Performance of high impedance resonators in dirty dielectric environments.

High-impedance resonators are a promising contender for realizing long-distance entangling gates between spin qubits. Often, the fabrication of spin qubits relies on the use of gate dielectrics which are detrimental to the quality of the resonator. Here, we investigate loss mechanisms of high-impedance NbTiN resonators in the vicinity of thermally grown SiO2 and Al2O3 fabricated by atomic layer deposition. We benchmark the resonator performance in elevated magnetic fields and at elevated temperatures and find that the internal quality factors are limited by the coupling between the resonator and two-level systems of the employed oxides. Nonetheless, the internal quality factors of high-impedance resonators exceed 103 in all investigated oxide configurations which implies that the dielectric configuration would not limit the performance of resonators integrated in a spin-qubit device. Because these oxides are commonly used for spin qubit device fabrication, our results allow for straightforward integration of high-impedance resonators into spin-based quantum processors. Hence, these experiments pave the way for large-scale, spin-based quantum computers.

Geometrical parameter combinations that correlate with early interaural cross-correlation coefficients in a performance hall.

The previous binaural data of the authors measured inside two multi-purpose performance halls are re-analyzed using regression in this study. It is done in an attempt to establish a framework that can improve the prediction of early interaural cross-correlation coefficients (IACCs), but with as little measurement effort and parameters as possible. The results show that regression models consist of linear combinations of polynomials of geometrical parameters, when used together with the measurement schemes suggested previously by the authors, are sufficient for predicting the IACCs to within engineering tolerance. The predictions are better than those obtained previously by the neural network approach of the authors. The relative importance of the geometrical parameters in the prediction of IACCs is also investigated.

Neural network predictions of acoustical parameters in multi-purpose performance halls.

A detailed binaural sound measurement was carried out in two multi-purpose performance halls of different seating capacities and designs in Hong Kong in the present study. The effectiveness of using neural network in the predictions of the acoustical properties using a limited number of measurement points was examined. The root-mean-square deviation from measurements, statistical parameter distribution matching, and the results of a t-test for vanishing mean difference between simulations and measurements were adopted as the evaluation criteria for the neural network performance. The audience locations relative to the sound source were used as the inputs to the neural network. Results show that the neural network training scheme using nine uniformly located measurement points in each specific hall area is the best choice regardless of the hall setting and design. It is also found that the neural network prediction of hall spaciousness does not require a large amount of training data, but the accuracy of the reverberance related parameter predictions increases with increasing volume of training data.

Pituitary phenotypes of mice lacking the notch signalling ligand delta-like 1 homologue.

The Notch signalling pathway ligand delta-like 1 homologue (Dlk1, also named Pref1) is expressed throughout the developing pituitary and becomes restricted to mostly growth hormone (GH) cells within the adult gland. We have investigated the role of Dlk1 in pituitary development and function from late embryogenesis to adulthood using a mouse model completely lacking the expression of Dlk1. We confirm that Dlk1-null mice are shorter and weigh less than wild-type littermates from late gestation, at parturition and in adulthood. A loss of Dlk1 leads to significant reduction in GH content throughout life, whereas other pituitary hormones are reduced to varying degrees depending on sex and age. Both the size of the pituitary and the proportion of hormone-producing cell populations are unchanged, suggesting that there is a reduction in hormone content per cell. In vivo challenge of mutant and wild-type littermates with growth hormone-releasing hormone and growth hormone-releasing hexapeptide shows that reduced GH secretion is unlikely to account for the reduced growth of Dlk1 knockout animals. These data suggest that loss of Dlk1 gives rise to minor pituitary defects manifesting as an age- and sex-dependent reduction in pituitary hormone contents. However, Dlk1 expression in other tissue is most likely responsible for the weight and length differences observed in mutant animals.

Effect of WEB 2086 on leukocyte adherence in response to hemorrhagic shock in rats.

