Journal of Pathology and Translational Medicine

Original Article

Post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury: Juan Carlos Alvarez Moreno, Hisham F. Bahmad, Christopher A. Febres-Aldana, Andrés Pirela, Andres Azuero, Ali Salami, Robert Poppiti; J Pathol Transl Med. 2021;55(6):369-379. Published online October 14, 2021; DOI: https://doi.org/10.4132/jptm.2021.08.03

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Background
Acute kidney injury (AKI) is a common cause of morbidity and mortality. It mainly targets the renal tubular epithelium with pathological changes, referred to as acute tubular injury. The latter is followed by a regenerative response that is difficult to visualize on routine hematoxylin and eosin (H&E) stains. In this study, we examined the regenerative capacity of renal tubules by correlating vimentin (VIM) immunohistochemical (IHC) expression and pathological findings of AKI and renal tubular regeneration (RTR) on H&E.
Methods
We reviewed 23 autopsies performed in the clinical setting of AKI and RTR. VIM expression was scored in the renal cortical tubular epithelium using a statistical cutoff ≥ 3% for high expression and < 3% for low expression.
Results
Of the 23 kidney tissues examined, seven (30.4%) had low VIM expression, and 16 (69.6%) had high VIM expression. Kidney tissues with evidence of AKI and RTR had significantly higher VIM expression. Renal peritubular microenvironment features showing regenerative changes on H&E were associated with high VIM expression. In the univariate model, kidney tissues with RTR were 18-fold more likely to have high VIM expression.
Conclusions
In conclusion, our findings suggest that VIM could serve as an IHC marker for RTR following AKI. However, correlation with H&E findings remains critical to excluding chronic tubular damage. Collectively, our preliminary results pave the way for future studies including a larger sample size to validate the use of VIM as a reliable biomarker for RTR.

Citations

Citations to this article as recorded by

Characterization of macrophages in ischemia–reperfusion injury-induced acute kidney injury based on single-cell RNA-Seq and bulk RNA-Seq analysis
Qin Wang, Yuxing Liu, Yan Zhang, Siyuan Zhang, Meifang Zhao, Zhangzhe Peng, Hui Xu, Hao Huang
International Immunopharmacology.2024; 130: 111754. CrossRef

Review

White Matter Injury of Prematurity: Its Mechanisms and Clinical Features: Young Ah Lee; J Pathol Transl Med. 2017;51(5):449-455. Published online August 11, 2017; DOI: https://doi.org/10.4132/jptm.2017.07.25

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Abstract PDF

A developing central nervous system is vulnerable to various insults such as infection and ischemia. While increased understanding of the dynamic nature of brain development allows a deeper insight into the pathophysiology of perinatal brain injury, the precise nature of specific fetal and neonatal brain injuries and their short- and long-term clinical consequences need special attention and further elucidation. The current review will describe the pathophysiological aspects and clinical significance of white matter injury of prematurity, a main form of perinatal brain injury in premature newborns, with a particular emphasis on its potential antenatal components.

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Pioglitazone Ameliorates Lipopolysaccharide-Induced Behavioral Impairment, Brain Inflammation, White Matter Injury and Mitochondrial Dysfunction in Neonatal Rats
Jiann-Horng Yeh, Kuo-Ching Wang, Asuka Kaizaki, Jonathan W. Lee, Han-Chi Wei, Michelle A. Tucci, Norma B. Ojeda, Lir-Wan Fan, Lu-Tai Tien
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Original Article

Chemotherapy-Associated Hepatopathy in Korean Colorectal Cancer Liver Metastasis Patients: Oxaliplatin-Based Chemotherapy and Sinusoidal Injury: Soo Jeong Nam, Jai Young Cho, Hye Seung Lee, Gheeyoung Choe, Ja June Jang, Yoo-Seok Yoon, Ho-Seong Han, Haeryoung Kim; Korean J Pathol. 2012;46(1):22-29. Published online February 23, 2012; DOI: https://doi.org/10.4132/KoreanJPathol.2012.46.1.22

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Abstract PDF

Background

Although chemotherapy-related hepatic injury has been reported in colorectal cancer liver metastasis (CRLM) patients, the morphologic changes caused by chemotherapeutic agents and the effect of chemotherapy on postoperative outcome remain ill-defined. A comprehensive review of the morphologic changes in the post-chemotherapy non-neoplastic liver was performed and the clinical effect of preoperative chemotherapy in CRLM patients was analyzed.

