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Relevant bibliographies by topics / Corticomedullary junction

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Journal articles

Academic literature on the topic 'Corticomedullary junction'

Author: Grafiati

Published: 7 June 2025

Last updated: 25 June 2025

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Journal articles on the topic "Corticomedullary junction"

1

BAUMGARTNER, BRUCE R., RENDON C. NELSON, WILLIAM E. TORRES, JOHN A. MALKO, JACK E. PETERSON, and MICHAEL E. BERNARDINO. "Renal Corticomedullary Junction." Investigative Radiology 24, no. 11 (1989): 884–87. http://dx.doi.org/10.1097/00004424-198911000-00008.

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2

Oda, Yasuhiro, Naoki Sawa, Junichi Hoshino, and Yoshifumi Ubara. "Linear Calcification along the Renal Corticomedullary Junction." Internal Medicine 59, no. 14 (2020): 1781. http://dx.doi.org/10.2169/internalmedicine.4414-20.

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3

Quimby, Jessica, Andrea Erickson, Shannon Mcleland, et al. "Renal Senescence, Telomere Shortening and Nitrosative Stress in Feline Chronic Kidney Disease." Veterinary Sciences 8, no. 12 (2021): 314. http://dx.doi.org/10.3390/vetsci8120314.

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Kidney tissues from cats with naturally occurring chronic kidney disease (CKD) and adult and senior cats without CKD were assessed to determine whether telomere shortening and nitrosative stress are associated with senescence in feline CKD. The histopathologic assessment of percent global glomerulosclerosis, inflammatory infiltrate, and fibrosis was performed. Senescence and nitrosative stress were evaluated utilizing p16 and iNOS immunohistochemistry, respectively. Renal telomere length was evaluated using telomere fluorescent in situ hybridization combined with immunohistochemistry. CKD cats were found to have significantly increased p16 staining in both the renal cortex and corticomedullary junction compared to adult and senior cats. Senior cats had significantly increased p16 staining in the corticomedullary junction compared to adult cats. p16 staining in both the renal cortex and corticomedullary junction were found to be significantly correlated with percent global glomerulosclerosis, cortical inflammatory infiltrate, and fibrosis scores. p16 staining also correlated with age in non-CKD cats. Average telomere length was significantly decreased in CKD cats compared to adult and senior cats. CKD cats had significantly increased iNOS staining compared to adult cats. Our results demonstrate increased renal senescence, telomere shortening, and nitrosative stress in feline CKD, identifying these patients as potential candidates for senolytic therapy with translational potential.

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4

Liu, Pei, Xuemei Lin, Xiangjun Chen, et al. "Neuronal Intranuclear Inclusion Disease-Related Neurotrophic Keratitis: A Case Report." Brain Sciences 12, no. 6 (2022): 782. http://dx.doi.org/10.3390/brainsci12060782.

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Neuronal intranuclear inclusion disease (NIID) is a rare and slowly progressive neurodegenerative disease characterized by the presence of eosinophilic neuronal intranuclear inclusions. The clinical manifestations of NIID are diverse, and the most common initial feature in cases of sporadic NIID is dementia. Herein, we report an adult female with keratitis as the initial presentation with subsequent bilateral limb tremor, gait disturbances, overemotional behavior, sweating and constipation. Diffusion-weighted imaging (DWI) showed hyperintensity in the bilateral fronto-parieto-occipital corticomedullary junction. Skin biopsy specimens revealed eosinophilic hyaline intranuclear inclusions in fibroblast cells, sweat gland cells and adipose cells. In vivo confocal microscopy of the cornea indicated the absence of corneal nerves in both affected eyes. The patient’s diagnosis of NIID was based on the presence of intranuclear inclusions in biopsied skin and the characteristic high-intensity signal in the corticomedullary junction obtained with DWI. This case report emphasizes that the clinical heterogeneity of NIID and an examination of the corneal nerves may offer valuable clues to its early diagnosis in some patients.

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5

Boyd, Richard L., Trevor J. Wilson, Harry A. Ward, and Kathy Mitrangas. "Phenotypic Characterization of Chicken Bursal Stromal Elements." Developmental Immunology 1, no. 1 (1990): 41–51. http://dx.doi.org/10.1155/1990/97618.

