Dhungana, Hiramani; Montaner, Joan; Koistinaho, Jari; Kanninen, Katja M.; Kaikkonen, Minna U.; Giugno, Rosalba; Heinäniemi, Merja; Malm, Tarja (2021)
    Ischemic stroke, the third leading cause of death in the Western world, affects mainly the elderly and is strongly associated with comorbid conditions such as atherosclerosis or diabetes, which are pathologically characterized by increased inflammation and are known to influence the outcome of stroke. Stroke incidence peaks during influenza seasons, and patients suffering from infections such as pneumonia prior to stroke exhibit a worse stroke outcome. Earlier studies have shown that comorbidities aggravate the outcome of stroke, yet the mediators of this phenomenon remain obscure. Here, we show that acute peripheral inflammation aggravates stroke-induced neuronal damage and motor deficits specifically in aged mice. This is associated with increased levels of plasma proinflammatory cytokines, rather than with an increase of inflammatory mediators in the affected brain parenchyma. Nascent transcriptomics data with mature microRNA sequencing were used to identify the neuron-specific miRNome, in order to decipher dysregulated miRNAs in the brains of aged animals with stroke and co-existing inflammation. We pinpoint a previously uninvestigated miRNA in the brain, miR-127, that is highly neuronal, to be associated with increased cell death in the aged, LPS-injected ischemic mice. Target prediction tools indicate that miR-127 interacts with several basally expressed neuronal genes, and of these we verify miR-127 binding to Psmd3. Finally, we report reduced expression of miR-127 in human stroke brains. Our results underline the impact of peripheral inflammation on the outcome of stroke in aged subjects and pinpoint molecular targets for restoring endogenous neuronal capacity to combat ischemic stroke.
  • O'Flynn, Joseph; Kotimaa, Juha; Faber-Krol, Ria; Koekkoek, Karin; Klar-Mohamad, Ngaisah; Koudijs, Angela; Schwaeble, Wilhelm J.; Stover, Cordula; Daha, Mohamed R.; van Kooten, Cees (2018)
    Properdin is the only known positive regulator of complement activation by stabilizing the alternative pathway convertase through C3 binding, thus prolonging its half-life. Recent in vitro studies suggest that properdin may act as a specific pattern recognition molecule. To better understand the role of properdin in vivo, we used an experimental model of acute anti-glomerular basement membrane disease with wild-type, C3-and properdin knockout mice. The model exhibited severe proteinuria, acute neutrophil infiltration and activation, classical and alternative pathway activation, and progressive glomerular deposition of properdin, C3 and C9. Although the acute renal injury was likely due to acute neutrophil activation, we found properdin deposition in C3-knockout mice that was not associated with IgG. Thus, properdin may deposit in injured tissues in vivo independent of its main ligand C3.
  • Khirug, Stanislav; Soni, Shetal; Saez Garcia, Marta; Tessier, Marine; Zhou, Liang; Kulesskaya, Natalia; Rauvala, Heikki; Lindholm, Dan; Ludwig, Anastasia; Molinari, Florence; Rivera, Claudio (2021)
    A striking result from epidemiological studies show a correlation between low alcohol intake and lower incidence for ischemic stroke and severity of derived brain injury. Although reduced apoptosis and inflammation has been suggested to be involved, little is known about the mechanism mediating this effect in vivo. Increase in intracellular chloride concentration and derived depolarizing GABAAR-mediated transmission are common consequences following various brain injuries and are caused by the abnormal expression levels of the chloride cotransporters NKCC1 and KCC2. Downstream pro-apoptotic signaling through p75NTR may link GABAA depolarization with post-injury neuronal apoptosis. Here, we show that changes in GABAergic signaling, Cl− homeostasis, and expression of chloride cotransporters in the post-traumatic mouse brain can be significantly reduced by administration of 3% ethanol to the drinking water. Ethanol-induced upregulation of KCC2 has a positive impact on neuronal survival, preserving a large part of the cortical peri-infarct zone, as well as preventing the massive post-ischemic upregulation of the pro-apoptotic protein p75NTR. Importantly, intracortical multisite in vivo recordings showed that ethanol treatment could significantly ameliorate stroke-induced reduction in cortical activity. This surprising finding discloses a pathway triggered by low concentration of ethanol as a novel therapeutically relevant target.
