Association between Intra-Circuit Activated Clotting Time and Incidence of Bleeding Complications during Continuous Renal Replacement Therapy using Nafamostat Mesilate : a Retrospective Pilot Observational Study

It has been proposed that anticoagulant activity during continuous renal replacement therapy with nafamostat mesilate can be monitored by using intra-circuit activated clotting time. However, it is still unclear whether activated clotting time would be useful for this purpose. We conducted a retrospective study and included 76 patients who required continuous renal replacement therapy using nafamostat mesilate. We obtained information for pre- and post-filter activated clotting times and bleeding complications. We calculated time-weighted average activated clotting time. We divided the patients into three activated clotting time groups (low, middle, high) according to the tertiles of pre- and post-filter activated clotting times. Regarding post-filter time-weighted average activated clotting time, the incidence of bleeding complications in the high activated clotting time group was significantly higher than those in the low and middle activated clotting time groups (p=0.04). The incidences of bleeding complications were not significantly different among the three groups according to pre-filter time-weighted average activated clotting time (p=0.35). In sensitive analysis, the duration on continuous renal replacement therapy without bleeding complications was significantly longer for filters with post-tw ACT<262 than for those with post-tw ACT≧262 (p=0.03). This result suggested that post-filter time-weighted average activated clotting time might be a good predictor of bleeding complications during continuous renal replacement therapy with nafamostat mesilate. Further study is required to refute or confirm our findings

Production of Functionally Deficient Dendritic Cells from HTLV-I-Infected Monocytes: Implications for the Dendritic Cell Defect in Adult T Cell Leukemia

AbstractAdult T cell leukemia (ATL) is induced by an infection with human T lymphotropic virus type I (HTLV-I) and is accompanied by immunodeficiency. Monocyte-derived immature dendritic cells (DCs) donated by 11 ATL patients were suppressed in the ability to take up fluorescein isothiocyanate (FITC)–dextran and were down-regulated in the expression of CD1a and CD86 antigens (Ags). Monocytes from the patients showed impaired expression of CD14 and HLA-DR Ags. These results suggest intrinsic abnormalities of monocytes and a defect of DC maturation in ATL patients. Therefore, we examined the influence of HTLV-I infection of monocytes on their differentiation to DCs. Monocytes obtained from healthy donors were susceptible to HTLV-I infection in vitro. HTLV-I-infected monocytes were down-regulated in the expression of CD14 Ags, and immature DCs obtained from them expressed CD1a poorly and were impaired in the ability to take up FITC–dextran. Mature DCs differentiated from these cells could not stimulate autologous CD4+ T cell or CD8+ T cell proliferation, even after being secondarily pulsed with HTLV-I at an immature DC stage. These results suggest that HTLV-I-infected monocytes cannot properly differentiate to DCs and that this might be one of the important mechanisms producing dysfunctional DCs in ATL patients

Molecular dissection and anatomical basis of dystonia : X-linked recessive dystonia-parkinsonism (DYT3)

Pathological findings in dystonia have been unclear. X-linked recessive dystonia-parkinsonism (XDP, DYT3), endemic in the Panay island, the Philippines, is characterized by the clinical onset with dystonia followed by parkinsonism. It provides a unique opportunity to explore the anatomical basis of dystonia, because it has discernible pathological changes even at its early phase of dystonia. After extensive searches for the anatomical basis in XDP, we found selective loss of striosomal neurons in the striatum in dystonic patients’ brain. Because striosomal neurons inhibit nigrostriatal dopaminergic neurons via GABAergic innervation, the striosomal lesion could account for dopamine excess in the striatum, which in turn causes a hyperkinetic state or dystonia. We also identified the causative gene as one of the general transcription factor genes, TAF1. XDP has certain similarities to Huntington disease not only in pathological and clinical findings, but also the molecular mechanism, which disturbs expression of genes essential for striatal neurons, such as DRD2. Therapeutic intervention may become possible through pharmacological measures that affect gene expression

Low-Temperature Characteristics of an AlN/Diamond Surface Acoustic Wave Resonator

Phonons confined in mechanical resonators can be coupled to a variety of quantum systems and are expected to be applied to hybrid quantum systems. Diamond surface acoustic wave (SAW) devices are capable of high efficiency in phonon interaction with color centers in diamond. The temperature dependence of the quality factor is crucial for inferring the governing mechanism of coupling efficiency between phonons and color centers in diamond. In this paper, we report on the temperature dependence of the quality factor of an AlN/diamond SAW device from room temperature to 5 K. The temperature dependence of the quality factor and resonant frequency suggests that the mechanism of SAW dissipation in the AlN/diamond SAW resonator at 5 GHz is the phonon-phonon scattering in the Akheiser region, and that further cooling can be expected to improve the quality factor. This result provides a crucial guideline for the future design of AlN/diamond SAW devices.Comment: 10 pages, 5 figure

Infiltration of T Lymphocytes and Expression of ICAM-1 in the Hippocampus of Patients with Hippocampal Sclerosis

We and others have previously shown that reactive microglia express the major histocompatibility complex (MHC) class I and class II antigens in the hippocampus of patients suffering from epilepsy. Although the MHC glycoproteins serve as restriction elements for T lymphocytes, there is little information available regarding T lymphocytes in hippocampal sclerosis. In the present study, we investigated T lymphocyte infiltration in human hippocampi in four cases of epilepsy with hippocampal sclerosis, as well as in four control cases without neurological disease. No CD8- or CD4-positive T lymphocytes were seen in hippocampi from the control cases. In contrast, CD8- and CD4-positive T lymphocytes had infiltrated into the hippocampi of patients with hippocampal sclerosis. In addition, expression of intercellular adhesion molecule-1 was diffusely upregulated in the hippocampi with hippocampal sclerosis. These results indicate that T lymphocyte infiltration is involved in the pathology of hippocampal sclerosis