Methods

Hematoxylin-eosin, Masson's trichrome and reticulin-stained slides from non-neoplastic livers obtained from 89 CRLM patients were analyzed, and the clinicopathologic features were correlated with the status of chemotherapy exposure.

Results

Histopathologic features of sinusoidal injury (sinusoidal dilatation, centrilobular perivenular fibrosis, parenchymal extinction lesions, small vessel obliteration, and hepatocyte plate disruption) were significantly more frequent in oxaliplatin-exposed livers (p<0.05). The extent of sinusoidal dilatation was positively correlated with increasing numbers of chemotherapy cycles (p=0.022). Abnormal preoperative liver function tests were more frequently seen (p<0.05) and postoperative total bilirubin was higher in the chemotherapy group (p=0.008). Postoperative morbidity was more common in the chemotherapy group (p=0.044).

Conclusions

Sinusoidal injury is frequently seen in oxaliplatin-treated livers, and its presence, especially when extensive, should be documented in surgical pathology practice. The recognition of sinusoidal injury may provide helpful guidelines for surgeons in deciding the extent of hepatic resection.

Citations

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Model establishment and microarray analysis of mice with oxaliplatin‑induced hepatic sinusoidal obstruction syndrome
Chen Zhu, Xinwei Cheng, Ping Gao, Qianyan Gao, Ximin Wang, Dong Liu, Xiuhua Ren, Chengliang Zhang
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Oxaliplatin-induced hepatic sinusoidal obstruction syndrome
Chen Zhu, Xiuhua Ren, Dong Liu, Chengliang Zhang
Toxicology.2021; 460: 152882. CrossRef
Hepatic steatosis in patients undergoing resection of colorectal liver metastases: A target for prehabilitation? A narrative review
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Protective effect of Korean red ginseng on oxaliplatin-mediated splenomegaly in colon cancer
Jeonghyun Kang, Joon Seong Park, Sung Gwe Ahn, Jin Hong Lim, Seung Hyuk Baik, Dong Sup Yoon, Kang Young Lee, Joon Jeong
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In Vitro

The Effects of Excitatory Amino Acids and Their Receptors on Neuronal Damage of Rat Brain in Hypoxic-Ischemic Encephalopathy.: Heasoo Koo; Korean J Pathol. 1995;29(5):545-562.

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Abstract: Since the role of excitatory amino acids such as glutamate and aspartate and their receptors mediating cellular injury through various mechanisms were known in hypoxic-ischemic injury and associated diseases of central nervous system, blocking agents for transmitter release or receptors have been tried to reduce the cellular damages and subsequent sequelae experimentally. Several in vitro studies suggested two kinds of glutamate neurotoxicity: (1) rapid toxicity due to influx of sodium or chloride with resultant cellular edema and consequent damage, which is associated with N-methyl-D-Aspartate(NMDA) as well as non-NMDA receptors, (2) calcium mediated delayed toxicity associated mainly with NMDA receptor. This study was conducted to investigate the role of rapid toxicity in hypoxic-ischemic injury. Early lesions of 30 minutes to 24 hours after hypoxic-ischemic insult were examined by autoradiography with radiolabelled glutamate and kainitic acid (KA) as well as light and electron microscopy. Late changes were evaluated on formaldehyde-acetic acid-methanol(FAM) fixed brain 1 week after the insult. Cornus ammonis(CA) l of hippocampus showed the highest density of NMDA receptors, which was decreased constantly from 2 hours to 24 hours. In contrast, CA3 of hippocampus showed the highest density of KA receptors, which was the lowest at 6 hour and increased thereafter. Light microscopic examination showed the worst changes during 30 minutes to 6 hours. After 1 week, most of the cases showed degeneration of neurons and CAI and CA3 did not show the difference. Electron microscopic examination showed marked degenerative changes of neurons as well as neuropils starting from 30 minutes after the insult. In conclusion, rapid toxicity mediated by non-NMDA(KA) receptor seen in CA3 lead to permanent damage in 1 week old lesion.

