The objective of this study was to describe a radiofrequency (RF) coil design for in vivo sodium magnetic resonance imaging (MRI) for use in small animals. Accumulating evidence has indicated the importance and potential of sodium imaging with improved magnet strength (> 7T), faster gradient, better hardware, multi-nucleus imaging methods, and optimal coil design for patient and animal studies. Thus, we developed a saddle-shaped sodium volume coil with a diameter/length of 30/30 mm. To evaluate the efficiency of this coil, bench-level measurement was performed. Unloaded Q value, loaded Q value, and ratio of these two values were estimated to be 352.8, 211.18, and 1.67, respectively. Thereafter, in vivo acquisition of sodium images was performed using normal mice (12 weeks old; n = 5) with a two-dimensional gradient echo sequence and minimized echo time to increase spatial resolution of images. Sodium signal-to-noise ratio in mouse kidneys (renal cortex, medulla, and pelvis) was measured. We successfully acquired sodium MR images of the mouse kidney with high spatial resolution (approximately 0.625 mm) through a combination of sodium-proton coils.
Suh, Sang Heon;Lee, Ko Eun;Park, Jeong Woo;Kim, In Jin;Kim, Ok;Kim, Chang Seong;Choi, Joon Seok;Bae, Eun Hui;Ma, Seong Kwon;Lee, Jong Un;Kim, Soo Wan
The Korean Journal of Physiology and Pharmacology
/
v.17
no.5
/
pp.435-440
/
2013
While the anti-apoptotic effect of paricalcitol has been demonstrated in various animal models, it is not yet clear whether paricalcitol attenuates the apoptosis in gentamicin (GM)-induced kidney injury. We investigated the effect of paricalcitol on apoptotic pathways in rat kidneys damaged by GM. Rats were randomly divided into three groups: 1) Control group (n=8), where only vehicle was delivered, 2) GM group (n=10), where rats were treated with GM (150 mg/kg/day) for 7 days, 3) PARI group (n=10), where rats were co-treated with paricalcitol (0.2 ${\mu}g/kg/day$) and GM for 7 days. Paricalcitol attenuated renal dysfunction by GM administration in biochemical profiles. In terminal deoxynucleotidyl transferase dUTP nick end labeling staining, increased apoptosis was observed in GM group, which was reversed by paricalcitol co-treatment. Immunoblotting using protein samples from rat cortex/outer stripe of outer medulla showed increased Bax/Bcl-2 ratio and cleaved form of caspase-3 in GM group, both of which were reversed by paricalcitol. The phosphorylated Jun-N-terminal kinase (JNK) expression was increase in GM, which was counteracted by paricalcitol. The protein expression of p-Akt and nitro-tyrosine was also enhanced in GM-treated rats compared with control rats, which was reversed by paricalcitol co-treatment. Paricalcitol protects GM-induced renal injury by antiapoptotic mechanisms, including inhibition of intrinsic apoptosis pathway and JNK.
In order to determine possible relationships between the renin-angiotensin system and nephron heterogeneity, we compared the response of renin release and the angiotensin-converting enzyme (ACE) activity from different areas of the rat kidney. We used the renal cortical slices from the capsular surface to the juxtamedullary junction. Slices from outer one-third of the cortex were designated as outer cortical slices (OC), middle one-third as midcortical slices (MC), and inner one-third as inner cortical slices (IC). The renal renin content markedly decreased from OC and MC to IC. The basal lenin release was higher in OC than in MC or IC. On the contrary the percent change of renin release in response to L-isoproterenol was significantly higher in MC than in OC or IC. By TMB-8, the renin release in MC by $231{\pm}21%$ was higher than OC by $171{\pm}19%$ or IC by $$162{\pm}19. Angiotensin II suppressed renin release in OC and MC by $68{\pm}2,\;71{\pm}4%$ respectively, but only $40{\pm}7%$ in IC. The ACE activity was higher in IC than in OC, MC, medulla and papilla. The present data indicate that renin content and basal lenin release gradulally decreased from outer (OC) to inner (IC) cortex. The renin release in response to beta-adrenergic agonist, L-isoproterenol and intracellular calcium antagonist, TMB-8 were higher in MC than in OC and IC, but angiotensin II suppressed renin release less in IC than in OC and MC. It is suggested that juxtaglomerular cells of outer, mid-and inner cortices show a difference in renin release response to the stimuli.
