90 research outputs found
Epidermal Growth Factor and Transforming Growth Factor-Ξ± Stimulate the Proliferation of Mouse Uterine Stromal Cells
Growth factors produced in the uterine endometrium are considered to be involved in the proliferation of the mouse uterine stromal cells induced by estradiol-17beta (E-2) and progesterone (P). The effect of epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha), one of EGF-related growth factors, on the proliferation of mouse uterine stromal cells was studied in a serum-free culture. The growth of the uterine stromal cells was measured by MTT assay. EGF was found to increase the number of uterine stromal cells in a dose-dependent manner. The DNA-replicating cells were investigated using the immunocytochemical detection of bromodeoxyuridine (BrdU)-labeled cells. EGF and TGF-alpha increased the percentage of BrdU-Iabeled cells in a dose-dependent manner. Administration of the combination of E-2 (10(-9) M) and P (10(-7) M) for 2 days increased the percentage of BrdU-Iabeled cells 2.3-fold. The stimulatory effect of EGF, TGF-a and the combination of E2 and P on DNA replication in the uterine stromal cells was repressed by RG-13022 (10(-5) M, the inhibitor of the EGF receptor tyrosine kinase). RT-PCR analysis of EGF-receptor-, TGF-alpha, and EGF-mRNA was carried,out in the cultured uterine stromal cells, and revealed the expression of those mRNAs. These data supported the hypothesis that uterine endometrial stromal growth induced by sex steroids required the EGF family of ligands such as EGF and TGF-alpha, both produced in the stromal cells, acting for DNA synthesis through EGF receptors
The effect of mood state on visual search times for detecting a target in noise:An application of smartphone technology
The study of visual perception has largely been completed without regard to the influence that an individualβs emotional status may have on their performance in visual tasks. However, there is a growing body of evidence to suggest that mood may affect not only creative abilities and interpersonal skills but also the capacity to perform low-level cognitive tasks. Here, we sought to determine whether rudimentary visual search processes are similarly affected by emotion. Specifically, we examined whether an individualβs perceived happiness level affects their ability to detect a target in noise. To do so, we employed pop-out and serial visual search paradigms, implemented using a novel smartphone application that allowed search times and self-rated levels of happiness to be recorded throughout each twenty-four-hour period for two weeks. This experience sampling protocol circumvented the need to alter mood artificially with laboratory-based induction methods. Using our smartphone application, we were able to replicate the classic visual search findings, whereby pop-out search times remained largely unaffected by the number of distractors whereas serial search times increased with increasing number of distractors. While pop-out search times were unaffected by happiness level, serial search times with the maximum numbers of distractors (n = 30) were significantly faster for high happiness levels than low happiness levels (p = 0.02). Our results demonstrate the utility of smartphone applications in assessing ecologically valid measures of human visual performance. We discuss the significance of our findings for the assessment of basic visual functions using search time measures, and for our ability to search effectively for targets in real world settings
Arachidonic Acid Drives Postnatal Neurogenesis and Elicits a Beneficial Effect on Prepulse Inhibition, a Biological Trait of Psychiatric Illnesses
Prepulse inhibition (PPI) is a compelling endophenotype (biological markers) for mental disorders including schizophrenia. In a previous study, we identified Fabp7, a fatty acid binding protein 7 as one of the genes controlling PPI in mice and showed that this gene was associated with schizophrenia. We also demonstrated that disrupting Fabp7 dampened hippocampal neurogenesis. In this study, we examined a link between neurogenesis and PPI using different animal models and exploring the possibility of postnatal manipulation of neurogenesis affecting PPI, since gene-deficient mice show biological disturbances from prenatal stages. In parallel, we tested the potential for dietary polyunsaturated fatty acids (PUFAs), arachidonic acid (ARA) and/or docosahexaenoic acid (DHA), to promote neurogenesis and improve PPI. PUFAs are ligands for Fabp members and are abundantly expressed in neural stem/progenitor cells in the hippocampus. Our results are: (1) an independent model animal, Pax6 (+/β) rats, exhibited PPI deficits along with impaired postnatal neurogenesis; (2) methylazoxymethanol acetate (an anti-proliferative drug) elicited decreased neurogenesis even in postnatal period, and PPI defects in young adult rats (10 weeks) when the drug was given at the juvenile stage (4β5 weeks); (3) administering ARA for 4 weeks after birth promoted neurogenesis in wild type rats; (4) raising Pax6 (+/β) pups on an ARA-containing diet enhanced neurogenesis and partially improved PPI in adult animals. These results suggest the potential benefit of ARA in ameliorating PPI deficits relevant to psychiatric disorders and suggest that the effect may be correlated with augmented postnatal neurogenesis
