Associations between dietary n-6 and n-3 fatty acids and arachidonic acid compositions in plasma and erythrocytes in young and elderly Japanese volunteers

<p>Abstract</p> <p>Background</p> <p>We reported that the compositions of arachidonic acid (ARA) in erythrocytes and plasma phospholipids (PL) in the elderly were lower than those in the young, though the ARA intake was nearly identical.</p> <p>Objective</p> <p>We further analyzed data in four study groups with different ages and sexes, and determined that the blood ARA levels were affected by the kinds of dietary fatty acids ingested.</p> <p>Methods</p> <p>One hundred and four healthy young and elderly volunteers were recruited. Dietary records together with photographic records from 28 consecutive days were reviewed and the fatty acid composition in plasma lipid fractions and erythrocyte PL was analyzed.</p> <p>Results</p> <p>No correlations for ARA between dietary fatty acids and blood lipid fractions were observed. A significant negative correlation between eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) intake and ARA composition in erythrocyte PL was observed. ARA composition in erythrocyte PL was significantly lower in elderly subjects than in young subjects, because EPA and DHA intake in elderly subjects was higher than in young subjects. However, after removing the effect of dietary EPA+DHA intake, the ARA composition in erythrocyte PL in elderly subjects was significantly lower than that in young subjects.</p> <p>Conclusions</p> <p>Changes in physical conditions with aging influenced the low ARA composition of erythrocyte in elderly subjects in addition to the effects of dietary EPA and DHA.</p

Increased Risk of Temporomandibular Joint Closed Lock: A Case-Control Study of ANKH Polymorphisms

Objectives: This study aimed to carry out a histological examination of the temporomandibular joint (TMJ) in ank mutant mice and to identify polymorphisms of the human ANKH gene in order to establish the relationship between the type of temporomandibular disorders (TMD) and ANKH polymorphisms.\ud \ud Materials and Methods: Specimens from the TMJ of ank mutant and wild-type mice were inspected with a haematoxylin and eosin staining method. A sample of 55 TMD patients were selected. Each was examined with standard clinical procedures and genotyping techniques.\ud \ud Results: The major histological finding in ank mutant mice was joint space narrowing. Within TMD patients, closed lock was more prevalent among ANKH-OR homozygotes (p = 0.011, OR = 7.7, 95% CI 1.6–36.5) and the elder (p = 0.005, OR = 2.4, 95% CI 1.3–4.3).\ud \ud Conclusions: Fibrous ankylosis was identified in the TMJ of ank mutant mice. In the human sample, ANKH-OR polymorphism was found to be a genetic marker associated with TMJ closed lock. Future investigations correlating genetic polymorphism to TMD are indicated

Id2 acts downstream of BMP signaling in chondrogenesis

Objectives: This study aimed to conduct a case-control investigation in maxilofacial morphogenesis, using a sample of Id2 homozygous knockout (KO) and wild-type (WT) mice. A special interest was to establish a relationship among Id2, BMP signals and chondrogenesis.\ud \ud Materials and Methods: Appropriate ethics approval has been received. Crania collected from mice at the age of 0 day, 2 weeks and 12 weeks were assessed with a Euclidean Distance Matrix Analysis method. Cultured synchondroses of the murine cranial base were inspected with a histological approach and examined with a reverse transcription polymerase chain reaction technique.\ud \ud Results: A shorter nasofrontal profile was seen in Id2 KO 12-week-olds but not 0-day-olds. The WT-KO gap in the skull length instead of the width increased with age. KO 2-week-olds showed a narrower hypertrophic zone and an inhibited proliferative zone in the presphenoid and the spheno-occipital synchondroses. Id2 expression in WT synchondroses was identified. Distribution of Type X collagen other than osteopontin was downregulated in Id2 KO samples. The WT murine cranial base showed a wider hypertrophic zone, a higher degree of ectopic hypertrophy and a larger number of proliferative chondrocytes in the presence of exogenous BMP2, BMP4 and BMP7, respectively. Such acquired growth was not detected in KO subjects. A 5-fold upregulation of Smad7 transcripts and a decrease in phosphorylation of Smad1-Smad5-and-Smad8-positive cells were identified in Id2 KO cartilage.\ud \ud Conclusions: Postnatal chondrogenesis was related to Id2 that acted downstream to enhance BMP signals by inhibiting Smad7 expression

ANKH polymorphisms and clicking of the temporomandibular joint in dental residents

Aim\ud \ud This study aimed to carry out a case-control research study to assess occurrence of clicking of the temporomandibular joint (TMJ) in order to establish the relationship between TMJ clicking and the genotype of "ANKH inorganic pyrophosphate transport regulator" (ANKH) polymorphisms.\ud \ud Materials and Method\ud \ud A sample of 41 first-year dental residents was selected. Each was examined using standard\ud clinical procedures and genotyping techniques.\ud \ud Results\ud \ud The participation rate was 91.8 %. The prevalence of TMJ clicking was 51.2 % (95 % CI:\ud 35.7–66.7 %). Occurrence of TMJ clicking was not related to age, gender and genotypes of ANKH-OR as well as ANKH-TR polymorphisms (p ≥ 0.165).\ud \ud Conclusion\ud \ud A similar distribution of ANKH genotypes in TMJ clicking and asymptomatic individuals has been\ud demonstrated by this study. A high percentage of TMJ clicking has been confirmed. Future investigations are indicated

