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Biomedical subjects

H Hayasawa

Publications and source records attributed to H Hayasawa.

46 records · Page 3Linked to original sources
PubMed1997

Lactoferrin as a suppressor of cell migration of gastrointestinal cell lines.

The effects of lactoferrin (Lf), an iron-binding glycoprotein, on cell migration were investigated. Lf inhibited the cell migration of three gastrointestinal cell lines (Caco-2 cells, AGS cells, and IEC-18 cells) in vitro. Both iron-saturated (holo) and iron-depleted (apo) Lf showed this inhibitory effect. Chelation of iron in the culture medium by desferrioxamine did not affect the activity of either form of Lf. A pepsin hydrolysate of Lf exhibited effectiveness similar to that of intact Lf. These results demonstrate a novel activity of Lf and suggest a potential role for this molecule in gastrointestinal wound healing, which is independent of its iron-binding capacity.

Adenocarcinoma↗
PubMed1997

Beta-lactoglobulin suppresses melanogenesis in cultured human melanocytes.

The effects of whey proteins from bovine milk on melanogenesis in cultured human melanocytes were examined. Among the major protein components of milk whey including beta-lactoglobulin (BLG), alpha-lactalbumin, serum albumin, and IgG, only BLG exhibited the depigmenting effect at a concentration of 1 mg/ml. Also, BLG suppressed the activity of tyrosinase in these cells. Retinol, to which BLG is known to bind, slightly increased the pigmentation of the cells at concentrations in the range of 1-100 nM, and retinoic acid, a metabolite of retinol, exhibited a strong pigmentation-promoting effect within the same concentration range. Treatment of the cells with 1 mg/ml BLG completely abrogated the pigmentation induced by these A vitamins. These results demonstrate a novel biological activity of BLG and suggest that this activity is dependent on its ability to bind retinol.

Animals↗
PubMed1997

Immunomodulatory effect of bovine lactoferrin pepsin hydrolysate on murine splenocytes and Peyer's patch cells.

The effects were examined of a pepsin hydrolysate of bovine lactoferrin on the proliferation of murine splenocytes. The hydrolysate enhanced [3H]thymidine uptake by splenocytes, but undigested bovine lactoferrin exerted an inhibitory effect. The hydrolysate had the ability to inhibit the blastogenesis that was induced by mitogens such as concanavalin A, phytohemagglutinin, and lipopolysaccharide; inhibition was similar to that with undigested lactoferrin. These results suggested that the hydrolysate contained both immunostimulatory and immunoinhibitory peptides. The stimulatory effect of the hydrolysate in the absence of mitogens was then explored in more detail using nonadherent splenocytes. The proliferative response of splenocytes to the hydrolysate was much greater in the fraction that was enriched with B cells than in the fraction that was enriched with T cells. The hydrolysate did not affect thymocyte proliferation. These data indicated that the adherent cells resembling macrophages and found among the splenocytes were not the target cells of the hydrolysate. The stimulatory effect of the hydrolysate was due to the activation of B cells by the hydrolysate and enhanced immunoglobulin production by splenocytes. Because the hydrolysate also enhanced the proliferation and immunoglobulin A production of Peyer's Patch cells, the immunostimulatory effect of the hydrolysate in vivo was examined using mice that had been orally immunized with cholera toxin. The concentrations of immunoglobulin A conjugated against cholera toxin in bile and in the intestinal contents of mice fed liquid diets containing 1% (wt/vol) lactoferrin hydrolysate were greater than those of mice fed control diets. This result suggested that the use of the lactoferrin hydrolysate is beneficial to enhance mucosal immunity.

Adjuvants, Immunologic↗
PubMed1997

[Epidemiological research on incidence of atopic disease in infants and children in relation to their nutrition in infancy].

Incidence and relative risk of atopic disease (atopic dermatitis; AD, bronchial asthma; BA, allergic rhinitis; AR) in Japanese infants and children in relation to their nutrition in infancy was analyzed from the data of the epidemiological survey which was conducted for 10,000 mothers of infants and children in 1993. A total of 4,610 replies were received: 2,714 from mothers of infants (12 months old) and 1,896 from mothers of children (2 years old). The subjects were allocated to following 3 groups based on their nutrition during first 3 months after birth; the breast-fed group (BF), the formula-fed group (EF), the mixed-fed group (MF). Incidence of atopic disease in BF, FF and MF was 23.5%, 22.2% and 21.8%, respectively and no statistical difference could be found among these 3 groups. AD was developed 17.0%, 14.4% and 13.9%; BA was 4.4%, 8.5% and 5.2%; AR was 4.9%, 6.5% and 5.8% in BF, FF and MF, respectively. Incidence of AD was significantly different between BF and MF (p < 0.01). Incidence of BA was also significantly different between BF and FF (p < 0.01). Risk of onset of BA and AR in FF was higher (adjusted odds ratio 2.2, 95% confidence interval 1.5-3.2 and adjusted odds ratio 1.5, 95% confidence interval 1.0-2.2, respectively) than that of BF controlled by age and family history with Cochran-Mantel-Haenzel test. With multiple logistic regression analysis, relative risk of the onset of BA in FF at the age of one year was 2.1, 95% confidence interval 1.2-3.5 and at the age of two years old was 2.5, 95% confidence interval 1.4-4.4. These results suggest that the breast-fed have certain suppression effects on incidence of bronchial asthma in infants and children.

Asthma↗
PubMed1996

Kappa-casein suppresses melanogenesis in cultured pigment cells.

