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Psychological palmar sweating is a phenomenon that occurs with emotional changes such as anxiety, fear, and anger. To identify the psychological anxiety and stress experienced by children visiting a dental office, we measured the amount of psychological palmar sweating using a sudorometer and obtained the following results. 1. Amount of sweating in dental office The amount of sweating was largest in both boys and girls when they were guided to the dental chair, followed by the period during tooth brushing and turbine sound. The least sweating occurred while they were in the waiting room. In boys, significant differences in sweating were seen between the times spent in the waiting room and when guided to the chair, and between the times when they were guided to the chair and taught tooth brushing. In girls, significant differences were seen between the times spent in the waiting room and when guided to the chair, between the times when guided to the chair and taught tooth brushing, and between being guided to the chair and turbine sound. 2. Amount of sweating by gender In the dental office, the amount of sweating was larger in girls than in boys during all times: while in the waiting room, when guided to the chair, during tooth brushing and turbine sound. However, no significant differences were seen between boys and girls. The method presented in our study maybe very useful to quantitatively understand the psychological state of children in dental offices who may be unable to express their own feelings well.

The objective of the study was to examine changes in palate section area, palate projection area and palate volume according to age. Using the maxillary dentition models, the palates of 10-, 12- and 14-year old children, who were in the early permanent dentition period, were measured threedimensionally using the semiconductor laser. Palate section areas between canines, the first premolars, second premolars and first molars became greater as children aged because the palate enlarged vertically with the growth and development of the maxilla. The palate projection area became greater as children aged because the palate enlarged laterally with the growth and development of the maxilla. The palate volume became greater as children aged because the palate enlarged laterally and vertically.

The objective of the study was to make three dimensional measurements of the maxillary palate of 3- and 4-year old children who have developed anterior cross bite of deciduous dentition using a semiconductor laser. The effects of anterior cross bite were examined on the interdentition section area, the intradentition projection area, and the palate volume. Compared with normal occlusion, anterior cross bite of deciduous dentition caused smaller interdentition section areas at the deciduous canines and the primary first molars, and greater interdentition section areas at the primary second molars and between the posterior margins of the primary second molars. The intradentition projection area at the anterior dentition was smaller in anterior cross bite than in normal occlusion. The intradentition projection area at the posterior dentition in anterior cross bite was nearly the same as that in normal occlusion. The anterior palate volume was smaller and the posterior palate volume was greater in anterior cross bite than in normal occlusion. The above results suggest that anterior cross bite in deciduous dentition suppresses anterior growth and accelerates posterior growth of the maxillary palate.

Inflammation in dental pulp tissue is associated with tissue degradation, and matrix metalloproteinases (MMPs) are believed to participate in this destruction. Elevated levels of some MMPs have been reported in inflamed pulp and periapical lesions. Moreover, in inflamed pulp, many kinds of inflammatory cytokines such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α, are released from inflammatory cells like macrophages, lymphocytes and neutrophils. In the present study, we examined whether TNF-α affected the production of MMP-2 in deciduous dental pulp fibroblasts and its signaling pathways utilizing gelatin zymography and western blotting analysis. TNF-α increased the expression of MMP-2 in a dose-dependent manner in deciduous dental pulp fibroblasts. LY294002 and Wortmannin, which are PI3-K (phosphoinositide 3-kinase) inhibitors, inhibited the MMP-2 production induced by TNF-α in deciduous dental pulp fibroblasts. Moreover, in deciduous dental pulp fibroblasts cultured with TNF-α, AKT (protein kinase B) was phosphorylated in a time-dependent manner with the maximum phosphorylation at 30 min, and LY294002 and Wortmannin abolished this phosphorylation of AKT in TNF-α-stimulated deciduous dental pulp fibroblasts. These results suggest that TNF-α may enhance pulp tissue destruction during pulp inflammation in part by regulating MMP-2, and that the AKT pathway is involved in MMP-2 production in deciduous dental pulp fibroblasts.

