BACKGROUND: Recruitment and homing cells into graft materials from host tissue is crucial for bone regeneration. METHODS: Highly porous, multi-level structural, hydroxyapatite bone void filler (HA-BVF) have been investigated to restore critical size bone defects. The aim was to investigate a feasibility of bone regeneration of synthetic HA-BVF compared to commercial xenograft (Bio-Oss). HA-BVF of 0.7 mm in average diameter was prepared via template coating method. Groups of animals (n = 6) were divided into two with normal (Sham) or induced osteoporotic conditions (Ovx). Subsequently, subdivided into three treated with HA-BVF as an experiment or Bio-Oss as a positive control or no treatment as a negative control (defect). The new bone formation was analyzed by micro-CT and histology. RESULTS: At 4 weeks post-surgery, new bone formation was initiated from all groups. At 8 weeks post-surgery, new bone formation in the HA-BVF groups was greater than Bio-Oss groups. Extraordinarily greater bone regeneration within the Ovx-HA group than Sham-Bio-Oss or Ovx-Bio-Oss group (p<0.05). CONCLUSION: This study suggests that the immediate wicking property of HA-BVF from host tissue activates a natural healing cascade without the addition of exogeneous factors or progenitor cells. HA-BVF may be an effective alternative for repairing bone defects under both normal and osteoporotic bone conditions.
Animals ; Bone Regeneration* ; Capillary Action* ; Durapatite ; Heterografts ; Methods ; Models, Animal* ; Osteogenesis ; Osteoporosis ; Rats* ; Stem Cells ; Transplants*

Background: This systematic review and meta-analysis aimed to evaluate the efficacy and cardiovascular safety of romosozumab compared with placebo. Methods: Randomized controlled trials (RCTs) were searched from Medline, EMBASE, Cochrane Central, and Web of Science until July 2022. Primary outcomes included the change in bone mineral density (BMD) from baseline at month 6. The secondary outcomes were the change of bone turnover markers (N-terminal propeptide of type 1 procollagen (P1NP); C-terminal telopeptide of type 1 collagen (CTX)) from baseline at month 3, and the incidence of cardiovascular adverse events for the total follow-up period. Results: A total of 7 RCTs on 8,370patients were included. Romosozumab showed better effects in improving BMD in both lumbar spine and femoral neck at month 6 (standardized mean difference, SMD 2.20 [95% CI: 1.89-2.52], SMD 0.63 [95% CI: 0.41-0.86]). In contrast to placebo, romosozumab significantly increased PINP levels and reduced CTX levels at month 3 (SMD 0.93 [95% CI: 0.65-1.22], SMD −1.03 [95% CI: −1.23~ −0.82]. However, there was no significant difference in the composite incidence of cardiovascular adverse events and major adverse cardiovascular events (OR 1.16 [95% CI: 0.82-1.65], OR 1.08 [95% CI: 0.75-1.56]). Conclusion This analysis showed that romosozumab significantly improved BMD compared to placebo and was beneficial for change in bone turnover markers. There is no significant difference in the incidence of cardiovascular adverse events compared to placebo.

Coronary artery ectasia is an uncommon disorder diagnosed in 1 to 4% of patients undergoing coronary arteriography. Coronary artery ectasia is often considered a variant of atherosclerotic coronary artery disease, although other causes should be considered. Complications from this disease usually occur as thrombo-embolic phenomena primarily due to thrombosis in the ectatic segment of the coronary artery. A 53-year old man was transferred to our ER, presenting with acute inferior wall infarction. Coronary angiogram showed a gigantic ectatic right coronary artery (RCA) with occlusion of the mid portion by a huge mural thrombus. We injected and infused glycoprotein IIb-IIIa inhibitor in the RCA, however the lysis of thrombus was minimal. Subsequently, we infused Urokinase into the RCA for 2 days. Follow-up angiography revealed partial lysis of the thrombus. The patient demonstrated no thrombo-embolic events during two months of coumadinization, and follow-up angiography revealed a complete lysis of the thrombus.
Angiography ; Coronary Artery Disease ; Coronary Vessels* ; Dilatation, Pathologic* ; Follow-Up Studies ; Glycoproteins ; Humans ; Infarction ; Middle Aged ; Myocardial Infarction* ; Thrombosis ; Urokinase-Type Plasminogen Activator ; Warfarin

