Biomedical subjects

Hajime Otani

Publications and source records attributed to Hajime Otani.

At least 19 recordsLinked to original sources

PubMed2006

Statin and resveratrol in combination induces cardioprotection against myocardial infarction in hypercholesterolemic rat.

Hypercholesterolemia (HC) is a common health problem that significantly increases risk of cardiovascular disease. Both statin (S) and resveratrol (R) demonstrated cardioprotection through nitric oxide-dependent mechanism. Therefore, the present study was undertaken to determine whether combination therapy with statin and resveratrol is more cardioprotective than individual treatment groups in ischemic rat heart model. The rats were fed with 2% high cholesterol diet and after 8 weeks of high cholesterol diet the animals were treated with statin (1 mg/kg bw/day) and resveratrol (20 mg/kg bw/day) for 2 weeks. The rats were assigned to: (1) Control (C), (2) HC, (3) HCR, (4) HCS and (5) HCRS. The hearts, subjected to 30-min global ischemia followed by 120-min reperfusion were used as experimental model. The left ventricular functional recovery (+dp/dt(max)) was found to be significantly better in the HCRS (1926+/-43), HCR (1556+/-65) and HCS (1635+/-40) compared to HC group (1127+/-16). The infarct sizes in the HCRS, HCS and HCR groups were 37+/-3.6, 43+/-3.3 and 44+/-4.2 respectively compared to 53+/-4.6 in HC. The lipid level was found to be decreased in all the treatment groups when compared to HC more significantly in HCS and HCRS groups when compared to HCR. Increased phosphorylation of Akt and eNOS was also observed in all the treatment groups resulting in decreased extent of cardiomyocyte apoptosis but the extent of reduction in apoptosis was more significant in HCRS group compared to all other groups. In vivo rat myocardial infarction (MI) model subjected to 1 week of permanent left descending coronary artery (LAD) occlusion documented increased capillary density in HCR and HCRS treated group when compared to HCS treatment group. We also documented increased beta-catenin translocation and increased VEGF mRNA expression in all treatment groups. Thus, we conclude that the acute as well as chronic protection afforded by combination treatment with statin and resveratrol may be due to pro-angiogenic, anti-hyperlipidemic and anti-apoptotic effects and long-term effects may be caused by increased neo-vascularization of the MI zone leading to less ventricular remodeling.

Animals↗

PubMed2006

Reducing postural sway by manipulating the difficulty levels of a cognitive task and a balance task.

Postural sway decreases when participants perform a balance task concurrently with a cognitive task. The present study examined whether this is based on the difficulty of the cognitive task, the difficulty of the balance task, or a combination of both. Participants completed easy and difficult Brooks' spatial and nonsense memory tasks in sitting and standing. Postural sway was measured while they performed one of three balance tasks concurrently with the Brooks' tasks and two control tasks. Performing the difficult cognitive task, yet not the easy cognitive task, was associated with a decrease in postural sway, F (3, 273)=3.53, MSE=0.007, p=0.015. The decrease was not influenced by the difficulty of the balance task. The difficulty level of the cognitive task was the critical factor that decreased sway in dual task conditions.

Adolescent↗

PubMed2006

Bovine beta-casein (1-28), a casein phosphopeptide, enhances proliferation and IL-6 expression of mouse CD19+ cells via Toll-like receptor 4.

This study was conducted to elucidate the target cells and receptors which participate in the mitogenic and interleukin (IL)-6-enhancing effect of bovine beta-casein (1-28), a casein phosphopeptide. When the spleen lymphocyte subset (CD4+, CD8+, and CD19+ cells) from C3H/HeN mice was cultured with the beta-casein (1-28), it exerted a dose-dependent mitogenic effect on CD19+ cells. The effect of beta-casein (1-28) was not apparent in the case of CD19+ cells from C3H/HeJ mouse. In addition, the effect was significantly inhibited by treating the C3H/HeN mouse-derived CD19+ cells with neutralizing antibody for toll-like receptor 4 (TLR4). Reverse transcription-polymerase chain reaction analysis showed that the beta-casein (1-28) exerted an IL-6-enhancing effect on the CD19+ cells. The effect was also abrogated in either C3H/HeJ mouse-derived CD19+ cell culture or the anti-TLR4 antibody-added culture. These results suggest that the beta-casein (1-28) stimulates both proliferation and IL-6 expression of CD19+ cells via TLR4.

