Clinical outcomes of patients with bilateral anterior disc displacement without reduction and erosive change of the temporomandibular joint after performance of unilateral arthrocentesis and stabilisation splint therapy.

The efficacy of a combination treatment of arthrocentesis and stabilisation splint for patients with bilateral anterior disc displacement without reduction (ADDWoR) and erosive change of the TMJ remains controversial. To evaluate clinical outcomes of patients with ADDWoR and erosive change of the TMJ after performance of unilateral arthrocentesis and stabilisation splint therapy. A retrospective study of 44 patients (37 females, 7 males, mean age of 34 years) with bilateral ADDWoR and erosive change of the TMJ were included in this study. Their clinical outcomes before and after arthrocentesis and stabilisation splint therapy were compared. Evaluation criteria were as follows: (a) Maximal mouth opening (MMO); (b) Right and left maximal lateral movement (RLM, LLM) and maximal protrusive movement (PM); (c) Visual analog scale (VAS) pain score during MMO, RLM, LLM and PM; and (d) VAS pain score during palpation of masticatory muscles. Wilcoxon signed-rank test, Mc Nemar test and paired t test were used for statistical analysis. Differences in VAS pain score between arthrocentesis and non-arthrocentesis sites were not statistically significant except MMO and LLM (P < .05) after 6 months. Differences in mean VAS pain scores for all variables between before arthrocentesis and 6 months follow-up in the arthrocentesis site were statistically significant. (P < .01). Unilateral arthrocentesis on more symptomatic TMJ and subsequent stabilisation splint therapy was highly successful for pain and achievement of normal range of mandibular movements in patients with both ADDWoR and bony change.

Clinical and Radiographic Performance of Rough Surfaced Implants Placed in the Atrophic Posterior Maxilla With Sinus Membrane Elevation Without Bone Grafting: A Prospective and Preliminary Study.

PURPOSE: The aim of the present prospective and preliminary study was to compare the clinical and radiographic outcomes of 2 types of rough surfaced implants after implant placement in the atrophic posterior maxilla with sinus membrane elevation without bone grafting using the crestal approach. PATIENTS AND METHODS: All clinical and radiographic records for 28 patients who had received 40 implants were included in the present study. The patients returned for radiographic and clinical examinations at 1, 3, and 6 months and every 6 months thereafter after implantation. Cone-beam computed tomography images were taken to evaluate the amount of bone gain in the maxillary sinus. Standardized periapical digital radiographs were taken to evaluate the changes in the crestal peri-implant bone level and peri-implant fixture radiolucency. RESULTS: The Kaplan-Meier survival estimates demonstrated a 100% probability of survival to 24 months. No significant differences were found in cervical bone loss (CBL) or residual bone height (RBH) between the TS III CA group and the TS III SA group during the 2-year follow-up period after implant placement. The CBL values according to gender, implant placement region, prosthesis type, and the time of implantation were not significantly different between the 2 groups. CONCLUSIONS: The results of the present preliminary study demonstrate that 2 types of rough surfaced implants placed in the atrophic posterior maxilla with sinus membrane elevation without a bone graft have good clinical and radiographic outcomes.

Influence of Fixture Thread Exposure on Marginal Bone Level Around Different Implant Systems: A Preliminary Study in Dogs.

PURPOSE: To evaluate the influence of implant neck structures on marginal bone loss around intentionally exposed implant fixtures by histomorphometric analysis. MATERIALS AND METHODS: Twenty-four implants representing 3 implant systems were placed in three dogs; an implant system with SLA surface without microthreads (group A); one with SLA + calcium surface without microthreads (group B); and one with SLA surface with microthreads (group C). The histomorphometric analyses for vertical defect length (VDL), infrabony defect height (IDH), and defect depth (DD) were performed at the buccal and lingual sides of each fixture. RESULTS: The VDL was lower in group A relative to groups B and C on the buccal and lingual sides. The IDH and DD were higher in group A than group C on the buccal and lingual sides; however, no statistically significant differences were noted between the groups in VDL, IDH, and DD on the buccal and lingual sides of the fixtures. CONCLUSIONS: In this preliminary study, marginal bone resorption pattern in the canine mandible varied according to the neck design of each implant fixture. Further studies with larger sample size are needed to confirm the effect of microthreads and surface roughness on the marginal bone loss at the exposed implant fixture.

