An immunoreactive xanthine oxidase protein-possessing xanthinuria and her family.

The presence of immunoreactive xanthine oxidase protein was proven in a xanthinuric patient, using a polyclonal antibody against xanthine oxidase. The antibody was raised against purified human liver xanthine oxidase in a rabbit. Double immunodiffusion method demonstrated the existence of an immunologically reactive xanthine oxidase which did not possess xanthine oxidase activity. In addition, urinary excretion of oxypurines in the patient and her family was investigated. The results indicated that a brother and a sister had xanthinuria.     

Suppression of Pseudomonas aeruginosa quorum-sensing systems by macrolides: a promising strategy or an oriental mystery?

A breakthrough in antibiotic chemotherapy for patients with chronic Pseudomonas aeruginosa pulmonary infections was brought about by findings in a patient with diffuse panbronchiolitis (DPB), who had been treated with erythromycin over a period of years. Recent clinical trials have demonstrated that long-term macrolide therapy can be used not only for DPB patients but also for those with other chronic infections, including patients with cystic fibrosis (CF). The pathogenesis of chronic P. aeruginosa infection is considered to arise from a bacterial cell-to-cell signaling mechanism, named “quorum-sensing”, which enables the bacteria to coordinately turn on and off their virulence genes through the production of autoinducer molecules. Accumulating evidence from clinical and basic science fields suggests the potential of macrolides as Pseudomonas quorum-sensing inhibitors. In this review, we briefly summarize the data on the clinical efficacy of macrolides in DPB and CF patients. Then we discuss the mechanisms of action of macrolides from the viewpoint of sub-minimum inhibitory concentration (sub-MIC) macrolide effects on P. aeruginosa, particularly the potential activity of this antibiotic to suppress the bacterial quorum-sensing system.     

Effect of Interleukin-10 on Gut-Derived Sepsis Caused by Pseudomonas aeruginosa in Mice

We evaluated the protective effect of interleukin-10 (IL-10) against murine gut-derived sepsis caused by Pseudomonas aeruginosa. Gut-derived sepsis was induced by administering cyclophosphamide and ampicillin while feeding P. aeruginosa to specific-pathogen-free mice. Treating mice with recombinant human IL-10 (rhIL-10) at 1.0 or 5.0 μg/mouse twice a day following the second cyclophosphamide administration significantly increased the survival rate compared to that of control mice treated with saline; however, treatment with rhIL-10 at 0.1 μg/mouse did not result in significant protection. Bacterial counts in the liver, spleen, and blood were all significantly lower in mice treated with rhIL-10 than in saline-treated control mice. Treatment with rhIL-10 significantly suppressed tumor necrosis factor alpha, interleukin-1β, interleukin-6, and gamma interferon levels in the serum of mice following induction of gut-derived sepsis. We also studied the effect of IL-10 on leukocyte recovery after cyclophosphamide treatment of mice. Administration of rhIL-10 intraperitoneally at 1.0 μg/mouse significantly accelerated the recovery of leukocytes in comparison with that of the group of saline-treated controls. These results indicate that IL-10 shows a protective effect against gut-derived P. aeruginosa sepsis. We suspect that the mechanism of this effect is that IL-10 regulates in vivo production of inflammatory cytokines. Furthermore, acceleration of leukocyte recovery by IL-10 after cyclophosphamide-induced depression may also play an important role in this protection.     

Rapid and sensitive mycoplasma detection system using image-based deep learning

Journal of Artificial Organs - A major concern in the clinical application of cell therapy is the manufacturing cost of cell products, which mainly depends on quality control. The mycoplasma test,...     

Evaluations for surrounding tissue incorporation after implantation of synthetic vascular prostheses in animal models

Journal of Artificial Organs - Incorporation of surrounding tissues after implantation of synthetic vascular prostheses potentially varies in accordance with implanted prostheses. To evaluate...     

Quantitative chest CT for subtyping chronic lung allograft dysfunction and its association with survival

Chronic lung allograft dysfunction (CLAD) is a major cause of mortality in lung transplant recipients. CLAD can be sub‐divided into at least 2 subtypes with distinct mortality risk characteristics: restrictive allograft syndrome (RAS), which demonstrates increased overall computed tomography (CT) lung density in contrast with bronchiolitis obliterans syndrome (BOS), which demonstrates reduced overall CT lung density. This study aimed to evaluate a reader‐independent quantitative density metric (QDM) derived from CT histograms to associate with CLAD survival. A retrospective study evaluated CT scans corresponding to CLAD onset using pulmonary function tests in 74 patients (23 RAS, 51 BOS). Two different QDM values (QDM1 and QDM2) were calculated using CT lung density histograms. Calculation of QDM1 includes the extreme edges of the histogram. Calculation of QDM2 includes the central region of the histogram. Kaplan‐Meier analysis and Cox regression analysis were used for CLAD prognosis. Higher QDM values were significantly associated with decreased survival. The hazard ratio for death was 3.2 times higher at the 75th percentile compared to the 25th percentile using QDM1 in a univariate model. QDM may associate with CLAD patient prognosis.