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Background and purpose:Na+/Ca2+ exchanger (NCX) inhibitors are known to attenuate myocardial reperfusion injury. However, the exact mechanisms for the cardioprotection remain unclear. The present study was undertaken to examine the mechanism underlying the cardioprotection by NCX inhibitors against ischaemia/reperfusion injury.Experimental approach:Isolated rat hearts were subjected to 35-min ischaemia/60-min reperfusion or 20-min ischaemia/60-min reperfusion. NCX inhibitors (3-30 μM KB-R7943 (KBR) or 0.3-1 μM SEA0400 (SEA)) were given for 5 min prior to ischaemia (pre-ischaemic treatment) or for 10 min after the onset of reperfusion (post-ischaemic treatment).Key results:With 35-min ischaemia/60-min reperfusion, pre- or post-ischaemic treatment with KBR or SEA neither enhanced post-ischaemic contractile recovery nor attenuated ischaemia- or reperfusion-induced Na+ accumulation and damage to mitochondrial respiratory function. With the milder model (20-min ischaemia/reperfusion), pre- or post-ischaemic treatment with 10 μM KBR or 1 μM SEA significantly enhanced the post-ischaemic contractile recovery, associated with reductions in reperfusion-induced Ca2+ accumulation, damage to mitochondrial function, and decrease in myocardial high-energy phosphates. Furthermore, Na+ influx to mitochondria in vitro was enhanced by increased concentrations of NaCl. KBR (10 μM) and 1 μM SEA partially decreased the Na+ influx.Conclusions and implications:The NCX inhibitors exerted cardioprotective effects during relatively mild ischaemia. The mechanism may be attributable to prevention of mitochondrial damage, possibly mediated by attenuation of Na+ overload in cardiac mitochondria during ischaemia and/or Ca2+ overload via the reverse mode of NCX during reperfusion.British Journal of Pharmacology (2007) 151, 963–978; doi:10.1038/sj.bjp.0707321; published online 4 June 2007 [ABSTRACT FROM AUTHOR]

summary The purpose of this study was to clarify the kinesiographs of chewing movement and masticatory efficiency before and after treatment in patients with non-reducing disk displacement of the temporomandibular joint (TMJ). Twenty patients who were diagnosed with unilateral non-reducing disk displacement of the TMJ were treated with pumping of the joint with injection of sodium hyaluronate. Chewing movement patterns in these patients were evaluated, using mandibular kinesiography (MKG) at their initial visit and at mean 19-month follow-up and the results were compared. Masticatory efficiency was also measured. As controls, 23 volunteers without TMJ dysfunction were employed. Far from the results of normal volunteers, chewing movement patterns of the patients on MKG did not show deviation to the chewing side in the TMJ-unaffected-side chewing in the horizontal plane. However, such patterns of the patients became similar to those of normal volunteers after treatment. Masticatory efficiency of the patients improved after treatment, though it was impaired at initial visit. The MKG and masticatory efficiency test appeared to be a useful method of comparing masticatory function before and after treatment in patients with non-reducing disk displacement of the TMJ. [ABSTRACT FROM AUTHOR]

SUMMARY The purpose of this study was to clarify the electromyographic property of chewing movement before and after treatment in patients with non-reducing disc displacement of the temporomandibular joint (TMJ). Twenty patients who were diagnosed with unilateral non-reducing disc displacement of the TMJ were treated by pumping and injection of sodium hyaluronate into the joint. Chewing movement in these patients was evaluated by electromyography (EMG) at the initial visit and at mean 19-month follow-up and the results were compared. Chewing movement in 23 normal controls were also examined. Duration of contraction, cycle time and integrated value at the initial visit which were different from those in the controls without TMJ dysfunction tended to be at the control level mean 19 months after treatment of pumping and injection of sodium hyaluronate into the joint in patients with non-reducing disc displacement of the TMJ. Electromyography appeared to be a method of documenting the chewing movement which was impaired at initial visit improved after treatment in patients with non-reducing disc displacement of the TMJ. [ABSTRACT FROM AUTHOR]

Summary Elastic fibres are thought to be very important for the function of various organs including the temporomandibular joint (TMJ). The current study was designed to examine changes in the elastic fibres of the TMJ following discectomy. The TMJs of six rabbits were surgically exposed, and the disc removed with a scalpel. Three untreated and three sham-operated rabbits were used as controls. Complete TMJs were removed in three rabbits 1 month and in three rabbits 3 months after discectomy and processed for histochemical demonstration of elastic fibres. In the TMJ 1 month after discectomy, osteoarthritic changes and a significant increase in the numbers of elastic fibres were observed in the condyle and articular eminence. In the TMJs 3 months after discectomy, they tended to revert to the levels in the condyle and articular eminence of the control TMJs. Our results show that after experimental discectomy, elastic fibres very often appear initially in the condyle and articular eminence, but they are destined to disappear later. This information may improve our understanding of the consequences of removal of the disc in clinical practice. [ABSTRACT FROM AUTHOR]

