Sedimentary environments of mangrove swamp in the Funaura Bay, Iriomote Island, Okinawa Prefecture, Southwest Japan

The distribution of conch shell contained in clastic sediments in the mangrove swamps in the Funaura Bay, Iriomote Island, Okinawa Prefecture was studied. The sediments in the mangrove swamp are mainly composed of up to 90% sands. The sand clasts are inferred to be derived from the sandstone of Miocene Yaeyama Group. The conch shells are richer in the muddy fraction than the sandy fraction. Many Terebralia palustris inhabit the mangrove swamp. However few dead shells were also observed in the sediments. Effect of selective transportation hermit crabs is considered to be the cause of this distribution

The implications of public school fees for educational performance and enrolment, with reference to the greater Durban area.

Thesis (M.T.R.P.)-University of Natal, Durban, 1999.This thesis is concerned with the implications of the new South African education system based on the South African Schools Act, No. 84 of 1996 for educational performance and learners' enrolment in public schools. Central to the argument are the unfavourable consequences of the charging of school fees at public schools for learners from poor families. This is analysed based on a survey conducted in the Durban Metropolitan area between September and November 1998. As a legacy of apartheid education, inequalities between population groups are still evident (Chapter 1). One of the aims of the Act is the redress of past inequalities and permission to charge fees at public schools is seen as a measure to supplement the resources provided by the State (Chapter 2). Implications of school fees for school finance and redress of past inequalities between ex-departments are often discussed. However, little attention has been given to the impact of charging fees on learners' enrolment, which is the main focus of this thesis. There is a contradiction between permitting the charging of fees at public schools and the insistence on compulsory attendance in the Act. Given the financial constraints of South African schools, most schools are likely to adopt school fees. There may be many learners who may not be able to afford fees. Although the Act provides measures to prevent poor learners from being refused admission, it is questionable whether the measures provided by the Act function properly in practice. There would be poor learners who are effectively excluded from advantaged schools which charge high school fees. Past inequalities would not necessarily be redressed under the new system. As a result ofthe implementation ofthe Act, a kind of semi-privatisation within the public school sector could be introduced (Chapter 3). Analysis based on the research in Durban supports these hypotheses to some degree (Chapter 4). Recent incidents regarding the refusal by some public schools to admit learners on the basis of the parents' inability to pay school fees indicate the importance of this issue. Equal access to a basic education cannot be guaranteed under the current situation. Chapter 5 presents an alternative to the current system. If the State provided all public schools with the minimum operation costs necessary to run daily activities, the school would be able to substitute voluntary contributions for school fees. One possible way to release resources for this purpose is a reduction in personnel expenditure, including an acceptance of much higher pupil/teacher ratios. Although this is a controversial issue, it is inevitable for any society to seek a more productive system if it faces financial constraints

ドウミャク コウカ ト コウシケッショウ

It is well known that four major risk factors for atherosclerosis include diabetes mellitus, hypertension, hyperlipidemia and smoking. Among these risk factors, management of hyperlipidemia, especially hyper-LDL cholesterolemia, has become to be strictly achieved by the appearance of statins. Many randomized control trials using statins have been performed, and the effectiveness in reduction of cardiovascular events is clearly established. Under these circumstances, we planed and performed the Shikoku Hyperlipidemia Study（SHS）to reveal how do we treat and what degree do we strictly manage patients with hyperlipidemia. Evidence obtained by The SHS study were 1）unmeasurement rates of serum cholesterol levels in categories B and C were 28.1% and 18.2%, respectively, 2）among patients in categories B and C who need to be treated by drugs, only 35.5% and 35.9% of patients in categories B and C were treated, respectively, 3）drugs medicated in such patients were mostly statins and a single kind of statin was administered, and 4）rate of successfully treated patients in category B was 40～50% and that in category C was 20～30%. When this analysis, which was performed based upon guideline published in 1997, was re-analyzed by new guideline published in 2002, rates of successfully treated patients in categories A, B1, B2, B3, B4, and C were 91.7%, 66.1%, 77.6%, 42.9%, 60.7%, and 32.6%, respectively. Pleiotropic effects of statins have been postulated, however, a couple of issues are still elusive ; that is, 1）can statins suppress the progression of atherosclerosis by the mechanism other than cholesterol lowering in humans? and 2）should statins be administered to patients for secondary and primary preventions against cardiovascular events to anticipate pleiotropic effects of statins?. Evidence obtained so far suggest that statins exert its pleiotropic effects via 1）enhancement of NO production by phosphorylation of eNOS, Akt and PI 3 kinase, 2） inhibition of Ras activation by reduction of farnesyl-pyrophosphate, and 3）inhibition of Rho family activation by reduction of geranylgeranyl-pyrophosphate, and that Heart Protection Study and ASCOT-LLA study revealed that additive benefits can be elicited when hyperlipidemic patients bearing many risk factors including diabetes mellitus were treated with statins. In conclusion, we need to treat patients with hyperlipidemia in consideration of the quality and quantity of risk factors for cardiovascular diseases