BACKGROUND: The pathogenesis of generalized microvascular injury after hemorrhagic shock is known to involve the generation of platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine [PAF]). The release of PAF is manifested in several ways, including by increased vascular permeability, altered vascular reactivity, and increased leukocyte adherence to the endothelium. WEB 2086 is a PAF antagonist that has been shown experimentally to improve survival after hemorrhagic shock. The purpose of this study was to examine the efficacy of WEB 2086 in attenuating leukocyte adherence before, during, and after hemorrhagic shock. METHODS: After a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mm Hg for 30 minutes in urethane-anesthetized rats. Mesenteric venules in a transilluminated segment of the small bowel were examined to quantitate leukocyte adherence using intravital microscopy. RESULTS: In sham-operated rats (control), there was minimal to no leukocyte adherence throughout the experiment. Hemorrhagic shock resulted in a significant increase in leukocyte adherence postshock during resuscitation (10.9 +/- 1.8 cells/100 microm, p < 0.01) when compared with controls. WEB 2086, when given before shock, significantly attenuated leukocyte adherence (0.1 +/- 0.08 cells/100 microm, p < 0.01) when compared with hemorrhagic shock alone. This effect of WEB 2086 on adherence could be demonstrated even when it was given during (3.5 +/- 0.9 cells/100 microm, p < 0.01) and 10 minutes into (5.8 +/- 1.1 cells/100 microm, p < 0.05) hemorrhagic shock. CONCLUSION: Our findings suggest that WEB 2086 may be of therapeutic benefit against the microvascular damage sustained after hemorrhagic shock.

The local effect of PAF on leukocyte adherence to small bowel mesenteric venules following intra-abdominal contamination.

We have previously demonstrated that intra-abdominal contamination increases neutrophil infiltration into the gastrointestinal tract. The purpose of our current study was twofold: 1) to determine if leukocyte adherence to the mesenteric microvasculature occurred by local peritoneal contamination or by systemic mechanisms; and 2) to assess the role of platelet activation factor (PAF) in this process. Rats underwent cecal ligation and puncture (CLP), and 4 h after the procedure we used intravital microscopy to visualize the mesenteric microcirculation. Cecal ligation and puncture increased leukocyte adherence (22.3+/-5.5 leukocytes/100 microm) vs. sham (2.3+/-0.9, P < 0.05). WEB-2086, a PAF receptor antagonist, prevented this increase (6.47+/-4.8, P < 0.05). To assess if leukocyte adherence was due to topical effects, we performed similar experiments with the small bowel exteriorized. In such cases, CLP did not increase leukocyte adherence (1.2+/-0.8 vs. 1.4+/-0.9). In addition, topical application of highly diluted fecal matter (1:1000) increased leukocyte adherence (4.8+/-1.2) vs. control (0.6+/-0.3, P < 0.05). Our study demonstrates that leukocyte adherence in the mesenteric microcirculation following intra-abdominal contamination is due to direct topical exposure to fecal matter, and it is mediated by PAF.

Effect of LFA-1beta antibody on leukocyte adherence in response to hemorrhagic shock in rats.

The activation and adherence of leukocytes to the venular endothelium are critical steps in the pathogenesis of generalized microvascular injury following hemorrhagic shock. Previous studies have shown that the integrins CD11/CD18 play a significant role in this interaction. The purpose of this study is to examine the efficacy of anti-LFA-1beta, an antibody to CD11a/CD18, in attenuating leukocyte adherence before, during, and after hemorrhagic shock. Following a control period, blood was withdrawn to reduce the mean arterial pressure to 40 mm Hg for 30 min in urethane-anesthetized rats. Mesenteric venules in a transilluminated segment of the small intestines were examined to quantitate leukocyte adherence using intravital microscopy. In sham-operated rats (control), there was minimal to no leukocyte adherence throughout the experiment. Hemorrhagic shock resulted in significant leukocyte adherence during resuscitation (10.8 +/- 1.7 cells/100 microm, P < 0.01) when compared to control. Anti-LFA-1beta, when given before hemorrhagic shock, significantly attenuated leukocyte adherence during resuscitation (1.1 +/- 0.8, P < 0.01) when compared with hemorrhagic shock alone. This protective effect of anti-LFA-1beta on leukocyte adherence was even demonstrated when it was given during (1.6 +/- 0.3, P < 0.01) and 10 min after hemorrhagic shock (5.8 +/- 0.4, P < 0.05). These results suggest that anti-LFA-1beta may be of potential therapeutic benefit against microvascular injury caused by hemorrhagic shock.