  • Rueda, Ferran; Borras, Eva; Garcia-Garcia, Cosme; Iborra-Egea, Oriol; Revuelta-Lopez, Elena; Harjola, Veli-Pekka; Cediel, German; Lassus, Johan; Tarvasmäki, Tuukka; Mebazaa, Alexandre; Sabido, Eduard; Bayes-Genis, Antoni (2019)
    Aims Cardiogenic shock (CS) is associated with high short-term mortality and a precise CS risk stratification could guide interventions to improve patient outcome. Here, we developed a circulating protein-based score to predict short-term mortality risk among patients with CS. Methods and results Mass spectrometry analysis of 2654 proteins was used for screening in the Barcelona discovery cohort (n = 48). Targeted quantitative proteomics analyses (n = 51 proteins) were used in the independent CardShock cohort (n = 97) to derive and cross-validate the protein classifier. The combination of four circulating proteins (Cardiogenic Shock 4 proteins-CS4P), discriminated patients with low and high 90-day risk of mortality. CS4P comprises the abundances of liver-type fatty acid-binding protein, beta-2-microglobulin, fructose-bisphosphate aldolase B, and SerpinG1. Within the CardShock cohort used for internal validation, the C-statistic was 0.78 for the CardShock risk score, 0.83 for the CS4P model, and 0.84 (P = 0.033 vs. CardShock risk score) for the combination of CardShock risk score with the CS4P model. The CardShock risk score with the CS4P model showed a marked benefit in patient reclassification, with a net reclassification improvement (NRI) of 0.49 (P = 0.020) compared with CardShock risk score. Similar reclassification metrics were observed in the IABP-SHOCK II risk score combined with CS4P (NRI =0.57; P = 0.032). The CS4P patient classification power was confirmed by enzyme-linked immuno-sorbent assay (ELISA). Conclusion A new protein-based CS patient classifier, the CS4P, was developed for short-term mortality risk stratification. CS4P improved predictive metrics in combination with contemporary risk scores, which may guide clinicians in selecting patients for advanced therapies.
  • Heliste, Juho; Jokilammi, Anne; Paatero, Ilkka; Chakroborty, Deepankar; Stark, Christoffer; Savunen, Timo; Laaksonen, Maria; Elenius, Klaus (2018)
    BackgroundReceptor tyrosine kinases (RTK) are potential targets for the treatment of ischemic heart disease. The human RTK family consists of 55 members, most of which have not yet been characterized for expression or activity in the ischemic heart.MethodsRTK gene expression was analyzed from human heart samples representing healthy tissue, acute myocardial infarction or ischemic cardiomyopathy. As an experimental model, pig heart with ischemia-reperfusion injury, caused by cardiopulmonary bypass,was used, from which phosphorylation status of RTKs was assessed with a phospho-RTK array. Expression and function of one RTK, ROR1, was further validated in pig tissue samples, and in HL-1 cardiomyocytes and H9c2 cardiomyoblasts, exposed to hypoxia and reoxygenation. ROR1 protein level was analyzed by Western blotting. Cell viability after ROR1 siRNA knockdown or activation with Wnt-5a ligand was assessed by MTT assays.ResultsIn addition to previously characterized RTKs, a group of novel active and regulated RTKs was detected in the ischemic heart. ROR1 was the most significantly upregulated RTK in human ischemic cardiomyopathy. However, ROR1 phosphorylation was suppressed in the pig model of ischemia-reperfusion and ROR1 phosphorylation and expression were down-regulated in HL-1 cardiomyocytes subjected to short-term hypoxia in vitro. ROR1 expression in the pig heart was confirmed on protein and mRNA level. Functionally, ROR1 activity was associated with reduced viability of HL-1 cardiomyocytes in both normoxia and during hypoxia-reoxygenation.ConclusionsSeveral novel RTKs were found to be regulated in expression or activity in ischemic heart. ROR1 was one of the most significantly regulated RTKs. The in vitro findings suggest a role for ROR1 as a potential target for the treatment of ischemic heart injury.
