The growth of high mobility heterostructures on (311)B GaAs

We demonstrate that the (311)B surface of GaAs can be used for the fabrication of high mobility (μ 2.4 × 10⁶ cm² V⁻¹ s⁻¹) two-dimensional electron gases, in which the mobility is found to be anisotropic with μ_{[ 33]} > μ_{[01 ]}. This paper reviews the magneto-transport properties of the (311)B system and sheds light on the nature of the scattering mechanisms determining the electron mobility. These results are of particular relevance to the current discussion of the nature of the {311} surface.

It is well known that a similar mobility anisotropy exists in hole gases grown on the (311)A surface, although attempts to interpret such results are complicated by the anisotropic and non-parabolic nature of the valence band structure. For electron gases grown on the (311)B surface we demonstrate experimentally (with ballistic focusing) that the Fermi surface is isotropic, leading to the conclusion that the most likely cause of the mobility anisotropy is anisotropic interface roughness scattering. This is also confirmed by measurements of mobility as a function of carrier density, which can be fitted by a simple interface roughness scattering theory.

Further experiments have demonstrated that ballistic quantization can be observed in both [ 33] and [01 ] directions, despite the large differences in anisotropic mobility.     

Biomechanical comparison of posterior internal fixation techniques for unstable pelvic fractures

Early reduction and rigid fixation of unstable vertical shear pelvic fractures has been shown to decrease the incidence of late sequelae and facilitate early mobilization. The results of fixation of the posterior pelvic ring without anterior fixation are unknown. The purpose of this study was to perform a biomechanical comparison of the most frequently used techniques of posterior fixation for unstable pelvic sacroiliac dislocations in conjunction with ipsilateral rami fractures, i.e., an unstable vertical shear injury. The four methods of posterior fixation tested included sacroiliac (SI) screws, anterior SI plates, transiliac bars, and a combination of SI screws and transiliac bars. Six cadaveric pelvises were tested in axial compression and torsion on a biaxial servohydraulic testing machine. Compared to the intact pelvis, single posterior methods of fixation provided approximately 70-85% resistance to axial and torsional loading. By combining SI screws with transiliac bars, approximately 90% of intact pelvic stability was achieved. Our results suggest that rigid posterior fixation of sacroiliac dislocations alone may obviate the need for additional complex anterior surgical procedures to fix rami fractures.     

Differential induction of c-Jun NH2-terminal kinase and c-Abl kinase in DNA mismatch repair-proficient and -deficient cells exposed to cisplatin

The c-Abl nonreceptor tyrosine kinase and the c-Jun NH2-terminal kinase (JNK/stress-activated protein kinase) are activated during the injury response to the DNA-damaging agent cisplatin. Loss of DNA mismatch repair activity results in resistance to cisplatin in human cancer cells, suggesting that the mismatch repair proteins function as a detector for cisplatin DNA adducts. To identify signaling pathways activated by this detector, we investigated the effect of the loss of DNA mismatch repair function on the ability of cisplatin to activate the JNK and c-Abl kinases. The results demonstrate that cisplatin activates JNK kinase 3.8 +/- 0.2-fold more efficiently in DNA mismatch repair-proficient than repair-deficient cells, and that activation of c-Abl is completely absent in the DNA mismatch repair-deficient cells. Furthermore, the results show that cisplatin-induced activation of JNK occurs through a stress-activated protein kinase/extracellular signal-regulated kinase kinase 1-independent mechanism. We conclude that activation of JNK and c-Abl by cisplatin is in part dependent upon the integrity of DNA mismatch repair function, suggesting that these kinases are part of the signal transduction pathway activated when mismatch repair proteins recognize cisplatin adducts in DNA.     

