Fibromyalgický syndrom (FMS) je stav nebo porucha, ale nikoliv nemoc. Není zcela objasněna příčina vzniku, ale dosavadní výzkumy naznačují, že jednou z příčin nebo dokonce hlavní příčinou je nerovnováha mozkových transmitérů , jejichž úlohou je kontrola bolesti, citlivosti a ovlivnění svalového metabolizmu. FMS vyžaduje velice komplexní terapii a komplexní diagnosti- ku. Je důležitá spolupráce s psychology a psychiatry pro případ upozornění na psychické poruchy maskované symptomatologií fibromyalgie. Na léčbě FMS se musí podílet jak lékaři, fyzioterapeuti a ergoterapeuti, tak psychologové, protože č stým neúspěchem léčby FMS je právě monoterapeutický přístup.
The fibromyalgic syndrome (FMS) is a condition or disorder but not a disease. The ethiological cause is not clarified up to now, but actual research sug- gests that one cause or even main cause could be imbalance of brain neurotransmitters, the role of which is pain and sensitivity control and influence of muscle metabolism. FMS required very complex therapy and complex diagnostics. Very important is the cooperation with psychologists, psychiatrists for the case of calling attention on psychical disorders masked by fibromyalgic symptomatology. Treatment of fibromyalgic has to be shared by physiotherapeutists and ergotherapeutists and psychologists too, because the failure of FMS treatment could be often caused by monotherapeutic attitude.
Acute myeloid leukemia (AML), a heterogeneous hematologic malignancy, has generally a poor prognosis despite the recent advancements in diagnostics and treatment. Genetic instability, particularly mutations in the FMS-like tyrosine kinase 3 (FLT3) gene, is associated with severe outcomes. Approximately 30 % of AML patients harbor FLT3 mutations, which have been linked to higher relapse and reduced survival rates. Traditional AML treatments employ cytarabine and anthracyclines drugs. Furthermore, the development of FLT3 inhibitors has significantly improved therapy for FLT3-mutated AML patients. For example, the introduction of midostaurin, the first FLT3 inhibitor, improved patient outcomes. However, resistant AML cell clones continue to pose a challenge to the success of AML treatment. This review discusses FLT3 kinase, mutations, and role in AML pathogenesis. It explores the molecular mechanisms of FLT3 activation, signaling pathways, and the structure and function of the FLT3 receptor. Current and emerging therapeutic approaches are presented, while highlighting the latest FLT3 inhibitors in clinical use, and strategies to overcome drug resistance. Future directions, including personalized therapies and novel drug designs, are examined to provide updated insights into FLT3-targeted treatments. This comprehensive review aims to guide clinicians and researchers in the development of innovative therapies to improve AML patient outcomes.
- MeSH
- Leukemia, Myeloid, Acute * drug therapy genetics MeSH
- Drug Resistance, Neoplasm drug effects MeSH
- Molecular Targeted Therapy * MeSH
- Protein Kinase Inhibitors * therapeutic use pharmacology MeSH
- Humans MeSH
- Mutation MeSH
- Antineoplastic Agents therapeutic use pharmacology MeSH
- Signal Transduction drug effects MeSH
- fms-Like Tyrosine Kinase 3 * antagonists & inhibitors genetics metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- MeSH
- Leukemia, Myeloid, Acute * diagnosis drug therapy MeSH
- Induction Chemotherapy methods MeSH
- Drug Therapy, Combination methods MeSH
- Humans MeSH
- Survival Rate MeSH
- Mutation MeSH
- Prognosis MeSH
- Antineoplastic Agents therapeutic use MeSH
- Risk Factors MeSH
- fms-Like Tyrosine Kinase 3 genetics MeSH
- Check Tag
- Humans MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
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Aims. The purpose of this study was to examine the effects of a six-month movement intervention program on the fundamental movement skills of preschool children and explore how parents of these children evaluate their children's skills. Sample and setting. The data collection was carried out for two years (2018–2020). An intervention group of 34 children and a control group of 31 children were recruited from 3–6 years (mean age=4.98; SD=0.87) of two preschools in the Czech Republic. FMS were tested by BOT-2 and parents of the children filled out the questionnaire about the demographic data and their estimation of their childrenʼs FMS. Statistical analysis. Mixed linear models were used to evaluate the effectiveness of the intervention program and the differences between the objective and subjective results of FMS were assessed by parametric (paired sample t-test) and nonparametric tests (Wilcoxon test). Results. The results revealed only one significant change in the FMS in the subscale of bilateral coordination (β=0.50; CI=0.17–0.82; p=0.003). Parents evaluated their childrenʼs FMS relatively accurately. Parents overestimated only the ability of the upper limb coordination (Z=-2.273, p=0.023). Limitations. Quasi-experimental design, number of participants, testing of preschool children and premature termination of data collection due to COVID-19 may be considered to be limiting