Leukocyte adherence and sequestration following hemorrhagic shock and total ischemia in rats.

The pathogenesis of generalized microvascular injury following hemorrhagic shock and total ischemia appears to be dependent on leukocytes interacting with the venular endothelium. The purpose of this study was to compare leukocyte adherence and sequestration following hemorrhagic shock with that of total ischemia in the small bowel mesentery of rats. Leukocyte adherence and sequestration was measured by direct visualization in vivo using intravital microscopy. In addition, sequestration was also quantitated by measuring tissue levels of myeloperoxidase, a marker of leukocyte infiltration. Mean arterial blood pressure was decreased to 40 mm Hg for 30 min (hemorrhagic shock group). In the total ischemia group, both the superior and inferior mesenteric arteries were clamped for 30 min followed by reperfusion. Hemorrhagic shock (9.4+/-1.5 cell/100 microm) and total ischemia (8.3+/-3 cell/100 microm) caused a statistically significant increases in leukocyte adherence 60 min postinsult as compared with controls (.9+/-1.5 cell/100 microm). However, the increase in leukocyte adherence appeared earlier and to a greater degree initially following total ischemia. Leukocyte sequestration as measured by intravital microscopy was significant only after total ischemia [(24.6+/-1.7 cell/(100 microm)2; p<.01] and not hemorrhagic shock [3.4+/-.6 cell/(100 microm)2] versus controls [2.2+/-.2 cell/(100 microm)2]. This difference in sequestration was also confirmed by tissue levels of myeloperoxidase. The results of this study suggest that the microvascular response following hemorrhagic shock is different than that of total ischemia, and caution is warranted when extrapolating the experimental results of one to the other.

Pallister-Killian syndrome: the first reported case in Hong Kong.

Pallister-Killian syndrome was first described in 1977 by Pallister, et al. It is a multiple congenital anomalies/mental retardation syndrome caused by mosaic tetrasomy of chromosome 12p. The chromosomal abnormality is often missed if only peripheral lymphocytes are examined, and bone marrow or cultured skin fibroblasts may be required for confirmation. Here we report the first case in Hong Kong.

Nonoperative treatment of biliary tract disease.

The rise of minimally invasive surgical techniques during the past 20 years has been one of the more dramatic developments in modern medicine. Minimally invasive procedures are now widely accepted for treatment of diseases involving many different organ systems. Minimally invasive procedures may be more common and more accepted in the treatment of diseases of the biliary tract than in any other area. The development of laparoscopic cholecystectomy serves as a benchmark for minimally invasive procedures, and it is now the standard of care for the treatment of cholelithiasis. Today, not only is laparoscopic cholecystectomy one of the most common operations performed in the United States, but many new techniques have been developed that allow minimally invasive treatment of a variety of biliary tract diseases. The development of nonoperative techniques for treatment of biliary tract disease has accompanied the rapid developments in minimally invasive surgical techniques. This article describes the nonoperative treatment of biliary tract disease.

PAF and CD18 mediate neutrophil infiltration in upper gastrointestinal tract during intra-abdominal sepsis.

Neutrophil infiltration is a critical event in the development of multiple organ failure during sepsis. We hypothesized that platelet-activating factor (PAF) release contributes to neutrophil infiltration in the gastrointestinal tract during sepsis. In the first experiments we administered exogenous PAF (1.56, 6.25, 25, and 100 ng . kg-1 . min-1 for 30 min) to urethan-anesthetized Sprague-Dawley rats. PAF was administered alone or in combination with either the PAF antagonist WEB-2086 (250 microg . kg-1 . min-1), a monoclonal antibody (MAb) to CD18, or a MAb to intercellular adhesion molecule 1 (ICAM-1). In separate groups of rats, cecal ligation and incision (CLI) was performed to create intra-abdominal sepsis, which we hypothesized would stimulate the release of endogenous PAF. CLI was performed in rats given either saline, WEB-2086, anti-CD18, or anti-ICAM-1 MAb. After these experiments, tissue myeloperoxidase (MPO) levels were determined as a marker of neutrophil infiltration. Both exogenous PAF and CLI induced significant increases in MPO activity in the stomach and duodenum. These increases were significantly attenuated by WEB-2086, anti-CD18 MAb, and anti-ICAM-1 MAb in both PAF- and CLI-treated rats. These results suggest that both the inflammatory mediator PAF and the CD18 integrins play a major role in neutrophil infiltration in the upper gastrointestinal tract during sepsis.

