The impact of wet cupping on haematological and inflammatory parameters in a sample of Jordanian team players.

Background/objective: The practice of complementary and alternative medicine has significantly gained acceptance worldwide, such as Al-Hijama, also known as cupping therapy. Despite the growing popularity of therapeutic cupping among athletes, little is known about the impact of cupping therapy on sports fields. The current study was designed to explore the effect of wet cupping therapy on the haematological and inflammatory parameters in Jordanian national team players. Methods: The procedure was carried out at a specialized centre for cupping in Amman on the morning of the 19th Rajab. The data were obtained from 14 healthy male participants aged between 21 and 22 years. The haematological and inflammatory parameters were assessed by comparing venous blood components before and after four weeks of wet cupping. Results: Complete blood count (CBC) analysis of venous blood samples four weeks after wet cupping showed a significant increase in the values of total white blood cells (WBCs), neutrophils, lymphocytes, red blood cells (RBCs), haematocrit, and haemoglobin as compared with venous blood samples before cupping. Blood film examination of venous blood samples post-cupping revealed normocytic normochromic RBCs; WBCs and platelets were unremarkable. Analysis of inflammatory markers post cupping showed a significant decrease in the monocyte/lymphocyte ratio (MLR) and platelet/lymphocyte ratio (PLR) but no differences in neutrophil/lymphocyte ratio (NLR). Conclusion: The findings of this study suggest that wet cupping has an indispensable influence on haematological and immunological parameters in athletes, where it reinforces cellular immunity, generates younger blood cells, and reduces inflammation markers. It is probable, therefore, that cupping improves sports performance and achievement. The evidence from this research adds to a growing body of literature on cupping therapy in sports.

Radioreparative Effect of Diode Laser on Leukopoiesis Recovery: A Pilot Study.

The aim of the present study was to investigate the effect of laser therapy on leukopoiesis recovery after irradiation with ionizing radiation. A dose of ionizing radiation was used that induced the hematological form of radiation sickness, reducing the number of blood cells. Subsequently, mice were treated with non-ionizing laser radiation. Based on the examination of the peripheral blood, the study found that laser therapy significantly impacted the number of eosinophils and basophils two weeks after irradiation. Laser therapy also led to the faster reparation of the lymphocyte lineage of white blood cells (WBCs). The research showed that the examined therapeutic laser had a long-term radioreparative effect on gamma-irradiated mice, improving the absolute counts of different lines of WBCs. The results of this study could have implications for the treatment of radiation sickness in humans.

Advantages of the Liposomal Form of Xymedon in Leukopoiesis Restoration against the Background of Myelosuppressive Therapy with Liposomal Antineoplastic Drugs in Experiment.

We analyzed advantages of the liposomal form of Xymedon (50 and 100 mg/kg) over free Xymedon (in the corresponding doses) in leukopoiesis restoration in rats with Walker-256 carcinoma treated with liposomal combination of doxorubicin (4 mg/kg) and cyclophosphamide (45 mg/kg) (single intravenous injection on day 11 after transplantation of tumor cells). Liposomal and free Xymedon were injected intravenously over 5 days starting from day 11 of the experiment. Changes in leukopoiesis in peripheral blood and myelograms were assessed on days 3 and 7 after chemotherapy. Liposomal Xymedon in both doses (unlike its free form) 2-fold increased the number of lymphocytes on day 3 after chemotherapy in comparison with the level observed after administration of liposomal cytostatics alone. Liposomal Xymedon in a dose of 50 mg/kg (but not 100 mg/kg) promoted the maintenance of monocyte count at the level of intact control on days 3 and 7 after chemotherapy. Liposomal Xymedon in a dose of 50 mg/kg and free Xymedon in a dose of 100 mg/kg equally stimulated the increase in myelocytes content in the bone marrow to the level of intact control on day 3 after chemotherapy, thus promoting restoration of granulocytopoiesis.

The milk thistle (Silybum marianum) compound Silibinin stimulates leukopoiesis from mouse embryonic stem cells.

