Publications by authors named "Takashi Oite"

Background: Nonspecific vaginitis, also known as Bacterial vaginosis, unlike genital candidiasis and trichomoniasis, is caused by microbiome breakdown. Döderlein's bacillus are gram-positive bacillus that form a microbiome, reproduce in the female vagina after gaining sexual maturity, secrete lactic acid, and prevent the growth of other vaginitis-causing bacteria. Clue cell are squamous epithelial cells with Gardnerella sp.

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Background: Extracorporeal membrane oxygenation (ECMO) is being increasingly used for mechanical support of respiratory and cardio-circulatory failure. An excessive systemic inflammatory response is observed during sepsis and after cardiopulmonary bypass (CPB) with similar clinical features. We hypothesized that hyperoxia condition encourages the systemic inflammatory response and organ disorder during ECMO.

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Background: Gap junctional intercellular communication is thought to play an important role in the maintenance of cell differentiation and homeostasis. Gap junctions connect glomerular mesangial cells to each other. In this study, we examined the glomerular expression of connexins (Cxs) 40 and 43 at both the protein and transcript levels in anti-Thy1.

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Background: Increasing evidence indicates that locally blocking renin-angiotensin system activity exerts a beneficial effect on glomerulonephritis (GN) progression leading to irreversible glomerulosclerosis. This is the first study on the pharmacological effect of the renal delivery of aliskiren, a direct renin inhibitor, in a progressive model of anti-Thy-1 GN.

Methods: Local blockade of renin activity was accomplished by subrenal capsular implantation of a collagen sponge with aliskiren.

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Background And Methods: There is increasing evidence that a change in glomerular hemodynamics may promote the development of glomerulosclerosis. In this study, we focused on the pharmacological effects of 2 contrasting agents, etodolac, a preferential cyclooxygenase-2 inhibitor, and beraprost sodium (BPS), a prostaglandin I(2) analog, delivered renally, on the disease course of progressive anti-Thy-1 (ATS) glomerulonephritis.

Results: Intravital microscopic analysis showed that the diameters of glomerular capillaries and glomerular blood flow in unilaterally nephrectomized (Nx) rats treated locally with BPS were significantly increased, as compared to those of Nx rats treated locally with normal saline (NS) or etodolac.

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Background: Previous studies have demonstrated that angiotensin Type I receptor blockade (ARB) reduces proteinuria, reverses glomerular injury and glomerulosclerosis in rat models of diabetic nephropathy and glomerulonephritis. However, the cellular and molecular mechanisms are unclear. To investigate the role of cells of the bone marrow (BM) in glomerular repair seen during ARB administration, we induced progressive glomerulosclerosis in enhanced green fluorescent protein BM chimeric rats by a single injection of anti-Thy 1.

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In this review, I introduce the strategy developed by our laboratory to explore the mechanisms of renoprotection against progressive glomerulosclerosis leading to renal death. First, I describe the experimental rat model in which disturbances of vascular regeneration and glomerular hemodynamics lead to irreversible glomerulosclerosis. Second, I discuss the possible mechanisms determining the progression of glomerulosclerosis and introduce a new imaging system based on intravital confocal laser scanning microscopy.

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Introduction: The nephro-protective effects of angiotensin II receptor blockers (ARBs) are widely known; however, there are few reports of long-term effects focusing on the renal vessels. We studied afferent arteriolar changes induced by the long-term administration of an ARB.

Materials And Methods: Thirty-two 6-week-old male Zucker fatty rats (ZFRs) were divided into following four groups (n = 8 in each): ZFR Group and ZFR+High Group fed a standard or high-salt diet, respectively; ZFR+ARB Group and ZFR+High+ARB Group fed a standard or high-salt diet with ARB (Olmesartan, 5 mg/kg/day), respectively.

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Background: Gap junction intercellular communication plays a fundamental role in various tissues and organs. Gap junctions transfer ions and molecules between adjacent cells and are formed by connexins (Cx). It is supposed that vascular conducted responses, which most likely spread through gap junctions in vascular beds, regulate microcirculatory blood flow and maintain vascular resistance.

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We attempted to clarify the effects of cyclohexenonic long-chain fatty alcohol (CHLFA) on the alterations of type 2 diabetes-induced nephropathy. Forty-week-old male Goto-Kakizaki (GK) and Wistar rats were divided into four groups of 6 to 8 animals. Group A consisted of eight Wistar rats and served as an age-matched control group.

