Cephalometric study of elderly with nearly intact dental arches

Objective: The purpose of this study was to investigate the craniofacial morphology of elderly people with many remaining teeth using cephalometric analysis. Subjects and methods: The subjects were 30 Japanese elderly who participated in the ‘8020 campaign 2001’ in Bunkyo Ward, Tokyo, organised by The Dental Association of Tokyo, as well as 30 Japanese young adults with normal occlusion. Lateral cephalograms of all subjects were analysed using the Coben method. Results: In the female elderly group, the lower face depth was smaller than in the younger adults. In the male elderly group, the height and depth of both the total face and the lower face were longer than in the younger group. In comparing the 8020 achievers with the younger group, the proportion of the lower facial height was greater than the upper facial height, and this finding was more pronounced in women than in men. Conclusion: For the lateral facial pattern of the elderly, a reduction of lower facial height because of tooth occlusal reduction was not apparent. It was clear that there are age differences for males and females; in addition, differences in the total face and lower face area of the elderly group were due to their having many remaining teeth over a long time period. Also, these changes were more apparent in women than in men, and it is clear that there is a male–female difference in ageing.     

Relationship of cariogenic bacteria levels with periodontal status and root surface caries in elderly Japanese

Objective: The relationship of the levels of cariogenic bacterial species with periodontal status and decayed root surfaces was investigated in elderly Japanese subjects. Methods: Three hundred and sixty‐eight individuals (each 75 years old) were examined for periodontal status (pocket depth, attachment loss), root surface caries and salivary levels of mutans streptococci (MS) and lactobacilli (LB). Results: Values >4 mm of attachment loss (rAL4) and for average attachment loss (aAL) of sites measured were significantly higher in subjects with LB than those without. Multiple regression analysis also showed a correlation between aAL and rAL4 values with the presence of LB (aAL p = 0.003; rAL4 p = 0.002). Further, multiple regression analysis of interacting factors regarding decayed root surfaces showed that LB carriers had a greater incidence of decayed root surface caries (p = 0.003), while MS and LB levels were correlated to the number of decayed root surfaces (LB p = 0.010; MS p = 0.026). Conclusion: Our results indicate that considerable attachment loss elevates the possibility of having LB, thus increasing the risk of root surface caries. It was also found that LB and MS measurements may be useful indicators of decayed root surfaces in elderly individuals with attachment loss.     

The distribution of myofibroblasts and CD34-positive stromal cells in normal renal pelvis and ureter and their cancers

In this article, we examined the distribution of myofibroblasts and CD34-positive stromal cells in normal renal pelvis and ureter and their cancers using immunohistochemistry. Eighteen tumors and normal tissues apart from the main tumor were examined. In the wall of normal renal pelvis and ureter, no myofibroblasts were observed through all layers, but CD34-positive stromal cells were observed in the deep area of lamina propria, muscular layer and adventitia. In the stroma of renal pelvic and ureteral cancers, myofibroblasts were distributed in fifteen tumors and were absent in three tumors. All three tumors containing no myofibroblasts in the stroma were non-invasive type and all invasive cancers contained myofibroblasts in the stroma. CD34-positive stromal cells were consistently absent in the stroma of cancers, irrespective of the invasiveness. Finally, myofibroblasts are major stromal components in renal pelvic and ureteral cancers, particularly in invasive cancers, and CD34-positive stromal cells are consistently absent or lost in the stroma of their cancers. These findings suggest that the invasion of renal pelvic and ureteral cancers may cause the phenotypic change of stromal cells.     

Bloom helicase and DNA topoisomerase IIIalpha are involved in the dissolution of sister chromatids

Bloom's syndrome (BS) is an autosomal disorder characterized by predisposition to a wide variety of cancers. The gene product whose mutation leads to BS is the RecQ family helicase BLM, which forms a complex with DNA topoisomerase IIIalpha (Top3alpha). However, the physiological relevance of the interaction between BLM and Top3alpha within the cell remains unclear. We show here that Top3alpha depletion causes accumulation of cells in G2 phase, enlargement of nuclei, and chromosome gaps and breaks that occur at the same position in sister chromatids. The transition from metaphase to anaphase is also inhibited. All of these phenomena except cell lethality are suppressed by BLM gene disruption. Taken together with the biochemical properties of BLM and Top3alpha, these data indicate that BLM and Top3alpha execute the dissolution of sister chromatids.     

