Study on Bearing Characteristics of Reciprocating Compressor for Refrigerator

In recent years, in order to reduce the energy consumption of refrigerators through reduction of input power and improved refrigeration capacity, reciprocating compressors are gradually converted to inverter type. Correspondingly, we have studied the sliding bearing characteristics of the crankshaft journal at variable speed which is the key to improving the efficiency of reciprocating compressor. Generally, the characteristics of a sliding bearing are explained with a Stribeck curve. In the fluid lubrication regime, there is sufficient lubricant between metal surfaces. As the rotational speed decreases, the viscous resistance is reduced and it will result in the reduction of friction coefficient. Conversely, it is widely known that further reduction of rotational speed will shift to boundary lubrication regime where the friction coefficient increases due to metal to metal contact. In the inverter reciprocating compressor, it is presumed that the sliding of crankshaft on bearing at high rotational speed is in fluid lubrication regime. The input power can be reduced with gradual decrease of friction coefficient by lowering rotational speed, but then the sliding characteristic of the crankshaft at each rotational speed was unclear such that when the speed is too low it will progress into the boundary lubrication regime. This paper explains our experimental study to obtain a Stribeck curve at low load, low speed, and low viscosity oil in inverter operation using a bearing tester that estimate sliding crankshaft on bearing. The results obtained enable the prediction of sliding characteristic of crankshaft and optimization of the bearing property in reciprocating compressor

Evolutionary inactivation of a sialidase in group B Streptococcus

Group B Streptococcus (GBS) is a leading cause of bacterial sepsis and meningitis in newborns. GBS possesses a protein with homology to the pneumococcal virulence factor, NanA, which has neuraminidase (sialidase) activity and promotes blood-brain barrier penetration. However, phylogenetic sequence and enzymatic analyses indicate the GBS NanA ortholog has lost sialidase function – and for this distinction we designate the gene and encoded protein nonA/NonA. Here we analyze NonA function in GBS pathogenesis, and through heterologous expression of active pneumococcal NanA in GBS, potential costs of maintaining sialidase function. GBS wild-type and ΔnonA strains lack sialidase activity, but forced expression of pneumococcal NanA in GBS induced degradation of the terminal sialic acid on its exopolysaccharide capsule. Deletion of nonA did not change GBS-whole blood survival or brain microvascular cell invasion. However, forced expression of pneumococcal NanA in GBS removed terminal sialic acid residues from the bacterial capsule, restricting bacterial proliferation in human blood and in vivo upon mouse infection. GBS expressing pneumococcal NanA had increased invasion of human brain microvascular endothelial cells. Thus, we hypothesize that nonA lost enzyme activity allowing the preservation of an effective survival factor, the sialylated exopolysaccharide capsule

Development of Health Promotion Programs based on the Salute Genetics Model

健康社会学者のアーロン・アントノフスキー (Aaron Antonovsky) は、健康を積極的に創出する要因の研究を展開し、この成果を健康生成論 (salute genetics oriented theory) として公表した。この理論に基づくヘルス・プロモーションは、ストレス社会で生活する我々の、健康の維持・増進に寄与することが期待される。本稿では健康生成モデルに基づく、一般の人々を対象にした心理教育プログラムのあり方について論考する。健康生成志向的な認知を促すグループワークでは、①ストレスの発生、およびSOCと健康の関連についての理解を深める知識教育、② SOCの自己理解、③ SOCの改善や変容を目的にしたに取り組みなどから構成されるプログラムが考えられる。Aaron Antonovsky, who was a health sociologist, investigated factors that promoted health and then published these results as the salute genetics-oriented theory. This theory is useful for health promotion for Japanese living in stressful environments. At this article, we discussed health promotion programs based on the salute genetics-oriented model. It was concluded that the programs were constructed of three elements: education about the salute genetics-oriented and general stress models, self-understanding of “sense of coherence” (SOC), and improvement of SOC

クロレラからの血圧降下作用糖蛋白質の検索(農芸化学部門)