The aim of the study was to measure three-dimensionally using the semiconductor laser to examine changes in palate section areas, palate projection areas and palate volumes for 5-year olds children with maxillary protrusion of primary dental arch induced by finger sucking. Because of pressure by fingers on the palate, the palate section areas between deciduous canines and between primary first molars in finger sucking children were greater than those in children with normal occlusion. The palate projection area in the anterior segment of the arch in finger sucking children was greater than that in normal occlusion children. The anterior palate volume in finger sucking children was greater than that in normal occlusion children. However, because of anterior traction of the palate by fingers in finger sucking, the palate section area between the posterior margin of the primary second molars in finger sucking children was smaller than that in normal occlusion children. The palate projection area between posterior segment of the arch in finger sucking children was smaller than that in normal occlusion children. The posterior palate volume in finger sucking children was smaller than that in normal occlusion children.

Dental pulp plays an important role in tooth vitality. Previous studies have indicated that stem cells can be isolated from dental pulp, and dental pulp exfoliated from deciduous teeth has become a useful alternative for dental tissue engineering because of its higher proliferation rate. In the present study, we analyzed the differences in gene expressions between human dental pulps exfoliated from deciduous and permanent teeth by DNA microarray assays. A scatter plot of mRNA levels based on fluorescent signals in human dental pulps from deciduous and permanent teeth indicated a dispersed distribution pattern. In a scatter plot of the genes, 2,573 genes were expressed at >2-fold higher levels in dental pulp from deciduous teeth, compared with permanent teeth. To confirm the microarray results, insulin-like growth factorbinding protein 5 (IGFBP5) and vascular endothelial growth factor A (VEGFA) showing higher mRNA expression levels were selected and analyzed for their mRNA levels by RT-PCR. Both the IGFBP5 and VEGFA mRNA levels were upregulated by about 3-fold in dental pulp from deciduous teeth compared with permanent teeth. Thus, the RT-PCR results for these genes were consistent with the microarray data. The dental pulps in deciduous and permanent teeth differ significantly with regard to their developmental processes, tissue structures and functions. The present findings using DNA microarray analyses to detect differences in the gene expressions of deciduous and permanent teeth may be useful for dental pulp tissue engineering.

The objective of the study was to examine changes in palate sectional areas, palate projection areas and palate volumes according to age. Using the maxillary dentition models, the palates of 7-, 8- and 9-year-old children, who were in the mixed dentition period, were measured threedimensionally using the semiconductor laser. The palate section areas, particularly between deciduous canines, primary first molars, primary second molars and first molars, increased with age, as the palate expanded vertically along with the growth and development of the maxilla. The palate projection areas increased with age, as the palate expanded laterally along with the growth and development of the maxilla. The palate volume increased with age, as the palate expanded laterally and vertically.

Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. Namely, macrophages are the main cells that secrete anti-inflammatory cytokines, such as IL-10. IL-10 is an important suppressive cytokine, produced by many kinds of immune cells, which plays a key role in the anti-inflammatory immune responses. Adenosine mediates many of its effects through one or more of four receptors, the adenosine A1, A2A, A2B, and A3 receptors, and it has been shown that A2A adenosine receptor (A2AR) is a critical part of the physiological negative feedback mechanism for limitation and termination of tissue-specific and systemic inflammatory responses. Mac-1 is an adhesion molecule required for apoptosis induced by other cell surface receptors, and is expressed on the surface of macrophages. Mac-1 expression is also necessary for the termination of an inflammatory reaction. To demonstrate how adenosine has its affects on macrophages to control inflammation, we evaluated the effects of adenosine in the RAW264 and THP-1 macrophage cell lines. Adenosine did not affect the proliferation in RAW264 cells regardless of the concentration. On the other hand, adenosine increased IL-10 production in RAW264 cells. Moreover, adenosine markedly increased the expression of CD11b, which is a Mac-1 alpha integrin. These results indicate that adenosine may affect the anti-inflammatory reactions in macrophages by enhancing the production of IL-10, and influence apoptosis by expression of CD11b.

