Search for Supersymmetry with Gauge-Mediated Breaking in Diphoton Events with Missing Transverse Energy at CDF II

accepted to Phys. Rev. LettWe present the results of a search for supersymmetry with gauge-mediated breaking and \NONE\to\gamma\Gravitino in the $\gamma\gamma$+missing transverse energy final state. In 2.6$\pm$0.2 \invfb of $p{\bar p}$ collisions at $\sqrt{s}$$=$1.96 TeV recorded by the CDF II detector we observe no candidate events, consistent with a standard model background expectation of 1.4$\pm$0.4 events. We set limits on the cross section at the 95% C.L. and place the world's best limit of 149\gevc on the \none mass at $\tau_{\tilde{\chi}_1^0}$$We present the results of a search for supersymmetry with gauge-mediated breaking and χ˜10→γG˜ in the γγ+missing transverse energy final state. In 2.6±0.2  fb-1 of pp̅ collisions at √s=1.96  TeV recorded by the CDF II detector we observe no candidate events, consistent with a standard model background expectation of 1.4±0.4 events. We set limits on the cross section at the 95% C.L. and place the world’s best limit of 149  GeV/c2 on the χ˜10 mass at τχ˜10≪1  ns. We also exclude regions in the χ˜10 mass-lifetime plane for τχ˜10≲2  ns.Peer reviewe

Measurements of branching fraction ratios and CP asymmetries in B+/- ->D_CP K+/- decays in hadron collisions

We reconstruct B+/- -> D K+/- decays in a data sample collected by the CDF II detector at the Tevatron collider corresponding to 1 fb-1 of integrated luminosity. We select decay modes where the D meson decays to either K- pi+ (flavor eigenstate) or K- K+, pi- pi+ (CP-even eigenstates), and measure the direct CP asymmetry A_CP+ = 0.39 +/- 0.17(stat) +/- 0.04(syst), and the double ratio of CP-even to flavor eigenstate branching fractions R_CP+ = 1.30 +/- 0.24(stat) +/- 0.12(syst). These measurements will improve the determination of the CKM angle gamma. They are performed here for the first time using data from hadron collisions.We reconstruct B±→DK± decays in a data sample collected by the CDF II detector at the Tevatron collider corresponding to 1  fb-1 of integrated luminosity. We select decay modes where the D meson decays to either K-π+ (flavor eigenstate) or K-K+, π-π+ (CP-even eigenstates), and measure the direct CP asymmetry ACP+=0.39±0.17(stat)±0.04(syst), and the double ratio of CP-even to flavor eigenstate branching fractions RCP+=1.30±0.24(stat)±0.12(syst). These measurements will improve the determination of the Cabibbo-Kobayashi-Maskawa angle γ. They are performed here for the first time using data from hadron collisions.Peer reviewe

Top Quark Mass Measurement in the lepton plus jets Channel Using a Matrix Element Method and in situ Jet Energy Calibration

A precision measurement of the top quark mass m(t) is obtained using a sample of t (t) over bar events from p (p) over bar collisions at the Fermilab Tevatron with the CDF II detector. Selected events require an electron or muon, large missing transverse energy, and exactly four high-energy jets, at least one of which is tagged as coming from a b quark. A likelihood is calculated using a matrix element method with quasi-Monte Carlo integration taking into account finite detector resolution and jet mass effects. The event likelihood is a function of mt and a parameter Delta(JES) used to calibrate the jet energy scale in situ. Using a total of 1087 events in 5.6 fb(-1) of integrated luminosity, a value of m(t) 173.0 +/- 1.2 GeV/c(2) is measured

Inclusive Search for Standard Model Higgs Boson Production in the WW Decay Channel using the CDF II Detector

