Whitening Efficacy of Chewing Gum Containing Sodium Metaphosphate on Coffee Stain: Placebo-controlled, Double-blind In Situ Examination.

This study aimed to evaluate the ability of chewing gum containing sodium metaphosphate (SMP) to remove coffee stains from enamel in situ. This was a double-blind (subjects, evaluators), parallel-group, crossover, randomized clinical trial with 30 healthy adult volunteers. Each participant held an appliance with a hydroxyapatite (HA) pellet on the lower lingual side of his or her mouth for two hours to allow pellicle formation. The appliances were subsequently immersed in coffee solution at 37°C for 48 hours. The color of the HA pellet before and after coffee immersion was measured using a spectrophotometer. The participant set the appliance and chewed two pieces of test gum, which contained 7.5 mg of SMP per piece, or control gum without SMP. Each cycle included five minutes of exposure to chewing gum, after which the appliances were placed in 100% relative humidity at room temperature for a 30-minute incubation. This cycle was repeated five times for each gum type. The color of the HA pellet was measured after each chewing cycle using the spectrophotometer. In addition, ΔE* values, which indicate the change in pellet color after each chewing cycle compared with after coffee immersion, were calculated. Data were analyzed using the paired t-test with Bonferroni adjustment to compare ΔE* values of control and test gum after each chewing cycle. The ΔE* values of test gum were significantly higher than those of control gum after all chewing cycles, excluding the first cycle (p<0.05). This finding indicates that test gum containing SMP was more effective at removing coffee stains from the HA pellet than control gum. We conclude that chewing gum containing SMP can effectively remove coffee stains from HA pellets. Thus, SMP is a promising agent to be further explored in tooth-cleaning studies.

Bond strength of simplified-step adhesives to enamel prepared with two different diamond burs.

BACKGROUND: Self-etching primers are reported to produce considerable etching on flat enamel surfaces. However, little is known about the influence of different enamel surface textures. In this study the influence of grinding enamel on bond strength of two all-in-one and one two-step adhesives was investigated. METHODS: Resin composite was bonded to the ground enamel of extracted human third molars that was reduced 0.5 mm from the buccal or lingual surfaces using either regular- or superfine-grit diamond burs with each of the three adhesives. After 24 hours in 37 degrees C water, the specimens were sectioned into slabs of 0.7 mm thickness, trimmed to an hourglass configuration, and subjected to microtensile bond strength (MTBS) testing. RESULTS: For all adhesive systems, MTBS to enamel ground with a regular-grit diamond bur was not significantly different from that with a superfine-grit diamond bur. The etching patterns of these adhesives were partly varied according to the aggressiveness of the adhesives. CONCLUSION: The use of two different burs does not affect the tensile bond strength of the adhesives to enamel.

Expression of cyclooxygenase-2 in human hyperplastic gastric polyps.

Cyclooxygenase (COX)-2, an inducible isoform of prostaglandin synthetase, has been reported to be a key molecular target of colon cancer prevention by nonsteroidal anti-inflammatory drugs. Recently, it has been shown that Helicobacter pylori (H. pylori) could induce COX-2 together with inflammatory cytokines. Although human hyperplastic gastric polyps disappeared or decreased in number and size after eradication of H. pylori, the mechanisms in this step, especially the roles of COX-2, have not been yet elucidated. The aims of the present study were to examine the expression and localization of COX-2 in human hyperplastic gastric polyps immunohistochemically. Twelve specimens of human hyperplastic gastric polyps were obtained from endoscopic polypectomy. The expression of the COX-2 protein was immunohistochemically examined on formalin-fixed and paraffin-embedded tissue sections using an anti-COX-2 antibody and an avidin-biotin complex method. Cells expressing COX-2 were further immunohistochemically identified using a specific antibody against macrophages (CD68), and myofibroblasts (alpha-smooth muscle actin). Immunoreactive COX-2 was predominantly and strongly expressed in interstitial cells in the sub-epithelial layer of 10 hyperplastic polyps. Semi-quantitative analysis revealed a significant increase in COX-2 expression in interstitial cells. The staining pattern of macrophages and myofibroblasts partly corresponded to that observed for COX-2 in hyperplastic gastric polyps. These results suggest that COX-2 in mesenchymal cells induced by H. pylori may play an important role in the tumorigenesis of human hyperplastic gastric polyps.

