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Aims/Introduction Incretin therapy is a common treatment for type 2 diabetes mellitus. We have previously reported an anti‐prostate cancer effect of glucagon‐like peptide‐1 receptor (GLP‐1R) agonist exendin‐4. The attenuation of cell proliferation in the prostate cancer cell line was dependent on GLP‐1R expression. Here, we examined the relationship between human prostate cancer severity and GLP‐1R expression, as well as the effect of forced expression of GLP‐1R using a lentiviral vector. Materials and Methods Prostate cancer tissues were extracted by prostatectomy and biopsy. GLP‐1R was overexpressed in ALVA‐41 cells using a lentiviral vector (ALVA‐41‐GLP‐1R cells). GLP‐1R expression was detected by immunohistochemistry and quantitative polymerase chain reaction. Cell proliferation was examined by growth curves and bromodeoxyuridine incorporation assays. Cell cycle distribution and regulators were examined by flow cytometry and western blotting. In vivo experiments were carried out using a xenografted model. Results GLP‐1R expression levels were significantly inversely associated with the Gleason score of human prostate cancer tissues. Abundant GLP‐1R expression and functions were confirmed in ALVA‐41‐GLP‐1R cells. Exendin‐4 significantly decreased ALVA‐41‐GLP‐1R cell proliferation in a dose‐dependent manner. DNA synthesis and G1‐to‐S phase transition were inhibited in ALVA‐41‐GLP‐1R cells. SKP2 expression was decreased and p27Kip1 protein was subsequently increased in ALVA‐41‐GLP‐1R cells treated with exendin‐4. In vivo experiments carried out by implanting ALVA‐41‐GLP‐1R cells showed that exendin‐4 decreased prostate cancer growth by activation of GLP‐1R overexpressed in ALVA41‐GLP‐1R cells. Conclusions Forced expression of GLP‐1R attenuates prostate cancer cell proliferation by inhibiting cell cycle progression in vitro and in vivo. Therefore, GLP‐1R activation might be a potential therapy for prostate cancer., Forced expression of glucagon‐like peptide‐1 receptor attenuates prostate cancer cell proliferation by inhibiting cell cycle progression both in vitro and in vivo. Glucagon‐like peptide‐1 receptor activation might be a potential therapy for not only type 2 diabetes, but also prostate cancer.

Summary Objective Low testosterone and hyperuricemia are associated with metabolic syndrome (MetS). However, little is known about the nature of the relationships between serum testosterone and sex hormone‐binding globulin (SHBG) concentrations, and hyperuricemia. Methods We evaluated the relationships between serum testosterone (calculated bioavailable testosterone [cbT], calculated free testosterone [cFT], SHBG, and total testosterone [TT]) and metabolic indices, including serum uric acid, in 363 Japanese males (mean age 51.1 ± 8.7 years) at routine health examinations. Results Participants with hyperuricemia (≥7.0 mg/dL) demonstrated lower adiponectin, cbT, cFT, SHBG, and TT, but a higher MetS prevalence and higher values of various MetS‐related parameters than those without hyperuricemia (

Individuals with spinal cord injury (SCI) have altered neurophysiology and present with symptoms that must be interpreted in the context of their specific neurologic injury. This is a case of a 16-year-old female adolescent with C5 American Spinal Injury Association Impairment Scale A SCI who presented with intractable nausea. Multiple etiologies for her nausea, including medication effect, metabolic and gastrointestinal disorders, autonomic dysreflexia, and mood disorder, were systematically ruled out. Due to the persistence of the patient's symptoms and suboptimal progression in her rehabilitation, a central nervous system etiology was investigated. Ultimately, atlantoaxial instability with odontoid compression on the medulla was identified and her refractory nausea resolved following an occiput to C2 fusion. To our knowledge, this is the first reported case of atlantoaxial instability causing intractable nausea due to brain stem compression in a patient with SCI. Level of Evidence: V.

