Search

Context. L-type ultra-cool dwarfs and brown dwarfs have cloudy atmospheres that could host weather-like phenomena. The detection of photometric or spectral variability would provide insight into unresolved atmospheric heterogeneities, such as holes in a global cloud deck. Indeed, a number of ultra-cool dwarfs have been reported to vary. Additional time-resolved spectral observations of brown dwarfs offer the opportunity for further constraining and characterising atmospheric variability.

Aims. In this paper we present the first results of a detailed spectroscopic and photometric analysis of the $V = 11.7^{\rm m}$eclipsing binary ASAS J052821+0338.5.

We present multi-color photometry and time resolved spectroscopy of OU Vir. The analysis of the quiescent light curve shows that OU Vir is characterized by i) strong cycle-to-cycle brightness variations, and ii) hot spot modulated light curve with grazing eclipse of the impact region. Colors are derived both in- and out- of eclipse. The time-resolved spectroscopy allows us to produce the radial velocity curve from the Hαaccretion disk emission line which possibly reveals only weak evidence for hot spot line emission. The hot spot is believed to be a turbulent optically thick region, producing mostly continuum emission.

APOGEE is a largescale, NIR, highresolution R∼ 20 000 spectroscopic survey of Galactic stars. It is one of the four experiments in SDSSIII. Because APOGEE will observe in the Hband, where the extinction is six times smaller than in V, it will be the first survey to pierce through Galactic dust and provide a vast, uniform database of chemical abundances and radial velocities for stars across all Galactic populations bulge, disk, and halo. The survey will be conducted with a dedicated, 300fiber, cryogenic, spectrograph that is being built at the University of Virginia, coupled to the ARC 2.5m telescope at Apache Point Observatory. APOGEE will use a significant fraction of the SDSSIII bright time during a threeyear period to observe, at high signaltonoise ratio SN> 100, about 100 000 giant stars selected directly from 2MASS down to a typical flux limit ofH< 13. The main scientific objectives of APOGEE are: 1 measuring unbiased metallicity distributions and abundance patterns for the different Galactic stellar populations, 2 studying the processes of star formation, feedback, and chemical mixing in theMilkyWay, 3 surveying the dynamics of the bulge and disk, placing constraints on the nature and influence of the Galactic bar and spiral arms, and 4 using extensive chemodynamical data, particularly in the inner Galaxy, to unravel its formation and evolution. © 2008 WILEYVCH Verlag GmbH & Co. KGaA, Weinheim

We previously reported that methoxychlor administration inhibits the activity of the hepatic, microsomal iodothyronine 5'-deiodinase, form I (ID-I; ). Our data further suggested that the inhibition was due to the covalent binding of a methoxychlor metabolite to a 56-kDa protein identified as ID-I (; ). This protein is 98% homologous to the thiol:protein disulfide oxidoreductase, form Q5 (ERp55;; ). Although at the time there was some controversy, most studies now suggest that ID-I is actually catalyzed by a 27-kDa selenoprotein that does not form adducts with methoxychlor (;; ). Because the 27-kDa protein is considered to be ID-I instead of ERp55, we have further examined the basis for the decreased ID-I activity observed after methoxychlor administration. Male, 150- to 200-g Sprague-Dawley rats were given methoxychlor (0-100 mg/kg/day) in corn oil by gavage for 14 days. ID-I was determined by a thyronine-specific immunoassay. Treated rats showed a significant 15% decline in total hepatic, microsomal protein at all doses. The ID-I-specific activity showed a linear decrease with increasing log doses of methoxychlor. The maximum decrease was 42% at 100 mg/kg/day. The 27-kDa protein specific content declined 37%. In rats given methoxychlor the ratios of the 27-kDa protein mRNA to the 18S ribosomal RNA declined from 2.2 +/- 0.27 x 10(-3) (controls) to 0.99 +/- 0.09 x 10(-3) (100 mg/kg/day). These data suggest that the decreased ID-I observed with chronic methoxychlor administration was due to decreased transcription or stability of the mRNA encoding the 27-kDa protein.

Discusses ways to get more out of DOS memory limitations, and examines the memory-addressing capabilities of the Intel microprocessors. Memory blocks; Expanded PC memory; Differences among expanded-memory boards; Using expanded memory; Expanded memory systems (EMS) without boards; Getting more physical memory; Software. INSET: The 640K-byte solution?;by J. Bertolucci..

