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.

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.

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.

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.

Local effects of 16, 16-dimethyl prostaglandin E2 on gastric blood flow and acid secretion.

The effects of luminal administration of 16, 16-dimethyl PGE2 on gastric blood flow and histamine-stimulated acid secretion were determined in a double-chambered preparation of canine fundic stomach. This model permitted simultaneous assessment of two segments of mucosa (17 cm2 each), one control and the other test, supplied by the same vascular pedicle. Topical application of 25 microgram 16, 16-dimethyl PGE2 in 15 ml HCl to the test chamber significantly increased mucosal blood flow of the test chamber from 1.2 +/- 0.1 to 2.5 +/- 0.5 ml/min (P less than 0.05) whereas no significant change in mucosal blood flow was noted in the control mucosa. Intravenous infusion of histamine at 1.0 microgram/kg/min stimulated comparable amounts of acid secretion in both segments of mucosa. The addition of 16, 16-dimethyl PGE2 (25 microgram in 15 ml of HCl) in the bathing solution of the test chamber significantly reduced histamine-stimulated acid secretion from 22.5 +/- 3.1 to 8.4 +/- 1.2 microEq/min (P less than 0.01) in the test mucosa whereas the control mucosa showed no evidence of secretory inhibition throughout the experiment. Since the control mucosa was supplied by the same vascular pedicle as the test mucosa, we concluded that the observed vasodilating and antisecretory effects of luminal administration of 16, 16-dimethyl PGE2 were local rather than systemic effects following its absorption from the stomach.

Effects of intra-arterial infusion of prostaglandin E1 on gastric secretion and blood flow.

The effect of intra-arterial infusion of Prostaglandin E1 (PGE1) on gastrict total and mucosal blood flow and acid secretion was studied in an exteriorized, chambered preparation of canine fundic stomach. Total gastric blood flow was measured simultaneously by venous outflow and by gamma-labeled microspheres. Mucosal blood flow also was measured by microspheres. Intra-arterial infusion of PGE1 at 1.0 microgram/min completely inhibited histamine-stimulated acid secretion. This inhibition was accompanied by a significant increase in both total (p less than 0.01) and mucosal blood flow (p less than 0.01). The ratio of mucosal to total blood flow remained unchanged during histamine stimulation (78 +/- 4%) and PGE1 inhibition (79 +/- 4%). The results suggest that inhibition of acid secretion can occur in the face of increased blood flow. This observation is contrary to the generally accepted concept that inhibition of acid secretion always is associated with a decrease is mucosal blood flow.

Effect of aspirin on epithelial cell membrane potentials of gastric fundic mucosa.

The effects of aspirin on epithelial cell membrane potentials of Necturus fundic mucosa were examined by in vitro experiments according to intracellular microelectrode techniques. Stable intracellular impalements were obtained with 15 to 50 M-ohm microelectrodes filled with 3M KCl. In neutral mucosal solutions (pH 7.0) aspirin (5.0 mM) resulted in a significant increase in apical cell membrane potential (Vmc) from -36.7 +/- 1.5 mV to -43.3 +/- 2.3 mV (p less than 0.001) and basolateral cell membrane potential (Vcs) from -42.7 +/- 1.8 mV to -50.6 +/- 2.4 (p less than 0.001). This hyperpolarization of the cell was associated with an increase in transmucosal potential from -5.8 +/- 0.7 to -7.4 +/- 0.9 (p less than 0.05) and an increase in the ratio of apical to basolateral membrane resistances from 5.1 +/- 1.2 to 8.8 +/- 1.9 (p less than 0.05). These changes were consistent with an increase in potassium conductance induced by the salicylate anion. In acidic mucosal solutions (pH 4.5) aspirin caused a reduction in Vmc and Vcs. This hypopolarization of the cell membrane is consistent with acidification of the epithelial cells. These observations support the proposed mechanisms of aspirin injury: (1) back diffusion of H+ into the cells and (2) influx of the salicylate anions into the cells, which may interfere with intracellular metabolism.