Interstitial Dup(1p) with findings of Kabuki make-up syndrome.

We describe a male patient with interstitial duplication of the short arm of chromosome 1 with breakpoints involving 1p13.1 and 1p22.1. The patient presented with some clinical findings of Kabuki make-up syndrome (KMS), including mental retardation, small head, eversion of the lateral part of lower eyelids, epicanthic folds, lateral flare of the eyebrows, short columella, and persistent fetal finger pads. This cytogenetic finding may provide clues for gene mapping of the syndrome.

Nitric oxide attenuates endothelin-1-induced vasoconstriction in canine stomach.

We previously observed that endothelin-1 (ET-1)-induced gastric vasoconstriction is enhanced after ischemia-reperfusion. The purpose of our present study was to examine the role of nitric oxide in regulating ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion. Using a mechanically perfused stomach segment from chloralose-anesthetized dogs, we examined 1) responses to NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with L-arginine, 2) whether L-NAME affects ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion, and 3) if spermine NONOate {1,3-propanediamine-N-[4-1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazi no] butyl; a nitric oxide donor} attenuates the augmented response to ET-1 after ischemia-reperfusion. Our results show that 1) L-NAME significantly increased baseline vascular resistance and this response was reduced by L-arginine, 2) ET-1-induced vasoconstriction was enhanced by L-NAME, and 3) administration of spermine NONOate during reperfusion largely attenuated the vasoconstrictor response to ET-1 after ischemia-reperfusion. Our findings are consistent with the hypothesis that nitric oxide modulates responses to ET-1 under normal conditions, and loss of this vasodilator after ischemia-reperfusion results in an augmented response to ET-1.

Superoxide dismutase attenuates effects of platelet-activating factor on gastric microcirculation.

This study examined the effect of Cu-Zn superoxide dismutase (SOD) on platelet-activating factor (PAF)-induced alterations of the gastric microcirculation. In separate experiments using an ex vivo canine gastric segment, changes in vascular resistance, filtration, and circulating neutrophil counts were measured during intra-arterial infusion of PAF (0.12 to 150 nM, n = 6) alone and with SOD (10 U/ml, n = 5). PAF produced dose-related increases in vascular resistance and filtration. SOD pretreatment attenuated changes in these measurements in response to 9 and 38 nM PAF. PAF also produced dose-related increases in the difference between arterial and venous neutrophil counts across the gastric segment. SOD significantly reduced this neutrophil flux at 0.5, 2, 9, and 38 nM PAF. Our results suggest that PAF causes both mucosal ischemia due to increased vascular resistance and microvascular injury as evidenced by increased filtration, as well as enhanced neutrophil adhesion to the microvasculature. The protective effects of SOD suggest that these responses to PAF involve the generation of oxygen-derived free radicals. In addition, these responses to PAF appear to be dependent upon circulating neutrophils.

Ischemia-reperfusion increases gastric motility and endothelin-1-induced vasoconstriction.

The purpose of our study was to 1) examine the effect of ischemia-reperfusion on gastric vascular resistance and motility, 2) determine whether endothelin-1 (ET-1)-induced vasoconstriction is enhanced after ischemia-reperfusion, and 3) assess the effect of superoxide dismutase (SOD) on these ischemia-reperfusion-induced alterations. These experiments used a mechanically perfused ex vivo gastric segment of chloralose-anesthetized dogs. We first evaluated the effect of varying the duration of total ischemia on reperfusion-induced changes in gastric vascular resistance and motility. In other experiments, responses to ET-1 (10(-10) M) were compared before and after 30-min ischemia and 30-min reperfusion, with saline or SOD (10 U/ml) infused intra-arterially to the stomach during reperfusion. Our results show that 1) after ischemia, vasodilation is seen initially on reperfusion followed by a slowly developing, progressive increase in vascular resistance, 2) the force of gastric contractions was reduced during ischemia but elevated immediately on reperfusion, 3) vasoconstrictor responses to ET-1 are enhanced after ischemia-reperfusion, and 4) SOD reduced the enhanced response to ET-1 and force of contractions. Our findings support the hypothesis that reactive oxygen metabolites contribute to augmented vascular reactivity and hypercontractility after ischemia-reperfusion.