We present a search for standard model (SM) Higgs boson production using ppbar collision data at sqrt(s) = 1.96 TeV, collected with the CDF II detector and corresponding to an integrated luminosity of 4.8 fb-1. We search for Higgs bosons produced in all processes with a significant production rate and decaying to two W bosons. We find no evidence for SM Higgs boson production and place upper limits at the 95% confidence level on the SM production cross section (sigma(H)) for values of the Higgs boson mass (m_H) in the range from 110 to 200 GeV. These limits are the most stringent for m_H > 130 GeV and are 1.29 above the predicted value of sigma(H) for mH = 165 GeV.We present a search for standard model (SM) Higgs boson production using pp̅ collision data at √s=1.96  TeV, collected with the CDF II detector and corresponding to an integrated luminosity of 4.8  fb-1. We search for Higgs bosons produced in all processes with a significant production rate and decaying to two W bosons. We find no evidence for SM Higgs boson production and place upper limits at the 95% confidence level on the SM production cross section (σH) for values of the Higgs boson mass (mH) in the range from 110 to 200 GeV. These limits are the most stringent for mH>130  GeV and are 1.29 above the predicted value of σH for mH=165  GeV.Peer reviewe

Measurement of the Lambda_b Lifetime in Lambda_b -> Lambda_c+ pi- Decays in p-pbar Collisions at sqrt(s) = 1.96 TeV

Submitted to Phys. Rev. LettWe report a measurement of the lifetime of the Lambda_b baryon in decays to the Lambda_C+ pi- final state in a sample corresponding to 1.1 fb^-1 collected in p-pbar collisions at sqrt(s) = 1.96 TeV by the CDF II detector at the Tevatron collider. Using a sample of about 3000 fully reconstructed Lambda_b events we measure tau(Lambda_b) = 1.401 +- 0.046 (stat) +- 0.035 (syst) ps (corresponding to c.tau(Lambda_b) = 420.1 +- 13.7 (stat) +- 10.6 (syst) um, where c is the speed of light). The ratio of this result and the world average B^0 lifetime yields tau(Lambda_b)/tau(B^0) = 0.918 +- 0.038 (stat and syst), in good agreement with recent theoretical predictions.We report a measurement of the lifetime of the Λb0 baryon in decays to the Λc+π- final state in a sample corresponding to 1.1  fb-1 collected in pp̅ collisions at √s=1.96  TeV by the CDF II detector at the Tevatron collider. Using a sample of about 3000 fully reconstructed Λb0 events we measure τ(Λb0)=1.401±0.046(stat)±0.035(syst)  ps (corresponding to cτ(Λb0)=420.1±13.7(stat)±10.6(syst)  μm, where c is the speed of light). The ratio of this result and the world average B0 lifetime yields τ(Λb0)/τ(B0)=0.918±0.038 (stat) and (syst), in good agreement with recent theoretical predictions.Peer reviewe

Measurement of the Top Quark Mass and ppbar -> ttbar Cross Section in the All-Hadronic Mode with the CDFII Detector

Submitted to Phys. Rev. DWe present a measurement of the top quark mass and of the top-antitop pair production cross section using p-pbar data collected with the CDFII detector at the Tevatron Collider at the Fermi National Accelerator Laboratory and corresponding to an integrated luminosity of 2.9 fb-1. We select events with six or more jets satisfying a number of kinematical requirements imposed by means of a neural network algorithm. At least one of these jets must originate from a b quark, as identified by the reconstruction of a secondary vertex inside the jet. The mass measurement is based on a likelihood fit incorporating reconstructed mass distributions representative of signal and background, where the absolute jet energy scale (JES) is measured simultaneously with the top quark mass. The measurement yields a value of 174.8 +- 2.4(stat+JES) ^{+1.2}_{-1.0}(syst) GeV/c^2, where the uncertainty from the absolute jet energy scale is evaluated together with the statistical uncertainty. The procedure measures also the amount of signal from which we derive a cross section, sigma_{ttbar} = 7.2 +- 0.5(stat) +- 1.0 (syst) +- 0.4 (lum) pb, for the measured values of top quark mass and JES.We present a measurement of the top quark mass and of the top-antitop (tt̅ ) pair production cross section using pp̅ data collected with the CDF II detector at the Tevatron Collider at the Fermi National Accelerator Laboratory and corresponding to an integrated luminosity of 2.9  fb-1. We select events with six or more jets satisfying a number of kinematical requirements imposed by means of a neural-network algorithm. At least one of these jets must originate from a b quark, as identified by the reconstruction of a secondary vertex inside the jet. The mass measurement is based on a likelihood fit incorporating reconstructed mass distributions representative of signal and background, where the absolute jet energy scale (JES) is measured simultaneously with the top quark mass. The measurement yields a value of 174.8±2.4(stat+JES)-1.0+1.2(syst)  GeV/c2, where the uncertainty from the absolute jet energy scale is evaluated together with the statistical uncertainty. The procedure also measures the amount of signal from which we derive a cross section, σtt̅ =7.2±0.5(stat)±1.0(syst)±0.4(lum)  pb, for the measured values of top quark mass and JES.Peer reviewe