BACKGROUND The clinical utility of stem cell therapy for peripheral artery disease has not been fully discussed, and one obstacle is limited donor supplies. In this study, we attempted to rescue mouse ischemic hind limb by xenotransplantation of neonatal porcine bone marrow-derived mesenchymal stem cells (npBM-MSCs). METHODS Neonatal porcine bone marrow-derived mesenchymal stem cells were transplanted to ischemic hind limbs of male C57BL/6J mice (npBM-MSCs group). Mice with syngeneic transplantation of mouse BM-MSCs (mBM-MSCs group) were also prepared for comparison. The angiogenic effects were evaluated by recovery of blood flow on laser Doppler imaging, histologic findings, and genetic and protein levels of angiogenic factors. RESULTS Regarding laser Doppler assessments, blood flow in the hind limb was rapidly recovered in the npBM-MSCs group, compared with that in the mBM-MSCs group (P = .016). Compared with the mBM-MSCs group, the npBM-MSCs group had early and prominent lymphangiogenesis [P

The circadian clock, which regulates cellular physiology, such as energy metabolism, resides in each cell level throughout the body. Recently, it has been elucidated that the cellular circadian clock is closely linked with cellular differentiation. Moreover, the misregulation of cellular differentiation in mouse embryonic stem cells (ESCs) induced abnormally differentiated cells with impaired circadian clock oscillation, concomitant with the post-transcriptional suppression of CLOCK proteins. Here, we show that the circadian molecular oscillation is disrupted in dysdifferentiation-mediated mouse kidney tumors induced by partial in vivo reprogramming, resembling Wilms tumors. The expression of CLOCK protein was dramatically reduced in the tumor cells despite the Clock mRNA expression. We also showed that a similar loss of CLOCK was observed in human Wilms tumors, suggesting that the circadian molecular clockwork may be disrupted in dysdifferentiation-mediated embryonal tumors such as Wilms tumors, similar to the in vivo reprogramming-induced mouse kidney tumors. These results support our previous reports and may provide a novel viewpoint for understanding the pathophysiological nature of cancers through the correlation between cellular differentiation and circadian clock.

Background A high prevalence of cancers in metabolic disorders, like metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM), recently has been noted, including prostate cancer (PC), which is androgen-sensitive. However, the pathological relationship among testosterone and insulin and insulin-like growth factor (IGF)-1 signaling in relation to MetS and T2DM with PC remains unclear. Methods Papers were reviewed, including those by the authors. Results In MetS or the initial stage of T2DM accompanying insulin resistance, insulin and IGF-1 signaling could be essential for PC growth. In the advanced stage of T2DM, the decrease in insulin secretion might work against PC growth. A decrease in testosterone concentration with T2DM also might suppress PC proliferation. Androgen deprivation therapy in patients with PC might increase the risk of MetS and/or T2DM and consequently cardiovascular events. Certain drugs for T2DM treatment, such as metformin and glucagon-like peptide-1 analog, potentially might be useful for the treatment of PC. Conclusion The improvement of insulin resistance appears to be essential for the prevention of PC growth. Further studies are needed to clarify the complicated pathophysiology of metabolic disorders in PC growth.

In order to investigate the effects of composite production and the role of the counter cation for metal phosphate conductors, changes in the solid-state nuclear magnetic resonance (NMR) spectra and magnetic relaxation times caused by the removal of volatile products and water washing were examined for various metal pyrophosphate (MP2 O7 -MO2 ; M = Sn, Si, Ti, and Zr). Acidic species could be detected by 1 H MAS NMR spectra for all the composites except ZrP2 O7 -ZrO2 that had the lowest conductivity. The 31 P DD-MAS NMR spectra for MP2 O7 -MO2 composites showed different signal patterns depending on the counter cations participating in the ion exchange as a result of different microstructures. Combinational analysis of 31 P DD-MAS and 31 P CP-MAS NMR spectra of the composites indicated that protonic bulk phosphates were observed at slightly lower fields than non-protonic bulk phosphates in all of the MP2 O7 -MO2 composites. After water washing, the acidic species and the protonic bulk phosphates of MP2 O7 -MO2 composites disappeared or were reduced to trace amounts. The T1 H values of the water-washed composites lengthened because of removal of orthophosphoric acid, although the T1 P values remained almost unchanged. The results of the solid-state NMR studies suggest that the protonic bulk phosphates of MP2 O7 -MO2 composites do not generally distribute in the bulk but exist in the interface between excess H3 PO4 and the bulk. Copyright © 2016 John Wiley & Sons, Ltd.

