Urinary prostaglandin D metabolite excretion during the first six months of life was significantly lower in breast-fed than formula-fed infants.

Aim: The metabolic changes that occur during the postnatal weaning period appear to be particularly important for future health, and breast milk is considered to provide the optimal source of infant nutrition. This pilot study from September 2013 to May 2015 examined the effect of breastfeeding on prostaglandin metabolism in healthy term infants.

Methods: Urine samples were collected from 19 infants at one month of age in the Juntendo University Hospital, Tokyo, Japan.

Association of zinc and copper with clinical parameters in the preterm newborn.

Background: Given that preterm infants are born at a time of rapid fetal growth, they are at risk of deficiency of essential nutrients for brain development, including zinc (Zn) and copper (Cu). This study evaluate the relationship between serum Cu or Zn, gestational age (GA) and anthropometric parameters at birth in preterm infants.

Methods: This was a retrospective study of infants <35 weeks' GA from January 2010 to August 2012.

A pilot study of the effect of human breast milk on urinary metabolome analysis in infants.

Background: This study aimed to examine the nutritional effect of breast feeding on healthy term infants by using urinary metabolome analysis.

Methods: Urine samples were collected from 19 and 14 infants at 1 and 6 months, respectively. Infants were separated into two groups: the breast-fed group receiving <540 mL/week of their intake from formula (n=13 at 1 month; n=9 at 6 months); and the formula-fed group receiving no breast milk (BM) (n=6 at 1 month; n=5 at 6 months).

The Ratio of Docosahexaenoic Acid and Arachidonic Acid in Infant Formula Influences the Fatty Acid Composition of the Erythrocyte Membrane in Low-Birth-Weight Infants.

Objective: The arachidonic acid (ARA) and docosahexaenoic acid (DHA) contents in the infant formula influence on the growth and development of low-birth-weight infants (LBWI). In Japan, many infant formulas are fortified only with DHA. We investigated the safety and efficacy of an infant formula (H2025A) fortified with DHA and ARA (DHA/ARA ratio of 2:1, the same as that in Japanese breast milk).

Amplitude-integrated electroencephalography in patients with acute encephalopathy with refractory, repetitive partial seizures.

We report amplitude-integrated EEG findings in two children with acute encephalopathy with refractory, repetitive partial seizures. Both patients had a febrile illness one week before the onset of seizure. They had reduction of consciousness and repetitive seizures refractory to first-line antiepileptic drugs.

Clustered subclinical seizures in a patient with acute encephalopathy with biphasic seizures and late reduced diffusion.

Using single-channel amplitude-integrated electroencephalography (aEEG), we monitored clustered seizures in a 12-month-old boy suffering from acute encephalopathy with biphasic seizures and late reduced diffusion (AESD). He was admitted to our hospital after losing consciousness and experiencing repeated seizures in association with fever. Although the patient's state of consciousness improved the next day, it declined on the fifth day of illness, and clinical seizures were observed.

Effects of ghrelin on growth and cardiac function in infants with congenital heart disease.

Background: Ghrelin has effects on appetite and growth. Recent reports suggest effects on cardiac function, but no study has evaluated the ghrelin levels of congenital heart disease (CHD) infants with heart failure. The purpose of the present study was therefore to investigate the relationship between ghrelin level and growth and cardiac function in CHD infants.

Usefulness of single-channel amplitude-integrated electroencephalography for continuous seizure monitoring in infancy: a case report.

We continuously monitored clustered seizures using single-channel amplitude-integrated electroencephalography (aEEG) in a 6-month-old girl with probable benign partial epilepsy in infancy (BPEI). The patient was admitted with clustered seizures, and aEEG using three disposable electrodes was started by a non-expert pediatrician. During the recording, seven seizures were detected.

Effects of alpha-linolenic acid on colonic secretion in rats with experimental colitis.

Background: Few studies have specifically examined the effects of n-3 polyunsaturated fatty acids (PUFAs) on intestinal water and ion secretion in ulcerative colitis (UC). The aim of this study was to examine the contribution of prostaglandins (PGs) and leukotrienes (LTs) to mucosal secretion in intestines with UC and to evaluate the effect of dietary n-3 PUFAs on diarrhea in UC.

Methods: We measured the short-circuit current (Isc), using the Ussing chamber method, and fatty acid composition in the colonic mucosa of rats with dextran sulfate sodium (DSS)-induced experimental colitis.

Suppression of azoxymethane-induced colon cancer development in rats by a cyclooxygenase-1 selective inhibitor, mofezolac.

We demonstrated recently that mofezolac, a cyclooxygenase-1 (COX-1) selective inhibitor, suppresses the development of azoxymethane (AOM)-induced colonic aberrant crypt foci in F344 rats and intestinal polyps in APC1309 mice. In the present study, we therefore investigated the effects of mofezolac on colon cancer development. Male F344 rats were injected subcutaneously with 15 mg/kg body weight of AOM in the back twice at 7-day intervals from 5 weeks of age, and fed a diet containing 600 or 1200 ppm mofezolac for 32 weeks, starting 1 day before the first dosing of AOM.

Prostaglandin E receptor EP3 deficiency modifies tumor outcome in mouse two-stage skin carcinogenesis.

We have recently shown that the prostaglandin E(2) (PGE(2)) receptor EP(3) plays an important role in suppression of colon cancer cell proliferation and that its deficiency enhances late stage colon carcinogenesis. Here we examined the effects of EP(3)-deficiency on two-stage skin carcinogenesis. 7,12-Dimethylbenz[a]anthracene (50 microg/200 microl of acetone) was thus applied to the back skin of female EP(3)-knockout and wild-type mice at 8 weeks of age, followed by treatment with 12-O-tetradecanoylphorbol-13-acetate (5 microg/200 microl of acetone) twice a week for 25 weeks.

