TADF and exciplex emission in a xanthone-carbazole derivative and tuning of its electroluminescence with applied voltage.

Materials showing white light emission have found applications in a variety of solid state devices especially in display technology. For white light emission, doping of red (R), green (G) and blue (B) emitters in a host matrix is commonly practised. However, finding RGB emitters of similar stability with homogenous doping is challenging. Furthermore, such devices suffer from color purity in the long run. Small organic light emitters, capable of colour tuning and having a broad emission spectrum are in high demand as they provide colour stability, reproducibility, a simple device geometry and high efficiency. Recently, it has been shown that the efficiency of OLEDs can be enhanced by employing thermally activated delayed fluorescence (TADF) materials. Here, we designed and synthesised a xanthone-carbazole based D-A-D material (Xan-Cbz) for TADF properties. Blue TADF emission, in neat thin films, at 470 nm was observed and further investigated by studying delayed fluorescence and lifetime measurements. In addition, a blend of Xan-Cbz with NPD shows exciplex emission at 525 nm in thin film. OLEDs based on Xan-Cbz were fabricated using several device configurations. OLEDs having the device configuration ITO/PEDOT:PSS/NPD/Xan-Cbz/Bphen/LiF-Al showed a luminance of 1.96 × 104 Cd m-2 (at a current density of 50 mA cm-2) and V ON at ∼6 V. Electroluminescence showed the features of both neat emission (470 nm) of Xan-Cbz and its exciplex (525 nm) with NPD. Further, colour tuning was observed as a function of applied voltage and the ratio of light intensity (I 525/I 470) of neat and exciplex emission was found to decrease with increasing voltage. Greenish-blue emission (CIE coordinates: 0.202, 0.382) from Xan-Cbz OLEDs was obtained. Xan-Cbz showed its neat emission (at 470 nm) in ITO/PEDOT:PSS/CBP/Xan-Cbz/Bphen/LiF-Al and pure exciplex emission (at 525 nm) in ITO/PEDOT:PSS/NPD:Xan-Cbz/Bphen/LiF-Al device configurations. Thus in this article we showed blue TADF emission, exciplex emission and voltage dependent color tuning in OLEDs based on a small organic emitter.

Aortic insufficiency and mitral regurgitation in patients with systemic lupus erythematosus and the antiphospholipid syndrome.

PURPOSE, PATIENTS, AND METHODS: Heart disease has not been well characterized in patients with systemic lupus erythematosus (SLE) and the antiphospholipid syndrome. During a prospective study of cerebrovascular disease in autoimmune disease and SLE, 11 lupus patients were identified with an antiphospholipid syndrome characterized by significant cardiac valvular disease in addition to cerebral infarction, deep vein thromboses, and thrombocytopenia. Patients were reviewed for criteria for systemic lupus and underwent echocardiographic studies and measurements of anticardiolipin antibodies, VDRL, and the lupus anticoagulant. RESULTS: Eight of the 11 patients had aortic insufficiency, two of whom had associated mitral regurgitation. Three patients had mitral regurgitation alone. Microscopic analysis of a surgically excised aortic valve indicated typical Libman-Sacks verrucous endocarditis. Infective endocarditis was ruled out in all patients. CONCLUSION: This report expands previous descriptions of antiphospholipid syndromes by describing a subset of lupus patients with significant aortic and mitral valvulitis in addition to circulating antiphospholipid antibodies, thrombocytopenia, and recurrent thromboses.

Alternative complement pathway in hypocomplementemic/normal C1s-C1 inhibitor complex patients with SLE.

To test whether alternative complement pathway activation explains normal C1s-C1 inhibitor complex in hypocomplementemic (low CH50cl) patients with systemic lupus erythematosus, we examined alternative pathway hemolytic complement (CH50alt) factor B, and Ba fragment in hypocomplementemic sera with normal and with elevated C1s-C1 inhibitor complex. Sera with and without high C1s-C1 inhibitor complex were similar in CH50cl, C3, and C4. There was little evidence for important alternative complement pathway activation in either group, but patients with classical pathway activation (elevated C1s-C1 inhibitor complex) had slightly lower CH50alt and slightly higher factor B and Ba compared to patients with normal C1s-C1 inhibitor complex. Pregnant patients did not differ from non-pregnant patients. Alternative complement pathway activation does not account for hypocomplementemia in this group of patients.

Pregnancy in systemic lupus erythematosus.

Experience with more than 150 pregnancies of women with systemic lupus erythematosus demonstrates that: many conventional measures of lupus activity, including complement, platelet count and urinary protein, are invalid during pregnancy; pregnancy does not cause lupus exacerbation; anti-phospholipid antibody is common and is closely associated with fetal loss, but is not the sole determinant factor of fetal loss; specific characteristics of anti-phospholipid antibody do not identify which antibody-positive women will have poor fetal outcome; prednisone therapy does not improve fetal prognosis; and neonatal lupus, diagnosed by rash and thrombocytopenia, is common but congenital heart block is rare.

