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Objectives: In this study, the correlation between anterior chamber depth (ACD) and corneal endothelial cell density (CECD) loss was evaluated, and an assessment was made of the safety and efficacy of the eight-chop technique in cataract surgery for patients with shallow anterior chamber (SAC) depth. Methods: The technique was applied to patients with SAC and normal ACD, defined as <3 mm and ≥3 mm, respectively. Best-corrected visual acuity (BCVA), intraocular pressure (IOP), CECD, coefficient of variation, percentage of hexagonal cells, and central corneal thickness were assessed pre- and postoperatively. Operative time, phaco time, aspiration time, cumulative dissipated energy (CDE), and volume of fluid used were recorded intraoperatively. Results: A total of 180 eyes from 99 patients (mean age, 74.8 ± 5.1 years; 28 men, 71 women) were analyzed. In the SAC group, the mean operative time, phaco time, aspiration time, CDE, and volume of fluid used were 4.7 min, 15.4 s, 65.6 s, 5.87, and 26.6 mL, respectively, demonstrating favorable surgical metrics. CECD loss was 1.3% at 7 weeks, 1.1% at 19 weeks, and 0.9% at 1 year, with no significant decrease after surgery in the SAC group. No correlation was observed between CECD loss and ACD in either group. Conclusions: These findings suggest that the eight-chop technique is a minimally invasive and effective approach that preserves corneal endothelial integrity, even in patients with SAC depth.

Objectives: This study aimed to evaluate the safety and efficacy of the eight-chop technique in cataract surgery in patients with pseudoexfoliation (PEX) syndrome and assess the intraoperative parameters, changes in corneal endothelial cells, intraocular pressure (IOP), and intraoperative complications. Methods: This technique was applied in patients with and without PEX syndrome. Preoperative and postoperative assessments were conducted on best-corrected visual acuity, IOP, corneal endothelial cell density (CECD), coefficient of variation, percentage of hexagonal cells, and central corneal thickness. Intraoperative recordings included operative time, phaco time, aspiration time, cumulative dissipated energy (CDE), and fluid of volume used. Results: We analyzed 150 eyes from 150 patients (mean age, 75.5 ± 5.7 years; 59 men, 91 women). In the PEX group, operative time, phaco time, aspiration time, CDE, and volume of fluid used were 6.7 min, 17.4 s, 85.2 s, 6.91 µJ, and 33.4 mL, respectively, demonstrating favorable surgical metrics. On the other hand, in the control group, operative time, phaco time, aspiration time, CDE, and volume of fluid used were 4.5 min, 14.3 s, 64.0 s, 5.83 µJ, and 25.5 mL, respectively. In addition, CECD losses were 3.7% at week 7 and 2.7% at week 19 in the PEX group and 2.7% and 1.6%, respectively, in the control group. Significant decreases were observed at 7 and 19 weeks postoperatively in the PEX and control groups. No eye in the PEX group required a capsular tension ring due to zonular dialysis. Conclusions: The eight-chop technique in cataract surgery demonstrates excellent intraoperative parameters in patients with PEX, is effective against zonular weakness, and does not require the use of a capsular tension ring. This technique will aid in establishing personalized treatment strategies and improve cataract management and treatment.

Objectives: To estimate the efficacy of the eight-chop technique in phacoemulsification surgeries for patients with hard nucleus cataracts by investigating the reduction of corneal endothelial cell density (CECD) after phacoemulsification and intraoperative parameters. Methods: Patients were categorized into three groups (Grade IV, IV plus, and V) according to the hardness of their lens nuclei. Surgeries were performed using the eight-chop technique. Key intraoperative metrics (operative time, phaco time, aspiration time, cumulative dissipated energy [CDE], and fluid volume used) were measured. Pre- and postoperative assessments included corrected-distance visual acuity, intraocular pressure (IOP), central corneal thickness, variation in the size of the endothelial cells, percentage of hexagonal cells, and CECD. Results: Overall, 89 eyes from 67 patients with cataracts were evaluated. The mean operative time, phaco time, aspiration time, CDE, and fluid volume used across Grades IV, IV plus, and V were 10.5 min, 38.9 s, 135.6 s, 19.2, and 53.0 mL, respectively. At 19 weeks postoperatively, the CECD decreased by 0.2%, 6.8%, and 9.6% for Grades IV, IV plus, and V, respectively, with an average decrease of 3.7%. Significant reductions in postoperative IOP were observed across all groups compared with preoperative IOP (p < 0.01). Loss of CECD significantly correlated with phaco time, CDE, and fluid volume (p = 0.027, p < 0.01, and 0.034, respectively). Conclusions: The eight-chop technique in phacoemulsification for hard nucleus cataracts resulted in minimal CECD loss. It may provide an effective surgical solution for patients with hard nucleus cataracts.