Arachidonic Acid Induces Both Na+ and Ca2+ Entry Resulting in Apoptosis

Marked accumulation of arachidonic acid ( AA) and intracellular Ca2+ and Na+ overloads are seen during brain ischemia. In this study, we show that, in neurons, AA induces cytosolic Na+ ([Na+](cyt)) and Ca2+ ([Ca2+](cyt)) overload via a non-selective cation conductance ( NSCC), resulting in mitochondrial [Na+](m) and [Ca2+](m) overload. Another two types of free fatty acids, including oleic acid and eicosapentaenoic acid, induced a smaller increase in the [Ca2+](i) and [Na+](i). RU360, a selective inhibitor of the mitochondrial Ca2+ uniporter, inhibited the AA-induced [ Ca2+ ](m) and [Na+](m) overload, but not the [Ca2+](cyt) and [Na+ ](cyt) overload. The [ Na+] m overload was also markedly inhibited by either Ca2+ -free medium or CGP3715, a selective inhibitor of the mitochondrial Na-cyt (+)-Ca-m(2+) exchanger . Moreover, RU360, Ca2+-free medium, Na+-free medium, or cyclosporin A (CsA) largely prevented AA-induced opening of the mitochondrial permeability transition pore, cytochrome c release, and caspase 3-dependent neuronal apoptosis. Importantly, Na+-ionophore/Ca2+- free medium, which induced [ Na+](m) overload, but not [Ca2+](m) overload, also caused cyclosporin A-sensitive mitochondrial permeability transition pore opening, resulting in caspase 3-dependent apoptosis, indicating that [Na+](m) overload per se induced apoptosis. Our results therefore suggest that AA-induced [Na +](m) overload, acting via activation of the NSCC, is an important upstream signal in the mitochondrial-mediated apoptotic pathway. The NSCC may therefore act as a potential neuronal death pore which is activated by AA accumulation under pathological conditions

Mechanism of Free Fatty Acids-Induced Mitochondrial Na+ and Ca2+ Overloads Resulting in Cell Apoptosis