Thermal defect healing of single-walled carbon nanotubes assisted by supplying carbon-containing reactants
We experimentally investigated the effect of carbon-containing reactants (C2H2) on healing the defects in single-walled carbon nanotubes (SWCNTs) by thermal processes at high temperatures (βΌ1100 Β°C). Introducing C2H2 notably improved the crystallinity of healed SWCNTs compared with the thermal process in Ar ambient without C2H2. The defect healing rate increased with increasing C2H2 partial pressure, and the healing effect of C2H2 was more remarkable for relatively thinner SWCNTs (<1.1 nm). Combined with the relevant theoretical work reported previously, we propose a healing model in which C2H2 helps to heal the vacancy defects and increases the healing rate at high temperatures.This is the version of the article before peer review or editing, as submitted by an author to Applied Physics Express. IOP Publishing Ltd is not responsible for any errors or omissions in this version of the manuscript or any version derived from it. The Version of Record is available online at https://doi.org/10.35848/1882-0786/acaaec
A Synthesis of (Β±)-Ipalbidine Using Sulfurcontrolled 6-Exo Selective Radical Cyclization of Ξ±-Phenylthio Amide
A Synthesis of (Β±)-Ipalbidine Using Sulfur-controlled 6-Exo Selective Radical Cyclization of Ξ±-Phenylthio Amide
Fabp7 Maps to a Quantitative Trait Locus for a Schizophrenia Endophenotype
Deficits in prepulse inhibition (PPI) are a biological marker for schizophrenia. To unravel the mechanisms that control PPI, we performed quantitative trait loci (QTL) analysis on 1,010 F2 mice derived by crossing C57BL/6 (B6) animals that show high PPI with C3H/He (C3) animals that show low PPI. We detected six major loci for PPI, six for the acoustic startle response, and four for latency to response peak, some of which were sex-dependent. A promising candidate on the Chromosome 10-QTL was Fabp7 (fatty acid binding protein 7, brain), a gene with functional links to the N-methyl-D-aspartic acid (NMDA) receptor and expression in astrocytes. Fabp7-deficient mice showed decreased PPI and a shortened startle response latency, typical of the QTL's proposed effects. A quantitative complementation test supported Fabp7 as a potential PPI-QTL gene, particularly in male mice. Disruption of Fabp7 attenuated neurogenesis in vivo. Human FABP7 showed altered expression in schizophrenic brains and genetic association with schizophrenia, which were both evident in males when samples were divided by sex. These results suggest that FABP7 plays a novel and crucial role, linking the NMDA, neurodevelopmental, and glial theories of schizophrenia pathology and the PPI endophenotype, with larger or overt effects in males. We also discuss the results from the perspective of fetal programming
Evaluation of Pax6 Mutant Rat as a Model for Autism
Autism is a highly variable brain developmental disorder and has a strong genetic basis. Pax6 is a pivotal player in brain development and maintenance. It is expressed in embryonic and adult neural stem cells, in astrocytes in the entire central nervous system, and in neurons in the olfactory bulb, amygdala, thalamus, and cerebellum, functioning in highly context-dependent manners. We have recently reported that Pax6 heterozygous mutant (rSey2/+) rats with a spontaneous mutation in the Pax6 gene, show impaired prepulse inhibition (PPI). In the present study, we further examined behaviors of rSey2/+ rats and revealed that they exhibited abnormality in social interaction (more aggression and withdrawal) in addition to impairment in rearing activity and in fear-conditioned memory. Ultrasonic vocalization (USV) in rSey2+ rat pups was normal in male but abnormal in female. Moreover, treatment with clozapine successfully recovered the defects in sensorimotor gating function, but not in fear-conditioned memory. Taken together with our prior human genetic data and results in other literatures, rSey2/+ rats likely have some phenotypic components of autism
Epidermal Growth Factor and Transforming Growth Factor-Ξ± Stimulate the Proliferation of Mouse Uterine Stromal Cells
Pharmacological targeting of bone marrow mesenchymal stromal/stem cells for the treatment of hematological disorders
Abstract The therapeutic effects of mesenchymal stromal/stem cells (MSCs) are mainly based on three characteristics: immunomodulation, tissue regeneration, and hematopoietic support. Cell therapy using culture-expanded MSCs is effective in some intractable bone and hemato-immune disorders; however, its efficacy is limited. In this article, we review the previous efforts to improve the clinical outcomes of cell therapy using MSCs for such disorders. We describe pharmacological targeting of endogenous bone marrow-derived MSCs as a crucial quality-based intervention to establish more effective MSC-based therapies
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