Examines Windows 3.1, the latest upgrade to Microsoft's graphical operating system. Discusses its five major areas of improvement. Enhancements; OS/2 2.0 update; Multimedia update.

Offers a look at the technological advances that have led to multimedia abilities. Looks at the computing demands of multimedia and coming products. Standards; Competition.

The mouse is a popular device used in many computer programs ranging from drafting to spreadsheet and word processor. Outlines the three basic mouse types and how they work.

On the basis of inhibition studies of the dealkylation of morphine and norcodeine, George and Tephly concluded that O-dealkylation and N-dealkylation are catalyzed by different enzymes. We have examined the microsomal dealkylation of 3-O-[1'-14Clethylmorphine by measuring HCHO colorimetrically and [1-14C]acetaldehyde radiometrically. We find that the KM for the O-de-ethylation is 57 muM, which is quite close to the KS(71 muM) for the type I binding of ethylmorphine in similar preparations. On the other hand, the KM for N-demethylation was 250 muM. Further, the N-demethylation was stoichiometric with the stimulation of both NADPH-cytochrome P-450 reductase and NADPH oxidase, whereas the sum of the N-demethylation and O-de-ethylation was significantly greater, suggesting that the O-de-ethylase activity does not involve stimulation of either of these two activities. Induction with phenobarbital increaesed N-demethylation 118% but did not affect O-de-ethylation. Finally, D2O inhibited the N-demethylase more than the O-de-ethylase.

We have examined the pharmacokinetic interaction between isradipine and lovastatin in six male and six female, healthy, normotensive, human subjects after a single dose and after treatment for 5 days. The isradipine plasma concentrations were determined by a radioimmunoassay and the lovastatin serum concentrations by gas chromatography-mass spectrometry (GC/MS) and by the inhibition of the 3-hydroxy-3-methylglutaric-coenzyme reductase activity. We found that the apparent serum concentrations of lovastatin were 4- to 6-fold higher in the reductase-inhibition assay than the GC/MS assay, suggesting that the bulk of the reductase inhibition is due to active metabolites. The peak and the time-to-peak concentrations were unaffected by the treatments, either after the first dose or after continued administration. In male subjects, after repeated doses of isradipine, the lovastatin area under the time-concentration curves (AUCs) decreased by 40% as determined by the GC/MS assay (P < .001) and 20% as determined by the reductase-inhibition assay (P < .0022). In the female subjects, isradipine treatment decreased the lovastatin AUCs as determined by the GC/MS assay, but this was not statistically significant due to a high variance. Furthermore, in the female subjects, isradipine had no effect on the lovastatin AUCs as determined by the reductase-inhibition assay. Because the lovastatin peak and the time-to-peak concentrations were unaffected by isradipine treatment, the decreased lovastatin AUCs were probably not due to altered intestinal absorption. More likely, because lovastatin has a high hepatic clearance, the decreased AUCs seen after isradipine treatment could be due to increases in the clearance of lovastatin secondary to increased hepatic blood flow.

• Dilevalol, the R-R optical isomer of labetalol, a nonselective β-antagonist with vasodilation from selective β2 agonism, was administered in sequential multiple bolus intravenous injections of 10 to 100 mg in total doses ranging from 35 to 585 mg (mean dose, 414 mg) to 101 patients with supine diastolic blood pressures above 120 mm Hg. Mean blood pressure was reduced from 200 (±3)/129 (±1) mm Hg to 149 (±2)/101 (±1) mm Hg, a mean reduction of 51/28 mm Hg. The therapeutic goal was established as a reduction in supine diastolic blood pressure to less than 100 mm Hg or a reduction of at least 30 mm Hg. This was achieved in 62 (61%) of 101 patients, with an additional 7 patients having a final supine diastolic blood pressure of 100 mm Hg. Treatment with dilevalol was less successful in black male patients than in the group at large. There was a tendency for older patients to respond better than younger patients. Prior recent treatment of patients with β-adrenergic antagonists decreased the effectiveness of the drug. Significant orthostatic hypotension was not noted. Sixty-four patients were transferred to oral dilevalol treatment in combination with a diuretic, and blood pressure in this group averaged 160/100 mm Hg after 1 month of therapy. Dilevalol appears to be a safe and effective drug that can be used intravenously successfully in the majority of patients with severe hypertension and provides an alternative to therapy with other agents. It also is a useful agent for oral treatment of these patients after successful intravenous therapy.(Arch Intern Med. 1989;149:2655-2661)

