ABSTRACT. The ICR-derived glomerulonephritis (ICGN) mouse, a new inbred mouse strain with a hereditary nephrotic syndrome, is considered to be a good model of human idiopathic nephrotic syndrome and notably exhibits proteinuria and hypoproteinemia from the neonatal stage. In chronic renal disorder (CRD), anemia is a major subsequent symptom (renal anemia). The precise cause of renal anemia remains unclear, primarily owing to the lack of appropriate spontaneous animal models for CRD. To establish adequate animal models for anemia with CRD, we examined the hematological-biochemical properties and histopathological characteristics. With the deterioration of renal function, ICGN mice developed a normochromic and normocytic anemia, and exhibited normochromic and microcytic at the terminal stage. The expression of erythropoietin (EPO) mRNA both in the kidneys and liver and the EPO leak into the urine were observed in ICGN mice, indicating a disrupted metabolism of EPO in ICGN mice. In addition, a lack of iron induced by the hemolysis in the spleen and the leak of transferrin into urine as proteinuria aggravated the anemic condition. In conclusion, the ICGN mouse is a good model for anemia with CRD. The ICR-derived glomerulonephritis (ICGN) mouse established in the National Institute of Infectious Diseases (NIID; Tokyo, Japan) is a novel inbred mouse strain with a hereditary nephrotic syndrome of unknown etiology, and considered to be a good model of human idiopathic nephrotic syndrome [13][14][15][16]. Homozygous ICGN mice show proteinuria at a young age, later develop hypoproteinemia, hyperlipidemia, severe anemia and systemic edema, and eventually die as a result of chronic renal disorder (CRD) [15]. Our previous studies [20][21][22][23]25] showed that most of the renal tubules expanded and many kinds of extracellular matrix (ECM) components, both interstitial and basement membrane components, abnormally accumulated in glomeruli and tubulointerstitium of ICGN mouse kidneys. The progress of fibrotic degeneration in ICGN mouse kidneys may be caused by overproduction of ECM components, inhibition of ECM breakdown, and decreased activities of matrix metalloproteinases [22]. Apoptotic cells or proliferating cells were detected only in the kidneys of ICGN mice but not those of normal ICR mice [25]. In the kidneys of ICGN mice, apoptotic cells with large round nuclei were observed only in the tubulointerstitium, and proliferating cells were detected in epithelial cells of distal renal tubules. Age-dependent increases in apoptotic cell and proliferating cell densities were also noted. Such irregular cellular kinetics may cause renal dysfunction in ICGN mice.Anemia with CRD (renal anemia) is a major subsequent symptom in patients with CRD. The hematocrit levels are less than 30% in CRD patients and the condition of renal anemia directly affects their quality of life [8,18]. The lack of appropriate animal models for CRD means that the precise cause of renal anemia is unknown, however, it has been established that the lack of ...
ABSTRACT. The ICR-derived glomerulonephritis (ICGN) mouse, a novel inbred mouse strain with a hereditary nephrotic syndrome, develops severe anemia associated with chronic renal failure. To reveal the pathogenic mechanism of anemia in ICGN mice, we subcutaneously administered recombinant human erythropoietin (rhEPO; 5 IU/mouse/day) or saline for 5 days to ICGN mice. In terminal-stage ICGN mice with severe anemia, rhEPO significantly increased hematocrit (Ht), red blood cells (RBC) and hemoglobin levels. Endogenous EPO levels in peripheral blood were reduced by rhEPO injection. No histopathological changes in bone marrow and kidneys w ere induced by rhEPO injection. Insufficiency of EPO may cause anemia in ICGN mice. KEY WORDS: anemia associated with chronic renal failure, erythropoietin, hereditary nephrotic mouse (ICGN).J. Vet. Med. Sci. 66 (7): [883][884][885][886] 2004 The Institute of Cancer Research (ICR)-derived glomerulonephritis (ICGN) mouse, an inbred mouse strain with a hereditary nephrotic syndrome, is considered to be a good model of human idiopathic nephrotic syndrome [9]. Homozygous ICGN mice show the typical symptoms