The effects of doped low-valence cations on the properties of the SnP2O7 proton conductor at ambient temperature are investigated from changes in solid-state NMR spectra and nuclear magnetic relaxation times. Although the T1H values increased with decreasing acidity as a result of cation exchange, the 1H chemical shifts moved to lower field in Al- and In-doped materials compared with undoped ones. Furthermore, the shifts changed to higher field in Mg-doped materials, suggesting the existence of different protonic species in those materials. The bulk phosphate chemical shifts in the 31P dipolar-decoupling MAS NMR spectra were very similar, regardless of the nature and amount of the doping species. On the other hand, by 1H/31P cross-polarization MAS NMR, P2O7 signals interacting with an interstitial proton [Q1(proton)] were observed in all the undoped and doped SnP2O7, while acidic P–OH-type phosphate signals [Q1(acid)] were additionally observed in the Mg-doped conductor. The different affinity of the proton with the dopants and phosphates caused lower conductivity and larger activation energy in the Mg-doped materials, compared with those in the In- and Al-doped materials. Copyright © 2014 John Wiley & Sons, Ltd.

Background and Objective Hydrogen sulfide ( H2S ) is a volatile sulfur compound responsible for physiological halitosis. H2S was also reported as having periodontal pathologic activities. Gingival crevicular epithelium is the first barrier against periodontal pathogens and their products; oral keratinocyte stem cells OKSCs play key roles in maintaining this barrier. The p53 pathway is responsible for regulating key biological events. Increased apoptosis and cell-cycle arrest of DNA repair can affect keratinocyte stem cells, having a direct impact on the architecture of the oral epithelial tissue. However, the link between H2S , p53 activity and OKSCs has not yet been fully explored. The main objective of the present study was to explore the implications of the p53 pathway in OKSCs following exposure to H2S . Material and Methods OKSCs were isolated from human gingival epithelium and incubated with physiological levels of H2S for 24 and 48 h. Apoptosis and the mitochondrial membrane potential were detected using flow cytometry. Cytochrome c, total p53, phosphorylated p53 and caspase activity were assessed using specific ELISAs. p53 Pathway gene activity was assayed using quantitative RT-PCR. Results The levels of apoptosis were significantly increased following incubation in the presence of H2S, especially after 48 h (36.95 ± 1.91% vs. 4.77 ± 0.74%). Caspases 9 and 3 were activated, whereas caspase-8 activity remained low. Total p53 activity and particularly phosphorylated p53 at serine 46, were significantly enhanced compared with controls (47.11 ± 9.84 units/mL vs. 1.5 ± 0 units/mL and 32.22 ± 10.23 units/mL vs. 0.15 ± 0 units/mL, respectively, at 48 h). Among p53 pathway genes, apoptosis-related genes [i.e. phosphatase and tensin homolog ( PTEN ), B-cell CLL/lymphoma 2 ( BCL2), sirtuin 3 ( SIRT3) and caspases]) were dramatically increased when compared with controls. Moreover, cell-cycle progression genes [i.e. E2F transcription factor (E2F) family and histone deacetylase ( HDAC )] and DNA-repair genes [i.e. growth arrest and DNA-damage-inducible, gamma ( GADD45G ) family and serine/threonine-protein kinase Chk2 ( CHEK2)] were also increased. Conclusion Following incubation with H2S , OKSCs express multiple p53-associated genes, including programmed cell death, cell-cycle control and DNA-repair genes.

Few reports show whether a high-fat (HF) dietary environment in the fetal period affects immune function or the development of lifestyle-related disease at maturity. We examined the influence of an HF dietary environment in the fetal period on postnatal metabolic and immune function. A total of 16 pregnant mice were given control (CON) diet and 16 were given HF diet in the gestational period, from mating to delivery. After delivery lactating mice were given either CON or HF diet, resulting in four groups. After weaning, the offspring mice were given the same diet that their mothers received during lactation. HF dietary intake in the postnatal period increased fat pad weights, serum glucose, and leptin levels. An HF diet in the fetal period resulted in fewer splenic lymphocytes, a thinner thymic cortex, and impaired antigen-specific immune reactions. Furthermore, tumor necrosis factor (TNF)-alpha production and serum triglyceride levels were elevated in the fetal HF group. In addition, the HF-HF group showed a consistent decrease in ovalbumin (OVA)-specific IgG and elevation of IgE, associated with advanced fatty changes in the liver. Results from this study suggest that HF environment during the fetal period induces epigenetic propensity toward obesity and immunological burden in part due to increased adipose tissue mass, significant reduction in the number of immune cells and decreased activities of immune cells.

