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Ahstract-U-Bus Air is a wireless communication standard for metering systems, targeting gas supplies with a multi-hop network function. As a multi-hop wireless network, U-Bus Air gathers meter reading information connected to a monitoring center. The terminal with the function of connecting to a monitoring center is called a gateway (GW). The multi-hop function is used to connect GWs; this reduces the cost of connecting wide-area wireless networks. However, the order of installing a new terminal is random because it is determined by timing of replacement on meter in individual homes on meters in individual homes. As a result, the installing location of GWs cannot be specified in advance. Consequently, any created network topology will exhibit redundancies, such as unnecessary GWs, or generate many small networks. In this paper, we propose two different redundancy reducing methods that use information of terminals on cloud to reconstruct a network topology. The proposed methods consists of three steps: gathering information, emulating the topology to reduce redundancy using cloud, and providing feedback to rebuild information of each smart meter. We perform a computer simulation to evaluate the packet delivery ratio (PDR) and the reduction ratio of the number of GWs. We confirm that the redundancy can be reduced by using the proposed methods without affecting the performance of the network topology.

Annelids as a group express a variety of phosphagen kinases including creatine kinase (CK), glyocyamine kinase (GK), lombricine kinase (LK), taurocyamine kinase (TK) and a unique arginine kinase (AK) restricted to annelids. In prior work, we have determined and compared the intron/exon organization of the annelid genes for cytoplasmic GK, LK, AK, and mitochondrial TK and LK (MiTK and MiLK, respectively), and found that these annelid genes, irrespective of cytoplasmic or mitochondrial, have the same 8-intron/9-exon organization strikingly similar to mitochondrial CK (MiCK) genes. These results support the view that the MiCK gene is basal and ancestral to the phosphagen kinases unique to annelids. To gain a greater understanding of the evolutionary processes leading to the diversity of annelid phosphagen kinases, we determined for the first time the intron/exon organization of a cytoplasmic CK gene from a polychaete as well as that of another polychaete MiCK gene. These gene structures, coupled with a phylogenetic analyses of annelid enzymes and assessment of the fidelity of substrate specificity of some these phosphagen kinases, provide insight into the pattern of radiation of the annelid enzymes. Annelid phosphagen kinases appeared to have diverged in the following order (earliest first): (1) cytoplasmic AK, LK and TK, (2) GK, and (3) mitochondrial MiLK and MiTK. Interestingly, phylogenetic analyses showed that the above phosphagen kinases appear to be basal to all CK isoforms (mitochondrial, cytoplasmic and flagellar CKs). This somewhat paradoxical placement of CKs most likely reflects a higher rate of evolution and radiation of the annelid-specific LK, TK and GK genes than the CK isoform genes.

We report on a patient with myelodysplastic syndrome (MDS) which resembled chronic myeloproliferative disorder (CMPD). A 67-year-old male was admitted to our hospital in June 1990. A diagnosis of refractory anemia with excess of blasts in transformation (RAEB-T) was based on the peripheral blood and bone marrow findings on admission. However, since thrombocytosis and bone marrow fibrosis was noted, the patient was diagnosed as MDS with myelofibrosis. Low-dose cytosine arabinoside therapy was performed. Although complete remission could not be achieved, a high quality of life could be maintained by appropriate transfusion. In January 1993, the patient was readmitted because of a marked increase in mature neutrophils, showing a moderate increase of blasts, chromosomal aberration (46,XY,12p-) and hepatosplenomegaly; but no fibrosis of bone marrow was observed. These findings suggested that neoplastic proliferation at the level more differentiated to granulocytic lineage occurred at the terminal stage and that his clinical feature was located between MDS and CMPD. This case may be important in considering various aspects of MDS.

We describe a patient with allergic granulomatous angitis who developed autoimmune hemolytic anemia (AIHA). A 44-year-old male had been suffering from bronchial asthma. On admission, laboratory tests revealed the presence of severe eosinophilia (21,500/microliters), elevation of total immunoglobulin E (IgE), high lactic dehydrogenase (LDH) and low haptoglobin levels, in addition to moderate reticulocytosis. During admission, the patient showed almost simultaneous occurrence of vasculitis in the extremities, severe hemolysis and exacerbation of asthma in relation to the progression of eosinophilia. Both IgM and IgG autoantibodies were considered to be responsible for hemolysis. Interestingly, serum levels of interleukin-4 (IL-4) and IL-5 were increased in association with eosinophilia and increased IgE production. These findings suggest that the AIHA in this patient is mediated or enhanced at least partly by high IL-4 and IL-5 production. Although AIHA in this syndrome is very rare, it should be considered as a clinical manifestation.

