Oversight of the Trade Act of 1988 : hearing before the Committee on Finance, United States Senate, One Hundred First Congress, first session.

Item 1038-A, 1038-B (MF).

Special analyses, budget of the United States Government.

Report covers fiscal year.

Upper Mississippi River navigation charts.

Includes maps of the Mississippi River above Cairo, Ill., and its tributaries.

Partners in flight : strategic plan.

Shipping list no.: 95-0092-P.

U.S. Marines at Twentynine Palms, California /

Includes bibliographical references.

Light Vehicle Obscuration Smoke System (LVOSS).

Mode of access: Internet.

Market based transit facility design : final report /

"DOT-T-89-12."

Imaging features of ocular adnexal lymphoproliferative disease

Purpose To evaluate the imaging characteristics of a cohort of patients with ocular adnexal lymphoproliferative disease (OALD). Methods A noncomparative retrospective review between 1992 and 1995 and prospective study from 1995 to 2005 of the clinical, imaging and treatment of 105 patients presenting to tertiary orbital referral centre presenting with OALD. Results One hundred and five patients (mean age 61 years, range 11-90 years) with equal gender distribution were included. Fifty-three were primary and 52 were secondary. Computed tomography (CT) usually showed a well-circumscribed lesion of greater than brain density, moulding to adjacent tissues with moderate enhancement. Aggressive histology was associated with bone destruction, while moulding was associated with indolent histology (P < 0.005). MRI in OALD showed intermediate signal intensity on T1- and T2-weighted images and moderate enhancement with gadolinium. Gallium scanning sensitivity to detect ocular adnexal disease was 25 and 57% for systemic involvement. Positron emission tomography (PET) upstaged (71%) of patients with systemic lymphoproliferative involvement, having a higher sensitivity than CT in detecting distant disease (86 vs 72%). Conclusions CT and/ or MRI are essential in the evaluation of OALD and can be used to establish that an orbital lesion may be lymphoprolifetaive in nature. Further, these imaging modalities may predict the behaviour of the lymphoma in certain cases. Gallium scanning provides no additional information to CT and does not influence patient treatment. PET represents an important addition to the assessment of OALD with real impact on patient management.

Heteronormativitet och homonationalism : En kritisk diskursanalys av Sverigedemokraternas hbtq-politik

I uppsatsen görs en kritisk diskursanalys ur ett hbtq-perspektiv av Sverigedemokraternas styrdokument, den partianknutna tidningen SD-Kuriren och några andra relevanta texter. Materialet har delats in i tre tidsperioder, 1989-1995, 1996-2002 och 2003-2015 och frågorna som ställs till materialet handlar om vilka problem, orsaker till problem och lösningar på problem som går att identifiera som centrala i de studerade texterna. De identifierade problemen under de olika perioderna är ”den låga nativiteten”, ”osundheten” och ”den hotade kärnfamiljen; samt ”den hotade kärnfamiljen och den därmed hotade nationen”. Alla dessa problem kan kopplas ihop med Sverigedemokraternas hbtq-politik. I ett andra steg i uppsatsen görs en kvantitativ studie över frekvensen av ett antal ur det studerade perspektivet centrala ord i partiets styrdokument och hur användningen av dessa ord varierar över tid. De studerade orden är sund, familj, naturlig, nation, moral, folk och nativitet. Ett par av resultaten är att användningen av ordet ”nation” är som mest frekvent i det senaste styrdokumentet, medan ordet ”sund” var mest vanligt under den mittersta av de studerade perioderna. I analysens sista del görs utblickar mot Sverigedemokraternas agerande på det hbtq-politiska området, under de senaste åren. Med hjälp av begreppen heteronormativitet, homonormativitet och homonationalism görs avslutningsvis ytterligare en läsning av texterna där exempel på alla dessa företeelser går att identifiera i materialet.

Activation of calcium-sensitive potassium channels in L6 skeletal myocytes by arginine vasopressin requires extracellular calcium

The effects of extracellular application of arginine vasopressin (AVP) upon membrane currents in L6 skeletal myocytes was investigated using the whole-cell configuration of the patch-clamp technique. At O mV AVP produced large amplitude, transient outward currents that reversed when the clamping potential was changed to -100 mV (negative to EK) The effects of alterations in the extracellular K+ concentration upon the current reversal potential suggested that the current elicited by AVP was carried mainly by K+ ions. Intracellular dialysis with 10 μM inositol 1,4,5-trisphosphate (InsP3) elicited similar currents but only in 6/14 cells. Inclusion of 5 mg ml-1 heparin in the intracellular solutions was ineffective at inhibiting the current responses to AVP. The AVP-induced current was totally abolished when the intracellular EGTA concentration was increased from 0.05 mM to 10 mM or Ca2+ was removed from the extracellular perfusing solution. These results suggest that AVP produces activation of a Ca2+-sensitive K+ conductance in L6 skeletal myocytes by a process dependent upon extracellular Ca2+ and not intracellular Ca2+ release. © 1995 Academic Press. All rights reserved.

