Effects of Tissue Temperature and Injury on ADC during Therapeutic Hypothermia in Newborn Hypoxic-Ischemic Encephalopathy.

BACKGROUND AND PURPOSE: ADC changes are useful in detecting ischemic brain injury, but mechanisms other than tissue pathology may affect the kinetic movement and diffusion of water molecules. We aimed to determine the effects of brain temperature on the corresponding ADC in infants undergoing therapeutic hypothermia. MATERIALS AND METHODS: Brain temperature and ADC values in the basal ganglia, thalamus, cortical GM, and WM were analyzed during and after therapeutic hypothermia. The study cohort was categorized as having no-injury or injury. Among infants without injury, the correlation between ADC values and temperature was analyzed using the Pearson correlation. Intrasubject comparison of ADC changes during and after therapeutic hypothermia were analyzed, excluding patients who had an MR image interval of >5 days to minimize the effects of injury evolution. RESULTS: Thirty-nine infants with hypoxic-ischemic encephalopathy were enrolled (23 no-injury; 16 injury). The median ADC was significantly lower during therapeutic hypothermia (837; interquartile range, 771-928, versus 906; interquartile range, 844-1032 ×10-6mm2/s; P < .001). There was no difference in the ADC between the no-injury and injury groups during therapeutic hypothermia (823; interquartile range, 782-868, versus 842; interquartile range, 770-1008 ×10-6mm2/s; P = .4). In the no-injury group, in which ADC is presumed least affected by the evolution of injury, the median ADC was significantly lower during therapeutic hypothermia (826; interquartile range, 771-866, versus 897; interquartile range, 846-936 ×10-6mm2/s; P < .001). There was a moderate correlation between temperature and ADC in the no-injury group (during therapeutic hypothermia: Spearman ρ, 0.48; P < .001; after therapeutic hypothermia: ρ, 0.4; P < .001). CONCLUSIONS: Aside from brain injury, reduced tissue temperature may also contribute to diffusion restriction on MR imaging in infants undergoing therapeutic hypothermia.

Upregulation of LINC00982 inhibits cell proliferation and promotes cell apoptosis by regulating the activity of PI3K/AKT signaling pathway in renal cancer.

OBJECTIVE: Previous studies have confirmed that lncRNAs are involved in the progression of multiple tumors. However, the role of lncRNAs in renal cancer remains unclear. Our study focused on investigating the expression and function of LINC00982 in renal cancer progression. PATIENTS AND METHODS: Quantitative Real time-polymerase chain reaction (qRT-PCR) assay was used to detect the expression of LINC00982 in renal cancer tissues and cell lines. LINC00982 expression was upregulated by transfecting with lentivirus. Western blot assay was used to detect the alteration expression levels of the relative protein involved PI3K/AKT signaling pathway. RESULTS: Downregulated LINC00982 expression was significantly observed in cancer samples when compared with the adjacent specimens, and was related to tumor size and TNM stage. Upregulation of LINC00982 inhibited proliferation and promoted apoptosis of ACHN and A-498 cell lines. LINC00982 could regulate the activity of PI3K/AKT signaling pathway. CONCLUSIONS: Upregulation of LINC00982 inhibits cell proliferation and promotes cell apoptosis by regulating the activity of PI3K/AKT signaling pathway in renal cancer.

[Determination of 8-methoxypsoralen in mouse plasma by high performance liquid chromatography and its application to pharmacokinetic study].

