Treatment of osteonecrosis of the femoral head using autologous cultured osteoblasts: a case report

<p>Abstract</p> <p>Introduction</p> <p>Osteonecrosis of the femoral head is a progressive disease that leads to femoral head collapse and osteoarthritis. Our goal in treating osteonecrosis is to preserve, not to replace, the femoral head.</p> <p>Case presentation</p> <p>We present the case of a patient with bilateral osteonecrosis of the femoral head treated with autologous cultured osteoblast injection.</p> <p>Conclusion</p> <p>Although our experience is limited to one patient, autologous cultured osteoblast transplantation appears to be effective for treating the osteonecrosis of femoral head.</p

Enhancement of protective immune responses by oral vaccination with Saccharomyces cerevisiae expressing recombinant Actinobacillus pleuropneumoniae ApxIA or ApxIIA in mice

We previously induced protective immune response by oral immunization with yeast expressing the ApxIIA antigen. The ApxI antigen is also an important factor in the protection against Actinobacillus pleuropneumoniae serotype 5 infection; therefore, the protective immunity in mice following oral immunization with Saccharomyces cerevisiae expressing either ApxIA (group C) or ApxIIA (group D) alone or both (group E) was compared with that in two control groups (group A and B). The immunogenicity of the rApxIA antigen derived from the yeast was confirmed by a high survival rate and an ApxIA-specific IgG antibody response (p < 0.01). The highest systemic (IgG) and local (IgA) humoral immune responses to ApxIA and ApxIIA were detected in group E after the third immunization (p < 0.05). The levels of IL-1β and IL-6 after challenge with an A. pleuropneumoniae field isolate did not change significantly in the vaccinated groups. The level of TNF-α increased in a time-dependent manner in group E but was not significantly different after the challenge. After the challenge, the mice in group E had a significantly lower infectious burden and a higher level of protection than the mice in the other groups (p < 0.05). The survival rate in each group was closely correlated to the immune response and histopathological observations in the lung following the challenge. These results suggested that immunity to the ApxIA antigen is required for optimal protection

Association between inhaler use and risk of haemoptysis in patients with non-cystic fibrosis bronchiectasis

Background and objective: Inhaled medications have been widely applied to patients with airflow limiting non-cystic fibrosis (non-CF) bronchiectasis. However, the association between the use of inhalers and the development of haemoptysis has rarely been explored. The objective of this study was to assess the association between the risk of haemoptysis and the use of inhalers in patients with non-CF bronchiectasis. Methods: A nested case-control study was performed using a national claims database from 1 January 2009 to 31 December 2011. Inhalers including inhaled corticosteroids (ICS), long-acting beta(2) agonists (LABA), long-acting muscarinic antagonists (LAMA), short-acting beta(2) agonists (SABA), short-acting muscarinic antagonists(SAMA) and their combinations were tested for the risk of clinically significant haemoptysis events. Results: Among the 62 530 eligible new users of inhalers with non-CF bronchiectasis, 6180 patients with haemoptysis and 27 486 strictly matched controls were selected. In the unadjusted analyses, SAMA, LAMA, SABA and ICS/LABA significantly increased the risk of haemoptysis. After adjustment for other inhaled respiratory medications, comorbidities, health-care utilization and concomitant medications, SAMA, SABA and LAMA consistently increased the risk of haemoptysis (SAMA: odds ratio (OR), 1.6; 95% confidence interval (CI), 1.1-1.4; LAMA: OR, 1.2; 95% CI: 1.1-1.2; SABA: OR, 1.2; 95% CI: 1.1-1.2). The association between anticholinergics (SAMA and LAMA) and risk of haemoptysis showed a dose-dependent trend (P for trend, &lt;0.001). Conclusions: The use of SABA and inhaled anticholinergics in patients with non-CF bronchiectasis increased the risk of haemoptysis. The risk-benefit ratio of inhaled bronchodilators should be considered in the haemoptysis-susceptible population.N

Inhaled bronchodilators and the risk of tachyarrhythmias

Background/objectives: There have been controversies about whether inhaled bronchodilators could increase the risk of clinically important tachyarrhythmias. We investigated the association between inhaled bronchodilators and the development of tachyarrhythmias, including atrial fibrillation and other paroxysmal tachyarrhythmias in real practice. Methods: We conducted a nested case-control study with the use of the nationwide insurance claims database of the Health Insurance Review and Assessment Service (Seoul, Republic of Korea). Overall, 3312 cases with newly developed tachyarrhythmias including atrial fibrillation and other paroxysmal tachyarrhythmias and 9732 matched (up to 1:5) controls were identified from 545,508 subjects without acute major cardiovascular events in the past year between January 1, 2011 and December 31, 2011. Conditional logistic regression analysis adjusted by comorbidities, cardiovascular drugs and healthcare utilization was performed. Results: In various multivariate models, the use of inhaled long-acting muscarinic antagonists (LAMAs) or longacting inhaled beta 2 agonists (LABAs) was significantly associated with tachyarrhythmias. Statistically significant effects of LAMAs on tachyarrhythmias were found only in the non-users of beta-blockers. We did not find a statistically significant difference in the impact of a LABA without a LAMA vs a LAMA without a LABA (aOR, 0.93; 95% CI, 0.74-1.18), or a multiplicative or additive interaction between a LABA and a LAMA. Conclusions: Inhaled LAMAs and LABAs were significantly and comparably associated with an increased risk of tachyarrhythmias. (C) 2015 Published by Elsevier Ireland Ltd.N

In Staphylococcus aureus, the Particulate State of the Cell Envelope Is Required for the Efficient Induction of Host Defense Responses

Upon microbial infection, host immune cells recognize bacterial cell envelope components through cognate receptors. Although bacterial cell envelope components function as innate immune molecules, the role of the physical state of the bacterial cell envelope (i.e., particulate versus soluble) in host immune activation has not been clearly defined. Here, using two different forms of the staphylococcal cell envelope of Staphylococcus aureus RN4220 and USA300 LAC strains, we provide biochemical and immunological evidence that the particulate state is required for the effective activation of host innate immune responses. In a murine model of peritoneal infection, the particulate form of the staphylococcal cell envelope (PCE) induced the production of chemokine (CX-C motif) ligand 1 (CXCL1) and CC chemokine ligand 2 (CCL2), the chemotactic cytokines for neutrophils and monocytes, respectively, resulting in a strong influx of the phagocytes into the peritoneal cavity. In contrast, compared with PCE, the soluble form of cell envelope (SCE), which was derived from PCE by treatment with cell wallhydrolyzing enzymes, showed minimal activity. PCE also induced the secretion of calprotectin (myeloid-related protein 8/14 [MRP8/14] complex), a phagocyte-derived antimicrobial protein, into the peritoneal cavity at a much higher level than did SCE. The injected PCE particles were phagocytosed by the infiltrated neutrophils and monocytes and then delivered to mediastinal draining lymph nodes. More importantly, intraperitoneally (i.p.) injected PCE efficiently protected mice from S. aureus infection, which was abolished by the depletion of either monocytes/macrophages or neutrophils. This study demonstrated that the physical state of bacterial cells is a critical factor for efficient host immune activation and the protection of hosts from staphylococcal infections