- MeSH
- Fecal Incontinence nursing MeSH
- Infections transmission MeSH
- Humans MeSH
- Health Care Costs MeSH
- Diarrhea complications prevention & control MeSH
- Aged MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Aged MeSH
- Publication type
- Case Reports MeSH
Background: Soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) are used in diagnosing preeclampsia (PE), but their potential in early prediction in pregnant women at 16 to 20 weeks gestation (WG) has remained unexplored. Methods: We retrospectively measured serum levels of sFlt-1 and PlGF in 120 pregnant women at 16 to 20 WG. Among these women, 16 had early-onset PE and 23 had late-onset PE. Results: Compared with normal pregnancy values, in the serum of women in whom PE later developed, sFlt-1 values increased (P <.001), values of PlGF decreased (P = .001), and the sFlt-1/PlGF ratio increased (P <.001) as early as 16 to 20 WG. Receiver operating characteristic (ROC) curve analysis for the sFlt-1/PlGF ratio at 16 to 20 WG showed an area under the curve (AUC) value of 0.863 (95% confidence interval [CI], 0.788-0.918), P <.001, sensitivity of 74.4%, and specificity of 86.6% for PE in general; and AUC of 0.970 (95% CI, 0.913-0.994), P <.001, sensitivity of 100%, and specificity of 81.5% for early-onset PE only. Also, we determined the 5th and 95th percentiles for sFlt-1, PlGF, and sFlt-1/PlGF ratio values of healthy pregnant women. Conclusion: sFlt-1 and PlGF and, in particular, the sFlt-1/PlGF ratio can detect PE as early as 16 to 20 WG-as long as 10 to 15 weeks before PE onset.
- MeSH
- Adult MeSH
- Humans MeSH
- Young Adult MeSH
- Placenta Growth Factor blood MeSH
- Pre-Eclampsia blood diagnosis MeSH
- Vascular Endothelial Growth Factor Receptor-1 blood MeSH
- Retrospective Studies MeSH
- Sensitivity and Specificity MeSH
- Pregnancy MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Young Adult MeSH
- Pregnancy MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- MeSH
- Leukemia, Myeloid, Acute * drug therapy genetics MeSH
- Gemtuzumab MeSH
- Humans MeSH
- Staurosporine therapeutic use MeSH
- fms-Like Tyrosine Kinase 3 genetics MeSH
- Check Tag
- Humans MeSH
- Publication type
- Letter MeSH
- Geographicals
- Czech Republic MeSH
Acute myeloid leukaemia (AML) is a complex haematological malignancy characterised by diverse genetic alterations leading to abnormal proliferation of myeloid precursor cells. One of the most significant genetic alterations in AML involves mutations in the FLT3 gene, which plays a critical role in haematopoiesis and haematopoietic homeostasis. This review explores the current understanding of FLT3 gene mutations and isoforms and the importance of the FLT3 protein in AML. FLT3 mutations, including internal tandem duplications (FLT3-ITD) and point mutations in the tyrosine kinase domain (FLT3-TKD), occur in 25-30% in AML and are associated with poor prognosis. FLT3-ITD mutations lead to constitutive activation of the FLT3 signalling pathway, promoting cell survival and proliferation. FLT3-TKD mutations affect the tyrosine kinase domain and affect AML prognosis in various ways. Furthermore, FLT3 isoforms, including shorter variants, contribute to the complexity of FLT3 biology. Additionally, nonpathological polymorphisms in FLT3 are being explored for their potential impact on AML prognosis and treatment response. This review also discusses the development of molecular treatments targeting FLT3, including first-generation and next-generation tyrosine kinase inhibitors, highlighting the challenges of resistance that often arise during therapy. The final chapter describes FLT3 protein domain rearrangements and their relevance to AML pathogenesis.
- MeSH
- Leukemia, Myeloid, Acute * genetics MeSH
- Humans MeSH
- Mutation genetics MeSH
- Protein Isoforms genetics MeSH
- fms-Like Tyrosine Kinase 3 genetics MeSH
- Protein-Tyrosine Kinases MeSH
- Cell Survival MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