We examined the immunohistochemical expressions of cell- cycle- and apoptosis-related factors to investigate the possible role of these factors in odontogenic keratocyst (OKC). Expression of cyclin D1 and p16 protein was detected in the basal and parabasal cells in lining epithelium of OKCs and was found more frequently in basal cell nevus syndrome (BCNS)-associated OKCs than in primary or recurrent OKCs. Positivity for p21 protein was detected in basal to superficial cells, whereas that for p27 protein was detected in parabasal to superficial cells in lining epithelium of OKCs. DNA topoisomerase lIα reacted with nuclei in basal and parabasal cells of the lining epithelium of OKCs. and positive cells were observed in BCNS associated OKCs significantly more frequently than in primary or recurrent OKCs. Expression of Fas in suprabasal to superficial cells and expression of Fast in basal and parabasal cells were detected in lining epithelium of OKCs. Immunoreactivity for caspase-3 was detected in basal to suprabasal or superficial cells in lining epithelium of OKCs. Single stranded (ss)DNA-positive nuclei were detected in superficial cells in lining epithelium of OKCs. Fas was more broadly distributed in BCNS-associated OKCs than in primary OKCs, and ssDNA-positive cells were observed in BCNS-associated OKCs significantly more frequently than in primary or recurrent OKCs. These results suggest that BCNS-associated OKCs might be a distinguishable entity from solitary OKCs. [ABSTRACT FROM AUTHOR]

The occlusal contact area, occlusal pressure, bite force, and masticatory efficiency were measured in 48 patients with anterior disc displacement (ADD) of the temporomandibular joint (TMJ). The results were compared with those of 30 normal controls without TMJ dysfunction. The values of occlusal contact area, bite force, and masticatory efficiency measured in patients with ADD were significantly smaller than those measured in the controls, although there was no difference in occlusal pressure between the two groups. The results of the measurements of 22 patients with ADD with reduction were also compared with those of 26 patients with ADD without reduction. There was no difference in any measurement between these patients subgroups. The analysis of occlusal contact area, bite force, and masticatory efficiency appeared to be useful methods in documenting the fact that masticatory function was impaired in patients with ADD of the TMJ. [ABSTRACT FROM AUTHOR]

An experimental psychological study was undertaken to assess the effect of a change in dietary habit upon behavioural development, using as a laboratory animal male Wistar rats maintained on natural foods and a processed food. Forty male Wistar rats were weaned at 21 days of age and divided into two equal groups. Group 1 was fed natural food (pressed wheat, dried fish, peanuts, cabbage and soybeans) and group 2 was fed powdered food. At 68 days of age, the rats were tested in a T-maze. The results showed that Group 1 excelled with regard to T-maze learning [ABSTRACT FROM AUTHOR]

Sjögren's syndrome is a systemic autoimmune disease characterized by reductions in salivary and lacrimal secretions. The mechanisms underlying these reductions remain unclear. We have previously shown that TNF-α plays an important role in the destruction of acinar structures. Here we examined TNF-α's function in the expression of aquaporin (AQP) 5 in human salivary gland acinar cells. Immortalized human salivary gland acinar (NS-SV-AC) cells were treated with TNF-α, and then the expression levels of AQP5 mRNA and protein were analysed. In addition, the mechanisms underlying the reduction of AQP5 expression by TNF-α treatment were investigated. TNF-α-treatment of NS-SV-AC cells significantly suppressed the expression levels of AQP5 mRNA and protein, and reduced the net fluid secretion rate. We examined the expression and activation levels of DNA methyltransferases (Dnmts) in NS-SV-AC cells treated with TNF-α. However, no significant changes were observed in the expression or activation levels of Dnmt1, Dnmt3a or Dnmt3b. Although we also investigated the role of NF-κB activity in the TNF-α-induced suppression of AQP5 expression in NS-SV-AC cells, we detected similar TNF-α suppression of AQP5 expression in non-transfected cells and in a super-repressor form of IκBα cDNA-transfected cell clones. However, interestingly, chromatin immunoprecipitation analysis demonstrated a remarkable decrease in levels of acetylated histone H4 associated with the AQP5 gene promoter after treatment with TNF-α in NS-SV-AC cells. Therefore, our results may indicate that TNF-α inhibition of AQP5 expression in human salivary gland acinar cells is due to the epigenetic mechanism by suppression of acetylation of histone H4., (© 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.)