Direct effect of endotoxin on the gastric mucosal microcirculation and electrical gradient.

The effects of intra-arterial infusion of E. coli endotoxin at 1.0 mg. per minute on the gastric total and mucosal blood flows, electrical potential difference, and ionic fluxes across the gastric mucosa were studied in an exteriorized, chambered preparation of canine fundic stomach. Gamma-labelled microsphere technique was used in addition to venous drainage and plasma aminopyrine clearance for the measurement of total and mucosal blood flow, respectively. In spite of normal systemic blood pressure throughout the experiment, E. coli endotoxin infusion caused a significant decrease in total gastric blood flow and in the fractional distribution of flow to the mucosae. There was no significant arteriovenous shunting of microspheres. Significant reduction in potential difference and hydrogen-ion back diffusion also was noted after endotoxin infusion, possibly as a consequence of reduced mucosal blood flow. The results indicate that significant gastric mucosal ischemia can occur and may represent a mechanism in the development of gastric erosions in endotoxemia, even in the absence of systemic hypotension.

Effect of aspirin, bile salt, and ethanol on canine gastric mucosal blood flow.

The effect of aspirin (20 mM.), sodium taurocholate (40 mM.), and ethanol (24 per cent w/v) on gastric mucosal blood flow was studied in an exteriorized, chambered preparation of canine fundic stomach. Gastric mucosal blood flow was measured by gamma-labeled microspheres and plasma aminopyrine clearance. All three test solutions caused a significant increase in microsphere-measured mucosal blood flow. The degree of increase in gastric mucosal blood flow was proportional to the severity of gross mucosal injury, being greatest with bile salt and least with ethanol. Plasma aminopyrine clearance determined only a small fraction of mucosal flow measured by microspheres following injury, particularly in sodium taurocholate and ethanol experiments, where the net hydrogen ion back diffusion was greatest. The results suggest that increased gastric mucosal blood flow may be a secondary defensive response to the damage caused by these irritants and that the plasma aminopyrine clearance is unreliable in quantitating mucosal blood flow changes in the presence of mucosal injury.

Controlled intragastric pH and cimetidine inhibition of histamine-stimulated gastric acid secretion in the dog.

This study tested a circulating intragastric titration system with an examination of the kinetics of cimetidine inhibition of histamine-stimulated gastric acid secretion of pH 7.0. Dogs were anesthetized, intubated with a biluminal nasogastric device, and connected to the titrating system. The dogs were stimulated with histamine at 0.0, 0.25, 0.50, 1.0, 2.0, and 4.0 microgram/kg/min IV. The dose variations were repeated on separate days with cimetidine infusion at 0.0, 20, and 40 microgram/kg/min IV. Calculated maximal response was 4.52 mEq/kg/hr. Histamine D50 was 0.60 microgram/kg/min. Cimetidine ID50 was 22.6 microgram/kg/min when histamine was given at 1.0 microgram/kg/min. Although acid secretion was higher than other published values, cimetidine inhibition kinetics were not significantly different from published values. A positive correlation was found between cimetidine ID50 and the logarithm of the histamine infusion rate. Our data suggest that (1) a simple circulating intragastric titration system can give accurate results in acid secretion studies, (2) increased gastric pH may enhance histamine-stimulated acid secretion, (3) neutralization of gastric contents does not interfere with cimetidine inhibition kinetics which is competitive, and (4) at artifically high rates of histamine infusion, cimetidine can actually increase acid secretion. We suggest that a circulating intragastric system may be tested in a surgical intensive care unit to evaluate potential clinical value in antiulcer therapy.

Effect of 16,16-dimethyl prostaglandin E2 on gastric epithelial cell membrane potentials and resistances.