The effects of bovine milk proteins on melanogenesis in B16 cells were examined. Both whey protein isolate and casein exhibited depigmenting properties. Among the major protein components of milk--including beta-lactoglobulin, alpha-lactalbumin, alpha-, beta-, and kappa-casein--only kappa-casein exhibited the depigmenting effect. However, the carboxyl terminal peptide of kappa-casein, glycomacropeptide, did not show this activity. Also, kappa-casein promoted the proliferation of the cells and inhibited the activity of tyrosinase in the cells. These results indicate that kappa-casein acts as a melanogenesis-suppressing modulator.

Animals↗
PubMed1994

Docosahexaenoic acid status of patients with extrahepatic biliary atresia.

Docosahexaenoic acid (DHA) is believed to be an important long-chain polyunsaturated fatty acid (LCPUFA), which may be essential for neurofunction in infants. Patients with extrahepatic biliary atresia (EBA) may have DHA deficiency secondary to fat malabsorption. The authors investigated DHA and other LCPUFA levels in plasma and red blood cell (RBC) phospholipids of patients after the Kasai portoenterostomy and after supplementation with essential fatty acids. Ten children aged 8 to 17 months (mean, 12.6 months) comprised the study group. Five were jaundiced and five had a normal bilirubin level. The patients received 1 mL/kg of fat emulsions (10% Intralipid, containing 50% linoleic acid and 9% alpha-linolenic acid) in addition to an age-appropriate diet. Additional supplements were ursodeoxycholic acid (UDCA) (15 mg/kg/d) and taurine (100 mg/kg/d). The percentages of DHA in both plasma and RBC phospholipids of patients in the jaundiced group were significantly lower than those of normal children. Patients in the jaundice-free group had significantly lower levels of DHA and higher levels of linoleic acid in both plasma and RBC phospholipids in comparison to the normal group. This study shows that postoperative EBA patient become DHA-deficient even when supplemented with fat emulsions (largely composed of linoleic acid) that contain DHA's precursor, alpha-linolenic acid. This demonstrates a deficiency in the long-chain acid desaturase activity of these patients. It is recommended that excessive/linoleic acid intake be avoided and that all EBA patients have small amounts of DHA added to their lipid supplementation.

Biliary Atresia↗
PubMed1994

Effects of ursodeoxycholic acid treatment on essential fatty acid deficiency in patients with biliary atresia.

To assess whether ursodeoxycholic acid (UDCA) treatment has any beneficial effect on essential fatty acid (EFA) deficiency in patients who have had a Kasai operation for extrahepatic atresia (EBA), responses of serum fatty acids to UDCA administration (15 mg/kg/d) were investigated in eight jaundice-free patients and in eight patients with jaundice (serum total bilirubin > or = 1.0 mg/dL). All patients were also given taurine supplementation (100 mg/kg/d). Serum fatty acid composition was determined before and 6 months after UDCA treatment. Serum total bile acid concentration and serum total bilirubin value, as a part of conventional liver function tests, were measured before and during UDCA therapy. Before UDCA treatment, the concentrations of linoleic acid and arachidonic acid were significantly lower (P > .05 for the former; P > .01 for the latter) in both the jaundice and jaundice-free groups than in the controls. After 6 months of treatment, the linoleic acid concentration significantly increased (P > .05), to the normal range, in the jaundice-free group, but not in the jaundice group. The arachidonic acid concentration did not increase significantly in either group. The serum total bile acid concentration was lower in six of the eight jaundice-free patients and in four of the eight jaundice patients. The serum total bilirubin value decreased in six of the eight jaundice-free patients and in four of the eight jaundice patients; however, the degree of improvement was not statistically significant in either group. No side effects developed, and there were no changes in blood chemistry values unrelated to liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Arachidonic Acid↗
PubMed1990

Prostaglandin and fatty acid metabolism in patients with extrahepatic biliary atresia.

The relationship between essential fatty acid (EFA) deficiency and disturbance of prostaglandin (PG) biosynthesis was studied in children after radical operation for extrahepatic biliary atresia (EBA). In addition, to investigate the method for treatment of postoperative EFA deficiency and disturbance of PG biosynthesis, the serum fatty acid and plasma PG levels were determined before and after supplementation of an EFA-rich powder (38 g of linoleic acid per 100 g of powder) through Suruga II enterostomy. Before administration of the EFA-rich powder, linoleic acid, arachidonic acid, PGE1, and PGF2 alpha levels were significantly lower in both good bile excretion and poor bile excretion groups than in the control group. After administration, linoleic acid and PGE1 levels significantly increased in the good bile excretion group as compared with the preadministration values. These results suggest that the supplementation of EFA-rich powder is an effective treatment for linoleic acid deficiency and disturbance of PGE1 biosynthesis in postoperative EBA patients.

Alprostadil↗
PubMed1986

Essential fatty acid deficiency in congenital biliary atresia: successful treatment to reverse deficiency.

Supplementation of lipid intake by infusion of solutions of essential fatty acid (EFA)-rich powder through Suruga II enterostomy was carried out for the treatment of EFA deficiency in nine children with postoperative congenital biliary atresia (CBA). Infusion of EFA-rich powder dissolved in excreted bile was effective in six patients except for a case who had a total bile acid concentration in the excreted bile that was less than critical micellar level. Administration of EFA-rich powder dissolved in a mixture of the patient's own bile and 1 to 2 mmol/L taurocholate (TC) solution corrected EFA deficiency in three children with total bile acid concentration lower than the critical level. Our results therefore show that infusion of EEA-rich lipid through Suruga II enterostomy after dissolving in the excreted bile is an effective treatment for EFA deficiency in postoperative patients with CBA, and that 1 to 2 mmol/L TC solution used as artificial bile facilitates lipid absorption in cases with total bile acid in the bile less than the critical micellar level.

Bile Acids and Salts↗