Evaluation of thermal pattern distributions in racehorse saddles using infrared thermography

The impact of a rider’s and saddle’s mass on saddle thermal pattern distribution was evalu ated using infrared thermography (IRT). Eighteen racehorses were ridden by four riders with their own saddle. Images of the saddle panels were captured at each of six thermographic examinations. On each image, six regions of interest (ROIs) were marked on the saddle panels. The mean temperature for each ROI was extracted. To evaluate the influence of load on saddle fit, 4 indicators were used: ΔTmax (difference between the mean temperature of the warmest and coolest ROI); standard deviation of the mean temperature of the six ROIs; right/left; bridging/rocking and front/back thermal pattern indicator. Incorrect saddle fit was found in 25 measurements (23.1%) with ΔTmax greater than 2˚C. The relationships between rider and saddle fit as well as saddle fit and horse were significant (p<0.001). An average ΔTmax in rider A was significantly higher than in other riders (p<0.001). The right/left thermal pattern differed significantly from the optimal value for riders A and B; while the bridging/rocking thermal pattern differed significantly from this value for riders A, C and D (p<0.05). Front saddle thermal pattern was most frequent for rider A (41.5%), whereas back saddle thermal pattern was most frequent for rider C (85.7%). Measurement of the mean temperature in 6 ROIs on saddle panels after training was helpful in assessing the influence of rider and saddle mass on saddle fit. IRT offered a non-invasive, rapid and simple method for assessing load on thermal pattern distribution in race saddles.info:eu-repo/semantics/publishedVersio

Comparing awareness of mental health issues and cognitive behavioural therapy in male and female UK Premier League academy soccer players and university students

The aim of this study was to obtain information regarding elite soccer academy players’ and university students’ awareness of common mental disorders and intervention options. A cross-sectional design compared perceptions of male and female Premier League soccer academy players with those of male and female university students using a custom-made questionnaire. The prevalence of experiences of anxiety and depression was high in all groups. Significantly less male soccer players had heard of cognitive behavioural therapy (CBT) or knew what CBT was compared with all other groups. Barriers to obtaining support for mental health concerns included not knowing how or when to seek help and what treatment entailed. Participants indicated that they would first turn to family and friends rather than coaches or professionals for help. A preference for CBT over counselling was indicated by the majority of the soccer players and students. The findings of this study can be applied during the development of suitable evidence-based interventions tailored for elite academy soccer players

Elite Academy Soccer Players’ Perceptions towards Cognitive Behavioural Therapy

The purpose of the present study was to address perceptions towards Cognitive Behavioural Therapy (CBT) in soccer. Twenty-four male, elite academy soccer players (M age = 20.04) completed a custom-made questionnaire which included education on CBT. The results found that: i) initially, only 8% of players had heard of CBT whilst only 4% of players knew what CBT was, ii) players strongly agreed that CBT should be offered to all players, iii) not knowing how/where to seek help was identified as the main barrier to CBT, iv) players indicated a preference for one-to-one and face-to-face CBT, as opposed to small-group or online-CBT, and v) players perceived they would receive most support from family/friends, and least support from teammates, if they were to undertake CBT. These findings demonstrate that whilst initial awareness and knowledge of CBT is low, general perceptions towards CBT are positive once athletes are educated on the area

Single Nucleotide Polymorphism in the LDHA Gene as a Potential Marker for the Racing Performance of Pigeons

The objective of the present study was to investigate the relationship between the g.2582481G>A, g.2583935G>A and g.2584057C>T single nucleotide polymorphisms (SNPs) within the lactate dehydrogenase A gene (LDHA) coding for lactate dehydrogenase isoform A and the racing performance of homing pigeons. As a measure of racing performance, we used the mean values of ace points won by individual birds during the whole season. The estimated heritability of the racing performance of pigeons was relatively low (h2=0.0596; SE=0.0249). The analysis performed for all race reports together showed that the factors such as gender, weather conditions at the start and at the end of the race affect the analyzed trait. Of the 3 single nucleotide polymorphisms, only the effect of the g.2582481G>A genotype on the performance of racing pigeons was significant. Statistical analysis indicated the difference in the value of ace points between the animals of GG and GA genotypes for the g.2582481G>A SNP. The study showed that the genotype homozygous for g.2582481A is linked to the highest mean value of ace points. Consequently, the relationship between the genotype for g.2582481G>A and the racing performance was shown

DNA methylation regulates expression of VEGF-R2 (KDR) and VEGF-R3 (FLT4)

