[Show abstract][Hide abstract] ABSTRACT: Anatomical variations of the biceps brachii have been described by various authors, but the occurrence of bilateral asymmetric supernumerary heads is rare and has not been reported. We found three accessory heads of the biceps brachii muscle on right arm and an anomalous third head of biceps brachii on left arm. The third, fourth, and fifth heads of right arm originated from the body of humerus at the insertion site of coracobrachialis and inserted into the distal part of biceps brachii short head in order. The third head of left arm originated from humerus at the insertion site of coracobrachialis and combined with the distal part of biceps brachii and continued to the proximal part of common biceps tendon. Understanding the existence of bilateral asymmetric supernumerary heads of biceps brachii may influence preoperative diagnosis and surgery on the upper limbs.
[Show abstract][Hide abstract] ABSTRACT: During potassium (K) depletion, many adaptive responses are likely mediated through a complex network that involves expression of a variety of genes. We identified that the Nrf2 gene was differentially expressed between normal and K-depleted rat kidney.
To investigate the effect of Nrf2 on colonic H/K-ATPase and kNBC1, overexpression of Nrf2 was carried out in 293T and CV1 cell lines, and experiments were conducted in low-K media. Sp family was cotransfected with Nrf2 to examine the relationship between the 2 molecules and their effect on ion transporters.
Ion transporters were activated by overexpression of Nrf2 and cotransfection of Nrf2 with Sp family genes showed additional enhancement of colonic H/K-ATPase and kNBC1 expression and their promoter activities. Pretreatment with low-K media increased the transcriptional activity of Nrf2, colonic H/K-ATPase and kNBC1. Furthermore, transfection of dominant-negative Nrf2 completely abolished low-K-mediated expression of the ion transporters.
These results suggest that Nrf2 mediates transcriptional activation of colonic H/K-ATPase and kNBC1 in response to K-depleted stress and augments Sp family-mediated expression of these ion transporters.
No preview · Article · Jun 2011 · Journal of nephrology
[Show abstract][Hide abstract] ABSTRACT: To identify genes that participate in the abortion process, normal pregnant uteri were compared to lipopolysaccharide (LPS)-induced abortion uteri. At day 6 of pregnancy, mice were treated with LPS at various time points to induce an abortion. Total RNAs were applied to a cDNA microarray to analyze genes with altered expression. At the early stage (2 hours) of LPS-induced abortion, upregulated genes were mainly composed of immune responsive genes, including Ccl4, Ccl2, Cxcl13, Gbp3, Gbp2, Mx2, H2-Eb1, Irf1 and Ifi203. Genes related to toll-like receptor signaling were also overexpressed. At late stages of abortion (12-24 hours), many genes were suppressed rather than activated, and these were mainly related to the extracellular matrix, cytoskeleton, and anti-apoptosis. Altered expression of several selected genes was confirmed by real time reverse transcription-polymerase chain reaction. The results demonstrated that many known genes were altered in the LPS-treated pregnant uterus, implying that the molecular mechanisms of the genes involved in LPS-induced abortion are complicated. Further analysis of this expression profile will help our understanding of the pathophysiological basis for abortion.
[Show abstract][Hide abstract] ABSTRACT: The dynamic exchange of histone lysine methylation status by histone methyltransferases and demethylases has been previously implicated as an important factor in chromatin structure and transcriptional regulation. Using immunoaffinity TAP analysis, we purified the WHISTLE-interacting protein complexes, which include the heat shock protein HSP90α and the jumonji C-domain harboring the histone demethylase JMJD1C. In this study, we demonstrate that JMJD1C specifically demethylates histone H3K9 mono- and di-methylation, and mediates transcriptional activation. We also provide evidence suggesting that both WHISTLE and JMJD1C performs functions in the development of mouse testes by regulating the expression of the steroidogenesis marker, p450c17, via SF-1-mediated transcription. Furthermore, we demonstrate that WHISTLE is recruited to the p450c17 promoter via SF-1 and represses the transcription of prepubertal stages of steroidogenesis, after which JMJD1C replaces WHISTLE and activates the expression of target genes via SF-1-mediated interactions. Our results demonstrate that the histone methylation balance mediated by HMTase WHISTLE and demethylase JMJD1C perform a transcriptional regulatory function in mouse testis development.
Full-text · Article · Oct 2010 · Nucleic Acids Research
[Show abstract][Hide abstract] ABSTRACT: 90K, a tumour-associated glycoprotein, interacts with galectins and has roles in host defence by augmenting the immune response, but the serum 90K level was suggested to indicate poor prognosis in several cancers. The cellular mechanisms of 90K action on colorectal cancer (CRC) cell motility and its effect on CRC progression were investigated.