  • Bhattarai, Niina; Korhonen, Eveliina; Toppila, Maija; Koskela, Ali; Kaarniranta, Kai; Mysore, Yashavanthi; Kauppinen, Anu (2020)
    Retinal pigment epithelial (RPE) cells maintain homeostasis at the retina and they are under continuous oxidative stress. Cigarette smoke is a prominent environmental risk factor for age-related macular degeneration (AMD), which further increases the oxidant load in retinal tissues. In this study, we measured oxidative stress and inflammatory markers upon cigarette smoke-derived hydroquinone exposure on human ARPE-19 cells. In addition, we studied the effects of commercial Resvega product on hydroquinone-induced oxidative stress. Previously, it was observed that Resvega induces autophagy during impaired protein clearance in ARPE-19 cells, for which it has the potential to alleviate pro-inflammatory pathways. Cell viability was determined while using the lactate dehydrogenase (LDH) and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, and the cytokine levels were measured using the enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS) production were measured using the 2′,7′-dichlorofluorescin diacetate (H2DCFDA) probe. Hydroquinone compromised the cell viability and increased ROS production in ARPE-19 cells. Resvega significantly improved cell viability upon hydroquinone exposure and reduced the release of interleukin (IL)-8 and monocytic chemoattractant protein (MCP)-1 from RPE cells. Resvega, N-acetyl-cysteine (NAC) and aminopyrrolidine-2,4-dicarboxylic acid (APDC) alleviated hydroquinone-induced ROS production in RPE cells. Collectively, our results indicate that hydroquinone induces cytotoxicity and increases oxidative stress through NADPH oxidase activity in RPE cells, and resveratrol-containing Resvega products prevent those adverse effects.
  • Dingemans, S. A.; Birnie, M. F. N.; Sanders, F. R. K.; van den Bekerom, M. P. J.; Backes, M.; van Beeck, E.; Bloemers, F. W.; van Dijkman, B.; Flikweert, E.; Haverkamp, D.; Holtslag, H. R.; Hoogendoorn, J. M.; Joosse, P.; Parkkinen, M.; Roukema, G.; Sosef, N.; Twigt, B. A.; van Veen, R. N.; van der Veen, A. H.; Vermeulen, J.; Winkelhagen, J.; van der Zwaard, B. C.; van Dieren, S.; Goslings, J. C.; Schepers, T. (2018)
    Background: Syndesmotic injuries are common and their incidence is rising. In case of surgical fixation of the syndesmosis a metal syndesmotic screw is used most often. It is however unclear whether this screw needs to be removed routinely after the syndesmosis has healed. Traditionally the screw is removed after six to 12 weeks as it is thought to hamper ankle functional and to be a source of pain. Some studies however suggest this is only the case in a minority of patients. We therefore aim to investigate the effect of retaining the syndesmotic screw on functional outcome. Design: This is a pragmatic international multicentre randomised controlled trial in patients with an acute syndesmotic injury for which a metallic syndesmotic screw was placed. Patients will be randomised to either routine removal of the syndesmotic screw or removal on demand. Primary outcome is functional recovery at 12 months measured with the Olerud-Molander Score. Secondary outcomes are quality of life, pain and costs. In total 194 patients will be needed to demonstrate non-inferiority between the two interventions at 80% power and a significance level of 0.025 including 15% loss to follow-up. Discussion: If removal on demand of the syndesmotic screw is non-inferior to routine removal in terms of functional outcome, this will offer a strong argument to adopt this as standard practice of care. This means that patients will not have to undergo a secondary procedure, leading to less complications and subsequent lower costs.
  • Soglia, Francesca; Petracci, Massimiliano; Puolanne, Eero (2020)
    The present study aims to measure the sarcomere lengths in normal broiler muscles and in non-lesion sites of breast muscles focally affected by Wooden Breast (WB). For this purpose, twenty Pectoralis major muscles (10 unaffected and 10 WB-focally affected cases) were sampled and used to measure sarcomere length by laser diffraction method. When compared with their unaffected counterpart, WB cases exhibited 13% longer sarcomeres (1.91 vs. 1.69 mu m; p <.001) measured within the non-lesioned site of the muscle. Although it is not simple to draw conclusions about the lesion properties based on the non-lesion area, but as the fibres are bound to each other, it may be reasonable to anticipate that the hardened consistency observed in WB is not ascribable to a more intense contraction of the sarcomeres. In addition, considering the current knowledge concerning this condition, it might be assumed that the longer sarcomeres observed in WB are not triggering the development of this condition but are rather a consequence of the profound alteration in the muscular structure resulting from it. Indeed, despite the outstanding improvements in the live and slaughtering traits, the selection programmes carried out in the past years have resulted in a reduced capillarization and impaired oxygen supply to the Pectoralis major of fast-growing hybrids thus affecting the physiology of its constituting fibres as well as maybe impairing their ability to synthetise new sarcomeres. This may result in a skeletal muscle injury, which would ultimately lead to necrosis and fibrosis.