Intracellular microelectrode techniques were employed to examine the effects of 16,16-dimethyl prostaglandin E2 (dmPGE2) on Necturus antral mucosa epithelial cell membrane potentials and resistances. Necturus antral mucosa was mounted in a modified Ussing chamber and stable intracellular impalements were obtained. Addition of 0.01 microgram/ml dmPGE2 to the mucosal solution produced an increase of the apical cell membrane potential (Vmc) from -44.3 +/- 3.1 to -53.5 +/- 3.8 mV (p less than 0.001) and of the basolateral cell membrane potential (Vcs) from -48.8 +/- 2.8 to -57.7 +/- 3.2 mV (p less than 0.001). This reversible, dose-dependent hyperpolarization of both cell membranes was accompanied by a decrease in the electrical resistance of the apical membranes (Ra) from 2550 +/- 250 omega/cm2 to 1870 +/- 210 omega/cm2 (p less than 0.05) and a decrease in the resistance of the basolateral membrane (Rb) from 1020 +/- 250 omega/cm2 to 630 +/- 80 omega/cm2 (p less than 0.05). In addition, there was an increase in the resistance of the shunt (intercellular junction, Rs), the major route of transepithelial ion flow, from 710 +/- 60 omega/cm2 to 750 +/- 80 omega/cm2 (p less than 0.05). Thus dmPGE2 increased the cell membrane potentials and reduced the ionic permeability of the intercellular junction.

Intracellular pH (pHi) in gastric surface epithelium is more susceptible to serosal than mucosal acidification.

Intracellular microelectrode techniques were used to examine the effects of mucosal or serosal acidification on intracellular pH (pHi) in gastric surface epithelial cells. Necturus antrum was mounted in a modified Ussing chamber, and pHi was determined from the difference between the potentials recorded by intracellular conventional and pH-sensitive microelectrodes. In tissues bathed with bicarbonate-buffered Ringer's solution (pH 7), acidification of the mucosal solution to pH 4.5 by isotonic replacement of the NaHCO3 with NaCl had no significant effects on pHi. In contrast, acidification of the serosal solution to pH 4.5 by replacing the bicarbonate reduced pHi from 7.32 +/- 0.04 to 6.95 +/- 0.06 (p less than 0.001, n = 8). Similarly, in tissues bathed with HEPES-buffered Ringer's solution (pH 7.0), pHi was unaffected by reducing the mucosal solution pH to 4.5 with HCl but fell 0.21 +/- 0.05 pH units (p less than 0.01, n = 7) during acidification of the serosal solution to pH 6. These results suggest that gastric epithelium is more sensitive to acidification from the serosal than the mucosal side. Such a finding is consistent with the concept of a gastric mucosal barrier to luminal acid. It may also explain the gastric epithelium's greater sensitivity to acute ulceration during systemic acidosis.

Comparison of gastric mucosal blood flow as measured by H2 gas clearance and microspheres during secretory stimulation and inhibition.

H2 clearance is a recently described method of measuring gastric mucosal blood flow that has great potential for clinical use. However, the effects of luminal pH and of secretory activity of the gastric mucosa on the accuracy of H2 clearance measurements have not been systematically examined. We therefore tested the validity of H2 clearance measurements at different pHs in both in vitro and in vivo systems. In addition, we compared measurements by H2 clearance and radioactive microspheres during stimulation and suppression of acid secretion. In vitro, H2 washout was relatively constant over a range of pHs from 2.0 to 8.0. In chambered segments of canine fundus in vivo, H2 clearance was not significantly affected by pH of the luminal solutions either in the resting state or at lower blood flows induced during infusion of vasopressin. Finally, there was a close correlation (r = 0.85; p less than 0.001) between H2 clearance and microsphere measurements under resting conditions, during intravenous histamine stimulation, and after infusion of cimetidine to suppress acid secretion. In summary, H2 clearance reliably and accurately measures gastric mucosal blood flow at different luminal pHs and under conditions that stimulate or suppress acid secretion.