Effect of rebamipide on prostaglandin receptors-mediated increase of inflammatory cytokine production by macrophages.

BACKGROUND: Rebamipide (Reb) is an anti-ulcer drug, and has unique properties such as anti-inflammatory action. We previously reported that prostaglandins (PGs) dramatically increased vascular endothelial growth factor (VEGF), a known angiogenic factor and a vascular permeable factor, by activated macrophages through specific PGE receptor and peroxisome proliferator-activated receptor gamma (PPARgamma, a nuclear receptor of PG) mediated process. Effects of PGs on the production of other cytokines such as interleukin (IL)-6 and IL-8 have been controversial. AIM: To clarify the anti-inflammatory roles of Reb, we examined the effect of Reb on PGE1- and 15-deoxy-Delta12, 14-PGJ2 (a potent PPARgamma ligand, 15d-PGJ2) -induced increase of VEGF production by macrophages. Additionally, effects of these PGs on the production of IL-6 and IL-8, and modulation of these actions by Reb were studied. METHODS: Phorbol 12-myristate 13-acetate-differentiated U937 cells were used as a human macrophage model (H-Mac). VEGF, IL-6, IL-8 and cAMP were measured by EIA. RESULTS: Reb suppressed PGE1-, but not 15d-PGJ2-, induced increase of VEGF production partially through decrease of cAMP formation. Reb suppressed PGE1 -, but not 15d-PGJ2-, induced increase of IL-6 and IL-8 production. CONCLUSION: Reb suppresses membrane, but not nuclear PG receptors mediated increase of inflammatory cytokine production, which may be involved in anti-ulcer action of this drug.

Review article: COX-2, prostanoids and colon cancer.

Epidemiological, experimental, and clinical studies have demonstrated that colon carcinogenesis may be prevented by nonsteroidal anti-inflammatory drugs (NSAIDs). Although controversy remains, recent studies, including ours, have revealed that NSAIDs suppress colon carcinogenesis at the adenoma stage where cyclooxygenase-2 (COX-2), a major molecular target in this action, is mainly expressed in interstitial cells but not in tumour cells. Therefore, it is unlikely that NSAIDs prevent colon cancer formation through modulating the functions of tumour cells. A more possible assumption is that NSAIDs suppress colon carcinogenesis through the inhibition of prostaglandin formation. However, the mechanisms by which prostanoids promote colon carcinogenesis have not been elucidated to date. A prostanoids act through both membrane receptors and nuclear receptors such as peroxisome proliferator receptor (PPAR) gamma or delta, one focus in this area is to investigate their roles in colon carcinogenesis, including the induction of growth factors.

Severe liver injury with hematological disorders following the injection of non-ionic contrast medium. A case report.

We describe a dramatic case of severe liver injury and hematological disorders following the injection of non-ionic contrast medium in a 49-year-old woman with endometrial cancer. This case developed into a fulminant hepatitis-like picture that required repeated plasmapheresis and hemodialysis.

Pro- and anti-apoptotic members of the Bcl-2 family in skeletal muscle: a distinct role for Bcl-2 in later stages of myogenesis.

Apoptotic myonuclei appear during myogenesis and in diseased muscles. To investigate cell death regulation in skeletal muscle, we examined how members of the Bcl-2 family of apoptosis regulators are expressed and function in the C2C12 muscle cell line and in primary muscle cells at different stages of development. Both anti-apoptotic (Bcl-W, Bcl-X(L)) and pro-apoptotic (Bad, Bak, Bax) members of the Bcl-2 family were expressed in developing skeletal muscle in vivo. Each was also expressed in embryonic (E11-12), fetal (E15-16), and neonatal muscle stem cells, myoblasts, and myotubes in vitro. In contrast, Bcl-2 expression was limited to a small group of mononucleate, desmin-positive, myogenin-negative muscle cells that were seen in fetal and neonatal, but not embryonic, muscle cell cultures. The cell surface protein Sca-1, which is associated with muscle and blood stem cells, was found on approximately 1/2 of these Bcl-2-positive cells. Loss of Bcl-2 did not affect expression of other family members, because neonatal muscles of wild-type and Bcl-2-null mice had similar amounts of Bcl-X(L), Bcl-W, Bad, Bak, and Bax mRNAs. Loss of Bcl-2 did have functional consequences; however, because neonatal muscles of Bcl-2-null mice had only approximately 2/3 as many fast muscle fibers as muscles in wild-type mice. Thus, Bcl-2 function is required for particular stages of fetal and postnatal myogenesis.

