Biological nitrogen removal over nitritation/denitritation using phenol as carbon source

A laboratory scale activated sludge sequencing batch reactor was operated in order to obtain total removal of influent ammonia (200; 300 and 500 mg NH3-N.L-1) with sustained nitrite accumulation at the end of the aerobic stages with phenol (1,000 mg C6H5OH.L-1) as the carbon source for denitrifying microorganisms during the anoxic stages. Ammonia removal above 95% and ratios of (NO2--N / (NO2--N + NO3--N)) ranging from 89 to 99% were obtained by controlling the dissolved oxygen concentration (1.0 mg O2.L-1) and the pH value of 8.3 during the aerobic stages. Phenol proved to be an adequate source of carbon for nitrogen removal via nitrite with continuous feeding throughout part of the anoxic stage. Nitrite concentrations greater than 70.0 mg NO2--N.L-1 inhibited the biological denitritation process.FAPESP (The State of São Paulo Research Foundation

Is the combination therapy of IKr-channel blocker and left stellate ganglion block effective for intractable ventricular arrhythmia in a cardiopulmonary arrest patient?

Background: We have previously reported that the defibrillation success rate of intravenous nifekalant hydrochloride (NIF), a pure IKr-channel (IKr: the rapid components of the delayed rectifier potassium current) blocker, was more than 75% for lidocaine-resistant ventricular tachycardia and fibrillation (VT/VF) in patients with out-of-hospital cardiopulmonary arrest (CPA). However, there was no effective treatment for the remaining 25% of patients in whom defibrillation was unsuccessful. We hypothesised that the combination therapy of NIF and left stellate ganglion block (LSGB) was useful for defibrillation in NIF-resistant VT/VF and investigated its efficacy in a retrospective study. Methods and results: We investigated sequentially 272 out-of-hospital CPA patients treated at Tokai University between April and December 2006. VT/VF occurred in 55 patients on arrival or during cardiopulmonary resuscitation (CPR). On the basis of our CPR algorithm, NIF was administered (0.15-0.3 mg/kg, i.v.) after the first direct-current cardioversion. NIF-resistant VT/VFs were observed in 15 out of 55 patients and LSGB was performed on 11 of these with administration of NIF. Sinus rhythm was restored in 7 patients following LSGB (64%) and complete recovery was achieved in 2 patients. In the non-LSGB group, however, all the patients died. Conclusions: The combination therapy of intravenous NIF and LSGB was useful for defibrillation in intractable VT/VF. It is a potential and innovative treatment strategy for IKr-channel blocker resistant VT/VF. (Cardiol J 2007; 14: 355-365

Two distinct prions in fatal familial insomnia and its sporadic form

Abstract Fatal familial insomnia is a genetic prion disease, which is associated with the aspartic acid to asparagine substitution at codon 178 of the prion protein gene. Although the hallmark pathological feature is thalamic and olivary degeneration, there is a patient with an atypical fatal familial insomnia without the hallmark feature. The cause of the pathological variability is unclear. We analysed a Japanese fatal familial insomnia kindred and compared one atypical clinicopathological fatal familial insomnia phenotype case and typical fatal familial insomnia phenotype cases with transmission studies using multiple lines of knock-in mice and with protein misfolding cyclic amplification. We also analysed the transmissibility and the amplification properties of sporadic fatal insomnia. Transmission studies revealed that the typical fatal familial insomnia with thalamic and olivary degeneration showed successful transmission only using knock-in mice expressing human–mouse chimeric prion protein gene. The atypical fatal familial insomnia with spongiform changes showed successful transmission only using knock-in mice expressing bank vole prion protein gene. Two sporadic fatal insomnia cases with thalamic and olivary degeneration showed the same transmissibility as the typical fatal familial insomnia phenotype. Interestingly, one sporadic fatal insomnia case with thalamic/olivary degeneration and spongiform changes showed transmissibility of both the typical and atypical fatal familial insomnia phenotypes. Protein misfolding cyclic amplification could amplify both typical fatal familial insomnia cases and sporadic fatal insomnia cases but not the atypical fatal familial insomnia phenotype or other sporadic Creutzfeldt–Jakob disease subtypes. In addition to clinical findings and neuropathological features, the transmission properties and the amplification properties were different between the typical and atypical fatal familial insomnia phenotypes. It is suggested that two distinct prions were associated with the diversity in the fatal familial insomnia phenotype, and these two prions could also be detected in sporadic fatal insomnia

