The buccal fat pad is specialized fat tissue located anterior to the masseter muscle and deep to the buccinator muscle. Possessing a central body and four processes it provides separation allowing gliding motion between muscles, protects the neurovascular bundles from injuries, and maintains facial convexity. Because of its many advantageous functions, the use of the buccal fat pad during oral and maxillofacial procedures is promoted for the reconstruction of defects secondary to tumor resection, and those defects resulting from oroantral fistula caused by dento-alveolar surgery or trauma. We used the pedicled buccal fat pad in the reconstruction of intraoral defects such as oroantral fistula, maxillary posterior bone loss, or defects resulting from tumor resection. Epithelization of the fat tissue began 1 week after the surgery and demonstrated stable healing without complications over a long-term period. Thus, we highly recommend the use of this procedure.
Adipose Tissue ; Masseter Muscle ; Muscles ; Oral Surgical Procedures ; Oroantral Fistula

BACKGROUND/AIMS: To determine the changes in body weight and bone mineral density in patients with ankylosing spondylitis (AS) receiving anti-tumor necrosis factor-alpha (TNF-alpha) treatment. METHODS: Thirty-one patients with AS (25 males and 6 females) who fulfilled the Modified New York Criteria for AS were included in this retrospective study. All patients had active disease that eventually required anti-TNF-alpha treatment. Each patient received anti-TNF-alpha treatment (etanercept 25 mg twice weekly or adalimumab 40 mg twice monthly) for more than 2 years. Body weight, disease activity as Bath ankylosing spondylitis disease activity index (BASDAI), C-reactive protein, erythrocyte sedimentation rate (ESR), lumbar bone mineral density (LBMD), and femoral bone mineral density (FBMD) were measured at baseline and at 1 and 2 years after initiating anti-TNF-alpha treatment. RESULTS: There was a significant increase in mean body weight at 1 year (1.1 +/- 3.8 kg) and at 2 years (1.7 +/- 4.8 kg) compared with baseline. The gains in mean BMD of the lumbar spine were significant at 1 year (0.4 +/- 0.4) and 2 years (0.5 +/- 0.7) compared with baseline. Mean BMD of the femur was also increased at 1 year (0.08 +/- 0.7) and 2 years (0.1 +/- 0.8) compared with baseline, but these differences were not statistically significant. There were significant decreases in BASDAI at 1 year (-3.3 +/- 2.8) and at 2 years (-3.6 +/- 2.8) compared with baseline. CONCLUSIONS: This study showed significant increases in body weight, lumbar BMD, and BASDAI at 1 year and 2 years in patients with ankylosing spondylitis after receiving anti-TNF-alpha treatment.
Antibodies, Monoclonal, Humanized ; Baths ; Blood Sedimentation ; Body Weight* ; Bone Density* ; C-Reactive Protein ; Cachexia ; Femur ; Humans ; Male ; Necrosis* ; Retrospective Studies ; Spine ; Spondylitis ; Spondylitis, Ankylosing* ; Adalimumab

BACKGROUND/AIMS: To determine the changes in body weight and bone mineral density in patients with ankylosing spondylitis (AS) receiving anti-tumor necrosis factor-alpha (TNF-alpha) treatment. METHODS: Thirty-one patients with AS (25 males and 6 females) who fulfilled the Modified New York Criteria for AS were included in this retrospective study. All patients had active disease that eventually required anti-TNF-alpha treatment. Each patient received anti-TNF-alpha treatment (etanercept 25 mg twice weekly or adalimumab 40 mg twice monthly) for more than 2 years. Body weight, disease activity as Bath ankylosing spondylitis disease activity index (BASDAI), C-reactive protein, erythrocyte sedimentation rate (ESR), lumbar bone mineral density (LBMD), and femoral bone mineral density (FBMD) were measured at baseline and at 1 and 2 years after initiating anti-TNF-alpha treatment. RESULTS: There was a significant increase in mean body weight at 1 year (1.1 +/- 3.8 kg) and at 2 years (1.7 +/- 4.8 kg) compared with baseline. The gains in mean BMD of the lumbar spine were significant at 1 year (0.4 +/- 0.4) and 2 years (0.5 +/- 0.7) compared with baseline. Mean BMD of the femur was also increased at 1 year (0.08 +/- 0.7) and 2 years (0.1 +/- 0.8) compared with baseline, but these differences were not statistically significant. There were significant decreases in BASDAI at 1 year (-3.3 +/- 2.8) and at 2 years (-3.6 +/- 2.8) compared with baseline. CONCLUSIONS: This study showed significant increases in body weight, lumbar BMD, and BASDAI at 1 year and 2 years in patients with ankylosing spondylitis after receiving anti-TNF-alpha treatment.
Antibodies, Monoclonal, Humanized ; Baths ; Blood Sedimentation ; Body Weight* ; Bone Density* ; C-Reactive Protein ; Cachexia ; Femur ; Humans ; Male ; Necrosis* ; Retrospective Studies ; Spine ; Spondylitis ; Spondylitis, Ankylosing* ; Adalimumab