Effect of prostaglandin E1 on vascular endothelial growth factor production by human macrophages and colon cancer cells.

We previously demonstrated that cyclooxygenase-2 (COX-2) was predominantly expressed in macrophages of sporadic human colonic adenomas; however, the role of COX-2-expressing cells during colon carcinogenesis has not yet been elucidated. In the present study, we showed the effect of PGE, on vascular endothelial growth factor (VEGF) production by PMA-differentiated U937 cells, a human macrophage model (H-Mac), and by human colon cancer cells T84. PGE1 dramatically induced VEGF production by H-Mac, but not that by T84. PGE1 significantly increased intracellular cAMP formation by H-Mac, but only modestly increased that by T84. 8-bromo-cAMP and cholera toxin also increased VEGF production by H-Mac. In contrast, neither of these agents modulated VEGF production by T84. EP2 and EP4 (PGE specific receptors) mRNA was expressed in both cells. PG dramatically increased VEGF production by activated macrophages, but not by cancer cells, through a specific PGE receptor-mediated process. These findings suggest that PGs produced by COX-2-expressing macrophages induce VEGF production by macrophages, but not by cancer cells, in an autocrine fashion.

Prostaglandins up-regulate vascular endothelial growth factor production through distinct pathways in differentiated U937 cells.

We previously reported that cyclooxygenase (COX)-2 was predominantly expressed in macrophages of human colonic adenomas (Int. J. Cancer 83, 470-475.). The role of prostaglandins (PGs) produced by COX-2-expressing macrophages in colon carcinogenesis is still unclear. Here we show that PGs up-regulate vascular endothelial growth factor (VEGF) production by activated macrophages through their specific receptors. mRNAs of both PGE-specific receptors and peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear receptor superfamily of ligand-dependent transcription factors, were expressed in phorbol 12-myristate 13-acetate-differentiated U937, a human macrophage model (H-Mac). Prostaglandin E(1) (PGE(1)) and 15-deoxy-Delta(12,14)-PGJ(2) (a potent PPARgamma ligand, 15d-PGJ(2)) dramatically increased VEGF production. The combination of PGE(1) and 15d-PGJ(2) additively increased VEGF production. In addition, PGE(1) significantly increased cAMP formation, whereas 15d-PGJ(2) did not affect cAMP formation. The effect of the combination of PGE(1) and 15d-PGJ(2) on cAMP formation was similar to that of PGE(1) alone. Unexpectedly, 15d-PGJ(2) also drastically increased IL-1beta production, an indicator of macrophage activation, although PGE(1) only mildly increased it. Additional enhancement of IL-1beta production was observed in the combination of PGE(1) and 15d-PGJ(2). These results suggest that PGs dramatically increased VEGF production by activated macrophages through specific PGE receptor and PPARgamma-mediated processes and that PGs may thereby promote tumor growth through VEGF production.

Microwave coagulation therapy: ex vivo comparison of MR imaging and histopathology.

