Structural investigations of amorphous metal-organic frameworks formed via different routes.

The structures of chemically identical amorphous zeolitic amorphous frameworks (ZIFs), which were prepared from crystalline ZIF-4 via three different routes, are compared by refining atomistic models against their neutron and X-ray total scattering data. The diffraction data are very similar at all but the lowest values of momentum transfer and this is reflected in the ability of models with the same continuous random network topology to fit the data from each of the three amorphous ZIFs. Despite this there are differences in the detail; the relative positions of the lowest-Q peak in the Zn-Zn partial structure factors are consistent with differences in the densities of the different amorphous samples, and peaks in the ZIF-4 glass total scattering structure factors are in general broader, suggesting shorter-ranged correlations.

Two-color pyrometry for low amplitude periodic heating.

Specimens subject to periodic heating must be probed for a calibrated temperature response if standard measurements of thermal diffusivity are to be extended to determine thermal conductivity. A variation on two-color pyrometry is developed to measure both the offset and harmonic amplitudes of temperature fluctuations caused by periodic heating. The requisite pyrometric formulae are derived for low amplitude heating using an expansion of the nonlinear thermal emission. Well-defined uncertainties in the temperature values are determined from experimental uncertainties in radiometric measurements. The accuracy demonstrated in this work is better than 2% for the temperature offset and 3%-8% for the fluctuating temperature amplitude.

Uncovering a reconstructive solid-solid phase transition in a metal-organic framework.

A nanoporous three-dimensional metal-organic framework (MOF), ZnPurBr undergoes a transition to a previously unreported high-temperature phase, ZnPurBr-ht. The transition, which proceeds without mass loss, is uncovered through the use of differential scanning calorimetry (DSC). The new crystal structure was solved using single-crystal X-ray diffraction, and the mechanical properties of both phases investigated by nanoindentation and density functional theory. The anisotropy of the calculated Young's moduli showed good agreement with the crystallographic alignment of the stiff purinate organic linker. The results provide a prototypical example of the importance of the use of DSC in the MOF field, where its use is not currently standard in characterization.

Porosity in metal-organic framework glasses.

The porosity of a glass formed by melt-quenching a metal-organic framework, has been characterized by positron annihilation lifetime spectroscopy. The results reveal porosity intermediate between the related open and dense crystalline frameworks ZIF-4 and ZIF-zni. A structural model for the glass was constructed using an amorphous polymerization algorithm, providing additional insight into the gas-inaccessible nature of porosity and the possible applications of hybrid glasses.

Linked Records of Children with Traumatic Brain Injury. Probabilistic Linkage without Use of Protected Health Information.

OBJECTIVE: Record linkage may create powerful datasets with which investigators can conduct comparative effectiveness studies evaluating the impact of tests or interventions on health. All linkages of health care data files to date have used protected health information (PHI) in their linkage variables. A technique to link datasets without using PHI would be advantageous both to preserve privacy and to increase the number of potential linkages. METHODS: We applied probabilistic linkage to records of injured children in the National Trauma Data Bank (NTDB, N = 156,357) and the Pediatric Health Information Systems (PHIS, N = 104,049) databases from 2007 to 2010. 49 match variables without PHI were used, many of them administrative variables and indicators for procedures recorded as International Classification of Diseases, 9th revision, Clinical Modification codes. We validated the accuracy of the linkage using identified data from a single center that submits to both databases. RESULTS: We accurately linked the PHIS and NTDB records for 69% of children with any injury, and 88% of those with severe traumatic brain injury eligible for a study of intervention effectiveness (positive predictive value of 98%, specificity of 99.99%). Accurate linkage was associated with longer lengths of stay, more severe injuries, and multiple injuries. CONCLUSION: In populations with substantial illness or injury severity, accurate record linkage may be possible in the absence of PHI. This methodology may enable linkages and, in turn, comparative effectiveness studies that would be unlikely or impossible otherwise.

Coating thermal diffusivity and effusivity measurement optimization using regression-based sensitivity.

Measurements of thermal diffusivity and thermal effusivity are critical to developing a complete description of thermal transport within thermal barrier coating systems. Thermal diffusivity and thermal effusivity of coatings can be measured nondestructively using the phase of photothermal emission analysis experimental measurement. However, the complexity of the regression analysis required in this measurement makes determining the uncertainties associated with the best-fit values nontrivial. The aim of this paper is to develop a framework to carry out this uncertainty analysis and to minimize the uncertainties in fitted parameters. It is shown that the physical model can be used as an effective tool for identifying and removing data points afflicted by excessive bias error, which can occur in the limits of the observational data. It is revealed that this reduction in the dataset offers a tradeoff between increasing agreement between the data and the model while reducing the uniqueness of fitted parameter values. The current analysis demonstrates that this situation can be treated as an optimization problem, whereby uncertainties in fitted parameters can be minimized.