A Study on Project-Based Learning from the Viewpoint of Organizational Knowledge Creation Theory

アクティブラーニングの1 つとしてPBL（problem/project-based learning）がある。PBL には問題解決学習（problem based learning）とプロジェクト学習（project based learning）の2 つがある。これまでPBL を対象とする研究は着実に蓄積されてきたが，PBL の理論的枠組みは未だ脆弱であることが指摘されている。そこで，本研究ではこの問題を克服するために，大学教育でのプロジェクト学習について，組織的知識創造理論から考察する。本研究の第1 の目的は，組織的知識創造理論がプロジェクト学習においても適用できることを確認することである。第2 の目的は，プロジェクト学習における教員の役割について，組織的知識創造理論から示唆を得ることである。本研究では，以下の3 ステップを踏む。まず，本研究の鍵概念である組織的知識創造理論を紹介する。次に，3 つのプロジェクト学習の事例を紹介し，組織的知識創造理論から分析する。最後に，組織的知識創造理論がプロジェクト学習においても適用できることについて，また，示唆されたプロジェクト学習における教員の役割について議論する。One form of active learning is PBL. There are two types of PBL: “problem-based learning” and “project-based learning.” Although a large number of studies have been on PBL, few studies have been conducted using surveys based on academic theories. Therefore, this paper discusses “project-based learning” from the viewpoint of organizational knowledge creation theory. The primary objective of this study is to apply organizational knowledge creation theory in the field of “project-based learning.” The secondary objective is to recommend teachers’ roles in “project-based learning” from the standpoint of organizational knowledge creation theory. The analysis includes three steps: first, a review of organizational knowledge creation theory; second, an examination of three case studies; and finally, a discussion on applying the theory to “project-based learning”, and suggesting teachers’ roles from this viewpoint

Reprint of "Gengi Ruijusho" in the Archives and Mausolea Department of the Imperial Household Agency

江戸後期の有職故実家である松岡行義の著作、『源氏類聚抄』(宮内庁書陵部蔵本) の翻刻を呈する。本書は、『源氏物語』に示された建築・調度・装束等に関する注釈書である。松岡行義 (1794-1848) による有職故実書は、平安期文献を重視する原点回帰の姿勢、絵画や図面等により対象を視覚化することに特徴がある。本書は、『源氏物語』の読解のみならず、平安期における生活文化への探求、一九世紀における有職故実学の諸相を知る上でも重要となろう。研究ノー

Overcoming minimal residual disease using intensified conditioning with medium-dose etoposide, cyclophosphamide and total body irradiation in allogeneic stem cell transplantation for Philadelphia chromosome-positive acute lymphoblastic leukemia in adults

