Search

Experiment E949 at Brookhaven National Laboratory has observed three new events consistent with the decay ${K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}\ensuremath{\nu}\overline{\ensuremath{\nu}}$ in the pion momentum region $140l{P}_{\ensuremath{\pi}}l199\text{ }\text{ }\mathrm{MeV}/c$ in an exposure of $1.71\ifmmode\times\else\texttimes\fi{}{10}^{12}$ stopped kaons with an estimated total background of $0.93\ifmmode\pm\else\textpm\fi{}0.17(\mathrm{stat}{)}_{\ensuremath{-}0.24}^{+0.32}(\mathrm{syst})$ events. This brings the total number of observed ${K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}\ensuremath{\nu}\overline{\ensuremath{\nu}}$ events to seven. Combining this observation with previous results, assuming the pion spectrum predicted by the standard model, results in a branching ratio of $\mathcal{B}({K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}\ensuremath{\nu}\overline{\ensuremath{\nu}})=({1.73}_{\ensuremath{-}1.05}^{+1.15})\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}10}$. An interpretation of the results for alternative models of the decay ${K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}+nothing$ is also presented.

An experimental upper limit on the branching ratio for the decay {pi}{sup 0}{r arrow}{nu}{bar {nu}} is set at 8.3{times}10{sup {minus}7} (90% C.L.). This decay is forbidden if neutrinos are purely left handed. The limit also applies to any decays of the {pi}{sup 0} to weakly interacting neutrals.

Three events for the decay K+-->pi+ nunu have been observed in the pion momentum region below the K+-->pi+pi0 peak, 140 pi+ nunu) = (1.73(-1.05)+1.15) x 10(-10) consistent with the standard model prediction.

Three events for the decay K+--pi+ nunu have been observed in the pion momentum region below the K+--pi+pi0 peak, 140Ppi199 MeV/c, with an estimated background of 0.93+/-0.17(stat.) -0.24+0.32(syst.) events. Combining this observation with previously reported results yields a branching ratio of B(K+--pi+ nunu) = (1.73(-1.05)+1.15) x 10(-10) consistent with the standard model prediction.

Experiment E949 at Brookhaven National Laboratory studied the rare decay K{sup +}-->pi{sup +} nu{ovr {nu}} and other processes with an exposure of 1.77 x 10{sup 12} k{sup +}'s. The data were analyzed using a blind analysis technique yielding one candidate event with an estimated background of 0.30 {+-} 0.03 events. Combining this result with the observation of two candidate events by the predecessor experiment E787 gave the branching ratio B(K{sup +}-->pi{sup +} nu{ovr {nu}}) = (1.47{sub -0.89}{sup +1.30}) x 10{sup -10}, consistent with the standard model prediction of (0.74 {+-} 0.20) x 10{sup -10}. This is a more detailed report of results previously published [V.V. Anisimovsky et al., Phys. Rev. Lett. 93, 031801 (2004)].

An upper limit on the branching ratio for the decay {ital K}{sup +}{r arrow}{pi}{sup +}{nu}{bar {nu}} is set at 3.4{times}10{sup {minus}8} (90% C.L.). In addition, a 90%-C.L. upper limit of 6.4{times}10{sup {minus}9} is set on the branching ratio for decays of the form {ital K}{sup +}{r arrow}{pi}{sup +}{ital X}{sup 0}, where {ital X}{sup 0} is any massless, weakly interacting neutral particle. Limits are also set for the case where {ital M}{sub {ital X}{sup 0}}{gt}0.

We report on a measurement of the {pi}{sup -} nuclear capture ratio on hydrogen and oxygen in water by two methods. The capture ratio is measured to be W{sub H{sub 2}}{sub O}=(4.45{+-}0.24)x10{sup -3}.

We report on a search for the free-decay component of {pi}{sup -} stopped in water and light materials. A nonzero value of this would be an indication of anomalous {nu}{sub e} contamination to the {nu}{sub e} and {nu}{sub {mu}} production at stopped-pion neutrino facilities. No free-decay component of {pi}{sup -} was observed in water, Beryllium, and Aluminum, for which upper limits were established at 8.2x10{sup -4}, 3.2x10{sup -3}, and 7.7x10{sup -3}, respectively.