Topochemical conversion of a dense metal-organic framework from a crystalline insulator to an amorphous semiconductor.

The topochemical conversion of a dense, insulating metal-organic framework (MOF) into a semiconducting amorphous MOF is described. Treatment of single crystals of copper(i) chloride trithiocyanurate, CuICl(ttcH3) (ttcH3 = trithiocyanuric acid), 1, in aqueous ammonia solution yields monoliths of amorphous CuI1.8(ttc)0.6(ttcH3)0.4, 3. The treatment changes the transparent orange crystals of 1 into shiny black monoliths of 3 with retention of morphology, and moreover increases the electrical conductivity from insulating to semiconducting (conductivity of 3 ranges from 4.2 × 10-11 S cm-1 at 20 °C to 7.6 × 10-9 S cm-1 at 140 °C; activation energy = 0.59 eV; optical band gap = 0.6 eV). The structure and properties of the amorphous conductor are fully characterized by AC impedance spectroscopy, X-ray photoelectron spectroscopy, X-ray pair distribution function analysis, infrared spectroscopy, diffuse reflectance spectroscopy, electron spin resonance spectroscopy, elemental analysis, thermogravimetric analysis, and theoretical calculations.

Flexibility of zeolitic imidazolate framework structures studied by neutron total scattering and the reverse Monte Carlo method.

The zeolitic imidazolate framework ZIF-4 undergoes an amorphization transition at about 600 K, and then transforms at about 700 K to ZIF-zni, the densest of the crystalline ZIFs. This series of long-range structural rearrangements must give a corresponding series of changes in the local structure, but these have not previously been directly investigated. Through analysis of neutron total diffraction data by reverse Monte Carlo modelling, we assess the changes in flexibility across this series, identifying the key modes of flexibility within ZIF-4 and the amorphous phase. We show that the ZnN4 tetrahedra remain relatively rigid, albeit less so than SiO4 tetrahedra in silicates. However, the extra degrees of freedom afforded by the imidazolate ligand, compared to silicate networks, vary substantially between phases, with a twisting motion out of the plane of the ligand being particularly important in the amorphous phase. Our results further demonstrate the feasibility of reverse Monte Carlo simulations for studying intermolecular interactions in solids, even in cases, such as the ZIFs, where the pair distribution function is dominated by intramolecular peaks.

Measurement of pulmonary artery diastolic pressure from a right ventricular pressure transducer in patients with heart failure.

Recent studies have demonstrated that pulmonary artery diastolic (PAD) pressure can be measured from a transducer positioned in the right ventricle (RV) based on the finding that PAD and RV pressures are equal at the time of pulmonary valve opening, which is associated with the time of maximum positive rate of pressure development (dP/dtmax) in the ventricle. The objective of this study was to assess the correlation between estimated PAD (ePAD) pressure, obtained through a RV transducer, and actual PAD (aPAD) pressure in patients with heart failure who have abnormal hemodynamics, reduced systolic function, and variable degrees of mitral regurgitation (MR) and tricuspid regurgitation (TR). Simultaneous measurements of pulmonary artery and RV pressures were obtained with a high-fidelity Millar catheter (Millar Instruments, Houston, TX) in 10 patients with New York Heart Association class III-IV heart failure who were being evaluated for cardiac transplantation. The overall correlation between ePAD and aPAD pressures was .92 (R2 = .878). This was not significantly different during the Valsalva maneuver (r = .96, R2 = .943), submaximal bicycle exercise (r = .87, R2 = .756), or infusions of dobutamine and nitroglycerin (r = .82, R2 = .730). The overall average difference between the average ePAD (24.6 +/- 7.0 mmHg) and aPAD (23.6 +/- 7.0 mmHg) pressures was 1.0 +/- 3.4 mmHg. The average difference between the two pressures in patients with mild to severe MR or TR was not different compared to those patients with no or trace MR or TR. The estimation of PAD pressure from an RV transducer is valid in patients with heart failure who have abnormal hemodynamics, reduced systolic function, and variable degrees of MR and TR. This correlation was observed at rest and during several provocative maneuvers. These data will be important for the development of a chronic, implantable hemodynamic monitor for patients with heart failure.