Dynamics of RhoA and ROKα translocation in single living cells

The RhoA-binding kinase (ROK) is one of the target kinases of RhoA and is known to play a critical role in regulating cytoskeletal rearrangement in cells. ROK translocates to the plasma membrane fraction; however, the mechanism of the translocation of ROK still remains obscure. To clarify the molecular mechanisms of the translocation of ROK, we co-transfected MDCK cells wity cyan fluorescent protein-tagged RhoA and yellow fluorescent protein-tagged ROKα, or their variants, and monitored the localization and translocation of the two different fluorescent tagged-molecules in single living cells during epithelial growth factor (EGF) stimulation. Both RhoA (wild-type) and ROKα (wild-type) translocated to ruffling membrane with EGF stimulation in several minutes. A ROKα mutant, in which Rho-binding ability is disrupted, is unable to translocate to the membrane with RhoA. However, RhoA mutant Q63L/C190R, an active form lacking membrane localization activity, abolished the translocation of wild-type ROKα, suggesting that the translocation of RhoA is critical for ROK translocation to the membrane. Another mutant lacking the pleckstrin homology domain failed in translocation as well. On the other hand, it was surprising that the kinase dead mutant succeeded in translocation to the membrane after EGF stimulation. Based on these results, we propose the following ROKα translocation mechanism. ROKα binds to RhoA in cytosol and translocates to the membrane based on the membrane-targeting ability of active RhoA. After ROKα associates with the membrane, the pleckstrin homology domain provides the stability of ROKα on the membrane. The activation of enzymatic activity or adenosine triphosphate binding, however, is not directly related to the translocation mechanism, although we found that the membrane association is critical for the activation of the kinase activity.     

Attenuation of mouse acute colitis by naked hepatocyte growth factor gene transfer into the liver

BACKGROUND: Hepatocyte growth factor (HGF) has multiple biological effects on a wide variety of cells. It modulates intestinal epithelial proliferation and migration, and critically regulates intestinal wound healing. AIMS: To investigate the therapeutic effect of HGF gene transfer, we introduced the HGF gene into the liver of mice with acute colitis. METHODS: The rat HGF expression plasmid vector, pCAGGS-HGF, was injected via the tail vein into C57BL/6 mice, followed by dosing with dextran sulfate sodium in distilled water. Firstly, the HGF gene was injected once on day 0. Secondly, the HGF gene was injected on day 0 and again on day 2. RESULTS: Injection of the HGF gene ameliorated colitis with inhibition of both loss of body weight and shortening of colon length. It protected the colon from epithelial erosions and cellular infiltration. Expression of mRNAs for IFN-gamma, IL18, and TNF-alpha was reduced in the colon. In contrast, expression of mRNA for IL-10 was increased. The numbers of BrdU-positive intestinal epithelial cells were increased, and the numbers of TUNEL-positive apoptotic cells were decreased. Furthermore, a second injection prolonged the elevation of serum HGF levels, and ameliorated the symptoms better than a single injection. The empty pCAGGS plasmid did not ameliorate acute colitis. CONCLUSIONS: HGF gene transfer attenuated acute colitis by facilitating intestinal wound repair as well as inhibiting inflammation, suggesting a new strategy for treatment of IBD.     

Synthesis of 3,6-bis[H-Tyr/H-Dmt-NH(CH2)m,n]-2(1H)pyrazinone derivatives: function of alkyl chain length on opioid activity

Dimeric opioid analogues linked to a pyrazinone platform, 3-[Tyr/Dmt-NH(CH2)m]-6-[Tyr/Dmt-NH(CH2)n]-2(1H)-pyrazinone (m, n=3 or 4), were synthesized. The Tyr-containing compound (m=4, n=3) exhibited mu-receptor affinity (K(i)mu; 7.58 nM) comparable to that of morphine, while the Dmt derivatives exhibited considerably higher affinity (K(i)mu; 0.021-0.051 nM) with corresponding agonism (IC50=1.79-4.93 nM). Interestingly one compound (m=4, n=3) revealed modest delta-opioid agonism; the converse analogue (m=3, n=4), however, was inactive in MVD assay.     

Generation of Mercury-Hyperaccumulating Plants through Transgenic Expression of the Bacterial Mercury Membrane Transport Protein MerC

The merC gene from Acidithiobacillus ferrooxidans functions as a mercury uptake pump. MerC protein localizes in the cytoplasmic membrane of plant cells. When Arabidopsis thaliana and tobacco plants were transformed with the merC gene under the control of the Cauliflower mosaic virus 35S promoter, the resulting overexpression of merC rendered the host plants hypersensitive to Hg²⁺ and they accumulated approximately twice as much Hg²⁺ ion as the wild type plants. Thus, bacterial mercuric ion transporters such as MerC may be useful molecular tools for producing transgenic plants that hyperaccumulate Hg²⁺ ion.     

Identification of mouse palmitoyl-coenzyme A Delta9-desaturase

Stearoyl-coenzyme A desaturase (SCD) catalyzes the desaturation of saturated fatty acids to monounsaturated fatty acids in mammalian cells. Currently, there are four known enzymatic isoforms (SCD1-SCD4) in the mouse genome. The physiological roles for multiple SCD isoforms and their substrate specificities are unknown at present. We report here distinct substrate specificities for the mouse SCD isoforms. Each SCD isoform was able to complement the ole1 mutation in Saccharomyces cerevisiae through heterologous expression of transgenic SCD. Fatty acid analysis showed that mouse SCD1, SCD2, and SCD4 desaturate both C18:0 and C16:0, whereas mouse SCD3 uses C16:0 but not C18:0. We identify SCD3 as a mammalian palmitotyl-CoA Delta9-desaturase, and its existence in mouse helps explain distinct physiological roles for each SCD isoform.