The change in the secretory immunoglobulin A (sIgA) level in saliva has received remarkable attention in recent years as an index of mental stress. Here, we examined its utility for assessing the stress caused by dental treatment. To achieve this, we measured salivary sIgA levels in children before and after dental treatment, and assessed their levels of stress by analyzing the change in salivary sIgA following treatment. Overall, 83% of the subjects showed a decrease in their salivary sIgA after treatment. Furthermore, the overall level of sIgA decreased significantly following dental treatment (p

We sent questionnaires to all the members (4,298 people) about the specialist pediatric dentistry system in Japan (Hereafter, termed specialists). The survey (1,129 dentists answered the questionnaire) revealed the following: 1.About 29% of the members who have qualifications for pediatric dentists, authorized by Japanese Society of Pediatric Dentistry (JSPD), hoped for a specialist qualification immediately. 2.Eighty point six percent of the members who do not have qualifications authorizing them as pediatric dentists answered that they wanted to take an examination to become a specialist as soon as they were qualified to take it. 3.Many members hoped that the examination to become a specialist would be strictly carried out. 4.Twenty-two point eight percent members thought that the qualifications for pediatric dentists authorized by Japanese Society of Pediatric Dentistry should be abolished after putting the specialist system into effect. 5.Fourteen percent of those that have the qualification of pediatric dentists, authorized by Japanese Society of Pediatric Dentistry, did not want to acquire the specialist title but they wanted to renew their current qualifications. 6.As dentists got older, the ratio of children patients (under 18 years old) tended to decrease. 7.However, about one-quarter, 112 members (about 10% of all) of dentists who are 50–69 years old (347 members) it occupied 34.7% of all treated exceeded 90% children patients.

The in vitro differentiation potential of rat dental pulp-derived cells into an osteoblastic lineage was examined. Induction was carried out under in vitro osteogenesis-inducing conditions used for mesenchymal stem cells from human bone marrow. We previously reported that the level of mineralization was high at 6 weeks after induction, as determined by von Kossa staining. In the present study, we quantitatively measured the alkaline phosphatase (ALP) activity after induction. The ratios of ALP-positive cells to total cells were 44.4 ± 1.0, 46.9 ± 0.9, 40.5 ± 0.5 and 21.0 ± 1.8% at 1, 2, 3 and 6 weeks after induction, respectively. The level of ALP activity was significantly decreased at 6 weeks after induction (p < 0.05). The stem cell markers STRO-1, SSEA-1, Nanog and Oct-3/4 were expressed in a subset of the cells, suggesting that stem cells were present. To elucidate gene regulation in the osteoblastic lineage of the cells, quantitative gene expression analyses were carried out using real-time RT-PCR. Col1a2 (collagen type I) and Bglap (osteocalcin) were up-regulated by about 1.7-fold and 1.3-fold, respectively, at 6 weeks after induction compared with their corresponding levels at 1 week. These results indicate that the cells differentiated into an osteoblastic lineage in parallel with decreasing ALP activity during induction. Moreover, the expressions of Col1a2 and Bglap were inversely correlated with Alpl (ALP) expression after induction, which was correlated with Bmp2 (bone morphogenetic protein 2) expression. Taken together, the findings indicate that these molecules contribute to the differentiation of rat dental pulp-derived cells into an osteoblastic lineage.