A sample of kinematically identified K{sup +}{yields}{pi}{sup +}{pi}{sup 0} decays obtained with the E949 detector was used to search for the helicity-suppressed decay {pi}{sup 0}{yields}{nu}{nu} resulting in an upper limit of 2.7x10{sup -7} at 90% confidence level. The upper limit is also applicable to {pi}{sup 0} decays into unknown weakly-interacting particles.

We report the results of a search for the decay ${K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}\ensuremath{\nu}\overline{\ensuremath{\nu}}$ in the kinematic region with ${\ensuremath{\pi}}^{+}$ momentum $140lPl195\mathrm{MeV}/c$ using the data collected by the E787 experiment at BNL. No events were observed. When combined with our previous search in this region, one candidate event with an expected background of $1.22\ifmmode\pm\else\textpm\fi{}0.24$ events results in a 90% C.L. upper limit of $2.2\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}9}$ on the branching ratio of ${K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}\ensuremath{\nu}\overline{\ensuremath{\nu}}.$ We also report improved limits on the rates of ${K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}{X}^{0}$ and ${K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}{X}^{1}{X}^{2}$ where ${X}^{0}{,X}^{1}{,X}^{2}$ are hypothetical, massless, long-lived neutral particles.

An additional event near the upper kinematic limit for K+ to pi+ nu nubar has been observed by Experiment E949 at Brookhaven National Laboratory. Combining previously reported and new data, the branching ratio is B(K+ to pi+ nu nubar)= 1.47 (+1.30, - 0.89) x 10-10 based on three events observed in the pion momentum region 211

An additional event near the upper kinematic limit for K+--pi(+)nunu; has been observed by experiment E949 at Brookhaven National Laboratory. Combining previously reported and new data, the branching ratio is B(K+--pi(+)nunu;)=(1.47(+1.30)(-0.89))x10(-10) based on three events observed in the pion momentum region 211P229 MeV/c. At the measured central value of the branching ratio, the additional event had a signal-to-background ratio of 0.9.

We have performed a search for the angular-momentum forbidden decay ${K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}\ensuremath{\gamma}$ with the E787 detector at BNL. No events were observed in the ${\ensuremath{\pi}}^{+}$ kinematic region around $227 \mathrm{MeV}/c.$ An upper limit on the branching ratio for the decay is determined to be $3.6\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}7}$ at $90%$ confidence level.

Additional evidence for the rare kaon decay ${K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}\ensuremath{\nu}\overline{\ensuremath{\nu}}$ has been found in a new data set with comparable sensitivity to the previously reported result. One new event was observed in the pion momentum region examined, $211lPl229\mathrm{MeV}/c$, bringing the total for the combined data set to two. Including all data taken, the backgrounds were estimated to contribute $0.15\ifmmode\pm\else\textpm\fi{}0.05$ events. The branching ratio is $B({K}^{+}\ensuremath{\rightarrow}{\ensuremath{\pi}}^{+}\ensuremath{\nu}\overline{\ensuremath{\nu}}){\phantom{\rule{0ex}{0ex}}=\phantom{\rule{0ex}{0ex}}1.57}_{\ensuremath{-}0.82}^{+1.75}\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}10}$.

Additional evidence for the rare kaon decay K+--pi+nu(nu) has been found in a new data set with comparable sensitivity to the previously reported result. One new event was observed in the pion momentum region examined, 211P229 MeV/c, bringing the total for the combined data set to two. Including all data taken, the backgrounds were estimated to contribute 0.15+/-0.05 events. The branching ratio is B(K+--pi+nu(nu)) = 1.57(+1.75)(-0.82)x10(-10).

Japanese guideline for the diagnosis and management of bronchial asthma was initially reported in 1998 and revised in 2000. This guideline was based on two former guidelines which were made by Japanese Allergology Society in 1993 and NIH.NHLBI in 1995 (GINA). New version of this guideline in 2000 pointed that the efficacy and adverse reaction of leukotriene receptor antagonists, the effectiveness of new inhaled corticosteroid (fluticasone propionate), and transdermal administration of beta-2 stimulant (tulobuterol hydrochloride). The precise evaluation of this guideline in terms of propriety, reliability, applicability and so on was not performed.

