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Aim The lateral pelvic lymph nodes are one of the major sites and sources of local recurrence ( LR) after surgery for rectal cancer. Salvage lateral pelvic lymph node dissection ( LPLD) is potentially curative, but the value of laparoscopic surgery in such cases is unknown. Our aim was to report the technical details of laparoscopic salvage LPLD for LR at these nodes after rectal cancer surgery. Method The study was based on nine patients who underwent laparoscopic salvage LPLD for LR at the lateral pelvic lymph nodes after surgery for rectal cancer. The safety and feasibility of this procedure were determined. Results The median operation time was 381 min and the median estimated blood loss was 130 ml. There were no conversions. Adjacent structures removed en bloc were the pelvic plexus in four patients, the internal iliac artery in seven patients and the seminal vesicle in one patient. The median number of metastatic lymph nodes was 1 (range 1-11). Conclusion Our novel technique of laparoscopic salvage LPLD for LR at the lateral pelvic lymph nodes is safe and feasible. [ABSTRACT FROM AUTHOR]

There are several reports suggesting that forward head posture is associated with temporomandibular disorders and restraint of mandibular growth, possibly due to mandibular displacement posteriorly. However, there have been few reports in which the condylar position was examined in forward head posture. The purpose of this study was to test the hypothesis that the condyle moves posteriorly in the forward head posture. The condylar position and electromyography from the masseter, temporal and digastric muscles were recorded on 15 healthy male adults at mandibular rest position in the natural head posture and deliberate forward head posture. The condylar position in the deliberate forward head posture was significantly more posterior than that in the natural head posture. The activity of the masseter and digastric muscles in the deliberate forward head posture was slightly increased. These results suggest that the condyle moves posteriorly in subjects with forward head posture. [ABSTRACT FROM AUTHOR]

In southern Kantoh, Japanese sika deer ( Cervus nippon) are distributed discontinuously due to large urban areas and developed road networks. To assess the impact of habitat fragmentation on sika deer subpopulations, we examined mitochondrial D-loop sequences from 435 individuals throughout southern Kantoh. About 13 haplotypes were detected, and their distributions revealed spatial genetic structure. Significant genetic differentiation was observed among seven of eight subpopulations. We found no significant correlation between pairwise F ST and geographical distance among subpopulations. Genetic diversity indices suggested that seven of eight subpopulations had probably experienced population bottlenecks in the recent past. Therefore, and in the light of the results of a nested clade analysis of these haplotypes, we conclude that recent fluctuations in population size and the interruption of gene flow due to past and present habitat fragmentation have played major roles influencing the spatial genetic structure of the sika deer population. This is the first evidence of spatial genetic population structure in the highly fragmented sika deer population in Honshu, Japan. [ABSTRACT FROM AUTHOR]

ABSTRACT The fatigue fracture surfaces of specimens of heat treated hard steels which failed in the regime of N = 10 5 to 5 × 10 8 cycles, were investigated by optical microscopy and SEM. Specimens having a longer fatigue life had a particular morphology beside the inclusion at the fracture origin. The particular morphology looked optically dark and in the previous paper it was named the Optically Dark Area, ODA. The roughness inside ODA is larger than outside ODA. The relative size of the ODA to the size of the inclusion at the fracture origin increases with increase in fatigue life. Thus, the ODA is considered to have a crucial role in the mechanism of ultra long life fatigue failure. Direct evidences of existence of hydrogen at the inclusion at fracture origin are presented. It is presumed that the ODA is made by the cyclic stress coupled with the hydrogen which is trapped by the inclusion at the fracture origin. To verify the influence of hydrogen, specimens containing different levels of hydrogen were prepared by different heat treatments. The results obtained by fatigue tests of these specimens suggest that the hydrogen trapped by inclusions is a crucial factor which causes the ultra long fatigue failure of high strength steels. Aspects of the double S–N curve are also discussed in terms of experimental methods, specimen size and statistical distribution of inclusions sizes. [ABSTRACT FROM AUTHOR]

Objective: The prominent side-effect of cyclosporin A, an immunosuppressive drug, in oral tissues is gingival outgrowth, although the exact mechanism underlying this side-effect is unclear. The main purposes of the present study were to determine whether cyclosporin A induced the gingival outgrowth by promoting proliferation of gingival cells and whether growth factors such as transforming growth factor-betas (TGF-betas), fibroblast growth factor-2 (FGF-2), platelet-derived growth factors (PDGFs), and insulin-like growth factors (IGFs) are involved in the possible changes in the proliferation of gingival cells induced by cyclosporin A., Methods: Cells isolated from rat gingival tissues were cultured with cyclosporin A or IGF-I for 3 days. The effects of cyclosporin A or IGF-I on the proliferation of cultured rat gingival cells were analyzed with a CellTiter 96 proliferation assay kit. The mRNA expression levels for TGF-betas, FGF-2, PDGFs, IGFs, insulin-like growth factor receptors (IGFRs), and insulin-like growth factor binding proteins (IGFBPs) in the rat gingival cells treated with cyclosporin A were measured using competitive reverse transcription-polymerase chain reaction (RT-PCR)., Results: Cyclosporin A induced 23-25% (p < 0.001) increases in the proliferation of rat gingival cells and approximately 130% (p < 0.05) and 60% (p < 0.05) elevations in the mRNA expression levels for TGF-beta1 and FGF-2, respectively. On the other hand, exogenous IGF-I induced 8-11% (p < 0.05) increases in the proliferation, but cyclosporin A induced 30-80% (p < 0.05-0.01) reductions in the mRNA expression levels for endogenous IGF-I, IGFR1, IGFBP2, IGFBP3, IGFBP5, and IGFBP6., Conclusions: Cyclosporin A stimulates the proliferation of rat gingival cells. TGF-beta1 and FGF-2 could be involved, but IGFs, IGFRs and IGFBPs could not be directly involved in this cyclosporin A induced-stimulation of the gingival cell proliferation.

We examined the effects of exogenous hepatocyte growth factor (HGF) on the differentiation and proliferation of tongue myoblasts by using an organ culture system of tongue obtained from mouse embryos at embryonic day (E) 13. Exogenous HGF induced reductions in the quantities of muscle creatine kinase and myogenin mRNAs and in the number of fast myosin heavy chain-positive myoblasts and myotubes, suggesting that HGF suppressed the differentiation of myoblasts in the cultured E13 tongues. Exogenous HGF induced no significant changes in the percentage of proliferating cell nuclear antigen (PCNA)-positive cell nuclei to total cell nuclei (labeling index) in the muscle portion of the cultured E13 tongue, suggesting that HGF did not affect the proliferation of myoblasts. Exogenous HGF induced the expression of myf5 mRNA but inhibited the expression of myoD mRNA. Since mouse tongue myoblasts are reported to complete proliferation by E13, it appears that exogenous HGF arrests myoblasts in the cell cycle and does not allow them to enter the differentiation process. This is achieved by controlling the expression of myf5 and myoD mRNAs, thus inhibiting the differentiation of tongue myoblasts.