Animals↗

PubMed2006

Oral ingestion of cow's milk immunoglobulin G stimulates some cellular immune systems and suppresses humoral immune responses in mouse.

Four-week-old male C3H/HeN mice were bred with diets consisting of ovalbumin alone (OVA, control diet) or mixtures of OVA and cow's milk immunoglobulin G (IgG-added diets) as a protein source for 4 or 5 weeks, and both the cellular and humoral immune properties of the mice were investigated. The number of interleukin (IL)-12+CD11b+ cells in spleens and the formation of superoxide by peritoneal macrophages were higher in mice given the IgG-added diet than in those given the control diet. The number of natural killer cells in Peyer's patches or spleens and the cytotoxic activity of spleen cells toward an erythroleukemia cell line, K562, were also higher in mice given the IgG-added diet. In contrast, the numbers of interferon-gamma+CD4+ and IL-4+CD4+ cells in Peyer's patches or spleens and the levels of total or OVA-specific intestinal IgA and serum IgG were significantly lower in mice given the IgG-added diet than in those given the control diet. In addition, the number of cells expressing CD19 in spleens was significantly higher in mice given the IgG-added diet. These results indicate that oral ingestion of cow's milk IgG may stimulate some innate cellular immune systems, while suppressing humoral adaptive immune responses in the mouse.

Administration, Oral↗

PubMed2006

Redox regulation of angiotensin II preconditioning of the myocardium requires MAP kinase signaling.

A recent study documented reactive oxygen species (ROS), generated through NADPH oxidase by angiotensin II (Ang II) with the activation of NADPH oxidase subunits, p22phox and gp91phox, to be responsible for the preconditioning effect of Ang II. The present study was designed to determine if similar to ischemic preconditioning (PC), mitogen-activated protein (MAP) kinases are also involved in Ang II PC of the heart. Isolated working rat hearts were perfused for 15 min with KHB (Krebs-Henseleit bicarbonate) buffer containing Ang II in the absence or presence of an Erk (1/2) inhibitor, PD 098059, a p38MAPK inhibitor, SB 202190, a JNK inhibitor, SP 600125 or a ROS scavenger, N-acetyl cysteine (NAC). All hearts were subsequently subjected to 30 min global ischemia followed by 2 h reperfusion with KHB buffer only. Cardioprotection was examined by determining infarct size, cardiomyocyte apoptosis and ventricular recovery. Redox and MAP kinase regulation were studied by determining the survival signaling mediated by Akt and Bcl-2. In consistent with previous results, Ang II preconditioned the heart as evidenced by improved postischemic ventricular recovery and reduced infarct size and decreases cardiomyocyte apoptosis. Ang II phosphorylated both Akt, Bcl-2 and Bad, which was blocked by NAC, PD 098059 or SP 600125, but not by SB 202190. NAC, PD 098059 and SP600125, but not SB202190, also abolished the cardioprotective effect of Ang II preconditioning. The results indicate that Ang II preconditioning is potentiated through MAP kinases that are regulated by redox signaling.

Angiotensin II↗

PubMed2006

Dystrophin is a possible end-target of ischemic preconditioning against cardiomyocyte oncosis during the early phase of reperfusion.

OBJECTIVE: Dystrophin is a sarcolemmal membrane protein that prevents the myocyte from oncosis induced by physical stress. Because ischemic preconditioning (IPC) protects mitochondria and prevents oncosis during reperfusion, we hypothesized that dystrophin is an end-target of IPC distal to mitochondrial protection. METHODS AND RESULTS: Isolated rat hearts were subjected to 30 min ischemia followed by reperfusion. IPC was introduced by 3 cycles of 5 min ischemia and 5 min reperfusion. The loss of sarcolemmal dystrophin and myocardial ATP during ischemia was comparable between the control and the IPC heart. Similar changes in sarcolemmal dystrophin and myocardial ATP were observed when the heart was treated with 2,4-dinitrophenol (DNP), an uncoupler of mitochondrial respiration, or oligomycin, an inhibitor of mitochondrial F1F0-ATPase. However, the IPC heart increased sarcolemmal dystrophin during reperfusion associated with an increase in tetramethylrhodamine ethylester (TMRE) uptake, an indicator of mitochondrial membrane potential (DeltaPsim), and myocardial ATP and inhibited myocyte oncosis. The increase in myocardial ATP and relocalization of dystrophin to the sarcolemma mediated by IPC was inhibited by treatment with DNP or oligomycin during reperfusion. In vitro experiments demonstrated that mitochondria isolated from the ischemic IPC heart increased ATP generation and facilitated relocalization of dystrophin from the insoluble to the soluble fractions in a manner sensitive to DNP and oligomycin. CONCLUSIONS: These results suggest that enhanced relocalization of dystrophin to the sarcolemma during reperfusion may be a mechanistic link between IPC-mediated improvement of mitochondrial function and its protection against oncosis during the early phase of reperfusion.