Evidence of massive neutrinos was sought in the ${\ensuremath{\pi}}^{+}\ensuremath{\rightarrow}{e}^{+}\ensuremath{\nu}$ decay spectrum with the background from the $\ensuremath{\pi}\ensuremath{\rightarrow}\ensuremath{\mu}\ensuremath{\rightarrow}e$ decay chain highly suppressed. Upper limits (90% C.L.) were set on the neutrino mixing parameter ${|{U}_{\mathrm{ei}}|}^{2}l{10}^{\ensuremath{-}7}$ in the mass region $50l{m}_{\ensuremath{\nu}}l130$ MeV/${\mathit{c}}^{2}$.

An upper limit on the branching ratio for the decay K{sup +}{r_arrow}e{sup +}{nu}{mu}{sup +}{mu}{sup {minus}} is set at 5.0{times}10{sup {minus}7} at a 90{percent} confidence level, consistent with predictions from chiral perturbation theory. {copyright} {ital 1998} {ital The American Physical Society}

To analyze the pulsatile movement of coronary arterial walls, intravascular ultrasound was used to measure the diameter changes in the arterial lumen of 32 patients with coronary artery disease (CAD group) and five patients with chest pain but no CAD (control group). Measurements were performed on segments of the proximal left anterior descending coronary artery that were angiographically nonstenotic. Following identification of the peak systolic and end-diastolic phases using intra-coronary pressure tracings, the luminal diameters were measured around the center at 4 degrees intervals using a computer-assisted image analyzer. The pulsatile diameter change (dD) and end-diastolic diameter (DD) at each interval were analyzed and compared between the CAD and control groups. Mean DD did not differ significantly between the CAD group (4.53 +/- 0.69 mm) and the control group (4.52 +/- 0.51 mm). In contrast, the mean dD in the CAD group (0.05 +/- 0.18 mm) was significantly lower than that of the control group (0.13 +/- 0.12 mm). The mean maximum and minimum standardized percentage pulsatile diameter changes were -10.6 +/- 6.2% and 16.2 +/- 5.9%, respectively, in the CAD group, and -2.7 +/- 4.6% and 11.7 +/- 1.3%, respectively, in the control group. The mean standard deviation of dD was significantly greater in the CAD group (0.182 +/- 0.05 mm) than in the control group (0.116 +/- 0.04 mm), which indicated dD in CAD patients varied to a greater degree than in control patients. The ratio dD/dP (dP : pulse pressure) was used as an index of vascular compliance at the site of measurement. The mean dD/dP was significantly smaller in the CAD group (1.1 +/- 2.5 x 10(-3) mm/mmHg) than in the control group (4.0 +/- 3.3 x 10(-3) mm/mmHg). Aniso-diametric wall movement in the coronary artery (as indicated by a negative dD during systolic expansion) was enhanced in the CAD group compared to the control group. This was probably caused by the early stages of the arterial sclerotic process as it progressed heterogeneously along the vessel wall. Thus, aniso-diametric movement, which is a functional abnormality of the coronary arterial wall, appears to antedate detectable morphological changes.

A 26-year-old woman was admitted to our hospital because of fever of unknown origin. She had been treated with prednisolone, elcatonin and alfacalcidol under the diagnosis of systemic lupus erythematosus (SLE) and aseptic necrosis of femoral bone head. Six months ago she began to have a fever and subsequently left low back pain, for which extensive examinations were performed in other hospital but their causes remained unclear. She was referred to our hospital for further evaluation and therapy in October 1995. Bacteriological, immunological or serological examinations did not reveal the origin of fever. CT and ultrasonic examination did not show any abnormality. However, MRI, which was taken for the evaluation of aseptic necrosis of femoral bone head, showed the abscess shadow in sacroiliac joint. Open biopsy was performed and Mycobacterium tuberculosis bacilli were detected from the abscess. To our best knowledge, this is the first report of SEE with tuberculosis sacroiliac arthritis.