BACKGROUND AIMS: An intensified conditioning regimen incorporating medium-dose etoposide (VP16) is an option for patients with acute lymphoblastic leukemia (ALL). However, the prognostic impacts of the addition of VP16 to cyclophosphamide (CY) and total body irradiation (TBI) in patients with Philadelphia chromosome-positive (Ph+) ALL with regard to minimal residual disease (MRD) status have not been elucidated. METHODS: The authors retrospectively compared the outcomes of patients with Ph+ ALL who underwent allogeneic transplantation following VP16/CY/TBI (n = 101) and CY/TBI (n = 563). RESULTS: At 4 years, the VP16/CY/TBI group exhibited significantly better disease-free survival (DFS) (72.6% versus 61.7%, P = 0.027) and relapse rate (11.5% versus 21.1%, P = 0.020) and similar non-relapse mortality (16.0% versus 17.2%, P = 0.70). In subgroup analyses, the beneficial effects of the addition of VP16 on DFS were more evident in patients with positive MRD status (71.2% versus 48.4% at 4 years, P = 0.022) than those with negative MRD status (72.8% versus 66.7% at 4 years, P = 0.24). Although MRD positivity was significantly associated with worse DFS in patients who received CY/TBI (48.4% versus 66.7%, P < 0.001), this was not the case in those who received VP16/CY/TBI (71.2% versus 72.8%, P = 0.86). CONCLUSIONS: This study demonstrated the benefits of the addition of VP16 in Ph+ ALL patients, especially those with positive MRD status. VP16/CY/TBI could be a potential strategy to overcome the survival risk of MRD positivity

Adult patients with Ph+ ALL benefit from conditioning regimen of medium‐dose VP16 plus CY/TBI

The medium-dose etoposide (VP16) added on cyclophosphamide (CY)/total body irradiation (TBI) is one of the intensified myeloablative conditioning regimens used in allogenic hematopoietic stem cell transplantation (allo-HSCT) for acute lymphoblastic leukemia (ALL). However, the patient subgroups who can actually benefit from VP16/CY/TBI compared to CY/TBI have not been precisely defined. Therefore, we conducted a multi-center retrospective study using the Japanese nationwide registry database to elucidate the efficacy of VP16/CY/TBI on post-transplant prognosis. Biological and clinical distinct subtypes (i.e., Philadelphia chromosome-positive (Ph+) and -negative (Ph−) ALL) were evaluated separately, which included 820 Ph+ and 1463 patients with Ph− ALL, respectively. Compared with the CY/TBI group, the VP16/CY/TBI group showed superior progression-free survival (PFS) in patients with Ph+ ALL (65% vs. 57% at 3 years after HSCT; adjusted hazard ratio (HR), 0.73; 95% confidence interval (CI), 0.55–0.98; p = 0.03), along with significantly reduced incidence of relapse (adjusted HR, 0.58; 95% CI, 0.37–0.90; p = 0.02) without the increase of non-relapse mortality (NRM). By contrast, in patients with Ph− ALL, VP16/CY/TBI did not improve PFS nor incidence of relapse; addition of VP16 reduced relapse (HR, 0.65; p = 0.06) in patients with Ph− ALL transplanted at CR1, while improved PFS was not observed (HR, 0.90; p = 0.52) due to increased NRM. This study demonstrated that VP16/CY/TBI is a more effective and well-tolerated regimen in comparison with CY/TBI in patients with myeloablative allo-HSCT for adult Ph+ ALL. Our findings can provide a novel algorithm for conditioning regimen selection in patients with adult ALL

Reprint of "Gengi Ruijusho 2 Hahaki-gi" in the Archives and Mausolea Department of the Imperial Household Agency

　前号に引き続き、江戸後期の有職故実家である松岡行義の著作、『源氏類聚抄』（宮内庁書陵部蔵本（函号））の翻刻を呈する。本書は、『源氏物語』に示された建築・調度・装束等に関する有職故実書である。松岡行義（一七九四―一八四八）による有職故実書は、平安期文献を重視する原点回帰の姿勢、絵画や図面等により対象を視覚化することに特徴がある。本書は、管見の限り、松岡行義による『源氏物語』の有職故実書のなかで、最も大部である。本書は、『源氏物語』の読解のみならず、平安期における生活文化への探求、一九世紀における有職故実学の諸相を知る上でも重要となろう。研究ノー