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Article Synopsis
  • The study investigates the effects of angiotensin II receptor blockers (ARB) on diabetic nephropathy, focusing on their role in reducing inflammation in the kidneys during early stages of the disease.
  • Local ARB treatment in diabetic rats resulted in lower levels of protein in urine and blood urea nitrogen, along with decreased infiltration of inflammatory cells in the kidneys.
  • The findings suggest that blocking the renin-angiotensin system locally could be an effective strategy for preventing the worsening of diabetic nephropathy.
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In this review, we introduce first our experimental rat model in which disturbances of vascular regeneration and glomerular hemodynamics lead to irreversible glomerulosclerosis. Secondly, we demonstrate a pivotal role for gap-junctional intercellular communication and adenosine triphosphate-dependent intercellular communication, via Ca++ signaling, in coordinating behavior of mesangial and juxtaglomerular cells. This has deepened our understanding of regulatory glomerular hemodynamics at the cellular and molecular levels.

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The juxtaglomerular apparatus (JGA) is a specialized contact region between the glomerulus and the cortical thick ascending limb that plays an active role in the maintenance of ion homeostasis and control of blood pressure. The JGA accommodates several different cell types, including vascular smooth muscle cells, endothelial cells, mesangial cells, macula densa cells, and renin-secreting juxtaglomerular granular cells. These cells, with the exception of the macular densa cells, are tightly coupled by gap junctions.

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We performed transfection using cationic liposome. According to the gene expression level, lined cells were divided into two groups, high and low. Introduced gene was monitored with a confocal laser-scanning microscope.

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The purpose of this study was to identify the endothelial cell antigens that react with circulating antiendothelial antibody (AECA) in mixed connective tissue disease (MCTD). We screened serum AECA reactivity in 23 patients with MCTD using a human glomerular endothelial cell (HGEC) cellular ELISA. Proteomics, two-dimensional gel electrophoresis and matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry were used to identify the endothelial cell antigens of HGECs that reacted with serum antibodies from MCTD patients.

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Enhanced intrarenal renin-angiotensin system (RAS) is implicated in the development and progression of renal injury. To investigate whether angiotensinogen (AGT) expression is involved in glomerular RAS activity and glomerular injury, we examined glomerular AGT expression and its correlation with expression of other RAS components, and levels of glomerular injury in samples from patients with immunoglobulin A nephropathy (IgAN) (23) and minor glomerular abnormalities (MGA) (8). Immunohistochemistry showed that AGT protein was highly expressed by glomerular endothelial cells (GEC) and mesangial cells in nephritic glomeruli of IgAN compared with glomeruli of MGA.

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Glomerular mesangial cells (MCs) are specialized vascular smooth muscle cells that play a critical role in the control of glomerular hemodynamics. One of the intriguing features of MCs is their extraordinary abundance in gap junctions (GJs). It has long been speculated that GJs may bridge MCs together and provide the mesangium with the characteristics of a functional syncytium.

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Background: Acute post-streptococcal glomerulonephritis (APSGN) is induced by glomerular deposition of nephritogenic streptococcal antigen-antibody complexes. Recently, a streptococcal antigen, nephritis-associated plasminogen receptor (NAPlr) was purified from ruptured streptococcal cell supernatants (RCS). However, the cellular and molecular mechanisms of NAPlr action on the glomerular vas culature are still unknown.

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Purpose: To maintain in vitro granulosa cell function by adenoviral-mediated FSHR gene transduction.

Methods: Rat granulosa cells were cultured and transduced with adenovirus carrying FSHR gene. The number of receptors and the rate of steroidogenesis were assessed.

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The gap junction plays an important role in the regulation of cell growth, migration, and differentiation. Platelet-derived growth factor (PDGF) is reported to be a potent inhibitor of gap junctional intercellular communication (GJIC). Short-term exposure of cells to PDGF causes rapid and transient disruption of GJIC without altering connexin43 (Cx43) protein level.

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Background: There is accumulating evidence that adult bone marrow (BM) cells show unexpected plasticity, and can differentiate into a wide range of specialized cells. In the case of intrinsic renal glomerular cells, BM-derived cells have been reported to differentiate into both mesangial cells and podocytes. However, there is controversy on recruitment of glomerular endothelial cells, although endothelial cells in other tissues are known to be recruited from the BM.

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Background: The experimental use of cultured endothelial cells derived from the microvasculature such as glomerular endothelial cells possesses many problems, including limited growth rates, heterogeneity and loss of specific cell properties dependent on culture passage. In this study, we attempted to establish immortalized, human glomerular endothelial cell (HGEC) lines.

Methods: HGECs of up to 5 passages were transformed by infection with simian virus (SV)-40.

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Background: An Experimental model of proliferative glomerulonephritis induced by an antibody against Thy-1 antigen has been established. However, the pathophysiologic role and the critical epitope of Thy-1 molecule for induction of mesangial cell dysfunction remain unknown. We have reported that monoclonal antibody 1-22-3 recognizes specific epitope which could transduce highly effective activation in mesangial cells.

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