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Background Electronic medical records (EMRs) are widely used, but in many cases, they are used within a network physically separated from the Internet. Multicenter clinical studies use Internet-connected electronic data capture (EDC) systems to collect data, where data entered into the EMR are manually transcribed into the EDC system. In addition, medical images for clinical research are also collected manually. Variations in EMRs and differing data structures among vendors hamper the use of data for clinical research. Methods We solved this problem by developing a network infrastructure for clinical research between Osaka University Hospital and affiliated hospitals in the Osaka area and introducing a clinical data collection system (CDCS). In each hospital's EMR network, we implemented a CRF reporter that accumulated data for clinical research using a template and then sent the data to a management server in the Osaka University Hospital Data Center. To organize the patient profile data and clinical laboratory data stored in each EMR for use in clinical research, the data are retrieved from the template by an interface module developed by each vendor, according to our common data output interface specification. The data entered into the CRF reporter template for clinical research are also recorded in the EMR progress notes and sent to the data management server. This network infrastructure can also be used as a medical image collection system that automatically collects images for research from PACS at each hospital. These systems are managed under common subject numbers issued by the CDCS. Results A network infrastructure was established among 19 hospitals, and a CRF reporter was incorporated into the EMR. A medical image transfer system was introduced in 13 hospitals. Since 2013, 28 clinical studies have been conducted using this system, and data for 9,987 cases have been collected as of December 31, 2020. Conclusion Incorporating a CRF reporter with medical image transfer system into the EMR has proven useful for collecting research data.

The Pro-His-Ser-Arg-Asn (PHSRN) sequence in fibronectin is a second cell-binding site that synergistically affects with Arg-Gly-Asp. The PHSRN peptide also induces cell invasion and accelerates wound healing. Here, we examined the sequence specificity of PHSRN on corneal epithelial migration using various synthetic peptides. Elongation and deletion analyses of Ac-PHSRN-NH(2) suggest that the five amino acid length was a minimum and essential sequence for promotion of rabbit corneal epithelial migration ex vivo. Additionally, alanine substituted analysis indicated that the Ser- and Arg-residues are critical for the biological activities. The Ser-Arg motif is involved in various biologically active peptides, suggesting that the unique sequence interacts with cellular receptor(s) and regulates biological functions. Further, the N-acetyl and C-amide of Ac-PHSRN-NH(2) contributed effectively for the chemical stability in tears. The Ac-PHSRN-NH(2) peptide has potential to use as a therapeutic reagent especially for corneal wound healing.

Glycerol-3-phosphate acyltransferase 1 (GPAT1) is a rate limiting enzyme in de novo glycerophospholipid synthesis. The murine GPAT1 promoter sequence (the "classical" sequence) was reported previously. However, the organization of this DNA sequence does not fully match the mouse genome sequences on NCBI/GenBank. Here we have identified net cis-acting promoter sequences for the mouse GPAT1 gene: promoter 1a which includes part of the classical sequence and the downstream promoter 1b. Promoter 1a facilitates transcription of two alternative GPAT1 transcript variants, GPAT1-V1 and V2, while promoter 1b produces a third transcript variant, GPAT1-V3. Upstream stimulating factor-1 (USF-1) controlled both promoters whereas sterol regulatory element-binding protein-1 (SREBP-1) exclusively regulated promoter 1a activity in vitro. Feeding increased GPAT1-V1 and V2, but not V3 mRNA levels in mouse liver. The obese condition of db/db mice did not alter the hepatic expression levels of any of the three GPAT1 variants. Feeding enhanced hepatic mRNA levels, intranuclear protein levels and promoter 1a-binding levels of SREBP-1, but not of USF-1. Thus, promoter 1a was exclusively activated by routine feeding in vivo. Our results indicate differential roles of the two promoters in the regulation of hepatic GPAT1 gene expression in mice.

We identified a novel alternative splicing event that constitutively produces a truncated active form of human sterol regulatory element-binding protein 1 (SREBP-1). A cDNA of this splicing variant (named SREBP-1Delta) contains a translational stop codon-encoding exon sequence between exons 7 and 8. It produces SREBP-1aDelta (470 a.a.) and SREBP-1cDelta (446 a.a.) proteins that lack transmembrane and C-terminal regulatory sequences necessary for localization of SREBP-1 to the endoplasmic reticulum. A luciferase reporter assay showed that SREBP-1aDelta and SREBP-1cDelta transactivated lipogenic gene promoters to the same extent as that induced by N-terminal active fragments of SREBP-1a and SREBP-1c, respectively. SREBP-1Delta mRNA is expressed in human cell lines as well as adipose and liver tissues. Expression levels ranged from 5% to 16% of total SREBP-1 expression. The ratio of SREBP-1Delta expression to total SREBP-1 expression in HepG2 cells was not affected by either insulin or high glucose treatment.