Thirteen patients met our criteria for severe acetaminophen hepatotoxicity over a 5-year study period. Six patients had therapeutic misadventures (not attempting suicide), and seven were attempting suicide. Five of six patients in the therapeutic misadventure group were chronic alcoholics, and three were taking other drugs reported to cause hepatic microsomal enzyme induction. In the suicide group, two of seven patients were alcoholics, and one patient was taking another inducing drug. All six patients in the therapeutic misadventure group had nausea, vomiting, or starvation, whereas two of seven patients in the suicide group had similar characteristics. Starvation could deplete the protective factor glutathione, thus augmenting hepatotoxicity. In the therapeutic misadventure group, four of six patients developed acute tubular necrosis, as compared to two of seven in the suicide group. One patient died in each group. Clinicians should be aware of these features as part of the spectrum of acetaminophen toxicity.

We have examined the analysis of pharmacodynamic data in normal subjects receiving propranolol, flecainide or the two together. We find that a second-order polynomial describes accurately the response of the left ventricular ejection fraction, cardiac output and vascular resistance of the subjects to these drugs. Both single dose and multiple doses of propranolol (80 mg 3 times a day) decreased the left ventricular ejection fraction and cardiac output, but increased the vascular resistance. On the other hand, single and multiple doses of flecainide (200 mg twice a day) decreased the left ventricular ejection fraction but did not affect either the cardiac output or vascular resistance. These data demonstrate the power of the polynomial formulation in analyzing pharmacodynamic data.

Nitrofurazone is shown to undergo an initial 1-electron (oxygen-sensitive) or 2- or more electron (oxygen-insensitive) reduction by partially purified nitroreductases from Escherichia coli. Nitrofurazone (50 micronM) is reduced by the oxygen-sensitive reductase to a nitro anion free radical as indicated by ESR and visible spectroscopy. The visible spectrum of the nitro anion free radical is characterized by an increase in absorption at 406 nm. In the presence of the oxygen-sensitive reductase, nitrofurazone stimulates superoxide formation and oxygen consumption. This enzyme gives a steady state radical concentration which is proportional to the square root of the enzyme concentration, suggesting that the nitrofurazone anion radical is an obligate intermediate in the reduction and that the radical decays by a nonenzymatic second order process. The oxygen-insensitive reductase does not form the nitro anion free radical nor in the presence of nitrofurazone does it stimulate oxygen consumption. Visible spectroscopy shows that nitrofurazone is reduced by the oxygen-sensitive reductase to a species with an absorption maximum at 335 nm, which has been previously identified as the amine. The oxygen-insensitive reductase reduces nitrofurazone to a previously identified cyano derivative with an absorption maximum at 280 nm. Rat hepatic microsomes appear to metabolize nitrofurazone in a manner similar to the oxygen-sensitive E. coli reductase.

The hypocholesterolemic cation resins, cholestyramine and colestipol, have variable effects on the absorption parameters of a number of lipophillic, anion drugs. Because of the unpredictable nature of this interaction, we have assessed in human volunteers the effect of these resins on the rate and total absorption of phenytoin. Our results indicate that these resins do not affect the absorption parameters of phenytoin and that special care does not have to be exercised when these agents are co-administered.

To expand on the recent single WFPC2 field obtained in the vicinity of this cluster, we have measured the luminosity function in a one-third by one-half degree field in the LMC with the 40 inch telescope at Siding Spring Observator. Combining our results with recent 4-meter and WFPC2 observations, we examine the constraints on the star formation history of the field from 108to 1010years ago. The simple model derived from the WFPC2 data with and increase in the star formation rate ~3 Gyrs ago fits the combined data. However, this rate increase seems to have been unique. This event notwithstanding, the smooth luminosity function from V = 16 to V = 22 suggests steady star formation rather than a star formation history dominated by intense bursts.