當腦部或心肌缺血 (ischemia) 或缺氧 (hypoxia) 時可觀察到花生四烯酸 (arachidonic acid, AA) 及其他不飽和脂肪酸 (unsaturated fatty acids)，例如 linoleic acid與oleic acid 會有大量堆積在肌肉細胞內之現象，而我發現如果在心肌細胞及神經細胞外直接給予這些脂肪酸，則細胞內的鈣離子與鈉離子會有過度負荷 (overloads) 而劇烈上升的情形。本研究的第一部分，我們由神經細胞的實驗結果得知，花生四烯酸會藉由打開非選擇性陽離子通道 (NSCC) 而引細胞質鈉離子與鈣離子的過度負荷，此結果將進一步導致粒線體 ( mitochondria) 內鈉離子與鈣離子過度負荷而顯著上升。而在另外兩種類型的游離脂肪酸，包括oleic acid與eicosapentaenoic acid 則可引起細胞內鈣離子與鈉離子的微幅上升。RU360為一種粒線體上鈣離子交換器的選擇性抑制劑，雖然可以顯著抑制經由花生四烯酸所造成的粒線體內鈣離子與鈉離子的劇烈上升，但是並不會影響胞質鈉離子與鈣離子的過度負荷。而粒線體鈉離子過度負荷的現象也可被無鈣培養液或一種粒線體上的鈉鈣離子交換器 (Na+cyt-Ca2+m exchanger) 的選擇性抑制劑CGP3715明顯抑制。因此RU360，無鈣培養液或cyclosporin A皆可非常大量去降低花生四烯酸所導致的粒線體通透移轉通道 (mPTP) 之開啟, 細胞色素C (cytochrome c) 的釋放與透過 caspase-3依存性的神經細胞凋亡。非常值得注意的是，單純在無鈣培養液的環境下用Na+-ionophore可引起細胞內鈉離子的過度負荷，儘管其對於細胞內鈣離子的上升並無影響，但同樣可以造成對CsA敏感的粒線體滲透轉換管道之開啟並且使神經細胞走向casapse-3依存性細胞凋亡的命運。此證據強烈顯示，只要細胞內鈉離子過度負荷的先決條件成立即可引起細胞凋亡。而我們的研究結果證實，花生四烯酸會藉由活化非選擇性陽離子通道而引發粒線體內鈉離子的過度負荷，這是一個藉由粒線體所導致細胞凋亡途徑上非常重要的上游訊號。而在病理情況下，經由花生四烯酸過量累積所啟動的非選擇性陽離子通道，將扮演潛在性神經細胞死亡管道的重要角色。 研究的第二部份則是想進一步釐清游離脂肪酸與造成心肌細胞凋亡之間的關連性。脂質代謝的異常已被證實在心肌細胞的損傷中扮演一個非常重要的角色。而游離脂肪酸，包括花生四烯酸、palmitic acid，oleic acid 與linoleic acid 大量堆樍則可在心肌細胞的缺血再灌流上出現。在本論文的第二部份，經由實驗發現花生四烯酸與游離脂肪酸皆會活化非選擇性陽離子通道，導致心肌細胞的細胞內包括鈣離子與鈉離子皆會有過度負荷的現象。而花生四烯酸引起鈣離子與鈉離子的過度負荷其百分之五十的有效濃度 (IC50) 分別為8 microM 與5 microM，而其他種類的游離脂肪酸若要引起鈉離子與鈣離子較為顯著的上升則需要較高的濃度(30 microM)。但是活性氧物種 (reactive oxygen species) 的過度生成與花生四烯酸的代謝產物則無影響。經由雷射共軛焦顯微鏡 (confocal microscopy) 的觀察發現，花生四烯酸會導致細胞質鈉離子與鈣離子的持續上升，結果使得粒線體內的鈉離子與鈣離子也同時劇烈的上升，如此將導致位於粒線體膜上的滲透轉換孔道的持續開啟，細胞色素c釋放與經由caspase-3所引發的細胞凋亡。相同細胞凋亡的效果也可在無鈣培養液的環境下給予Na+-ionophore使細胞質與粒線體內Na+大量上升來達成。此處理雖然對於細胞質與粒線體鈣離子的上升並無貢獻，但是卻足以引起細胞質與粒線體鈉離子過度負荷而劇烈上升的效應。藉由電子顯微鏡的觀察顯示，抑制粒線體鈉離子的過度負荷可以有效地降低粒線體膜的破裂崩解的程度，證實粒線體內鈉離子的過度負荷為經由花生四烯酸與游離脂肪酸所導致心肌細胞凋亡途徑上非常重要的上游訊號。此花生四烯酸與游離脂肪酸很可能扮演內生性離子管道 (endogenous ionophores) 的角色，它會活化非選擇性陽離子通道，當缺血再灌流的情況發生時造成心肌及神經細胞死亡的結果。There is ample evidence that marked accumulation of free fatty acids, including arachidonic acid (AA), linoleic acid and oleic acid, during ischemia - reperfusion in the brain. n the first part of my study, I found that AA induced cytosolic Na+ ([Na+]cyt) and Ca2+ ([Ca2+]cyt) overload via a non-selective cation conductance (NSCC), resulting in mitochondrial [Na+]m and [Ca2+]m overload in cerebellar neurons. Moreover, oleic acid and eicosapentaenoic acid also induced a small increase in the [Ca2+]i and [Na+]i. A selective inhibitor of the mitochondrial Ca2+ uniporter, RU360, inhibited the AA-induced [Ca2+]m and [Na+]m overload, but not the [Ca2+]cyt and [Na+]cyt overload. The [Na+]m overload was also markedly inhibited by either Ca2+-free medium or CGP3715, a selective inhibitor of the mitochondrial Na+cyt-Ca2+m exchanger. Furthermore, RU360, Ca2+-free medium, Na+-free medium, or cyclosporin A (CsA) largely prevented AA-induced opening of the mitochondrial permeability transition pore (mPTP), cytochrome c (cytC) release, and