OBJECTIVE: To establish a high performance liquid chromatography (HPLC) method for the determination of 8-methoxypsoralen (8-MOP) in mouse plasma and apply it to a pharmacokinetic study of 8-MOP. METHODS: 8-MOP was separated on a Waters Symmetry18 column (250 mm × 4.6 mm, 5 µm) and determined by HPLC using isocratic elution, and 5-methoxypsoralen was used as internal standard. The mobile phase consisted of methanol-water (55:45, V/V) at a flow rate of 1.0 mL/min. The excitation and emission wavelength of fluorescence detector were set at 334 nm and 484 nm respectively, and the internal standard method was used for quantitative analysis. In the study, 60 healthy ICR male mice were randomly divided into twelve groups. The mice in control group were administered intragastrically with 1% Tween 80, and the mice in the other eleven groups were administered intragastrically with 8-MOP (40 mg/kg). Plasma concentrations of 8-MOP in the mice at different time points after treatment were determined by HPLC. Pharmacokinetic parameters were calculated by DAS 2.0 software. RESULTS: The calibration curve of 8-MOP was linear with a correlation coefficient of 0.999 3 over the concentration range of 0.05 to 10 mg/L, and the limit of detection was 0.015 mg/L. The average recoveries of 8? MOP at three different concentrations (0.10, 0.50, 2.5 mg/L) were from 92.5% to 100.6%. The intra-day precision of 8-MOP was from 3.3% to 8.2%, while the inter-day precision was from 3.4% to 6.7% at three spiked concentration levels. The extraction recoveries of 8-MOP were from 90.9% to 92.0%, and the plasma samples could be stored at -80°C for 15 days at least at three spiked concentration levels. 8-MOP could be detected in mouse plasma 5 min after intragastrical administration to the mice (1.4 mg/L). The concentration of 8-MOP in the mouse plasma reached a maximum 2 h after administration, and 8-MOP could still be detected 24 h after administration (1.1 mg/L). t1/2 was (39.21±3.65) h, Cmax was (2.31±0.02) mg/L, tmax was (2.00±0.00) h, and AUC0-t was (33.34±1.19) (h×mg)/L. CONCLUSION: The proposed method is accurate and simple,suitable for pharmacokinetics of 8-MOP in mice.

Hemodynamic reference for neonates of different age and weight: a pilot study with electrical cardiometry.

OBJECTIVE: Electrical cardiometry (EC) is an impedance-based monitor that provides noninvasive, real-time hemodynamic assessment. However, the reference values for neonates have not been established. STUDY DESIGN: EC (Aesculon) was applied to hemodynamically stable preterm and term infants. Hemodynamic variables included cardiac output (CO), cardiac index (CI), stroke volume (SV) and heart rate (HR). Their gestational age (GA), weight and body surface area (BSA) were recorded. RESULTS: A total of 280 neonates were studied. Their GA ranged from 26(5/7) to 41(4/7) weeks, weight 800 to 4420 g and BSA 0.07 to 0.26 m(2). CO was positively correlated to GA, weight and BSA (r=0.681, 0.822, 0.830, respectively; all P<0.001). Using regression analysis, CO was most significantly correlated to BSA. Mean CI was 2.55±0.37 l min(-1) per m(2). CONCLUSION: Hemodynamic reference by EC is notably distinct among neonates of diverse maturity. CO is most closely correlated to BSA.

Comparison of the Therapeutic Effects and Side Effects of Oral Iron Supplements in Iron Deficiency Anemia.

OBJECTIVE: Iron deficiency anemia is an important public health issue, especially for infants, children, and women with menorrhagia. Oral iron supplements are the cheapest, safest, and most effective treatment. This study compared the therapeutic and side effects of ferrous and ferric in iron deficiency anemia. METHODS: This was a retrospective study on data collected between April 2012 and October 2013 for patients with iron deficiency anemia who continuously took oral ferric for over one month and then switched to oral ferrous due to poor therapeutic effects. The exclusion criteria were the use of other oral or injected iron preparations, erythropoietin, or vitamin B12. RESULTS: A total of 41 participants were recruited. The average participant age was 44.76±16.89 years; most participants were females (95.1%; 39/41); the average daily dose of oral ferric (139.02±49.39 mg) was higher than that of ferrous (96.34±23.43 mg). Repeated measures: mixed model analyses were conducted to examine patients' clinical blood test values. The results showed that the mean blood test values for all patients significantly increased after switching to ferrous (p<0.01, with the exception of mean corpuscular hemoglobin). One patient experienced gastrointestinal discomfort and diarrhea after switching to ferrous. CONCLUSION: This study found that blood test values improved after iron deficiency anemia female patients who displayed poor therapeutic effects with oral ferric switched to ferrous. Literature review showed that the risk for gastrointestinal problems with ferrous is higher than that with ferric. However, no significant difference was found in this study.

HLA-DPB1 and anti-HBs titer kinetics in hepatitis B booster recipients who completed primary hepatitis B vaccination during infancy.

