Bone marrow mesenchymal cells: polymorphism associated with transformation of rough endoplasmic reticulum.

To understand the behavior and function of bone-marrow mesenchymal cells (BMMCs), we overviewed the morphological presentation of BMMCs in bone-marrow granules (b-BMMCs), isolated BMMCs (i-BMMCs), and BMMCs (c-BMMCs) cultured in H4434 methylcellulose semisolid and MEM media. All samples were derived from bone-marrow aspirates of 30 patients with hematocytopenia. Light microscopy exhibited b-BMMCs and i-BMMCs characterized by abundant cytoplasm and irregular shape in bone-marrow smears, as well as c-BMMCs in culture conditions.

Generation of fractals as Duffing equation orbits.

Dynamics are constructed for fractals utilizing the motion associated with Duffing equation. Using the paradigm of Fatou-Julia iteration, we develop iterations to map fractals accompanied with a criterion to ensure that the image is again a fractal. Because of the close link between mappings, differential equations and dynamical systems, one can introduce dynamics for fractals through differential equations such that they become points of the solution trajectory.

MEG2 is regulated by miR-181a-5p and functions as a tumour suppressor gene to suppress the proliferation and migration of gastric cancer cells.

Background: Protein-tyrosine phosphatase MEG2 (MEG2) is a classic tyrosine-specific protein tyrosine phosphatase (PTP). It has been reported that MEG2 participates in the carcinogenesis of the breast and liver. However, functions of MEG2 in gastric cancer remain poorly understood.

Silencing of β1 integrin regulates airway remodeling by regulating the transcription of SOCE‑associated genes in asthmatic mice.

The incidence of asthma is increasing globally; however, current treatments are only able to cure a certain proportion of patients. There is an urgent need to develop novel therapies. β1 integrin serves a role in the pathophysiology of asthma through the development of airway remodeling.

miR-208a-3p suppresses cell apoptosis by targeting PDCD4 in gastric cancer.

Programmed cell death 4 (PDCD4) is a novel tumor suppressor gene and a promising target for anticancer therapies. PDCD4 is frequently downregulated in various human cancers; however, the molecular mechanism accounting for the loss expression of PDCD4 in cancers is not fully understood. In this study, we identified specific targeting sites for miR-208a-3p in the 3'-untranslated region (3'-UTR) of the PDCD4 gene which regulated PDCD4 expression.