2,4-Dinitrophenol↗

PubMed2006

Role of mechanical stress in the form of cardiomyocyte death during the early phase of reperfusion.

BACKGROUND: The hypothesis that mechanical stress during reperfusion produces myocyte oncosis and inhibits apoptosis was tested in the present study. METHODS AND RESULTS: Isolated and perfused rat hearts were subjected to 30 min ischemia followed by 150 min reperfusion. In the control-reperfusion heart, the form of myocyte death was a mixture of apoptosis only, oncosis only, and both apoptosis and oncosis. Apoptotic myocytes contained mitochondria that maintained membrane potential (Deltapsim), whereas oncotic myocytes contained only Deltapsim-collapsed mitochondria. Treatment with the contractile blocker 2,3-butanedione monoxime (BDM) during reperfusion increased caspase-3 activity and produced predominantly apoptosis. However, withdrawal of BDM provoked oncosis in terminal deoxynucleotide nick-end labeling (TUNEL)-positive myocytes. Myocardial stretch by inflating an intraventricular balloon at the time of reperfusion with BDM increased only oncotic myocytes, whereas the same mechanical stress 120 min after reperfusion increased oncotic myocytes positive for TUNEL. Increased mechanical stress at the time of reperfusion by treatment with isoproterenol or hyposmotic buffer inhibited caspase-3 activity and increased only oncotic myocytes. Co-treatment with the caspase-3 inhibitor, Ac-DEVD-CHO, and BDM during reperfusion inhibited myocyte apoptosis and oncosis but did not inhibit oncosis after withdrawal of BDM. CONCLUSIONS: These results suggest that mechanical stress is a critical determinant of the form of myocyte death during the early phase of reperfusion.

Animals↗

PubMed2006

Effects of intravenous administration of tissue plasminogen activator before thrombectomy in patients with acute myocardial infarction.

BACKGROUND: Myocardial salvage after acute myocardial infarction (AMI) largely depends on the removal of infarct-related thrombus. Although both thrombolysis and thrombectomy are effective strategies to remove thrombus, there is a paucity of reports regarding the benefit of the combination therapy. Therefore, the efficacy of intravenous administration with mutant tissue plasminogen activator (Mt-PA) before thrombectomy and ordinary percutaneous coronary intervention (PCI) was evaluated. METHODS AND RESULTS: Consecutive 44 AMI patients without contraindication of Mt-PA were enrolled in the study and randomly assigned to thrombectomy with Mt-PA pre-administration (group T) or thrombectomy alone (group N). Although Thrombolysis in Myocardial Infarction (TIMI) grade before PCI and TIMI myocardial perfusion grade immediately after PCI were significantly greater in group T (p<0.05), there was no improvement of left ventricular ejection fraction immediately and 6 months after PCI. CONCLUSIONS: These results suggest that intravenous administration with Mt-PA before thrombectomy had no significant benefit in the salvage of infracted myocardium over thrombectomy alone, despite improvement of coronary microcirculation immediately after PCI.

Acute Disease↗

PubMed2006

Stimulatory effect of lactic acid bacteria from commercially available Nozawana-zuke pickle on cytokine expression by mouse spleen cells.

We investigated the effect of lactic acid bacteria (LAB) isolated from eight samples of commercially available Nozawana-zuke, a traditional Japanese pickle, on cytokine expression by mouse spleen cell cultures. The 12 isolated strains of LAB (Nz1-Nz12), which were identified as genus Lactobacillus or Leuconostoc by the API50CHL test, enhanced the expression of interferon (IFN)-gamma with 6 h of culture. Ten of these 12 LAB, particularly Nz8, enhanced interleukin (IL)-12 p40 expression. The actinase E- and Benzonase-treated or untreated cell wall fraction of Nz8 enhanced both IFN-gamma and IL-12 p40 expression, while the cell plasma fraction had little effect. In the presence of anti-toll like receptor 4 antibody, the effect of the cell wall fraction of Nz8 was significantly abrogated. These results suggest that some LAB from Nozawana-zuke have a T helper 1-type immunoenhancing effect.