Previously we reported significant associations of the human leukocyte antigen (HLA)-DPB1 05:01 with memory against hepatitis B (HB) vaccination. However, the effects of HLA-DPB1 on antibodies to hepatitis B surface antigen (anti-HBs) kinetics were not explored. We followed up a cohort of 1974 HB booster recipients and quantified their 1-month and 1-year post-booster anti-HBs titers. A total of 681 subjects were randomly selected and typed for HLA-DPB1. We found that male subjects, undetectable pre-booster titers, and 05:01 homozygotes led to significantly lower post-booster anti-HBs titers. The geometric means (95% confidence interval (CI)) of 1-month post-booster anti-HBs titers were 4.68 (2.69-8.12), 23.01 (14.96-35.40) and 50.06 (27.20-92.13) mIU ml(-1) for subjects carrying two, one and no HLA-DPB1 05:01 allele. The corresponding figures for 1-year post-booster anti-HBs titers were 1.26 (0.73-2.18), 4.72 (3.08-7.25) and 7.32 (3.75-13.56) mIU ml(-1). There were significant associations of post-booster anti-HBs titers with the number of HLA-DPB1 risk and protective alleles. Among booster responders, anti-HBs decay rates were significantly reduced in subjects who had detectable pre-booster anti-HBs titers and the HLA-DPB1 05:01 allele. Our results indicated that HLA-DPB1 influences the kinetics of anti-HBs. The long-term memory against hepatitis B surface antigen (HBsAg) and the residual serum titers of anti-HBs after HB vaccination may be influenced by different mechanisms as evidenced by their inverse trend of associations with the 05:01 allele.

Generation of pseudonondiffracting optical beams with superlattice structures.

We demonstrate an approach to generate a class of pseudonondiffracting optical beams with the transverse shapes related to the superlattice structures. For constructing the superlattice waves, we consider a coherent superposition of two identical lattice waves with a specific relative angle in the azimuthal direction. We theoretically derive the general conditions of the relative angles for superlattice waves. In the experiment, a mask with multiple apertures which fulfill the conditions for superlattice structures is utilized to generate the pseudonondiffracting superlattice beams. With the analytical wave functions and experimental patterns, the pseudonondiffracting optical beams with a variety of structures can be generated systematically.

The combinatorial effect of different Equex STM paste concentrations, cryoprotectants and the straw-freezing methods on the post-thaw boar semen quality.

This study was to evaluate the combinatorial effect (14 treatments, A-N) of different Equex STM paste concentrations, cryoprotectants and the straw-freezing method on the post-thaw boar semen quality. Two ejaculates were collected from each of nine boars (three boars from each of three breeds). Semen was diluted in extenders with different concentrations of Equex STM paste and different cryoprotectants [glycerol or dimethylacetamide (DMA)] before cryopreserving via liquid nitrogen or dry ice. Motility, viability, percentage of spermatozoa with intense acrosomal staining and with normal morphology of post-thaw sperm were evaluated. The qualities of thawed semen were best preserved in treatment H (extender with 0.5% Equex STM paste and 5% glycerol and freezing by dry ice) and were worst in treatment B (extender with 0% Equex STM paste and 5% DMA and freezing by dry ice). Significant difference (p < 0.05) was present in post-thawed sperm motility (63% vs 27%), sperm viability (70% vs 33%) and sperm acrosomal integrity rate (68% vs 29%) between treatments H and B. However, sperm proportion with normal morphology showed no significant difference among treatments (66% vs 66%; p > 0.05). Moreover, statistical analysis suggests that no significant difference was present in semen quality among breed or individual donors (p > 0.05). These findings suggest that Equex STM paste improved the cryosurvival efficiency of boar sperm, and the favourable straw-freezing method changes between glycerol and DMA.

Defect solitons in two-dimensional optical lattices.

We report on the existence and stability of solitons in a defect embedded in a square optical lattice based on a photorefractive crystal with focusing saturable nonlinearity. These solitons exist in different bandgaps due to the change of defect intensity. For a positive defect, the solitons only exist in the semi-infinite gap and can be stable in the low power region but not the high power region. For a negative defect, the solitons can exist not only in the semi-infinite gap, but also in the first gap. With increasing the defect depth, these solitons are stable within a moderate power region in the first gap while unstable in the entire semi-infinite gap.

Netrin-1 attenuates ischemic stroke-induced apoptosis.