Regional gastric mucosal blood flow after parietal cell vagotomy in dogs.

In this study we used the recently validated H2 clearance method to perform endoscopic measurements of gastric mucosal blood flow (MBF) in anesthetized dogs before and after parietal cell vagotomy (PCV). Under resting conditions, MBF in the gastric corpus before PCV was 72 +/- 5 ml/min/100 gm. This was not altered significantly at 4, 8, or 16 weeks after PCV, and there were not significant long-term changes in MBF on the greater or lesser curvatures of the corpus individually. Before PCV infusion of pentagastrin (8 micrograms/kg/hr) elicited increases in corpus MBF to 104 +/- 4 ml/min/100 gm, accompanied by increases in gastric acid output from resting levels of 2.1 +/- 0.9 to 38.6 +/- 2.4 mEq/hr (p less than 0.001). PCV significantly reduced pentagastrin-stimulated acid secretion by 50%, and secretory inhibition was accompanied by significant reductions in pentagastrin-stimulated MBF in the corpus. Pentagastrin did not alter antral MBFs before or after PCV. In summary PCV does not elicit significant long-term changes in resting MBF in different regions of the gastric corpus, and PCV significantly diminishes increases in acid output and corpus MBF that are normally stimulated by pentagastrin. These observations suggest that alterations in gastric MBF after PCV may be attributable to alterations in acid secretion.

Intravenous cholangiography in the diagnosis of acute cholecystitis.

We reviewed our experience with intravenous cholangiography in the evaluation of 70 patients with suspected acute cholecystitis. Twenty-one of these patients had visualization of the biliary ducts without opacification of the gallbladder, a roentgenographic finding that was considered diagnostic of acute cholecystitis. Twenty of the 21 patients were noted to have acute cholecystitis during exploratory laparotomy. The remaining patient had a normal gallbladder, but was found to have a liver abscess. Opacification of the gallbladder with evidence of gallstones was found in eight patients; all had acute cholecystitis. Visualization of the gallbladder without gallstones was found in 22 patients, revealing no acute cholecystitis in this group. Many of these patients were admitted to the hospital with a primary diagnosis of acute cholecystitis and were spared an unnecessary surgical exploration. Nineteen patients had nonvisualization of the gallbladder and biliary ducts. This roentgenographic finding may be caused by acute intra-abdominal conditions other than cholecystitis and caution is warranted in its interpretation. This test has been found to be a reliable adjunct in the work-up of patients with suspected acute cholecystitis.

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.

Thomas G Orr Memorial Lecture. Pathogenesis, prophylaxis, and treatment of stress gastritis.

In the last decade, significant progress has been made in understanding the basic mechanisms involved in the development of acute stress gastritis. Many of the experimental observations have been applied in our clinical approaches to patients at high risk. A strong impression exists among investigators that efforts to improve ventilatory support, correct abnormalities in cardiac output and intravascular volume, and maintain adequate nutrition in critically ill patients may have contributed to the decreased incidence and prevalence of stress gastritis over the past decade. In addition, reduction of intragastric acidity, either by titration with antacids or administration of H2 antagonists, further prevented stress gastritis in these patients. We have every reason to believe that progress will continue at the same rate in the decades before us in this area of investigation.

Jaundice in patients with acute cholecystitis. Its validity as an indication for common bile duct exploration.

Our study demonstrates that (1) mild to moderate jaundice is frequently seen in patients with acute cholecystitis; (2) severe degrees of jaundice were seen in two patients without the presence of common duct stone or recognizable obstruction of the common bile duct; (3) only one of forty-one patients with acute cholecystitis had common bile duct stone; (4) jaundice does not appear to be a compelling reason for choledochotomy; and (5) less invasive technics such as intravenous and intraoperative cholangiography should suffice to exclude the possibility of common bile duct stone in patients with acute cholecystitis.