Ru Yx

Multiple Organ Invasion by Viruses: Pathological Characteristics in Three Fatal Cases of the 2009 Pandemic Influenza A/H1N1

To further understand the pathological characteristics of multiple organ involvement of the 2009 pandemic influenza A/H1N1 infection, tissues of bronchial mucosa, lung, myocardium, gastrocnemius, and liver from 3 patients with fatal A/H1N1 infections were investigated by light microscopy and transmission electron microscopy. In all 3 patients, bronchial mucosa showed necrotizing bronchiolitis, epithelial necrosis and desquamation, and squamous metaplasia, while lung consolidation or fibrosis was identified. Myocardium and gastrocnemius exhibited focal necrosis and fibrosis, surrounded by muscle cells showing features of cell damage. In liver, there was widespread fatty degeneration and necrosis, most often around the central lobular vein and portal area. Viral particles were found in all samples, frequently located in endothelium, epithelium, and muscle cells. The observations demonstrate that in fatal cases of A/H1N1 infection, viruses not only infect the respiratory system, but also engage in multiple organ invasions, causing pathologic changes.

On the Maturation of Megakaryocytes: A Review with Original Observations on Human In Vivo Cells Emphasizing Morphology and Ultrastructure

Abstract Megakaryocytes engage in the synthesis of a variety of molecular and macromolecular constituents to build-up characteristic megakaryocyte structure and form proplatelets in a series of cells from megakaryocyte precursors to the fully matured cell. The process is illustrated in this review by light microscope morphology and transmission electron microscopy, which emphasizes new findings in human in vivo megakaryocytes, thereby making a contrast with the abundant literature on megakaryocytes from experimental animal and human in vitro material. Four stages are identified and described, based on the development of characteristic structures including α-granules, dense granules (dense-core granules), the demarcation membrane system (DMS), and proplatelets. The mechanism of DMS development is discussed, in terms of hypotheses suggesting origin from the plasma membrane, and contributions of membrane from the Golgi apparatus and endoplasmic reticulum. The formation of the marginal zone is also discussed, which is suggested to result from a circumscription of the peripheral organelle-free cytoplasmic fringe by peripheral circular cytoskeletal elements such as cytoplasmic actin and microtubules.

Morphologic Characteristics of Blastic Plasmacytoid Dendritic Cell Neoplasm: A Case Report

Abstract Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare aggressive lymphoma derived from plasmacytoid dendritic cells or precursor dendritic cells. Despite some 240 reported cases, its morphology and especially ultrastructure has not been satisfactorily studied. A case is reported of a 13 year old boy, who, despite chemotherapy, died within a 12-month period. The electron microscopy findings – microvillous processes, nuclei with slight irregularities, a moderate amount of heterochromatin, and rough endoplasmic reticulum in the form of long, narrow profiles, often in parallel arrangements – taken together, serve to distinguish BPDCN from other neoplastic cells, such as monocytes, plasma cells and the cells of chronic lymphocyte leukemia.

CIAPIN1 targets Na+/H+ exchanger 1 to mediate K562 chronic myeloid leukemia cells’ differentiation via ERK1/2 signaling pathway

CIAPIN1 (cytokine-induced antiapoptotic inhibitor 1) was recently identified as an essential downstream effector of the Ras signaling pathway. However, its potential role in regulating myeloid differentiation remains unclear. In this study, we found depletion of CIAPIN1 by shRNAs led to granulocytic differentiation of K562 cells. Meanwhile, the decrease of NHE1 and up-regulation of phosphorylated ERK1/2 were observed after CIAPIN1 depletion. Interestingly, targeted inhibition of NHE1 further promoted the differentiation of K562 cells with CIAPIN1 silencing. Accordingly, ectopic expression of NHE1 reversed this phenotype. Furthermore, ERK1/2 inhibition with the chemical inhibitor, PD98059, abolished CIAPIN1 silencing-induced differentiation of K562 cells after NHE1 inhibition. Thus, our results revealed important mechanism that CIAPIN1 targeted NHE1 to mediate differentiation of K562 cells via ERK1/2 pathway. Our findings implied CIAPIN1 and NHE1 could be new targets in developing therapeutic strategies against leukemia.