In the present study we tested the protective effects of netrin-1 in stroke and investigated the potential underlying mechanisms. When we performed middle cerebral artery occlusion (MCAO) on adult mice, up-regulation of the receptor uncoordinated gene 5H2 (UNC5H2) but not its ligand netrin-1 was detected with RT-PCR and immunohistochemistry. Injection of netrin-1, 1 day after MCAO, significantly reduced infarct volume at 3 days after MCAO as revealed by functional magnetic resonance imaging. The ischemic cortex was preserved when netrin-1 was continuously administered. Fluoro-Jade and terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling staining showed that netrin-1 reduced the number of dying neurons and apoptotic cells after MCAO. Ischemia-induced p53 expression was attenuated by netrin-1. We also tested the ability of netrin-1 to attract intrinsic neuronal stem cells to the infarct area. Both DCC and UNC5H2 were expressed in neurosphere culture and netrin-1 attracted stem cells in an in vitro transwell assay. However, in vivo netrin-1 administration did not enhance the MCAO-induced stem cell migration toward the infarct area. Our study shows that UNC5H2 expression was elevated after MCAO and administration of netrin-1 protected infarct tissue from p53-mediated apoptosis. These data indicate that the p53/dependent receptor pathway is involved in ischemic stroke pathology and suggest possible new stroke therapies.

17Beta-estradiol induced Ca2+ influx via L-type calcium channels activates the Src/ERK/cyclic-AMP response element binding protein signal pathway and BCL-2 expression in rat hippocampal neurons: a potential initiation mechanism for estrogen-induced neuroprotection.

Our group and others have demonstrated that 17beta-estradiol (E2) induces neurotrophic and neuroprotective responses in hippocampal and cortical neurons which are dependent upon the Src/extracellular signal-regulated kinase (ERK) signaling pathways. The purpose of this study was to determine the upstream mechanism(s) that initiates the signaling cascade leading to E2-inducible neuroprotection. We tested the hypothesis that E2 activates rapid Ca(2+) influx in hippocampal neurons, which would lead to activation of the Src/ERK signaling cascade and up-regulation of Bcl-2 protein expression. Using fura-2 ratiometric Ca(2+) imaging, we demonstrated that E2 induced a rapid rise of intracellular Ca(2+) concentration ([Ca(2+)](i)) within minutes of exposure which was blocked by an L-type Ca(2+) channel antagonist. Inhibition of L-type Ca(2+) channels resulted in a loss of E2 activation of the Src/ERK cascade, activation of cyclic-AMP response element binding protein (CREB) and subsequent increase in Bcl-2. Real-time intracellular Ca(2+) imaging combined with pERK immunofluorescence, demonstrated that E2 induced [Ca(2+)](i) was coincident with ERK activation in the same neuron. Small interfering RNA knockdown of CREB resulted in a loss of E2 activation of CREB and subsequent E2-induced increase of Bcl-2 expression. We further demonstrated the presence of specific membrane E2 binding sites in hippocampal neurons. Together, these data indicate that E2-induced Ca(2+) influx via the L-type Ca(2+) channel is required for E2 activation of the Src/ERK/CREB/Bcl-2 signaling. Implications of these data for understanding estrogen action in brain and use of estrogen therapy for prevention of neurodegenerative disease are discussed.

A direct mixed-body boundary element method for packed silencers.

Bulk-reacting sound absorbing materials are often used in packed silencers to reduce broadband noise. A bulk-reacting material is characterized by a complex mean density and a complex speed of sound. These two material properties can be measured by the two-cavity method or calculated by empirical formulas. Modeling the entire silencer domain with a bulk-reacting lining will involve two different acoustic media, air and the bulk-reacting material. Traditionally, the interior silencer domain is divided into different zones and a multi-domain boundary element method (BEM) may be applied to solve the problem. However, defining different zones and matching the elements along each interface is tedious, especially when the zones are intricately connected. In this paper, a direct mixed-body boundary element method is used to model a packed silencer without subdividing it into different zones. This is achieved by summing up all the integral equations in different zones and then adding the hypersingular integral equations at interfaces. Several test cases, including a packed expansion chamber with and without an absorbing center bullet, and a parallel baffle silencer, are studied. Numerical results for the prediction of transmission loss (TL) are compared to experimental data.

MCI-186: further histochemical and biochemical evidence of neuroprotection.

