Demineralized Frozen-dried Allogeneic Bone Blocks with Suture Fixation Technique for reconstruction of maxillary alveolar bone deficiency: A Case Series.

PURPOSE: This study aims to evaluate the clinical outcomes of using demineralized freeze-dried allogeneic bone blocks (DFDABB) combined with the periosteal vertical mattress suture (PVMS) technique for the reconstruction of severe horizontal alveolar bone deficiencies in the maxilla. METHOD: In continuous horizontal maxillary defects cases, bone augmentation was performed using DFDABB and deproteinized bovine bone matrix (DBBM) filling the interstice. Subsequently, a resorbable collagen membrane was carefully placed over the graft surface, and both the membrane and bone graft were firmly secured using the periosteal vertical mattress suture technique (PVMS). Linear changes were assessed through superimposed cone-beam computed tomography (CBCT) scans obtained before the operation and after a healing period of 6-10 months. RESULTS: A total of 7 female patients with ten bone blocks and 13 implants were included in this study. One of the wounds was slightly ruptured postoperatively without infection, and all implants showed successful osseointegration. The average alveolar ridge width at a point 5 mm below the crest was 4.52 ± 2.03 mm before bone graft and 9.79 ± 1.57 mm after implantation, with an average increase of 5.26 ± 1.97 mm. Similarly, at a point 10 mm below the crest, the pre-graft alveolar ridge width measured 7.23 ± 3.60 mm, and post-implantation, it expanded to 11.81 ± 2.90 mm, showing an average gain of 4.58 ± 2.01 mm. CONCLUSION: This case series demonstrates the successful application of DFDABB combined with the PVMS technique to achieve adequate bone width for implantation at severe continuous horizontal bone deficiency of the maxilla. DFDABB with the PVMS technique resulted in superior horizontal bone gain during maxillary bone augmentation with horizontal continuity deficiency. However, further studies are necessary to validate these findings.

Syringaresinol attenuates Tau phosphorylation and ameliorates cognitive dysfunction induced by sevoflurane in aged rats.

Cognitive dysfunction following anesthesia with agents such as sevoflurane is a significant clinical problem, particularly in elderly patients. This study aimed to explore the protective effects of the phytochemical syringaresinol (SYR) against sevoflurane-induced cognitive deficits in aged Sprague-Dawley rats and to determine the underlying mechanisms involved. We assessed the impact of SYR on sevoflurane-induced cognitive impairment, glial activation, and neuronal apoptosis through behavioral tests (Morris water maze), immunofluorescence, Western blotting for key proteins involved in apoptosis and inflammation, and enzyme-linked immunosorbent assays for interleukin-1ß, tumor necrosis factor-α, and interleukin-6. SYR treatment mitigated sevoflurane-induced cognitive decline, reduced microglial and astrocyte activation (decreased Iba-1 and GFAP expression), and countered neuronal apoptosis (reduced Bax, cleaved-caspase3, and cleaved-PARP expression). SYR also enhanced Sirtuin-1 (SIRT1) expression and reduced p-Tau phosphorylation; these effects were reversed by the SIRT1 inhibitor EX527. SYR exerts neuroprotective effects on sevoflurane-induced cognitive dysfunction by modulating glial activity, apoptotic signaling, and Tau phosphorylation through the SIRT1 pathway. These findings could inform clinical strategies to safeguard cognitive function in patients undergoing anesthesia.

A Germinal Center Checkpoint of AIRE in B Cells Limits Antibody Diversification.

In response to antigens, B cells undergo affinity maturation and class switching mediated by activation-induced cytidine deaminase (AID) in germinal centers (GCs) of secondary lymphoid organs, but uncontrolled AID activity can precipitate autoimmunity and cancer. The regulation of GC antibody diversification is of fundamental importance but not well understood. We found that autoimmune regulator (AIRE), the molecule essential for T cell tolerance, is expressed in GC B cells in a CD40-dependent manner, interacts with AID and negatively regulates antibody affinity maturation and class switching by inhibiting AID function. AIRE deficiency in B cells caused altered antibody repertoire, increased somatic hypermutations, elevated autoantibodies to T helper 17 effector cytokines and defective control of skin Candida albicans. These results define a GC B cell checkpoint of humoral immunity and illuminate new approaches of generating high-affinity neutralizing antibodies for immunotherapy.