Biomedical subjects

Jin Kim

Publications and source records attributed to Jin Kim.

At least 37 records · Page 2Linked to original sources

PubMed2006

Increased expression of renal aquaporin water channels in spontaneously hypertensive rats.

AIMS: The present study was aimed to determine whether there exists an altered regulation of aquaporin (AQP) water channels in hypertension. METHODS: Male spontaneously hypertensive rats (SHR) aged 10-12 weeks were used. Age-matched Wistar-Kyoto (WKY) rats served as control. The abundance of AQP1-4 proteins in the kidney was determined by Western blot analysis. The protein expression and activity of adenylyl cyclase were also determined. RESULTS: The medullary expression of AQP2 and AQP3 proteins was increased in SHR compared with that in WKY rats. The expression of AQP1 protein was also significantly increased in the inner medulla, while that of AQP4 was not. Immunohistochemistry of AQP2 revealed that principal cells of the collecting duct have strong immunoreactivity, the degree of which was augmented with prominent apical labeling in SHR. The plasma level of arginine vasopressin (AVP) was higher in SHR; the adenylyl cyclase activity stimulated by AVP was augmented, along with increased expression of type VI adenylyl cyclase. The urine was more concentrated with its volume decreased in SHR. CONCLUSION: The expression of AQP1-3 channels is increased in the kidney, in association with enhanced activity of the AVP/cAMP pathway, in SHR.

Adenylyl Cyclases↗

PubMed2006

An unusual odontogenic cyst with diverse histologic features.

An unusual odontogenic cyst, which was originally believed to be a clinical dentigerous cyst associated with an impacted mandibular third molar, was found histologically to demonstrate the characteristics of a glandular odontogenic cyst with para- and orthokeratinization. These histologic diversities were interpreted as a reflection of the pluripotentiality of the epithelial remnants of the mandibular third molars or dentigerous cyst epithelium. It is possible that it has the capacity to induce the formation of cysts in both squamous and glandular epithelium.

Aged↗

PubMed2006

Surgical outcomes for gastric cancer in the upper third of the stomach.

INTRODUCTION: The proportion of gastric cancers affecting the upper third of the stomach has been increasing. At our surgical service we perform total and proximal gastrectomy for this condition. The purpose of this study was to investigate the surgical outcome of the two operative procedures and determine an optimal surgical approach. METHODS: Data from 147 patients who underwent resection for gastric cancer affecting the proximal one-third of the stomach were retrospectively analyzed. The patients were classified into a total gastrectomy (TG) group or a proximal gastrectomy (PG) group, and the clinicopathologic characteristics and surgical results were compared. We analyzed survival rates using Kaplan-Meier methods and made comparisons using a log-rank test across the same stage of the gastric cancer. RESULTS: From 1992 to 2000, a total of 104 total gastrectomies and 43 proximal gastrectomies for gastric cancer affecting the upper one-third of the stomach were performed. Our investigation revealed significantly different clinicopathologic characteristics in Borrmann type, length of the resection margin, degree of lymph node dissection, and lymph node stage. During the procedure, a combined resection of other organs was performed in 30 TG and 27 PG patients. Postoperative complications developed in 15 TG and 22 PG patients. The cancer recurrence rate was 4.8% for the TG group and 39.5% for the PG group; it was highest when the length of the proximal resection margin was < 1 cm. When we compared 5-year survival rates between the two groups, each at the same cancer stage, a significant difference was noted for stage III and IV gastric cancers. CONCLUSIONS: Proximal gastrectomy may be performed during the early stage of proximal gastric cancer; but because of the high frequency of complications and cancer recurrence, an additional procedure should be expected afterward. When the cancer stage is advanced, total gastrectomy should be performed with sufficient length of the proximal resection margin.

Cardia↗

PubMed2006

Inflammatory myofibroblastic tumor of the kidney in a child: report of a case.

Inflammatory myofibroblastic tumor (IMT), also known as inflammatory pseudotumor, is an uncommon benign tumor that has been reported in various locations throughout the body, but rarely in the kidney. To our knowledge, only 22 cases of renal IMT have been described in the literature. Renal IMT in children is difficult to differentiate from a malignancy such as Wilms' tumor. We report a case of a 9-year old girl with a left renal mass mimicking malignancy on preoperative diagnostic images, which was pathologically revealed to be an IMT. We review the literature and discuss the pathophysiology and clinical features of this unusual tumor.