Genetic and molecular pathogenesis of hereditary hemorrhagic telangiectasia

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder characterized by vascular dysplasia and hemorrhage. The pathogenesis regarding heterogeneity of vascular malformations in patients with HHT has been obscure, although it has become possible to partially explain the pathogenesis from the identification of two distinct genes, endoglin and ALK-1. Endoglin and ALK-1 are type III and type I TGF-β receptors, respectively, and are exclusively expressed on vascular endothelial cells. Binding of TGF-β to the type II TGF-β receptor on endothelial cells, which is accelerated in the presence of endoglin, phosphorylates type I TGF-β receptors, ALK-5 and ALK-1, and phosphorylated ALK-5 and ALK-1 activate the downstream proteins Smad2/3 and Smad1/5, respectively. These activated Smad proteins dissociate from the type I TGF-β receptor, bind to Smad4, and enter the nucleus to transmit TGF-β signaling by regulating transcription from specific gene promoters involved in angiogenesis. Therefore, a balance between these two signaling pathways via ALK-5 and ALK-1 plays an important role in determining the properties of endothelial cells during angiogenesis. Mutations of endoglin and ALK-1 genes are genetic pathogenesis of HHT type 1 and HHT type 2, respectively. To date, at least 29 and 17 different kinds of mutations in endoglin and ALK-1, respectively, have been found, including missense, nonsense, frameshift, and deletion mutations. The precise mechanisms of vascular abnormalities elicited by these mutations observed in HHT patients are still uncertain, although elucidation of the mechanism of intracellular signal transduction and the change in targeted gene expressions using mutant recombinant endoglin or ALK-1 proteins and knockout mice will enable us to understand the genetic and molecular pathogenesis of HHT and to effectively treat patients with HHT

Cross-priming for antitumor CTL induced by soluble Ag + polyI:C depends on the TICAM-1 pathway in mouse CD11c+ /CD8α+ dendritic cells

PolyI:C is a nucleotide pattern molecule that induces cross-presentation of foreign Ag in myeloid dendritic cells (DC) and MHC Class I-dependent proliferation of cytotoxic T lymphocytes (CTL). DC (BM or spleen CD8α(+)) have sensors for dsRNA including polyI:C to signal facilitating cross-presentation. Endosomal TLR3 and cytoplasmic RIG-I/MDA5 are reportedly responsible for polyI:C sensing and presumed to deliver signal for cross-presentation via TICAM-1 (TRIF) and IPS-1 (MAVS, Cardif, VISA) adaptors, respectively. In fact, when tumor-associated Ag (TAA) was simultaneously taken up with polyI:C in DC, the DC cross-primed CTL specific to the TAA in a syngenic mouse model. Here we tested which of the TICAM-1 or IPS-1 pathway participate in cross-presentation of tumor-associated soluble Ag and retardation of tumor growth in the setting with a syngeneic tumor implant system, EG7/C57BL6, and exogenously challenged soluble Ag (EG7 lysate) and polyI:C. When EG7 lysate and polyI:C were subcutaneously injected in tumor-bearing mice, EG7 tumor growth retardation was observed in wild-type and to a lesser extent IPS-1(−/−) mice, but not TICAM-1(−/−) mice. IRF-3/7 were essential but IPS-1 and type I IFN were minimally involved in the polyI:C-mediated CTL proliferation. Although both TICAM-1 and IPS-1 contributed to CD86/CD40 upregulation in CD8α(+) DC, H2K(b)-SL8 tetramer and OT-1 proliferation assays indicated that OVA-recognizing CD8 T cells predominantly proliferated in vivo through TICAM-1 and CD8α(+) DC is crucial in ex vivo analysis. Ultimately, tumor regresses > 8 d post polyI:C administration. The results infer that soluble tumor Ag induces tumor growth retardation, i.e., therapeutic potential, if the TICAM-1 signal coincidentally occurs in CD8α(+) DC around the tumor

View of physicians on and barriers to patient enrollment in a multicenter clinical trial: experience in a Japanese rural area

<p>Abstract</p> <p>Background</p> <p>Clinical trials in the general practice setting are important for providing evidence on the effectiveness and safety of different agents under various conditions. In conducting these trials, the participation of physicians and patient recruitment are important issues. Various investigations in the literature have reported views and attitudes of physicians on various types of clinical trials. Nevertheless, there is still little information concerning physicians participating in a clinical trial and among them, those who could not recruit any patients (unsuccessful physician recruiters).</p> <p>Methods</p> <p>In 2003, we collaborated in a large-scale multicenter study of Japanese hypertensive patients (COPE Trial). In Tokushima University Hospital and 18 other medical institutions, we investigated the views and attitudes of unsuccessful physician recruiters in comparison with successful physician recruiters, using a questionnaire.</p> <p>Results</p> <p>The questionnaire was provided by mail to 47 physicians and 27 (57%) responded. The response rate was 79% for successful physician recruiters compared to 43% (P = 0.014) for unsuccessful physician recruiters. More successful physician recruiters (73%) than unsuccessful physician recruiters (42%) stated they had participated and enrolled patients in previous multicenter clinical trials. A significantly higher number of successful physician recruiters than unsuccessful physician recruiters (42%; P = 0.040) considered the presence of a support system with clinical research coordinators (CRC) as the reason for participation (80%). A large number of unsuccessful physician recruiters experienced difficulty in obtaining informed consent (67%), whereas a significantly smaller number of successful physician recruiters experienced such difficulty (20%; P = 0.014). The difficulties experienced by unsuccessful physician recruiters in the trial were as follows: inability to find possible participants (100%), difficulty in obtaining informed consent (58%), cumbersome procedures (58%), difficulty in long-term follow up (33%), and insufficient tools for explanation and obtaining informed consent (8%).</p> <p>Conclusion</p> <p>This survey showed that successful physician recruiters consider a support system with CRC of value, and that they are skillful in obtaining informed consent. These views and attitudes may have originated from past experience involving clinical trials. In this regard, we need to develop an infrastructure to enlighten physicians on this support system for the promotion of clinical trials.</p

