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Background Coronavirus disease 2019 (COVID‐19) pandemic has affected the lives of young and old people. Most reports on pediatric cases suggest that children experience fewer and milder symptoms than adults do. This is the first nationwide study that focused on pediatric cases reported by pediatricians, including those with no or mild symptoms, in Japan. Methods We analyzed the epidemiological and clinical characteristics, and transmission patterns of 840 pediatric (

Background CD26 is a T-cell costimulatory molecule with dipeptidyl peptidase IV (DPPIV) activity in its extracellular region. The relevance of sCD26 levels and disease activity has been reported in rheumatic or infectious disease. For certain metabolic and endocrine conditions, DPPIV inhibitors were recently developed as a new class of antidiabetic drugs that act by inhibiting DPPIV, the enzyme that inactivates incretin hormone. Higher levels of sCD26 in diabetic patients have been shown to be associated with a poor clinical response to DPPIV inhibitors, with sCD26/DPPIV being an adipokine that may impair insulin sensitivity. With the increasing use of serum sCD26 and DPPIV enzyme activity as biomarkers with potential clinical implications, accurate measurements of serum sCD26 levels and DPPIV enzyme activity are needed. Methods We compare two commercially widely available and an in-house enzyme-linked immunosorbent assays (ELISAs) for measurement of serum sCD26 in healthy or diabetic human sera. Results The significant discrepancies among the results obtained from commercially available and the in-house sCD26 assays were found. We also observed that a linear correlation between serum sCD26 level and DPPIV enzyme activity exists with the in-house ELISA, while the commercial ELISAs demonstrate a lack of consistency between serum sCD26 level and DPPIV enzyme activity. Conclusion These data strongly suggest that new commercial assays for sCD26 plasma levels need detailed evaluation and validation with samples from clinically well-characterized patients, and results obtained from these newer assays should be compared to those obtained from well-established in-house assays such as our assay or other validated sCD26 ELISA assays.

N,N-Di(arenesulfonyl)-N′,N′-dimethyl-hydrazines, readily prepared from arenesulfonyl chlorides and N,N-dimethylhydrazine, were heated at 120°C in chlorobenzene to give S-aryl arenethiosulfonates, ArSSO2Ar, in good yields.

When benzyl, allyl, and propargyl ethers were treated with tert-butyl hydroperoxide and a catalytic amount of iron(III) acetylacetonate, tert-butyl peroxyacetals were produced in good to excellent yields, via C-H bond functionalization. This method is also applicable to ethylene acetals of unsaturated aldehydes to give peroxyorthoesters.

Treatment of 2-alken-4-ynoates with methyl- or aryl-Grignard reagents and iron(II) chloride (10 mol%) afforded 5-methyl- or 5-aryl-3,4-alkadienoates in good yields as a single isomer after aqueous work-up. Likewise, (2-alken-4-ynoyl)oxazolidinones afforded (5-methyl-3,4-alkadienoyl)oxazolidinones. The aldol-type reaction with acetone was also possible in place of the hydrolytic work-up.

Summary Background Cytokine imbalance and cellular migration to inflammatory sites are critical components of allergic diseases. Redirecting cytokine imbalance and inhibiting cell migration therefore represent important therapeutic strategies for the treatment of these disorders. Objectives To study the in vitro effect of ebastine, a novel non-sedating H1 receptor antagonist, on cytokine secretion and migration of activated T cells, as well as production of pro-inflammatory cytokines by macrophages. Methods Peripheral T cells obtained from healthy volunteers were cultured in wells coated with the combination of anti-CD3 monoclonal antibody (mAb) and anti-CD26 mAb, anti-CD3 mAb and anti-CD28 mAb, or anti-CD3 mAb with PMA, in the presence or absence of ebastine. T cell proliferation and the production of cytokines were measured by [3H]thymidine incorporation assay and ELISA, respectively. In addition, transendothelial migration of T cells and production of pro-inflammatory cytokines by macrophages were examined. Results Ebastine inhibited T cell proliferation and the production of IL-4, IL-5, IL-6, and TNF-α by T cells under each co-stimulatory condition tested, whereas it exhibited no effect on the production of IL-2 or IFN-γ. In addition, T cell migration and the production of such pro-inflammatory cytokines as TNF-α and IL-6 by macrophages were inhibited by ebastine. Conclusions These results indicate that ebastine has a specific inhibitory effect on Th2-type cytokine production. Moreover, ebastine inhibited T cell migration and pro-inflammatory cytokine production by T cells and macrophages, suggesting that ebastine might be useful for the treatment of T cell-mediated allergic inflammatory disorders, including asthma, atopic dermatitis, and Th2-type autoimmune diseases.