Prostaglandin E2 stimulates urokinase-type plasminogen activator receptor via EP2 receptor-dependent signaling pathways in human AGS gastric cancer cells.

Aberrant expression of urokinase-type plasminogen activator receptor (uPAR) has been observed in human gastric cancers. Prostaglandin E2 (PGE2 ), whose biosynthesis is catalyzed by cyclooxygenase-2 (COX-2), is implicated in cancer metastasis; however, the cellular and molecular mechanisms of PGE2 -driven uPAR expression are yet to be elucidated in human gastric cancer AGS cells. In this study, we showed that PGE2 induces uPAR expression in concentration- and time-dependent manners. Furthermore, using antagonists and siRNA, we found that among the four subtypes of PGE2 receptors, EP2 receptors are involved in PGE2 -induced uPAR expression. PGE2 induced the activation of Src, epidermal growth factor receptor (EGFR), c-Jun NH2 -terminal kinase (JNK), extracellular signal-regulated kinase (Erk), and p38 mitogen activated protein kinase (p38 MAPK). Specific inhibitor and mutagenesis studies showed that Src, EGFR, JNK1/2, and Erk1/2 are involved in PGE2 -induced uPAR expression. PGE2 induces EP2-dependent phosphorylation of Src, while the activation of Src-dependent EGFR leads to the phosphorylation of JNK1/2 and Erk1/2. Deletion and site-directed mutagenesis studies demonstrated the involvement of transcription factor activator protein (AP)-1 and nuclear factor-kappa B (NF-κB) in PGE2 -induced uPAR expression. EGFR-dependent MAPKs (JNK1/2 and Erk1/2) function as the upstream signaling molecules in the activation of AP-1 and NF-κB, respectively. AGS cells pre-treated with PGE2 showed remarkably enhanced invasiveness, which was partially abrogated by uPAR-neutralizing antibodies. To the best of our knowledge, this is the first report that PGE2 -induced uPAR expression, which stimulates invasiveness of human gastric cancer AGS cells, is mediated by the EP2 receptor-dependent Src/EGFR/JNK1/2, Erk1/2/AP-1, and Src/EGFR/JNK1/2, Erk1/2/NF-κB cascades. © 2016 Wiley Periodicals, Inc.

Clinical and Retrospective Evaluation of 4.1- or 4.3-mm-Diameter Implants Placed Immediately in the Molar Region: A Preliminary Study.

PURPOSE: The purpose of this study was to evaluate the clinical and radiographic performance of 4.1- or 4.3-mm-diameter implants placed immediately in the molar region. MATERIALS AND METHODS: Twenty-nine patients (14 men and 15 women, aged 21-71 years) received 38 implants that were placed immediately in the molar region. Of the implants, 19 (50%) were placed in the maxilla and 19 (50%) in the mandible. Thirty-eight prostheses (19 single restoration and 19 partial fixed prostheses) were fabricated. The diameter of the implant type was 4.1 mm (15 implants, 39%) or 4.3 mm (23 implants, 61%). Clinical and radiographic assessments of implants, prostheses, and peri-implant tissues were performed at 1 month, 3 months, and 6 months and then every 6 months after definitive restoration. RESULTS: Kaplan-Meier survival estimates showed a 97.4% probability of implant survival to 36 months. The mean time of implant follow-up was 36 months, with a maximum of 75 months and minimum of 4 months. Cement dissolution occurred in 1 partial fixed prosthesis. Screw loosening occurred in 2 single-crown restorations in 1 patient. No abutment, screw, or implant fixture fractures were observed during the follow-up periods. The mean cervical bone loss of 38 implants measured 0.31 ± 0.06 mm mesially and 0.31 ± 0.07 mm distally 1 year after implant installation. There were no significant differences in implant survival and cervical bone loss based on anatomic location, gender, and prosthesis type. CONCLUSIONS: This study describes successful outcomes after the use of 4.1- or 4.3-mm-diameter implants placed immediately in the molar region. Further comprehensive maintenance practices and follow-up schedules are required.