The impact of 90K was analysed by combining cell cultures, in vitro assays, and immunohistochemistry.
Secreted 90K suppresses CRC cell invasion, but this action of 90K is masked through binding with extracellular galectins. A novel pathway is identified comprising a secretory 90K and a CD9/CD82 tetraspanin web; in this pathway, 90K interacts with CD9/CD82, suppresses the Wnt/beta-catenin signal via a novel proteasomal-ubiquitination mechanism of beta-catenin that is dependent on ISG15 (interferon-stimulated gene-15) modification (ISGylation) but not on glycogen synthase kinase 3beta (GSK-3beta) and Siah/Adenomatous polyposis coli (APC). In a syngeneic mouse colon tumour model, tumour growth and lung metastasis were increased with 90K knockdown. In colon tissues from stage IV human CRC and invading cancer cells of corresponding metastatic liver tissues, in which beta-catenin and galectin expression was higher, immunostained 90K and CD9/CD82 were lower than in adjacent hepatic tissues or colon tissues from stage I.
90K itself has antitumour activity in CRC cells via suppression of Wnt signalling with a novel mechanism of ISGylation-dependent ubiquitination of beta-catenin when it interacts with CD9/CD82, but is downregulated in advanced CRC tissues. The data suggest a strategy of strengthening this novel pathway with concomitant knockdown of galectins as a potential therapeutic approach to CRC progression.
[Show abstract][Hide abstract] ABSTRACT: To investigate the anti-angiogenic effects of photodynamic therapy with verteporfin in a rabbit model of corneal neovascularization.
One week after suturing, the localization of verteporfin in the neovascularized cornea was examined through fluorescent microscopy 1 hr after administration. Rabbits were treated with one or two times of photodynamic therapy with verteporfin at 1-week intervals. Analysis of corneal neovascularization was performed by biomicroscopic and histological examinations.
Fluorescent microscopy showed green fluorescence in the vascular walls and interstitial tissue of the corneal stroma. The mean percentages of neovascularized corneal area at 3 days, 1 week, and 2 weeks after one time of photodynamic therapy were 90.3% +/- 3.5%, 71.6% +/- 6.2%, and 43.6% +/- 15.1% in treated eyes and 96.4% +/- 1.9% (p = 0.10), 88.6% +/- 4.6% (p = 0.01), and 76.8% +/- 4.4% (p < 0.01) in control eyes, respectively. The mean percentages 3 days, 1 week, and 2 weeks after two times of photodynamic therapy were also significantly lower in treated eyes compared with control eyes. In quantitative histological examination at 1 and 2 weeks after therapy, treated eyes showed significantly less neovascular area and number of vessels than control eyes.
Photodynamic therapy with verteporfin is a safe and useful procedure to reduce experimental corneal neovascularization and can be used to inhibit angiogenesis in the cornea.
No preview · Article · Apr 2006 · Current Eye Research
[Show abstract][Hide abstract] ABSTRACT: The tyramide signal amplification (TSA) technique has been shown to detect scarce tissue antigens in light and electron microscopy. In this study we applied the TSA technique at the electron microscopic level to pre-embedding immunocytochemistry. This protocol was compared to the non-amplified protocol. With the TSA protocol, the labeling of GM130, a cis-Golgi matrix protein, was tested in a cell line and found to be highly sensitive and more enhanced than that with the simple protocol. Moreover, the gold particles were well localized to the cis-side of the Golgi apparatus in both the TSA and the simple protocol.
Full-text · Article · Mar 2005 · Journal of Histochemistry and Cytochemistry
[Show abstract][Hide abstract] ABSTRACT: To investigate whether intracavernosal injection of vascular endothelial growth factor (VEGF) can restore erectile function in the aging rat.
Ten young (4-5 months) and 30 old (24 months) Sprague-Dawley male rats were used. The old rats were divided into 3 groups: vehicle-only (phosphate buffered saline plus 0.1% bovine serum albumin; n = 10), VEGF 1 microg/kg (n = 10), and VEGF 10 microg/kg (n = 10). At 2 and 4 weeks after treatment, erectile function and histology were evaluated by hemodynamic study, histomorphometric analysis, and immunohistochemistry.
After 4 weeks of treatment, the ratio of peak intracavernosal pressure to systemic arterial blood pressure in response to neurostimulation was significantly higher in both the VEGF 1 microg/kg (79.9 +/- 7.7%) and the VEGF 10 microg/kg group (76.8 +/- 5.8%) compared to the vehicle-only group (63.1 +/- 8.5%; p < 0.05). The percentage of cavernosal smooth muscle was significantly higher in the VEGF 10 microg/kg group (16.1 +/- 1.4%) compared to the vehicle-only group (12.8 +/- 2.2%; p = 0.047). VEGF treatment in old rats increased e-NOS and VEGF expression in both treatment groups.
