We have previously reported the presence of an apyrase in Mimosa pudica. However, only limited information is available for this enzyme. Thus, in this study, the apyrase was purified to homogeneity. The purified enzyme had a molecular mass of around 67 kD and was able to hydrolyze both nucleotide triphosphate and nucleotide diphosphate as substrates. The ratio of ATP to ADP hydrolysis velocity of the purified protein was 0.01 in the presence of calcium ion, showing extremely high substrate specificity toward ADP. Thus, we designated this novel apyrase as MP67. A cDNA clone of MP67 was obtained using primers designed from the amino acid sequence of trypsin-digested fragments of the protein. In addition, rapid amplification of cDNA ends-polymerase chain reaction was performed to clone a conventional apyrase (MpAPY2). Comparison of the deduced amino acid sequences showed that MP67 is similar to ecto-apyrases; however, it was distinct from conventional apyrase based on phylogenetic classification. MP67 and MpAPY2 were expressed in Escherichia coli, and the recombinant proteins were purified. The recombinant MP67 showed high substrate specificity toward ADP rather than ATP. A polyclonal antibody raised against the recombinant MP67 was used to examine the tissue distribution and localization of native MP67 in the plant. The results showed that MP67 was ubiquitously distributed in various tissues, most abundantly in leaves, and was localized to plasma membranes. Thus, MP67 is a novel ecto-apyrase with extremely high substrate specificity for ADP.

This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

We must need uniform heating in microwave ovens. To remove unevenness.it is important to analyze the electromagmtic field distribution in the cavity of microwave ovens. and to optimize it.Generally. we m u s t use three-dimensional analysis in microwave over^ and often face the problem of exceeding computer resouras available. So we adopt the Fl-TD method, which has an advantage of using computer memories over other s~ace dividing methods. mch as FEM.But the FD-TD method is mainly used for transient analysis, and not often for steady state analysis. So we first investigate in judgement on mvergence to steady state, then compare the calculated electromagnetic energy distribution with experimental heating unevennes;. We see that they fairly resemble each other. Figure I shows the model of a microwave oven which we analyze. We set fr-2.464MHz. and as;ume that only TElo mode can propagate in the exciting rectangular waveguide. The waveguide is mat&& at the source. II .MCWL FOR ANALYSISThe observing plane is at 40.0mm above the bottcm of the cavity. We use rectangular cells with the smallest cell size Ad=5mm and tire step At=1/(2.464x1Ogx50)sec. which satisfies the Courant stability condition".The operational memory is about 12hlbytes. and Bv times for calculating 30.000 time steps are 270 sec. by using our slpercomputer. I.GoN\IERCINXTO STE4DY SATE Figure 2 shows the energy flow at a cross section of the waveguide as shown in figure 1 . We calculate the su11 of the Pointirg's vector in this c r m section and integrate over ax: period which m r r m to 50 time steps. So this figure shows the relatihip between energy flow and 0-7803-2009-3/941$4.00 0 1994 IEEE. 1806

No abstract

ObjectivesTo elucidate the risk of cardiovascular event occurrence followingStreptococcus pneumoniaeinfection.DesignRetrospective cohort study using a LIFE Study database.SettingThree municipalities in Japan.ParticipantsMunicipality residents who were enrolled in either National Health Insurance or the Latter-Stage Elderly Healthcare System from April 2014 to March 2020.ExposureOccurrence ofS. pneumoniaeinfection.Primary outcome measuresOccurrence of one of the following cardiovascular events that led to hospitalisation afterS. pneumoniaeinfection: (1) coronary heart disease (CHD), (2) heart failure (HF), (3) stroke or (4) atrial fibrillation (AF).ResultsS. pneumoniae-infected patients were matched with non-infected patients for each cardiovascular event. We matched 209 infected patients and 43 499 non-infected patients for CHD, 179 infected patients and 44 148 non-infected patients for HF, 221 infected patients and 44 768 non-infected patients for stroke, and 241 infected patients and 39 568 non-infected patients for AF. During follow-up, the incidence rates for the matched infected and non-infected patients were, respectively, 38.6 (95% CI 19.9 to 67.3) and 30.4 (29.1 to 31.8) per 1000 person-years for CHD; 69.6 (41.9 to 108.8) and 50.5 (48.9 to 52.2) per 1000 person-years for HF; 75.4 (48.3 to 112.2) and 35.5 (34.1 to 36.9) per 1000 person-years for stroke; and 34.7 (17.9 to 60.6) and 11.2 (10.4 to 12.0) per 1000 person-years for AF. Infected patients were significantly more likely to develop stroke (adjusted HR: 2.05, 95% CI 1.22 to 3.47; adjusted subdistribution HR: 1.94, 95% CI 1.15 to 3.26) and AF (3.29, 1.49 to 7.26; 2.74, 1.24 to 6.05) than their non-infected counterparts.ConclusionsS. pneumoniaeinfections elevate the risk of subsequent stroke and AF occurrence. These findings indicate that pneumococcal infections have short-term effects on patients’ health and increase their midterm to long-term susceptibility to serious cardiovascular events.