Tunneled Catheter–Associated Atrial Thrombi: Successful Treatment with Chronic Anticoagulation

Tunneled dialysis catheter–associated right atrial thrombus (RAT) is a rarely reported complication. We reviewed hospital records of 10 patients from a teaching hospital dialysis unit, in whom RAT was diagnosed by trans‐esophageal echocardiography (TEE). Patients were treated with chronic anticoagulation (heparin followed by warfarin) and followed over time. The group included 7 women; 6 patients were African American, 3 were Caucasian, and 1 was Hispanic. The average age was 52.1 ± 15.3 years. The most common presenting symptom was poor catheter flow on hemodialysis followed by fever and chills. On average, the patients had had 3.4 ± 2.7 catheter insertions before diagnosis of RAT, and the tunneled dialysis catheter (TC) had been in place for a mean of 91 ± 89.4 days when the thrombi were diagnosed. Trans‐thoracic echocardiography (2‐D echo) was done in 4 patients, but it identified RAT in only 1 patient. The catheter tip was at the junction of the superior vena cava and right atrium (SVC/RA) in most patients. Thrombolysis (unsuccessful) was attempted with urokinase in 3 patients, complicated in 2 patients by hemorrhage. After anticoagulation, 90% of the RAT resolved on repeated TEE. One patient had persistent RAT for 23 weeks and underwent surgical thrombolysis, but died postoperatively. We conclude that RAT is a frequently missed complication of a TC. Positioning the tip of the TC at the SVC/RA junction may not prevent RAT. Trans‐esophageal echocardiography is a more sensitive diagnostic tool than 2‐D echo and should be obtained early. Most patients can be successfully treated with anticoagulation alone. Thrombolytic therapy and surgical thrombolysis have high morbidity and mortality.     

Gibbs energy of formation of nickel chromite

The equilibrium partial pressure of oxygen for a system containing coexisting NiCr₂O₄, Cr₂O₃, and Ni was determined at 1000 to 1300 K using the electrochemical technique. Yttria-stabilized zirconia was employed as a solid-state electrolyte in the open-circuit electromotive force (EMF) measurements. Results were compared to the reported data in the literature. The standard Gibbs energy of NiCr₂O₄ at 1000 to 1300 K was determined to be ΔG°_f(NiCr₂O_{4)=-1327.2+0.314T±2.874 (kJ/mole)}     

Huntingtin-associated protein 1 (HAP1) interacts with the p150Glued subunit of dynactin

Huntington's disease (HD) is an inherited neurodegenerative disease caused by expansion of a polyglutamine repeat in the HD protein huntingtin. Huntingtin's localization within the cell includes an association with cytoskeletal elements and vesicles. We previously identified a protein (HAP1) which binds to huntingtin in a glutamine repeat length-dependent manner. We now report that HAP1 interacts with cytoskeletal proteins, namely the p150 Glued subunit of dynactin and the pericentriolar protein PCM-1. Structural predictions indicate that both HAP1 and the interacting proteins have a high probability of forming coiled coils. We examined the interaction of HAP1 with p150 Glued . Binding of HAP1 to p150 Glued (amino acids 879-1150) was confirmed in vitro by binding of p150 Glued to a HAP1-GST fusion protein immobilized on glutathione-Sepharose beads. Also, HAP1 co-immunoprecipitated with p150 Glued from brain extracts, indicating that the interaction occurs in vivo . Like HAP1, p150 Glued is highly expressed in neurons in brain and both proteins are enriched in a nerve terminal vesicle-rich fraction. Double label immunofluorescence experiments in NGF-treated PC12 cells using confocal microscopy revealed that HAP1 and p150 Glued partially co-localize. These results suggest that HAP1 might function as an adaptor protein using coiled coils to mediate interactions among cytoskeletal, vesicular and motor proteins. Thus, HAP1 and huntingtin may play a role in vesicle trafficking within the cell and disruption of this function could contribute to the neuronal dysfunction and death seen in HD.     

8-ns CMOS 64 K×4 and 256 K×1 SRAMs

SRAMs (static random-access memory) with a 64 K×4 and 256 K×1 structure and with 8-ns access time have been developed on a 1.0-μm CMOS process. Circuits are designed with source-coupling techniques to achieve high speed with small signal swings, using only CMOS devices. A metal option permits selection of the 64 K×4 or 256 K×1 configuration. The same core architecture has also been used to generate ×8 and ×9 designs. An output-enable (OE) version achieves 3-ns response time. As system speeds have recently increased toward 100-MHz operation, the need for address transition detection (ATD) has diminished as a means for improving the SRAM speed/power ratio. This trend in SRAM design stems mainly from the fact that AC current becomes the most significant fraction of the total current. Accordingly, the design described here employs a purely static path through the entire SRAM, with no requirement of ATD at any point. The resulting DC current is countered with a combined strategy of array subdivision, small-signal techniques, and active preamplification at key points in the data path     

Effect of fatigue loading on the modal properties of composite structures and its utilization for prediction of residual life

The design of composite structures for fatigue loading utilizes S-N curves to predict the fatigue life based on coupon testing. Due to the complex manufacturing process, the initial fabrication inconsistencies may cause the predicted number of cycles to failure to be off by one or two orders of magnitude. An experimental method is developed to predict the residual fatigue life of composite structures and continuously refine the prediction during the service life of these structures. Global effects on modal parameters, natural frequencies and damping ratios are investigated during the fatigue process. The Random Decrement signal processing technique is used. Changes of modal parameters are correlated with the prediction of fatigue failure life for selected graphite/epoxy composite specimens. The nature of the proposed method lends itself to real-time applications, especially, in service structures, as a nondestructive indicator.     

Optimum Downlink Power Control of a DS-CDMA System via Convex Programming

An optimum downlink power control that maximizes the user-capacity of a Direct Sequence-Code Division Multiple Access (DS-CDMA) cellular system is proposed based on a convex programming method. First, the downlink beamforming weights for the base-station antenna-array are designed based on the maximum Signal-Interference-Ratio (SIR) criterion. Then by optimizing the downlink power subject to a fixed total transmit power constraint, we further increase the Signal-Interference-Noise-Ratio (SINR) at the mobile terminal, thus increasing the capacity of the system. With the same methodology, we can also minimize the required transmit power while satisfying the SINR threshold constraints. Additionally, a robust downlink power control approach for mitigating the performance degradation due to channel estimates error is also proposed. Computer simulations are given to demonstrate the improvement of downlink capacity, received SINR, robustness, and the minimization of the required transmit power for a DS-CDMA system with antenna-array at the base-station.