Role of prostaglandins in angiotensin II-induced gastric vasoconstriction.

The purpose of our study was to examine the role of prostaglandins in angiotensin II (ANG II)-induced gastric vasoconstriction. ANG II produced statistically significant, dose-related increases in vascular resistance of a mechanically perfused ex vivo stomach segment of chloralose-anesthetized dogs. We next examined the effect of cyclooxygenase inhibitors on responses to ANG II. Indomethacin (10 mg/kg), which blocked the vasodilator response to intra-arterial arachidonic acid, augmented the maximal increase in perfusion pressure during ANG II infusion. Similar results were found using a different cyclooxygenase inhibitor, meclofenamic acid. In the final experiments we used an enzyme immunoassay to measure 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) plasma concentrations. ANG II produced dose-related increases in gastric venous but not arterial levels of 6-keto-PGF1 alpha, the major metabolite of prostacyclin. Our results are consistent with the hypothesis that release of vasodilatory prostaglandins attenuates the vasoconstrictor response to ANG II in the gastric microcirculation.

Phosphoramidon attenuates big endothelin-1-induced vasoconstriction in canine stomach.

We compared the effects of endothelin-1 and its precursor, big endothelin-1, on vascular resistance of a blood-perfused ex vivo stomach segment of chloralose-anesthetized dogs. In separate groups of dogs, endothelin-1 or big endothelin-1 was infused intra-arterially directly to the gastric segment. Endothelin-1 caused statistically significant dose-related increases in gastric vascular resistance at final blood concentrations of 0.15-10 nM. Although each dose was given for only 5 min, endothelin-1 at concentrations > 0.6 nM caused sustained responses with vascular resistance remaining above control values for approximately 45-90 min. In contrast, however, big endothelin-1 caused a small but statistically significant vasoconstriction only at the highest concentration (10 nM). In other experiments, using 15-min peptide infusions, we found that pretreatment with phosphoramidon, an inhibitor of endothelin-converting enzyme, markedly reduced response to big endothelin-1 but not to endothelin-1. Our results demonstrate that endothelin-1, but not big endothelin-1, is a potent vasoconstrictor of the canine gastric microcirculation. In addition, it appears that big endothelin-1 is degraded to endothelin-1 in the stomach by a phosphoramidon-sensitive metalloproteinase.

Characteristics of basolateral Cl- transport by gastric surface epithelium in Necturus antral mucosa.

Conventional and ion-selective microelectrodes were used to characterize transport of Cl- across the basolateral cell membranes of gastric surface epithelium in isolated preparations of gastric antrum of Necturus. Conventional, voltage-sensing electrodes were used to evaluate changes in membrane potentials and resistances during removal of Cl- from the nutrient perfusate. Liquid ion exchanger Cl(-)-selective microelectrodes were constructed and validated to measure intracellular Cl- activity (aiCl). Our data indicate that 1) aiCl (range 12-25 mM) is close to that predicted if Cl- is distributed across the cell membranes by electrochemical equilibrium, 2) aiCl is not influenced by changes in luminal Cl- content but is susceptible to changes in nutrient Cl- content, 3) Cl- conductances cannot be detected in the basolateral membrane and changes in membrane potentials do not influence aiCl, and 4) Cl- accumulation across the basolateral membrane depends on Na+ and the level of [K+] in the nutrient solution. Inhibition of K(+)-dependent Cl- accumulation, in the absence of nutrient Na+ or in the presence of the inhibitor bumetanide, was demonstrated. These findings suggest that basolateral Na(+)-K(+)-Cl- cotransport is important in regulating cell Cl- levels in surface cells of the gastric antrum in Necturus.