Suppression of azoxymethane-induced colon cancer development in rats by a prostaglandin E receptor EP1-selective antagonist.

Prostaglandin E(2) is involved in colon carcinogenesis through its binding to the PGE(2) receptor subtypes EP(1), EP(2), EP(3) and EP(4). We have demonstrated that administration of ONO-8711, an EP(1)-selective antagonist, suppresses development of AOM-induced ACF in C57BL/6 mice and F344 rats. ONO-8711 also reduced the numbers of intestinal polyps in Min mice.

Prostaglandin E receptor subtype EP(1) deficiency inhibits colon cancer development.

Prostaglandin E(2) exerts its biological activity through binding to its membrane receptors, E-prostanoid (EP) receptors. Our previous finding that lack of EP(1) receptor inhibits the early stages of colon carcinogenesis led us to investigate whether EP(1) receptor deficiency reduces colon cancer development induced by azoxymethane (AOM) using EP(1) receptor knockout mice. At 6 weeks of age 33 homozygous EP(1)-deficient (EP(1)(-/-)) mice and 28 wild-type (EP(1)(+/+)) mice were given i.

Carcinogenicity of aminophenylnorharman, a possible novel endogenous mutagen, formed from norharman and aniline, in F344 rats.

A novel mutagenic compound, 9-(4'-aminophenyl)-9H- pyrido[3,4-b]indole (aminophenylnorharman, APNH), is shown to be formed by the in vitro enzymatic reaction of 9H-pyrido[3,4-b]indole (norharman) and aniline. APNH generates DNA adducts (dG-C8-APNH), and is potently genotoxic to bacteria and mammalian cells. APNH has also been demonstrated to be formed in vivo from norharman and aniline, and suggested to be a new type of endogenous mutagenic compound.

Combined effects of cyclooxygenase-1 and cyclooxygenase-2 selective inhibitors on intestinal tumorigenesis in adenomatous polyposis coli gene knockout mice.

As with cyclooxygenase (COX)-2, genetic disruption of COX-1 gene or pharmacologic inhibition of its activity has been shown to decrease the number of intestinal polyps in Apc gene-deficient mice. The present study was designed to investigate the combined effects of COX-1 and COX-2 selective inhibitors on spontaneous polyp formation in APC1309 female mice. The animals were treated with 300 or 600 ppm mofezolac (a COX-1 selective inhibitor) alone, 200 or 400 ppm nimesulide (a COX-2 selective inhibitor) alone, 300 ppm mofezolac plus 200 ppm nimesulide, 600 ppm mofezolac plus 400 ppm nimesulide, or 10 ppm indomethacin (a dual-COX inhibitor) in the diet from 7 weeks of age for 4 weeks.

Concomitant suppression of hyperlipidemia and intestinal polyp formation in Apc-deficient mice by peroxisome proliferator-activated receptor ligands.

Epidemiological studies have shown a positive association of colon cancer with hyperlipidemia. Furthermore, signaling generated by peroxisome proliferator-activated receptor (PPAR) alpha and gamma ligands, suggested to be candidate tumor preventive agents, has been shown to lower serum triglyceride levels. In the present study, we assessed hyperlipidemia in Apc-deficient mice, model animals for human familial adenomatous polyposis, and examined the effects of pioglitazone and bezafibrate, respectively, PPARgamma and PPARalpha agonists, on both hyperlipidemia and intestinal polyposis.

Combined effects of prostaglandin E receptor subtype EP1 and subtype EP4 antagonists on intestinal tumorigenesis in adenomatous polyposis coli gene knockout mice.

Previous studies have shown that prostaglandin E(2) (PGE(2)) is involved in intestinal carcinogenesis through its binding to the PGE(2) receptor subtypes EP(1) and EP(4) and activation of downstream pathways. ONO-8711 and ONO-AE2-227, prostaglandin E receptor subtype EP(1)- and EP(4)-selective antagonists, respectively, are known to suppress formation of intestinal polyps in adenomatous polyposis coli gene-deficient mice. The present study was designed to investigate the combined effects of EP(1) and EP(4) antagonists on spontaneous polyp formation in APC1309 mice in order to determine the contribution of each receptor to intestinal tumorigenesis.

Inhibitory effects of mofezolac, a cyclooxygenase-1 selective inhibitor, on intestinal carcinogenesis.

Cyclooxygenase (COX)-2, one enzyme isoform responsible for producing prostanoids from arachidonic acid, contributes to colon carcinogenesis. Recently, genetic disruption of COX-1, the other isoform, was shown to decrease the number of intestinal polyps and prostaglandin E(2) levels in intestinal mucosa, like the case with COX-2 gene disruption, in Min mice. We therefore investigated whether a COX-1 selective inhibitor, mofezolac, suppresses intestinal carcinogenesis in rodents.

Involvement of prostaglandin E receptor subtype EP(4) in colon carcinogenesis.

Accumulating evidence indicates that overproduction of prostanoids attributable to overexpression of cyclooxygenase-2 (COX-2) plays an important role in colon carcinogenesis. We have shown recently that the prostaglandin (PG) E receptor, EP(1), but not EP(3), is involved in mouse colon carcinogenesis. In line with our previous study, here we examined the role of prostanoid receptors in colon carcinogenesis using six additional lines of knockout mice deficient in prostanoid receptors EP(2), EP(4), DP, FP, IP, or TP.