Background/Objectives: To analyze corneal endothelial changes and intraocular pressure (IOP) after phacoemulsification combined with the eight-chop technique and intraoperative parameters in patients with diabetes mellitus. Methods: The eyes of patients with cataracts who underwent phacoemulsification were analyzed in this study. Based on their hemoglobin A1c levels, patients were divided into two groups. The eight-chop technique was used for cataract surgery. The operative time, the phaco time, the aspiration time, the cumulative energy dissipated, and the volume of fluid used were determined. Best corrected visual acuity, IOP, corneal endothelial cell density (CECD), central corneal thickness (CCT), coefficient of variation (CV), and percentage of hexagonal cells (PHC) were recorded before and after surgery. Results: Overall, 181 eyes of 138 patients with cataracts were evaluated. In the diabetes group, the CECD loss rates were 5.1%, 3.9%, and 2.1% at 7 weeks, 19 weeks, and 1 year postoperatively, respectively. In the control group, the CECD loss rates were 2.8%, 2.6%, and 1.2% at 7 weeks, 19 weeks, and 1 year postoperatively, respectively. Significant differences in the percentage decrease in CECD were observed between the two groups at 7 and 19 weeks postoperatively. Significant differences in the CV and PHC were observed preoperatively and postoperatively between the diabetes and control groups (p < 0.01 or p = 0.01, 0.02). Significant differences were also observed between CV and PHC preoperatively, at 19 weeks, and 1 year postoperatively in the diabetes and control groups (p < 0.01). At 1 year postoperatively, IOP reduction rates were 8.0% and 11.2% in the diabetes and control groups, respectively. Conclusions: CECD loss was minimal with the eight-chop technique; however, the diabetes group showed a higher percentage decrease than the control group up to 19 weeks postoperatively. In addition, although IOP decreased in both groups after surgery, the percentage decrease was significantly different at 1 year postoperatively. This study suggests that the corneal endothelial cells of diabetic eyes may be more fragile than those of normal eyes and that the long-term postoperative IOP-lowering effect may be attenuated. These findings will contribute to advances in personalized treatment strategies for patients with diabetes.

Sema3A, a member of the semaphorin family of proteins, is shown to regulate bone remodelling indirectly by modulating sensory nerve development in mice. A role for sensory nerves in bone remodelling The semaphorins are diffusible proteins involved in the development of the nervous system, organs and blood vessels, as well as in immunity. Osteoblasts and osteoclasts express semaphorin family members, and it has been shown recently that semaphorin 3A (Sema3A) can regulate bone remodelling by acting locally. Here Toru Fukuda et al . demonstrate that Sema3A regulates bone remodelling in vivo indirectly by modulating sensory nerve development. Semaphorin 3A (Sema3A) is a diffusible axonal chemorepellent that has an important role in axon guidance 1 , 2 , 3 , 4 , 5 . Previous studies have demonstrated that Sema3a −/− mice have multiple developmental defects due to abnormal neuronal innervations 6 , 7 . Here we show in mice that Sema3A is abundantly expressed in bone, and cell-based assays showed that Sema3A affected osteoblast differentiation in a cell-autonomous fashion. Accordingly, Sema3a −/− mice had a low bone mass due to decreased bone formation. However, osteoblast-specific Sema3A-deficient mice ( Sema3a col1 −/− and Sema3a osx −/− mice) had normal bone mass, even though the expression of Sema3A in bone was substantially decreased. In contrast, mice lacking Sema3A in neurons ( Sema3a synapsin −/− and Sema3a nestin −/− mice) had low bone mass, similar to Sema3a −/− mice, indicating that neuron-derived Sema3A is responsible for the observed bone abnormalities independent of the local effect of Sema3A in bone. Indeed, the number of sensory innervations of trabecular bone was significantly decreased in Sema3a synapsin −/− mice, whereas sympathetic innervations of trabecular bone were unchanged. Moreover, ablating sensory nerves decreased bone mass in wild-type mice, whereas it did not reduce the low bone mass in Sema3a nestin −/− mice further, supporting the essential role of the sensory nervous system in normal bone homeostasis. Finally, neuronal abnormalities in Sema3a −/− mice, such as olfactory development, were identified in Sema3a synasin −/− mice, demonstrating that neuron-derived Sema3A contributes to the abnormal neural development seen in Sema3a −/− mice, and indicating that Sema3A produced in neurons regulates neural development in an autocrine manner. This study demonstrates that Sema3A regulates bone remodelling indirectly by modulating sensory nerve development, but not directly by acting on osteoblasts.