Intracavernosal injection of VEGF appears to restore smooth muscle integrity and improve erectile function in aged rats.
No preview · Article · Oct 2004 · European Urology
[Show abstract][Hide abstract] ABSTRACT: To examine whether zinc accumulation occurs during retinal neuronal death after pressure-induced ischemia in rats and whether pyruvate protects against such death.
To induce transient retinal ischemia, intraocular pressure was increased above systolic pressure for 65 minutes. Pyruvate was administered through the tail vein for 12 hours after ischemia to determine its effect on degeneration of retinal neurons. Retinas were removed and sectioned, and zinc accumulation was visualized with N-(6-methoxy-8-quinolyul)-p-carboxybenzoyl-sylphonamide (TFL-Zn) fluorescence microscopy, and neuronal death was determined with acid fuchsin staining. For in vitro studies, retinal cell cultures were prepared from newborn rat pups and used for experiments at days in vitro (DIV) 7 to 10.
After retinal ischemia, staining revealed that most zinc-accumulating neurons were injured neurons, suggesting that endogenous zinc may contribute to ischemic neuronal death in the retina. In vitro studies showed that 15 minutes of exposure to 300 to 500 microM zinc resulted in the death of a substantial number of retinal cells in culture, and that this death was preceded by poly(ADP-ribose) polymerase (PARP)-mediated depletion of nicotinamide-adenine dinucleotide (NAD+) and adenosine triphosphate (ATP). Pyruvate, but not lactate, protected against this zinc-induced cell death in vitro. Consistent with this finding, in vivo studies showed that compared with control rats, pyruvate-treated rats had a substantial reduction in the number of cells showing signs of cell death.
The present results suggest endogenous zinc contributes to retinal cell death after ischemia. Pyruvate potently protected against zinc toxicity in cultured rat retinal cells and reduced ischemia-induced cell death in rat retinas.
[Show abstract][Hide abstract] ABSTRACT: To investigate the antiproliferative effects of the subconjunctival injection of human RAD50 (hRAD50) on fibroblasts after glaucoma filtering surgery.
After glaucoma filtering surgery in normal rabbit eye, the subconjunctival injection of hRAD50 was performed. Morphologic changes in the subconjunctival area of hRAD50-treated eyes were compared with those of mitomycin C (MMC)-treated and control eyes using light and electron microscopy. Results. Two weeks after hRAD50 treatment (2 microg), the conjunctival epithelium increased in thickness and had many tonofilaments, but the basal lamina was intact. The subconjunctival fibroblasts exhibited a granular endoplasmic reticulum without distension. Most of the collagen bundles and fibers around the fibroblasts disappeared, and apoptotic cells with many fragmented nuclei and condensed chromatin were observed. Four weeks after hRAD50 treatment, the findings were similar with those of 2 weeks except for a slight increase in the number of collagen bundles and fibers and the appearance of macrophages. In MMC-treated eyes, the conjunctival epithelium also increased in thickness and had many tonofilaments. However, intercellular spaces were widened and the basal lamina was interrupted in some areas. Most of the collagen bundles and fibers were shortened, and apoptotic cells were also observed.
These results demonstrate that the histologic antiproliferative effects of local hRAD50 on the conjunctival fibroblasts are similar to those of MMC, but without damage to the basal lamina of the conjunctival epithelium, and suggest that hRAD50 may be useful as a possible antifibroblastic agent for glaucoma filtering surgery. However, further investigations are needed to test for possible systemic complications, which so far have not been reported.
No preview · Article · Apr 2004 · Current Eye Research
[Show abstract][Hide abstract] ABSTRACT: Previous reports showed that human RAD50 (hRAD50) gene delivery induced regression of an experimental rat tumor and porcine neointimal hyperplasia. In this study, we examined the effects of hRAD50 on the morphological changes and migration of endothelial cells (EC) as possible mechanisms by which hRAD50 might block angiogenesis. Quantitative image analysis revealed significant inhibition of the number and total area of blood vessels in rat tumor tissues following hRAD50 gene delivery. hRAD50 distorted actin and tubulin arrangements, and significantly reduced the F/G-actin ratio and increased the nitric oxide (NO) production in the primary cultured human EC. These effects were blocked by pretreatment with L-NAME (N(G)-nitro-L-arginine-methyl ester), a NO synthase inhibitor. FACScan analysis showed that NO was involved in the necrosis and apoptosis of EC by hRAD50. hRAD50 also inhibited EC migration in an in vitro wound-healing model. These results indicate that NO-dependent cytoskeletal changes and inhibition of EC migration contribute to the suppression of angiogenesis by hRAD50 delivery in vivo.