Yuji Hatakeyama

Anthropogenic pressures and climate change are altering coastal environments and the body condition and biochemical composition of marine organisms. In the field, however, many environmental factors vary simultaneously, and the pathways through which individual factors act are difficult to separate. We sampled seawater and Pacific oysters (Crassostrea gigas), an important fishery species, at 22 coastal sites in northeastern Japan in late spring 2023 and 2024, and measured physical and chemical variables of environmental and oyster samples. We used redundancy analysis (RDA) and a Bayesian network (BN) to distinguish factors directly associated with oyster condition from those linked to it through other variables. The RDA showed differences among sites and between years. In the BN, cumulative water temperature was negatively related to the oyster condition index (CI), whereas indices of food quantity and quality showed no direct association. Particulate organic carbon was positively associated with total dry mass, suggesting that food availability relates to overall growth rather than to condition. Salinity was negatively related to CI only indirectly, through the arachidonic acid proportion and nitrogen-to-carbon ratio of soft tissue, consistent with an osmoregulatory response. A second salinity-linked pathway appeared in the carbon stable isotope ratios of particulate organic matter and oyster soft tissue, indicating a shift from riverine to oceanic food source. Physicochemical environmental variables such as water temperature and salinity were more closely associated with CI than food limitation. The BN separated directly associated factors from candidate indirect pathways, providing a foundation for generating causal hypotheses regarding coastal ecosystem responses.

Amelogenin is one of the enamel matrices secreted by ameloblasts. A mutation of the amelogenin gene can cause hereditary dental enamel defects known as amelogenesis imperfecta (AI). Since lysosome-associated membrane protein-1 (LAMP-1), -3 (LAMP-3), and 78kDa glucose-related protein (Grp78) were identified as binding proteins of amelogenin, several studies have suggested the involvement of these binding proteins with the cell kinetics of ameloblasts in normal or abnormal conditions. The purpose of this study is to investigate the distribution of these amelogenin binding proteins in the ameloblast cell differentiation of mice with a point mutation of the amelogenin gene (Amelx*). The incisors of Amelx* mice had a white opaque color and the tooth surface was observed to be rough under a scanning electron microscope. Among the sequential ameloblast cell differentiation in the Amelx* mice, the shape of ameloblasts at the transition stage was irregular in comparison to those in wild-type (WT) mice. Immunostaining of Grp78 revealed that the whole cytoplasm of the transition stage ameloblasts was immunopositive for Grp78 antibody, while only the distal part of cell was positive in the WT mice. Furthermore, in the Amelx* mice, the cytoplasm of the transition stage ameloblasts was immunopositive for LAMP-1 and LAMP-3. These results suggest that Amelx* may cause the abnormal distribution of amelogenin binding proteins in the cytoplasm of ameloblasts.

Purpose We aimed to evaluate the incidence of (and risk factors for) postoperative pregabalin and/or limaprost to treat persistent numbness and/or pain of the lower extremities after lumbar spinal stenosis (LSS) surgery. Methods Medical records of 329 patients (168 men, 161 women; average age 70 years) were retrospectively reviewed for data on the duration of LSS diagnosis; LSS disease; preoperative medication (limaprost, pregabalin, or combined limaprost/pregabalin; duration); symptoms; preoperative/postoperative intermittent claudication (IC); operation type; and postoperative medication and period. Results Limaprost, pregabalin, and combined limaprost/pregabalin were prescribed preoperatively for 43%, 7%, and 5% of patients, respectively. At an average of 21 months postoperatively, limaprost, pregabalin, and combined therapy were prescribed in 11%, 8%, 4% of patients, respectively. Medication requirement was significantly lower postoperatively than preoperatively (P < 0.0001). Significant risk factors for required postoperative medication were required preoperative medication (odds ratio [OR] 3.088, 95% confidence interval [CI] 1.679 to 5.681]; postoperative period (OR 1.063, 95% CI 1.031 to 1.096); and postoperative IC (OR 3.868, 95% CI 1.481 to 10.103). A negative impact from postoperative medication was seen in patients who had undergone decompression surgery (OR 0.589, 95% CI 0.377 to 0.918). Conclusions Overall, 23% of LSS patients required medication for pain and/or numbness at 21 months postoperatively. Significant factors portending required postoperative medication were preoperative medication, longer postoperative period, and postoperative IC. A negative influence from postoperative medication was seen in patients who had undergone decompression surgery without fusion.

Recently, we reported that toll-like receptor (TLR)2 and TLR4 localized on the glomerular endothelium in the glomeruli of streptozotocin (STZ)-induced type 1 diabetic mice and high fat diet feed-induced type 2 diabetic mice, and that periodontal pathogen Porphyromonas gingivalis LPS (Pg-LPS) administration lowered the survival rate of diabetic mice. The present study aims to examine the effect of TLR4 blocking on the suppression of Pg-LPS-induced diabetic nephropathy. The survival rate and morphological/biochemical features for streptozotocin-induced diabetic mice with Pg-LPS and TLR4 blocker eritoran administration were investigated by reporter gene assay, urine and blood analysis, immunohistochemistry, and real time-PCR. All of the diabetic mice administered Pg-LPS were euthanized within the survival period of almost all of the diabetic mice. The blood urea nitrogen and creatinine, expression of TLR2 and TGF-b, and type 1 collagen accumulation, in the diabetic mice increased significantly with the Pg-LPS administration. In spite of the limited TLR4 activation with Pg-LPS, the TLR4 blocker eritoran decreased blood urea nitrogen and creatinine, and raised the survival rate of the Pg-LPS-administered diabetic mice slightly. The high expression levels of TLR2, TGF-b, and type 1 collagen in Pg-LPS-administered diabetic mice decreased with eritoran. Nuclear STAT3 which enhances TLR2 expression was detected in the TLR2-expressing glomeruli of diabetic mice. The TLR2 and STAT3 gene expression increased by the Pg-LPS administration but decreased with eritoran. These may suggest that Pg-LPS-induced diabetic nephropathy is mainly dependent on TLR2 signaling on glomerular endothelial cells, and that TLR4 blocker eritoran may play a role to slow the progress of diabetic nephropathy.

Ameloblastoma is a locally invasive benign epithelial odontogenic tumor and its histopathological structures are similar to the enamel organ. Although various studies have investigated cell proliferation in ameloblastoma to elucidate the biological behavior and clinicopathological mechanisms, it remains poorly understood. The studies on the development of the enamel organ reports that FGF-9, -10, and TGF-β1 are strongly involved in dental epithelial cell differentiation and cell proliferation. In this study, we attempt to evaluate the effect of these growth factors on ameloblastoma cells. Both collagen-coated and normal plastic cell culture plate cell growth curves were steeper in the presence of growth supplement than in the absence of growth supplement. The presence of TGF-β1 at each dose (1 to 10 ng/ml), however, suppressed the number of cells cultured on the collagen-coated plate but made no significant difference on the normal plastic plate. The number of cells was increased in the presence of FGF-10 at 100 ng/ml, but not in the presence of FGF-9 after 48 h culture. These results suggest that FGF-10 and TGF-β1 play distinct roles in the cell proliferation of human ameloblastoma cells.