CD146 is a potential immunotarget for neuroblastoma

Neuroblastoma, the most common extracranial solid tumor of childhood, is thought to arise from neural crest-derived immature cells. The prognosis of patients with high-risk or recurrent/refractory neuroblastoma remains quite poor despite intensive multimodality therapy; therefore, novel therapeutic interventions are required. We examined the expression of a cell adhesion molecule CD146 (melanoma cell adhesion molecule [MCAM]) by neuroblastoma cell lines and in clinical samples and investigated the anti-tumor effects of CD146-targeting treatment for neuroblastoma cells both in vitro and in vivo. CD146 is expressed by 4 cell lines and by most of primary tumors at any stage. Short hairpin RNA-mediated knockdown of CD146, or treatment with an anti-CD146 polyclonal antibody, effectively inhibited growth of neuroblastoma cells both in vitro and in vivo, principally due to increased apoptosis via the focal adhesion kinase and/or nuclear factor-kappa B signaling pathway. Furthermore, the anti-CD146 polyclonal antibody markedly inhibited tumor growth in immunodeficient mice inoculated with primary neuroblastoma cells. In conclusion, CD146 represents a promising therapeutic target for neuroblastoma

Skuteczność terapii złożonej polegającej na podaniu blokera kanału IKr oraz wykonaniu blokady zwoju gwiaździstego w leczeniu opornych arytmii komorowych u chorych z zatrzymaniem krążenia

Wstęp: W poprzednich doniesieniach autorzy niniejszej pracy dowiedli, że współczynnik skuteczności defibrylacji przy jednoczesnym dożylnym podaniu chlorowodorku nifekalantu (NIF) - selektywnego blokera kanałów szybkiej składowej opóźnionego prostującego prądu potasowego (IKr) wynosił powyżej 75% dla opornego na lignokainę częstoskurczu lub migotania komór (VT/VF) w przebiegu pozaszpitalnego zatrzymania krążenia (CPA). Jednakże dla pozostałych 25% chorych, u których wykonana defibrylacja okazała się nieskuteczna, nie znaleziono efektywnych metod leczenia. Autorzy niniejszej pracy sugerują, że zastosowanie złożonej terapii polegającej na dożylnym podaniu NIF oraz wykonaniu blokady lewego zwoju gwiaździstego (LSGB) jest użyteczne w przypadku defibrylacji VT/VF opornego na działanie NIF. Na podstawie własnych badań retrospektywnych podjęto także próbę oceny skuteczności tej terapii. Metody i wyniki: Do badania włączono kolejnych 272 chorych przyjętych do Kliniki Kardiologii Uniwersytetu Tokai w okresie od kwietnia do grudnia 2006 roku z powodu pozaszpitalnego zatrzymania krążenia. U 55 pacjentów (podczas przyjęcia lub też w przebiegu resuscytacji krążeniowo-oddechowej) stwierdzono VT/VF. Zgodnie z samodzielnie wypracowanymi przez autorów pracy algorytmami prowadzenia resuscytacji krążeniowo-oddechowej NIF (w dawce 0,15-0,3 mg/kg) podawano dożylnie po pierwszej próbie kardiowersji. Oporne na działanie NIF częstoskurcze komorowe/migotania komór wystąpiły u 15 spośród 55 pacjentów. U 11 chorych z powyższej grupy wykonano LSGB oraz podano dożylnie NIF. U 7 osób (64%) po zabiegu LSGB uzyskano powrót rytmu zatokowego. Całkowity powrót do zdrowia zanotowano u 2 chorych. Jednakże w grupie, w której nie wykonano zabiegu blokady lewego zwoju gwiaździstego (grupa nie-LSBG), zmarli wszyscy pacjenci. Wnioski: Terapia złożona polegająca na dożylnym podaniu NIF oraz wykonaniu LSGB okazała się użyteczna w przypadku defibrylacji opornego VT/VF. Jest to potencjalna i innowacyjna strategia leczenia opornego na selektywne blokery kanałów IKr częstoskurczu komorowego/ migotania komór. (Folia Cardiologica Excerpta 2007; 2: 524-536