Piperine inhibits IL-1ß-induced IL-6 expression by suppressing p38 MAPK and STAT3 activation in gastric cancer cells.

Piperine, a kind of natural alkaloid found in peppers, has been reported to exhibit anti-oxidative and anti-tumor activities, both in vitro and in vivo. Interleukin-6 (IL-6) is an important cytokine that activates the signal transduction, promotes tumor cell metastasis, and induces malignancy, including in gastric cancer. However, the effects of piperine on IL-6 expression in gastric cancer cells have not yet been well defined. In this study, we investigated the effects of piperine on the IL-6 expression, and examined the underlying signaling pathways via RT-PCR, promoter studies and Western blotting in human gastric cancer TMK-1 cells. Our results showed that piperine inhibited interleukin-1ß (IL-1ß)-induced IL-6 expression in a dose-dependent manner. In addition, piperine also inhibited IL-6 promoter activity. Experiments with mitogen-activated protein kinase (MAPK) inhibitors and dominant negative mutant p38 MAPK indicated that p38 MAPK was essential for IL-6 expression in the TMK-1 cells. Additionally, signal transducer and activator of transcription 3 (STAT3) was also involved in the IL-1ß-induced IL-6 expression in gastric cancer cells. Piperine inhibited IL-1ß-induced p38 MAPK and STAT3 activation and, in turn, blocked the IL-1ß-induced IL-6 expression. Furthermore, gastric cancer cells pretreated with IL-1ß showed markedly enhanced invasiveness, which was partially abrogated by treatment with IL-6 siRNA, piperine, and inhibitors of p38 MAPK and STAT3. These results suggest that piperine may exert at least part of its anti-cancer effect by controlling IL-6 expression through the suppression of p38 MAPK and STAT3.

Protective effect of diet supplemented with rice prolamin extract against DNCB-induced atopic dermatitis in BALB/c mice.

BACKGROUND: Rice prolamin has been reported to possess antioxidative, anti-inflammatory and immune-promoting properties. This study is aimed to examine the protective effects of dietary rice prolamin extract (RPE) against dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD)-like skin lesions in mice. METHODS: BALB/c mice were fed diet supplemented with 0-0.1 % RPE for 6 weeks. For the last 2 weeks, 1 % or 0.2 % DNCB was applied repeatedly to the back skin of mice to induce AD-like lesions. Following AD induction, the severity of skin lesions was examined macroscopically and histologically. In addition, the serum levels of IgE, IgG1 and IgG2a were determined by ELISA, and the mRNA expression of IL-4 and IFN-γ in the skin was determined by real-time PCR. RESULTS: Dietary RPE suppressed the clinical symptoms of DNCB-induced dermatitis as well as its associated histopathological changes such as epidermal hyperplasia and infiltration of mast cells and eosinophils in the dermis. RPE treatment also suppressed the DNCB-induced increase in transepidermal water loss. Dietary RPE inhibited the DNCB-induced enhancement of serum IgE and IgG1 levels, whereas it increased the serum IgG2a level in DNCB-treated mice. In addition, dietary RPE upregulated the IFN-γ mRNA expression and downregulated the IL-4 mRNA expression in the skin of DNCB-treated mice. CONCLUSIONS: The above results suggest that dietary RPE exerts a protective effect against DNCB-induced AD in mice via upregulation of Th1 immunity and that RPE may be useful for the treatment of AD.

Clinical outcomes of patients with unilateral internal derangement of the temporomandibular joint following arthrocentesis and stabilization splint therapy.