Summary In order to explore the question if dopamine β-hydroxylase inhibitor alone has a disulfiram-like effect on alcohol, fusaric acid, a potent inhibitor of dopamine β-hydroxylase, was administered to 23 gamma alcoholics. The alcohol-test was made twice, prior to administration of fusaric acid and after one week of the treatment. Significant effects of the agent on reaction to alcohol were observed in the symptom of flushing of face, a fall in blood pressure, change of the taste, and feeling of getting drunk. These symptoms were more slight than those of the alcohol-disulfiram reaction. However, it was emphasized that the mechanism of the alcohol-disulfiram reaction is not explained by only a transient hyperacetaldehydemia, but may be also related to the metabolism of both catecholamines and serotonin. Further clinical studies are needed to assess therapeutic use of te compound in the treatment of chronic alcoholism. The fusaric acid was supplied from Banyu Pharmaceutical Co. Ltd. with a favor of Professor Hamao Umezawa, Director of Institute of Biseibutsu Kagaku to meet with the request of one of the authors, Motoi Ogata, M.D.

Chromosome studies was conducted on 15 patients with adult T-cell leukemia. Cells with chromosomal abnormality were seen in 14 of the 15 patients. The modal chromosome number was near diploid range in all the patients. The most common abnormality was 14q+ marker chromosome and partial deletion of the long arm of chromosome 6, i.e., 6q-, which were seen in eight and seven cases, respectively. Donor chromosomes involved in the 14q+ marker chromosome varies, i.e., Yq, #5p, #5q, #9q, #10q or #12q, except for two patients whose donor chromosome origins were unable to determine. The break point in 14q+ marker chromosome was band at q32. The 6q- chromosome was due to a deletion in one patient and interstitial deletion in six patients. A 14q- chromosome having break point at q24 was found in one patient and duplication of Yq chromosome in two patients. In addition, four patients showed a 5q- chromosome or a 9q- chromosome which was due to a translocation or deletion. The significance of these chromosome abnormalities was discussed.

高齢者白血病至適治療体系の確立を目的とし, 今回70歳以上の高齢者ANLLを対象に aclarubicin (ACR) 単独療法を試み, その臨床効果を検討した. 対象は未治療ANLL15例〔男女比13:2, 年齢71～84歳 (中央値76歳)〕で, 病型はAML6例, AMoL5例, AMMoL2例, EL2例でうち2例が hypoplastic leukemia であった. 入院時未血所見は各々中央値でRBC223×104/cmm (142～414×104/cmm), Hb7.4g/dl (4.5～13.8g/dl), WBC10,400/cmm (1,300～179,000/cmm), 白血病細胞百分率32% (0～98%), Thr. 6.6×104/cmm (2.8～49.5×104/cmm), 骨髄所見ではN.C. C.38.0×104/cmm (3.3～103.4×104/cmm), 白血病細胞百分率62.3% (29.0～96.6%), Ebl18.6% (1.2～32.6%) あった. ACRは14mg/m2/日, 2時間の点滴静注で7～10日間の連日投与を原則とし, 末梢血並びに骨髄所見により適宜2コース目を施行した. その結果CRは評価可能12例中5例, 42%に得られたが, hypoplastic leukemia を除くとCR率は10例中5例, 50%で, 病型別検討ではAML, ELにCR例は認められなかったがAMoLでは4例中3例, 75%, AMMoLでは2例中2例と, AMoL, AMMoLに高いCR率が認められた. CR到達に要したACRの総量は140～400mg (中央値200mg), CR到達日数は24～97日 (中央値28日), 60年7月現在でのCR期間は1.3～11.3月 (中央値7.5月), CR例における生存期間は6.6～15.6月 (中央値10月+) であった. 副作用では12例中食思不振9例, 嘔気・嘔吐3例と消化器障害が全例に認められたが循環器障害, 肝障害は認められなかった. 合併症では感染症が8例 (敗血症2例, 肺炎3例, 不明3例), 消化管出血が3例に認められた.高齢者白血病の増加とともにその治療体系の確立が要求されているが, 70歳以上の高齢者ANLL, 特にAMoL, AMMoLに対するACR単独療法は評価し得る治療法と考えられる.

The vitamin B12 levels of cerebrospinal fluid were assayed microbiologically (Lactobacillus leichmannii method) using samples from 44 patients with various neurological disorders, 4 patients with megalo-blastic anemia and 34 controls. Twenty-seven controls that did not receive vitamin B12 showed a mean cerebrospinal fluid vitamin B12 level of 21.5 pg/ml (range: 0-60). No decrease in cerebrospinal fluid vitamin B12 level was seen in patients with subacute myelo-optico-neuropathy (SMON). High levels of cerebrospinal fluid vitamin B12 were observed only in the patients receiving long term administration of the vitamin. Intrathecal administration of vitamin B12 caused only a slight increase in serum vitamin B12 level after four hours. The existence of a blood brain barrier for vitamin B12 was suggested.