Measurement of intracellular calcium in cell populations loaded with aequorin: neurokinin-1 responses in U373MG cells

Changes in intracellular calcium concentration are important in mediating a wide variety of physiological responses. Recently there has been renewed interest in the use of aequorin, a protein from jellyfish that emits light when calcium is bound, to measure calcium levels in cells. We have loaded populations of cells from the human glioma line, U373MG, with aequorin. Lysis of aequorin-loaded but not control cells with detergent resulted in a luminescence signal that was dependent on extracellular calcium. Aequorin-loaded cells responded to substance P, histamine, or the calcium ionophore, ionomycin, with an increase in luminescence. Signals in response to detergent, ionomycin, or substance P could be detected up to 48 h after cells were loaded with aequorin. Other neurokinin-1 agonists but not agonists at neurokinin-2 or neurokinin-3 receptors produced luminescence signals. Neurokinin-1 antagonists inhibited the substance P-induced signal. The aequorin-loading procedure worked well with U373MG cells but not with AR42J, CHO, IMR-90, or WI-38 cells.     

Biochemical characterization of the human arsenite-stimulated ATPase (hASNA-I)

Arsenic is a potent toxin and carcinogen. In prokaryotes, arsenic detoxification is accomplished by chromosomal and plasmid-borne operon-encoded efflux systems. We have previously reported the cloning of hASNA-I, a human homologue of arsA encoding the ATPase component of the Escherichia coli arsenite transporter. Purified glutathione S-transferase (GST)-hASNA-I fusion protein was biochemically characterized, and its properties were compared with those of ArsA. The GST-hASNA-I exhibited a basal level of ATPase activity of 18.5 +/- 8 nmol/min/mg in the absence of arsenite. Arsenite produced a 1.6 +/- 0.1-fold stimulation of activity (p = 0. 0044), which was related to an increase in Vmax; antimonite did not stimulate activity. Two lines of evidence suggest that an oligomer is the most likely native form of hASNA-I. First, lysates of human embryo kidney 293 cells overproducing recombinant hASNA-I produced a single monomeric 37-kDa band on SDS-polyacrylamide gel electrophoresis (PAGE) and two distinct species when analyzed using nondenaturing PAGE. Second, chemical cross-linking of the 63-kDa GST-hASNA-I resulted in the formation of dimeric and tetrameric protein forms. The results indicate that hASNA-I is a distinct human arsenite-stimulated ATPase belonging to the same superfamily of ATPases represented by the E. coli ArsA protein.     

Effect of acute dietary fibre supplementation on colonic pH in healthy volunteers

Two patients presented with a tumor involving mainly the supplementary motor area or the premotor cortex. Shortly after tumor resection, each developed transient impairment of voluntary movements. An electromyogram, with the skin electrodes placed over the muscles of the upper arms and forearms, demonstrated aberrant ipsilateral, contralateral or bilateral muscle activation during unilateral motor tasks in both patients. The bilateral activation was more prominent in the patient who had an intact dominant hemisphere. The present study suggests for the first time the importance of non-primary motor areas of the human brain in activating the proper set of muscles on the proper side of the body.     

Effect of exercise on acid-base status and ventilatory kinetics

OBJECTIVES: To study the clinical spectrum of an acute severe encephalopathy occurring in 2 patients after recovery from falciparum malaria infection and to compare it with the reported clinical features of the postmalaria neurological syndrome. DESIGN: Case report. SETTING: Tertiary care hospital. PATIENTS: Two patients presented with acute onset of fluctuating motor aphasia, severe generalized myoclonus, and postural tremor. Additional signs were cerebellar ataxia, and in 1 patient, generalized epileptic seizures. Magnetic resonance imaging of the brain revealed patchy white matter lesions in 1 patient. Clinically, the patients' conditions continued to worsen until corticosteroids were introduced, the use of which induced a rapid, albeit incomplete, recovery. CONCLUSIONS: We describe a new, severe variant of the still poorly defined postmalaria neurological syndrome. We propose a preliminary classification of this syndrome, according to its clinical characteristics, as follows: a mild or localized form, characterized by isolated cerebellar ataxia or postural tremor; a diffuse, but relatively mild encephalopathic form, characterized by acute confusion or epileptic seizures; and a severe, corticosteroid-responsive encephalopathy that is characterized by motor aphasia, generalized myoclonus, postural tremor, and cerebellar ataxia.