BACKGROUND: The management of internal derangement (ID) of the TMJ is challenging because of multiple etiologic factors and varying degrees of severity. The aim of this study was to evaluate the clinical outcomes of patients with unilateral ID treated with arthrocentesis and stabilization splint therapy during a 6-month period. METHODS: A total of 105 patients (87 females, 18 males) with unilateral ID were included in this study. Patients were divided into unilateral anterior disc displacement with reduction (ADDwR) and unilateral anterior disc displacement without reduction (ADDwoR). Patients with ADDwoR were subdivided according to the erosive bone changes. Objective parameters on mandibular movement and subjective parameters on pain were obtained and assessed. Their clinical outcomes before and after arthrocentesis and stabilization splint therapy were compared with the chi-square, Fisher's exact test, paired t-test, or Wilcoxon singed-rank test. RESULTS: All objective parameters of unilateral ID patients significantly increased at the 6-month follow-up. The differences in mean visual analog scale (VAS) pain scores were statistically significant in all subjective variables (p < 0.01). In joints with ADDwoR, preoperative maximal mouth opening, and maximal protrusive movement in both groups, with erosive and non-erosive changes were significantly increased after 6 months (p < 0.01). However, right and left maximal lateral movement increased after treatment in both groups but without significant differences. All VAS pain scores on jaw movement and palpation of associated muscles showed a significant decrease regardless of erosive changes. CONCLUSIONS: The combination of arthrocentesis and subsequent stabilization splint therapy was shown to be highly effective in pain reduction and improvement of mandibular movements in both unilateral ADDwR and ADDwoR, as well as in cases with both erosive and non-erosive bony changes associated with unilateral ADDwoR.

Redox Regulation of PTEN by Reactive Oxygen Species: Its Role in Physiological Processes.

Phosphatase and tensin homolog (PTEN) is a tumor suppressor due to its ability to regulate cell survival, growth, and proliferation by downregulating the PI3K/AKT signaling pathway. In addition, PTEN plays an essential role in other physiological events associated with cell growth demands, such as ischemia-reperfusion, nerve injury, and immune responsiveness. Therefore, recently, PTEN inhibition has emerged as a potential therapeutic intervention in these situations. Increasing evidence demonstrates that reactive oxygen species (ROS), especially hydrogen peroxide (H2O2), are produced and required for the signaling in many important cellular processes under such physiological conditions. ROS have been shown to oxidize PTEN at the cysteine residue of its active site, consequently inhibiting its function. Herein, we provide an overview of studies that highlight the role of the oxidative inhibition of PTEN in physiological processes.

Redox Regulation of Phosphatase and Tensin Homolog by Bicarbonate and Hydrogen Peroxide: Implication of Peroxymonocarbonate in Cell Signaling.

Phosphatase and tensin homolog (PTEN) is a negative regulator of the phosphoinositide 3-kinases/protein kinase B (PI3K/AKT) signaling pathway. Notably, its active site contains a cysteine residue that is susceptible to oxidation by hydrogen peroxide (H2O2). This oxidation inhibits the phosphatase function of PTEN, critically contributing to the activation of the PI3K/AKT pathway. Upon the stimulation of cell surface receptors, the activity of NADPH oxidase (NOX) generates a transient amount of H2O2, serving as a mediator in this pathway by oxidizing PTEN. The mechanism underlying this oxidation, occurring despite the presence of highly efficient and abundant cellular oxidant-protecting and reducing systems, continues to pose a perplexing conundrum. Here, we demonstrate that the presence of bicarbonate (HCO3-) promoted the rate of H2O2-mediated PTEN oxidation, probably through the formation of peroxymonocarbonate (HCO4-), and consequently potentiated the phosphorylation of AKT. Acetazolamide (ATZ), a carbonic anhydrase (CA) inhibitor, was shown to diminish the oxidation of PTEN. Thus, CA can also be considered as a modulator in this context. In essence, our findings consolidate the crucial role of HCO3- in the redox regulation of PTEN by H2O2, leading to the presumption that HCO4- is a signaling molecule during cellular physiological processes.

The Role of Oxidative Inactivation of Phosphatase PTEN and TCPTP in Fatty Liver Disease.

Alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are becoming increasingly prevalent worldwide. Despite the different etiologies, their spectra and histological feature are similar, from simple steatosis to more advanced stages such as steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Studies including peroxiredoxin knockout models revealed that oxidative stress is crucial in these diseases, which present as consequences of redox imbalance. Protein tyrosine phosphatases (PTPs) are a superfamily of enzymes that are major targets of reactive oxygen species (ROS) because of an oxidation-susceptible nucleophilic cysteine in their active site. Herein, we review the oxidative inactivation of two tumor suppressor PTPs, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and T-cell protein tyrosine phosphatase (TCPTP), and their contribution to the pathogenicity of ALD and NAFLD, respectively. This review might provide a better understanding of the pathogenic mechanisms of these diseases and help develop new therapeutic strategies to treat fatty liver disease.