Animals↗

PubMed2006

Segregation accuracy in item-method directed forgetting across multiple tests.

Two experiments examined recall across tests following item-method directed-forgetting instructions and the varying of presentation duration of items at study. For both immediate testing (Experiment 1) and delayed testing (Experiment 2), accurate recall of remember instruction items (R-items) exceeded the accurate recall of forget instruction items (F-items). However, some F-items from study were inaccurately recalled as R-items and R-items from study as F-items. Inaccurate recall persisted across tests for both immediate and delayed recall and increased across tests for immediate recall. We view the R-item advantage in accurate recall as consistent with the account they receive more rehearsal at study than do F-items. We view inaccurate recall as reflecting the bias to report items retrieved on an immediate test lacking instructional tags as F-items. On delayed tests, items retrieved lacking instructional tags are first assessed against a criterion point on a memory-strength continuum and those with strength above the criterion reported as R-items and those below the criterion as F-items.

Humans↗

PubMed2005

Opposing effect of p38 MAP kinase and JNK inhibitors on the development of heart failure in the cardiomyopathic hamster.

OBJECTIVE: p38 MAP kinase (p38 MAPK) and c-Jun NH2-terminal kinase (JNK) have been implicated in the pathophysiology of heart failure. We investigated the effects of chronic treatment with p38 MAPK and JNK inhibitors on the development of heart failure in dilated cardiomyopathy (DCM) hamster heart. METHODS AND RESULTS: BIO14.6 hamster hearts showed markedly increased p38 MAPK and JNK activities at 6 weeks of age when there was no significant increase in the area of fibrosis, heart weight/body weight, left ventricular (LV) chamber dilation and LV dysfunction. p38 MAPK and JNK activities were attenuated at 26 weeks of age and abolished at 40 weeks of age in BIO14.6 hamster hearts. BIO14.6 hamsters and the control BIOF1B hamsters were chronically treated (i.p.) with the p38 MAPK inhibitors, SB203580 (1 mg/kg/day) and FR167653 (3 mg/kg/day), or the JNK inhibitor, SP600125 (1 mg/kg/day) or vehicle for 20 weeks starting from 6 weeks of age. Treatment of BIO14.6 hamster hearts with SB203580 and FR167653 reduced the number of TUNEL-positive myocytes, the area of fibrosis and heart weight/body weight associated with a significant decrease of LV dimension and an increase in LV ejection fraction and LV contractility compared to the vehicle-treated counterpart. In contrast, treatment with SP600125 increased the number of TUNEL-positive myocytes and the area of interstitial fibrosis associated with aggravation of LV chamber dilation and LV dysfunction. CONCLUSIONS: These results suggest that chronic treatment with p38 MAPK and JNK inhibitors produces opposing effects on the development of heart failure in the DCM hamster heart.

Animals↗

PubMed2005

Role of F-actin organization in p38 MAP kinase-mediated apoptosis and necrosis in neonatal rat cardiomyocytes subjected to simulated ischemia and reoxygenation.

Activation of p38 mitogen-activated protein (MAP) kinase (MAPK) has been implicated in the mechanism of cardiomyocyte (CMC) protection and injury. The p38 MAPK controversy may be related to differential effects of this kinase on apoptosis and necrosis. We have hypothesized that p38 MAPK-mediated F-actin reorganization promotes apoptotic cell death, whereas it protects from osmotic stress-induced necrotic cell death. Cultured neonatal rat CMCs were subjected to 2 h of simulated ischemia followed by reoxygenation. p38 MAPK activity measured by phosphorylation of MAP kinase-activated protein (MAPKAP) kinase 2 was increased during simulated ischemia and reoxygenation. This was associated with translocation of heat shock protein 27 (HSP27) from the cytosolic to the cytoskeletal fraction and F-actin reorganization. Cytochrome c release from mitochondria, caspase-3 activation, and DNA fragmentation were increased during reoxygenation. Robust lactate dehydrogenase (LDH) release was observed under hyposmotic (140 mosM) reoxygenation. The p38 MAPK inhibitor SB-203580 abrogated activation of p38 MAPK, translocation of HSP27, and F-actin reorganization and prevented cytochrome c release, caspase-3 activation, and DNA fragmentation. Conversely, SB-203580 enhanced LDH release during hyposmotic reoxygenation. The F-actin disrupting agent cytochalasin D inhibited F-actin reorganization and prevented cytochrome c release, caspase-3 activation, and DNA fragmentation, whereas it enhanced LDH release during hyposmotic reoxygenation. When CMCs were incubated under the isosmotic condition for the first 15 min of reoxygenation, SB-203580 and cytochalasin D increased ATP content of CMCs and prevented LDH release after the conversion to the hyposmotic condition. These results suggest that F-actin reorganization mediated by activation of p38 MAPK plays a differential role in apoptosis and protection against osmotic stress-induced necrosis during reoxygenation in neonatal rat CMCs; however, the sarcolemmal fragility caused by p38 MAPK inhibition can be reversed during temporary blockade of physical stress during reoxygenation.