Original Articles

HgCl2 Toxicity on Cultured Renal Tubular Cells of Rabbit.: Jung Young Lee, Seong Beom Lee, Suk Hyung Lee, Won Sang Park, Nam Jin Yoo, Sang Ho Kim, Choo Soung Kim; Korean J Pathol. 1995;29(5):615-623.

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Abstract: To understand the mechanism of cell injury when exposed to HgCl2, monitoring of cytosolic ionized free Ca2+([Ca2+]i), viability test, measurement of the amount of ATP, and Ca-ATPase activity were evaluated in cultured rabbit renal tubular cells(RTC) exposed to HgCl2. The results were as follows: 1) HgCl2 was cytotoxic to rabbit RTC at all doses except 10 uM and the rate of killing displayed a dose- and time-dependent relationship. 2) The absence of extracellular Ca provided partial protection from irreversible injury induced by HgCl2. 3) The increasing pattem of [Ca2+]i varied according to the concentrations of HgCl2. At the low concentrations of HgCl2 (2.5-10 microM), the level of [Ca2+]i increased slowly over the flat 2-3 min and then achieved plateau-state. In contrast, at the high concentrations of HgCl2 (25-100 microM) the level of [Ca2+]i achieved peak within 1 min and then decreased to a plateau state under normal concentrations. 4) The level of ATP was decreased to 27.5% of that of normal control cells within 3 min by using a treatment of 100 microM HgCl2. 5) HgCl2 did not affect the Ca2+ ATPase activity by enzyme histochemical observation. These findings suggest that the elevation of [Ca2+]i in response to the HgCl2-induced injury is an important event in accelerating injury that ultimately leads to cell death. But other possibilities such as HgCl2 might have direct deleterious effects on the also should be considered.

Correlation between Transforming Growth Factor-beta and Procollagen III with Regenerative Activity in Acute Liver Injury, and the Effect of Prostaglandin E2.: Nam Hoon Cho, Chan Il Park; Korean J Pathol. 1996;30(5):367-387.

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Abstract PDF: Transforming growth factor-beta (TGF-beta) plays an important role in hepatic fibrogenesis. It is thought to inhibit regeneration of the hepatocytes. The aim of this present study was to clarify the correlation of TGF-beta, collagen type III (PIIINP) and the regenerating activity of hepatocytes, and the effect of prostaglandin E2 (PgE2) on them in acute liver injury. Two hundred and sixteen male Sprague-Dawley rats, weighing 200g on average, were divided into six experimental groups and two control groups; group I-CCl4 only administration, group II-partial hepatectomy(PH) only, group III-PH following CCl4 administration, group IV-olive oil only administration, group V-sham operation, group VI-CCl4 administration with pretreatment of PgE2, group VII- PH with pretreatment of PgE2, and group VIII- PH following CCl4 administration with pretreatment of PgE2. Five rats were sacrificed at 12, 24, 36, 48, 96 and 168 hours after the administration of CCl4 or PH in each experimental group. The liver was tested with immunohistochemical stain for proliferating cell nuclear antigen (PCNA) and in situ hybridization for TGF-beta. Radioimmunoassay for serum PIIINP was also performed. The results were as follows: TGF-beta was expressed mainly in the perisinusoidal cells and periportal mesenchymal cells. The TGF-beta positive cells were most numerous in the combined group of CCl4 plus PH. TGF-beta expression tended to have an inverse relation, with the PCNA index in all experimental groups. The PCNA index was highest in the CCl4 only group and lowest in the combined group of CCl4 plus PH. The PH only group showed a peak PCNA index at 48 hours. In the CCl4 only group and the combined group of CCl4 plus PH, serum PIIINP appeared to increase at 12 hours or more after the expression of hepatic TGF-beta. Pretreatment of PgE2 revealed that TGF-beta precipitously disappeared at 48-96 hours after insult. PgE2 influenced the vanishing period, not the emerging time of TGF-beta and had a remarkable effect on the amount of TGF-beta especially in the PH following CCl4 administration group, which resulted in significant accentuation of PCNA indices. In conclusion, PH of the prior injured liver induces a marked increase of TGF-beta followed by a significant suppression of regeneration of the remaining liver, and PgE2 overtly suppresses the expression of TGF-beta.