15-Deoxy-Δ 12,14 -prostaglandin J 2 (15dPGJ 2 ), which is a ligand for peroxisome proliferatoractivated receptor γ (PPARγ), induced apoptosis of several human tumors including gastric, lung, colon, prostate and breast. However, the role of PPARγ signals in other types of cancer cells such as leukemia, except solid cancer cells, is still unclear. The aim of this study was to evaluate the ability of 15dPGJ 2 on the proliferation of the human T cell leukemia cell line MOLT-4F. 15dPGJ 2 at 5 μM stimulated proliferation in MOLT-4F at 1 to 3 days after incubation. In contrast, 15dPGJ 2 at concentrations of above 10 μM inhibited proliferation. PGD 2 , PGJ 2 and Δ 12 -PGJ 2 (APGJ 2 ), which are precursors of 15dPGJ 2 , had similarly proliferative effects, whereas they showed anti-proliferatioe effects at high concentrations. Both SB203580, a p38 mitogen-activated protein kinase (MAPK) inhibitor, and LY294002, a phosphoinositide 3-kinase (PI3K) inhibitor, prevented proliferation accelerated by 15dPGJ 2 and its three precursors in MOLT-4F. In contrast, PD98059, an extracellular signal-related kinase 1/2 inhibitor, did not affect proliferation accelerated by 15dPGJ 2 and its three precursors. Immunoblotting analysis revealed that PGD 2 at 5 μM, PGJ 2 at 5 μM, APGJ 2 at 1 μM and 15dPGJ 2 at 5 μM potentiated the expression of cyclin A, without affecting the expression of Cdk inhibitors including p18, p21, and p27 in MOLT-4F. These results suggest that PGD 2 , PGJ 2 , ΔPGJ2 and 15dPGJ 2 may, through the activation of p38 MAPK and/or PI3K, potentiate the expression of cyclin A, leading to acceleration of proliferation in MOLT-4F.

Adenosine and ATP have been implicated in the regulation of inflammatory responses. Furthermore, adenosine and ATP affect cell growth, cell differentiation, and apoptosis. The aim of this study was to evaluate the differentiation-inducing effects of adenosine and ATP on human monocytic leukemia U937 cells. Adenosine at 10 -3 M markedly induced differentiation in leukemia U937 cells as assessed by evaluating the expression of CD11b. Similarly, ATP at 10 -4 and 10 -3 M significantly induced differentiation in U937 cells. Simultaneously, adenosine at 10 -3 M and ATP at 10 -4 and 10 -3 M significantly inhibited the cell number in U937 cells. Next, we evaluated the effects of adenosine and ATP on U937 cells differentiated by differentiation inducers all-trans retinoic acid (ATRA), 1,25-dihydroxy-vitamin D 3 , (VD 3 ) and phorbol. 12-myristate 13-acetate (PMA). Interestingly, adenosine at 10 -4 and 10 -3 M significantly potentiated ATRAinduced CD11b expression. However, ATRA failed to affect adenosine at 10 -3 M-induced CD11b expression. Similarly, ATP at 10 -4 and 10 -3 M significantly potentiated ATRA-induced CD11b expression. In addition, ATRA potentiated ATP-induced CD11b expression. In contrast, VD 3 and PMA further increased the expression of CD11b in the presence of adenosine or ATP, respectively. These results suggest that adenosine and ATP may induce differentiation in human leukemia U937 cells, and may further increase ATRAinduced differentiation in U937 cells.

15-Deoxy-Δ12,14-prostaglandin J2 (15dPGJ2), which is a ligand for peroxisome proliferator-activated receptor γ (PPARγ), induced apoptosis of several human tumors including gastric, lung, colon, prostate, and breast. However, the role of PPARγ signals in other types of cancer cells (e.g., leukemia) except solid cancer cells is still unclear. The aim of this study is to evaluate the ability of 15dPGJ2 to modify the proliferation of the human leukemia cell line THP-1. 15dPGJ2 at 5 μM stimulated the proliferation in THP-1 at 24 to 72 h after incubation. In contrast, 15dPGJ2 at concentrations above 10 μM inhibited the proliferation through the induction of apoptosis. PGD2, PGJ2, and Δ12-PGJ2 (ΔPGJ2), precursors of 15dPGJ2, had similar proliferative effects at lower concentrations, whereas they induced apoptosis at high concentrations. 15dPGJ2 and three precursors failed to induce the differentiation in THP-1 as assessed by using the differentiation marker CD11b. FACScan analysis revealed that PGD2 at 5 μM, PGJ2 at 1 μM, ΔPGJ2 at 1 μM and 15dPGJ2 at 5 μM all accelerated cell cycle progression in THP-1. Immunoblotting analysis revealed that PGD2 at 5 μM and 15dPGJ2 at 5 μM inhibited the expression of phospho-p38, phospho-MKK3/MKK6, and phospho-ATF-2, and the expression of Cdk inhibitors including p18, p21, and p27 in THP-1. In contrast, PGJ2 at 1 μM and ΔPGJ2 at 1 μM did not affect their expressions. These results suggest that 15dPGJ2 and PGD2 may, through inactivation of the p38 mitogen-activated protein kinase pathway, inhibit the expression of Cdk inhibitors, leading to acceleration of the THP-1 proliferation. Keywords:: THP-1, proliferation, 15-deoxy-Δ12,14-prostaglandin J2, prostaglandin D2, p38