Actins↗

PubMed2005

Isoflurane induces second window of preconditioning through upregulation of inducible nitric oxide synthase in rat heart.

The second window of preconditioning (SWOP) induced by inhalation of volatile anesthetics has been documented in the rat heart and is triggered by nitric oxide synthase (NOS), but involvement of NOS in the mediator phase of isoflurane-induced SWOP has not been demonstrated. We tested the hypothesis that isoflurane-induced SWOP is mediated through upregulation of inducible NOS (iNOS). Rats inhaled 0.75 minimum alveolar concentration (MAC) isoflurane, 1.5 MAC isoflurane, or O2 for 2 h. After 24, 48, 72, and 96 h, the isolated heart was perfused with buffer and subjected to 30 min of ischemia followed by 2 h of reperfusion. Inhalation of 0.75 and 1.5 MAC isoflurane significantly limited infarct size after ischemia-reperfusion 24-72 h after isoflurane inhalation. The maximum effect was obtained 48 h after inhalation of 1.5 MAC isoflurane. Postischemic left ventricular function was improved only 48 h after inhalation of 1.5 MAC isoflurane. iNOS expression and activity in the heart were increased 24-72 h after inhalation of 1.5 MAC isoflurane; this increase was less pronounced after inhalation of 0.75 MAC isoflurane. A selective iNOS inhibitor, 1400W (10 microM), abolished iNOS activation and cardioprotection induced 48 h after inhalation of 1.5 MAC isoflurane. These results suggest that isoflurane inhalation induces SWOP after 24-72 h through overexpression and activation of iNOS in the rat heart.

Administration, Inhalation↗

PubMed2005

Integrated pharmacological preconditioning and memory of cardioprotection: role of protein kinase C and phosphatidylinositol 3-kinase.

Although protein kinase C (PKC) and phosphatidylinositol 3 (PI3)-kinase are implicated in cardioprotective signal transduction mediated by ischemic preconditioning, their role in pharmacological preconditioning (PPC) has not been determined. Cultured neonatal rat cardiomyocytes (CMCs) were subjected to simulated ischemia for 2 h followed by 15 min of reoxygenation. PPC of CMCs consisted of administration of 50 microM adenosine, 50 microM diazoxide, and 50 microM S-nitroso-N-acetylpenicillamine (SNAP), each alone or in combination, for 15 min followed by 30 min of washout before simulated ischemia. Although PKC-epsilon and PI3-kinase were significantly activated during treatment with adenosine, activation of these kinases dissipated after washout. In contrast, PPC combined with adenosine, diazoxide, and SNAP elicited sustained activation of PKC-epsilon and PI-3 kinase after washout. The combined-PPC, but not the single-PPC, protocol conferred antiapoptotic and antinecrotic effects after reoxygenation. The PKC inhibitor chelerythrine (5 microM) or the PI3-kinase inhibitor LY-294002 (10 microM) given during the washout period partially blocked the activation of PKC-epsilon and PI3-kinase mediated by the combined-PPC protocol, whereas combined addition of chelerythrine and LY-294002 completely inhibited activation of PKC-epsilon and PI3-kinase. Chelerythrine or LY-294002 partially blocked antiapoptotic and antinecrotic effects mediated by the combined-PPC protocol, whereas combined addition of chelerythrine and LY-294002 completely abrogated antiapoptotic and antinecrotic effects. These results suggest that the combined-PPC protocol confers cardioprotective memory through sustained and interdependent activation of PKC and PI3-kinase.