Cigarette smoking is a leading risk factor for atherosclerosis. Endothelial injury may be the initial event in this process. The carcinogenic metabolites of the polycyclic aromatic hydrocarbons found in cigarette smoke tars could cause this injury. We tested this model by examining the effect of 3-methylcholanthrene administration on aortic polycyclic aromatic hydrocarbon metabolism. Immunoblotting with a monoclonal antibody (mAb 1-7-1) specific for cytochromes CYPIA1 and CYPIA2 showed that aortic microsomes from treated, but not from control, animals contained CYPIA1; the CYPIA1 was primarily in the endothelium. Aortic microsomes from induced animals metabolized benzo[a]pyrene (BaP) to the 7R,8S,9,10-tetrahydrotetrol-, 7,8-dihydrodiol-, 1,6 quinone-, 3,6 quinone-, 6,12 quinone-, 3-hydroxy-, and 9-hydroxy-BaP. mAb 1-7-1 inhibited the formation of the tetrahydrotetrol, the dihydrodiol-BaP, and the 3-hydroxy-BaP but did not inhibit the quinones or the 9-hydroxy-BaP. Arachidonic acid did not affect metabolism. These data suggest that the aortas of induced animals metabolize the BaP in cigarette smoke to carcinogenic and toxic products and that this metabolism may initiate vessel injury and lead to the accelerated atherosclerosis seen in cigarette smokers.

In previous studies we have observed that the Km for ethylmorphine N-demethylase was only 50 to 100 microM in the isolated hepatocyte as opposed to 250 to 340 microM in isolated microsomes. These data suggested that either the drug is actively transported into the cell or that the enzymes in the cell had a reduced turnover number. Our current study indicates that ethylmorphine is transported into the hepatocyte with a Km of 250 microM and Tm of 20 nmol/min 10(6) cells. On the basis of temperature and inhibitor studies, this would appear to be active transport. When the turnover number of the ethylmorphine N-demethylase was decreased by reducing the oxygen from 20% of the gas phase to 5%, the activity was partially uncompetitively inhibited with the Km decreasing from 182 to 105 microM. The Vm decreased from 1.85 nmol/min 10(6) to 0.71 nmol/min 10(6) cells. These data suggest that the low Km we initially observed was probably due to active transport of the substrate into the hepatocyte. Further, our observations indicate that the effects of oxygen pressure on the kinetic parameters should be considered in predicting in vivo kinetics from in vitro studies.

Plots of reciprocal initial rate of formaldehyde formation as a function of reciprocal ethylmorphine concentration provide parallel lines for oxygen concentrations ranging from 5.41 to 211 microM, and the apparent Km values for ethylmorphine at these extremes are 167 and 417 microM, respectively. Similarly, the apparent Km for O2 decreases from 7.69 microM at 2 mM ethylmorphine to 3.64 microM at 0.2 mM ethylmorphine. Reciprocal plots of 1/Km app and 1/Vm for ethylmorphine against 1/[O2] give Km values for O2 of 9.35 microM and 9.09 microM, respectively. Similar plots give Km values for ethylmorphine of 0.28 mM and 0.36 mM. Similarly, NADH causes an uncompetitive stimulation. These data suggest that hepatic microsomal ethylmorphine N-demethylase follows parallel plot sequential kinetics. These results, along with studies of other workers, suggest that cytochrome P-450 forms an active complex with O2 which is stable for at least many milliseconds.

Numerous in vitro studies have indicated that acetaminophen is activated by mouse hepatic microsomal cytochrome P450 to form N-acetylbenzoquinone imine. This in turn covalently binds through a Michael addition to protein sulfhydryl and amino groups. Although acetaminophen adducts of several cytosolic proteins have been purified after its administration in vivo, no adducts of specific microsomal proteins have been reported. We find that, after the in vitro incubation of mouse hepatic microsomes with [ring-¹⁴C]acetaminophen in the presence of an NADPH generating system, 95% of the bound radioactivity was associated with adducts to three intraluminal microsomal proteins:  calreticulin and the two forms of thiol:protein disulfide oxidoreductase, Q2 and Q5. The acetaminophen bound to 0.35, 1.32, and 0.25 mol/mol of the three proteins, respectively. Sequencing of the ¹⁴C-labeled tryptic peptides indicated that the acetaminophen bound to lysine 103 of Q2, lysines 202, 209 or 210 and 354 of Q5 and lysines 233 or 239 of calreticulin. No adducts of cysteine residues were observed. Our data might suggest that acetaminophen hepatotoxicity results from the formation of the reactive metabolite within the endoplasmic reticulum. This then binds to these essential proteins and blocks the posttranslational modification of secretory and membrane proteins. This inhibition could then lead to cellular injury and death.