Background: The mechanisms responsible for activation and proliferation of lining epithelium involved in inflammatory processes in periapical inflammatory lesions remain unclear. In this study, the expression and distribution of inducible nitric oxide synthase (iNOS) and heat shock proteins (HSPs) were immunohistochemically investigated in periapical inflammatory lesions., Methods: Control specimens of periodontal ligaments including Malassez epithelial rests from seven teeth and periapical inflammatory lesions (15 apical granulomas (AGs), 16 radicular cysts (RCs), and 10 residual radicular cysts (RRCs)) were prepared and examined by the standard streptavidin-biotin peroxidase complex method using anti-iNOS rabbit polyclonal antiserum, and anti-HSP27, -HSP60, -HSP70 mouse monoclonal antibodies., Results: Immunoreactivity for iNOS was detected in macrophages, lymphocytes, and endothelial cells of granulation tissue and in lining epithelium of periapical inflammatory lesions. Malassez epithelial rests showed no or slight staining for iNOS. The epithelial staining intensity of iNOS in RCs was greater than that in Malassez epithelial rests and RRCs. Immunoreactivity for HSP27 was recognized in inflammatory cells, endothelial cells and lining epithelium of periapical inflammatory lesions and in Malassez epithelial rests. HSP60 was detected in some lymphocytes of granulation tissue and in lining epithelium of periapical inflammatory lesions, whereas Malassez epithelial rests showed no staining for HSP60. Epithelial HSP60 reactivity was more intense in RCs than in RRCs. HSP70 was expressed in lymphocytes, endothelial cells and lining epithelium of periapical inflammatory lesions and in Malassez epithelial rests. The staining intensity of HSP70 in Malassez epithelial rests was slightly lower than that in lining epithelium of RCs and RRCs., Conclusions: These data demonstrate that the expressions of iNOS, HSP60, and HSP70 are involved in inflammatory processes and might play a role in the activation and proliferation of lining epithelium, leading to progression of periapical inflammatory lesions.

Objective: Our previous results suggested that suppression of tumor necrosis factor alpha (TNFalpha)-induced matrix metalloproteinase 9 (MMP-9) could prevent the destruction of acinar tissue in the salivary glands of patients with Sjögren's syndrome (SS). The present study was undertaken to investigate the effect of cepharanthine on the suppression of TNFalpha-induced MMP-9 production in NS-SV-AC, an SV40-immortalized normal human acinar cell clone., Methods: After pretreatment with or without cepharanthine, NS-SV-AC cells were treated with TNFalpha alone or with a combination of TNFalpha and cepharanthine. The expression of MMP-9 was then examined at the protein and messenger RNA levels. In addition, the effect of cepharanthine on the morphogenetic behavior of NS-SV-AC cells cultured on type IV collagen-coated dishes in the presence of TNFalpha was examined., Results: Although TNFalpha induced the production of MMP-9 in NS-SV-AC cells, this production was greatly suppressed when cells were pretreated with cepharanthine, followed by treatment with both TNFalpha and cepharanthine. In addition, cepharanthine suppressed the TNFalpha-stimulated NF-kappaB activity by partly preventing the degradation of IkappaBalpha protein in NS-SV-AC cells. When NS-SV-AC cells were seeded on type IV collagen-coated dishes in the presence of both TNFalpha and plasmin, type IV collagen interaction with the cells was lost and the cells entered apoptosis. However, pretreatment with cepharanthine restored the aberrant in vitro morphogenesis of the NS-SV-AC cells., Conclusion: These results may indicate a molecular mechanism by which cepharanthine is able to protect against the destruction of the acinar structure in salivary glands from patients with SS.

Objective: We have previously shown that specific enhancement in acinar cells of proteolytic activity induced by tumor necrosis factor alpha (TNFalpha) may be responsible for the destruction of the acinar structure in the salivary glands of patients with Sjögren's syndrome. Because matrix metalloproteinase 9 (MMP-9) is regulated by nuclear factor kappaB (NF-kappaB), we investigated the effect of a super-repressor form of inhibitor of nuclear factor kappaBalpha (srIkappaBalpha) on the suppression of TNFalpha-induced MMP-9 production in acinar cells., Methods: Two srIkappaBalpha complementary DNA (cDNA)-transfected acinar cell clones (ACMT-6 and ACMT-7) and 1 empty vector-transfected cell clone (ACpRc-1) were established. After treatment of cell clones with TNFalpha, the expression of MMP-9 was examined. In addition, the effect of TNFalpha on cell growth and the morphogenetic behavior of cell clones cultured on type IV collagen-coated dishes were examined., Results: TNFalpha induced the production of MMP-9 in the ACpRc-1 cell clone, but greatly suppressed MMP-9 production in ACMT-6 and ACMT-7 clones. No apparent cytotoxic effect of TNFalpha treatment was observed in these cell clones. When ACpRc-1 cells were seeded on type IV collagen-coated dishes in the presence of both TNFalpha and plasmin, type IV collagen interaction with the cells was lost and the cells entered apoptosis. However, even when ACMT-6 and ACMT-7 cells were cultured under the same culture conditions as those for ACpRc-1, these cell clones attached to the substrate and grew consistently without showing apoptosis. Conclusion. These observations indicate that suppression of TNFalpha-induced MMP-9 production by the introduction of srIkappaBalpha cDNA corrected the aberrant in vitro morphogenesis of acinar cells grown on type IV collagen.