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Biomedical subjects

H Ishida

Publications and source records attributed to H Ishida.

At least 379 records · Page 21Linked to original sources
PubMed1998

[The investigation of surgical procedures for post infarcted ventricular septal defects: a comparison between Daggett and David method].

Post infarcted ventricular septal perforations (VSP) has diverse clinical and pathological manifestations and the surgical results in severe cases have not yet been satisfactory. In the past we had performed the procedure of Daggett. However since 1992 we have also introduced the procedure of infarction exclusion technique proposed by David which involves plastering the ventricular cavity in a large patch without infarcted myotomy. We reported 5 cases treated with David method, 5 cases with Daggett method, and their results were compared. There were four mortality cases in Daggett method and three in David method. No significant difference was observed regarding the surgical mortality. However, there were different post-operative features between the two groups. In Daggett method patients had prolonged heart failure and LOS. In David method patients, had no severe LOS, but residual shunt were recognized in two cases. We think that the emergence of residual shunt in David method was probably due to suturing without prior removal of the damaged fragile infarcted myocardium. In Daggett method there were death cases caused by LOS and postoperative heart failure but without residual shunts. Despite its recent growing popularity for treating VSP, our experience suggests that residual shunt is an important issue remains to be solved in David method.

Aged↗
PubMed1998

[Computer-assisted education of laboratory medicine based on common disease database and electric RCPC system using Internet technology].

We are developing computer-assisted instruction systems (CAI) for efficient education of laboratory medicine. To practice evidence-based laboratory medicine and put the education along the way, we gathered a large number of clinical records and constructed a database of clinical symptoms and signs of major diseases. We also constructed a web-based RCPC system featuring interactive multimedia materials and Q/A sessions to guide the students along important points in laboratory interpretations. We have been using these systems for 5th grade medical students and evaluated the effectiveness of them for the students to obtain knowledge regarding laboratory diagnosis. Although we still have a lot of aspects to improve, students showed interests in them and used them willingly. We believe that these CAI systems contribute to raise students' ability of problem solving in laboratory medicine.

Computer-Assisted Instruction↗
PubMed1997

Cataract development induced by repeated oral dosing with FK506 (tacrolimus) in adult rats.

FK506 (tacrolimus), a potent immunosuppressant, is used for inhibiting allograft rejection in the organ transplantation field. In a preclinical toxicity study in rats, FK506 induced various toxicities, including renal and pancreatic injuries. One of these toxic findings was cataract, and we have found that cataract appeared in rats dosed orally with FK506 for 13 weeks and more. Therefore, to better elucidate the onset mechanism of FK506-induced cataract, we measured biochemical parameters, such as sorbitol, Na,K-ATPase and glutathione in the lens of rats. Rats were dosed with FK506 in oral daily doses of 0.2, 1 or 5 mg/kg for 13 weeks, the lowest dose of which approximated the expected clinical dosage. Cataract developed in the 5-mg/kg/day group, with an incidence of 25%, whereas no cataract formation was observed in the 0.2- or 1-mg/kg/day groups. Five mg/kg/day led an increase of sorbitol and a decrease of reduced type glutathione, but did not affect Na,K-ATPase activity of the lens. FK506 is known to have diabetogenicity mediated through pancreatic injury, which appears as vacuolation of islet cell in rats. Five mg/kg/day of FK506 induced an elevation of blood glucose associated with glucose intolerance, and decrease of both basal insulin level and insulin content in the pancreas, and the changes were in parallel with the cataract development in the present study. On the other hand, diabetic parameters did not change in the 0.2- or 1-mg/kg/day groups. These observation suggest that diabetes developed in the rats dosed with 5 mg/kg/day of FK506. Coadministration of a novel aldose reductase inhibitor, Zenarestat, at an oral dose of 50 mg/kg/day resulted in a reduction of incidence of the FK506-induced cataract and a decrease of sorbitol levels in the lens when compared to that in the lens of rats dosed with 5 mg/kg/day of FK506. These results suggest that FK506-induced cataract in rats is due to an accumulation of sorbitol in the lens, secondary to the diabetogenic effect of FK506. FK506 treatment at the doses of 0.2 and 1 mg/kg/day neither affected parameters indicative of diabetes nor induced cataract in rats, suggesting that the cataract would not develop with FK506 if diabetic parameters were kept under control.

Administration, Oral↗
PubMed1997

First total synthesis of ganglioside GT1a alpha.