We compared the findings of magnetic resonance (MR) images and pathological examination to determine whether or not MR images reflect pathological changes following microwave coagulation therapy (MCT) on liver tissue. We used microwave (generating frequency 2450 Mhz, wave length 12 cm, output 50 W, 60 second duration) to irradiate six canine livers under general anesthesia. After the animals were sacrificed, the livers were resected. The irradiated regions were cut with margins and divided into two pieces, one for MR study, and the other for pathological examination. The findings were compared. From the center to the marginal layer, the irradiated region presented 4/3 laminal patterns on T1/T2-weighted images: low/high, high/low, very high/high, and iso-low/high intensity. On gradient-echo imaging, the irradiated regions presented no decreasing signals using several echo time lengths. With hematoxylin and eosin stain, MR laminar patterns reflected the histopathological changes, as follows: a tissue loss area surrounding the inserted needle, low/high; decreased sinusoidal width with/without necrotic tissue, high/low; sinusoidal width dilation at the periphery, very high/high; and fatty degenerated tissue surrounding the irradiated area at the boundary of the normal hepatocytes, iso-low/high. The MR signal intensity, which reflected the histopathological changes, presented tissue characterization after MCT, and the macromolecular hydration effect influenced the high intensity on T1-weighted images.

Microtensile bond strength to dentin and cavity adaptation of Cerec 2 inlay restoration.

PURPOSE: To examine the bond strength of Cerec 2 inlays both to dentin surface by microtensile testing and to cavity walls by cavity adaptation in Class II restorations, using three luting materials. MATERIAL AND METHODS: VitaMark II disc was bonded to the coronal dentin surface with Clapearl DC (Clearfil DC)/Linerbond IIsigma (Linerbond 2V), AP-X/Linerbond IIsigma or Fluorocement (Panavia F)/ED Primer. After 24-hr storage in water, microtensile bond strengths (MTB) were measured. Additionally, Cerec inlays were luted to the MO cavities prepared in molars with the same materials. After thermocycling (x2000), the restorations were sectioned mesio-distally. Gap formation was microscopically examined along the cavity walls. RESULTS: There was no significant difference in MTB among the materials (Clapearl DC: 20.89 +/- 4.58 MPa, AP-X: 24.22 +/- 5.97 MPa, Fluorocement: 19.82 +/- 6.43 MPa, Scheffé, P > 0.05). The frequency of gap formation was higher in AP-X than in Clapearl DC and Fluorocement (chi2-test, P < 0.05). Debonding occurred more often at the luting material/dentin interface than at the inlay/luting material interface (Sign test, P < 0.05).

The role of laparoscopic US and laparoscopic US-guided aspiration biopsy in the diagnosis of multicentric hepatocellular carcinoma.

BACKGROUND: Detection of small hepatocellular carcinomas has become possible with improvements in various diagnostic imaging techniques. However, intraoperative US can detect lesions not visualized by any preoperative imaging study in which case it is difficult to determine whether the lesion is a hepatocellular carcinoma. METHODS: Nodular lesions detected by laparoscopic US in 186 patients with hepatocellular carcinoma were examined and we evaluated the diagnostic ability of laparoscopic US to detect multicentric hepatocellular carcinoma. RESULTS: One hundred thirty-four new nodular lesions were detected by laparoscopic US in 64 (34.4%) of 186 patients. Aspiration biopsy under laparoscopic US guidance was performed on the 134 nodules, and 28 nodules in 23 (12.4%) of the 186 patients were histologically diagnosed as hepatocellular carcinoma. Of these 23 patients, 18 had been diagnosed with solitary hepatocellular carcinoma before laparoscopic US. One hundred six of the newly detected lesions were initially diagnosed as noncarcinomatous nodules, but the diagnosis of 10 of these lesions was changed to hepatocellular carcinoma during follow-up that was as long as 96 months. CONCLUSIONS: Laparoscopic US is useful in the initial diagnosis of hepatocellular carcinoma and impacts treatment selection by more accurately defining the presence of multicentric hepatocellular carcinomas.

Laparoscopic cholecystectomy in gallstone patients with acute cholecystitis.