Background and Objective: Volatile sulfur compounds are the main cause of halitosis. Hydrogen sulfide is one of these volatile sulfur compounds and the principal malodorous compound in physiological halitosis. Periodontally pathogenic activities of hydrogen sulfide have been previously reported. Hydrogen sulfide induces apoptotic cell death in aorta smooth muscle cells and in other tissues. Apoptosis plays an important role in the onset and progress of periodontitis. The objective of this study was to determine whether hydrogen sulfide causes apoptosis in human gingival fibroblasts. Material and methods: Necrotic cells were detected using a lactate dehydrogenase assay. Apoptosis was ascertained using a histone-complexed DNA fragment assay and flow cytometry. The level of caspase 3, a key enzyme in apoptotic signaling, was also measured, and the effects of hydrogen sulfide on reactive oxygen species and superoxide dismutase were assessed. DNA damage caused by hydrogen sulfide was examined by means of single-cell gel electrophoresis. Results: After 72 h of incubation with 100 ng/mL of hydrogen sulfide, necrosis was found in less than 10% of human gingival fibroblasts, whereas apoptosis was significantly increased (p

Bone marrow stem cells develop into haematopoietic and mesenchymal lineages, but have not been known to participate in steroidogenic cell production. Steroidogenic factor 1 (SF-1), also designated adrenal 4 binding protein (Ad4BP), is an essential orphan nuclear receptor for steroidogenesis as well as for adrenal and gonadal gland development. In the present study, we revealed that the adenovirus-mediated forced expression of SF-1 can transform cultured primary long-term cultured bone marrow cells into steroidogenic cells, showing the de novo synthesis of multiple steroid hormones in response to adrenocorticotropic hormone (ACTH). This finding may provide an initial step in innovative autograft cell transfer therapy for steroid hormone deficiencies.

There is growing interest in beta-catenin and its role in various human cancers. We recently reported that 2-amino-3-methylimidazo[4,5-f]quinoline (IQ)- and 1,2-dimethylhydrazine (DMH)-induced colon tumors in the rat contain mutations in Ctnnb1, the gene for beta-catenin, but the mutation spectrum was influenced by postinitiation exposure to chlorophyllin (CHL) and indole-3-carbinol (I3C) [Blum et al., Carcinogenesis 2001;22:315-320]. The present paper describes a follow-up study in which all of the target organs for IQ- and DMH-induced tumorigenesis were screened; Ctnnb1 mutations were found in 44 of 119 DMH-induced colon tumors, six of 13 IQ-induced colon tumors, 28 of 81 DMH-induced small intestine tumors, none of five IQ-induced small intestine tumors, four of 106 IQ-induced liver tumors, none of 14 DMH-induced Zymbal's gland tumors, none of 24 IQ-induced Zymbal's gland tumors, and none of 29 IQ-induced skin tumors. In tumors from rats given carcinogen alone, or carcinogen plus CHL or I3C, Ctnnb1 mutations frequently substituted amino acids adjacent to Ser33, a critical Ser/Thr residue in the glycogen synthase kinase-3beta regulatory domain of beta-catenin. However, substitution of critical Ser/Thr residues themselves was detected in only three of 24 (12.5%) of the tumors from rats given carcinogen alone, compared with 23 of 58 (40%) of the tumors from rats given carcinogen and treated postinitiation with I3C or CHL (P < 0.02). More than 50 of the colon tumors with wild-type beta-catenin were examined further for their Apc status; the overall frequency of Apc mutations was

Whole sunflower seeds (Helianthus annuus L.) were exposed to microwaves for 6, 12, 20 or 30 min at a frequency of 2450 MHz. The hulls were then stripped from the seeds. Molecular species and fatty acid distributions of triacylglycerols (TAGs), isolated from total lipids in the hulls, were analyzed by a combination of argentation thin-layer chromatography (TLC) and gas chromatography. A modified argentation TLC procedure, developed to optimize the separation of the TAGs, provided 10 different groups of TAGs, based on both the degree of unsaturation and the total fatty acid chain-length. Dilinoleolein (29.5-30.2 wt-%), trilinolein (18.2-24.2 wt-%), dilinoleopalmitin and dilinoleostearin (17.0-18.1 wt-%), palmitoleolinolein and stearoleolinolein (11.4-14.0 wt-%) and dioleolinolein (7.5-8.6 wt-%) were the main TAGs detected after microwave roasting. However, roasting caused a significant decrease (p Des graines entieres de tournesol sont exposees a des micro-ondes pendant 6, 12, 20 ou 30 min a une frequence de 2450 MHz. Les enveloppes sont ensuite enlevees des graines. Les especes moleculaires et les distributions en acides gras des triacylglycerols, isoles a partir des lipides des enveloppes, sont analysees a la fois par chromatographie en couche mince et chromatographie gazeuse.