A comparative histological and immunohistochemical study of wound healing following incision with a scalpel, CO2 laser or Er,Cr:YSGG laser in the guinea pig oral mucosa.

PURPOSE: This study was undertaken to compare wound healing following incisions with either a scalpel, CO(2) laser or Er,Cr:YSGG laser in Guinea pig oral mucosa. MATERIALS AND METHODS: Three types of wounds were randomly introduced with either a stainless steel scalpel, CO(2) laser or Er,Cr:YSGG laser in the buccal mucosa of each of 22 Guinea pigs. Four Guinea pigs were sacrificed on day 1, day 3 and day 5 post-surgery. Five Guinea pigs were sacrificed on day 7 and day 14 post-surgery. Biopsy samples from each oral mucosa wound were examined and the expression of TNF-α and TGF-ß1 was determined by immunohistochemical staining. RESULTS: At day 3 post-surgery, the histological pattern of the healing process was similar in the scalpel and Er,Cr:YSGG laser wounds and there were more ulcerations present in the CO(2) laser wounds than in the scalpel and Er,Cr:YSGG laser wounds. The level of TNF-α expression was twice in the laser wounds that in the scalpel wounds. A higher level of TGF-ß1 expression was seen at day 7 post-surgery and a lower level at day 14 post-surgery in the CO(2) laser wounds than in the scalpel and Er,Cr:YSGG laser wounds. CONCLUSIONS: The Er,Cr:YSGG laser has many advantages for oral surgery due to a low inflammatory response and minimal damage of the tissue. Although a CO(2) laser has better hemostatic ability, its use causes greater tissue damage than a scalpel and Er,Cr:YSGG laser. However, further larger studies would be needed before fully endorsing its widespread use.

Treatment outcome analysis of speedy surgical orthodontics for adults with maxillary protrusion.

INTRODUCTION: The purposes of this study were to quantify the treatment outcomes of speedy surgical orthodontic treatment for adults with maxillary protrusion and to identify the key factors influencing the efficacy of speedy surgical orthodontic biomechanics. METHODS: Twenty-four adults with maxillary or bimaxillary protrusion were treated with speedy surgical orthodontics, including maxillary perisegmental corticotomy followed by the orthopedic en-masse retraction against C-palatal miniplate anchorage. The average total treatment time was 20 months (range, 11-42 months). Lateral cephalograms were taken at pretreatment, just after the perisegmental corticotomy, and at posttreatment to evaluate the skeletal and soft-tissue changes. The Pearson correlation analysis was used to identify the relationships between hard-tissue, soft-tissue, and perisegmental corticotomy variables. RESULTS: The maxillary central incisors were retracted by 9.19 ± 0.31 mm and retroclined by 19.73° ± 1.17°. The change of the maxillary alveolar ridge angle was 13.97° ± 1.04°. The extrusion tendency of the retracted maxillary incisors was minimal, measured as 1.17 ± 0.36 mm. The width of the buccal corticotomy showed statistically significant correlations with the angular change of the maxillary central incisors and the maxillary alveolar ridge angle. The retrusion of the maxillary central incisors and the maxillary alveolar ridge angle were the 2 hard-tissue variables that most closely correlated with retrusion of the upper lip. CONCLUSIONS: Speedy surgical orthodontic treatment can be an effective modality for adults with severe maxillary protrusion.

A framework for treatment of autism using affective computing.

It is known that as many as 1 in 91 children are diagnosed with autistic spectrum disorder. Since the children with autism usually do not express their own emotional status, it is needed to develop a novel technology to sense their emotional status and give proper psychological treatment. This article presents a framework of the treatment system for children with autism using affective computing technologies.

Redox Regulation of PTEN by Peroxiredoxins.

