The thermodynamics of volatilization of chromic oxide: Part II. the species CrO2 CI{8in2}

A study has been made, using the transpiration technique, of the volatility of chromic oxide in oxygen-chlorine-argon mixtures in the temperature range 627 to 977°C. Under the conditions of the experiments, the volatilization is shown to occur by the reaction Cr₂O₃(s) + 2Cl₂(g) + 1/2O₂(g) = 2CrO₂Cl₂(g). The standard Gibbs free energy change is given by AG° = 90,900(±1200) + 16.46(±1.2)TJ, where the reference state for the gases is one standard atmosphere. Combination of this work with previous structural studies leads to a value for the heat of formation of CrO₂Cl₂ (g) at 298 K of + 518.2 (±2) kJ/mole.     

Chromoxyd im Gleichgewicht mit Eisen-Chrom-Legierungen bei 1600 °C

Sauerstoffsättigung in Eisen-Chrom-Legierungen. Abhängigkeit des Chromgehaltes in der Schmelze vom Sauerstoffpartialdruck der Gasphase. Zusammensetzung des Chromoxydes im Gleichgewicht mit Eisen-Chrom-Legierungen. Der Aktivitätskoeffizient von Chrom in der Schmelze.     

Suboptimal regulator design of linear systems with quantized controls

This short paper presents a design technique for determining a suboptimal feedback control law for linear systems actuated by the quantized control signals. This control law is easily implemented in the form of the switching hyperplanes characterized by a nonlinear matrix difference equation for discrete-time systems or by a differential equation for continuous-time systems. The properties of this control law are investigated in detail.     

Efficient subspace-based algorithm for adaptive bearing estimation and tracking

In some practical applications of array processing, the directions of the incident signals should be estimated adaptively, and/or the time-varying directions should be tracked promptly. In this paper, an adaptive bearing estimation and tracking (ABEST) algorithm is investigated for estimating and tracking the uncorrelated and correlated narrow-band signals impinging on a uniform linear array (ULA) based on the subspace-based method without eigendecomposition (SUMWE), where a linear operator is obtained from the array data to form a basis for the space by exploiting the array geometry and its shift invariance property. Specifically, the space is estimated using the least-mean-square (LMS) or normalized LMS (NLMS) algorithm, and the directions are updated using the approximate Newton method. The transient analyses of the LMS and NLMS algorithms are studied, where the "weight" (i.e., the linear operator) is in the form of a matrix and there is a correlation between the "additive noise" and "input data" that involve the instantaneous correlations of the received array data in the updating equation, and the step-size stability conditions are derived explicitly. In addition, the analytical expressions for the mean-square error (MSE) and mean-square deviation (MSD) learning curves of the LMS algorithm are clarified. The effectiveness of the ABEST algorithm is verified, and the theoretical analyses are corroborated through numerical examples. Simulation results show that the ABEST algorithm is computationally simple and has good adaptation and tracking abilities.     

Site-directed mutagenesis of surfactant protein A reveals dissociation of lipid aggregation and lipid uptake by alveolar type II cells

Surfactant protein A (SP-A) binds to dipalmitoylphosphatidylcholine (DPPC) and induces phospholipid vesicle aggregation. It also regulates the uptake and secretion of surfactant lipids by alveolar type II cells. We introduced the single mutations Glu195-->Gln (rE195Q), Lys201-->Ala (rK201A) and Lys203-->Ala (rK203A) for rat SP-A, Arg199-->Ala (hR199A) and Lys201-->Ala (hK201A) for human SP-A, and the triple mutations Arg197, Lys201 and Lys203-->Ala (rR197A/K201A/K203A) for rat SP-A, into cDNAs for SP-A, and expressed the recombinant proteins using baculovirus vectors. All recombinant proteins avidly bound to DPPC liposomes. rE195Q, rK201A, rK203A, hR199A and hK201A function with activity comparable to wild type SP-A. Although rR197A/K201A/K203A was a potent inducer of phospholipid vesicle aggregation, it failed to stimulate lipid uptake. rR197A/K201A/K203A was a weak inhibitor for lipid secretion and did not competed with rat [125I]SP-A for receptor occupancy. From these results, we conclude that Lys201 and Lys203 of rat SP-A, and Arg199 and Lys201 of human SP-A are not individually critical for the interaction with lipids and type II cells, and that Glu195 of rat SP-A can be replaced with Gln without loss of SP-A functions. This study also demonstrates that the SP-A-mediated lipid uptake is not directly correlated with phospholipid vesicle aggregation, and that specific interactions of SP-A with type II cells are involved in the lipid uptake process.     