Child↗

PubMed2006

Molecular and biochemical characterization of hemoglobinase, a cysteine proteinase, in Paragonimus westermani.

The mammalian trematode Paragonimus westermani is a typical digenetic parasite, which can cause paragonimiasis in humans. Host tissues and blood cells are important sources of nutrients for development, growth and reproduction of P. westermani. In this study, a cDNA clone encoding a 47 kDa hemoglobinase of P. westermani was characterized by sequencing analysis, and its localization was investigated immunohistochemically. The phylogenetic tree prepared based on the hemoglobinase gene showed high homology with hemoglobinases of Fasciola hepatica and Schistosoma spp. Moreover, recombinant P. westermani hemoglobinase degradaded human hemoglobin at acidic pH (from 3.0 to 5.5) and its activity was almost completely inhibited by E-64, a cysteine proteinase inhibitor. Immunohistochemical studies showed that P. westermani hemoglobinase was localized in the epithelium of the adult worm intestine implying that the protein has a specific function. These observations suggest that hemoglobinase may act as a digestive enzyme for acquisition of nutrients from host hemoglobin. Further investigations may provide insights into hemoglobin catabolism in P. westermani.

Amino Acid Sequence↗

PubMed2005

Inhibitory effect of pravastatin on transforming growth factor beta1-inducible gene h3 expression in a rat model of chronic cyclosporine nephropathy.

BACKGROUND/AIMS: Overexpression of transforming growth factor beta1-inducible gene h3 (betaig-h3) is associated with renal scarring in several models of renal disease. We investigated the inhibitory effect of pravastatin on betaig-h3 expression in a rat model of chronic cyclosporin A (CsA)-induced nephropathy. METHODS: Adult Sprague Dawley rats kept on a low salt diet (0.05% sodium) were treated daily for 4 weeks with vehicle (olive oil, 1 ml/kg), CsA (15 mg/kg) or both CsA and pravastatin (20 mg/kg in drinking water). The effect of pravastatin on betaig-h3 expression was evaluated using in situ hybridization, immunohistochemistry, and immunoblotting. Functional parameters, histopathology (tubulointerstitial fibrosis, TIF, and arteriolopathy), and levels of transforming growth factor beta1 (TGF-beta1) and endothelial nitric oxide synthase were compared for the different treatment groups. RESULTS: Co-administration of pravastatin significantly inhibited betaig-h3 mRNA production and gene expression within the tubulointerstitium of the CsA-treated kidneys, and this paralleled an attenuation of TIF (12.7 +/- 2.2 vs. 35.9 +/- 5.4%, p < 0.01 vs. CsA) and the expression of TGF-beta1 mRNA (279 +/- 40 vs. 719 +/- 85%, p < 0.01 vs. CsA). Pravastatin treatment reduced endothelial nitric oxide synthase protein levels and reversed the renal dysfunction caused by CsA. Neither CsA nor pravastatin affected total serum cholesterol or triglyceride levels in the treatment groups. CONCLUSION: Pravastatin thus effectively abrogated the upregulation of betaig-h3 gene expression and associated TGF-beta1 production, and this was associated with attenuated TIF in this model of chronic CsA-induced nephropathy.

Animals↗

PubMed2005

Cryopreservation of human teeth for future organization of a tooth bank--a preliminary study.

This study was aimed at evaluating whether cryopreserved teeth can be used for future transplantation by examining the viability and differentiation capability of periodontal ligament (PDL) cells and measuring the hardness of dental hard tissue. Fifty-four teeth were divided into two groups, control and frozen teeth. A MTT assay and a TUNEL assay were performed for the examination of the viability and apoptotic death of PDL cells. Immunohistochemical staining for alkaline phosphatase was performed to observe whether the differentiation capability of PDL cells was maintained by the freezing and thawing procedure. Hardness was measured to detect whether dental hard tissue was affected by the freezing conditions. The MTT and TUNEL assays showed no significant difference in the viability of PDL cells between the two groups. The differentiation capability of PDL cells was maintained in frozen teeth as evidenced by alkaline phosphatase staining. The hardness of frozen teeth was not changed, but a longitudinal fracture was found in 25% of the frozen group. The viability and differentiation capability of PDL cells were maintained in a frozen environment; however, it is thought that a new cryopreservation method preventing fracture of dental hard tissue should be developed for clinical application.