Peroxisome proliferator-activated receptor γ (PPARγ) is expressed in several human tumors including gastric, lung, colon, prostate and breast. However, the role of PPARγ signals in leukemia is still unclear. The aim of this study is to evaluate the ability of 15-deoxy-Δ12,14-prostaglandin J2 (15dPGJ2), that is a ligand for PPARγ, on proliferation of human leukemia cell line U937. 15dPGJ2 at 5 µmol/l stimulated the proliferation. In contrast, 15dPGJ2 at concentrations of >10 µmol/l inhibited the proliferation through the induction of apoptosis. PGD2, PGJ2 and Δ12-PGJ2 (ΔPGJ2), those are precursors of 15dPGJ2, had similarly proliferative effects, whereas they showed antiproliferative effects at high concentrations. FACScan analysis revealed that PGD2 at 5 µmol/l, PGJ2 at 1 µmol/l, ΔPGJ2 at 1 µmol/l and 15dPGJ2 at 5 µmol/l, all accelerated cell cycle progression. Immunoblotting analysis revealed that PGD2 at 5 µmol/l and 15dPGJ2 at 5 µmol/l inhibited the expression of phospho-p38, phospho-MKK3/MKK6 and phospho-ATF-2, and the expression of Cdk inhibitors including p18, p27. In contrast, PGJ2 at 1 µmol/l and ΔPGJ2 at 1 µmol/l did not affect the expression of them. These results suggest that 15dPGJ2 and PGD2 may, through inactivation of the p38 MAPK pathway, inhibit the expression of Cdk inhibitors, leading to acceleration of proliferation.

Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During an infection, lipopolysaccharide (LPS) stimulates macrophages to produce proinflammatory cytokines. Recently, it has been shown that A 2 a adenosine receptor (A 2 aR) is a critical part of the physiological negative feedback mechanism for the limitation and termination of tissue-specific and systemic inflammatory responses. It was useful and meaningful to gain information about interaction between LPS, which generates the inflammation, and adenosine receptors, which terminate the inflammation. However, very little, if anything, is known about the effect of bacterial LPS on the expression of A 2 aR during an infection of bacteria. The aim of this study is to evaluate the effects of adenosine, ATP and LPS on the expression of A 2 aR and toll-like receptor 4 (TLR 4), which is a receptor for LPS, in the mouse macrophage cell line RAW 264. Adenosine and ATP failed to affect proliferation in RAW 264 cells, whereas LPS increased proliferation. Adenosine significantly potentiated the expression of TLR 4, but not of A 2 aR. ATP and LPS markedly potentiated the expression of A 2 aR and TLR 4, respectively. Moreover, adenosine and ATP did not affect the expression of A 2 aR and TLR 4 in the presence of LPS, respectively. This study revealed that adenosine, ATP and LPS affect the expression of A 2 aR and TLR 4 in macrophages.

Prostaglandin D2 (PGD2) acts via the adenyl cyclase-coupled receptor for PGD2 (DP receptor). Here we present evidence that BW245C, a DP receptor agonist, modulates macrophage functions related to natunal immunity. BW245C inhibited macrophage chemotaxis at concentrations of 0.1 to 10μM and phagocytosis of Escherichia coli by macrophages at a concentration of 10μM. In addition, BW245C inhibited the production of superoxide anions by PMA-stimulated macrophages at concentrations of 0.1 to 10μM and nitrite production by LPS-stimulated macrophages at a concentration of 10μM. In contrast, BW245C potentiated the production of TNF-α, a pro-inflammatory cytokine, by LPS-stimulated macrophages at concentrations of 1 to 10μM. These results suggest that PGD2 may modulate macrophage functions related to natural immunity via the DP receptor.