PURPOSE: Glioblastoma (GBM) is classified as one of the most aggressive and lethal brain tumor. Great strides have been made in understanding the genomic and molecular underpinnings of GBM, which translated into development of new therapeutic approaches to combat such deadly disease. However, there are only few therapeutic agents that can effectively inhibit GBM invasion in a clinical framework. In an effort to address such challenges, we have generated anti-SEMA3A monoclonal antibody as a potential therapeutic antibody against GBM progression. MATERIALS AND METHODS: We employed public glioma datasets, Repository of Molecular Brain Neoplasia Data and The Cancer Genome Atlas, to analyze SEMA3A mRNA expression in human GBM specimens. We also evaluated for protein expression level of SEMA3A via tissue microarray (TMA) analysis. Cell migration and proliferation kinetics were assessed in various GBM patient-derived cells (PDCs) and U87-MG cell-line for SEMA3A antibody efficacy. GBM patient-derived xenograft (PDX) models were generated to evaluate tumor inhibitory effect of anti-SEMA3A antibody in vivo. RESULTS: By combining bioinformatics and TMA analysis, we discovered that SEMA3A is highly expressed in human GBM specimens compared to non-neoplastic tissues. We developed three different anti-SEMA3A antibodies, in fully human IgG form, through screening phage-displayed synthetic antibody library using a classical panning method. Neutralization of SEMA3A significantly reduced migration and proliferation capabilities of PDCs and U87-MG cell line in vitro. In PDX models, treatment with anti-SEMA3A antibody exhibited notable tumor inhibitory effect through down-regulation of cellular proliferative kinetics and tumor-associated macrophages recruitment. CONCLUSION: In present study, we demonstrated tumor inhibitory effect of SEMA3A antibody in GBM progression and present its potential relevance as a therapeutic agent in a clinical framework.
Antibodies ; Brain ; Brain Neoplasms ; Cell Line ; Cell Movement ; Computational Biology ; Dataset ; Down-Regulation ; Genome ; Glioblastoma* ; Glioma ; Heterografts ; Humans ; Immunoglobulin G ; In Vitro Techniques ; Kinetics ; Macrophages ; Mass Screening ; Methods ; RNA, Messenger ; Semaphorin-3A

Background: Carvedilol is one of the most effective beta-blockers in reducing ventricular tachyarrhythmias and mortality in patients with heart failure. One of the possible antiarrhythmic mechanisms of carvedilol is the suppression of store overload-induced Ca2+ release, especially for the triggered activity. Objectives: Premature ventricular complex (PVC) originating from the ventricular outflow tract (OT) is the most common form of idiopathic PVC, and its main mechanism is related to triggered activity. We evaluate the efficacy of carvedilol to suppress the OT PVC. Methods: The electronic medical records at our hospital were screened to identify OT PVC patients treated with carvedilol. Clinical, electrocardiographic, and Holter monitoring studies were reviewed. Results: A total of 25 patients who underwent Holter monitoring before and after carvedilol administration were found and enrolled. The mean age of the patients was 54.9 ± 13.9 years, and the mean dose of carvedilol was 18.2 ± 10.2 mg (sustained release formulation, 8/16/32 mg). The 24-h burden of PVC in 18 (72%) of 25 patients was significantly reduced from 12.2 ± 9.7% to 4.4 ± 6.7% (P = 0.006). In seven patients, the burden of PVC was changed from 7.1 ± 6.1% to 9.8 ± 8.4% (P = 0.061). There was no difference in age, carvedilol dose, duration of treatment, ventricular function, and left atrial size between responding and non-responding groups. Conclusion In this retrospective pilot study, treatment with carvedilol showed PVC suppression in 72% of patients. Now, we are conducting a prospective, randomized, multicenter study to evaluate the effect of carvedilol on OT PVC (Clinical trial registration: FOREVER trial, Clinical-Trials.gov: NCT03587558).