Alkaline Phosphatase↗

PubMed2005

Effect of FTY720 on chronic cyclosporine nephropathy in rats.

BACKGROUND: Long-term treatment with cyclosporine A (CsA) causes tubulointerstitial inflammation and fibrosis in the kidney. To define the role of lymphocytes in this process, the novel lymphocyte-specific inhibitor FTY720 was administered to rats with experimental model of chronic CsA nephropathy. METHODS: Sprague-Dawley rats were treated daily for 4 weeks with CsA (7.5 mg/kg), or both CsA and FTY720 (0.125 mg/kg). The effects of FTY720 on CsA-induced renal injury were evaluated using renal function tests and histopathology, and the expression of mediators of CsA-induced renal injury (osteopontin, transforming growth factor-beta1 [TGF-beta1], betaig-h3, and angiotensin II). RESULTS: FTY720 treatment significantly decreased T-lymphocyte accumulation in kidneys compared with CsA treatment alone. FTY720 treatment improved not only CsA-induced renal dysfunction but also renal histopathology, demonstrated by decreased macrophage infiltration and interstitial fibrosis. Increased osteopontin, TGF-beta1, betaig-h3, and angiotensin II expression in CsA-treated rat kidneys were decreased with FTY720 treatment. CONCLUSIONS: FTY720 treatment prevents CsA-induced renal injury.

Angiotensin II↗

PubMed2005

Characterization of newly established oral cancer cell lines derived from six squamous cell carcinoma and two mucoepidermoid carcinoma cells.

Since genetic abnormalities of human cancer are greatly geographically dependent, cultural and environmental backgrounds are thought to be closely related to the carcinogenic process. In the present study, eight human cell lines were established by culture from untreated carcinomas of the oral cancer, of which five were from primary oral squamous cell carcinomas (OSC), one from a mucoepidermoid carcinoma (MEC) and one each originating from metastatic OSC and MEC. All the studied tumor lines grew as monolayers, and showed: i) an epithelial origin by the presence of cytokeratin, and ii) tumorigenic potential in nude mice. Western blot analysis revealed i) over expression of EGFR in six of the cell lines ii) decreased expression of E-cadherin in six cell lines compared to normal human oral mucosa. A mutational analysis showed: point mutations of p53 at exon 7, with transversion, and at exon 8, with transition. These well-characterized human YD cell lines should serve as useful tools in the study of the molecular pathogenesis and biological characteristics of head and neck cancer cells, and in the future testing of new therapeutic reagents for oral cancer.

Adult↗

PubMed2005

Increased apical targeting of renal ENaC subunits and decreased expression of 11betaHSD2 in HgCl2-induced nephrotic syndrome in rats.

Nephrotic syndrome is often accompanied by sodium retention and generalized edema. We hypothesize that dysregulation of the epithelial sodium channel (ENaC) and/or of sodium (co)transporters may be responsible for the increased sodium retention associated with HgCl(2)-induced nephropathy. In addition, we examined the hypothesis that the expression of type 2 11beta-hydroxysteroid dehydrogenase (11betaHSD2) is reduced, contributing to the enhanced mineralocorticoid activity. Membranous nephropathy was induced in Brown Norway rats by repeated injections of HgCl(2) (1 mg/kg sc), whereas the control group received only vehicle. After 13 days of treatment, the abundance of ENaC subunits, sodium (co)transporters, and 11betaHSD2 in the kidney was examined by immunoblotting and immunohistochemistry. HgCl(2) treatment induced marked proteinuria, hypoalbuminemia, decreased urinary sodium excretion, and ascites. The protein abundance of alpha-ENaC was increased in the cortex/outer stripe of outer medulla (OSOM) and inner stripe of the outer medulla (ISOM). The protein abundances of beta-ENaC and gamma-ENaC were decreased in the cortex/OSOM while increased in the ISOM. Immunoperoxidase microscopy demonstrated increased targeting of ENaC subunits to the apical plasma membrane in the distal convoluted tubule, connecting tubule, and cortical and medullary collecting duct segments. Moreover, 11betaHSD2 abundance was decreased in cortex/OSOM and ISOM. The protein abundances of type 3 Na/H exchanger (NHE3), Na-K-2Cl cotransporter (NKCC2), and thiazide-sensitive Na-Cl cotransporter (NCC) were decreased. Moreover, the abundance of the alpha-1 subunit of the Na-K-ATPase was decreased in the cortex/OSOM and ISOM but remained unchanged in the inner medulla. These results suggest that increased apical targeting of ENaC subunits combined with diminished abundance of 11betaHSD2 may contribute to sodium retention associated with HgCl(2)-induced nephrotic syndrome. The decreased abundance of NHE3, NKCC2, NCC, and Na-K-ATPase may play a compensatory role in promoting sodium excretion.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗

PubMed2005

Ultrastructural localization of UT-A and UT-B in rat kidneys with different hydration status.

Urea transport in the kidney is mediated by a family of transporter proteins, including renal urea transporters (UT-A) and erythrocyte urea transporters (UT-B). We aimed to determine whether hydration status affects the subcellular distribution of urea transporters. Male Sprague-Dawley rats were divided into three groups: dehydrated rats (WD) given minimum water, hydrated rats (WL) given 3% sucrose in water for 3 days before death, and control rats given free access to water. We labeled kidney sections with antibodies against UT-A1 and UT-A2 (L194), UT-A3 (Q2), and UT-B using preembedding immunoperoxidase and immunogold methods. In control animals, UT-A1 and UT-A3 immunoreactivities were observed throughout the cytoplasm in inner medullary collecting duct (IMCD) cells, and weak labeling was observed on the basolateral plasma membrane. UT-A2 immunoreactivity in the descending thin limbs (DTL) was observed mainly on the apical and basolateral membranes of type I epithelium, and very faint labeling was observed in the long-loop DTL at the border between the outer and inner medulla. UT-A1 immunoreactivity intensity was markedly lower, and UT-A3 immunoreactivity was higher in IMCD of WD vs. controls. UT-A2 immunoreactivity intensities in the plasma membrane and cytoplasm of type I, II, and III epithelia of DTL were greater in WD vs. controls. In contrast, UT-A1 expression was greater and UT-A2 and UT-A3 expressions were lower in WL vs. controls. The subcellular distribution of UT-A in DTL or IMCD did not differ between control and experimental animals. UT-B was expressed in the plasma membrane of the descending vasa recta of both control and experimental animals. UT-B intensity was higher in WD and lower in WL vs. controls. These data indicate that changes in hydration status over 3 days affected urea transporter protein expression without changing its subcellular distribution.

Animals↗

PubMed2005

Cyclosporine-induced renal injury induces toll-like receptor and maturation of dendritic cells.

BACKGROUND: The toll-like receptor (TLR) is stimulated by not only pathogen-associated molecular patterns but also endogenous TLR ligands provided by injured cells. The influence of cyclosporine A (CsA)-induced renal injury on TLR expression and subsequent signaling pathway was evaluated. METHODS: Induction of chronic CsA nephropathy was made by administering CsA (15 mg/kg/day) for 28 days in rats. The TLR2 and TLR4 mRNA and protein expression, TLR-signaling pathway (MYD88, NF-kappaB and AP-1), putative TLR ligand (heat shock protein 70 [HSP70]), and maturation of dendritic cells were evaluated in CsA-treated rat kidneys. RESULTS: Long-term CsA treatment upregulated TLR2 and TLR4 mRNA and protein expression on renal tubular cells, and these were accompanied by increased MYD88, NF-kappaB and AP-1 expression. Putative TLR ligand (HSP70) was also significantly increased in CsA-treated rat kidney compared with vehicle-treated rat kidney. CsA-treatment increased expression of TNF-alpha mRNA, the number of dendritic cells, and expression of MHC class II antigen. Double-labeling of markers of dendritic cells and MHC class II antigen revealed that matured dendritic cells increased in CsA-treated rat kidney. CONCLUSIONS: CsA-induced renal injury stimulates components of innate immunity, and this finding suggests close association between CsA-induced renal injury and activation of innate immunity.

Animals↗

PubMed2005

Long-term and sustained COMP-Ang1 induces long-lasting vascular enlargement and enhanced blood flow.