A time spectrum of surface muons from the decay {pi}{sup +}{r_arrow}{mu}{sup +}{nu} ({ital P}{sub {mu}}{sup +}=30 MeV/{ital c}) was measured using a secondary beam channel as a spectrometer, yielding the pion lifetime {tau}{sub {pi}}=26.0231{plus_minus}0.0050 (stat){plus_minus}0.0084(syst) ns.

Eosinophils generate and release leukotrienes C4 and B4 (LTC4, LTB4) and platelet activating factor (PAF), all of which have the capacity to cause inflammation and tissue injury in the airways. This study has examined the effects of a new 5-lipoxygenase inhibitor, 6-hydroxy-2-(4-sulfamoylbenzylamino)-4,5,7-trimethylbenzothiazo le hydrochloride (CAS 120164-49-0, E6080) on the release of LTC4, LTB4 and PAF by human eosinophils, Eosinophils stimulated by 1 mumol/l calcium ionophore A23187 for 15 min released 37.5 +/- 2.2 ng, 2.3 +/- 0.3 ng and 4.0 +/- 0.3 pmol per 10(6) cells of immunoreactive LTC4, LTB4 and PAF, respectively (mean +/- SEM, n = 4). LTC4 and LTB4 releases were inhibited dose-dependently by the addition of E6080 to the cell suspension. The IC50 values were 0.26 mumol/l for LTC4 and 0.23 mumol/l for LTB4. PAF release was not inhibited. These results suggest that E6080 is a potent inhibitor of LTC4 and LTB4 release from eosinophils and may provide a protective effect against bronchoconstriction during late-phase asthmatic responses.

Study of rare decays is an important approach for exploring physics beyond the Standard Model (SM). The branching ratio of the helicity suppressed pion decays, R = , is one of the most accurately calculated decay process involving hadrons and has so far provided the most stringent test of the hypothesis of electron-muon universality in weak interactions. The branching ratio has been calculated in the SM to better than 0.01% accuracy to be RSM = 1.2353(1) × 10 . The PIENU experiment at TRIUMF, which started taking physics data in September 2009, aims to reach an accuracy five times better than the previous experiments, so as to confront the theoretical calculation at the level of ±0.1%. If a deviation from the RSM is found, "new physics" beyond the SM, at potentially very high mass scales (up to 1000 TeV), could be revealed. Alternatively, sensitive constraints on hypotheses can be obtained for interactions involving pseudoscalar or scalar interactions. So far, 4 million π+ → e+ νe ue events have been accumulated by PIENU. This paper will outline the physics motivations, describe the apparatus and techniques designed to achieve high precision and present the latest results.

To determine whether IL-5 is locally produced in the bronchial mucosa of asthmatics, and to ascertain the precise cell type producing this cytokine, we examined bronchial biopsies by non-radioactive in situ hybridization and immunohistochemistry. IL-5 cDNA probes were labeled with digoxigenin-dUTP and hybridized to frozen or paraffin tissue sections. Hybridization signals were visualized by an immunohistochemistry technique. An IL-5-producing T cell clone derived from a patient with adult T cell leukemia was used as a positive control. Specific hybridization signals for IL-5 mRNA were observed in the bronchial mucosa of symptomatic asthmatics. No hybridization signal was detected in the control subject in whom no underlying disease was found. Immunohistochemical staining of serial sections using a panel of monoclonal antibodies directed against lymphocyte subsets strongly suggested that cells expressing mRAN for IL-5 were T cells. These results suggest that a cell-cell interaction between T cells and eosinophils through IL-5 may play an important role in the airway inflammation in asthma.

In order to evaluate the role of tumor necrosis factor alpha (TNF alpha) in the recruitment of eosinophils and neutrophils into the tissues, we studied the effect of TNF alpha on the migration of those cells in vitro, employing a modified Boyden's chamber technique. TNF alpha induced a significant migration of human eosinophils in a dose-dependent manner, and the preincubation of eosinophils with TNF alpha enhanced platelet activating factor (PAF)-induced eosinophil migration. Checkerboard analysis revealed that the eosinophil migration induced by TNF alpha was mainly due to chemokinesis. On the other hand, TNF alpha induced neither neutrophil migration nor enhancement of PAF-induced neutrophil migration. These results indicate that TNF alpha possesses a chemokinetic effect on human eosinophils and that TNF alpha augments the migration of eosinophils by PAF.