Recent report (Maret, S., Franken, P., Dauvilliers, Y., Ghyselinck, N.B., Chambon, P., Tafti, M., 2005. Retinoic acid signaling affects cortical synchrony during sleep. Science 310, 111-113.) has suggested that vitamin A (retinol and its derivatives) is genetically involved in the electroencephalogram (EEG) delta oscillation during sleep. However, this finding has not yet been confirmed by other studies. In this study, we attempted to record the sleep EEG and behavior, and to quantify striatal monoamines in mice fed a vitamin A-deficient (VAD) diet for 4 weeks, in order to clarify the linkage between the delta oscillation and vitamin A. VAD mice demonstrated a significant decrease in the delta power of the EEG. However, 6-h sleep deprivation caused the recovery of the delta power in VAD mice to a level similar to that of the control. VAD also caused the decrease of spontaneous activity throughout 24-h period. Furthermore, dihydroxyphenylacetic acid, a metabolite of dopamine, was decreased significantly in the striatal tissue of VAD mice. Our present results suggest that the deficiency of vitamin A causes the attenuation of delta power in NREM sleep and spontaneous activity. These attenuations may be related to the alteration of striatal dopaminergic function.

The water–fine SiO2 particle suspension with a narrow-size distribution (mean diameter of 2.97 μm , standard deviation of 0.03 μm ) was heated in a rectangular vessel from a vertical wall and cooled from the opposing vertical wall. Temperature distribution and local particle concentration of the suspension were measured under various temperature differences between the opposing vertical walls. It was found that behaviors of natural convection in the suspension were classified into five patterns. The critical wall temperature difference that would give rise to change of the natural convection pattern decreased as the initial particle concentration decreased.

The RING finger (C3HC4-type zinc finger) is a variant zinc finger motif presents in a new family of proteins. A new member of the RING finger family was identified and its cDNA structures were determined in human and mouse. The predicted protein consisting of a 144 amino acid residues is very conservative between the two species and contains a canonical RING-H2 finger motif (C3H2C2) at the carboxyl-terminal region. The genes were designated as RNF11/Rnf11 for RING finger protein 11. A single 2.4-kb transcript of mouse Rnf11 was ubiquitously expressed in various fetal and adult mouse tissues by the Northern blot analysis. The human RNF11 gene was mapped on chromosome 1p31-p32 region, where frequent alterations have been observed in T-cell acute lymphoblastic leukemia.

In order to investigate the effects of additives on the active sites of β-(VO)2P2C7 catalyst, a series of promoted VPO catalysts, prepared by the impregnation of VOHPO4.0.5H2O with solutions containing promoter elements, were characterized with BET, XRD, and NARP (NO-NH3 Rectangular Pulse) technique, and their catalytic properties were examined with the continuous flow reaction of the selective oxidation of n-butane. The structure of catalyst and the number of surface V=O species as the active sites are discussed in relation to the promoter and the preparation procedure, and the catalytic property is discussed in relation to the structural factors and the active sites.

The effect of promoters on the activity and selectivity of the active sites was investigated in the selective oxidation of benzene over vanadium pentoxide catalysts. The activity per surface area is increased by addition of MoO3, WO3, P2O5 and SnO2, but the activity of each redox sites, i.e., turnover frequency (TF), was not. This indicates that the promoters enhanced the activity by increasing the redox sites, such as the surface V O species. The selectivity to maleic anhydride (MA) was improved by the addition of MoO3, WO3 and P2O5, while it was lowered by SnO2. The effect on the selectivity was discussed in the light of the electronegativity of promoter cations. The additions of MoO3, WO3 and P2O5, of which the cations are more electronegative than V5+, decreased TF of the production of carbon oxides more seriously than that of MA. On the other hand, the addition of less electronegative cation, i.e., Sn4+, increased TF of the production of carbon oxides at the sacrifice of MA.

The electronic nature of the catalysis in the NO-NH 3 reaction on vanadium oxide catalyst has been investigated using the CNDO/2 method. The calculations have shown that NH 3 is stably chemisorbed on the Bronsted acid site on the catalyst, whereas NO is hardly chemisorbed, which is in accordance with experiment. The charge distributions and bond energies of the system composed of NO and NH 3 absorbed on the catalyst have been calculated for various states on the reaction coordinate. The calculated results have indicated that electrons on the adsorbed NH 3 transfer to the antibonding orbitals of NO at the transition state to dissociate the NO bond. This dissociation has been shown to lead to the formation of N 2 , H 2 O, and V—OH species. Furthermore, the calculations have supported the validity of the Eley-Rideal mechanism experimentally proposed.