  • Niemelä, Markus; Niemelä, Onni; Bloigu, Risto; Bloigu, Aini; Kangastupa, Päivikki; Juvonen, Tatu (2020)
    Purpose: While extreme physical exertion is known to induce changes in the status of inflammation comparisons of the responses for various mediators of inflammation after acute bouts of high-intensity exercise have been limited. Subjects and Methods: We examined the responses in serum levels of novel inflammatory proteins, calprotectin, suPAR, CD163, and pro- and anti-inflammatory cytokines in 12 physically active volunteers (10 men, 2 women, mean age 37 +/- 14 years) before and after completing various types of extreme physical exertion (marathon run, half-marathon run or 24-h cross-country skiing). For comparisons, the levels of the biomarkers were also measured at rest in 30 healthy controls (25 men, 5 women, mean age 42 +/- 12 years) with low or sedentary activity. Results: Extreme physical exertion induced significant increases in serum calprotectin (p <0.0005), suPAR (p <0.01), CD163 (p <0.05), IL-6 (p <0.0005), IL-8 (p <0.01) and IL-10 (p <0.0005) (pre- vs 3h-post-exercise). These responses were found to normalize within 48 hours. While the increases in blood leukocytes were of similar magnitude following the different types of exercise, markedly more pronounced responses occurred in serum TNF-alpha (p <0.01), IL-8 (p <0.01) and CD163 (p <0.05) in those with more intense activity. In 3-h post-exercise samples significant correlations were observed between serum calprotectin and IL-6 (r(s) = 0.720, p <0.01), IL-10 (r(s) = 0.615, p <0.05), TNF-alpha (r(s) = 0.594, p <0.05), suPAR (r(s) = 0.587, p <0.05) and blood leukocytes (r(s) = 0.762, p <0.01). Conclusion: The present results suggest distinct exercise-intensity dependent changes in mediators of inflammation (including calprotectin, suPAR and CD163) following extreme physical exertion. Our findings indicate that there is a major reversible impact of high-intensity physical exertion on the status of inflammation.
  • Ervasti, Jenni; Kivimäki, Mika; Head, Jenny; Goldberg, Marcel; Airagnes, Guillaume; Pentti, Jaana; Oksanen, Tuula; Salo, Paula; Suominen, Sakari; Jokela, Markus; Vahtera, Jussi; Zins, Marie; Virtanen, Marianna (2018)
    Aims To estimate differences in the strength and shape of associations between alcohol use and diagnosis-specific sickness absence. Design A multi-cohort study. Participants (n = 47 520) responded to a survey on alcohol use at two time-points, and were linked to records of sickness absence. Diagnosis-specific sickness absence was followed for 4-7 years from the latter survey. Setting and participants From Finland, we had population cohort survey data from 1998 and 2003 and employee cohort survey data from 2000-02 and 2004. From France and the United Kingdom, we had employee cohort survey data from 1993 and 1997, and 1985-88 and 1991-94, respectively. Measurements We used standard questionnaires to assess alcohol intake categorized into 0, 1-11 and > 11 units per week in women and 0, 1-34 and > 34 units per week in men. We identified groups with stable and changing alcohol use over time. We linked participants to records from sickness absence registers. Diagnoses of sickness absence were coded according to the International Classification of Diseases. Estimates were adjusted for sex, age, socio-economic status, smoking and body mass index. Findings Women who reported drinking 1-11 units and men who reported drinking 1-34 units of alcohol per week in both surveys were the reference group. Compared with them, women and men who reported no alcohol use in either survey had a higher risk of sickness absence due to mental disorders [rate ratio = 1.51, 95% confidence interval (CI) = 1.22-1.88], musculoskeletal disorders (1.22, 95% CI = 1.06-1.41), diseases of the digestive system (1.35, 95% CI = 1.02-1.77) and diseases of the respiratory system (1.49, 95% CI = 1.29-1.72). Women who reported alcohol consumption of > 11 weekly units and men who reported alcohol consumption of > 34 units per week in both surveys were at increased risk of absence due to injury or poisoning (1.44, 95% CI = 1.13-1.83). Conclusions In Finland, France and the United Kingdom, people who report not drinking any alcohol on two occasions several years apart appear to have a higher prevalence of sickness absence from work with chronic somatic and mental illness diagnoses than those drinking below a risk threshold of 11 units per week for women and 34 units per week for men. Persistent at-risk drinking in Finland, France and the United Kingdom appears to be related to increased absence due to injury or poisoning.