Small pancreatic cancers (longest diameter < or =2 cm) have been regarded as preliminary to early pancreatic cancer, which was thought to be highly curable. During our experience since 1989, we evaluated 542 cases of pancreatic cancer. Among them we found 74 cases of tumors < or =2 cm in diameter, small pancreatic cancer (TS1 pancreatic cancer). Well-differentiated adenocarcinomas (18.9%) and absence of symptoms (8.1%) were more frequent in patients with TS1 than in those with larger pancreatic tumors. Only 16 of the 74 patients (21.6%) with small pancreatic cancers had T1 tumors. According to the International Union Against Cancer (UICC) staging, only 11 patients (14.9%) were stage IA: their 5-yr survival rate was 23.3% and their median survival was 30.0 months. Among these 11 patients, 3 had tumors <1 cm; their median survival time was 30.0 months and their 5-yr survival rate was 50.0%. These findings may indicate that 'small' pancreatic cancer is not equivalent to 'early' pancreatic cancer.
Adenocarcinoma/pathology ; Adenocarcinoma, Mucinous/pathology ; Adenocarcinoma, Papillary/pathology ; Adult ; Aged ; CA-19-9 Antigen/metabolism ; Carcinoembryonic Antigen/metabolism ; Carcinoma/pathology ; Carcinoma, Adenosquamous/pathology ; Carcinoma, Pancreatic Ductal/pathology ; Female ; Humans ; Korea/epidemiology ; Male ; Middle Aged ; Neoplasm Staging ; Pancreatic Neoplasms/immunology/mortality/*pathology ; Prognosis ; Survival Rate ; Tumor Burden

Hereditary pancreatitis is a rare, autosomal dominant, inherited disease characterized by recurrent attacks of acute pancreatitis with the development of chronic pancreatitis and an increased risk of pancreatic cancer. R122H or N29I mutation in cationic trypsinogen (protease serine 1, PRSS1) gene causes hereditary pancreatitis. R122H mutation is the most common mutation that causes pancreatitis by preventing deactivation of trypsin within the pancreas and prolonging its action. Three members of the family, the patient, her elder son, and her niece experienced recurrent attacks of pancreatitis. We analyzed five exons of the PRSS1 gene in DNA samples of five family members including her husband and younger son who were asymptomatic. We found out that four members of the family, the patient, her two sons, and her niece, had R122H mutation in the exon 3 of PRSS1 gene. Finally, we diagnosed hereditary pancreatitis in two households in the same family.
Adolescent ; Adult ; Amino Acid Substitution ; Cholangiopancreatography, Endoscopic Retrograde ; Female ; Humans ; *Mutation ; Pancreatitis, Chronic/*diagnosis/*genetics ; Pedigree ; Sequence Analysis, DNA ; Tomography, X-Ray Computed ; Trypsinogen/*genetics

New insight in the field of chronic pancreatitis was provided by the discovery of protease serine 1 (PRSS1) mutation, inherited by autosomal dominant trait in hereditary pancreatitis. Serine protease inhibior, Kazal type 1 (SPINK1) is a potent protease inhibitor which prevents premature intrapancreatic activation of trypsin and pancreatic autodigestion. Strong associations of SPINK1 mutation and different forms of pancreatitis were suggested. However, it is unlikely that SPINK1 mutation alone can cause chronic pancreatitis. This mutation acts as a disease-modifier or plays a role within polygenic or multifactorial models. A 23 year-old young woman with chronic pancreatitis was recently discovered to have SPINK1 N34S heterozygous mutation cosegregated with two intronic mutations, IVS1-37T>C and IVS3-69insTTTT, during the evaluation for potential cause of chronic idiopathic pancreatitis. The same mutation was identified in her mother. This is the first report in Korea suggesting that SPINK1 mutation would be a possible cause of chronic pancreatitis in a patient with familial background.
Adult ; Amino Acid Substitution ; Carrier Proteins/*genetics ; Cholangiopancreatography, Endoscopic Retrograde ; Family ; Female ; Heterozygote ; Humans ; *Mutation ; Pancreatitis, Chronic/*diagnosis/*genetics ; Sequence Analysis, DNA ; Tomography, X-Ray Computed