Application of anti-BMP antibodies to immunohistochemical examination of fibrous dysplasia

Objective: Fibrous dysplasia of bone (FD) is a benign developmental disorder of bone in which normal bone is replaced by fibrous tissue, containing trabeculae of immature woven bone. This disease has been classified into three types: monostotic (MFD), polyostotic (PFD), and McCune–Albright syndrome (MAS). Occurring in multiple adjacent craniofacial bones (craniofacial FD) is considered to be an MFD lesion. Surgical reduction is performed for form revision after having observed the progress until adulthood, but postoperative recurrence cases are not rare, there is a report of malignant progression to osteosarcoma, and the clinical phenotypes are generally various. This study aimed to identify the relationship between clinical futures of FD and expression of bone morphogenetic protein (BMP) subtypes.\ud \ud Methods: We studied 10 cases (9 MFD cases and 1 McCune–Albright syndrome case) diagnosed with fibrous dysplasia in our hospital, and immunohistochemical examinations of the excised sample from each case with anti-BMP-2, 4, 6, and 7 antibodies were performed.\ud \ud Results: 5 MFD cases and 1 MAS case underwent reoperation, and the case that had the most number of operations was 9 times in the MFD case. Malignant transformations were not identified. BMP-4, 6, and 7 expressions were positive in all cases, but the expression of BMP-2 was positive only in 6 MFD cases. BMP-2 negative cases tended to undergo reoperation.\ud \ud Conclusions: The variable expression of BMP-2 demonstrated in the current study was suggested to be a useful indication for clinical activity and convalescence of the lesions

TM2D3, a mammalian homologue of Drosophila neurogenic gene product Almondex, regulates surface presentation of Notch receptors

Abstract Notch signaling is an evolutionarily conserved mechanism required for numerous types of cell fate decisions in metazoans. It mediates short-range communication between cells with receptors and ligands, both of which are expressed on the cell surfaces. In response to the ligand-receptor interaction, the ligand and the extracellular domain of the Notch receptor (NECD) in the complex are internalized into ligand-expressing cells by endocytosis, a prerequisite process for the conformational change of the membrane proximal region of Notch to induce critical proteolytic cleavages for its activation. Here we report that overexpression of transmembrane 2 (TM2) domain containing 3 (TM2D3), a mammalian homologue of Drosophila melanogaster Almondex (Amx), activates Notch1. This activation requires the ligand-binding domain in Notch1 and the C-terminal region containing TM2 domain in TM2D3. TM2D3 physically associates with Notch1 at the region distinct from the ligand-binding domain and enhances expression of Notch1 on the cell surface. Furthermore, cell surface expression of Notch1 and Notch2 is reduced in Tm2d3-deficient cells. Finally, amx-deficient Drosophila early embryos exhibit impaired endocytosis of NECD and Delta ligand, for which surface presentation of Notch is required. These results indicate that TM2D3 is an element involved in Notch signaling through the surface presentation

Id2 controls chondrogenesis acting downstream of BMP signaling during maxillary morphogenesis

Maxillofacial dysmorphogenesis is found in 5% of the population. To begin to understand the mechanisms required for maxillofacial morphogenesis, we employed the inhibitors of the differentiation 2 (Id2) knock-out mouse model, in which Id proteins, members of the regulator of basic helix-loop-helix (bHLH) transcription factors, modulate cell proliferation, apoptosis, and differentiation. We now report that spatially-restricted growth defects are localized at the skull base of Id2 KO mice. Curiously, at birth, neither the mutant Id2 KO nor wild-type (WT) mice differed, based upon cephalometric and histological analyses of cranial base synchondroses. In postnatal week 2, a narrower hypertrophic zone and an inhibited proliferative zone in presphenoid synchondrosis (PSS) and spheno-occipital synchondrosis (SOS) with maxillary hypoplasia were identified in the Id2 mutant mice. Complementary studies revealed that exogenous bone morphogenetic proteins (BMPs) enhanced cartilage growth, matrix deposition, and chondrocyte proliferation in the WT but not in the mutant model. Id2-deficient chondrocytes expressed more Smad7 transcripts. Based on our results, we assert that Id2 plays an essential role, acting downstream of BMP signaling, to regulate cartilage formation at the postnatal stage by enhancing BMP signals through inhibiting Smad7 expression. As a consequence, abnormal endochondral ossification was observed in cranial base synchondroses during the postnatal growth period, resulting in the clinical phenotype of maxillofacial dysmorphogenesis