The authors have determined the binding parameters for [14C] lidocaine to several preparations of purified human serum alpha 1-acid glycoprotein (AAG) and human serum albumin (HSA). The authors find that the average Kd for the three different purified AAG preparations was 15.2 +/- 0.5 microM, with an average of 0.567 +/- 0.009 binding sites (N) per AAG molecule, when the concentration of AAG was determined by a standard colorimetric protein assay. The number of binding sites per AAG increased to 0.99 +/- 0.06 when the concentration of AAG was determined immunologically. On the other hand, delipidized AAG had a Kd of 28.0 microM, with an N of 1.72 based on the immunological assay. Various preparations of HSA had Kd/N values ranging from 4.3 to 17.3 mM. The number of binding sites per HSA molecule could not be determined because the maximum concentration of lidocaine that can be used is 10 mM, which is only approximately equal to the Kd. The Kd to HSA was so low and the capacity so high that, at therapeutic concentrations, the binding was in the linear range. Solutions containing both purified AAG and HSA had Kd values of 30.2 +/- 1.8 microM, with 2.01 +/- 0.04 binding sites per AAG molecule. With HSA and delipidized AAG, the Kd was 60 microM, with 3.16 sites per delipidized AAG molecule. This increase in the binding parameters appeared to be due to a direct interaction between the two proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

The mechanism of the azo reduction of sulfonazo III and amaranth by the rat hepatic monooxygenase system was studied. Air strongly inhibited (greater than 95%) the enzymatic reduction of both azo compounds; a 100% CO atmosphere inhibited amaranth reduction (greater than 90%) but only slightly inhibited sulfonazo III reduction (13%). The addition of 50 microM sulfonazo III to microsomal incubations stimulated oxygen consumption, NADPH oxidation, and adrenochrome formation, whereas 100 microM amaranth did not. The reduction potentials of these two azo compounds were also very different (amaranth, E = -0.620 V; sulfonazo III, E = -0.265 V versus normal hydrogen electrode). The organic mercurial mersalyl converted cytochrome P-450 to cytochrome P-420 (68%) and markedly decreased NADPH-cytochrome P-450(c) reductase activity (97%) in microsomal preparations, presumably by inactivating or destroying functional sulfhydryl groups important for the catalytic activity of these enzymes. GSH was used to restore, and NADP+ to protect, the activities of the monooxygenase components from the effects of mersalyl. The data indicate that inactivation of NADPH-cytochrome P-450(c) reductase inhibits sulfonazo III and amaranth reduction, whereas inactivation of cytochrome P-450 inhibits only amaranth reduction. Furthermore, the reduction of sulfonazo III by purified microsomal NADPH-cytochrome P-450(c) reductase was significantly faster than the rate of reduction of amaranth. These studies demonstrate that two distinct sites of azo reduction exist in the monooxygenase system and that not all azo compounds are reduced by cytochrome P-450.

We have previously found that for acetaminophen kinetic differences exist between the hepatic microsomal catalyzed protein binding and cysteine conjugation. We have also observed that the protein binding of acetaminophen is only to intralumenal proteins. Together these data suggested that two pools of the reactive metabolite, N-acetyl-p-benzoquinone imine (NABQI), are formed during the oxidative metabolism of acetaminophen: one on the cytosolic surface and the other within the lumen of the microsomes. This would indicate that some of forms of cytochrome P450 (CYP) catalyzing NABQI formation have their active site on the cytosolic surface and others on the lumenal surface. We have examined this question by comparing the rates of cysteine conjugation and protein binding of acetaminophen by microsomes from lymphoblasts transfected with the cDNAs for human CYPs. We found that CYP2D6 catalyzed only cysteine conjugation; CYP1A2 and 3A4 catalyzed only protein binding; CYP2E1 catalyzed both; and CYP1A1, CYP2A6 and CYP2B6 catalyzed neither. These data suggest that CYP2D6 has its active site only on the cytosolic surface; CYP1A2 and CYP3A4 only on the lumenal surface; and CYP2E1 has catalytic sites on both the lumenal and cytosolic surfaces of the membrane. In mouse studies we have found that ethanol administration increased acetaminophen protein binding by 265% but cysteine conjugation by only 61%. CYP2E1 and CYP2B increased, whereas CYP3A decreased and the others did not change. These data suggest that in control mice CYP2E1 catalyzes the bulk of protein binding, whereas CYP2D catalyzes slightly more cysteine conjugation than does CYP2E1.