Measurement of pulmonary artery diastolic pressure from the right ventricle.

OBJECTIVES: This study evaluated the feasibility of estimating pulmonary artery end-diastolic pressure from within the right ventricle. If feasible, this could have important implications for long-term hemodynamic monitoring. BACKGROUND: Right ventricular pressure at the time of pulmonary valve opening closely approximates pulmonary artery end-diastolic pressure. Because maximal first derivative of right ventricular pressure (dP/dt) can be easily measured, if it occurs at or very near pulmonary valve opening, right ventricular pressure at maximal right ventricular dP/dt would be an estimation of pulmonary artery end-diastolic pressure. METHODS: In 10 patients undergoing routine right and left heart catheterization, simultaneous measurements were made using micromanometers in the right ventricle and pulmonary artery at baseline, during isometric work and Valsalva maneuver. Right ventricular pressure at maximal right ventricular dP/dt was considered the estimated pulmonary artery end-diastolic pressure and was compared with the actual pulmonary artery end-diastolic pressure. RESULTS: At baseline, estimated and actual pulmonary artery end-diastolic pressures were (mean +/- SD) 17.7 +/- 6.6 and 16.7 +/- 6.7 mm Hg, respectively (p = NS). During isometric stress, estimated and actual pulmonary artery end-diastolic pressures were 30.4 +/- 12.7 and 28.4 +/- 10.1 mm Hg, respectively (p = NS). During Valsalva maneuvers, estimated and actual pulmonary artery end-diastolic pressures were 36.5 +/- 17.8 and 38.0 +/- 16.1 mm Hg, respectively (p = NS). CONCLUSIONS: Although more extensive testing is necessary to evaluate validity in different physiologic and pathologic situations, it appears that right ventricular pressure at maximal right ventricular dP/dt can provide accurate estimation of pulmonary artery end-diastolic pressure.

Right ventricular pressure during ventricular arrhythmias in humans: potential implications for implantable antitachycardia devices.

Implantable defibrillators use algorithms based on ventricular electrographic data to detect the onset and termination of arrhythmias, but these algorithms do not always differentiate hemodynamically stable from unstable arrhythmias. Although, ideally, left ventricular function should be used to assess the hemodynamic state, right ventricular pulse pressure can be assessed in humans on a long-term basis with a transvenous lead. The potential utility of right ventricular pulse pressure to assess hemodynamic stability was studied in 22 patients with induced ventricular arrhythmias. Right ventricular pressure was measured with use of a transvenous right ventricular endocardial pacing lead with a piezoelectric bender pressure sensor 3 cm from its tip. Single ventricular premature paced beats administered in up to a bigeminal frequency did not alter the mean right ventricular pulse pressure (control 33.7 +/- 26, bigeminy 35.7 +/- 26 mm Hg). Twenty-one episodes of induced ventricular tachycardia were studied in the electrophysiology laboratory. Five seconds after tachycardia induction, hemodynamically stable ventricular tachycardia had a longer cycle length (294 +/- 41 ms) and the right ventricular pulse pressure ratio was higher (0.55 +/- 0.26) than that in unstable ventricular tachycardia (cycle length 256 +/- 55 ms, p = 0.06; pulse pressure ratio 0.26 +/- 0.09, p less than 0.05). Twenty episodes of ventricular fibrillation were induced in eight patients. One second after induction, right ventricular pulse pressure decreased from 25 +/- 5 to 6 +/- 3 mm Hg (p less than 0.05). On the first beat after defibrillation, right ventricular pulse pressure increased to 24 +/- 14 mm Hg, a level not significantly different from that before the induction of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cross-talk in bipolar pacemakers.

Investigation of dual chamber pacing and sensing interactions at high rates is becoming increasingly important with the advent of sensor driven dual chamber pacemakers. The present study was designed to investigate the pacemaker and lead interactions that will affect cross-talk during high rate atrial and ventricular pacing. The study was divided into two phases, phase one investigated the mechanisms of cross-talk using standard pacemaker circuitry and various electrode types in a canine model. In six dogs with complete heart block, dual chamber pacing was carried out with four lead types at increasing pacing rates, while output of the ventricular sense amplifier of a pacemaker breadboard was monitored. Ventricular sense amplifier output signals (n = 332) progressively increased from 31.5 +/- 18.3 mV at 100 ppm to 102 +/- 55 mV at 160 ppm. Smooth platinum-iridium and platinized leads were statistically different at higher pacing rates (P less than 0.05). This signal level is sufficient to lead to a ventricular sensing event. In a second phase of the study, the incidence of cross-talk at high pacing rates was studied in patients with implantable dual chamber bipolar pacemakers. In 166 clinical trials on 106 patients with the same pacemaker, there was evidence of cross-talk in 1/59 cases at 110 ppm and 3/47 at 130 ppm, but none at higher rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in vascular capacity in awake dogs in response to carotid sinus occlusion and administration of catecholamines.