De novo protein synthesis in eukaryotes is mainly controlled at the level of gene transcription by transcription factors in the nucleus. In this communication, the expression and nuclear localization of the Rel/NF-κB family member p65 in nuclear and cytosolic fractions of the brain and retina from streptozotocin (STZ) -injected diabetic rats were determined in order to evaluate the possibility that the transportation of Rel/NF-κB family members from the cytoplasm to the nucleus could play a role in diabetes. Immunoblotting assays with a specific antibody revealed a much higher expression of immunoreactive p65 in nuclear fractions than in cytosolic fractions of the cerebral cortex, hippocampus, midbrain and cerebellum after diabetes induction by STZ administration. In contrast, STZ administration suppressed the p65 nuclear localization detected in the striatum, hypothalamus, medulla-pons and retina. These results suggest that STZ-inlected diabetic rats show differential alterations in the nuclear localization of p65 protein in the brain and retina.

Lipopolysaccharides (LPS) of Porphyromonas gingivalis have been implicated in the initiation and development of periodontal diseases. In a previous study, we investigated the signal transduction pathway of P. gingivalis and demonstrated that LPS stimulates the production of interleukin (IL)-6 in human gingival fibroblasts (HGFs), which in turn activates osteoclasts in vitro. The cytokine, IL-10, was initially described as cytokine synthesis inhibitory factor. In this study, we examined that effect of IL-10 on P. gingivalis LPS-induced human gingival fibroblast production of IL-6. LPS-induced IL-6 production was inhibited by IL-10 in a dose-dependent manner. Flow cytometric analysis showed that HGFs bind to fluorescein-isothiocyanate (FITC) labeled IL-10. Western blotting analysis demonstrated the expression of IL-10 receptor on the cell surface of these cells. Engagement of LPS initiated the protein tyrosine phosphorylation of several intracellular proteins including extracellular signal-regulated kinase 2 (ERK2), and these events were suppressed by IL-10. These results suggest that IL-10 inhibits the inflammatory response via the IL-10 receptor in P. gingivalis LPS-initiated periodontal diseases.

Proteases produced by Porphyromonas gingivalis are believed to contribute to the pathogenesis of periodontal diseases. Here the cytotoxic effects of a purified preparation of a P. gingivalis protease with trypsin-like specificity were tested on human gingival fibroblasts in vitro. The active protease induced apoptotic cell death in the fibroblasts, as indicated by DNA fragmentation and the expression of 7A6 antigen. Thus, the production of proteases by periodontopathic bacteria could be an important factor in the induction of apoptosis of host cells in the aetiology of periodontal diseases.

We purified and characterized a protease from Actinobacillus actinomycetemcomitans. The protease was isolated from the culture supernatant by sonication in phosphate-buffered 3-[(3 cholamidopropyl)dimethylammonio]-1-propanesulfonate (CHAPS). The protease was purified by acetone precipitation, followed by column chromatography with Arginine Sepharose 4B, DEAE Sepharose CL-6B, Sephacryl S-200HR and HiTrap Q. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the purified protease showed a clear band at approximately 50 kDa. The protease showed trypsin-like activity with hydrolytic activity for the synthetic substrates N alpha-benzoyl-DL-arginine p-nitroanilide (BApNA) and N alpha benzoyl-DL-lysine p-nitroanilide (BLpNA). The activity of the protease was stable at pH 7.0 to approximately 8.0. The activity of the protease was inhibited by leupeptin, phenylmethylsulfonyl fluoride (PMSF), and EDTA, but was not affected by dithiothreitol (DTT), cysteine, 2-mercaptoethanol, pepstatin or soybean trypsin inhibitor. These data suggest that this protease is a serine protease or metallo protease. This enzyme extensively degraded collagen type I and fibronectin.