クロレラから, 血圧降下作用物質が部分精製された。生クロレラの細胞壁破砕物を冷アセトンにて脱脂脱色後, 冷水抽出物が得られた。冷水抽出物の80%エタノール不溶性画分に降圧作用が認められた。80%エタノール不溶性画分のBio-Gel P-60ゲルロ過, DEAE-セルロースクロマトグラフィーにより, ほぼ均一な降圧画分D-IIが得られた。画分D-IIの分子量は, 約80,000と推定された。画分D-IIを, 13週令の血圧180∿190mmHgのSHRに0.5mg/100g体重の割合で腹腔内投与すると, 1時間後に140∿160mmHgという血圧になり, 強い降圧効果が認められた。画分D-IIは, ガラクトース, マンノース, グルコサミンを含む糖蛋白質で, アスパラギン酸, グルタミン酸, アラニン, プロリンの含量が高く, 塩基性アミノ酸が少なかった。The antihypertensive material was partially purified from chlorella. Cell wall of chlorella was destroyed with Dyno-mill. After defatted and decolored with cold aceton, water extract was obtained from chlorella by the extraction at 4℃ for 24 hours. 80% ethanol precipitate from water extract was fractionated by Bio-Gel P-60 gel filtration followed by DEAE-cellulose chromatatography. About 50mg of antihypertensive fraction D-II were obtained from 10g of chlorella. The molecular weight of fraction D-II was about 80,000 dalton. The blood pressure of spontaneously hypertensive rat (13 weeks of age) was decreased from 185 to 150mmHg, when fraction D-II was injected intraperitoneally at the concentration of 0.5mg/100g of body weight. Fraction D-II contained galactose, mannose and glucosamine. The contents of aspartic acid, glutamic acid, alanine and proline in fraction D-II were large

Hydrogen peroxide produced by oral Streptococci induces macrophage cell death.

Hydrogen peroxide (H2O2) produced by members of the mitis group of oral streptococci plays important roles in microbial communities such as oral biofilms. Although the cytotoxicity of H2O2 has been widely recognized, the effects of H2O2 produced by oral streptococci on host defense systems remain unknown. In the present study, we investigated the effect of H2O2 produced by Streptococcus oralis on human macrophage cell death. Infection by S. oralis was found to stimulate cell death of a THP-1 human macrophage cell line at multiplicities of infection greater than 100. Catalase, an enzyme that catalyzes the decomposition of H2O2, inhibited the cytotoxic effect of S. oralis. S. oralis deletion mutants lacking the spxB gene, which encodes pyruvate oxidase, and are therefore deficient in H2O2 production, showed reduced cytotoxicity toward THP-1 macrophages. Furthermore, H2O2 alone was capable of inducing cell death. The cytotoxic effect seemed to be independent of inflammatory responses, because H2O2 was not a potent stimulator of tumor necrosis factor-α production in macrophages. These results indicate that streptococcal H2O2 plays a role as a cytotoxin, and is implicated in the cell death of infected human macrophages

Hydrogen peroxide contributes to the epithelial cell death induced by the oral mitis group of streptococci.

Members of the mitis group of streptococci are normal inhabitants of the commensal flora of the oral cavity and upper respiratory tract of humans. Some mitis group species, such as Streptococcus oralis and Streptococcus sanguinis, are primary colonizers of the human oral cavity. Recently, we found that hydrogen peroxide (H2O2) produced by S. oralis is cytotoxic to human macrophages, suggesting that streptococcus-derived H2O2 may act as a cytotoxin. Since epithelial cells provide a physical barrier against pathogenic microbes, we investigated their susceptibility to infection by H2O2-producing streptococci in this study. Infection by S. oralis and S. sanguinis was found to stimulate cell death of Detroit 562, Calu-3 and HeLa epithelial cell lines at a multiplicity of infection greater than 100. Catalase, an enzyme that catalyzes the decomposition of H2O2, inhibited S. oralis cytotoxicity, and H2O2 alone was capable of eliciting epithelial cell death. Moreover, S. oralis mutants lacking the spxB gene encoding pyruvate oxidase, which are deficient in H2O2 production, exhibited reduced cytotoxicity toward Detroit 562 epithelial cells. In addition, enzyme-linked immunosorbent assays revealed that both S. oralis and H2O2 induced interleukin-6 production in Detroit 562 epithelial cells. These results suggest that streptococcal H2O2 is cytotoxic to epithelial cells, and promotes bacterial evasion of the host defense systems in the oral cavity and upper respiratory tracts