The bioactivity of 3-methyl-1-phenyl-pyrazolin-5-one (MCI-186) was examined based on histochemical changes in drastic global ischemic rat brains. Rats with mean arterial blood pressure reduction were subjected to 60 min cerebral ischemia/80 min reperfusion. Infusion of MCI-186 at 3.0 mg/Kg reduced brain infarction from 21 +/- 4% (saline control, n= 15) to 11 +/- 3% (n=16, p<0.05). By comparison, infusion of up to 20 mg/Kg propyl galalate (PG)--a well documented antioxidant--produced an infarct percentage of 14 +/- 5% (n=8), close to the saline control. Biochemically, the neuroprotective effect of MCI-186 was demonstrated by diminishing the release of creatine kinase (CK) in serum from 3363 +/- 608 U/L (n=14) in saline control to 1989 +/- 293 U/L (n= 15) in MCI group (p<0.05), while PG did not lower the activity of CK significantly. MCI-186 behaves as a free radical scavenger by suppressing the formation of superoxide anion in xanthine oxidase (XO)-hypoxanthine (HP) system (p<0.05). Our data supported our contention that MCI-186 has potent anti-stroke effect with antioxidant activities.

Morin hydrate: a potential antioxidant in minimizing the free-radicals-mediated damage to cardiovascular cells by anti-tumor drugs.

The co-incubation of morin hydrate with either doxorubicin or mitomycin C could minimize the toxicity of these anti-tumor drugs on cardiovascular cells, such as red blood cells, human umbilical vein endothelial cells (ECV304) and primary mouse cardiomyocytes, whereas morin hydrate did not lower the cytotoxicity of the drugs on human hepatocellular carcinoma cells (HepG2). Morin hydrate may not exert its antioxidant effect by enhancing the antioxidant enzymatic activity because it did not cause any induction on the mRNA levels of manganese superoxide dismutase expression in ECV304 cells and HepG2 cells.

Targeting of aminopeptidase N to bile canaliculi correlates with secretory activities of the developing canalicular domain.

We have used human hepatoma cell lines as an in vitro model to study the development of hepatic bile canaliculi (BC). Well-differentiated hepatoma cells cultured for 72 hours could develop characteristic spheroid structures at sites of cell-cell contact that contained tight junctions and various membrane protein markers, resembling BC found in vivo. Intact cytoskeleton was essential for this differentiation process. In the coculture experiments in which cells of different origins were populated together, BC only formed between hepatic cells and preferentially among well-differentiated cells. Poorly differentiated hepatoma cells never formed BC among themselves, but could be induced to undergo canalicular differentiation by interacting with well-differentiated cells. During BC morphogenesis, integral canalicular membrane proteins were gradually delivered and accumulated at the developing BC. Among them, targeting of aminopeptidase N (APN) seemed to correlate with activation of certain secretory functions. Specifically, only APN-positive BC supported excretion of fluorescein diacetate (FDA) and 70-kd dextran, but had no relationship with secretion of horseradish peroxidase (HRP). Targeting of another BC protein, dipeptidyl peptidase IV (DPPIV), on the other hand, bore no association with any secretory activity examined. In addition, inhibition of enzymatic activity of APN could perturb canalicular differentiation without affecting cell proliferation. Our results suggest that targeting of APN proteins may reflect or even play an important role in the development and functional maturation of the canalicular structures.

Aortic endothelial cells damaged by a nitric oxide donor and protected by flavonoids.

Cultured porcine aortic endothelial cells (PAEC) were exposed to four concentrations (0.00 mM - 5.00 mM) of 3-Morpholino-sydnonimine-hydrochloride (SIN-1, a nitric oxide donor). SIN-1 demonstrated a dose dependent cytotoxicity against PAEC as indicated by the thiobarbituric acid (TBA) assay. Morphologically and biochemically, the presence of selected flavonoids (morin, quercetin, or catechin) was shown to protect the PAEC from SIN-1 toxicity. Protection levels determined from the TBA assay were significant (p<0.05) for all flavonoids, with morin at 72+/-8%. Quercetin and catechin had comparable protective activities of 54+/-6% and 43+/-3%, respectively. This study supports the contention that SIN-1 is cytotoxic to PAEC and that antioxidants such as flavonoids may attenuate such toxicity.

CpABC, a Cryptosporidium parvum ATP-binding cassette protein at the host-parasite boundary in intracellular stages.