The present study was designed to characterize the dopamine D3 receptor agonist R(+)-7-hydroxy-N,N-di-n-propyl-2-aminotetralin (R(+)-7-OH-DPAT)-induced changes in locomotor activity in mice. Although R(+)-7-OH-DPAT (0·01–10 mg/kg) produced a significant decrease in horizontal and vertical motility within 15 min after the start of behavioural measurements, the dopamine D1 receptor antagonist R(+)-SCH23390 (0·05 mg/kg) and the dopamine D3 receptor antagonist (+)-UH232 (10 mg/kg) had no antagonistic effects on the R(+)-7-OH-DPAT (3 mg/kg)-induced hypomotility, while the dopamine D2 receptor antagonist S(−)-sulpiride (20 mg/kg) augmented it. Although R(+)-7-OH-DPAT (0·01–1 mg/kg) had no marked effects on horizontal or vertical motility, higher doses (3 and 10 mg/kg) of the drug produced a significant increase in horizontal or vertical motility from 30 to 90 min after the start of the behavioural measurements. S(−)-sulpiride (20 mg/kg) and (+)-UH232 (10 mg/kg) almost completely inhibited the R(+)-7-OH-DPAT (3 mg/kg)-induced hypermotility, whereas the antagonistic effects of R(+)-SCH23390 (0·05 mg/kg) were partial. These results suggest that the R(+)-7-OH-DPAT-induced hypermotility is mediated principally via dopamine D2 and D3 receptors, whereas it is unlikely that the hypomotility results from the activation of presynaptic dopamine D2 or D3 receptors. Copyright © 1999 John Wiley & Sons, Ltd.

1 In the present study, we examined whether deprivation of oestrogens by ovariectomy could modify learning and memory deficits caused by a continuous intracerebroventricular (i.c.v.) infusion of amyloid beta-peptide (Abeta), the major constituent of senile plaques in AD. 2 Neither long-term (3 months) nor short-term (1 month), deprivation of oestrogens by ovariectomy caused a significant impairment in spatial learning and memory in a water maze and spontaneous alternation behaviour in a Y-maze. 3 A continuous i.c.v. infusion of Abeta-(1-42) caused spatial learning and memory deficits in both ovariectomized and sham-operated rats. 4 The Abeta-induced working memory deficits were significantly potentiated in ovariectomized rats compared with sham-operated rats when mnemonic ability was examined 3 months after ovariectomy. 5 These results suggest that long-term deprivation of oestrogens induced by ovariectomy increases susceptibility to memory deficits produced by Abeta-(1-42) in rats.

Amyloid beta-peptide (A beta), the major constituent of the senile plaques in the brains of patients with Alzheimer's disease, is cytotoxic to neurons and has a central role in the pathogenesis of the disease. Previous studies have suggested that oxidative stress is involved in the mechanisms of A beta-induced neurotoxicity in vitro. In the present study, we examined whether oxidative stress contributes to learning and memory deficits caused by continuous intracerebroventricular infusion of A beta-(1-42). In the A beta-(1-42)-infused rats, spontaneous alternation behaviour in a Y-maze and spatial memory in a water maze task were significantly impaired, as compared with A beta-(40-1)-infused control rats. The retention of passive avoidance learning was also significantly impaired by treatment with A beta-(1-42). Potent antioxidants idebenone and alpha-tocopherol prevented the behavioural deficits in Y-maze and water maze, but not passive avoidance, tasks in A beta-(1-42)-infused rats when they were repeatedly administered by mouth once a day from 3 days before the start of A beta infusion to the end of behavioural experiments. Lipid peroxide levels in the hippocampus and cerebral cortex of A beta-(1-42)-infused rats did not differ from those in control animals, and neither idebenone nor alpha-tocopherol affected the lipid peroxide levels. These results suggest that treatment with antioxidants such as idebenone and alpha-tocopherol prevents learning and memory deficits caused by A beta.