The milk thistle compound Silibinin (i.e., a 1:1 mixture of Silybin A and Silybin B) stimulates vasculogenesis of mouse embryonic stem (ES) cells. Because vasculogenesis and leukopoiesis are interrelated, the effect of Silibinin on leukopoiesis of ES cells was investigated. Treatment of differentiating ES cells with hydrosoluble Silibinin-C-2',3-dihydrogen succinate dose-dependent increased the number of CD18+ , CD45+ , and CD68+ cells, indicating leukocyte/macrophage differentiation. Silibinin treatment activated phosphoinositide 3-kinase (PI3K), AKT (protein kinase B), signal transducer and activator of transcription 3 (STAT3), stimulated hypoxia-induced factor-1α (HIF-1α), and vascular endothelial growth factor receptor 2 (VEGFR2) expression and raised intracellular nitric oxide (NO). Western blot experiments showed that upon coincubation with either the PI3K inhibitor LY294002, the STAT3 inhibitor Stattic, the AKT antagonist AKT inhibitor VIII, or the NO inhibitor L-NAME, the Silibinin-induced expression of CD18, CD45, and CD68 was abolished. Moreover, the stimulation of HIF-1α and VEGFR2 expression was blunted upon STAT3 and PI3K/AKT inhibition. Treatment of differentiating ES cells with L-NAME abolished the stimulation of VEGFR2 and VE-cadherin expression achieved with Silibinin, indicating that NO is involved in vasculogenesis and leukocyte differentiation pathways. In summary, the data of the present study demonstrate that Silibinin stimulates leukocyte differentiation of ES cells, which is associated to vasculogenesis and regulated by PI3K/AKT-, STAT3-, and NO-mediated signaling.

An Integrative multi-lineage model of variation in leukopoiesis and acute myelogenous leukemia.

BACKGROUND: Acute myelogenous leukemia (AML) progresses uniquely in each patient. However, patients are typically treated with the same types of chemotherapy, despite biological differences that lead to differential responses to treatment. RESULTS: Here we present a multi-lineage multi-compartment model of the hematopoietic system that captures patient-to-patient variation in both the concentration and rates of change of hematopoietic cell populations. By constraining the model against clinical hematopoietic cell recovery data derived from patients who have received induction chemotherapy, we identified trends for parameters that must be met by the model; for example, the mitosis rates and the probability of self-renewal of progenitor cells are inversely related. Within the data-consistent models, we found 22,796 parameter sets that meet chemotherapy response criteria. Simulations of these parameter sets display diverse dynamics in the cell populations. To identify large trends in these model outputs, we clustered the simulated cell population dynamics using k-means clustering and identified thirteen 'representative patient' dynamics. In each of these patient clusters, we simulated AML and found that clusters with the greatest mitotic capacity experience clinical cancer outcomes more likely to lead to shorter survival times. Conversely, other parameters, including lower death rates or mobilization rates, did not correlate with survival times. CONCLUSIONS: Using the multi-lineage model of hematopoiesis, we have identified several key features that determine leukocyte homeostasis, including self-renewal probabilities and mitosis rates, but not mobilization rates. Other influential parameters that regulate AML model behavior are responses to cytokines/growth factors produced in peripheral blood that target the probability of self-renewal of neutrophil progenitors. Finally, our model predicts that the mitosis rate of cancer is the most predictive parameter for survival time, followed closely by parameters that affect the self-renewal of cancer stem cells; most current therapies target mitosis rate, but based on our results, we propose that additional therapeutic targeting of self-renewal of cancer stem cells will lead to even higher survival rates.

Stimulation of vasculogenesis and leukopoiesis of embryonic stem cells by extracellular transfer RNA and ribosomal RNA.

OBJECTIVE: Cell injury releases nucleic acids supporting inflammation and stem cell activation. Here, the impact of extracellular ribonucleic acid, especially transfer RNA (ex-tRNA), on vasculogenesis and leukopoiesis of mouse embryonic stem (ES) cells was investigated. APPROACH AND RESULTS: ex-tRNA, whole cell RNA and ribosomal RNA (ex-rRNA) but not DNA increased CD31-positive vascular structures in embryoid bodies. Ex-tRNA and ex-rRNA increased numbers of VEGFR2(+), CD31(+) and VE-cadherin(+) vascular cells as well as CD18(+), CD45(+) and CD68(+) cells, indicating leukocyte/macrophage differentiation. This was paralleled by mRNA and protein expression of hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor-165 (VEGF165) and neuropilin 1 (NRP1), phosphorylation of phosphatidyl inositol 3-kinase (PI3K) and VEGF receptor 2 (VEGFR2) as well as mRNA expression of α-smooth muscle actin (α-SMA). ex-tRNA was taken up by endosomes, increased expression of the pro-angiogenic semaphorin B4 receptor plexin B1 as well as the ephrin-type B receptor 4 (EphB4) and ephrinB2 ligand and enhanced cell migration, which was inhibited by the VEGFR2 antagonist SU5614 and the PI3K inhibitor LY294002. This likewise abolished the effects of ex-tRNA on vasculogenesis and leukopoiesis of ES cells. Ex-tRNA increased NOX1, NOX2, NOX4 and DUOX2 mRNA and boosted the generation of superoxide and hydrogen peroxide which was inhibited by radical scavengers, the NADPH oxidase inhibitors apocynin, VAS2870, ML171, and plumbagin as well as shRNA silencing of NOX1 and NOX4. CONCLUSIONS: Our findings indicate that ex-tRNA treatment induces vasculogenesis and leukopoiesis of ES cells via superoxide/hydrogen peroxide generated by NADPH oxidase and activation of VEGFR2 and PI3K.