UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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.

An older patient with stage II bladder carcinoma presented with 1 week of fatigue and 2 days of dyspnea on exertion. He was receiving carboplatin/gemcitabine with 6 mg of pegylated G-CSF chemotherapy; his white blood cell count was elevated, hemoglobin low, and ferritin notably increased. What is the diagnosis and what would you do next?

暂无摘要。

Myelosuppression is a predominant side-effect of radiotherapy, which manifests as the lower activity of blood cell precursors in bone marrow. Though progress in anti-myelosuppression has been made by the application of growth factors e.g., the granulocyte colony-stimulating factor (G-CSF), the side-effects (e.g., bone-pain, liver injury, and lung toxicity) limit their applications in clinic. Herein, we developed a strategy of efficiently normalizing leukopoiesis using gadofullerene nanoparticles (GFNPs) against myelosuppression triggered by radiation. Specifically, GFNPs with high radical-scavenging abilities elevated the generation of leukocytes and alleviated the bone marrow\'s pathological state under myelosuppression. Notably, GFNPs potentiated the differentiation, development, and maturation of leukocytes (neutrophils, lymphocytes) in radiation bearing mice even better than what G-CSF did. In addition, GFNPs had little toxicity towards the main organs including the heart, liver, spleen, lung, and kidney. This work provides an in-depth understanding of how advanced nanomaterials mitigate myelosuppression by regulating leukopoiesis.

The granulocyte colony-stimulating factor receptor (G-CSFR), encoded by the CSF3R gene, is involved in the production and function of neutrophilic granulocytes. Somatic mutations in CSF3R leading to truncated G-CSFR forms are observed in acute myeloid leukemia (AML), particularly those subsequent to severe chronic neutropenia (SCN), as well as in a subset of patients with other leukemias.
This investigation introduced equivalent mutations into the zebrafish csf3r gene via genome editing and used a range of molecular and cellular techniques to understand the impact of these mutations on immune cells across the lifespan.
Zebrafish harboring truncated G-CSFRs showed significantly enhanced neutrophil production throughout successive waves of embryonic hematopoiesis and a neutrophil maturation defect in adults, with the mutations acting in a partially dominant manner.
This study has elucidated new insights into the impact of G-CSFR truncations throughout the life-course and created a bone fide zebrafish model for further investigation.

During acute infectious and inflammatory conditions, a large number of neutrophils are in high demand as they are consumed in peripheral organs. The hematopoietic system rapidly responds to the demand by turning from steady state to emergency granulopoiesis to expedite neutrophil generation in the bone marrow (BM). How the hematopoietic system integrates pathogenic and inflammatory stress signals into the molecular cues of emergency granulopoiesis has been the subject of investigations. Recent studies in the field have highlighted emerging concepts, including the direct sensing of pathogens by BM resident or sentinel hematopoietic stem and progenitor cells (HSPCs), the crosstalk of HSPCs, endothelial cells, and stromal cells to convert signals to granulopoiesis, and the identification of novel inflammatory molecules, such as C/EBP-β, ROS, IL-27, IFN-γ, CXCL1 with direct effects on HSPCs. In this review, we will provide a detailed account of emerging concepts while reassessing well-established cellular and molecular players of emergency granulopoiesis. While providing our views on the discrepant results and theories, we will postulate an updated model of granulopoiesis in the context of health and disease.

Neutrophils are key pathogen exterminators of the innate immune system endowed with oxidative and non-oxidative defense mechanisms. More recently, a more complex role for neutrophils as decision shaping cells that instruct other leukocytes to fine-tune innate and adaptive immune responses has come into view. Under homeostatic conditions, neutrophils are short-lived cells that are continuously released from the bone marrow. Their development starts with undifferentiated hematopoietic stem cells that pass through different immature subtypes to eventually become fully equipped, mature neutrophils capable of launching fast and robust immune responses. During severe (systemic) inflammation, there is an increased need for neutrophils. The hematopoietic system rapidly adapts to this increased demand by switching from steady-state blood cell production to emergency granulopoiesis. During emergency granulopoiesis, the de novo production of neutrophils by the bone marrow and at extramedullary sites is augmented, while additional mature neutrophils are rapidly released from the marginated pools. Although neutrophils are indispensable for host protection against microorganisms, excessive activation causes tissue damage in neutrophil-rich diseases. Therefore, tight regulation of neutrophil homeostasis is imperative. In this review, we discuss the kinetics of neutrophil ontogenesis in homeostatic conditions and during emergency myelopoiesis and provide an overview of the different molecular players involved in this regulation. We substantiate this review with the example of an autoinflammatory disease, i.e. systemic juvenile idiopathic arthritis.

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.

Integration of external signals and B-lymphoid transcription factor activities organise B cell lineage commitment through alternating cycles of proliferation and differentiation, producing a diverse repertoire of mature B cells. We use single-cell transcriptomics/proteomics to identify differentially expressed gene networks across B cell development and correlate these networks with subtypes of B cell leukemia. Here we show unique transcriptional signatures that refine the pre-B cell expansion stages into pre-BCR-dependent and pre-BCR-independent proliferative phases. These changes correlate with reciprocal changes in expression of the transcription factor EBF1 and the RNA binding protein YBX3, that are defining features of the pre-BCR-dependent stage. Using pseudotime analysis, we further characterize the expression kinetics of different biological modalities across B cell development, including transcription factors, cytokines, chemokines, and their associated receptors. Our findings demonstrate the underlying heterogeneity of developing B cells and characterise developmental nodes linked to B cell transformation.

The ubiquitin-proteasome system plays important roles in various biological processes as it degrades the majority of cellular proteins. Adequate proteasomal degradation of crucial transcription regulators ensures the proper development of neutrophils. The ubiquitin E3 ligase of Growth factor independent 1 (GFI1), a key transcription repressor governing terminal granulopoiesis, remains obscure. Here we report that the deficiency of the ring finger protein Interferon regulatory factor 2 binding protein 2a (Irf2bp2a) leads to an impairment of neutrophils differentiation in zebrafish. Mechanistically, Irf2bp2a functions as a ubiquitin E3 ligase targeting Gfi1aa for proteasomal degradation. Moreover, irf2bp2a gene is repressed by Gfi1aa, thus forming a negative feedback loop between Irf2bp2a and Gfi1aa during neutrophils maturation. Different levels of GFI1 may turn it into a tumor suppressor or an oncogene in malignant myelopoiesis. Therefore, discovery of certain drug targets GFI1 for proteasomal degradation by IRF2BP2 might be an effective anti-cancer strategy.