Sparing and enhancing dose protraction effects for radiation damage to the aorta of wild-type mice.

Purpose: Our previous work indicated the greater magnitude of damage to the thoracic aorta at 6 months after starting 5 Gy irradiation in descending order of exposure to X-rays in 25 fractions > acute X-rays > acute γ-rays > X-rays in 100 fractions ≫ chronic γ-rays, in which the limitations of the study included a lack of data for fractionated γ-ray exposure. To better understand effects of dose protraction and radiation quality, the present study examined changes after exposure to γ-rays in 25 fractions, and compared its biological effectiveness with five other irradiation regimens.

Materials And Methods: Male C57BL/6J mice received 5 Gy of Cs γ-rays delivered in 25 fractions spread over six weeks.

Temporal Changes in Sparing and Enhancing Dose Protraction Effects of Ionizing Irradiation for Aortic Damage in Wild-Type Mice.

In medical and occupational settings, ionizing irradiation of the circulatory system occurs at various dose rates. We previously found sparing and enhancing dose protraction effects for aortic changes in wild-type mice at 6 months after starting irradiation with 5 Gy of photons. Here, we further analyzed changes at 12 months after stating irradiation.

Vascular Damage in the Aorta of Wild-Type Mice Exposed to Ionizing Radiation: Sparing and Enhancing Effects of Dose Protraction.

During medical (therapeutic or diagnostic) procedures or in other settings, the circulatory system receives ionizing radiation at various dose rates. Here, we analyzed prelesional changes in the circulatory system of wild-type mice at six months after starting acute, intermittent, or continuous irradiation with 5 Gy of photons. Independent of irradiation regimens, irradiation had little impact on left ventricular function, heart weight, and kidney weight.

Bach1 plays an important role in angiogenesis through regulation of oxidative stress.

Bach1 is a known transcriptional repressor of the heme oxygenase-1 (HO-1) gene. The purpose of this study was to determine whether angiogenesis is accelerated by genetic ablation of Bach1 in a mouse ischemic hindlimb model. Hindlimb ischemia was surgically induced in wild-type (WT) mice, Bach1-deficient (Bach1) mice, apolipoprotein E-deficient (ApoE) mice, and Bach1/ApoE double-knockout (Bach1/ApoE) mice.

Daily Low-intensity Pulsed Ultrasound Ameliorates Renal Fibrosis and Inflammation in Experimental Hypertensive and Diabetic Nephropathy.

The estimated morbidity rate of chronic kidney disease is 8% to 16% worldwide, and many patients with chronic kidney disease eventually develop renal failure. Thus, the development of new therapeutic strategies for preventing renal failure is crucial. In this study, we assessed the effects of daily low-intensity pulsed ultrasound (LIPUS) therapy on experimental hypertensive nephropathy and diabetic nephropathy.

Ionizing Irradiation Induces Vascular Damage in the Aorta of Wild-Type Mice.

There has been a recent upsurge of interest in the effects of ionizing radiation exposure on the circulatory system, because a mounting body of epidemiological evidence suggests that irradiation induces cardio- and cerebrovascular disease at a much lower dose and lower dose rate than previously considered. The goal of our project is to determine whether dose protraction alters radiation effects on the circulatory system in a mouse model. To this end, the use of wild-type mice is pivotal albeit without manifestation of vascular diseases, because disease models (e.

Serum-Free Medium Enhances the Immunosuppressive and Antifibrotic Abilities of Mesenchymal Stem Cells Utilized in Experimental Renal Fibrosis.

Serum used in culture medium brings risks of immune reactions or infections and thus may hinder using ex vivo expanded mesenchymal stem cells (MSCs) for medical treatment. Here, we cultured MSCs in a serum-free medium (SF-MSCs) and in a medium containing 10% fetal bovine serum (10%MSCs) and investigated their effects on inflammation and fibrosis. MSC-conditioned medium suppressed transforming growth factor-β1-induced phosphorylation of Smad2 in HK-2 cells, with no significant difference between the two MSCs.

Prior neonatal isolation reduces induction of NGF mRNA and decreases GDNF mRNA in the hippocampus of juvenile and adult rodents subjected to immobilization stress.

Numerous studies have demonstrated that early adverse experiences are associated with the development of susceptibility to stress later in life. Although it is known that early experience of adversity, such as neonatal isolation, maternal separation, and low maternal care, enhances the activity of the hypothalamo-pituitary-adrenalaxis in rodents, the detailed mechanism underlying stress susceptibility induced by early adversity remains to be elucidated. Since neurotrophins have been shown to have a neuroprotective effect, we examined the influence of repeated neonatal isolation on expression of nerve growth factor (NGF), glia cell-derived neurotrophic factor (GDNF), and neurotrophin-3 mRNA in the hippocampus of juvenile and adult rats subsequently exposed immobilization stress, using real-time quantitative PCR and in situ hybridization.

Neonatal isolation changes the expression of IGF-IR and IGFBP-2 in the hippocampus in response to adulthood restraint stress.

Early adverse experiences are thought to contribute to the development of stress vulnerability, and to increase the onset of stress-related psychiatric disorders in stressful environments in adulthood. One plausible molecular mechanism of stress vulnerability is the modulation of neurotrophic factor signal transduction in the hippocampus by early adversity. In the present study we investigated the influence of neonatal isolation (NI) with or without adulthood single restraint stress (SRS) on the expression of several growth factor-related genes in the rat hippocampus using a cDNA microarray, real-time quantitative PCR, and Western blot.

Effect of neonatal isolation on the noradrenergic transduction system in the rat hippocampal slice.

Numerous studies suggest that early adverse experiences induce neurochemical, morphological, and functional changes in the hippocampus in adolescence and adulthood. The aim of this study was to identify the influence of neonatal isolation (NI) on noradrenaline (NA)-mediated intracellular calcium ([Ca(2+)](i)) mobilization. To measure [Ca(2+)](i), we used the Ca(2+)-sensitive dye fura-2 and analysis by fluorescence microscopy.

Influence of immobilization stress on the levels of CaMKII and phospho-CaMKII in the rat hippocampus.

The phosphorylation of calcium/calmodulin-dependent protein kinase (CaMK) II, induced by an increase in the intracellular Ca2+ concentration, is involved in the alteration of brain functions such as memory formation. In the present study, we examined the influence of various immobilization stress paradigms on the phosphorylation of CaMKII (phospho-CaMKII) and CaMKII levels in the rat hippocampus. Immunoblot and immunohistochemical analyses were performed to examine the levels of CaMKII and phospho-CaMKII.

Influence of immobilization stress on the expression and phosphatase activity of protein phosphatase 2A in the rat brain.

Background: Protein phosphatase 2A (PP2A) is a major kinase phosphatase that plays an important role in regulating the activities of protein kinase cascades. It has been revealed that stress changes neuronal gene expression by activating these cascades. We examined the expression of the catalytic subunit C and serine and threonine phosphatase activity of PP2A in the rat frontal cortex and hippocampus following various immobilization stress paradigms.