caspase-3-dependent neuronal apoptosis. Importantly, Na+-ionophore/Ca2+-free medium, which induced [Na+]m overload, but not [Ca2+]m overload, also caused CsA-sensitive mPTP opening, resulting in caspase-3 dependent apoptosis, indicating that [Na+]m overload per se induced apoptosis. Our results therefore suggest that AA-induced [Na+]m overload, acting via activation of the NSCC, is an important upstream signal in the mitochondrial-mediated apoptotic pathway. The NSCC may therefore act as a potential neuronal death pore which is activated by AA accumulation under pathological conditions. isturbances in lipid metabolism have been suggested to play an important role in myocardial damage. Marked accumulation of free fatty acids (FFAs), including arachidonic acid (AA), palmitic acid, oleic acid, and linoleic acid, also occurs during post-ischemia and reperfusion (post-I/R) in the heart. In the second part of my study is to investigate possible mechanism of the myocyte apoptosis mediated by free fatty acids. Here, I shows that AA also activated a novel non-selective cation conductance (NSCC), resulting in both intracellular Ca2+ and Na+ overload in cultured ventricular myocytes. The EC50 of the AA-induced Ca2+ and Na+ overload was 8 microM and 5 microM, respectively. A higher concentration (30 microM) of other FFAs was required to induce significant Na+/Ca2+ overload. Overproduction of reactive oxygen species (ROS) and AA metabolites was not involved. Using confocal microscopy, I showed that AA caused sustained [Na+]cyt and [Ca2+]cyt overload, resulting in [Na+]m and [Ca2+]m overload, which induced opening of the mPTP, cytochrome c release, and caspase-3-mediated apoptosis. Similar apoptotic effects were seen using Na+-ionophore cocktail/Ca2+-free medium, which induced [Na+]cyt and [Na+]m, but not [Ca2+]cyt and [Ca2+]m overload. Electron microscopy showed that inhibition of [Na+]m overload prevented disruption of the mitochondrial membrane, indicating that [Na+]m overload is also an important upstream signal in AA- and FFAs-induced myocyte apoptosis. n summary, FFAs including AA may therefore act as endogenous ionophores, which activate an NSCC, resulting in both myocyte and neuronal cell death seen in post-I/R.口試委員會審定書 ……………… i謝 ……………………………… iiontents ……………………………… ivbstract in Chinese (中文摘要)………1bstract ……………………………… 4hapter 1 Introduction ………………7hapter 2 Materials and Methods………11hapter 3 Arachidonic acid induced both Na+ and Ca2+ entry resulting in apoptosis ……… 19esults ………………………………20iscussion ……………………………… 27igures ………………………………31hapter 4 Free fatty acids act as endogenous ionophores, resulting in Na+ and Ca2+ influx and myocyte apoptosis………………………………47esults ………………………………48iscussion ………………………………56igures ………………………………60hapter 5 Concluding Remarks and prospectives …………80hapter 6 References ………………………………8