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is known as a tumor suppressor gene that is frequently mutated in numerous human cancers and inherited syndromes. PTEN functions as a negative regulator of PI3K/Akt signaling pathway by dephosphorylating phosphatidylinositol (3, 4, 5)-trisphosphate (PIP3) to phosphatidylinositol (4, 5)-bisphosphate (PIP2), which leads to the inhibition of cell growth, proliferation, cell survival, and protein synthesis. PTEN contains a cysteine residue in the active site that can be oxidized by peroxides, forming an intramolecular disulfide bond between Cys124 and Cys71. Redox regulation of PTEN by reactive oxygen species (ROS) plays a crucial role in cellular signaling. Peroxiredoxins (Prxs) are a superfamily of peroxidase that catalyzes reduction of peroxides and maintains redox homeostasis. Mammalian Prxs have 6 isoforms (I-VI) and can scavenge cellular peroxides. It has been demonstrated that Prx I can preserve and promote the tumor-suppressive function of PTEN by preventing oxidation of PTEN under benign oxidative stress via direct interaction. Also, Prx II-deficient cells increased PTEN oxidation and insulin sensitivity. Furthermore, Prx III has been shown to protect PTEN from oxidation induced by 15s-HpETE and 12s-HpETE, these are potent inflammatory and pro-oxidant mediators. Understanding the tight connection between PTEN and Prxs is important for providing novel therapies. Herein, we summarized recent studies focusing on the relationship of Prxs and the redox regulation of PTEN.

A comparative study of wound healing following incision with a scalpel, diode laser or Er,Cr:YSGG laser in guinea pig oral mucosa: A histological and immunohistochemical analysis.

OBJECTIVE: This study compared wound healing following incisions with either a scalpel, a diode laser or an Er,Cr:YSGG laser in guinea pig oral mucosa. MATERIAL AND METHODS: Three types of wound were made randomly with either a stainless-steel scalpel, a diode laser or an Er,Cr:YSGG laser in the buccal mucosa of 24 guinea pigs. Five guinea pigs were sacrificed on each of Days 1, 3, 5 and 7 post-surgery. Four guinea pigs were sacrificed on Day 14 post-surgery. Biopsy samples from each oral mucosa wound were examined using light microscopy and the expression of tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta1 was determined by immunohistochemical staining. The expression of TNF-alpha and TGF-beta1 was evaluated by calculating the percentage of positively stained cells and immunostaining intensity was evaluated using a scale ranging from 0 to 3. RESULTS: Infiltration of inflammatory cells decreased rapidly at Day 5 post-surgery in all three groups of animals. The highest level of TNF-alpha expression was found at Day 1 post-surgery for the diode laser wounds. The intensity of TNF-alpha immunostaining was highest at Day 3 post-surgery and lowest at Day 7 post-surgery for all three groups of animals. For the scalpel wounds, a lower level of TGF-beta1 expression was seen until Day 3 post-surgery and a higher level from Day 7 post-surgery compared to laser wounds. The intensity of TGF-beta1 immunostaining was highest at Day 1 post-surgery for the diode laser wounds. CONCLUSIONS: The diode laser is considered a good cutting device for oral mucosa; however, more tissue damage occurs than with the use of a scalpel or an Er,Cr:YSGG laser. Larger studies will be needed before fully endorsing the widespread use of the diode laser.

Redox regulation of tumor suppressor PTEN in cell signaling.

Phosphatase and tensin homologs deleted on chromosome 10 (PTEN) is a potent tumor suppressor and often dysregulated in cancers. Cellular PTEN activity is restrained by the oxidation of active-site cysteine by reactive oxygen species (ROS). Recovery of its enzymatic activity predominantly depends on the availability of cellular thioredoxin (Trx) and peroxiredoxins (Prx), both are important players in cell signaling. Trx and Prx undergo redox-dependent conformational changes through the oxidation of cysteine residues at their active sites. Their dynamics are essential for protein functionality and regulation. In this review, we summarized the recent advances regarding the redox regulation of PTEN, with a specific focus on our current state-of-the-art understanding of the redox regulation of PTEN. We also proposed a tight association of the redox regulation of PTEN with Trx dimerization and Prx hyperoxidation, providing guidance for the identification of novel therapeutic targets.

MRI findings of patients with temporomandibular joint internal derangement: before and after performance of arthrocentesis and stabilization splint.