We investigated the molecular epidemiology and biological characteristics of wild measles viruses isolated since 1984 in Japan. The circulating measles virus was of genotype C1 before 1985, D3 from 1987 to 1990, and D5 from 1990 to 1997. It was replaced by the same cluster of Chicago-type D3 strain from 1997 to 1999. In 2000, D5 recirculated with sporadic cases caused by genotype H1. The H1 genotype became dominant in 2001 with a minor distribution of D5. No significant difference was observed in neutralizing titers against C1, D3, D5, and H1 when we used sera having high neutralizing titers. However, some D3 and H1 strains were not completely neutralized with low levels of neutralizing antibody, and maintaining high levels of measles antibodies would be required for the control measles outbreaks.

Objective We have previously reported that the anti-6C2 monoclonal antibody (mAb) defines a subset of human CD4+ memory T cells. The present study sought to determine the nature of the 6C2 molecule and the function associated with 6C2+ T cells, and to examine whether this T cell subset is involved in the pathophysiology of rheumatoid arthritis (RA). Methods Cytofluorographic analysis was performed for identification of T cell surface molecules displaying a distribution similar to that of the 6C2 molecule. T cells in the synovial fluid of RA patients were examined for expression of the 6C2 molecule. Transendothelial migratory activity was assessed by assay using monolayers of human endothelial cells. Specific reactivity of the anti-6C2 mAb was determined by immunoblotting on gangliosides separated by thin-layer chromatography, and flow cytometric analysis of the cells transfected with complementary DNA (cDNA) was performed for determination of the glycosyltransferases involved in biosynthesis of the gangliosides. Results On human peripheral T cells, the 6C2 molecule was distributed, by and large, in a pattern similar to that of CDw60, or O-acetyl-GD3. The majority (>70%) of synovial fluid T cells from patients with RA were found to be 6C2 positive, and those 6C2+ T cells exhibited a transendothelial migratory capacity that was inhibited by pretreatment of T cells with anti-6C2 mAb. Moreover, treatment of T cells with neuraminidase resulted in a loss of 6C2 expression as well as a reduction in the transendothelial migratory activity. Anti-6C2 mAb reacted specifically with GD3, but not with O-acetyl-GD3. The reactivity of anti-6C2 mAb was induced on the cell surface only by transfection with cDNA for GD3 synthase. Conclusion The 6C2 molecule is a disialoganglioside, GD3, and is present on a subset of T cells with transendothelial migratory capacity. The 6C2/GD3 molecules, as well as 6C2/GD3+ T cells, appear to play a role in T cell migration and in the inflammation of RA.

The presented reaction is limited to N,N-Di(arenesulfonyl)hydrazines and does not work with N,N-Di(alkylsulfonyl)hydrazines.

Background Cytokine imbalance is thought to be one of the causes for allergic diseases. The effect of anti-allergic drugs on cytokine production from T cells should be examined in a convenient way. Objectives To study the in vitro effect of terfenadine, a prototype non-sedating H1 receptor antagonist, on cytokine production from activated T cells. Methods T cells were cultured in the presence of terfenadine on anti-CD3 mAb and anti-CD26 mAb-coated wells, anti-CD3 mAb and anti-CD28 mAb-coated wells, and anti-CD3 mAb wells with PMA. T-cell proliferation, along with the concentrations of interleukin (IL) -2, interferon (IFN) -gamma, IL-4, and IL-5 were measured. Results Terfenadine inhibited T-cell proliferation and IL-4 and IL-5 production under each costimulatory condition tested, whereas it had no effect on IL-2 and IFN-gamma production. Conclusions These results indicate that terfenadine has a specific inhibitory effect on TH2-type cytokine production induced by several ways of costimulatory activation.

Treatment of 2-alken-4-ynoates with methyl- or aryl-Grignard reagents and iron(II) chloride (10 mol%) afforded 5-methyl- or 5-aryl-3,4-alkadienoates in good yields as a single isomer after aqueous work-up. Likewise, (2-alken-4-ynoyl)oxazolidinones afforded (5-methyl-3,4-alkadienoyl)oxazolidinones. The aldol-type reaction with acetone was also possible in place of the hydrolytic work-up.

— An advanced screen for use with LCD/LCoS/DMD rear-projection TV has been developed. A lenticular lens having a pitch of 64 μm has been developed without loss in any other optical property. A 70% black-stripe ratio was obtained by optimizing the patterning process, which maintains high contrast. As described in this paper, the FC-Screen manufacturing technology has been further developed.

An advanced screen for application on LCD/LCoS/DMD Rear Projection TV was developed. We achieved a lenticular lens of pitch 64 μm pitch without loss of contrast and any other optical properties. As described in this paper, our FC-Screen manufacturing technology was further developed.

An advanced screen (fine-pitch FC-Screen) for application on LCD/DLP rear projection TV was developed. A lenticular lens of pitch 98 μm was achieved without loss of contrast and other optical properties. That is effective for high-definition imaging as well as reduction of moire.

