Vascular cell adhesion molecule-1 (CD106) is cleaved by neutrophil proteases in the bone marrow following hematopoietic progenitor cell mobilization by granulocyte colony-stimulating factor

BAD is a proapoptotic member of the BCL-2 family of proteins, which play a major role in regulating apoptosis in cytokine-dependent hematopoietic cells. The function of BAD is regulated by reversible phosphorylation. Deprivation of survival factors induces BAD dephosphorylation, resulting in apoptosis. Serine-threonine phosphatase activity dephosphorylated BAD in interleukin-3-dependent FL5.12 lymphoid cells. Inhibition of PP2A activity by treatment of cells with PP2A-selective inhibitors, okadaic acid and fostriecin, prevented BAD dephosphorylation in these cells. Conversely, BAD dephosphorylation was not inhibited by the PP1-selective inhibitor tautomycin. In cell-free extracts, BAD phosphatase activity was also inhibited by the PP2A-selective inhibitors okadaic acid and fostriecin, but not by the PP1-specific protein inhibitor I-2. Dissociation of 14-3-3 from BAD was a prerequisite for BAD dephosphorylation in vitro, suggesting a mechanism by which 14-3-3 can regulate the activation of the proapoptotic function of BAD in vivo. Significantly, the inhibition of BAD phosphatase activity rescued cell death induced by survival factor withdrawal in FL5.12 cells expressing wild-type BAD but not phosphorylation-defective mutant BAD. These data indicate that PP2A, or a PP2A-like enzyme, dephosphorylates BAD and, in conjunction with 14-3-3, modulates cytokine-mediated survival.     

Coat protein gene sequence of tobacco mosaic virus encodes a host response determinant.

The common strain and tomato strain of tobacco mosaic virus (TMV) are known to be closely related to each other. However, plants with the N' gene, such as Nicotiana sylvestris and Nicotiana tabacum L. cv. Bright Yellow, respond differently to infections by these viruses. In the N' plants, TMV-OM (common strain) spreads systemically with mosaic symptoms, whereas TMV-L (tomato strain) induces the necrotic response of plants, causing local lesions. To reveal the viral factor of TMV-L inducing the necrotic response, we have constructed several recombinant viruses between the two strains, in which TMV-L RNA was partly replaced by TMV-OM RNA. The recombinant viruses having the coat protein gene sequence of TMV-OM in place of TMV-L produced no necrotic local lesions but spread systemically with mosaic symptoms in the N' plants. On the other hand, the recombinant viruses having TMV-OM-derived sequences other than the coat protein gene sequence, and in which the coat protein gene sequence of TMV-L still remained, produced necrotic local lesions. These observations indicate that the viral factor of TMV-L responsible for the necrotic response of the N' plants is coded in the coat protein gene sequence.     

Correction to: Agarotetrol: a source compound for low molecular weight aromatic compounds from agarwood heating

Journal of Natural Medicines - In the original publication of the article, under the paragraphs “Collection of volatile compound” and “Analysis of essential oil and...     

Effects of angiogenic factors and 3D-microenvironments on vascularization within sandwich cultures

The in vitro fabrication of vascularized tissue is a key challenge in tissue engineering, but little is known about the mechanisms of blood-capillary formation. Here we investigated the mechanisms of in vitro vascularization using precisely-controlled 3D-microenvironments constructed by a sandwich culture using the cell-accumulation technique. 3D-microenvironments controlled at the single layer level showed that sandwich culture between more than 3 fibroblast-layers induced tubule formation. Moreover, the secretion of angiogenic factors increased upon increasing the number of sandwiching layers, which induced highly dense tubular networks. We found that not only angiogenic factors, but also the 3D-microenvironments of the endothelial cells, especially apical side, played crucial roles in tubule formation in vitro. Based on this knowledge, the introduction of blood and lymph capillaries into mesenchymal stem cell (MSC) tissues was accomplished. These findings would be useful for the in vitro vascularization of various types of engineered organs and studies on angiogenesis.     

Cytomegalovirus (CMV) antigenaemia for rapid diagnosis and monitoring of CMV-associated disease after bone marrow transplantation

A technique for the rapid detection of cytomegalovirus (CMV) antigen-positive blood leucocytes (CMV antigenaemia) was evaluated in 15 marrow transplant patients as a means of diagnosis and for monitoring CMV-associated disease. CMV antigenaemia was determined by direct immunoperoxidase staining of leucocytes with a peroxidase-labelled monoclonal antibody, HRP-C7, which binds an immediate-early antigen of human CMV.
CMV antigenaemia occurred in 7/15 marrow transplant patients (47%) and was initially detected between 4 and 6 weeks after transplantation. CMV-associated diseases developed in 3/15 patients (20%). All patients with CMV-associated disease had a relatively large number of CMV antigen-positive leucocytes, exceeding 10 per 50000 white blood cells (WBCs). In the remaining 12 patients, CMV antigen-positive leucocytes were less than 10 per 50000 WBCs or were undetectable. CMV-associated disease did not develop in these patients during the period of monitoring. CMV antigen-positive leucocytes were detected more frequently in patients who developed acute graft-versus-host disease (GVHD) or haemorrhagic cystitis than in those without such complications. CMV antigens were detectable from 1 to 4 weeks before the onset of CMV-associated disease which allowed initiation of ganciclovir treatment at an early stage. The degree of CMV antigenaemia paralleled the clinical symptoms and signs, higher degrees of antigenaemia being associated with more significant disease. Thus, the detection of CMV antigen-positive blood leucocytes is useful for the diagnosis and monitoring of CMV-associated disease following bone marrow transplantation.     