A 5‐fluorouracil (5‐FU)‐resistant subline of human colon cancer HT‐29 cells was developed by repeated 1‐h exposure in vitro to 5‐FU. This subline (HT‐29/5‐FU/S) had 8‐fold resistance to 5‐FU in a 1‐h exposure assay. However, it had rather increased sensitivity to 5‐FU when assayed after a continuous 96‐h exposure to it. Significantly less 5‐fluorouridine‐5′‐triphosphate was produced in the resistant cells, leading to a lower level of 5‐FU incorporation into the cellular RNA. The reduced activity of orotate phosphoribosyltransferase might explain these results. In contrast, the HT‐29/5‐FU/S cells were more sensitive to the inhibition of in situ thymidylate synthase (TS) by 5‐FU than were the parent cells. The lower in situ TS activity may have made HT‐29/5‐FU/S cells more sensitive to TS inhibition by 5‐FU as compared with the parent cells. The fact that HT‐29/5‐FU/S was more resistant to short‐term 5‐FU exposure but more sensitive to long‐term exposure than the parent line confirmed the existence of different modes of action of 5‐FU, depending on the exposure time.

A total of 221 responses were obtained from a survey of international students in Japan, regarding the facilitative effects of social network formation on their adjustment. Regression analyses were conducted to explore the relationships among four types of adjustment revealed in a preceding study (“general adjustment,”“self-control,”“affiliative” and “dependent”), network size, demographic variables, expected social support, etc. For each adjustment type, predictive variables were identified. Two of the variables that showed network effects on adjustment were Japanese language proficiency and race (Asians vs. Westerners). From these results, it would appear that social network formation does facilitate adjustment, and insight into the effect of adjustment type and demographic variables on network functions was obtained. Furthermore, the actual conditions regarding network formation of international students in Japan were revealed.

To reveal morphological changes in bamboo constituents induced by delignification and hemicelluloses removal processes, changes in chemical composition and dynamics were examined at molecular- to nano-scales, using scanning electron microscopy images, attenuated total reflection infrared spectra, solid state nuclear magnetic resonance spectra, and relaxation time analysis at multiple hierarchical levels. Boiling removed spherical particles from the parenchymal cells of bamboo, leaving the cells containing water that had infiltrated into the nanostructure composed of carbohydrates and lignin. Treatment of the boiled bamboo with NaClO2 solution removed most of lignin, leaving hemicellulose chains that made the parenchymal cells stretch. In contrast, treatment of the boiled bamboo with NaOH solution removed both hemicellulose and lignin, with the result that parenchymal cells shrank in the cross-section direction. Furthermore, treatment of the delignified bamboo with NaOH solution demolished the parenchymal cells due to complete removal of hemicellulose and lignin. A nanostructural model proposed on the basis of molecular- to nano-scale analyses was consistent with the changes of vascular bundles and parenchymal cells. © 2013 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2014, 131, 40243.

The palladium-catalyzed regioselective allylic amination of the α-trifluoromethyl group-substituted allyl acetate has been accomplished using Pd(OAc)2/DPPE and [Pd(π-allyl)(cod)]BF4/DPPF as catalysts. The selective formation of the γ-product was attained in the presence of Pd(OAc)2/DPPE, while the α-product was obtained using [Pd(π-allyl)(cod)]BF4/DPPF. We also succeeded in the regioselective synthesis of the enantiomerically enriched aminated product from chiral allyl acetate using Pd(OAc)2/DPPE and [Pd(π-allyl)(cod)]BF4/(S)-BINAP. Furthermore, we found that kinetic resolution had occurred during the isomerization step from the γ-type product to the α-type product by the [Pd(π-allyl)(cod)]BF4/(S)-BINAP catalyst.

In a study of risk factors for coronary heart disease (CHD) in Japanese schoolchildren, serum cholesterol and triglyceride were measured in 3813 fasting schoolchildren ages 6 to 18 years, and simultaneously serum high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) were measured in a randomly selected subsample of 2579 children. Mean and standard deviations as well as the fifth, 50th and 95th percentiles for serum cholesterol, triglyceride, HDLC and LDL-C for males and females were summarized by the age groups. The percentage of serum cholesterol levels higher than 200 mg/dl and triglyceride levels higher than 140 mg/dl by sex and age were also shown. In the light of the present results, it is concluded that the serum cholesterol, triglyceride, HDL-C and LDL-C levels are suggested to be on the same level with those in the United States. Accordingly, the present results also appear to emphasize the importance of further studies on the serum lipid and lipoprotein levels in Japanese children, as they are emphasized in the Western countries with high CHD mortality rates.