Abstract Background Vascular Endothelial Growth Factors (VEGFs) and their receptors (VEGF-Rs) are important regulators for angiogenesis and lymphangiogenesis. VEGFs and VEGF-Rs are not only expressed on endothelial cells but also on various subtypes of solid tumors and leukemias contributing to the growth of the malignant cells. This study was performed to examine whether VEGF-R2 (KDR) and VEGF-R3 (FLT4) are regulated by DNA methylation. Methods Real-time (RT) PCR analysis was performed to quantify KDR and FLT4 expression in some ninety leukemia/lymphoma cell lines, human umbilical vein endothelial cells (HUVECs) and dermal microvascular endothelial cells (HDMECs). Western blot analyses and flow cytometric analyses confirmed results at the protein level. After bisulfite conversion of DNA we determined the methylation status of KDR and FLT4 by DNA sequencing and by methylation specific PCR (MSP). Western blot analyses were performed to examine the effect of VEGF-C on p42/44 MAPK activation. Results Expression of KDR and FLT4 was observed in cell lines from various leukemic entities, but not in lymphoma cell lines: 16% (10/62) of the leukemia cell lines expressed KDR, 42% (27/65) were FLT4 positive. None of thirty cell lines representing six lymphoma subtypes showed more than marginal expression of KDR or FLT4. Western blot analyses confirmed KDR and FLT4 protein expression in HDMECs, HUVECs and in cell lines with high VEGF-R mRNA levels. Mature VEGF-C induced p42/44 MAPK activation in the KDR- /FLT4+ cell line OCI-AML1 verifying the model character of this cell line for VEGF-C signal transduction studies. Bisulfite sequencing and MSP revealed that GpG islands in the promoter regions of KDR and FLT4 were unmethylated in HUVECs, HDMECs and KDR + and FLT4 + cell lines, whereas methylated cell lines did not express these genes. In hypermethylated cell lines, KDR and FLT4 were re-inducible by treatment with the DNA demethylating agent 5-Aza-2'deoxycytidine, confirming epigenetic regulation of both genes. Conclusions Our data show that VEGF-Rs KDR and FLT4 are silenced by DNA methylation. However, if the promoters are unmethylated, other factors (e.g. transactivation factors) determine the extent of KDR and FLT4 expression

BCR-ABL1-independent PI3Kinase activation causing imatinib-resistance

<p>Abstract</p> <p>Background</p> <p>The <it>BCR-ABL1 </it>translocation occurs in chronic myeloid leukemia (CML) and in 25% of cases with acute lymphoblastic leukemia (ALL). The advent of tyrosine kinase inhibitors (TKI) has fundamentally changed the treatment of CML. However, TKI are not equally effective for treating ALL. Furthermore, <it>de novo </it>or <it>secondary </it>TKI-resistance is a significant problem in CML. We screened a panel of <it>BCR-ABL1 </it>positive ALL and CML cell lines to find models for imatinib-resistance.</p> <p>Results</p> <p>Five of 19 <it>BCR-ABL1 </it>positive cell lines were resistant to imatinib-induced apoptosis (KCL-22, MHH-TALL1, NALM-1, SD-1, SUP-B15). None of the resistant cell lines carried mutations in the kinase domain of <it>BCR-ABL1 </it>and all showed resistance to second generation TKI, nilotinib or dasatinib. STAT5, ERK1/2 and the ribosomal S6 protein (RPS6) are <it>BCR-ABL1 </it>downstream effectors, and all three proteins are dephosphorylated by imatinib in sensitive cell lines. TKI-resistant phosphorylation of RPS6, but responsiveness as regards JAK/STAT5 and ERK1/2 signalling were characteristic for resistant cell lines. PI3K pathway inhibitors effected dephosphorylation of RPS6 in imatinib-resistant cell lines suggesting that an oncogene other than <it>BCR-ABL1 </it>might be responsible for activation of the PI3K/AKT1/mTOR pathway, which would explain the TKI resistance of these cells. We show that the TKI-resistant cell line KCL-22 carries a PI3Kα E545G mutation, a site critical for the constitutive activation of the PI3K/AKT1 pathway. Apoptosis in TKI-resistant cells could be induced by inhibition of AKT1, but not of mTOR.</p> <p>Conclusion</p> <p>We introduce five Philadelphia-chromosome positive cell lines as TKI-resistance models. None of these cell lines carries mutations in the kinase domain of <it>BCR-ABL1 </it>or other molecular aberrations previously indicted in the context of imatinib-resistance. These cell lines are unique as they dephosphorylate ERK1/2 and STAT5 after treatment with imatinib, while PI3K/AKT1/mTOR activity remains unaffected. Inhibition of AKT1 leads to apoptosis in the imatinib-resistant cell lines. In conclusion, Ph+ cell lines show a form of imatinib-resistance attributable to constitutive activation of the PI3K/AKT1 pathway. Mutations in <it>PIK3CA</it>, as observed in cell line KCL-22, or PI3K activating oncogenes may undelie TKI-resistance in these cell lines.</p