Characterization of a volume-sensitive chloride current in rat osteoblast-like (ROS 17/2.8) cells

1. During osmotic swelling, cultured osteoblastic cells (ROS 17/2.8) exhibited activation of large amplitude Cl- currents in the whole-cell configuration of the patch-clamp technique. Effects of hypotonic shock on cell volume and membrane conductance were rapidly reversed on return to isotonic conditions. 2. Voltage command pulses in the range -80 to +50 mV produce instantaneous activation of Cl- currents. At potentials more positive than +50 mV the current exhibited time-dependent inactivation. The instantaneous current-voltage relationship was outwardly rectifying. 3. The anion permeability sequence of the induced current was SCN- (2.2) > I- (1.9) > Br- (1.5) > Cl- (1.0) > F- (0.8) > gluconate- (0.2). This corresponds to Eisenman's sequence I. 4. The volume-sensitive Cl- current was effectively inhibited by the Cl- channel blockers 4,4'-diisothiocyanatostilbene-2,2-disulphonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB). Outward currents were more effectively suppressed by DIDS than inward currents. The concentrations for 50% inhibition (IC50) of outward and inward currents were 81 and 298 μM, respectively. NPPB was equally effective at inhibiting outward and inward currents (IC50 of 64 μM). The current was relatively insensitive to diphenylamine-2-carboxylate (DPC), 500 μM producing only 22.5 ± 4.0% inhibition. 5. Inhibitors of protein kinase A (H-89, 1 μM) and tyrosine kinase (tyrphostin A25, 200 μM) were without effect upon activation of Cl- currents in response to hypotonic shock. Under isotonic conditions, elevation of intracellular Ca2+ by ionomycin (1 μM) or activation of protein kinase C by 12-O-tetradecanoylphorbol 13-acetate (TPA, 0.1 μM) failed to evoke increases in basal Cl- conductance levels. 6. It is concluded that an outwardly rectifying Cl- conductance is activated upon osmotic swelling and may be involved in cell volume regulation of ROS 17/2.8 cells.

Studies on the neurotoxicity of 6,7-dihydroxy-1-methyl-1,2,3,4-tetrahydroisoquinoline (salsolinol) in SH-SY5Y cells

We have studied the hypothesis that 6,7-dihydroxy-1-methyl-1,2,3,4-tetrahydroisoquinoline (salsolinol) is neurotoxic. Salsolinol induced a significant time and dose related inhibition of 3[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide; thiazoyl blue (MTT) reduction, and increased lactate dehydrogenase release (LDH) release from human SH-SY5Y neuroblastoma cells, at concentrations within the range of 1-methyl-4-phenylpyridinium (MPP+) cytotoxicity, in vitro. Cytotoxicity was not inhibited by the addition of antioxidants, monoamine oxidase inhibitors or imipramine. In confluent monolayers, salsolinol stimulated catecholamine uptake with EC50 values of 17 muM and 11 muM, for noradrenaline and dopamine, respectively. Conversely, at concentrations above 100 muM, salsolinol inhibited the uptake of noradrenaline and dopamine, with IC50 values of 411 muM and 379 muM, respectively. The inhibition of catecholamine uptake corresponded to the increase displacement of [3H]nisoxetine from the uptake 1 site by salsolinol, as the Ki (353 muM) for displacement was similar to the IC50 (411 and 379 muM) for uptake. Salsolinol stimulated catecholamine uptake does not involve the uptake recognition site, or elevation of cAMP, cGMP, or inhibition of protein kinase C. Salsolinol also inhibited both carbachol (1 mM) and K+ (100 mM, Na+ adjusted) evoked released of noradrenaline from SH-SY5Y cells, with IC50 values of 500 muM and 120 muM, respectively. In conclusion, salsolinol appears to be cytotoxic to SH-SY5Y cells, via a mechanism that does not require uptake 1, bioactivation by monoamine oxidase, or membrane based free radical damage. The effects of salsolinol on catecholamine uptake, and the mechanism of toxicity require further investigation.

Characterization of tumour necrosis factor alpha release by human granulocytes in response to procainamide challenge

The role of human granulocytes in the promotion of procainamide (PA) toxicity in vitro has been studied and one of the agents responsible for DNA strand scission and cell death in human target cells has been characterized. Crude peripheral blood mononuclear cells (cPBMNs) isolated by density centrifugation, and the lymphocyte cell lines--CCRF-HSB2 and WIL-2NS--were exposed to PA, and DNA strand breaks were quantified by fluorescent analysis of DNA unwinding. Therapeutic plasma concentrations of PA (0-50 microM) caused dose-dependent cytotoxicity, determined by dye exclusion, and strand breaks in cPBMNs incubated for 3 and 1.5 hr at 37 degrees, respectively. Using 50 microM PA a five-fold increase in DNA strand breaks was observed after 1.5 hr, with significant induction of strand breaks also being observed for 10 and 25 microM concentrations. Toxicity was much reduced in lymphocyte cell lines (maximal killing = 3.0% at 50 microM PA compared with 13.2% in cPBMNs). A similar decrease in toxicity was observed where N-acetyl procainamide (NAPA) was substituted for PA (less than 50% of strand breaks at all concentrations). Further investigations showed that the presence of a contaminating granulocyte population in the cPBMN fraction was responsible for the induction of PA toxicity. Incubation of a highly enriched granulocyte population with PA for 1 hr prior to exposure to purified peripheral blood mononuclear cells (pPBMNs) led to the complete restoration of the toxic effects. The resulting cyto- and genotoxicity were not significantly different to levels observed in cPBMNs. Significantly, incubation of granulocytes with NAPA did not induce toxicity in target pPBMNs. Ultrafiltration of granulocyte supernatants led to the identification of two toxic fractions of < 3000 and > 30,000 Da. Temporal studies showed that the toxicity associated with the < 3000 Da fraction appeared during the first 10-15 min incubation with PA whereas the > 30,000 Da fraction did not display significant toxicity until the 40-60 min period. Further assessment of the nature of these agents indicated that the 30,000 Da fraction was a protein. SDS-PAGE analysis showed an inducible 17,800 Da species appearing in granulocyte supernatants after 40 min incubation with PA. Dot blot analysis indicated that tumour necrosis factor alpha (TNF alpha) was present in the > 30,000 Da fraction. Evidence that TNF alpha was the high-molecular weight species responsible for PA-induced toxicity was obtained from neutralization assays employing an anti-TNF alpha antibody.(ABSTRACT TRUNCATED AT 400 WORDS)