Extracellular Matrix and Astrocytic Response during Regeneration following Cryogenic Injury in Adult Rat Cerebral Cortex.: Soo Im Choi, Woo Ick Yang, Tae Seung Kim; Korean J Pathol. 1996;30(6):473-486.

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Abstract PDF: Astrocytes are the most numerous cellular elements in the cerebrum, and they normally have a very slow turnover rate. But during regeneration after injury, they proliferate markedly resulting in astrogliosis. The extracellular matrix in the central nervous system is present in the vessel walls and in the external glia limitans as a basal lamina. The presence of an intact extracellular matrix framework is important in regeneration after injury. Understanding the properties of astrocytic proliferation will be helpful to find out new treatment for functional recovery in the central nervous system. In this study, after cryogenic injury was performed on the cerebral cortex in rats, changes in astrocytes and the extracellular matrix were observed using light microscopy, immunohistochemical stain for glial fibrillary acidic protein(GFAP), proliferating cell nuclear antigen(PCNA), fibronectin, laminin, and type IV collagen, autoradiography and electron microscopy. The results were as follows; 1) The coagulative necrosis, which followed cryogenic injury on the cerebral cortex was healed, forming a new pia mater above the lesion. 2) Some of the PCNA positive cells were astrocytes and some of the GFAP positive cells showed a positive reaction to PCNA. 3) Proliferating astrocytes labelled by autoradiography or immunohistochemical stain for PCNA reached maximal numbers 3days after the injury and they were no longer found 2 weeks after injury. 4) In autoradiography with immunohistochemical stain for GFAP, about 1% of GFAP positive astrocytes were labelled by autoradiography and in double immunohistochemical stain for PCNA and GFAP, about 8-16% of GFAP positive astrocytes were also stained by PCNA. 5) In immunohistochemical stain for fibronectin, laminin and type IV collagen, laminin and type IV collagen were present in the newly formed blood vessel walls and fibronectin showed a diffuse positive reaction within the lesion. The new pia mater was formed within 2 weeks after the injury. 6) On electron microscopic examination, basal lamina material was found in the vessel wall 1 week after the injury and at 2 weeks, a nearly complete and continuous basal lamina was formed although the thickness was uneven. According to these findings, astrocytes in the cerebral cortex of adult rats proliferate very early in the regenerative period after cryogenic injury. At 2 weeks after the injury, this regeneration ceases and the damaged basal lamina of pia mater and vessel wall were reconstituted.

Protective Effects of Captopril in Radiation-Induced Renal Injury in Rats.: Ji Yeon Bae, Eun Sook Chang, Ok Bae Kim; Korean J Pathol. 2000;34(3):214-224.

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Abstract PDF: The angiotensin I converting enzyme inhibitor (Captopril) has recently been studied extensively in various experimental models of radiation injury and has proven its protective effects in various organs, such as the lungs, gastrointestinal tract, and kidneys. Twenty-three Sprague-Dawley rats were divided into experimental and control group. The experimental group was divided into two large groups: the first one received a single dose of 18 Gy irradiation from an electron beam on the local field of the kidney region only, and the second group received captopril per oral continuously after the same doses of irradiation. The second experimental group was divided into four subgroups by captopril doses: 62.5 mg/l, 125 mg/l, 250 mg/l, and 500 mg/l, respectively. On light and electron microscopy, the kidneys of the irradiated rats with no captopril treatment showed diffuse glomerular contraction, congestion with occlusion and focal necrosis of the endothelial, and mesangial cells. The tubules showed ballooning degeneration, desquamation, and diffuse coagulation necrosis. Captopril treated rats, especially those given a high dose (more than 250 gm/l), revealed a marked reduction of the tubular and glomerular injuries. There was a statistically significant difference in the degree of renal injury among the experimental groups (p<0.05). The result of this study suggests that an administration of high dose captopril might prevent radiation-induced renal injury, especially in the early post-irradiation period.