The intracellular parasite Cryptosporidium parvum develops inside a vacuole at the apex of its epithelial host cell. The developing parasite is separated from the host cell cytoplasm by a zone of attachment that consists of an extensively folded membranous structure known as the feeder organelle. It has been proposed that the feeder organelle is the site of regulation of transport of nutrients and drugs into the parasite. In this report, we localize an approximately 200-kDa integral membrane protein, CpABC, from Cryptosporidium parvum to the host-parasite boundary, possibly the feeder organelle. The predicted amino acid sequence of CpABC has significant structural similarity with the cystic fibrosis conductance regulator and the multidrug resistance protein subfamily of ATP-binding cassette proteins. This is an example of a parasite-encoded transport protein localized at the parasite-host interface of an intracellular protozoan.

Cyclosporin analogs inhibit in vitro growth of Cryptosporidium parvum.

Cyclosporine and nonimmunosuppressive cyclosporin (CS) analogs were demonstrated to be potent inhibitors of the growth of the intracellular parasite Cryptosporidium parvum in short-term (48-h) in vitro cultures. Fifty-percent inhibitory concentrations (IC50s) were 0.4 microM for SDZ 033-243, 1.0 microM for SDZ PSC-833, and 1.5 microM for cyclosporine. Two other analogs were less effective than cyclosporine: the IC50 of SDZ 205-549 was 5 microM, and that of SDZ 209-313 was 7 microM. These were much lower than the IC50 of 85 microM of paromomycin, a standard positive control for in vitro drug assays for this parasite. In addition, intracellular growth of excysted sporozoites that had been incubated for 1 h in cyclosporine was significantly reduced, suggesting that the drug can inhibit sporozoite invasion. The cellular activities of the CS analogs used have been characterized for mammalian cells and protozoa. The two analogs that were most active in inhibiting C. parvum, SDZ PSC-833 and SDZ 033-243, bind weakly to cyclophilin, a peptidyl proline isomerase which is the primary target of cyclosporine and CS analogs. However, they are potent modifiers of the activity of the P glycoproteins/ multidrug resistance (MDR) transporters, members of the ATP-binding cassette (ABC) superfamily. Hence, both cyclophilin and some ABC transporters may be targets for this class of drugs, although drugs that preferentially interact with the latter are more potent. Cyclosporine (0.5 microM) had no significant chemosensitizing activity. That is, it did not significantly increase sensitivity to paromomycin, suggesting that an ABC transporter is not critical in the efflux of this drug. Cyclosporine at concentrations up to 50 microM was not toxic to host Caco-2 cells in the CellTiter 96 assay. The results of this study complement those of studies of the inhibitory effect of cyclosporine and CS analogs on other apicomplexan parasites, Plasmodium falciparum, Plasmodium vivax, and Toxoplasma gondii.

Morin hydrate: a better protector than purpurogallin of corneal endothelial cell damage induced by xanthine oxidase and SIN-1.

PURPOSE: Free radicals are responsible for tissue injury in corneal preservation and transplantation. Morin hydrate, a flavonoid from Brazil wood, has been shown to be cytoprotective in several types of cells. The aim of this study was to investigate the effectiveness of morin hydrate on rabbit corneal endothelial cells against damage induced by oxyradicals and nitric oxide. METHODS: Corneal endothelial cell cultures were prepared from New Zealand white rabbits, using standard microcarrier technique. Two free-radical-generating systems were used-17 IU/L xanthine oxidase/1 mM hypoxanthine and 5 mM 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1, a nitric oxide-donating agent). RESULTS: Over 95% of cultured corneal endothelial cells necrosed within 3.6 +/- 1.5 min after exposure to xanthine oxidase/hypoxanthine. Adding morin hydrate delayed cell necrosis to 5.8 +/- 0.3 min (0.25 mM morin hydrate), 13.3 +/- 5.0 min (0.5 mM), and 41.5 +/- 8.6 min (1.0 mM). Exposed to nitric oxide generated by SIN-1, cells necrosed by 9.5 +/- 2.5 min, versus 14.1 +/- 1.3 min (0.25 mM morin hydrate), 27.2 +/- 2.0 min (0.5 mM), and 43.3 +/- 5.4 min (1.0 mM). Morin hydrate significantly prolonged survival of cells compared to equimolar concentrations of purpurogallin, Trolox, or ascorbate (P < 0.01). CONCLUSION: This study demonstrates that morin hydrate behaves as a broad-spectrum antioxidant: it scavenges not only xanthine oxidase/hypoxanthine-generated oxyradicals, but also nonenzymatic, nitrogen-derived radicals, better than those above mentioned antioxidants. This property of morin hydrate may help prevent free radical damage in corneal preservation solutions.