The authors have recently found that the hepatic, microsomal ATP-dependent Ca++ pump activity is decreased through oxidation by cytochrome P-450-generated reactive oxygen species. This inhibition is reversed by reduced glutathione and only partially reversed by reactive oxygen scavengers. In view of these observations, the authors have sought to determine whether norepinephrine could regulate the Ca++ pump by differential modulation of the oxidative and reductive pathways. They find that, in the presence of superoxide dismutase (15 micrograms/ml), catalase (65 micrograms/ml), reduced glutathione (5 mM) and NADP+ (0.39 mM), the pump activity was maximal 142% of no norepinephrine at 10(-11) to 10(-10) M norepinephrine and decreased with increasing concentrations of norepinephrine. NADPH had no effect on uptake at 10(-11) M norepinephrine, but, between 10(-10) and 10(-8) M norepinephrine, it significantly decreased uptake compared with NADP+. At 10(-7) to 10(-6) M norepinephrine, with either NADP+ or NADPH, the uptake was significantly lower than at other norepinephrine concentrations. This decrease in the uptake seen at 10(-7) to 10(-6) M norepinephrine disappeared on the addition of 0.25 microM l-(S)-propranolol. The NADPH inhibition of the pump was blocked by imidazole-histidine buffer but not by inhibitors of mitochondrial metabolism. ATP and norepinephrine had little effect on mitochondrial uptake. These studies suggest that norepinephrine may modulate the hepatic, microsomal ATP-dependent Ca++ pump through alterations in the balance between oxidative and reductive pathways.

A sensitive and convenient radioassay for the in vitro determination of ethylmorphine N-demethylase and O-de-ethylase activity has been developed. Ethylmorphine[6-3H] was prepared by reduction of the corresponding morphinone in nearly quantitative yield. After incubation with hepatic microsomes from male rats, the reaction was terminated by the addition of 5 ml of acetone. The sample was saturated with potassium acetate and extracted twice with acetone giving complete extraction of the radiolabeled ethylmorphine and its metabolites. After the combined organic phases were evaporated, the samples were dissolved in methanol and applied to a Silica Gel GF plate with subsequent development in ethyl acetate-methanol-concentrated NH4OH. The amount of radioactivity detected for the morphine and norethylmorphine bands at zero time was approximately 0.05% of the original amount of labeled ethylmorphine added to the incubation media. Similarly, the Km values were 52 and 250 microns for the O- and N-dealkylation respectively, while the Vmax values were 5.0 and 1.8 nmol/mg of protein per min. Finally, with this assay we have observed constant specific activity for both the N- and O-dealkylation of ethylmorphine[6-3H] with as little as 10 micrograms of microsomal protein per ml of incubation media.

Previous in vivo and in vitro studies have indicated that the Km for phenytoin hydroxylation is about 30 microM. Yet, the drug shows dose-dependent kinetics suggesting a Km of about 5 microM. The present studies indicate the discrepancy is not due to active transport of the drug in the hepatocyte or a decrease in the Km due to the low pO2 of the portal vein leading to uncompetitive inhibition. Studies in both hepatocytes and microsomes indicate the presence of a high affinity hydroxylase with a Km of 2 to 5 microM. These data suggest that this enzyme is the one primarily involved in the metabolism of phenytoin.