Adenosine↗

PubMed2005

Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580.

p38 MAP kinase activation is known to be deleterious not only to mitochondria but also to contractile function. Therefore, p38 MAP kinase inhibition therapy represents a promising approach in preventing reperfusion injury in the heart. However, reversal of p38 MAP kinase-mediated contractile dysfunction may disrupt the fragile sarcolemma of ischemic-reperfused myocytes. We, therefore, hypothesized that the beneficial effect of p38 MAP kinase inhibition during reperfusion can be enhanced when contractility is simultaneously blocked. Isolated and perfused rat hearts were paced at 330 rpm and subjected to 20 min of ischemia followed by reperfusion. p38 MAP kinase was activated after ischemia and early during reperfusion (<30 min). Treatment with the p38 MAP kinase inhibitor SB-203580 (10 microM) for 30 min during reperfusion, but not the c-Jun NH(2)-terminal kinase inhibitor SP-600125 (10 microM), improved contractility but increased creatine kinase release and infarct size. Cotreatment with SB-203580 and the contractile blocker 2,3-butanedione monoxime (BDM, 20 mM) or the ultra-short-acting beta-blocker esmorol (0.15 mM) for the first 30 min during reperfusion significantly reduced creatine kinase release and infarct size. In vitro mitochondrial ATP generation and myocardial ATP content were significantly increased in the heart cotreated with SB-203580 and BDM during reperfusion. Dystrophin was translocated from the sarcolemma during ischemia and reperfusion. SB-203580 increased accumulation of Evans blue dye in myocytes depleted of sarcolemmal dystrophin during reperfusion, whereas cotreatment with BDM facilitated restoration of sarcolemmal dystrophin and mitigated sarcolemmal damage after withdrawal of BDM. These results suggest that treatment with SB-203580 during reperfusion aggravates myocyte necrosis but concomitant blockade of contractile force unmasks cardioprotective effects of SB-203580.

Animals↗

PubMed2005

Emotional stimuli, divided attention, and memory.

The emotion-memory literature has shown that negative emotional arousal enhances memory. S. A. Christianson (1992) proposed that preattentive processing could account for this emotion-memory relationship. Two experiments were conducted to test Christianson's theory. In Experiment 1, participants were exposed to neutral and negative arousing slides. In Experiment 2, participants were exposed to neutral, negative arousing, and positive arousing slides. In both experiments, the aforementioned variable was factorially combined with a divided-attention or non-divided-attention condition. The authors predicted that, in contrast to the nondivided condition, dividing attention would adversely impact neutral and positive stimuli more than negative stimuli. The hypothesis was supported; participants recalled more high negative-arousal slides than positive or neutral slides when their attention was divided rather than nondivided.

Adolescent↗

PubMed2005

Remembering a nuclear accident in Japan: did it trigger flashbulb memories?

Flashbulb memories are vivid memories of the details surrounding the discovery of an emotional event. We investigated whether the nuclear accident that occurred in Japan in 1999 produced flashbulb memories among people who lived near the accident site. A questionnaire was distributed twice (approximately 3 weeks after the accident and 1 year later) to (1) the residents of the communities surrounding the accident site, (2) the students at a university near the accident site, and (3) the students at two universities far away from the accident site. Flashbulb memory holders were defined as those individuals who showed consistent memories between test and retest. The results indicated that only a small percentage of participants formed flashbulb memories. Further, no age-related decline was found. Flashbulb memories were distinguished by perfect or near perfect scores on four attributes: source, place, activity, and people. The results also indicated that the ratings on emotional reactions, personal consequentiality, and surprise did not differentiate between the flashbulb and non-flashbulb memory holders. In contrast, the flashbulb memory holders reported rehearsing more than the non-flashbulb memory holders. These results supported the notion that flashbulb memories are formed through rehearsal rather than at encoding. However, it is also possible that rehearsal was a result of the flashbulb memory.

Adult↗

PubMed2005

Lycopene, tomatoes, and coronary heart disease.

Tomato and its major antioxidant component lycopene have recently been focused as important antioxidant nutrients because of their ability to reduce reactive oxygen species and to provide health benefits. Most of the studies were undertaken to determine the usefulness of lycopene against cancer and cardiovascular diseases. Epidemiological studies, however, yielded conflicting results. This study was undertaken to compare cardioprotective abilities of tomato juice and lycopene. Rats were gavaged either tomato juice or lycopene for 3 weeks. At the end of 3 weeks, isolated hearts were subjected to 30 min ischemia followed by 2 h of reperfusion. Both tomato juice and lycopene reduced the extent of lipid peroxidation; but only tomato juice, but not lycopene, improved post-ischemic ventricular function, and reduced myocardial infarct size and cardiomyocyte apoptosis. The results indicated for the first time that tomato juice, but not lycopene, possesses cardioprotective ability.

Animals↗