Changes in cardiac filling pressure (central venous pressure) were measured following carotid occlusion and infusions of catecholamines in awake dogs while cardiac output was held constant. After carotid occlusion in dogs with vagi blocked, central venous pressure increased about 0.8 mm Hg (an estimated decrease in vascular capacity of 2.4 ml/kg). Carotid occlusion before vagal block or following vagal block and beta-adrenergic block with propranolol caused no significant changes in central venous pressure. Phenylephrine (0.1-2.0 micrograms/min per kg) caused dose-dependent increases in arterial pressure, but changed central venous pressure (ca. 2.5 mm Hg) only at the highest doses. Epinephrine in doses (0.03-0.51 micrograms/min per kg) that caused little change in arterial pressure increased central venous pressure up to 5.3 mm Hg (an estimated decrease in vascular capacity of 12.0 ml/kg); this response was attenuated about 50% by propranolol. Isoproterenol (0.01-0.40 micrograms/min per kg) decreased arterial pressure and caused changes in central venous pressure similar to those seen with epinephrine. These responses were abolished by propranolol. Vascular compliance, determined from the change in central venous pressure following known changes in vascular blood volume, averaged 3.0 +/- 0.6 ml/mm Hg per kg. In the conscious, resting dog, both alpha- and beta-adrenergic receptors are involved in the reflex control of cardiac filling pressure. The beta-adrenergic responses predominate.

Active hepatic capacitance responses to neural and humoral stimuli in dogs.

Active changes in hepatic capacitance were studied in pump-perfused dog livers during hepatic nerve stimulation or during intrahepatic arterial infusion of histamine (0.01-1 mg/l) or epinephrine (0.05 mg/l). Hepatic nerve stimulation at 5 pulses/s (pps) reduced hepatic blood volume by 76 +/- 39 (SD) ml/kg tissue and decreased the apparent hepatic compliance 36% from a control value of 25.6 +/- 9.3 ml.kg-1.mmHg-1, with constant flow perfusion. With a constant hepatic arterial pressure, 5 pps stimulation decreased hepatic arterial flow to 16% of control; the volume expelled was 91 +/- 33 ml/kg. Epinephrine caused hepatic artery constriction, the active expulsion of 71 ml/kg of blood, and a decrease of about 30% in hepatic compliance. Histamine dramatically reduced the hepatic vascular compliance, decreased the portal venous conductance, increased hepatic arterial conductance, and caused the apparent hepatic blood volume to double. Increased hepatic venous pressure, hepatic nerve stimulation, epinephrine, and, especially, histamine caused a significant filtration of fluid from the hepatic vasculature. We conclude that significant active capacitance changes and transsinusoidal fluid filtration can be induced in the canine liver by neural and hormonal stimuli.

Beat-by-beat control of cardiac output in awake dogs with atrioventricular block.

In dogs with atrioventricular block and implanted ascending aortic flow probes, cardiac output can be controlled on each beta. The procedure is implemented through on-line use of a digital computer. The algorithm has three steps: 1) aortic flow is measured and integrated to give stroke volume; 2) at the end of ejection, the program computes how long the current beat must be to keep cardiac output at a target level; and 3) the ventricle is stimulated at the proper time. Cardiac output can be controlled over a range of 60-110% of normal in a resting dog. This range can be expanded by combining hemorrhage or volume infusion with the control procedure.

Hepatic capacitance responses to changes in flow and hepatic venous pressure in dogs.