Integrin activation is associated with conformational regulation. In this study, we developed a system to evaluate conformational changes in α 4 β 7 integrin. We first inserted the PA tag into the plexin-semaphorin-integrin (PSI) domain of β 7 chain, which reacted with an anti-PA tag antibody (NZ-1) in an Mn 2+ -dependent manner. The small GTPase Rap1 deficiency, as well as chemokine stimulation and the introduction of the active form of Rap1, Rap1V12, enhanced the binding of NZ-1 to the PA-tagged mutant integrin, and increased the binding affinity to mucosal addressing cell adhesion molecule-1 (MAdCAM-1). Furthermore, we generated two kinds of hybridomas producing monoclonal antibodies (mAbs) that recognized Mn 2+ -dependent epitopes of β 7 . Both epitopes were exposed to bind to mAbs on the cells by the introduction of Rap1V12. Although one epitope in the PSI domain of β 7 was exposed on Rap1-deficienct cells, the other epitope in the hybrid domain of β 7 was not. These data indicate that the conversion of Rap1-GDP to GTP exerts two distinct effects stepwise on the conformation of α 4 β 7 . The induction of colitis by Rap1-deficient CD4 + effector/memory T cells suggests that the removal of constraining effect by Rap1-GDP on α 4 β 7 is sufficient for homing of these pathogenic T cells into colon lamina propria (LP).

The differentiation and function of osteocytes are controlled by surrounding cells and mechanical stress; however, the detailed mechanisms are unknown. Recent findings suggest that IL-33 is highly expressed in periodontal tissues in orthodontic tooth movement. The present study aimed to elucidate the effect of IL-33 on the expression of regulatory factors for bone remodeling and their molecular mechanisms in the osteocyte-like cell line MLO-Y4. MLO-Y4 cells were treated with IL-33, and the activation of intracellular signaling molecules and transcriptional factors was determined using Western blot analysis and chromatin immunoprecipitation assay. IL-33 treatment enhanced the expression of IL-6 in MLO-Y4 cells, which was suppressed by the knockdown of the IL-33 receptor ST2L. Additionally, IL-33 treatment induced activation of NF-κB, JNK/AP-1, and p38 MAPK signaling pathways in MLO-Y4 cells. Moreover, pretreatment with specific inhibitors of NF-κB, p38 MAPK, and JNK/AP-1 attenuated the IL-33-induced expression of IL-6. Furthermore, chromatin immunoprecipitation indicated that IL-33 increased c-Jun recruitment to the IL-6 promoter. Overall, these results suggest that IL-33 induces IL-6 expression and regulates osteocyte function via activation of the NF-κB, JNK/AP-1, and p38 MAPK pathways through interaction with ST2L receptors on the plasma membrane.