Interruption or prolonged reduction and subsequent restoration of blood flow into the kidney triggers the generation of a burst of reactive oxygen species (ROS), leading to injury in the tubular epithelial cells. In this study, we determined whether methanol extract of goat's-beard (Aruncus dioicus) (extract) could prevent this ischemia/reperfusion injury. When in vitro radical scavenging activity of the extract was measured using a DPPH radical quenching assay, the extract displayed slightly lower activity than ascorbic acid. One hour after administration of the extract (400 mg/kg) by intraperitoneal injection in rats, renal ischemia/reperfusion injury was generated by clamping the left renal artery for forty minutes, followed by 24 hr restoration of blood circulation. Prior to clamping the left renal artery, the right renal artery was removed. Compared with the vehicle-treated group, pretreatment with the extract significantly reduced the tubular epithelial cell injury by 37% in the outer medulla region, and consequently reduced serum creatinine concentration by 39%. Reduction in the cell injury was mediated by attenuation of Bax/Bcl-2 ratio, inhibition of caspase-3 activation from procaspase-3, and subsequent reduction in the number of apoptotic cells. Thus, goat's-beard (Aruncus dioicus) might be developed as a prophylactic agent to prevent acute kidney injury.
Oh, Jeong Min;Jung, Eun Sun;Choi, Koh Eun;Heo, Jong Won;Kim, Hyun Tae;Ryu, Ju Young;Lee, Kang Wook;Cha, Ji Yun;Seol, In Chan;Cho, Hyun Kyoung;Yoo, Ho Ryong;Cho, Min Kyoung;Kim, Yoon Sik
Journal of Physiology & Pathology in Korean Medicine
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v.30
no.4
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pp.289-299
/
2016
This study is aimed to report two cases of chronic kidney disease treated with Korean traditional medicine. We treated the patients with traditional herbal medicine and other treatments including acupuncture. We measured serum creatinine, estimated glomerular filtration rate(eGFR), blood urea nitrogen(BUN), albumin, red blood cell count(RBC), hemoglobin for several times during admission. Case 1 patient was diagnosed with right medulla infarction, bladder stone, chronic kidney disease. The symptoms were quadriplegia, right side dysesthesia, drowsiness and edema. Case 2 patient was diagnosed with acute cerebral infarction, hypertension, chronic kidney disease. The symptoms were right side weakness, delusion, anorexia, low back pain. Case 1 patient was hospitalized for 80 days, and case 2 patient was for 31 days. Korean traditional medicine decreased serum creatinine and BUN level, improved eGFR, increased RBC and hemoglobin. The symptoms of chronic kidney disease such as edema, general body weakness and anorexia were also improved. These cases suggest that Korean traditional medicine can be effective and safe for patients with chronic kidney disease.
Mongolian gerbil (Meriones unguiculatus) has been as an model animal for studing the neurological disease such as stroke and epilepsy because of the congenital incompleteries in Willis circle, as well as the investigation of water metabolism because of the long time-survival in the condition of water-deprived desert condition, compared with other species animal. Aquaporin 2 (AQP2) expressed at the surface of principal cells in collecting duct results from an equilibrium between the AQP2 in intracellular vesicles and the AQP2 on the plasma membrane. Aquaporin 4 (AQP4), which is expressed in cell in a wide range of organ, is also present in the collecting duct principal cells where this is abundant in the basolateral plasma membranes and represent potential exit pathways from the cell for water entering via AQP2. In this research, we divide 3 groups of which each group include the 5 animals. In the study of 7 or 14 days water restricted condition, we investigated the AQP2 and AQP4 by using a quantitative immunohistochemistry in the kidney. The results obtained in this study were summarized as followings. AQP2 is abundant in the apical plasma membrane and apical vesicles in the collecting duct principal cell and at rare abundance in connecting tubules. In the water-deprived Mongolian gerbil kidney, expression of AQP2 was continuosly increased in the cortical collecting duct and inner medullary collecting duct. This increase was both the apical region and cytoplasm. AQP4 is mainly expressed in the inner medulla, although some expression is also noted in the more proximal segment. In the water-deprived Mongolian gerbil kidney, AQP4 was also increased in the inner medullary collecting duct. Immunoactivity was increased in entire inner medullary collecting duct and newly detected in cytoplasm of principal cell. These findings suggest that increased levels of AQP2 and AQP4 in the cortical and inner medulalry collecting duct may play a important role for maintain fluid balance in the water-deprived kidney.
A 9-year-old, male, Doberman pinscher dog with 5-month history of intermittent hematuria, vomiting and glucosuria was referred to local animal hospital. Abdominal ultrasonography showed an irregular and hyperechoic mass in the renal medulla of the enlarged left kidney. Grossly atrophied renal cortex and medulla and marked hydronephrosis were observed on the cut surface of kidney. A single, numerous papillary projected, pedunculated mass 4~5.5 cm in diameter was occupied in renal pelvis, and extended from pelvis to the inlet of ureter. Histopathologically, the mass had numerous papillary structures with arboriform pattern. These papillae were consisted of fibro-vascular stalks that were lined by multiple layers of neoplastic urothelium (transitional epithelium) with marked cellular atypia. Immnohistochemical (IHC) staining demonstrated that the neoplastic cells showed strong positive reactions for cytokeratin (CK) 7, CK 19, CK clone MNF116 and CK high molecular weight, but negative signals for CK 8 low molecular weight. Based on the gross findings, histopathology and CKs profile using IHC staining, this mass was diagnosed as renal pelvis transitional cell carcinoma in a dog.