Epigenetic regulation of CD44 in Hodgkin and non-Hodgkin lymphoma

<p>Abstract</p> <p>Background</p> <p>Epigenetic inactivation of tumor suppressor genes (TSG) by promoter CpG island hypermethylation is a hallmark of cancer. To assay its extent in human lymphoma, methylation of 24 TSG was analyzed in lymphoma-derived cell lines as well as in patient samples.</p> <p>Methods</p> <p>We screened for TSG methylation using methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) in 40 lymphoma-derived cell lines representing anaplastic large cell lymphoma, Burkitt lymphoma (BL), diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), Hodgkin lymphoma and mantle cell lymphoma (MCL) as well as in 50 primary lymphoma samples. The methylation status of differentially methylated <it>CD44 </it>was verified by methylation-specific PCR and bisulfite sequencing. Gene expression of <it>CD44 </it>and its reactivation by DNA demethylation was determined by quantitative real-time PCR and on the protein level by flow cytometry. Induction of apoptosis by anti-CD44 antibody was analyzed by annexin-V/PI staining and flow cytometry.</p> <p>Results</p> <p>On average 8 ± 2.8 of 24 TSG were methylated per lymphoma cell line and 2.4 ± 2 of 24 TSG in primary lymphomas, whereas 0/24 TSG were methylated in tonsils and blood mononuclear cells from healthy donors. Notably, we identified that <it>CD44 </it>was hypermethylated and transcriptionally silenced in all BL and most FL and DLBCL cell lines, but was usually unmethylated and expressed in MCL cell lines. Concordant results were obtained from primary lymphoma material: <it>CD44 </it>was not methylated in MCL patients (0/11) whereas <it>CD44 </it>was frequently hypermethylated in BL patients (18/29). In cell lines with <it>CD44 </it>hypermethylation, expression was re-inducible at mRNA and protein levels by treatment with the DNA demethylating agent 5-Aza-2'-deoxycytidine, confirming epigenetic regulation of <it>CD44</it>. CD44 ligation assays with a monoclonal anti-CD44 antibody showed that CD44 can mediate apoptosis in CD44⁺lymphoma cells. <it>CD44 </it>hypermethylated, CD44^-lymphoma cell lines were consistently resistant towards anti-CD44 induced apoptosis.</p> <p>Conclusion</p> <p>Our data show that <it>CD44 </it>is epigenetically regulated in lymphoma and undergoes <it>de novo </it>methylation in distinct lymphoma subtypes like BL. Thus <it>CD44 </it>may be a promising new epigenetic marker for diagnosis and a potential therapeutic target for the treatment of specific lymphoma subtypes.</p

Detekcja jałówek z trudnymi porodami za pomocą sztucznych sieci neuronowych z uwzględnieniem genotypów ERalfaBGLI, ERalfa-SNABI i CYP19-PVUII

The aim of this study was to detect heifers with dystocia using artificial neural networks (ANN). A total of 531 calving records of Holstein-Friesian heifers of Black-and-White strain and 8 diagnostic variables were used. The output variable was the class of calving difficulty: difficult or easy. Perceptrons with one (MLP1) and two (MLP2) hidden layers and radial basis function (RBF) networks were investigated. The root mean square error and the structure of selected ANN (number of neurons in the input, hidden and output layers) were 0.22, 10-4-1; 0.25, 10-17-17-1 and 0.19, 10-25-1 for MLP1, MLP2 and RBF, respectively. The percentage of correctly recognized heifers with difficult and easy calvings and that of correctly diagnosed heifers from both categories for the training and validation sets were approx. 90%. The same values for the test set were 75-83%, 82–88% and 82–86%, respectively. In both cases, no significant differences in these proportions were found. The following variables contributed most to the detection of heifers with dystocia: gestation length, BCS index, CYP19-PvuII and ERα-BglI genotypes and percentage of HF genes in heifer’s genotype.Celem niniejszej pracy była detekcja jałówek z trudnymi porodami przy użyciu sztucznych sieci neuronowych (SSN).Wykorzystano w tym celu dane o 531 wycieleniach jałówek rasy polskiej holsztyńsko-fryzyjskiej odmiany czarno-białej oraz 8 zmiennych diagnostycznych. Zmienną wyjściową była klasa trudności porodu: trudny lub łatwy. Analizowano perceptrony z jedną (MLP1) i dwoma (MLP2) warstwami ukrytymi oraz sieci o radialnych funkcjach bazowych (RBF). Pierwiastek błędu średniokwadratowego oraz struktura wybranych SSN (liczba neuronów w warstwach wejściowej, ukrytej i wyjściowej) były następujące: 0,22, 10-4-1; 0,25, 10-17-17-1 i 0,19, 10-25-1 odpowiednio dla MLP1, MLP2 i RBF. Odsetek prawidłowo rozpoznanych jałówek z trudnymi i łatwymi porodami oraz odsetek prawidłowo zdiagnozowanych jałówek z obu kategorii dla zbioru uczącego i walidacyjnego wynosiły ok. 90%.Wartości te dla zbioru testowego wynosiły odpowiednio: 75–83%, 82–88% i 82–86%. W obu przypadkach nie stwierdzono istotnych statystycznie różnic między tymi proporcjami. Następujące zmienne miały największy wkład w detekcję jałówek z trudnymi porodami: długość ciąży, indeks BCS, genotypy CYP19-PvuII i ERα-BglI oraz procentowy udział genow hf w genotypie jałówki