Hazards of lupus pregnancy.

Fetal death occurs in about 1/3 of pregnancies in patients with systemic lupus erythematosus (SLE). It is largely predicted by lupus anticoagulant (estimated by activated partial thromboplastin time) and/or antibody to cardiolipin. These antibodies are not synonymous. Neonatal lupus appears in a minority of infants born to women with antibody to the Ro/La antigens. Hypocomplementemia is common in SLE pregnancies, as in pregnancy induced hypertension. Lupus exacerbation is uncommon either during or after pregnancy. Prematurity and fetal death are the greatest hazards.

Prednisone does not prevent recurrent fetal death in women with antiphospholipid antibody.

Effects of therapy, antibody titer, and pregnancy history on pregnancy outcome were evaluated in pregnancies of women with antiphospholipid antibody. Prior fetal death and a high antiphospholipid antibody titer (greater than 40 IgG phospholipid units) contributed independently, in an additive manner, to current fetal loss. Twenty-one pregnancies occurred in asymptomatic women who had both prior fetal death and a high IgG antiphospholipid antibody titer. In this very high-risk group, 9 of 11 (82%) of pregnancies treated with prednisone, 10 to 60 mg/day, ended in fetal death, compared with 5 of 10 (50%) not treated with prednisone (p approximately 0.01, life-table analysis). Of pregnancies treated with aspirin, 80 mg/day, 9 of 14 (64%) treated and 5 of 7 (71%) not treated with prednisone had a fetal death (difference not significant). Prednisone does not improve, and may worsen, current fetal outcome in asymptomatic pregnant women with a high antiphospholipid antibody titer and prior fetal death.

Corticosteroid use and abuse by medical practitioners for arthritis and related disorders in Pakistan.

A total of 256 consecutive patients attending our out-patient clinic in Islamabad, Pakistan, with complaints of pain in or around the joints were evaluated for use of corticosteroids prescribed by medical practitioners they had seen earlier. The appropriateness of such prescriptions and their consequent effects were assessed. Of the 256 patients, 110 (i.e. 42.5%) were identified as steroid users; some of them were suffering from conditions known to be unresponsive to this form of therapy. One hundred and one of the 256 patients had rheumatoid arthritis and 67% of these had been using steroids, mostly in an irrational manner. The general practitioners and consultants (all non-rheumatologists) were responsible for the majority of steroid prescriptions. Steroid side-effects were observed in 42/110 (38.2%) cases. This prevalent practice in Pakistan is a reflection of the state of affairs in developing countries, and indicates a need for improvement and better regulation of health care in such countries.

Hypocomplementemia with low C1s-C1 inhibitor complex in systemic lupus erythematosus.

Ninety-three serum and plasma samples from 45 patients with systemic lupus erythematosus were analyzed for the complex formed by C1s and its inhibitor, as well as for C3, C4, C4a desarginine, and staphylococcal protein A-bound immune complexes. There were statistically significant correlations between C1s-C1 inhibitor complex and CH50, between C1s-C1 inhibitor complex and C4, and between C1s-C1 inhibitor complex and C4a desarginine. Serial studies were performed on 24 patients over a period of 6 months. Seven of 21 patients with hypocomplementemia had persistently normal levels of C1s-C1 inhibitor complex, 7 had transiently abnormal levels of C1s-C1 inhibitor complex, and 7 had sustained abnormal levels of C1s-C1 inhibitor complex. Two of 3 pregnant patients with normal levels of complement had abnormal levels of C1s-C1 inhibitor complex. Staphylococcal protein A-bound immune complexes demonstrated no correlation with any of the complement assays. Complement activation, as measured by C1s-C1 inhibitor complex, is often a transient phenomenon in systemic lupus erythematosus patients with persistent hypocomplementemia.

Characteristics of high-titer IgG antiphospholipid antibody in systemic lupus erythematosus patients with and without fetal death.

Although high-titer IgG antiphospholipid antibody (aPL) is a predictor of mid-pregnancy fetal death in women with systemic lupus erythematosus (SLE), some SLE patients with high-titer aPL carry pregnancies normally, and to term. To determine potential antibody differences between IgG aPL-positive women with and without fetal death, we studied aPL isotype, subclass, anticoagulant activity, phospholipid specificity, and antibody avidity in selected sera from pregnant SLE patients with high-titer IgG aPL. For controls, we selected sera from pregnant SLE patients who had negative results on tests for IgG aPL (with and without fetal loss). None of the specified antibody characteristics distinguished between the aPL-positive patient groups, nor were other specificities defined in IgG aPL-negative sera from women with fetal death. Although high-titer aPL is a good predictor of fetal death, currently known characteristics, other than a high titer of aPL, do not identify which women will experience this complication.

Lysophosphatidylethanolamine is the antigen to which apparent antibody to phosphatidylethanolamine binds.