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

Ulcerative colitis (UC) is a chronic idiopathic inflammatory disorder of the colon with a variable clinical course of exacerbation and remission. Extraintestinal manifestations of UC, including hematological disorders, such as the rare immune thrombocytopenic purpura (ITP), may be the presenting symptoms. We encountered the case of a 23-year-old man with UC who showed typical symptoms and endoscopic findings. Despite receiving steroid treatment, the patient developed severe thrombocytopenia. He was diagnosed with ITP, characterized by autoimmunity, a demonstrated low platelet count, normal bone marrow, positivity for autoantibody to platelet membrane antigen, and no splenomegaly. We initiated high dose intravenous immunoglobulin immediately for treatment of his steroid-refractory thrombocytopenia. The patient's hematochezia and platelet count improved following immunoglobulin treatment. After discharge, the patient's platelet count was maintained at a stable level and his condition was good. This case suggests that immunoglobulin therapy may be useful for treatment of ITP in UC.
Autoimmunity ; Blood Platelets ; Bone Marrow ; Colitis, Ulcerative* ; Colon ; Gastrointestinal Hemorrhage ; Humans ; Immunization, Passive ; Immunoglobulins ; Membranes ; Platelet Count ; Purpura, Thrombocytopenic, Idiopathic* ; Splenomegaly ; Thrombocytopenia ; Young Adult

PURPOSE: Genetic variations among prostate cancer (PCa) patients who underwent radical prostatectomy (RP) and pelvic lymph node dissection were evaluated to predict lymph node invasion (LNI). Exome arrays were used to develop a clinicogenetic model that combined clinical data related to PCa and individual genetic variations. MATERIALS AND METHODS: We genotyped 242,186 single-nucleotide polymorphisms (SNPs) by using a custom HumanExome BeadChip v1.0 (Illumina Inc.) from the blood DNA of 341 patients with PCa. The genetic data were analyzed to calculate an odds ratio as an estimate of the relative risk of LNI. We compared the accuracies of the multivariate logistic model incorporating clinical factors between the included and excluded selected SNPs. The Cox proportional hazard models with or without genetic factors for predicting biochemical recurrence (BCR) were analyzed. RESULTS: The genetic analysis indicated that five SNPs (rs75444444, rs8055236, rs2301277, rs9300039, and rs6908581) were significant for predicting LNI in patients with PCa. When a multivariate model incorporating clinical factors was devised to predict LNI, the predictive accuracy of the multivariate model was 80.7%. By adding genetic factors in the aforementioned multivariate model, the predictive accuracy increased to 93.2% (p=0.006). These genetic variations were significant factors for predicting BCR after adjustment for other variables and after adding the predictive gain to BCR. CONCLUSIONS: Based on the results of the exome array, the selected SNPs were predictors for LNI. The addition of individualized genetic information effectively enhanced the predictive accuracy of LNI and BCR among patients with PCa who underwent RP.
Aged ; Biomarkers, Tumor/*genetics ; Biopsy ; DNA, Neoplasm/genetics ; Exome ; Gene Frequency ; Genome ; Genotype ; Humans ; Lymph Node Excision ; Lymph Nodes/pathology ; Lymphatic Metastasis ; Male ; Middle Aged ; *Models, Genetic ; Neoplasm Invasiveness ; Polymorphism, Single Nucleotide ; Predictive Value of Tests ; Prospective Studies ; Prostatectomy ; Prostatic Neoplasms/*genetics/pathology/surgery