CD82, a member of tetraspan family (tetraspanin), is a multifunctional molecule that is involved in cell activation, costimulation, and cell spreading of T cells. Here we show that immobilized anti-CD82 monoclonal antibody (mAb) as well as anti-alpha4beta1 integrin mAb induced tyrosine phosphorylation of pp105/Crk-associated substrate lymphocyte type (Cas-L) in human peripheral T cells and H9 cells. Furthermore, one of anti-CD82 mAb (8E4), which induces homotypic aggregation of T cells and H9 cells but has no costimulatory activity, partially inhibited very late antigen (VLA)-4 integrin ligand-mediated costimulation of T cells, whereas it failed to inhibit VLA-5 integrin ligand-mediated costimulation. To further elucidate the relationship between CD82- and VLA-4-mediated signaling pathways we defined the IL-2 production by the costimulation of Jurkat T cells with marginal amount of Cas-L, and subsequently found that mAb against CD82 had strong costimulatory activity to CD3/TCR, whereas mAb against beta1 failed to do so in those cells. We have further demonstrated that this discrepancy between beta1 integrin- and CD82-mediated costimulation partly lies in differential activation of NF-AT, AP-1, and NF-kappaB in Jurkat T cells. In this study, although some functional overlap exists, we provide evidence for distinctive signaling of CD82- and beta1 integrin-mediated costimulation at the transcriptional level of IL-2 gene.

The objective of the present research was to investigate the mechanism of the hemorrhagic tendency known to be associated with the administration of antibiotics. To do this from the viewpoints of the supply and utilization of vitamin K, studies were carried out in newborn infants and in germ-free mice. The reasons for the selection of newborns were that their intestinal bacterial flora is easily changed by the administration of antibiotics and that it is easy to monitor their oral food intake. Germ-free mice were selected because they do not have intestinal bacteria. Forty newborn infants were each given one of the antibiotics latamoxef (LMOX), cefmenoxime (CMX), cefotaxime (CTX) and ceftazidime (CAZ), and the establishment of most bacteria in the intestinal tract was delayed, with the exception of the enterococci, and sometimes S. epidermidis, which are insensitive to these antibiotics. PIVKA II, which is an indicator of vitamin K deficiency, was detected in 72% of the patients treated with LMOX and in 48% of the CMX-treated patients. Conversely, all 16 patients who were treated with either CTX or CAZ were negative for PIVKA II. The correlation between the incidence of a positive result for PIVKA II and the oral food intake was investigated. It was found that 11 of 16 infants (68%) fed no milk or fed breast milk became positive for PIVKA II. In contrast, only 4 (16%) of 24 infants fed formula milk became positive for PIVKA II. The importance of the intestinal bacteria and the oral food intake was confirmed by the fact that the hepaplastin test value was prolonged when methyltetrazolyl-thiomethyl (MTT) was administered to germ-free mice and to normal mice on a vitamin-K-free diet. On the basis of these experimental findings, it is surmised that the association between antibiotic therapy and the development of a hemorrhagic tendency is a result of a complex interaction of various factors, i.e., a decrease in oral food intake, a decrease in the count of the normal bacterial flora of the intestinal tract, and the presence of an MTT group in the structure of the administered antibiotic.

One of the factors in the deterioration of the reconstructed image of the single-photon emission CT (SPECT) is the respective characteristics of the collimator used in the detection of the γ-ray. The characteristics depend on the shape and material of the collimator, and produce shiftvariant blurs on the reconstructed image. This kind of error cannot be eliminated by the deconvolution, which regards the blur as shift-invariant. This paper discusses the effect in the spatial frequency domain, and it is shown that the effect of the blur by collimator can be approximated analytically by a shift-invariant blur on the annular ring determined for each frequency. A method of improving the quality of the reconstructed image is proposed utilizing this property. By the numerical simulation using a computer, it is verified that the proposed method is effective independently of the attenuation and quantization noise.

Single-photon emission CT is one of the most useful techniques in nuclear medicine, wherein a radioisotope material is injected into the body and by external detection of the radiated y-ray the RI distribution on an arbitrary layer (slice) is reconstructed from the data, permitting visual representation of physiological information. Longitudinal imaging is one of such techniques. The object is regarded as composed of layered RI distributions. From the y-ray projection data obtained by y-ray detectors placed parallel to the layer, the RI distribution at each slice is reconstructed. In longitudinal imaging, however, the projection data are observed only along a particular direction and the working range of the detector is restricted, leading to blur and degradation of the reconstructed image. This paper discusses the quality degradation inherent in longitudinal imaging and proposes a reconstruction algorithm which employs the contour information of the object in the reconstruction computation to make correction for the quality. The result of numerical simulation is also reported.