Effects of Active Hexose Correlated Compounds on Drug Induced Liver Injury in Mice.: Ki Ouk Min, Hi Jeong Kwon, Eun Joo Seo, Jeana Kim, Seok Jin Kang, Byung Kee Kim; Korean J Pathol. 2000;34(7):509-515.

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Abstract PDF: AHCC (Active Hexose Correlated Compounds), which was at first extracted from cultured broth of Basidiomycotina, is known to be one of the Biological Response Modifiers (BRM). We examined the protective effects of AHCC on carbon tetrachloride (CCl4) and thioacetamide (TAA)-induced liver injury in mice. The AHCC pretreatment prevented the suppression of several physiological and biochemical parameters in the mice injected with CCl4 or TAA for 5 days. The liver weights and serum ALT and AST levels were increased by CCl4 or TAA, the degree of which was significantly reduced with the AHCC pretreatment. The AHCC pretreatment induced increasing activity of GST (glutathione s-transferase) and showed an increasing tendency of P450 and EROD (ethoxyresorufin o-dealkylation). The AHCC pretreatment also showed negative effects against the suppression of drug metabolizing enzymes, such as P450, EROD, and GST induced by CCl4 or TAA. AHCC pretreatment showed protective effects with significant inhibition of fatty change, inflammation, and necrosis in CCl4 and TAA intoxicated mice liver. The present study suggests that the protective effect of AHCC pretreatment might be related to the protection of liver from the drug induced liver injury in mice model.

Distribution of Free Radicals in Reperfusion Injury after Transient Brain Ischemia.: Eunkyoung Kwak, Hyungho Suh, Jiyoung Park, Yunsup Kum, Taein Park, Jungwan Kim, Yoonkyung Sohn; Korean J Pathol. 2000;34(11):893-900.

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Abstract PDF: Free radicals are known as an important factor which may act on reperfusion injury after transient or permanent brain ischemia. Numerous studies about cytotoxic function of free radical have been done. Most of these studies demonstrate the function of free radical in reperfusion injury by using radical scavenger or antioxidant as inhibitor of radicals. We used a modification of Karnovsky's Mn2 /diaminobenzidine (DAB) technique to demonstrate intravascular free radicals following transient occlusion and reperfusion of one middle cerebral artery in Sprague-Dawley rats. The MCA was occluded for 2 hours using an intraluminal suture method. The reperfusion time after transient ischemia was 1 hour, 6 hours, and 24 hours, respectively. Animals were perfused transcardially with solution containing Mn2 and DAB. After DAB perfusion, the brains were removed promptly, sectioned in frozen, and stained with methylene blue for light microscopic examination. Upon light microscopic examination, free radicals were confined within intravascular lumen and the amount of deposits increased according to the duration of reperfusion. Upon electron microscopic examination, free radicals were located in nuclear membrane and membrane of mitochondria and RER, and demonstrated as electron dense deposits. In addition, cell processes of the neuron revealed an electron dense deposits beneath the inner side of the membrane. In conclusion, free radicals demonstrated in the reperfusion injury area indicate that free radical acts as an important cytotoxic factor. Intracellular localization of free radicals may explain the relationship between free radical and delayed neuronal injury.

The Effect of Ischemic Preconditioning in Rat Liver: The Expression of Interleukin-1 and Nuclear Factor-B.: Kum Yoon Seup, Soo Kyoung Lee, Sun zoo Kim, Eun Kyoung Kwak, Ji Young Park, Tae In Park, Han Ik Bae, Yoon Kyung Sohn, In Soo Suh; Korean J Pathol. 2002;36(4):238-242.