A first total synthesis of ganglioside GT1a alpha (IV3III6II3)Neu5AcGg4Cer) is described. The suitably protected sialyl alpha-(2-->6) ganglioside was glycosylated with the phenylthioglycoside of sialic acid in the presence of N-iodosuccinimide (NIS)-trimethylsilyl trifluoromethanesulfonate (TMSOTf), followed by further glycosylation with the methyl thioglycoside promoted by dimethyl(methylthio)sulfonium triflate (DMTST), to give the heptasaccharide. The oligosaccharide obtained was converted into the title ganglioside by the introduction of ceramide and then complete deprotection.

Antigens, Surface↗
PubMed1997

Sialyl-Lewis(x) sequence 6-O-sulfated at N-acetylglucosamine rather than at galactose is the preferred ligand for L-selectin and de-N-acetylation of the sialic acid enhances the binding strength.

Oligosaccharide sequences based on sialyl-Lewis(x) with 6-O-sulfation at galactose (6'-sulfo) or at N-acetylglucosamine (6-sulfo) and expressed on high endothelial venules are considered likely endogenous ligands for the leukocyte adhesion molecule, L-selectin. In the course of high performance TLC of three hexaglycosylceramides 6'-sulfo sialyl Lewis(x), 6-sulfo sialyl Lewis(x), and 6',6-bis-sulfo sialyl Lewis(x), synthesized chemically for selectin recognition studies, two minor byproducts were detected and isolated from each parent compound. By liquid secondary ion mass spectrometry these were identified as isomers containing a de-N-acetylated sialic acid or having a modified carboxyl group. Binding experiments with the parent compounds and the non-sulfated sialyl Lewis(x) glycolipid show that 6-sulfation potentiates, whereas 6'-sulfation virtually abolishes L-selectin binding. Thus the hierarchy of binding strengths were 6-sulfo sialyl > sialyl = 6',6-bis-sulfo sialyl >> 6'-sulfo sialyl Lewis(x). Whereas modification of the sialic acid carboxyl group markedly impaired L-selectin binding, de-N-acetylation resulted in enhanced binding. The natural occurrence on high endothelial venules of this 'super-active' de-N-acetylated form of 6-sulfo sialyl Lewis(x), and related structures, now deserves investigation.

Acetylation↗
PubMed1997

The prognostic significance of p53 and bcl-2 expression in lung adenocarcinoma and its correlation with Ki-67 growth fraction.

BACKGROUND: The p53 and bcl-2 gene deregulations are frequently involved in several types of epithelial malignancy. The aims of this study were to determine the relationships between the Ki-67 labeling index (LI) and the expression of p53 and bcl-2 protein in lung adenocarcinoma and to investigate the clinicopathologic features of the tumors and the prognostic significance of p53 and bcl-2. METHODS: Immunohistochemical staining for p53, bcl-2, and Ki-67 was performed on paraffin embedded sections from 114 lung adenocarcinomas from patients who had been treated with complete and potentially curative surgery. To define a cutoff value for p53 immunopositivity, 37 of 114 tumors were examined for p53 gene mutations using cDNA sequencing. The results were compared with clinical outcomes. RESULTS: Expression of p53 protein was defined as nuclear staining in more than 20% of tumor cells, and the concordance rate between p53 expression and gene mutation was 73%. Expression of p53 (39%) was significantly associated with higher Ki-67 LI (P < 0.001) and with several poor prognostic factors, such as poor histologic grade of differentiation (P < 0.05), lymphatic permeation (P < 0.001), and vascular permeation (P < 0.001). Expression of bcl-2 (38%) was significantly associated with favorable T classification (P < 0.001) and smaller tumor size (<2 cm) (P < 0.05) and tended to be associated with lower Ki-67 LI (P = 0.054). In univariate analysis, p53 expression was significantly correlated with poor prognosis (53% vs. 90% at 5 years, P < 0.001) and bcl-2 expression with favorable prognosis (90% vs. 68% at 5 years, P < 0.05). Proliferative activity was highest when only p53 was expressed; by contrast, proliferative activity was lowest when only bcl-2 was expressed. Among four groups of patients, the group that was positive only for p53 had the shortest survival; this difference was statistically significant. Multivariate analysis showed that T classification (P = 0.002), vascular permeation (P = 0.011), and p53 expression (P = 0.03) were independent prognostic factors. CONCLUSIONS: The results of this study indicated an inverse relationship between the proliferative activity of p53 and bcl-2. Expression of p53 was an independent factor associated with poor prognosis, whereas bcl-2 expression was associated with favorable prognosis.