Purpose : To investigate the effects of angiotensin II inhibition on the epithelial to mesenchymal transition (EMT) in the developing kidney, we tested the expression of EMT markers and nestin in angiotensin converting enzyme (ACE) inhibitor-treated kidneys. Methods : Newborn rat pups were treated with enalapril (30 mg/kg/d) or a vehicle for 7 days. Immunohistochemistry for the expression of ${\alpha}$-smooth muscle actin (SMA), E-cadherin, vimentin, and nestin were performed. The number of positively-stained cells was determined under 100 magnification in 10 random fields. Results : In the enalapril-treated group, ${\alpha}SMA-positive$ cells were strongly expressed in the dilated tubular epithelial cells. The number of ${\alpha}SMA-positive$ cells in the enalapril-treated group increased in both the renal cortex and medulla, compared to the control group (P<0.05). The expression of E-cadherin-positive cells was dramatically reduced in the cortical and medullary tubular epithelial cells in the enalapril-treated group (P<0.05). The number of vimentin- and nestin-positive cells in the cortex was not different in comparisons between the two groups; however, their expression increased in the medullary tubulointerstitial cells in the enalapril-treated group (P<0.05). Conclusion : Our results show that ACE inhibition in the developing kidney increases the renal EMT by up-regulating ${\alpha}SMA$ and down-regulating E-cadherin. Enalapril treatment was associated with increased expression of vimentin and nestin in the renal medulla, suggesting that renal medullary changes during the EMT might be more prominent, and ACE inhibition might differentially modulate the expression of EMT markers in the developing rat kidney.
Renal size(length, width and height) of rabbits was measured by radiographs and nephrosonograms and compared with actual size. After measuring on the radiographs and nephrograms, both kidneys were removed from the body and actual size was also measured. On radiographs, right kidney was observed at the T13-L2 vertebrae and left kidney was at L2-L4 vertebrae. On nephrosonograms, the renal cortex was visible as small, homogenous echoes that were hypoechoic relative to the surrounding tissues, whereas the renal medulla was anechoic to slightly hypoechoic. The actual length, width and height of the left kidney were $35.84{\pm}3.12(mean{\pm}SD)$, $23.52{\pm}3.21$, $15.11{\pm}2.58cm$, respectively, whereas those of the right kidney were $36.02{\pm}3.42$, $23.69{\pm}3.50$ and $14.13{\pm}3.55cm$, respectively. On radiographs, the length and width of both kidneys were a little magnified(102-104%) when compared to actual size. On nephrosonograms, the length, width and height of bothkidneys were lessened(70-96 %) when compared to actual size. The length and width of kidney were 1.85 and 1.25 times the length of the second lumbar vertebrae on the ventrodorsal view. In correlation and correlation coefficient of body weight with the renal size, the body weight and renal size were significantly correlated with each other other(p<0.01) and the correlation coefficents of body weight with left, right and both Kindneys were 0.748, 0.794 and 0.859, respectively.
This study investigated the localization and changes in the concentration of injected mercury in the kidney, liver, and spleen of mice. To evaluate changes in the concentration of mercury over time, the mice were euthanized 10, 150, and 300 days post-treatment. Localization of accumulated mercury was identified by the autometallography method. Mercury was densely located in the supranuclear cytoplasm of epithelial cells of proximal tubules of the kidney but was not detected in the glomerulus 10 days post-treatment. In the liver, mercury was mainly found in hepatocytes around the portal vein and in sinusoidal Kupffer cells 10 days post-treatment. Mercury was scattered throughout both white and red pulp of the spleen 10 days post-treatment. In terms of changes in the concentration of mercury, the levels were lower in the renal cortex and medulla 150 and 300 days post-treatment as compared with those 10 days post-treatment. Mercury was found at low concentrations in liver hepatocytes 150 and 300 days post-treatment. The mercury concentration was also low in both the white and red pulp of the spleen 150 and 300 days post-treatment. Therefore, the concentrations of accumulated mercury in the kidney, liver, and spleen 150 and 300 days post-treatment were lower than those 10 days post-treatment. We identified the localization of mercury in cells and tissues of several organs and observed that accumulated mercury in organs decreased naturally over time.
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