Eosinophils, which are prominent inflammatory cells in the asthmatic airway, are attracted to the airway by several chemoattractants. At present, eosinophil chemotaxis is studied employing the Boyden Millipore chamber system in vitro. In the Boyden method, the number of migrated cells are evaluated by direct microscopic observation of individual cells. This microscopic procedure usually requires much time and it is difficult to obtain objective results. Therefore, we have developed a new fractional measurement technique, using the image analyzing system connected with a color video camera and a computer for counting the eosinophils which have migrated into a filter. Using this system with the Boyden method, migrated cells were observed more objectively and quickly. Therefore, this image analyzing system with the Boyden method, may be a useful technique for the fractional measurement of migrated eosinophils in a sample mixture of eosinophils and neutrophils.

In order to clarify the role of leukotriene in the antigen-induced asthmatic response, we carried out mite-antigen, leukotriene D4 (LTD4) and histamine inhalation tests in 21 mite-sensitive atopic asthma patients, and investigated the relationship between the bronchial responsiveness to mite (PD20-Mite) and that to LTD4 and histamine (PD20-LTD4, PD20-Hist). We then compared PD20-LTD4 and PD20-Hist between the groups with and without late asthmatic response (LAR), and investigated the relationship between the peak percentage fall of FEV1.0 in LAR (magnitude of LAR) and PD20-LTD4 and PD20-Hist. There were significant correlations between PD20-LTD4 and PD20-Mite (r = 0.590, p0.01), and between PD20-Hist and PD20-Mite (r = 0.669, p0.001). The bronchial responsiveness to LTD4 and histamine was significantly higher in the group with LAR. In addition, PD20-LTD4 showed a significant negative correlation with the magnitude of LAR (r = 0.724, p0.001). Furthermore we analyzed the relationship between PD20-LTD and the ratio of the magnitude of LAR to that of IAR (immediate asthmatic response), because there was a significant correlation between the magnitude of IAR and that of LAR (r = 0.842, p0.001) in 16 asthmatic patients with dual asthmatic response, and found that the correlation coefficient was also very high (r = -0.836, p0.001). These results suggest an important role of leukotriene in the antigen-induced asthmatic response.

Identification of G-proteins and coupling of PAF receptors to G-proteins have been examined in the membranes of human blood eosinophils and neutrophils. Heterotrimeric G-proteins, Gi and GS, were present in both cell types, as demonstrated by immunoblotting and ADP-ribosylation with pertussis toxin. In addition, a group of low molecular mass (18-28 kDa) monomeric G-proteins was also identified. Pertussis toxin and GTP gamma S attenuated the specific binding of [3H]PAF, suggesting the occurrence of coupling between pertussis toxin-sensitive Gi protein and PAF receptors in eosinophils and neutrophils.

Compared to PAF-induced platelet aggregation, the chemotactic response to PAF of human eosinophils requires higher PAF concentrations, suggesting a lower binding affinity of PAF for the eosinophil. To test this possibility, we examined the binding of PAF by human eosinophils. The dose range of unlabeled PAF required to produce inhibition of [3H]PAF binding was roughly the same as that for induction of chemotaxis, and was much higher than that in platelets as reported in the literature. These results indicate that the affinity of PAF for the eosinophil is considerably less than that for the platelet, and may explain the higher EC50 for eosinophil chemotaxis.

Experiment 787, now in progress at Brookhaven National Laboratory (BNL), is designed to measure the process K+→π+νν. A preliminary upper limit for this process was recently obtained Γ(K+→π+νν/Γ(K+→all)