Adenocarcinoma↗
PubMed1997

Mechanism of beta-adrenergic agonist-induced transmural transport of glucose in rat small intestine. Regulation of phosphorylation of SGLT1 controls the function.

The perfusion of rat small intestine with 10 microM epinephrine (Epi) or 10 microM norepinephrine resulted in significant increases in the amount of 3-O-[methyl-3H]-D-glucose transported from the mucosal to serosal side. The Epi-induced increases in glucose transport were coupled with selective increases in beta-adrenoceptor density in the mucosal membranes. Treatment with 0.1 microM okadaic acid increased glucose transport even in the absence of Epi, but that with 1 microM staurosporine or 60 microM N-[2-(methylamino)ethyl]-5-isoquinoline-sulfonamide dihydrochloride completely inhibited the increases in glucose transport induced by 10 microM Epi or 10 microM dibutyryl cAMP. The maximal binding sites (Bmax) of [3H]phlorizin in brush border membrane (BBM) from tissues perfused with Epi was increased, showing increases in the binding ability of the Na+/glucose cotransporter (SGLT1) to glucose. Phosphorylation and dephosphorylation of BBM with protein kinase A (PKA) and alkaline phosphatase resulted in increases and decreases in Bmax of [3H]phlorizin, respectively. The phosphorylation state of SGLT1 immunoprecipitated from BBM incubated with [gamma-32P]ATP-Mg2+ and PKA, and the analysis of phosphoamino acids composed of SGLT1 in rats given [32P]orthophosphate indicate the presence of potential sites for PKA-mediated phosphorylation of SGLT1 at serine. These findings indicate that the regulation of phosphorylation of SGLT1 leads to an alteration of its function and results in the control of glucose transport in the rat small intestine.

Adrenergic beta-Agonists↗
PubMed1997

Suppressive effects of tranilast on the expression of inducible cyclooxygenase (COX2) in interleukin-1beta-stimulated fibroblasts.

We investigated the effects of tranilast on inducible cyclooxygenase (COX2)-mediated prostaglandin E2 (PGE2) production and enzyme induction in interleukin-lbeta (IL-1beta)-stimulated cultured dermal fibroblasts. IL-1beta enhanced PGE2 production in cultured fibroblasts. Tranilast did not affect constitutive cyclooxygenase (COX1) or COX2 activity in non-stimulated or IL-lbeta-stimulated fibroblasts. However, the COX2 expression induced by IL-1beta was inhibited by tranilast. This result, that IL-1beta-induced COX2 expression was suppressed by tranilast, was confirmed by immunohistochemical analysis. Thus, it is possible for tranilast to regulate PGE2 production by inhibiting COX2 induction.

Anti-Allergic Agents↗
PubMed1997

Gastric inhibitory polypeptide activates MAP kinase through the wortmannin-sensitive and -insensitive pathways.

The signal transduction pathways of a cloned human gastric inhibitory polypeptide (GIP) receptor have been investigated in CHO cells stably expressing this receptor. Exposure of GIP receptor expressing cells to GIP significantly increased MAP kinase activity. Time course analysis showed that a rapid and marked increase in MAP kinase activation was detected and that this activation reached maximal levels 10 min after the addition of GIP. Dose-response analysis showed that GIP activated MAP kinase activity in a dose-dependent manner with an ED50 value of 5.9 x 10(-10) M of GIP. Wortmannin, a potent inhibitor of phosphatidylinositol 3-kinase (PI3-kinase), partially inhibited GIP-induced MAP kinase activation, suggesting that GIP activates MAP kinase through two different, wortmannin-sensitive and -insensitive pathways. It has been demonstrated that in CHO cells cAMP attenuates MAP kinase activity by inhibiting Raf-1. Since GIP elevates intracellular cAMP, we examined the effects of cAMP on MAP kinase activation. Interestingly, forskolin, which increased intracellular cAMP levels, significantly inhibited MAP kinase activation by GIP, but did not affect MAP kinase activation by GIP in the presence of wortmannin, suggesting that the wortmannin-sensitive pathway activates an MAP kinase cascade at or above the level of Raf-1 and that the wortmannin-insensitive pathway activates an MAP kinase cascade below the level of Raf-1. These findings demonstrate that the GIP receptor is linked to the MAP kinase cascade via at least two different pathways.