Competence-induced protein Ccs4 facilitates pneumococcal invasion into brain tissue and virulence in meningitis

Streptococcus pneumoniae is a major pathogen that causes pneumonia, sepsis, and meningitis. The candidate combox site 4 (ccs4) gene has been reported to be a pneumococcal competence-induced gene. Such genes are involved in development of S. pneumoniae competence and virulence, though the functions of ccs4 remain unknown. In the present study, the role of Ccs4 in the pathogenesis of pneumococcal meningitis was examined. We initially constructed a ccs4 deletion mutant and complement strains, then examined their association with and invasion into human brain microvascular endothelial cells. Wild-type and Ccs4-complemented strains exhibited significantly higher rates of association and invasion as compared to the ccs4 mutant strain. Deletion of ccs4 did not change bacterial growth activity or expression of NanA and CbpA, known brain endothelial pneumococcal adhesins. Next, mice were infected either intravenously or intranasally with pneumococcal strains. In the intranasal infection model, survival rates were comparable between wild-type strain-infected and ccs4 mutant strain-infected mice, while the ccs4 mutant strain exhibited a lower level of virulence in the intravenous infection model. In addition, at 24 hours after intravenous infection, the bacterial burden in blood was comparable between the wild-type and ccs4 mutant strain-infected mice, whereas the wild-type strain-infected mice showed a significantly higher bacterial burden in the brain. These results suggest that Ccs4 contributes to pneumococcal invasion of host brain tissues and functions as a virulence factor

Streptococcal H2O2 inhibits IgE-triggered degranulation of RBL-2H3 mast cell/basophil cell line by inducing cell death.

Mast cells and basophils are central players in allergic reactions triggered by immunoglobulin E (IgE). They have intracellular granules containing allergic mediators (e.g., histamine, serotonin, inflammatory cytokines, proteases and β-hexosaminidase), and stimulation by IgE-allergen complex leads to the release of such allergic mediators from the granules, that is, degranulation. Mast cells are residents of mucosal surfaces, including those of nasal and oral cavities, and play an important role in the innate defense system. Members of the mitis group streptococci such as Streptococcus oralis, are primary colonizers of the human oral cavity. They produce hydrogen peroxide (H2O2) as a by-product of sugar metabolism. In this study, we investigated the effects of streptococcal infection on RBL-2H3 mast cell/basophil cell line. Infection by oral streptococci did not induce degranulation of the cells. Stimulation of the RBL-2H3 cells with anti-dinitrophenol (DNP) IgE and DNP-conjugated human serum albumin triggers degranulation with the release of β-hexosaminidase. We found that S. oralis and other mitis group streptococci inhibited the IgE-triggered degranulation of RBL-2H3 cells. Since mitis group streptococci produce H2O2, we examined the effect of S. oralis mutant strain deficient in producing H2O2, and found that they lost the ability to suppress the degranulation. Moreover, H2O2 alone inhibited the IgE-induced degranulation. Subsequent analysis suggested that the inhibition of degranulation was related to the cytotoxicity of streptococcal H2O2. Activated RBL-2H3 cells produce interleukin-4 (IL-4); however, IL-4 production was not induced by streptococcal H2O2. Furthermore, an in vivo study using the murine pollen-induced allergic rhinitis model suggested that the streptococcal H2O2 reduces nasal allergic reaction. These findings reveal that H2O2 produced by oral mitis group streptococci inhibits IgE-stimulated degranulation by inducing cell death. Consequently, streptococcal H2O2 can be considered to modulate the allergic reaction in mucosal surfaces