The photon energy spectra from radiative muon capture on {sup 12}C, {sup 16}O, and {sup 40}Ca have been measured using a time projection chamber as a pair spectrometer. The branching ratio for radiative muon capture is sensitive to {ital g}{sub {ital p}}, the induced pseudoscalar coupling constant of the weak interaction. Expressed in terms of the axial-vector weak coupling constant {ital g}{sub {ital a}}, values of {ital g}{sub {ital p}}/{ital g}{sub {ital a}}=5.7{plus minus}0.8 and {ital g}{sub {ital p}}/{ital g}{sub {ital a}}=7.3{plus minus}0.9 are obtained for {sup 40}Ca and {sup 16}O, respectively, from comparison with phenomenological calculations of the nuclear response. From comparison with microscopic calculations, values of {ital g}{sub {ital p}}/{ital g}{sub {ital a}}=4.6{plus minus}1.8, 13.6{sub {minus}1.9}{sup +1.6}, and 16.2{sub {minus}0.7}{sup +1.3} for {sup 40}Ca, {sup 16}O, and {sup 12}C, respectively, are obtained. The microscopic results are suggestive of a renormalization of the nucleonic form factors within the nucleus.

To evaluate the role of eosinophils in the pathogenesis of bronchial asthma, we measured eosinophil cationic protein (ECP), one of the eosinophil granule proteins. Serum ECP levels were measured by radioimmunoassay in asthmatic (n = 59) and non-asthmatic (n = 47) patients. Preliminary study showed that ECP levels were time-dependently increased in the blood samples until 3 hr. Based on the findings, we determined to measure serum ECP levels at 30 min after blood sampling. Serum ECP levels and blood eosinophil counts in asthmatic patients were significantly higher than those in non-asthmatic patients (p less than 0.01). There was also a positive correlation between serum ECP levels and blood eosinophil counts in patients with asthma (r = 0.46, p less than 0.001). No significant difference was observed in either serum ECP levels or blood eosinophil counts in asthmatic patients classified by clinical type and severity. Blood eosinophil counts in patients with asthma attacks were significantly greater than in those in remission (p less than 0.05), but no significant difference was observed in serum ECP levels between these groups, suggesting an enhanced elimination of ECP during attack. Serum alpha-2 macroglobulins, which bind to ECP and may function as scavengers for ECP, were not significantly different in these group. These results suggest that serum ECP levels may not be a direct indicator of eosinophil activation or degranulation in the pathogenesis of asthma.

To evaluate the acute effects of anti-asthmatic drugs in vitro, we examined the modulation of various anti-asthmatic drugs in therapeutic concentrations on PAF-induced human eosinophil chemotaxis. Aminophylline (20 micrograms/ml) and Isoproterenol (10 nM) inhibited PAF (3 X 10(-8) M)-induced eosinophil chemotaxis nearly 30%, whereas no inhibitory effects were observed by Dexamethasone (0.1 microM), Tranilast, Ketotifen or Azelastine. Aminophylline (20 micrograms/ml) also inhibited LTB4 (3 X 10(-8) M)-induced eosinophil chemotaxis nearly 30%, whereas it did not inhibit chemotaxis induced by zymosan (5 mg/ml)-activated serum. These results indicate that anti-asthmatic drugs except for aminophylline and isoproterenol, when used acutely in therapeutic concentrations, have no striking inhibitory effects on PAF-induced eosinophil chemotaxis. These results further suggest the possibility that there are different mechanisms in eosinophil chemotaxis induced by PAF, LTB4 or by C5a.

To elucidate the role of eosinophils, neutrophils and lymphocytes for the development of bronchial hyperresponsiveness (BHR) following antigen exposure, we have developed a guinea pig model of BHR. Guinea pigs immunized by repeated exposure to aerosolized ovalbumin (OA) were intravenously given metopirone, a cortisol synthesis inhibitor, 24 hrs before and 30 min before antigen challenge, and to prevent death from immediate severe bronchoconstriction, chlorpheniramine maleate was also injected. After antigen challenge with high dose of OA, LAR occurred in twelve of fifteen animals (80%) and the bronchial responsiveness to acetylcholine (Ach) was significantly increased. Histologic examination at 72 h showed a significant increase in the number of eosinophils but not neutrophils within the tracheal walls. However, there was no significant correlation between the change in bronchial responsiveness to Ach at 24 h and the number of eosinophil in the tracheal wall at 72 h. When guinea pigs were treated with Cyclosporin A or FK506, T-lymphocyte selective immunosuppressive agents, from the beginning of immunization period, both eosinophil infiltration and an increase in bronchial responsiveness were inhibited. These results suggest that eosinophils and T-lymphocytes may play an important role in the development of bronchial hyperresponsiveness.

