Single center experience of cell-free and concentrated ascites reinfusion therapy in malignancy related ascites.

Cell-Free and Concentrated Ascites Reinfusion Therapy (CART) is expected to improve patients' symptoms related to ascites. Use of a patient's own proteins in ascites might reduce the risk of infection. However, several reports have described that reinfusion of concentrated ascites might elevate body temperature. The aim of this study is to examine the safety and efficacy of the CART system performed exclusively on patients with malignancies. In this retrospective cohort observational study, we examined 81 CART processes performed on 24 patients with malignancies. Data were collected from medical records and records during processing of ascites. We investigated the effectiveness and adverse events during the procedures. The amount of ascites processed was 2.6 ± 1.4 L on average. The concentration ratio was 9.31 ± 5.45 on average. We found an increase in the urine volume after the procedure, which was significantly related to the amount of reinfused protein. The body temperature increased by 0.44°C. Systolic blood pressure decreased by 4 mm Hg after paracentesis, but no significant difference was found between the pressure before paracentesis and after reinfusion. In platelet counts, no significant change was observed. After all, no clinically significant adverse event was confirmed during CART procedures. Results show that CART can be performed safely even on patients with malignancy-related ascites and that the procedure might improve diuresis.

Effectiveness of using clinical guidelines for conducting palliative care family meetings in Japan.

PURPOSE: The purpose of this study is to pilot test the effectiveness of using recently developed clinical guidelines from Australia for conducting palliative care family meetings in Japan. METHODS: Palliative care family meetings were conducted using clinical guidelines with 15 primary family carers of cancer patients who were admitted to an acute care hospital in Japan. Using the pre-family meeting questionnaire, the primary carers were asked to write key concerns to discuss during the family meetings and rate their concerns via a numerical rating scale: how upset/worried they were about the problem, frequency in which problem occurs, life interference with the problem, and the confidence to deal with the problem. Within 3 days after the meeting, the primary carers were asked to complete the post-meeting questionnaire to evaluate the effectiveness of the family meeting. RESULTS: There was a significant improvement in family carers' psychological well-being in the post-meeting questionnaires compared to the pre-meeting questionnaires as follows: how upset/worried they were about the problem, t(14) = 3.1071, p < 0.000011; frequency in which problem occurs, t(14) = 3.2857, p < 0.000013; life interference with the problem, t(14) = 2.7857, p < 0.000008; and the confidence to deal with the problem, t(13) = -2.3007, p < 0.005480. CONCLUSIONS: In accordance with the study aims, we were able to demonstrate the utility of a questionnaire as an essential tool to plan and conduct effective communication between health professionals and primary family carers in Japanese cancer patients. This pilot test should be followed up with a larger sample and a controlled trial.

Contribution of CCR4 and CCR8 to antigen-specific T(H)2 cell trafficking in allergic pulmonary inflammation.

BACKGROUND: Recruitment of antigen-specific T(H)2 cells into the lung is critical for the development of allergic airway inflammation. Although CCR4 and CCR8 are preferentially expressed on T(H)2 cells and CCR4, CCR8, and CXCR3 ligands are increased in asthma, the specific relative contribution of these receptors to antigen-specific T(H)2 cell trafficking into the allergic lung is not known. OBJECTIVE: To determine the relative contribution of the chemokine receptors CCR4, CCR8, and CXCR3 to antigen-specific T(H)2 cell trafficking in a murine model of allergic pulmonary inflammation. METHODS: We used adoptive transfer experiments to compare the trafficking of wild-type antigen-specific T(H)2 cells with antigen-specific T(H)2 cells deficient in CCR4, CCR8, or CXCR3. RESULTS: CCR4-deficient antigen-specific T(H)2 cells failed to traffic efficiently into the lung and the airways. In contrast, CCR8-deficient antigen-specific T(H)2 cells accumulated in these sites. Trafficking of CXCR3-deficient antigen-specific T(H)2 cells and CCR4-deficient and CCR8-deficient antigen-specific T(H)1 cells were comparable to their wild-type counterparts. Approximately 60% of IL-4-producing antigen-specific T cells expressed CCR4. Disruption of CCR4-mediated antigen-specific T(H)2 cell trafficking decreased the levels of T(H)2-type cytokines in the airways and reduced airway eosinophilia and mucus production. CONCLUSIONS: Our study demonstrates that CCR4 is required for the efficient entry of antigen-specific T(H)2 cells into the lung and the airways in a murine model of allergic pulmonary inflammation.

Airway hyper-reactivity mediated by B-1 cell immunoglobulin M antibody generating complement C5a at 1 day post-immunization in a murine hapten model of non-atopic asthma.

Contact skin immunization of mice with reactive hapten antigen and subsequent airway challenge with the same hapten induces immediate airflow obstruction and subsequent airway hyper-reactivity (AHR) to methacholine challenge, which is dependent on B cells but not on T cells. This responsiveness to airway challenge with antigen is elicited as early as 1 day postimmunization and can be adoptively transferred to naïve recipients via 1-day immune cells. Responses are absent in 1-day immune B-cell-deficient JH(-/-) mice and B-1 B-cell-deficient xid male mice, as well as in recipients of 1-day immune cells depleted of cells with the B-1 cell phenotype (CD19(+) B220(+) CD5(+)). As B-1 cells produce immunoglobulin M (IgM), we sought and found significantly increased numbers of anti-hapten IgM-producing cells in the spleen and lymph nodes of 1-day immune wild-type mice, but not in xid mice. Then, we passively immunized naive mice with anti-hapten IgM monoclonal antibody and, following airway hapten challenge of the recipients, we showed both immediate airflow obstruction and AHR. In addition, AHR was absent in complement C5 and C5a receptor-deficient mice. In summary, this study of the very early elicited phase of a hapten asthma model suggests, for the first time, a role of B-1 cells in producing IgM to activate complement to rapidly mediate asthma airway reactivity only 1 day after immunization.