Vascular enlargement is a characteristic feature of angiopoietin-1 (Ang1)-induced changes in adult blood vessels. However, it is unknown whether tissues having Ang1-mediated vascular enlargement have more blood flow or whether the enlargement is reversible. We have recently created a soluble, stable and potent Ang1 variant, COMP-Ang1. In the present study, we investigated the effects of varied dose and duration of COMP-Ang1 on vascular enlargement and blood flow in the tracheal microvasculature of adult mice and explored a possible mechanism of long-lasting vascular enlargement. We found that COMP-Ang1 administered by adenoviral vector induced long-lasting vascular enlargement and increased tracheal blood flow. In contrast, short-term administration of COMP-Ang1 recombinant protein induced transient vascular enlargement that spontaneously reversed within a month. In both cases, the vascular enlargement resulted from endothelial proliferation. The COMP-Ang1-induced vascular remodeling is mediated mainly through Tie2 activation. Sustained overexpression of Tie2 could participate in the maintenance of vascular changes. Together, our findings indicate that sustained treatment with COMP-Ang1 can produce long-lasting vascular enlargement and increased blood flow.

Adenoviridae↗

PubMed2005

Combined effects of losartan and pravastatin on interstitial inflammation and fibrosis in chronic cyclosporine-induced nephropathy.

BACKGROUND: Statins and angiotensin II type I receptor blockers have synergistic effects on vascular smooth-muscle-cell proliferation and the progression of renal diseases. We evaluated whether combined treatment with losartan (LSRT) and pravastatin (PRVT) affords superior protection compared with their respective monotherapies in treating chronic cyclosporine (CsA)-induced nephropathy in rats. METHODS: Rats maintained on a low salt diet were given vehicle, CsA (15 mg/kg), CsA and LSRT (10 mg/kg), CsA and PRVT (5 mg/kg), or a combination of CsA, LSRT, and PRVT for 28 days. Basic parameters (renal function, systolic blood pressure, serum high-sensitivity C-reactive protein [hs-CRP], and lipid profiles), histopathology (arteriolopathy, tubulointerstitial fibrosis, and inflammatory cell infiltration), and inflammatory and fibrotic factors (intrarenal CRP, angiotensin II, osteopontin, and transforming growth factor [TGF]-beta1) were studied. RESULTS: LSRT or PRVT treatment significantly attenuated the histopathologic changes induced by CsA, and combined treatment with LSRT and PRVT further decreased these parameters compared with giving each drug alone. Increased levels of angiotensin II, intrarenal CRP, osteopontin, and TGF-beta1 in CsA-treated rat kidney were reduced by treatment with either LSRT or PRVT and were further decreased by the combination of the two drugs. There were no significant differences in systolic blood pressure or serum lipid parameters between groups. CONCLUSIONS: Combined treatment with LSRT and PRVT provided synergistic effects in attenuating inflammatory and fibrotic processes in a rat model of chronic CsA-induced nephropathy, and this effect was independent of their hypolipidemic and hypotensive actions.

Animals↗

PubMed2005

Ischemia-reperfusion injury activates innate immunity in rat kidneys.

BACKGROUND: There is growing evidence of a role of the immune system in the pathophysiology of ischemia-reperfusion (I/R) injury, but the influence of I/R injury on innate immunity is still undetermined. METHODS: Sprague-Dawley rats were used. I/R injury was induced by clamping both renal arteries for 45 min, and the rats were killed 1, 3, 5, and 7 days later. Activation of innate immunity was evaluated in terms of the expression of toll-like receptor (TLR) 2 or TLR4 mRNAs and protein, by the level of the TLR ligand (heat shock protein [HSP] 70), and maturation of dendritic cells by double-label immunohistochemistry of dendritic cells for major histocompatibility complex (MHC) class II antigen. RESULTS: I/R injury increased TLR2 and TLR4 mRNA and protein expression, and they were mainly observed on renal tubular cells. I/R injury also produced endogenous TLR ligand (HSP70) on renal tubular cells. I/R injury increased not only the numbers of dendritic cells but also the production of MHC class II antigen in dendritic cells, suggesting maturation of these cells. Activation of innate immunity was observed at day 1, peaked at days 3 to 5 after I/R injury, and thereafter gradually decreased. CONCLUSIONS: I/R injury rapidly activates the innate immune response.

Animals↗

PubMed2005

Preconditioning with 1,25-dihydroxyvitamin D3 protects against subsequent ischemia-reperfusion injury in the rat kidney.