Improved On-Site Characterization of Arsenic in Gypsum from Waste Plasterboards Using Smart Devices

The impurities in waste plasterboards, a product of ethical demolition, are a serious problem for their recycling. Plasterboards, the wall materials used in old buildings, are often recycled into gypsum powder for various applications, including ground stabilization. However, this powder contains various chemical impurities from the original production process of the gypsum itself, and such impurities pose a risk of polluting the surrounding soil. Here, we present a simple method for verifying the presence of arsenic, a harmful element in recycled gypsum that is suitable for use at demolition sites. First, we developed a simple pretreatment method using a cation-exchange resin to dissolve insoluble gypsum suspended in water by exploiting a chemical equilibrium shift, and we estimated the quantity suitable for releasing the arsenic from arsenic-containing gypsum. This pretreated solution could then be tested with a conventional arsenic test kit by observing the color changes in the test paper using the image sensor of a smart device. This simple method could determine a wide range of arsenic quantities in the gypsum, which would be helpful for monitoring arsenic in recycled gypsum powder, thereby supporting the development of a safe circular economy for waste plasterboards.     

Epstein-Barr Virus-positive Intestinal Diffuse Large B-cell Lymphoma in a Japanese Patient with Celiac Disease: First Reported Case and a Literature Review

A 60-year-old Japanese woman was diagnosed with celiac disease (CeD) and treated with a gluten-free diet. For five years, she had a good clinical course. However, she complained of inappetence and nausea. Colonoscopy revealed ulcerative tumors in the terminal ileum. A histological examination of biopsy specimens from the ulcerative tumor showed diffuse infiltration of large atypical lymphocytes. Immunohistologically, the atypical lymphoid cells were positive for cluster of differentiation (CD)10 and CD20. Many Epstein-Barr virus-encoded small RNA (EBER)-positive atypical lymphocytes were detected by in situ hybridization. This represents the first reported case of Epstein-Barr virus-positive intestinal diffuse large B-cell lymphoma complicated with CeD.     

Reelevation of parathyroid hormone level after parathyroidectomy in patients with primary hyperparathyroidism: importance of decreased renal parathyroid hormone sensitivity

BACKGROUND: We hypothesized that impaired peripheral sensitivity to parathyroid hormone (PTH) may play a role in reelevation of PTH after successful operation for primary hyperparathyroidism (pHPT). METHODS: Factors affecting reelevation of PTH were determined in 90 patients who underwent parathyroidectomy for pHPT. PTH/nephrogenous cyclic adenosine monophosphate ratio, as an index of renal resistance to PTH, was examined in relation to factors shown to influence reelevation of PTH. RESULTS: Serum PTH levels were elevated above the upper limit of normal in 23 patients (26%) at 1 week and in 39 patients (43%) at 1 month after parathyroidectomy. These 39 normocalcemic patients with elevated serum PTH at 1 month after parathyroidectomy had a higher preoperative serum level of PTH and lower serum phosphate and 25-hydroxyvitamin D (25OHD) concentrations than those with normal PTH (n = 59). Elevated PTH and low 25OHD were shown by multivariate analysis to be significant predictors of reelevation of PTH. Renal resistance to PTH was higher in patients with vitamin D deficiency or renal insufficiency than in patients with normal serum vitamin D concentrations or normal renal function, and it increased according to increases in levels of PTH. CONCLUSIONS: The mechanism of PTH reelevation in patients with pHPT after successful parathyroidectomy appears to be renal resistance to PTH.     

Ischemic heart disease associated with bortezomib treatment combined with dexamethasone in a patient with multiple myeloma

A 79-year-old female patient with multiple myeloma who had no prior cardiac disease history developed an acute myocardial infarction on day 5 after receiving bortezomib and dexamethasone (BD). After treatment of coronary stenoses by stents, she received another course of BD therapy and developed angina pectoris on day 5 after the therapy. Bortezomib’s antitumor effect is due to the inhibition of proteasome activity. This inhibition may increase endothelial progenitor cell apoptosis and decrease endothelial nitric oxide synthase/nitric oxide (eNOS/NO), thus leading to coronary spasm. It is, therefore, important to carefully monitor patients being treated with bortezomib for the potential occurrence of ischemic heart disease.