EPD FOR COMPOSITE CATHODE LAYER IN ALL-SOLID-STATE LITHIUM ION BATTERY BASED ON SULFIDE ELECTROLYTE

All-solid-state lithium ion batteries (LIBs), in which liquid-organic electrolytes are replaced with solid state inorganic electrolytes, are expected to be the optimal rechargeable batteries in the next generation because of their higher energy density, cycle stability and ignition safety. In order to develop all-solid-state LIBs with practical performance, controlling architecture in electrode layer consisting of active materials and solid electrolyte, to obtain good contact of the solids interfaces, with high packing ratio is necessary. However, there are few studies on controlled fabrication of macrostructure. We would like to propose a novel method which is employs electrophoretic deposition (EPD) for preparing composite cathode layer, with LiNi1/3Mn1/3Co1/3O2 (NMC) and 75Li2S-25P2S5 (LPS) used as the cathodic active material and solid electrolyte, respectively. The EPD technique can be used to prepare a cathodic layer with a desired structure because its equipment set up is simple but can be used to obtain complex composite structures. Please click Additional Files below to see the full abstract

INCS suppresses H1R gene expression

The purpose of this study is to examine the effect of intranasal corticosteroid (INCS) administration on histamine H1 receptor (H1R) gene expression in the nasal mucosa of healthy participants and the effects of dexamethasone on basal and histamine-induced H1R mRNA expression, and histamine-induced phosphorylation of extracellular signal-regulated kinase (ERK) in HeLa cells. Sixteen healthy participants were given INCS once daily for a week. After pretreatment of dexamethasone, HeLa cells were treated with histamine. Levels of H1R mRNA and phosphorylation of ERK were measured using real time PCR and immunoblot analysis, respectively. Levels of H1R mRNA in the nasal mucosa of healthy participants receiving INCS was significantly decreased. Dexamethasone suppressed basal levels of H1R mRNA, and histamine-induced up-regulation of H1R mRNA and ERK phosphorylation in HeLa cells. These data suggested that corticosteroid inhibited both basal transcription and histamine-induced transcriptional activation of H1R through its suppression of ERK phosphorylation in the signaling pathway involved in H1R gene transcription. It is further suggested that pre-seasonal prophylactic administration of INCS suppresses both basal and pollen-induced upregulation of H1R gene expression in the nasal mucosa of patients with pollinosis, leading to prevention of the exacerbation of nasal symptoms during peak pollen season

Adverse effect of donor-specific anti-human leukocyte antigen (HLA) antibodies directed at HLA-DP/-DQ on engraftment in cord blood transplantation

[Background aims] While donor-specific anti-human leukocyte antigen (HLA) antibodies (DSAs) in the recipient before transplantation are associated with graft failure in cord-blood transplantation (CBT), effects of DSAs other than against HLA-A, -B or -DRB1 on transplantation outcomes remained poorly understood. [Methods] We retrospectively analyzed 567 single-unit CBT recipients to evaluate impact of DSAs against HLA-DP and -DQ on CBT outcomes. [Results] Among 143 recipients (25.2%) who had anti-HLA antibodies, nine harbored DSAs against HLA-DP or -DQ. DSAs against HLA-DP or -DQ were associated with a significantly lower neutrophil engraftment rate (55.6% versus 91.8%, P = 0.032) and with a marginally lower platelet engraftment rate (46.7% versus 75.3%, P = 0.128) at day 100 after transplantation, compared with patients without anti-HLA antibodies. Time to neutrophil and platelet engraftment in patients with DSAs for HLA-DP or -DQ was significantly longer than that in patients without anti-HLA antibodies (median, 25 versus 21 days, P = 0.002 in neutrophil; median 61 versus 46 days, P = 0.014 in platelet). Cumulative incidence of bacterial infection at day 100 was significantly greater (88.9% versus 57.1%, P = 0.024), and re-transplant-free survival was marginally lower (55.6% versus 76.8%, P = 0.132) in patients with DSAs against HLA-DP or -DQ, compared with those without anti-HLA antibodies. These findings suggest that DSAs against HLA-DP or -DQ lead to unfavorable engraftment, which may increase risk of bacterial infection, and reduce survival soon after CBT. [Conclusions] Our results suggest the importance of evaluating DSAs against HLA-DP and -DQ in recipients before selecting CB units