BACKGROUND/AIM: Induction of heat shock protein 70 (HSP70) is important in the tolerance of subsequent ischemia-reperfusion (I/R) injury. The aim of this study was to evaluate the effect of HSP70 induction by 1,25-dihydroxyvitamin D3 (VD3) on subsequent I/R injury in rats. METHODS: HSP70 was induced in Sprague-Dawley rats by VD3 treatment for 7 days, and the effect of VD3 pretreatment on subsequent I/R injury was evaluated in terms of renal function, tubular necrosis score, tumor necrosis factor alpha mRNA expression, mitogen-activated protein kinase expression, and proliferating cell nuclear antigen expression. RESULTS: VD3 treatment increased HSP70 expression which was localized to renal tubular cells in the outer medulla. Pretreatment with VD3 before I/R injury resulted in (1) decreased blood urea nitrogen and serum creatinine levels; (2) decreased tubular cell necrosis; (3) increased tubular cell proliferation as determined by proliferating cell nuclear antigen expression; (4) decreased tumor necrosis factor alpha mRNA expression, and (5) increased extracellular signal regulated protein kinase and decreased c-Jun N-terminal kinase expression. CONCLUSION: Our study demonstrates that VD3 is a nontoxic inducer of HSP70 and exerts a protective effect against subsequent I/R injury.

Animals↗

PubMed2005

Attenuation of interstitial inflammation and fibrosis by recombinant human erythropoietin in chronic cyclosporine nephropathy.

BACKGROUND: Evidence suggests that recombinant human erythropoietin (rHuEPO) protects neurons and cardiomyocytes from acute insults. We investigated the protective effect of rHuEPO on cyclosporine (CsA)-induced renal injury. METHODS: CsA (15 mg/kg/day) was given to rats for 1 or 4 weeks, and rHuEPO was concurrently administered at a dose of 100 units/kg (thrice weekly). Effects of rHuEPO on CsA-induced renal injury were evaluated with tubulointerstitial fibrosis (TIF) score, macrophage infiltration, expression of proinflammatory and profibrotic cytokines, and apoptotic cell death. RESULTS: Administration of rHuEPO decreased TIF score and the number of macrophages, which increased significantly in CsA-treated rat kidneys. At the molecular level, rHuEPO treatment decreased proinflammatory mediators (osteopontin and C-reactive protein) and profibrotic mediators (transforming growth factor-beta1 and transforming growth factor-beta1-inducible gene-h3). Increased apoptotic cell death in CsA-treated rat kidneys was significantly decreased with rHuEPO cotreatment, and apoptosis-related genes were regulated in favor of cell survival (increased Bcl-2 and suppressed caspase-3). CONCLUSION: rHuEPO has a renoprotective effect against chronic CsA-induced renal injury.

Animals↗

PubMed2005

The effect of human serum albumin on the extended storage of human oral keratinocyte viability under mild hypothermia.

Isolated oral keratinocytes in suspension provide a number of advantages for use in maxillofacial surgery, however, the poor stability of this cell preparation at physiological temperatures is an apparent barrier preventing their use. The purpose of the present study was to evaluate whether human serum albumin (HSA) could serve as an effective constituent of a storage medium to enhance human oral keratinocyte (HOK) viability under conditions of mild hypothermia. Primary human oral keratinocytes were isolated from small pieces of the non-inflamed gingival tissues obtained during the extraction of the third molars of patients. HOK were cultured on collagen type I-coated culture dishes in keratinocyte growth medium (KGM). After the trypsinization of a culture dish (passage 2 or 3), freshly isolated HOK were stored for 24, 48, and 72 h at 4 degrees C or at room temperature in KGM, saline, Dulbecco's modified Eagle's medium (DMEM), saline supplemented with 10% HSA or DMEM supplemented with 10% (v/v) HSA under one atmosphere pressure. After storage, HOK cell survival was determined by dye exclusion using trypan blue and colony-forming assay and cell cycle change was obtained by flow cytometry. Highest cell viability was obtained in saline supplemented with 10% HSA and DMEM supplemented with 10% (v/v) HSA at 4 degrees C and at room temperature. Under these conditions no significant decline in keratinocyte viability was observed for at least 48 h. The cell cycle profiles of these cells were also maintained for at least 48 h at room temperature. These observations demonstrate that HSA might be better at preserving the viability of HOK stored under hypothermic and mild hypothermic conditions up to 48 h.

Antioxidants↗