Prevalence of myofascial pain syndrome in patients with incurable cancer.

BACKGROUND: Myofascial pain syndrome (MPS) is a condition that involves skeletal muscles. It is caused by overload or disuse of muscles and is characterized by extreme tenderness in the muscles with taut bands. Treatment for MPS is different from that for cancer-related pain. Cancer patients have many factors that cause restriction of body movement and posture. Although cancer patients appear to demonstrate risk factors for MPS, its prevalence has not been reported in patients with incurable cancer. This study was conducted to investigate the prevalence of MPS in patients with incurable cancer. METHODS: A retrospective chart review. The data for patients with incurable cancer who received palliative care at our department between September 2015 and March 2016 were investigated. We examined the prevalence of MPS, which was diagnosed on the basis of the Rivers criteria (RC) and Simons criteria (SC). We also examined the following factors associated with MPS: performance status (PS), use of medical devices, and primary cancer sites. The primary outcome was the prevalence of MPS based on RC. Secondary outcomes included the prevalence of MPS based on SC and the relationship between MPS and either PS or medical devices. RESULTS: Thirty-four patients with incurable cancer were identified. MPS based on RC or SC was detected in 10 (29%) and 20 (59%) patients, respectively. Twenty-two of 34 patients who complained of pain, 10 (45%) had MPS based on RC and 20 (90%) had MPS based on SC. Age and central venous port were risk factors for MPS by multivariate analysis. CONCLUSION: A very high prevalence of MPS was detected in our study population. MPS should be considered when patients with incurable cancer complain of pain.

Breakthrough fungemia due to Candida fermentati with fks1p mutation under micafungin treatment in a cord blood transplant recipient.

The prophylactic use of antifungal drugs in allogeneic hematopoietic cell transplant recipients has revealed that the rate of non-albicans candidemia has increased. We herein report the case of a patient with adult T-cell leukemia who developed candidemia due to Candida fermentati during micafungin treatment after cord blood transplantation. The isolate was identified on day 47 by sequencing of the internal transcribed spacer region of the ribosomal RNA gene. The sequencing of the hot spot region of fks1p of isolate revealed naturally occurring amino acid substitutions, which conferred reduced echinocandin susceptibility. This case highlights that breakthrough candidemia due to C. fermentati occurred in a patient receiving micafungin treatment.

Effect of Cell Seeding Conditions on the Efficiency of In Vivo Bone Formation.

PURPOSE: To optimize methods for seeding cells on granular-type beta-tricalcium phosphate (ß-TCP). MATERIALS AND METHODS: Bone marrow stromal cells were obtained from rat long bones and cultured in flasks with Minimum Essential Medium, Alpha Modification (αMEM) supplemented with 10% fetal bovine serum (FBS), dexamethasone, ascorbic acid, ß -glycerophosphate, and antibiotics. The influence of differential cell seeding densities and dynamic cell seeding conditions (rotation) was investigated using different sizes of ß -TCP granules and a subcutaneous implantation model. RESULTS: Higher cell seeding densities contributed to efficient in vivo bone formation. The rotational seeding did not affect the efficiency but contributed to the uniformity. Although the granule size did not affect the efficiency under the conditions used in this study, large granules showed more uniform distribution of bone regeneration, while small granules showed nonuniform but dense bone formation. Mixtures of relatively large and small granules may be beneficial for both uniform and efficient bone regeneration. CONCLUSION: These findings may contribute to stable bone tissue engineering with bone marrow stromal cells and ß -TCP granules as a scaffold.

Imatinib mesylate directly impairs class switch recombination through down-regulation of AID: its potential efficacy as an AID suppressor.

Activation-induced cytidine deaminase (AID) is essential for class switch recombination and somatic hypermutation. Its deregulated expression acts as a genomic mutator that can contribute to the development of various malignancies. During treatment with imatinib mesylate (IM), patients with chronic myeloid leukemia often develop hypogammaglobulinemia, the mechanism of which has not yet been clarified. Here, we provide evidence that class switch recombination on B-cell activation is apparently inhibited by IM through down-regulation of AID. Furthermore, expression of E2A, a key transcription factor for AID induction, was markedly suppressed by IM. These results elucidate not only the underlying mechanism of IM-induced hypogammaglobulinemia but also its potential efficacy as an AID suppressor.

JTE-607, a multiple cytokine production inhibitor, ameliorates disease in a SCID mouse xenograft acute myeloid leukemia model.

OBJECTIVE: Accumulating findings suggest that in acute myeloid leukemia (AML) patients, proinflammatory cytokines and growth factors play important roles in the proliferation and survival of AML cells in an autocrine and paracrine manner, leading to deterioration of AML. JTE-607 is a multiple cytokine inhibitor that potently suppresses production of proinflammatory cytokines. In the present study, we investigated the potency of JTE-607 as an antileukemic agent by exploiting a SCID mouse acute leukemia model. METHODS: SCID mice injected with anti-asialo-GM1 antibody were exposed to sublethal total-body irradiation at a dose of 3 Gy and then inoculated intravenously with AML cells. JTE-607 was administered using osmotic minipumps. The effects of JTE-607 on mouse survival time, human interleukin (IL)-8 levels in mouse plasma, and proportion of human CD45(+) cells in the bone marrow were studied. RESULTS: The survival time of the mice was strictly dependent on the number of U-937 cells proliferating in vivo. Administration of JTE-607 during the initial 7 days significantly prolonged survival of the mice, suggesting killing activity of JTE-607 against AML cells in vivo. Delayed administration of JTE-607 also prolonged the survival of mice bearing established leukemia with an effect comparable to the maximum tolerable dose of cytarabine. Flow cytometer analysis of bone marrow cells revealed decreased number of human CD45(+) cells. Human IL-8 level was also reduced by JTE-607. CONCLUSION: Our results indicate that JTE-607 has potential to be a new class of antileukemic drug that exerts inhibitory activities against both the proliferation and proinflammatory cytokine production of AML cells.

Severe immune dysfunction after lethal neutron irradiation in a JCO nuclear facility accident victim.

The optimal treatment for the hematological toxicity of acute radiation syndrome (ARS) is not fully established, especially in cases of high-dose nonuniform irradiation by mixed neutrons and gamma-rays, because estimation of the irradiation dose (dosimetry) and prediction of autologous hematological recovery are complicated. For the treatment of ARS, we performed HLA-DRB1-mismatched unrelated umbilical cord blood transplantation (CBT) for a nuclear accident victim who received 8 to 10 GyEq mixed neutron and gamma-ray irradiation at the JCO Co. Ltd. nuclear processing facility in Tokaimura, Japan. Donor/ recipient mixed chimerism was attained; thereafter rapid autologous hematopoietic recovery was achieved in concordance with the termination of immunosuppressants. Immune function examined in vitro showed recovery of the autologous immune system was severely impaired. Although the naive T-cell fraction and the helper T-cell subtype 1 fraction were increased, the mitogenic responses of T-cells and the allogeneic mixed leukocyte reaction were severely suppressed. Endogenous immunoglobulin production was also suppressed until 120 days after the accident. Although skin transplantation for ARS was successful, the patient died of infectious complications and subsequent acute respiratory distress syndrome 210 days after the accident. These results suggest that fast neutrons in doses higher than 8 to 10 Gy cause complete abrogation of the human immune system, which may lead to fatal outcome even if autologous hematopoiesis recovers. The roles of transplantation, autologous hematopoietic recovery, chimerism, immune suppression, and immune function are discussed.