Primitive Erythropoiesis Is Regulated by miR-126 via Nonhematopoietic Vcam-1+ Cells

SummaryPrimitive erythropoiesis defines the onset of hematopoiesis in the yolk sac of the early embryo and is initiated by the emergence of progenitors assayed as colony-forming cells (EryP-CFCs). EryP-CFCs are detected for only a narrow window during embryonic development, suggesting that both their initiation and termination are tightly controlled. Using the embryonic stem differentiation system to model primitive erythropoiesis, we found that miR-126 regulates the termination of EryP-CFC development. Analyses of miR-126 null embryos revealed that this miR also regulates EryP-CFCs in vivo. We identified vascular cell adhesion molecule-1 (Vcam-1) expressed by a mesenchymal cell population as a relevant target of miR-126. Interaction of EryP-CFCs with Vcam-1 accelerated their maturation to ßh1-globin+ and Ter119+ cells through a Src family kinase. These findings uncover a cell nonautonomous regulatory pathway for primitive erythropoiesis that may provide insight into the mechanism(s) controlling the developmental switch from primitive to definitive hematopoiesis

Research on Control Methods of Planar Motors based on the Modal Forces

There is tight electromagnetic and mechanical coupling among planar motor (PM) 6- degree of freedom (DOF) motions for photolithography in semiconductor manufacturing. For the purpose of achieving decoupled control of the 6-DOF motions, this paper presents the current-controlled model of linear motor (LM) as the actuators, the concept of the actuator forces and the modal forces, and the decoupled dynamics model based on the modal forces. Under some reasonable assumptions on the prototype motor kinematics and structure parameters, the modal forces method successfully decouples the 6-DOF dynamics models and all the dynamics models become simple 2nd order linear systems which can be controlled with multiform linear controller. For the prototype motor, the transformation matrices between the modal forces and the actuator forces are derived and the current-controlled block diagram is presented

Study on the Dynamics of Laser Gyro Strapdown Inertial Measurement Unit System Based on Transfer Matrix Method for Multibody System

The dynamic test precision of the strapdown inertial measurement unit (SIMU) is the basis of estimating accurate motion of various vehicles such as warships, airplanes, spacecrafts, and missiles. So, it is paid great attention in the above fields to increase the dynamic precision of SIMU by decreasing the vibration of the vehicles acting on the SIMU. In this paper, based on the transfer matrix method for multibody system (MSTMM), the multibody system dynamics model of laser gyro strapdown inertial measurement unit (LGSIMU) is developed; the overall transfer equation of the system is deduced automatically. The computational results show that the frequency response function of the LGSIMU got by the proposed method and Newton-Euler method have good agreements. Further, the vibration reduction performance and the attitude error responses under harmonic and random excitations are analyzed. The proposed method provides a powerful technique for studying dynamics of LGSIMU because of using MSTMM and its following features: without the global dynamics equations of the system, high programming, low order of system matrix, and high computational speed

Giant breast phyllodes tumor with silent thromboembolism: A case report

Abstract Background Phyllodes tumor (PT) is a solid fibroepithelial breast lesion with proliferation of stromal and epithelial elements, usually presents with a rapidly expanding feature. Venous thromboembolism (VTE) have been reported to increase the burden in terms of mortality and morbidity of malignant tumor, and associate with worsened survival. However, benign PTs with silent thromboembolism that have not yet been reported, we report an unusual case of massive benign PT that grew on the left side of the breast in a cauliflower‐shaped form and presented severe chronic blood loss and deep VTE. Case A 37‐year‐old woman with uncontrolled pain presented a rapidly enlarging left breast mass, measuring approximately 30 × 20 × 15 cm3 that first started 25 years ago. color Doppler ultrasound showed a large mass lesion on the left breast and deep VTE, several enlarged lymph nodes in the left axilla and mediastinum, which presented a malignant character. However, the biopsies of the mass did not show evidence of malignancy and the pathology result was considered to be benign PT. The patient was treated with an inferior vena cava and anticoagulation, the operation was arranged according to the surgical procedure, the patient recovered very well after mastectomy. Conclusion This case is unique in that the giant breast mass presented with malignant character, was eventually pathologically confirmed to be benign PT, and it's rare that the benign tumor accompanied with silent thromboembolism. This finding describes the atypia features of giant benign PT and reminds the surgeon to consider the factor of VTE and risk when encountering ulcerative benign breast tumor and avoid excessive treatment

MAPK6-AKT signaling promotes tumor growth and resistance to mTOR kinase blockade.

Mitogen-activated protein kinase 6 (MAPK6) is an atypical MAPK. Its function in regulating cancer growth remains elusive. Here, we reported that MAPK6 directly activated AKT and induced oncogenic outcomes. MAPK6 interacted with AKT through its C34 region and the C-terminal tail and phosphorylated AKT at S473 independent of mTORC2, the major S473 kinase. mTOR kinase inhibitors have not made notable progress in the clinic. Our identified MAPK6-AKT axis may provide a major resistance pathway. Besides repressing growth, inhibiting MAPK6 sensitized cancer cells to mTOR kinase inhibitors. MAPK6 overexpression is associated with decreased overall survival and the survival of patients with lung adenocarcinoma, mesothelioma, uveal melanoma, and breast cancer. MAPK6 expression also correlated with AKT phosphorylation at S473 in human cancer tissues. We conclude that MAPK6 can promote cancer by activating AKT independent of mTORC2 and targeting MAPK6, either alone or in combination with mTOR blockade, may be effective in cancers