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Platelets and the clinical course of Crohn's disease

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Background. Crohn’s disease (CD) is a chronic, autoimmune, inflammatory bowel disease (IBD) characterised by periods of exacerbations and remissions. Autoimmune disorders caused by undetermined factors lead to inflammation in the intestinal mucosa. Presently, there is a growing interest in the role of platelets in the assessment of inflammatory lesions in CD. Accordingly, the aim of this study was to answer the question of whether routinely measured platelet indices: concentration of platelets (PLT), the mean platelet volume (MPV), plateletcrit (PCT) could become biomarkers for monitoring the course of CD. Material and methods. In the study programme, there were enrolled 100 patients with a diagnosed CD with a different clinical course, disease location and heterogeneous therapy. In all patients, there were collected blood and stool samples for the assessment of CRP, blood count and fecal calprotectin evaluation. The clinical state of each patient was classified using the Harvey-Bradshaw index. Results. The study showed a positive, statistically significant correlation between fecal calprotectin, CRP, WBC, the Harvey-Bradshaw index and the number of platelets and PCT. Furthermore, the analysis showed a statistically significant negative correlation between MPV and the number of WBC, CRP and fecal calprotectin. Conclusions. Our study showed that platelet indices are a valuable, non-invasive and widely accessible method to assess mucosal healing and the clinical status of the patient.
The quantity and quality of spears from asparagus plants infected with Asparagus virus 2 was lower in comparison to healthy plants. The total number of spears was decreased in 16% and mass of spears in 24.7%. Asparagus virus 2 reduced the number of marketable spears in 31.9%, and increased the number of unmarketable spears in 20.2%. The green mass of stem brushes of infected plants was reduced in 19.4% in field conditions and in 20% in seedlings growing in a greenhouse.
INTRODUCTION: Motor impairment is fundamental feature of Parkinson’s disease (PD). There are several reports on the beneficial effect of physical training on the PD symptoms reduction, however the mechanisms underlying this improvement are not known The selection of an appropriate animal model is crucial to demonstrate positive effect of physical effort on motor function, because even despite extensive loss of dopaminergic neurons the detection and quantification of motor impairment is difficult. AIM(S): The purpose of the study was to examine the efficacy of physical training in reversing the expected motor impairment in chronic MPTP mice model of parkinsonism. METHOD(S): C57BL/6 mice were treated for five weeks with 12,5 mg/kg MPTP in combination with 250 mg/kg probenecid. Mice were subdivided into: 1) control sedentary; 2) control trained (10 weeks); 3) MPTP sedentary (non-exercised with PD); 4) early trained MPTP (10 weeks: before, during, and after the induction of PD), and 5) late trained MPTP (10 weeks, started after the induction of PD). To assess motor performance rotarod, open field and inverted horizontal grid tests were performed before MPTP treatment, after the completion of intoxication and when the training was finished. RESULTS: MPTP did not impair motor function. We observed improvement of motor performance in rotarod and open field test in MPTP, early trained mice. Some enhancement of motor skills in rotarod test was observed also for MPTP non-exercised mice. In horizontal grid test the only parameter significantly influenced by MPTP treatment was the total number of touches and we did not observe the impact of physical training on the reduction of this parameter. CONCLUSIONS: We did not observe the impact of MPTP and physical training alone on motor performance in mice model of parkinsonism. However, there has been a certain improvement in some of the motor parameters in both groups of MPTP treated mice, which performed physical training. FINANCIAL SUPPORT: NCN grant 2014/15/B/ NZ4/05041
A defi cit in the cholinergic system of the basal forebrain (BF) is thought to contribute to the development of cognitive symptoms of dementia. Forebrain cholinergic neurons are highly dependent on nerve growth factor (NGF) for phenotype maintenance. Attempts to prevent age-associated cholinergic vulnerability and deterioration therefore represent a crucial point for pharmacotherapy in the elderly. The pharmacological induction of endogenous NGF synthesis in the brain could be an elegant way to overcome application problems. Therefore, the present experiment was undertaken to determine the infl uence of prolonged pharmacological stimulation of NGF biosynthesis on learning and memory in aged rats. To address these issues we used young (4-month-old) and aged (28-month-old) rats in which we stimulated endogenous NGF biosynthesis by treatment with clenbuterol (β2-adrenergic receptors agonist). The cognitive behavior of the young and aged rats was assessed in the long-lasting “Non-Matching to Position Test”. Our data suggest that in aged rats, clenbuterol positively affects cognitive processes related to formation of associations established in recognition memory and discrimination tasks. In addition, NGF signifi cantly improved morphological parameters of BF cholinergic cells in aged rats. These data suggest that endogenous NGF induction restores the age-related decline of the cholinergic system activity in rats, resulting in improvement of water maze performance in old animals.
Both intensive training and bed confinement impair orthostatic tolerance, however, moderate training may exert beneficial effect on cardiovascular adjustment to gravitational stimuli. It was hypothesized that moderate training attenuates effects of bed rest. To test this assumption 24 healthy male volunteers aged 20.8±0.9 yrs were subjected to 6° head down bed rest (HDBR) for 3 days before and after 6 weeks of moderate endurance training. Before and after HDBR graded LBNP tests (-15, -30, -50 mmHg) were performed. During these tests heart rate (HR), stroke volume (SV), blood pressure (BP), plasma catecholamines, ACTH, adrenomedullin, atrial natriuretic peptide, plasma renin activity (PRA) and hematocrit were determined. HDBR did not systematically influence LBNP tolerance up to -50 mmHg, but it enhanced rates of reduction of SV, cardiac output and systolic BP and increased elevations of HR and PRA. Training did not alter significantly effects of HDBR on LBNP-induced changes in HR, SV, CO and TPR but it attenuated decrease in systolic BP and diminished increases in plasma noradrenaline and PRA. In conclusion, training has negligible effect on the HDBR-induced changes in central hemodynamics during LBNP but may increase vascular sensitivity to some vasoconstricting factors.
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