Periodontitis is a biofilm-driven inflammatory disease in which conventional indices (probing depth, clinical attachment level, and radiographs) quantify tissue destruction without capturing the biology of infection. In this review, we synthesized microbiological diagnostics, from chairside tools to omics. We outline sampling strategies and emphasize the quantitative monitoring of bacterial load. Enzymatic assays (e.g., N-benzoyl-DL-arginine-2-naphthylamide hydrolysis assay test) measure functional activity at the point of care. Immunological methods include rapid immunochromatography for Porphyromonas gingivalis and enzyme-linked immunosorbent assay for the high-throughput measurement of bacterial antigens. Molecular platforms encompass quantitative polymerase chain reaction (qPCR) (TaqMan, SYBR, multiplex panels; propidium monoazide quantitative-qPCR for viable cells), checkerboard DNA–DNA hybridization for semi-quantitative community profiling, loop-mediated isothermal amplification (LAMP)/molecular beacon-LAMP for portable isothermal detection, and microarrays. Complementary modalities such as fluorescent in situ hybridization, next-generation sequencing, and Fourier transform infrared spectroscopy provide spatial, ecological, and biochemical resolutions. We discuss the limitations of current approaches, including sampling bias, presence–activity discordance, semi-quantitation, method biases, limited strain/function resolution, low-biomass artifacts, and lack of validated cutoffs. To address these challenges, we propose a pragmatic hybrid strategy: site-specific quantitative panels combined with activity and host-response markers interpreted alongside clinical metrics under standardized quality assurance/quality control. Priorities include outcome-linked thresholds, strain-aware/functional panels, robust point-of-care chemistry, and harmonized protocols to enable personalized periodontal care.

Both Achilles and masticatory muscle tendons are large load-bearing structures, and excessive mechanical loading leads to hypertrophic changes in these tendons. In the maxillofacial region, hyperplasia of the masticatory muscle tendons and aponeurosis affect muscle extensibility resulting in limited mouth opening. Although gene expression profiles of Achilles and patellar tendons under mechanical strain are well investigated in rodents, the gene expression profile of the masticatory muscle tendons remains unexplored. Herein, we examined the gene expression pattern of masticatory muscle tendons and compared it with that of Achilles tendons under tensile strain conditions in the Japanese macaque Macaca fuscata . Primary tenocytes isolated from the masticatory muscle tendons (temporal tendon and masseter aponeurosis) and Achilles tendons were mechanically loaded using the tensile force and gene expression was analyzed using the next-generation sequencing. In tendons exposed to tensile strain, we identified 1076 differentially expressed genes with a false discovery rate (FDR) < 10 −10 . To identify genes that are differentially expressed in temporal tendon and masseter aponeurosis, an FDR of < 10 −10 was used, whereas the FDR for Achilles tendons was set at > 0.05. Results showed that 147 genes are differentially expressed between temporal tendons and masseter aponeurosis, out of which, 125 human orthologs were identified using the Ensemble database. Eight of these orthologs were related to tendons and among them the expression of the glycoprotein nmb and sphingosine kinase 1 was increased in temporal tendons and masseter aponeurosis following exposure to tensile strain. Moreover, the expression of tubulin beta 3 class III, which promotes cell cycle progression, and septin 9, which promotes cytoskeletal rearrangements, were decreased in stretched Achilles tendon cells and their expression was increased in stretched masseter aponeurosis and temporal tendon cells. In conclusion, cyclic strain differentially affects gene expression in Achilles tendons and tendons of the masticatory muscles.

Background This study was conducted to determine gender differences in the relationship between extracurricular sports activities (ECSA) and low back pain (LBP) in children and adolescents. Methods In a cohort analysis of a 6-year birth cohort annual survey, students were followed from the fourth to sixth grades of elementary school (E4–E6; 9–12 years old) through the first to third grades of junior high school (J1–J3; 12–15 years old). All students completed annual questionnaires on ECSA and LBP. The odds ratio (OR) and 95% confidence interval (CI) were calculated to assess the association strength between ECSA and LBP. We also calculated the population attributable fraction (PAF), which was defined as the proportion of students with ECSA-related LBP among all students with LBP. Results ECSA was significantly associated with LBP only in grade J3 among boys (OR: 2.00, 95% CI: 1.47–2.71). On the other hand, among girls, ECSA was significantly associated with LBP in grades E5 (OR: 1.48, 95% CI: 1.00–2.20), E6 (OR: 1.91, 95% CI: 1.33–2.75), and J3 (OR: 1.81, 95% CI: 1.26–2.61). Among boys, PAF was similar in all grades (range, 10–16%), whereas among girls, the PAF varied (− 11 to 29%) and was significantly higher in girls than in boys in grades E5 (19.0% vs. 1.1%, P  < 0.01) and E6 (28.8% vs. 12.8%, P  < 0.01). Conclusions Although there was a link between ECSA and LBP in both boys and girls, girls were more susceptible to ECSA-related LBP, especially in grades E5 and E6.