Androstadienes↗
PubMed1997

Design and synthesis of potent antitumor 5,4'-diaminoflavone derivatives based on metabolic considerations.

Recently, we reported that 5,4'-diaminoflavone (1) exhibits potent and specific growth-inhibitory activity against the estrogen receptor (ER)-positive human breast cancer cell line MCF-7. However, when compound 1 was incubated with S-9 mix, its metabolites were observed. Moreover, addition of S-9 mix to the medium caused the drastic decrease in activity of compound 1. Since the 6-, 8-, and 3'-positions were considered to be metabolized oxidatively in vivo from MO calculations, a series of 5,4'-diaminoflavone derivatives substituted at such putative metabolic positions with various functional groups were synthesized aiming at the metabolically stable derivatives. Among them, 5,4'-diamino-6,8,3'-trifluoroflavone (14d) exhibited strong growth-inhibitory activity against MCF-7 cells even in the presence of S-9 mix. Moreover, orally administered compound 14d completely suppressed the growth of MCF-7 inoculated into nude mice, and the effect was more potent than that of compound 1. In addition to ER-positive breast cancer cells, compound 14d exhibited growth-inhibitory activity against a panel of human cancer cell lines including a part of ER-negative breast, endometrial, ovarian, and liver cancers. From these results, fluorine introduction to the putative metabolic positions of compound 1 was elucidated to be effective in the enhancement of the in vivo antitumor activity, probably due to the block of the metabolic deactivation.

Animals↗
PubMed1997

A synthetic approach to the c-series gangliosides containing sialyl-alpha(2-->8)sialyl-alpha(2-->8)sialic acid: synthesis of ganglioside GT4, alpha(2-->6) GT4 and GT3.

Trimeric sialic acid [Neu5Ac alpha(2-->8)Neu5Ac alpha(2-->8)Neu5Ac, 1] residue-containing gangliosides, GT4, alpha(2-->6)GT4 and GT3, have been synthesized for the first time. Methyl [phenyl] 5-acetamido-8-O-[5-acetamido-8-O-(5-acetamido-4, 7, 8, 9-tetra-O-acetyl-3, 5-dideoxy-D-glycero-alpha-D-galacto-2-nonulopyranosylono-1", 9'-lactone)-4,7-di-O-acetyl-3,5-dideoxy-D- glycero-alpha-D-galacto-2-nonulopyranosylono-1',9-lactone]-4,7-di- O-acetyl -3,5-dideoxy-2-thio-D- glycero-D-galacto-2-nonulopyranosid]onate (3) was prepared from 1, via lactonization, methyl esterification of the carboxyl group at the reducting end, O-acetylation and conversion of the anomeric acetoxy group into a phenylthio group. Iodonium-promoted glycosylation of 3 with 2-(trimethylsilyl)ethyl 2,6-di-O-benzyl-beta-D-galactopyranoside (5), 2-(trimethylsilyl)ethyl 3-O-benzyl-beta-D-galactopyranoside (6), 2-(trimethylsilyl)ethyl 2-O-benzoyl-3-O-benzyl-beta-D-galactopyranoside (9), and 2-(trimethylsilyl)ethyl 2, 3-di-O-benzyl-beta-D-galactopyranoside (11) gave the corresponding tetrasaccharides (13-15, 17) having the (Neu5Ac)3-Gal structure. The peracylated oligosaccharides 18 and 24 derived from 13 and 17, and the previously reported lactose derivative 29 were converted into the alpha-trichloroacetimidates 20, 26 and 31, and coupled with (2S,3R,4E)-2-azido-3-O-benzoyl-4-octadecene-1,3-diol (21) to afford the corresponding beta-glycosides 22, 27 and 32. These protected azidosphingosine derivatives were each transformed into the target gangliosides GT4, alpha(2-->6)GT4 and GT3 via selective reduction of the azido group, subsequent coupling with octadecanoic acid, O-deacylation and saponification of the methyl ester and lactone groups.

Carbohydrate Sequence↗
PubMed1997

Effects of concanavalin A on chondrocyte hypertrophy and matrix calcification.