It remains controversial whether patients with gallstones with acute cholecystitis should be operated on early, or whether surgery should be delayed until the acute phase subsides. To help resolve this question, we retrospectively studied 109 patients with acute cholecystitis, 56 of whom underwent laparoscopic cholecystectomy after acute cholecystitis had subsided (delayed group) and 53 of whom underwent early laparoscopic cholecystectomy--within 7 days after admission (early group). On admission, the inflammatory findings in the two groups were very similar; however, at operation, the inflammatory findings were alleviated in the delayed group, while they remained unchanged in the early group. The mean operative time for the two groups was very similar. As for intraoperative complications, there was no conversion to laparotomy in either group, and there were no major complications in either group. The total hospital stay was 37.7 +/- 14.4 days for the delayed group and 12.7 +/- 2.0 days for the early group, showing a highly significant difference (P < 0.001). Early laparoscopic cholecystectomy seems to be better than delayed treatment for patients with gallstones with acute cholecystitis.

Prognosis of small hepatocellular carcinoma after laparoscopic ethanol injection.

BACKGROUND: Most patients with hepatocellular carcinoma have underlying cirrhosis, and this impairment of liver function makes hepatectomy difficult, prompting the use of other modalities such as transcatheter arterial embolization and percutaneous ethanol injection. METHODS: Laparoscopic ethanol injection was performed in 48 previously untreated patients with hepatocellular carcinoma smaller than 2 cm in diameter. Long-term survival was evaluated. RESULTS: In 12 patients, hepatocellular carcinoma was not detected by trans-cutaneous ultrasonography but could be demonstrated by laparoscopic ultrasonography. Laparoscopic ethanol injection did not cause serious complications in any patient. The mean hospital stay after ethanol injection was 8.6 days (4 to 15 days). The cumulative survival rate was 86.7% at 3 years and 60.0% at 5 years. According to the Child-Pugh classification, the cumulative survival rate at 5 years was 87.9% for class A, 65.7% for class B, and 28.6% for class C. CONCLUSIONS: The long-term prognosis for patients with small hepatocellular carcinoma treated solely by laparoscopic ethanol injection is satisfactory but still dependent on underlying liver function.

Microwave coagulation therapy on hepatomas: CT and MR appearance after therapy.

Laparoscopic microwave coagulation (LMC) for hepatocellular carcinomas (HCCs) was performed on 26 HCCs in 17 patients. Contrast-enhanced CT (CECT) and MR images (T1-weighted imaging [T1WI], T2WI, gadolinium-diethylenetriamine pentaacetic acid [Gd-DTPA] T1WI) were obtained to determine changes over time. The irradiated center exhibited low to moderate intensity with surrounded high intensity (HI) on T2WI and Gd-DTPA T1WI. On T1WI, lesions showed four patterns of intensity: uniform HI (30.8%), arcuate HI (26.9%), mainly low with spot HI (30.8%), and isointensity to hypointensity (11.5%). Follow-up imaging at more than 170 days revealed isointensity to hypointensity on T1WI (96.2%) and reduced HI on T2-weighted imaging (T2WI) and Gd-DTPA T1WI. All lesions became less conspicuous and were reduced in volume. HCC shows time-related changes in signals and size after LMC. Identifying the irradiated lesion is necessary to estimate the adequacy of treatment by comparison with the pretherapeutic image.

The role of endoscopic balloon sphincteroplasty in patients with gallbladder and bile duct stones.

We clarified the significance of endoscopic balloon sphincteroplasty (EBS) in the therapeutic treatment of biliary tract stones in the present era of laparoscopic cholecystectomy (LC). Patients with cholecysto-choledocholithiasis (n = 33) were treated by EBS. After endoscopic retrograde cholangiography (ERC), a balloon catheter (8 mm in diameter and 3 cm in width) was inserted into the bile duct using a guidewire, and positioned at the sphincter of Oddi. After inflating the balloon catheter, bile duct stones were removed by mechanical lithotripsy, a basket catheter, or a balloon catheter. In all patients, bile duct stones were removed by EBS without endoscopic sphincterotomy. No complication occurred except for 2 cases of mild pancreatitis, which was resolved within 48 hours. Twenty-four patients underwent LC before or after EBS. The remaining 9 patients did not undergo LC due to a poor-risk status for general anesthesia. None of them, however, experienced cholecystitis or colicky attacks after EBS. The combination of EBS and LC is an excellent method for treating cholecysto-choledocholithiasis.