Histiocytic differentiation in acute monocytic leukemia

ABSTRACT Myeloid histocytes of dendritic cells (DCs), Langerhans cells (LCs), and macrophages in varied tissues, as leukemic blasts in acute monoblastic and monocytic leukemia (AML-M5a and M5b), are derived from monocyte progenitors in bone marrow. Based on DC induction from hematopoietic stem cells, myeloid progenitors, and monocytes, and occasional expressions of histocyte-related antigens (HRAs) in M5, we presume some M5 cases share histiocytic phenotypes originally. To clarify the conception, 93 M5 cases were tested with antibodies for HRAs, CD1a, CD163, S100, fascin, and langerin by immunostaining, and their morphologic characteristics were studied by light and transmission electron microscopy. The study revealed that 23 M5 cases were positive for two or more kinds of HRAs and shared a serial of histocytic immunophenotype and morphologic features, which were closely associated with M5b subtype and expression of CD14 in M5.

Platelet production of megakaryocyte: A review with original observations on human in vivo cells and bone marrow.

ABSTRACT Megakaryocytes (MKs) build characteristic structures to produce platelets in a series of steps. Although mechanisms of demarcation membrane system (DMS) and open canalicular system transformation have been proposed based on experimental studies in recent decades, the related evidence is lacking in human cells in vivo. The present review describes and discusses the development of MKs, transformation of DMS, and the release and maturation of proplatelets based on our observation of human MKs in vivo and bone marrow biopsy by light microscope and transmission electron microscope. Four stages were subdivided from megakaryoblasts to matured cells; presumption of DMS transformation from endoplasmic reticulum and Golgi apparatus were evidenced in contrast to another presumption of DMS transformation from plasma membrane in this review. Effectors of interaction between hematopoietic cells, the sucking and shearing force of sinus blood flow on movement of MKs, and release of proplatelets were emphasized. Additionally, the mechanism of secondary splitting of proplatelets in circulation was demonstrated ultrastructurally. These findings and conceptions might significantly promote our understanding of the mechanism of platelet production in human in vivo cells.

Activation of Monocyte-Derived Cells in the Bone Marrow of Myelodysplastic Syndrome

Abstract Object: To study the relationship between monocyte/histiocyte activation and myelodysplastic syndrome (MDS). Methods: Analyzing ultrastructure and myeloperoxidase reaction of nucleated cells in bone marrow from 59 cases of MDS by transmission electron microscopy. Four groups of MDS were subdivided on the basis of their content of activated inflammatory cells – morbid hematopoiesis with minimal inflammatory cell activation (MH-MICA); MDS with monocytic system activation (MSA); MDS with lymphocyte activation (LCA); and MDS with granulocyte activation (GCA). Results: About 20, 22, 7, and 10 cases were classified as MH-MICA (34%), MSA (37%), LCA (12%), and GCA sub-types (17%), respectively. About 3, 5, 0, and 3 cases from MH-MICA, MSA, LCA, and GCA, respectively, underwent leukemic transformation within 2 years. Conclusion: The findings suggest that activation of inflammatory cells in bone marrow is an important feature of MDS, and that monocytes/histocytes are perhaps the most prominent cellular participants in the pathogenesis of MDS.

Myofibroblast Transformation in Metastatic Extramedullary Chronic Myeloid Leukemia: A Case Report

Primary and metastatic carcinomas have a reactive stroma characterized by many myofibroblasts. These cells have also been documented in nonepithelial malignancies, such as sarcomas, malignant melanoma, and lymphoid tumors but in generally far fewer numbers. In non-Hodgkins lymphoma, Hodgkins disease, and leukemia, myofibroblasts are rather rarely documented. In particular, there appear to be no reports of myofibroblasts in either primary bone-marrow/peripheral blood leukemia or secondary deposits of leukemia. In this paper, a case of a relapsed chronic myeloid leukemia appearing in an inguinal lymph node is described, containing many myofibroblasts. The case is detailed and presented with a discussion on the role of myofibroblasts in the progression of nonepithelial cancers.