Surgical repair of coronary sinus type partial anomalous pulmonary venous drainage with intact atrial septum

A method to prevent co-elution of steroid sulfates with proteins in serum from the pre-column in column-switching HPLC was developed. The pre-column, a polymer-coated mixed function column, was used for ion-pair chromatography with 5 mM tetra-n-butylammonium (TBA) ion. As steroid sulfates, estriol 3-sulfate, dehydroepiandrosterone 3-sulfate and pregnenolone 3-sulfate were used. Human serum (25 microl) was diluted with mobile phases including 5, 100 and 500 mM TBA ion, and then injected directly into the pre-column. The peak areas of the steroid sulfates in serum samples were compared with those of the steroid standards without serum. When 25/microl of serum was diluted with mobile phase including 100 or 500 mM TBA ion, the steroid sulfates in serum were retained in the pre-column; however, the steroid sulfates from the same sample diluted with mobile phase containing 5 mM TBA ion were not retained in the pre-column. Addition of an excess amount of counter ion (TBA ion) into the serum sample made it possible to retain the steroid sulfates in the pre-column. This method was applied to column-switching HPLC for measurement of steroid sulfates in serum using a semi-microcolumn as the analytical column.     

Thermodynamics of phosphorus in carbon-saturated manganese-based alloys

The interaction coefficient of phosphorus with silicon in a Mn-Si-C_sat alloy has been measured at 1573 K, equilibrating CaC₂, C, and Ca₃P₂ in a quartz capsule to keep the phosphorus partial pressure as high as 33.7 Pa. The activity coefficient of phosphorus in the melts increases with increasing silicon content, and the interaction parameter between silicon and phosphorus in the melts at carbon saturation ε^Si_P, C_sat was found to be 10.4. The activity of phosphorus in a carbon-saturated Fe-Mn alloy was also determined at temperatures of 1573 to 1673 K using a chemical equilibration technique between BaO-BaF₂ fluxes and Fe-Mn-C_sat with manganese mass contents ranging from 0 to 85.3 %. A slight decrease in the activity coefficient of phosphorus in Fe-Mn-C_sat alloys was observed with increasing manganese content, as a reflection of a stronger interaction between manganese and phosphorus than that between iron and phosphorus. The value for e^Mn_P,Csat was found to be -0.0029 between 1573 and 1673 K.     

Case report: fibrolamellar hepatocellular carcinoma in a Japanese woman: a case report and review of Japanese cases

There have been few reports on cerebral arteriovenous malformation (AVM) of newborns. We present here an interesting case of occult AVM diagnosed 17 years after an episode of acute subdural hematoma in the neonatal period. The cause of subdural hematoma had remained unclear and the patient had suffered from an intractable epilepsy of 17 years duration. Seizures were mainly characterized by drop attacks and included other seizure types such as complex partial seizure and generalized tonic clonic seizure. The symptoms had gradually become worse and the intervals between the occurrences of symptoms had become shorter. An interictal scalp EEG showed a focal spike in the left temporoparietal lobe. CT and MRI of that region demonstrated a porencephalic cyst which was supposed to have resulted from an old hematoma. There were no vascular abnormalities in angiography. Temporoparietal craniotomy and a corticogram were performed. The cortex with a focus was resected and the disappearance of a focal spike in the corticogram was confirmed during operation. Microscopically the cortex included AVM with gliosis. The initial postoperative course was good and seizures disappeared immediately after the operation. However, the symptoms of drop attacks observed before operation began to occur again 3 months later. The fact of postoperative recurrence suggests that the long history of the patient's seizures originating from AVM may have produced secondary epileptic foci.     

Lead discovery of inhibitors of the dihydrofolate reductase domain of Plasmodium falciparum dihydrofolate reductase-thymidylate synthase

A three-dimensional structure model of the dihydrofolate reductase (DHFR) domain of the bifunctional DHFR-thymidylate synthase of Plasmodium falciparum was used as a basis for computational screening of commercially available compounds for candidate inhibitors. Compounds which can stably dock to the model with strong ionic hydrogen bonds via protonation by an aspartic acid residue at the bottom of the active site were identified through docking simulation. Among compounds thus identified, 21 were assayed for inhibitory activity towards the recombinant DHFR domain. Two compounds, 2-amino-1,4-dihydro-4,4,7,8-tetramethyl-s-triazino(1,2-a)benzimida zole and Trp-P-2, inhibited the recombinant P. falciparum DHFR domain with Ki values of 0.54 and 8.7 microM, respectively. Kinetic analysis showed that these compounds competitively inhibited the enzyme with respect to the substrate dihydrofolate. These findings support the validity of both the modeled structure and the docking results. Furthermore, these compounds serve as leads for developing new DHFR inhibitors, since their skeletal structures are different from any of known DHFR inhibitors. This paper also reveals a new biological activity of Trp-P-2, a potent mutagen.