We examined the relationship between collagen crosslinking techniques and dentinum reinforcement. In the present study, the tensile tests, imbibition test and antienzyme test were performed on collagen films mainly composed of type I collagen after ultraviolet irradiation and immersion in tannic acid and glutaraldehyde. The elastic modulus increased with the reaction time, but reduction of elongation at breaking point and increased stiffness were observed. This tendency was enhanced by ultraviolet irradiation. Tannic acid treatment resulted in slower crosslinking than the other two techniques. Antienzyme activity was markedly increased by treatment with tannic acid and glutaraldehyde.

Our previous study reported that an osteopontin-derived peptide SVVYGLR activates the adhesion, migration and tube formation abilities of endothelial cells in vitro. The present study investigated angiogenesis due to synthetic SVVYGLR and mutant peptides in vivo. Mutant peptides (n = 7) were synthesized by substituting alanine (A) for one of the 7 amino acids comprising SVVYGLR. In dorsal air sac assay, mouse dorsal skin 5 days after implantation of a chamber filled with SVVYGLR had approximately the same number of newly formed blood vessels to that filled with vascular endothelial growth factor (VEGF). The ability of angiogenesis due to SVVAGLR was significantly lower than that due to other 6 mutant peptides and SVVYGLR. This indicates that tyrosine (Y) plays an important role in angiogenesis due to SVVYGLR.

Peroxisome proliferator-activated receptor gamma (PPARgamma) is expressed in several human tumors including gastric, lung, colon, prostate and breast. However, the role of PPARgamma signals in leukemia is still unclear. The aim of this study is to evaluate the ability of 15-deoxy-Delta12,14-prostaglandin J2 (15dPGJ2), that is a ligand for PPARgamma, on proliferation of human leukemia cell line U937. 15dPGJ2 at 5 micromol/l stimulated the proliferation. In contrast, 15dPGJ2 at concentrations of10 micromol/l inhibited the proliferation through the induction of apoptosis. PGD2, PGJ2 and Delta12-PGJ2 (DeltaPGJ2), those are precursors of 15dPGJ2, had similarly proliferative effects, whereas they showed antiproliferative effects at high concentrations. FACScan analysis revealed that PGD2 at 5 micromol/l, PGJ2 at 1 micromol/l, DeltaPGJ2 at 1 micromol/l and 15dPGJ2 at 5 micromol/l, all accelerated cell cycle progression. Immunoblotting analysis revealed that PGD2 at 5 micromol/l and 15dPGJ2 at 5 micromol/l inhibited the expression of phospho-p38, phospho-MKK3/MKK6 and phospho-ATF-2, and the expression of Cdk inhibitors including p18, p27. In contrast, PGJ2 at 1 micromol/l and DeltaPGJ2 at 1 micromol/l did not affect the expression of them. These results suggest that 15dPGJ2 and PGD2 may, through inactivation of the p38 MAPK pathway, inhibit the expression of Cdk inhibitors, leading to acceleration of proliferation.

Herein, we suggest that Streptococcus mutans lipoteichoic acid-induced death of dental pulp cells on human deciduous teeth is caused by apoptosis. We provide evidence for the causal role of apoptosis in this process by demonstrating an increase in the proportion of fragmented DNA in such dental pulp cells, which results in a ladder pattern of DNA fragmentation. Additionally, Streptococcus mutans lipoteichoic acid-induced apoptotic cell death is suppressed by caspase inhibitor. Collectively, these findings suggest that Streptococcus mutans lipoteichoic acids may cause apoptosis in human dental pulp cells, and serve as an important factor in pulpitis.

Wistar strain rats fed low calcium diets (1, 2, 3,4, 6 and 8 weeks) exhibited changes in secretory function of whole saliva. In particular, there were changes in salivary flow rate, total salivary protein, amylase enzyme activity, salivary amylase content and the level of cyclic AMP in the parotid gland acinar cell. Although there were no changes for the first 3 weeks, the levels increased at week 4 and decreased at week 6. The wet weight of the parotid gland started to decrease at week 4. These results suggest that when fed low calcium diets for long periods of time, rats develop defective salivary secretion.