of nephrosis [10][11][12] and exhibit severe glomerular and tubulointestitial fibrosis [14]. Age-dependent increases in apoptotic cell and proliferating cell densities were also observed in the kidneys of ICGN mice [15]. Renal deterioration eventually leads to death as a result of chronic renal disorder (CRD). Moreover, ICGN mice develop a marked anemia with the deterioration of renal function [16]. Anemia associated with chronic renal failure is a major subsequent symptom that appears in the earlier stages of renal disease. It is a normochromic and normocytic anemia with hypoplastic bone marrow. The anemia associated with chronic renal failure is initially mild and inconsequential, however, ultimately it directly affects quality of life [3,13].Twenty week-age homozygous ICGN mice were prepared by mating homozygous males (nep/nep) and heterozygous females (nep/-), and age-and sex-matched ICR mice, were purchased from Clea Japan (Tokyo, Japan) as healthy controls. They received humane care as outlined in the "Guide for the Care and Use of Laboratory Animals" (Kyoto University Animal Care Committee according to NIH No. 86-23; revised 1999). Peripheral blood samples were obtained from the cervical vein under ether anesthesia and used for hematological and biochemical analyses. Hematological analyses were performed using an automatic counter (K-4500; Sysmex Co., Kobe, Japan), as were serum biochemical analyses (Fuji Drichem 3500V; Fuji Film, Tokyo, Japan), according to the manufacturer's instructions.Based on serum creatinine (sCre) levels, ICGN mice were categorized into three groups (latent, progressing and terminal) [14][15][16]. Briefly, ICGN mice with less than 0.34 mg/dl of sCre (mean plus SD of healthy ICR mice: 0.27 plus 0.07) were categorized as being in the latent stage. ICGN mice with 0.35-0.54 mg/dl (twice the mean of ICR mice) and those with more than 0.55 mg/dl were class...
We observed the pulsar PSR J1648−4611 with Suzaku. Two X-ray sources, Suzaku J1648−4610 (Src A) and Suzaku J1648−4615 (Src B), were found in the field of view. Src A is coincident with the pulsar PSR J1648−4611, which was also detected by the Fermi Gamma-ray Space Telescope. A hard-band image indicates that Src A is spatially extended. We found point sources in the vicinity of Src A by using a Chandra image of the same region, but the point sources have soft X-ray emission and cannot explain the hard X-ray emission of Src A. The hard-band spectrum of Src A can be reproduced by a power-law model with a photon index of 2.0 +0.9 −0.7 . The X-ray flux in the 2-10 keV band is 1.4 × 10 −13 erg cm −2 s −1 . The diffuse emission suggests a pulsar wind nebula around PSR J1648−4611, but the luminosity of Src A is much larger than that expected from the spin-down luminosity of the pulsar. Parts of the very-high-energy γ-ray emission of HESS J1646−458 may be powered by this pulsar wind nebula driven by PSR J1648−4611. Src B has soft emission, and its Xray spectrum can be described by a power-law model with a photon index of 3.0 +1.4 −0.8 . The X-ray flux in the 0.4-10 keV band is 6.4 × 10 −14 erg s −1 cm −2 . No counterpart for Src B is found in literatures.
Infections caused by Edwardsiella tarda (E. tarda), particularly musculoskeletal ones, have rarely been reported in humans. Here, we report the case of a 77-year-old man with thoracic spondylitis caused by E. tarda. The patient had back pain without neurological symptoms for several weeks. He had a history of diabetes, prostate cancer, and pancreatic cancer with hepatic metastasis. Computed tomography (CT) revealed endplate erosion at the T1/2 disk (Fig. 1a), whereas magnetic resonance imaging (MRI) revealed bone edema in the T1-2 vertebrae and fluid accumulation in the T1/2 disk (Fig. 1b, c). Furthermore, laboratory examination revealed hyperleukocytosis and high C-reactive protein levels.Subsequently, empiric antimicrobial therapy with intravenous piperacillin/tazobactam (4.5 g every 8 h) was started for thoracic spondylitis (Fig. 2), and CT-guided drainage was performed at the T1/2 disk level. A few days later, blood, urine, and abscess cultures became positive for
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