The effect of changes in inflow and hepatic venous pressure (Phv) on the hepatic vascular bed was studied in denervated, pump-perfused canine livers. Hepatic arterial, portal venous, and hepatic venous pressures and flows were continuously monitored as was the hepatic venous hematocrit (Hct). The hepatic venous outflow, which averaged 1179 +/- 356 (SD) ml x min-1 x kg tissue-1 at control conditions, was controlled by a servosystem set to keep Phv at the desired level. Hepatic volume changes (delta V) were determined by integration of the difference between hepatic inflow (Fin) and outflow (Fhv). Over the range of Phv of 0-15 mmHg, the delta V-to-delta Phv ratio (apparent compliance C) was linear; C = 19.8 ml x mmHg-1 x kg tissue-1. These increases in Phv caused transient and plateau increases in Hct of 1.26 and 0.42%/mmHg, respectively. Varying inflow over the range of 0-156% of control by changing hepatic arterial and/or portal venous flow(s) resulted in delta V of 0.066 ml/kg per ml x min-1 x kg tissue-1 change in flow. We conclude that changes in Fin as well as changes in Phv cause changes in liver volume; and that a significant fraction of the volume shift accompanying changes in Phv is due to transsinusoidal plasma movement.

Linearity of the vascular pressure-volume relationship of the canine intestine.

To test whether the pressure-volume relationship of the canine small intestinal vasculature is linear over the normal range of portal venous pressures (5 to 35 mm Hg), we used two methods to measure volume: (1) the integral of inflow minus outflow (IFD), and (2) tissue activity of 51Cr-labeled erythrocytes (Cr-51). Venous pressures were changed in steps of 5 mm Hg with a servo-controlled system. The tissue was perfused at a constant rate. With venous pressures of 3.6 to 38.6 mm Hg, the vascular compliance was 2.19 +/- 0.42 (SD) ml/kg x mm Hg using IFD, and 1.87 +/- 0.50 ml/kg x mm Hg using Cr-51. Although a quadratic term significantly improved the fit, the effect was small (less than 3 ml/kg with a 30 mm Hg venous pressure change). The control blood volume of the intestinal loop at a venous pressure of 8.6 +/- 1.5 (SD) mm Hg was 86.2 +/- 19.1 ml/kg tissue weight using the mean transit time of a step input of indocyanine green at a perfusion pressure of 106 +/- 29 mm Hg and a flow of 556 +/- 147 ml/min x kg. We conclude that there is no significant change in compliance over the normal venous pressure range of 5-35 mm Hg.

Actively circulating blood volume in endotoxin shock measured by indicator dilution.

To estimate the size of the actively circulating blood volume of splenectomized dogs during control conditions and after endotoxin infusion, the pattern of concentration changes of 51Cr-labeled erythrocytes and 125I-labeled albumin was monitored. A dual exponential equation was fitted to the data. The total red blood cell and albumin volumes of distribution were determined from the slow exponential disappearance curves. The active red blood cell and albumin volumes were 89.8 +/- 5.3% and 92.0 +/- 2.0% of the total volumes, respectively. After endotoxin shock (mean arterial blood pressure 49.1 +/- 17.8 mmHg) the active volumes fell to only 60.0 +/- 10.3% and 56.2 +/- 20.0% of the total volumes, respectively. The fast-mixing time constants were similar (3.1 +/- 1.4 min and 2.5 +/- 2.7 min, respectively) and did not change significantly during the endotoxin shock, indicating that the albumin tag mixed into its larger volume of distribution as rapidly as the cells mixed into their indicated volume. We conclude that 1) an active blood volume can be distinguished, 2) it decreases for both red blood cells and albumin in endotoxin shock, and 3) a major part of the "extravascular plasma volume," as estimated by albumin dilution, is in the actively circulating circulation.

Vascular capacitance of dog intestine using mean transit time of indicator.

Changes in vascular volume of dog jejunum caused by norepinephrine, isoproterenol, or acetylcholine at constant=flow perfusion, were compared to changes in volume caused by changes in blood flow or venous pressure. Vascular volume was measured by indicator dilution mean transit time, using a step input of indocyanine green (125 microgram/min). Venous pressure was held at 10 mmHg; control arterial pressure was about 110 mmHg. At a control flow of 521 ml/min.kg of tissue, the vascular volume was 104 +/- 14 (SD) ml/kg of tissue. Reducing flow by 75 percent caused the volume to decrease by 29 percent (--31 ml/kg); maximal norepinephrine infusion at constant flow and venous pressure decreased the vascular volume by 24 percent, and a 10-mmHg reduction in venous outflow pressure caused a 25 percent (--27 ml/kg) reduction. On the other hand, isoproterenol (100 microgram/liter) at constant flow caused a 245 percent increase in conductance and only a 12 percent increase in vascular volume. Thus, active venoconstriction, changes in venous pressure, or changes in flow independently may cause changes in vascular volume of the intestine. Active smooth muscle changes in the venous capacitance vessels are not necessarily correlated with changes in the arterial resistance vessels.