Resting chondrocytes do not usually undergo differentiation to the hypertrophic stage and calcification. However, incubating these cells with concanavalin A resulted in 10-100-fold increases in alkaline phosphatase activity, binding of 1,25(OH)2-vitamin D3, type X collagen synthesis, 45Ca incorporation into insoluble material, and calcium content. On the other hand, other lectins tested (including wheat germ agglutinin, lentil lectin, pea lectin, phytohemagglutinin-L, and phytohemagglutinin-E) marginally affected alkaline phosphatase activity, although they activate lymphocytes. Methylmannoside reversed the effect of concanavalin A on alkaline phosphatase within 48 h. Concanavalin A did not increase alkaline phosphatase activity in articular chondrocyte cultures. In resting chondrocyte cultures, succinyl concanavalin A was as potent as concanavalin A in increasing alkaline phosphatase activity, the incorporation of [35S]sulfate, D-[3H]glucosamine, and [3H]serine into proteoglycans, and the incorporation of [3H]serine into protein, although concanavalin A, but not succinyl concanavalin A, induced a rapid change in the shape of the cells from flat to spherical. These findings suggest that concanavalin A induces a switch from the resting, to the growth-plate stage, and that this action of concanavalin A is not secondary to changes in the cytoskeleton. Chondrocytes exposed to concanavalin A may be useful as a novel model of endochondral bone formation.

Alkaline Phosphatase↗
PubMed1997

Characterization of a cartilage-derived 66-kDa protein (RGD-CAP/beta ig-h3) that binds to collagen.

A 66-kDa collagen fiber-associated protein (RGD-CAP) was isolated from a fiber-rich fraction of pig cartilage by ultrafiltration and collagen-affinity chromatography. Amino acid sequencing and cDNA cloning indicated that the RGD-CAP is identical or closely related to beta ig-h3 protein which is induced in human adenocarcinoma cells by transforming growth factor-beta (TGF-beta) (Skonier, J., Neubauer, M., Madisen, L., Bennett, K., Plowman, G.D., and Purchio, A.F. (1992) DNA Cell. Biol. 11, 511-522). The RGD-CAP, as well as beta ig-h3, has the RGD sequence in the C-terminal region. The native RGD-CAP bound to type I, II, and IV collagens even in the presence of 1 M NaCl. A recombinant preparation of RGD-CAP expressed in Escherichia coli cells also bound to collagen but not to gelatin. The RGD-CAP mRNA was expressed in chondrocytes throughout all stages, although the expression level was highest during the prehypertrophic stage. In addition, TGF-beta increased the RGD-CAP mRNA level in chondrocyte cultures. Since RGD-CAP transcripts were found in most tissues, this novel collagen-binding protein may play an important role in cell-collagen interactions in various tissues including developing cartilage.

Amino Acid Sequence↗
PubMed1997

Sulfated sialyl Lewis X, the putative L-selectin ligand, detected on endothelial cells of high endothelial venules by a distinct set of anti-sialyl Lewis X antibodies.

Endothelial cells of high endothelial venules (HEV) in human peripheral lymph nodes expressed a distinct type of sialyl Lewis X antigen, which was detected preferentially with a set of anti-sialyl Lewis X antibodies, 2F3, 2H5 and HECA-452 in immunohistochemistry, while another set of anti-sialyl Lewis X antibodies, FH-6 and CSLEX-1, failed to detect it. The adhesion of cells expressing L-selectin to HEV was inhibited by members of the former set of antibodies in Stamper-Woodruff assays performed on frozen sections of human peripheral lymph nodes. Transfection of a cultured endothelial cell line with a human alpha1-->3 fucosyltransferase, Fuc-T VII, resulted in the expression of a distinct type of sialyl Lewis X antigen having the reactivity similar to that of HEV; i.e., the antigen appearing on the transfectant clone was detectable only with the set of 2F3, 2H5 and HECA-452, but not with the set of FH-6 and CSLEX-1. Treatment of transfectant cells with sodium chlorate, a metabolic inhibitor of sulfation, resulted in reactivity to the members of the latter set of antibodies, suggesting that sulfation of sialyl Lewis X moiety was the cause of the discrepancy in the reactivity of the anti-sialyl Lewis X antibodies. When tested against various authentic sulfated sialyl Lewis X determinants, 6-sulfo sialyl Lewis X and 6,6'-bis-sulfo sialyl Lewis X were found to be reactive to the antibodies, 2F3, 2H5 and HECA-452, but not with antibodies FH-6 and CSLEX-1, suggesting that the distinct type of sialyl Lewis X determinant on the HEV endothelial cells and Fuc-T VII-transfected endothelial cell clone are mainly 6-sulfo and/or 6,6'-bis-sulfo sialyl Lewis X determinants.