We examined the effects of FK-506, a potent immunosuppressive agent, on the development of late asthmatic response (LAR) and on the increased bronchial responsiveness to acetylcholine following LAR in guinea pig model of asthma. Guinea pigs sensitized by repeated inhalation of ovalbumin (OA) were intravenously given metopiron 24 hours before and 30 minutes before antigen challenge and to prevent death from immediate severe bronchoconstriction, chlorpheniramine maleate was also injected. When we defined LAR as the responses with a two-fold increase in respiratory resistance during the late phase of antigen challenge, twelve out of fifteen control animals demonstrated apparent LAR. However, when guinea pigs were treated with FK-506 from the beginning of immunization period, the development of LAR was completely inhibited, although similar magnitude of immediate bronchoconstriction was observed, and a subsequent increase in bronchial responsiveness was significantly blocked. We also measured bronchial responsiveness to acetylcholine before, 24 and 72 hours after antigen challenge. FK-506-treated animals inhibited an increase in bronchial responsiveness to acetylcholine. These results suggest that the involvement of cell-mediated immunity may be important in the development of LAR and an increase in bronchial responsiveness.

Bronchial eosinophilia is a characteristic of asthma. To elucidate the mechanisms of eosinophil accumulation in the airways, the time course of eosinophil infiltration in the airway mucosa after antigen inhalation was examined in actively sensitized and passively sensitized guinea pig models of asthma. The lungs and tracheae were removed at intervals after antigen challenge, fixed and stained. The eosinophil infiltration was quantitated in the tracheal walls by counting the number of cells per square millimeter. Guinea pigs sensitized by intraperitoneal injection of ovalbumin (OA) responded to a single exposure to aerosolized OA with biphasic infiltration of eosinophils in the tracheal walls; a striking early-phase which peaked at 6 hr and a delayed-phase which peaked at 24 hr and persisted for as long as 5 days. These kinetics were different from those observed with passively sensitized animals which showed only early-phase infiltration. Administration of CV-6209, a specific PAF antagonist, before and 12 hrs after antigen challenge significantly (p less than 0.01) inhibited the early-phase but not the delayed-phase eosinophil infiltration in actively sensitized animals. In contrast, when guinea pigs were treated with Cyclosporin A, a T lymphocyte-selective immunosuppressive agent, throughout the immunization period, the delayed-phase but not the early-phase infiltration was significantly (p less than 0.01) inhibited. These results suggest that PAF may contribute to early-phase and T cell factor(s) may contribute to delayed-phase eosinophil infiltration of the airways.

We have previously demonstrated that Cyclosporin A (CyA), a T lymphocyte-selective immunosuppressive agent, reduced the delayed-phase bronchial eosinophil infiltration after antigen challenge in a guinea pig model of asthma. In the present study, we studied the effects of CyA on antigen-induced late asthmatic response (LAR) and bronchial hyperresponsiveness following LAR. Guinea pigs immunized by repeated exposure to aerosolized ovalbumin (OA) were intravenously given metopirone, a cortisol synthesis inhibitor, 24 hours before and 30 minutes before antigen challenge, and to prevent death from immediate severe bronchoconstriction, chlorpheniramine maleate was also injected. After antigen challenge with high dose of OA, LAR occurred in twelve of fifteen animals (80%) and the bronchial responsiveness to acetylcholine was significantly increased. However, when guinea pigs were treated with CyA from the beginning of immunization period, the development of LAR was completely inhibited, although similar magnitude of immediate bronchoconstriction was observed, and a subsequent increase in bronchial responsiveness was partially but significantly blocked. Since CyA has been shown to suppress activation of guinea pig T lymphocytes and their production of lymphokines, these results suggest that T cell factor(s) may be important for the elicitation of LAR and the antigen-induced bronchial hyperresponsiveness.

