Long Lasting Local and Systemic Inflammation after Cerebral Hypoxic ischemia in Newborn Mice

Abstract Neonatal sepsis (NS) is a severe syndrome in newborns induced by infections, the initiation and development of which are closely related to the function of miRs. In the current study, the anti-NS effects of berberine, a functional component in Traditional Chinese medicine (TCM), were assessed by focusing on its interaction with miR-132-3p-mediated signaling. NS model was induced using cecal slurry (CS) and handled with berberine. The changes in survival rate, intestinal structure, systemic inflammation, miR-132-3p level, and activities of FOXA1 and NF-κB pathways were detected. The data showed that berberine increased survival rate of NS mice. The intestinal injures induced by CS were also attenuated by berberine, which was associated with the inhibited production of systemic IL-6, IL-1β, and TNF-α. At molecular level, the expression of miR-132-3p was up-regulated, suppressing the expressions of FOXA1, p-IκBα, and p65, while inducing the expression of IκBα. The effects of berberine on NS-induced impairments were blocked by the injection of miR-132-3p antagomir, which reduced survival rate, exacerbated intestinal injuries, induced systemic inflammation, and re-activated FOXA1 and NF-κB pathways. Collectively, the findings outlined in the current study indicated that berberine had solid protective effects on newborn mice against NS-induced symptoms, and the effects depended on the up-regulation of miR-132-3p.

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Altered thymic epithelial cells may be decisive for Moloney virus-induced lymphoma development

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100077499 ◽

1983 ◽

Vol 41 ◽

pp. 784-785

Author(s):

U.I. Heine ◽

G.R.F. Krueger ◽

E. Munoz ◽

A. Karpinski

Keyword(s):

Epithelial Cells ◽

Leukemia Virus ◽

Light And Electron Microscopy ◽

Tumor Development ◽

Current Evidence ◽

Thymic Epithelial Cells ◽

Thymic Tissue ◽

Newborn Mice ◽

Moloney Leukemia Virus ◽

Differentiation Block

Infection of newborn mice with Moloney leukemia virus (M-MuLV) causes a T-cell differentiation block in the thymic cortex accompanied by proliferation and accumulation of prethymic lymphoblasts in the thymus and subsequent spreading of these cells to generate systemic lymphoma. Current evidence shows that thymic reticular epithelial cells (REC) provide a microenvironment necessary for the maturation of prethymic lymphoblasts to mature T-lymphocytes by secretion of various thymic factors. A change in that environment due to infection of REC by virus could be decisive for the failure of lymphoblasts to mature and thus contribute to lymphoma development.We have studied the morphology and distribution of the major thymic cell populations at different stages of tumorigenesis in Balb/c mice infected when newborn with 0.2ml M-MuLV suspension, 6.8 log FFU/ml. Thymic tissue taken at 1-2 weekly intervals up to tumor development was processed for light and electron microscopy, using glutaraldehyde-OsO4fixation and Epon-Araldite embedding.

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Reversal of cardiomyopathy resulting from prenatal exposure to ethanol

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100113469 ◽

1984 ◽

Vol 42 ◽

pp. 716-717

Author(s):

C. Uphoff ◽

C. Nyquist-Battie

Keyword(s):

Prenatal Exposure ◽

Heart Development ◽

Membrane Integrity ◽

Ethanol Exposure ◽

Prenatal Ethanol Exposure ◽

Pathological Changes ◽

Prenatally Exposed ◽

Inner Mitochondrial Membrane ◽

Fetal Alcohol ◽

Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

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