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Abstract PDF: BACKGROUND
A short period of ischemia and reperfusion, called ischemic preconditioning, protects various tissues against subsequent sustained ischemic insult. Apoptosis of hepatocytes and sinusoidal endothelial cells are a critical mechanisms of injury in the ischemic liver. Because nuclear factor-B (NF-B) has a significant role in the cell survival, we hypothesized that ischemic preconditioning protects by inhibition of apoptosis through the expression of NF-B, induced by interleukin-1 (IL-1), which is known for enhancement of its transcription and activation.
METHODS
We induced ischemia and reperfusion on rat liver, and performed in situ terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labelling assay and polymerase chain reaction for IL-1 mRNA and NF-B mRNA.
RESULTS
Apoptosis of hepatocytes and sinusoidal endothelial cells, assessed by in situ TUNEL assay, was significantly reduced with preconditioning. The expression of IL-1 mRNA and NF-B mRNA are seen on discrete monoclonal bands around 344 and 356 base pairs, in comparison with normal rat liver, but, there was no significant difference between the ischemia-reperfusion group and the preconditioning group.
CONCLUSIONS
We suggest that ischemic preconditioning confers dramatic protection against prolonged ischemia via inhibition of apotosis through the expression of IL-1 inducing NF-B and its activation. However, we need further study in the activity of NF-B, such as nucleotide shift assay, because the activity of NF-B is regulated by binding of the inhibitory protein, IB.

Effects of Selective Cyclooxygenase-2 Inhibitor NS-398 Pretreatment on the Rat Spinal Cord after Contusion Injury.: Hyeon Dae Cheong, Joo Kyung Sung, In Suk Ham, Ku Seong Kang, Joung Ok Kim, Jung Wan Kim, Tae In Park, Yoon Kyung Sohn; Korean J Pathol. 2006;40(4):255-262.

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Abstract PDF: BACKGROUND
Secondary spinal cord injury (SCI) that follows an initial mechanical insult can exacerbate the overall damage, limit the restorative processes and eventually lead to an in- creased neurological deficit. We hypothesized that selective inhibition of cyclooxygenase-2 (COX-2) may decrease the delayed cell death, and so this will contribute to decreased level of the secondary injury.
METHODS
The dorsal surface of the cord at the T9 level was subjected to weight drop impact using a 10 g rod. To block COX-2 activation, a selective COX-2 inhibitor (NS-398) was administered (5 mg/kg, i.p.) 15 min prior to SCI. The COX-1, COX-2, Caspase-3 and PGE2 expressions were measured by real time quantitative RT-PCR and fluorescence immunostaining.
RESULTS
Many activated caspase-3 positive cells were observed at 6 h and they increased until 72 h after SCI. The expression of COX-2 peaked at 6 h after SCI, while the COX-1 expression was unaffected. The principal cells that showed a COX-2 expression were the neurons and microglia. Pretreatment with NS-398 caused a significant decrease in the expression of prostaglandin E2 and activated caspase-3 positive cells after SCI.
CONCLUSION
These data suggest that COX-2 is one of the main factors related with the pathologic deficits from secondary SCI.

Effects of Calcitriol on Delayed Neuronal Damage of Hippocampus in Transient Global Ischemia Model of Mature Gerbil.: Hye Jin Park, Hea Soo Koo, Woon Sup Han, Kyung Kyu Choi; Korean J Pathol. 2003;37(5):307-315.

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Abstract PDF: BACKGROUND
It is well documented that calcium ions perform a major role in neuronal degeneration in cerebrovascular disease and the other degenerative diseases, and that 1,25-dihydroxyvitamin D3 (D3) has the dose-dependent protective effects. This study was performed to examine the effects of different D3 dosages against delayed neuronal damage of the hippocampus.
METHODS
Mature mongolian gerbils were injected with either 0.8 microgram/kg/day (group 2) for 5 days or 1.0 microgram/kg/day for 8 days (group 3) prior to the 10 min ligation of the bilateral common carotid arteries. Immunohistochemical expression for the glial cell line-derived neurotrophic factor (GDNF), the basic fibroblast growth factor (bFGF) and the platelet-derived neurotrophic factor (PDNF) was observed in the D3-injected (0.8 microgram/kg/day for 5 days) group.
RESULTS
Group 2 showed a highly significant attenuation of delayed neuronal damage in the lateral CA1 region at 7 days after reperfusion. Group 3 showed unilateral or bilateral hemispheric infarcts 24 h after the onset of reperfusion. The D3-injected group showed a markedly increased bFGF expression level.
CONCLUSION
The dose-dependent effect of D3 suggests the importance of determining the appropriate D3 dose for clinical applications. Although the mechanism(s) of neuroprotection by D3 remains unclear, D3 may facilitate a reduction in ischemia-induced oxidative stress via the activation of the neurotrophic factors, including bFGF and GDNF.