The proto-planetary nebula, CRL 2688, has been imaged through a wideband filter centered at 606 nm (F606W) with the Wide Field Planetary Camera 2 onboard the HubbleSpaceTelescope. CRL 2688 is the prototypical bipolar reflection nebula in which a star is surrounded by a dense, flattened cocoon of dust seen nearly edge-on and starlight escapes preferentially along the polar directions producing a pair of bright nebulosities, one above and one below the equatorial plane. We find a pair of radial "searchlight beams" emerging from within the dusty cocoon which intersect at the position expected for the central star when extrapolated inside the cocoon. The beams are crisscrossed by a large number of roughly round arcs with their center of curvature in the vicinity of the central star. The arcs are not systematically elongated along the polar axis of the nebula, as would be expected in the current model of CRL 2688 where the nebular density decreases with latitude.

Mixed-function oxidase activity, when measured by the N-demethylation of ethylmorphine or the hydroxylation of aniline, is significantly higher in the smooth hepatic endoplasmic reticulum than in the rough. In the rabbit the smooth membrane/rough membrane activity ratios are significantly greater than 1 whether the activities are expressed per g. of liver (ratio 5), per mg. of protein (ratio 3–5), per μg. of phospholipid phosphorus (ratio 2), per unit of cytochrome P-450 (ratio 1·7) or per unit of NADPH–cytochrome c reductase activity (ratio 2). On the other hand, if the activities are normalized to the NADPH–cytochrome P-450 reductase, there is no significant difference between the rough and smooth membranes. These results suggest that, in the rabbit, the rate-limiting step is the reduction of cytochrome P-450. In contrast, in the rat the difference in activities can be explained by differences in the concentration of cytochrome P-450.

The problem of sensitivity of specified terminal conditions to parameter variations is examined for three types of optimal systems: 1) open loop control 2) closed loop (feedback) control 3) closed loop control for trajectories neighboring an optimal open loop control trajectory. A method is proposed and illustrated for including the specification of sensitivity in open loop design. This is in contrast to analyzing sensitivity after the design has been completed. Open loop controls have some disadvantages from a sensitivity viewpoint. First of all, placing a constraint on the sensitivity will generally result in degradation of the performance. Furthermore, it may not even be possible to constrain the sensitivity to certain parameters. Closed loop controls would be expected to have superior sensitivity properties. Indeed it is proved that for a class of linear feedback systems, there is a finite range of parameter variations which have no effect on the terminal conditions. Furthermore, any bounded changes in some parameters have no effect on the terminal conditions. The results for the linear feedback laws are also applicable to neighboring optimal control systems at least in the case of small parameter variations.

Covers recent developments in personal computer hardware and software, and how the virtual PC is evolving. Looks at Microsoft's Windows 3.1, IBM's OS/2 2.0, and Intel's new X86 family of chips.

Offers a look at several new and on-the-horizon computer industry products and services. Includes the Personal Digital Assistant (PDA), the Virtual Press Conference and the Dycam Digital Still Camera Model 1. Developers; Uses; Prices.

Looks at the latest happenings in the computer industry and their implications. Includes: A ten-year agreement between IBM and Intel to design new 80x86 ICs; The formation of the trade association Power Open by IBM, Apple and Motorola; LAN-tastic 4.0 small-office network.

Examines the evolution and the use of pen-based computers, which were developed at Xerox Palo Alto Research Center (PARC) in 1968, by Alan Kay. The typical pen-based machine is the size of a notebook PC and uses its screen for both input and output. Hardware; Software; Operation-related products.

Offers a look at recent happenings in the computer industry including: software updates by IBM, Apple and Microsoft; the Novell acquisition of Digital Research; release of the SAA7199 multi-standard video encoder chip.

Opinion. Explains the author's bias against the Amiga PC and his favoritism toward IBM-compatible machines. Also comments on recently released PC products.

Discusses how the release of Windows 3.0 software nearly a year ago has impacted virtually all other software. Looks at the resulting good and bad products, including Windows 3.1, Excel 3.0 and BeckerTools 2.0. INSET: XGA update (IBM's new XGAvideo adapter).;Chips ahoy! (AM386....

Traces the evolution of video terminals and personal computers. Performance; Interfaces; Color and pixels; PC video modes; Resolution; Future outlook. INSET: Hercules' graphics station card..

Opinion. Traces the evolution of standards in radio electronics and relates it to the development of personal computers and their software.