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Many, if not all, of the different phases of intrabursal B-cell maturation are controlled by the stromal components. We have used an extensive panel of mAb to provide a detailed phenotypic profile of these cells. Antigenic specificities were defined for the entire surface epithelium, interfollicular surface epithelium, follicle-associated epithelium, basement membrane, basement membrane-associated epithelium. Several mAb were specific for the medulla, including those reactive with the stellate network of epithelial cells, isolated macrophages, and granular, apparently secreted antigens. One of these, MUI-92, appears to be bursa-specific. Two mAb reacted strongly with stellate cortical macrophages, one of which weakly stained similar cells in the medulla. MHC-class II antigens were expressed on endothelium of the corticomedullary junction, macrophagelike cells in the cortex, and medulla and B lymphocytes predominantly in the cortex. Collectively, these mAb have demonstrated the antigenically distinct nature of discrete regions in the bursa, but also the continuity of the surface epithelium with the corticomedullary junction and medulla. They represent excellent reagents for defining the stromal cell contribution to B-cell development.

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6

Rakow-Penner, Rebecca, Bert Glader, Huanzhou Yu, and Shreyas Vasanawala. "Adrenal and renal corticomedullary junction iron deposition in red cell aplasia." Pediatric Radiology 40, no. 12 (2010): 1955–57. http://dx.doi.org/10.1007/s00247-010-1824-2.

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7

Olsen, A., J. Hansen Højhus, and G. Steffensen. "Renal Medullary Cystic Disease." Acta Radiologica 29, no. 5 (1988): 527–29. http://dx.doi.org/10.1177/028418518802900507.

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Medullary cystic disease (MCD) is an uncommon renal disease with adult onset and autosomal inheritance, eventually progressing to terminal renal failure. It may be difficult to identify because of insufficient diagnostic tools. At urography, the same ring- shaped accumulation of contrast medium at the corticomedullary junction was observed in two patients (mother and son) suffering from MCD. To our knowledge this observation has not been reported before.

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8

Zachariah, M. A., and J. G. Cyster. "Neural Crest-Derived Pericytes Promote Egress of Mature Thymocytes at the Corticomedullary Junction." Science 328, no. 5982 (2010): 1129–35. http://dx.doi.org/10.1126/science.1188222.

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9

Kim, Jinyong, Su-Hyun Park, and Hye-Rim Shin. "Neuronal Intranuclear Inclusion Disease Presented with Acute Aphasia." Journal of the Korean Neurological Association 42, no. 4 (2024): 348–52. http://dx.doi.org/10.17340/jkna.2024.0059.

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Neuronal intranuclear inclusion disease (NIID) is a rare disorder with slowly progressive neurodegeneration. Major clinical presentation is dementia, but some patients can have episodic symptoms. This is a rare case of NIID presented with acute aphasia. A 62-years-old male visited emergency room presenting with aphasia. On brain magnetic resonance imaging, a U-shaped diffusion high signal intensity lesion in bilateral frontal corticomedullary junction was observed. A skin biopsy showed intranuclear cytoplasmic inclusion bodies, so he was diagnosed as NIID.

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10

Jeong, Ayeong, Youngho Kim, Ho-Sung Ryu, Man-Hoon Han, and Jong-Mok Lee. "Neuronal Intranuclear Inclusion Disease with Abnormal Peripheral Nerve Conduction." Journal of the Korean Neurological Association 40, no. 2 (2022): 156–59. http://dx.doi.org/10.17340/jkna.2022.2.9.

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A 70-year-old female presented with progressive gait disturbance. Neurologic examination revealed sensory impairment, hyporeflexia, and sensory ataxia. Nerve conduction study demonstrated mildly decreased velocity in motor nerves. Brain magnetic resonance imaging showed high signal intensities in the corticomedullary junction on diffusion weighted imaging. Neurocognitive function test implied mild cognitive impairment. Based on eosinophilic intranuclear inclusions in pathology, neuronal intranuclear inclusion disease was confirmed. Neuronal intranuclear inclusion needs to be considered when abnormal nerve conduction studies are consistent with abnormal brain imaging findings.

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