Evidence of massive neutrinos was sought in the {pi}{sup +}{implies}{mu}{sup +}{ital x} decay spectrum in the mass region {ital M}{sub {ital x}}=30{endash}33.91 MeV/{ital c}{sup 2}. Upper limits on the branching ratio {ital R}{sub {mu}}{sub {ital x}}{le}(4{endash}6){times}10{sup -}{sup 5} (90{percent} C.L.) were set for this region, which correspond to the neutrino mixing parameter {vert_bar}{ital U}{sub {mu}}{sub {ital x}}{vert_bar}{sup 2}{much_gt}10{sup -}{sup 3}{endash}10{sup -}{sup 4}. {copyright} {ital 1995 The American Physical Society.}

A description of the detector and of preliminary results of work in progress in its performance is presented here for an experiment to study the decay of K + → π + ν ν .

Limits on the lepton-flavor-violating reactions ${\ensuremath{\mu}}^{\mathrm{\ensuremath{-}}}$+Z\ensuremath{\rightarrow}${e}^{\mathrm{\ensuremath{-}}}$+Z and ${\ensuremath{\mu}}^{\mathrm{\ensuremath{-}}}$+Z\ensuremath{\rightarrow}${e}^{+}$+(Z-2), muon-electron and muon-positron conversion, have been obtained from a search performed at TRIUMF using a time-projection chamber. Upper limits (90% C.L.) for the branching ratios compared to ordinary muon capture for a titanium target are R---(Ti)=\ensuremath{\Gamma}(${\mathrm{\ensuremath{\mu}}}^{\mathrm{\ensuremath{-}}}$Ti\ensuremath{\rightarrow}${\mathit{e}}^{\mathrm{\ensuremath{-}}}$Ti)/\ensuremath{\Gamma}(${\mathrm{\ensuremath{\mu}}}^{\mathrm{\ensuremath{-}}}$Ti capture)4.6\ifmmode\times\else\texttimes\fi{}${10}^{\mathrm{\ensuremath{-}}12}$ and ${\mathit{R}}_{+}$(Ti)=\ensuremath{\Gamma}(${\mathrm{\ensuremath{\mu}}}^{\mathrm{\ensuremath{-}}}$Ti\ensuremath{\rightarrow}${\mathit{e}}^{+}$Ca*)/\ensuremath{\Gamma}(${\mathrm{\ensuremath{\mu}}}^{\mathrm{\ensuremath{-}}}$Ti capture).1.7\ifmmode\times\else\texttimes\fi{}${10}^{\mathrm{\ensuremath{-}}10}$ A smaller data set obtained using a lead target yielded ${R}_{\mathrm{\ensuremath{-}}}$(Pb)4.9\ifmmode\times\else\texttimes\fi{}${10}^{\mathrm{\ensuremath{-}}10}$. The implications of these results for extensions of the standard model which allow lepton-flavor violation are discussed.

A new isomer with a half-life of 62 ± 5 ms was observed in 205Po by the reaction 209Bi (p, 5n)205mPo. Prompt and delayed spectra of γ-rays and internal conversion electrons were measured using Ge(Li) and Si(Li) detectors. The 1461 keV isomer decays by an E3 transition with an energy of 580.8 keV and the spin-parity is assigned as 19 2 − .

An upper limit on the branching ratio of the decay {ital K}{sup +}{r arrow}{pi}{sup +}H, {ital H}{r arrow}{mu}{sup +}{mu}{sup {minus}} is set at 1.5{times}10{sup {minus}7} at the 90% confidence level, for a Higgs-boson mass in the interval 220{lt}{ital m}{sub {ital H}}{lt}320 MeV/{ital c}{sup 2}. In addition, 90%-confidence-level upper limits on the branching ratios of the decays {ital K}{sup +}{r arrow}{pi}{sup +}{mu}{sup +}{mu}{sup {minus}} and {ital K}{sup +}{r arrow}{mu}{sup +}{nu}{mu}{sup +}{mu}{sup {minus}} are set at 2.3{times}10{sup {minus}7} and 4.1{times}10{sup {minus}7}, respectively.

The cross section of the pair production in germanium at 1064 keV, only 42 keV above threshold, has been measured with the use of a Ge(Li) detector. The obtained cross section is 0.182 mb/atom and has a large deviation from the theoretical value by \O{}verb\o{}, Mork, and Olsen. The present result suggests that the screening effect of atomic electrons has a large contribution to the pair-production cross section near threshold.