PURPOSES: The purpose of this study was to evaluate the clinical outcome and magnetic resonance imaging (MRI) changes of patients with temporomandibular joint (TMJ) internal derangement before and after performance of arthrocentesis and stabilization splint therapy. PATIENTS AND METHODS: Thirty-three patients with unilateral TMJ internal derangement that was successfully treated were included in this study. The clinical outcome and changes in the disc position, disc mobility, disc morphology, joint effusion, bone marrow edema pattern in the mandibular condyle, and the degenerative change before and after arthrocentesis and stabilization splint therapy were compared using MRI. RESULTS: The average maximum mouth opening (MMO) was increased and the average pain during MMO was decreased significantly after treatment. The disc position, disc mobility, and joint effusion were significantly improved after treatment. CONCLUSION: The results in this study indicate that arthrocentesis and stabilization splint therapy provide significant improvement in the clinical outcome, disc position, disc mobility and joint effusion.

Native low density lipoprotein increases the production of both nitric oxide and reactive oxygen species in the human umbilical vein endothelial cells.

BACKGROUND: Nitric oxide synthases (NOSs) are a unique family of enzymes that catalyze the production of nitric oxide (NO) from L-arginine. Atherogenic action of oxidized low-density lipoproteins (oxLDL) may be mediated partly by the formation of NO in endothelial cells. OBJECTIVE: The objective of this study was to identify sources of reactive oxygen species (ROS) causing native LDL (nLDL)-induced senescence of cultured human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were treated with nLDL and NO production was assessed using Griess reagent as substrate and spectrophotometry in the absence or presence of specific inhibitors of endothelial NOS (eNOS) and inducible NOS (iNOS). In addition, expression levels of eNOS and iNOS were measured with ELISA and western blotting, and ROS was evaluated using 2',7'-dichlorofluorescin diacetate (DCF-DA) and a fluorescence microplate reader. RESULTS: NO formation in nLDL-treated HUVECs was significantly increased. Long-term treatment with nLDL up-regulated both eNOS and iNOS proteins. Such increase of NO production in HUVECs induced by nLDL was significantly suppressed by treatment with iNOS-selective inhibitor 1400 W, but not by the eNOS-selective inhibitor L-NIO. Native LDL treatment uncoupled Hsp90, the regulatory binding protein of eNOS, from the enzyme in HUVECs. Native LDL also significantly increased ROS production in HUVECs. CONCLUSION: These findings suggest that oxidative stress originated from induction of iNOS and eNOS could be a causative factor for nLDL-induced senescence of HUVECs.

Effects of chitosan oligosaccharide (COS) on the glycerol-induced acute renal failure in vitro and in vivo.

The purpose of this study was to investigate the effects of chitosanoligosaccharide (COS) on the change of inflammatory response, renal function factor, and renal oxidative stress in glycerol-induced ARF in vitro and in vivo. The molecular weight of COS was approximately below 10 kDa with 90% degree of deacetylation. Renal proximal tubular cells were treated with only COS (0, 0.01, 0.025, 0.05, 0.075 and 0.1%) or COS in the presence of glycerol (4mM). And rats were administered with glycerol (50%, 8 ml/kg) by intramuscular injection for the induction of ARF. For identification the protection effect of COS in the glycerol-induced ARF, rats were administered by COS (0.05 and 0.1%) using P.O. injection. The enzymatic activity of the released RDPase was assayed by the fluorometric method. The level of TNF-alpha in kidney or the culture medium was quantified using ELISA kit (R&D Systems, Minneapolis, USA) and, nitrite concentration was determined by the Griess reaction. We showed that COS stimulated the production of TNF-alpha, NO and the released RDPase. Glycerol increased the concentration of RDPase in kidney and decreased the released RDPase in proximal tubular cells. And, glycerol increased the production of NO, TNF-alpha, creatinine, and MDA, and decreased SOD. However, COS recovered the glycerol-induced inflammatory response, renal function factor, and antioxidant effect in kidney. COS had the antioxidant activity and the anti-inflammatory effect. And maybe that characteristics could help recover the glycerol-induced ARF.