Animals↗
PubMed1997

Angiotensin II inhibits protein kinase A-dependent chloride conductance in heart via pertussis toxin-sensitive G proteins.

BACKGROUND: Angiotensin II receptors are reported to be abundant in the guinea pig ventricle; their coupling to adenylate cyclase in the heart, however, remains controversial. Therefore, we investigated the effect of angiotensin II on Cl- conductance activated by cAMP-dependent protein kinase. METHODS AND RESULTS: After minimizing the contribution of other ionic currents, exposure of single guinea pig ventricular cells to isoproterenol (40 to 50 nmol/L; 36 degrees C) elicited a typical protein kinase A-dependent Cl- conductance. Subsequent application of angiotensin II reduced the isoproterenol-induced conductance with an IC50 of 0.24 +/- 0.08 nmol/L. Angiotensin II also inhibited the Cl- currents, which were activated through stimulation of adenylate cyclase by forskolin and histamine receptors. CV-11974 (1 mumol/L), an antagonist selective for the angiotensin type 1 receptor, prevented the effect of angiotensin II. Angiotensin II did not inhibit the current that had been persistently activated by intracellular GTP gamma S (100 mumol/L), a nonhydrolyzable guanine nucleotide, plus isoproterenol. In addition, prior incubation of myocytes with pertussis toxin prevented the angiotensin II inhibitory action. Cl- conductance, when activated directly by intracellular dialysis with cAMP (1 mmol/L), was not affected by angiotensin II. Radioimmunologic measurement of cellular cAMP in the dissociated myocytes showed that angiotensin II inhibited the isoproterenol-induced increase of cAMP. CONCLUSIONS: Angiotensin II receptors negatively couple to adenylate cyclase via pertussis toxin-sensitive G proteins, thereby inhibiting cardiac protein kinase A-dependent Cl- conductance.

Adenylate Cyclase Toxin↗
PubMed1997

Prevention of adenocarcinoma colon 26-induced cachexia by interleukin 10 gene transfer.

A s.c. injection of a mouse colon adenocarcinoma cell line, colon 26 clone 20, induced cachexia, as evidenced by progressive weight loss and severe hypoglycemia. Several lines of evidence indicate that a pro-inflammatory cytokine, interleukin 6 (IL-6), plays a major role, albeit partially, in the establishment of cachexia in this model. Because IL-10 can potentially inhibit the production of pro-inflammatory cytokines including IL-6, we evaluated the effects of IL-10 gene transfer on the establishment of cachexia. IL-6 transcript was detected at tumor sites of mice inoculated with parental or control vector transfectant cells, and serum IL-6 levels were markedly increased in these mice. The injection of parental cells into IL-6-deficient mice induced cachexia with elevated serum IL-6 levels comparable to wild-type mice, indicating that tumor cells are a major source of IL-6. The inoculation of IL-10-transfectant cells kept IL-10 mRNA expression at tumor sites and induced the elevation in serum IL-10 levels without affecting the growth rates of colon 26 cells both in vitro and in vivo. However, the implantation with IL-10-transfectant cells reduced the expression of IL-6 mRNA at the tumor sites and the elevation in serum IL-6 levels. Concomitantly, mice inoculated with IL-10-transfectant cells did not exhibit progressive weight loss, a reduction in food intake, or severe hypoglycemia, which was observed in mice inoculated with parental or control vector-transfectant cells. Collectively, these results suggest that IL-10 gene transfer prevented the occurrence of cachexia with a concomitant inhibition of IL-6 production at the tumor sites.

Animals↗
PubMed1997

Cranial variation in prehistoric human skeletal remains from the Marianas.

Nonmetric cranial variation and facial flatness of the Pacific and circum-Pacific populations are investigated. The peoples of the Marianas, eastern Polynesia and Hawaii form a cluster and show affinities in terms of nonmetric cranial variation with the Southeast and East Asians rather than with the Jomon-Ainu, a view which is widely supported by others. Facial flatness analysis also indicates that Polynesians have different patterns of facial prominence as compared with the Jomon-Ainu. These results increase the difficulty of accepting the Jomon-Pacific cluster proposed by Brace and his coworkers. Although genetic and nonmetric cranial variation reveal relatively close relationships, the Mariana skeletons are markedly different in facial flatness and limb bone morphology from those of Polynesians.

Anthropology, Physical↗