Ultrastructural Study of Amiodarone-Associated Lung Injury.: Eun Yung Kim, Sang Han Lee, Yoon Kyung Sohn, Tae Joong Sohn; Korean J Pathol. 1995;29(1):10-23.

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Abstract PDF: Amiodarone, an antiarrhythmic drug, may exert pulmonary toxicity in some patients but the pathogenesis is not clear. This study was carried out to investigate the pathogenetic mechanism of pulmonary injury induced by amiodarone at dose of 100 mg/kg/day given to rats by intraperitoneal injection for 3 weeks. And the preventive effects of concomitantly injected steroid (10 mg/kg/day) on amiodarone induced pulmonary injury was also studied using bronchoalveolar lavage, light microscopy and transmission electron microscopy. The results obtained were summarized as follows: Mild lymphocytosis of bronchoalveolar lavage fluid was found in all experimental groups. Intracytoplasmic lamellar body formation was found in all types of pulmonary cells and type II pneumocytes revealed the earliest abnormal lamellar body formation. The capillary endothelial cells showed cellular swelling and detachment from underlying basement membrane at early phase of experiment and the edema of alveolar wall and interstitium were noted. Interstitial fibrosis and proliferation of type II pneumocytes were noted at late phase. The lungs of steroid injected groups revealed accumulation of lamellar bodies in all types of pulmonary cells but interstitial fibrosis was not occurred. These findings support the concept that amiodarone is responsible for a drug-induced phospholipidosis and directly toxic to pulmonary endothelial and epithelial cells. And steroid may regress the progression of amiodarone induced pulmonary injury.

Experimental Study of the Progressive Glomerulosclerosis Induced by Long-term Administration of Puromycin Aminonucleoside in Rats.: Mi Kyung Kim, Hyun Soon Lee; Korean J Pathol. 1993;27(1):1-10.

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Abstract PDF: Pathogenetic mechanisms of progressive glomerulosclerosis are not clear. We studied the long-term(10 weeks) effects of puromycin aminonucleoside(PAN) in Sprague-Dawley rats with or without uninephrectomy(UN). Compared to rats with PAN injections only, rats with uninephrectomy and PAN injections showed significantly higher serum levels of urea nitrogen(153 +/- 155 mg/dl vs. 16 +/- 4 mg/dl, p<0.01), ceatinine(2.96 +/- 1.21 mg/dl vs. 0.92 +/- 0.36 mg/dl, p<0.01), cholesterol(466 +/- 125 mg/dl vs. 94 +/- 27 mg/dl, p<0.01), and triglyceride(337 +/- 237 mg/dl vs. 111 +/- 36 mg/dl, p<0.05) as well as increased amounts of proteinuria(428 +/- 90 mg/day vs. 136 +/- 130 mg/day, p<0.01). Lesions of focal segmental glomerulosclerosis(FSGS) were more frequently observed in rats with UN and PAN injections than rats with PAN infections only(39.5 +/- 17.2% vs. 4.3 +/- 4.7%, p<0.01). Ultrastructural examination of the glomeruli from rats with UN and PAN injections revealed severe epithelial cell changes including foot process effacement, vaculoar change or pseudocyst formation and focal detachment of epithelial cells from the underlying basement membrane. The results suggest that chronic nephrosis induced by PAN showed functional and morphologic features similar to those of human FSGS. Cytotoxic effect of PAN on the glomerular epithelial cells may be an initiating factor for the development of FSGS. which may be aggravated by some hemodynamic changes induced by uninephrectomy.

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