Because binding of antiphospholipid antibody (aPL) to phosphatidylethanolamine (PE) is central to the definition of the antigenic epitope targeted by aPLs, we examined the binding of aPL-positive SLE sera to PE under various conditions. No serum bound to PE uncontaminated with lysophosphatidylethanolamine (1PE), but many aPL-positive sera bound to 1PE-contaminated PE and to 1PE coated onto an ELISA plate. Absorption studies indicated partial cross-reactivity between PE containing 1PE and cardiolipin. We conclude that clinical aPLs do not bind to PE. Prior reports to the contrary most likely represent binding of aPL to PE's degradation product, 1PE.

IgG but not IgM anti-phospholipid antibody binding is temperature dependent.

We examined the effect of temperature on the measurement of enzyme-linked immunosorbent assay (ELISA)-defined human polyclonal antiphospholipid antibody. Both IgG and IgM antibodies were easily demonstrable when sera were incubated on phospholipid-coated ELISA plates at 4-22 degrees C. When incubations were done at 37-45 degrees C IgG antibody binding markedly decreased but IgM antibody binding did not. Warming the phospholipid-coated ELISA plate alone, the serum alone, the buffer alone, or the blocking reagent alone had no effect. When the antigen content of the wells was increased fourfold the effect of warming still occurred. The effect of warmth was reversible and was seen with affinity-purified antibody as well as with whole serum. Phospholipid vesicles in suspension, however, absorbed antibody in a dose-dependent fashion at 4, 22, and 42 degrees C. These results indicate that antibody binding to phospholipid is temperature dependent when phospholipid is adherent to the solid phase. Whether the change in IgG-phospholipid interaction results from a change in antigen or in antibody remains unknown.

Antibody to cardiolipin, lupus anticoagulant, and fetal death.

We compared the concordance and predictive powers of activated partial thromboplastin time (APTT) and of IgG and IgM antibody to cardiolipin (aCL), for predicting fetal death in 50 pregnant women with systemic lupus erythematosus (SLE) and/or lupus anticoagulant. Overall concordance of any abnormal determination of aCL during pregnancy with any abnormal determination of APTT was 76% (0.05 less than p less than 0.10). Fetal death occurred in 6/12 (50%) of patients with high APTT compared to 5/20 (16%) of patients with low APTT; fetal death occurred in 10/13 (77%) of patients with abnormal aCL and in 2/37 (5%) of patients with normal aCL. Sensitivity for predicting fetal death was .55 for APTT and .85 for aCL; specificity was .81 for APTT and .92 for aCL. Abnormalities of APTT and aCL are sufficiently frequently discordant to prevent equation of the 2 assays. ACL is the better assay for predicting fetal death.

Characteristics of IgG antiphospholipid antibodies in patients with systemic lupus erythematosus and syphilis.

To evaluate the similarities and differences of antiphospholipid antibodies (aPL) in systemic lupus erythematosus (SLE) and syphilis, we studied 20 SLE and 16 syphilis high titer IgG aPL sera for antibody isotype, avidity, phospholipid specificity, light chain and IgG subclass. Syphilis aPL had lower avidity, with kappa light chain and IgG1 and IgG3 predominance, in contrast to higher avidity, with lambda light chain and IgG2 and IgG4 predominance in SLE aPL. Phospholipid specificities were similar. SLE and syphilis aPL both recognize phospholipid epitopes but differ in important antibody characteristics.

Antibody to cardiolipin as a predictor of fetal distress or death in pregnant patients with systemic lupus erythematosus.

During a prospective study of pregnancies in women with systemic lupus erythematosus, we examined the relation between antibody to cardiolipin, measured by the enzyme-linked immunosorbent assay, and midpregnancy fetal distress, identified by abnormal results of antepartum fetal heart-rate testing or by fetal death. All of nine patients with lupus and this complication had abnormally high antibody levels (mean, 212.3 +/- 55.3 units), as compared with values in normal nonpregnant women (28.2 +/- 10.1 units). None of 12 pregnant patients with lupus but without this complication had antibody levels above 50 units (mean, 27.5 +/- 3.4 units; P less than 0.005 vs. women with lupus and fetal distress); 4 of 12 pregnant subjects without lupus had antibody levels above 50 units (mean, 42.5 +/- 11.0), and fetal death occurred in the subject with the highest level. The mean antibody level in 12 nonpregnant patients with lupus was 117.4 +/- 35.0 units. Two patients who had lupus anticoagulant but not clinical lupus, both with histories of prior fetal death, also had high antibody levels; fetal death occurred in one, and spontaneous fetal bradycardia in the other. Antibody to cardiolipin was loosely linked to a history, but not the simultaneous presence, of demonstrable lupus anticoagulant or thrombocytopenia, and could be detected as early in pregnancy as either anticoagulant or thrombocytopenia. We conclude that measurement of antibody to cardiolipin is the most sensitive assay to predict fetal distress or death in patients with systemic lupus erythematosus and may be of pathogenetic importance in this syndrome.