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We report on the observation of the excitation/emission spectrum of a dendrimer-encapsulated gold nanocluster; the synthesis of Au-PAMAM was based on reduction of HAuCl4 x 3 H2O co-dissolved in methanol together with fourth-generation OH-terminated PAMAM.
Electrospray ionization of a mixture of the two gold phosphine chlorides, R3PAuCl (R = Ph and Me), silver nitrate and the amino acid N,N-dimethylglycine (DMG) yields a range of gold containing cluster ions including: (R3P)Au(PR'3)+; (R3PAu)(R'3PAu)Cl+ and (R3PAu)(R'3PAu)(DMG-H)+ (where R = R' = Ph; R = R' = Me; R = Me and R' = Ph). Collision induced dissociation (CID) of the (R3PAu)(R'3PAu)(DMG-H)+ precursor ions yielded the hitherto unknown gold hydride dimers (R3PAu)(R'3PAu)H+. The gas-phase chemistry of these dimers was studied using ion-molecule reactions, collision induced dissociation, electronic excitation dissociation (EED) and DFT calculations on the (H3PAu)2H+ model system. A novel phosphine ligand migration was found to occur prior to fragmentation under CID conditions and this was supported by DFT calculations, which revealed a transition state with a bridging phosphine ligand.
Novel amphiphilic trithiolates possess excellent properties for gold nanoparticle (AuNP) stabilization and functionalization and cannot be replaced by exchange reactions.
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We report the case of a woman with a characteristic transient skin rash, fever, severe polyarthritis, hepatosplenomegaly, lymphadenopathy and myalgia. The clinical and laboratory data led to a diagnosis of adult-onset Still's disease. The elevated levels of serum ferritin and caeruloplasmin could be important as diagnostic indicators.
In autoimmune thrombocytopenia, platelet-associated IgG (PA-IgG) frequently displays specificity against glycoprotein (GP) IIbIIIa and/or GP IbIX. Because in a high proportion of patients positive PA-IgG may not be explained by these GP specificities, studies on other target proteins are needed. We studied the presence of GP V-specific PA-IgG by direct monoclonal antibody-specific immobilization of platelet antigens (MAIPA) with the monoclonal antibody SW16. We focused on 69 consecutive random patients with histories of thrombocytopenia who were strongly positive for PA-IgG detected by the direct platelet immunofluorescence test (PIFT). PA-IgG against GP V (ratio > or = 1.5) was noted in 15 (22%) patients. The degree of PA-IgG measured by PIFT, and of GP IIbIIIa-and/or GP IbIX-specific PA-IgG measured by direct MAIPA, correlated directly with the GP V-specific PA-IgG (P < 0.001). In one patient, GP V-specific antibodies were associated with quinidine-induced thrombocytopenia. Although this patient had strongly positive GP V-specific PA-IgG, she remained negative in GP IIbIIIa- and GP IbIX-specific direct MAIPA. Two patients studied because of thrombocytopenia associated with gold therapy had strongly positive GP V-specific PA-IgG. In one patient with rheumatoid arthritis and severe gold-induced thrombocytopenia, the amount of GP V-specific PA-IgG decreased during the recovery phase. Thus, GP V may represent an important target antigen in autoimmune-mediated thrombocytopenia, especially in drug-induced thrombocytopenia.
OBJECTIVE: To provide a review of the renal toxicity of disease-modifying antirheumatic drugs (DMARDs) currently used for the treatment of rheumatoid arthritis. METHODS: Papers in American and European medical journals related to renal toxicity of DMARDs used for the treatment of rheumatoid arthritis were reviewed. Specific DMARDs reviewed were cyclosporine, gold, D-penicillamine, methotrexate, azathioprine, antimalarials, sulfasalazine, leflunomide, etanercept, infliximab, and DMARD combination therapy. RESULTS: The renal toxicity of DMARDs varies widely. Cyclosporine, gold, and D-penicillamine all have a serious potential for renal side effects, particularly in the elderly or in patients with compromised renal function. Concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs) increases the potential for renal damage. In contrast, methotrexate, azathioprine, antimalarials, sulfasalazine, leflunomide, etanercept, and infliximab have relatively little renal toxicity. CONCLUSIONS: The potential for renal toxicity should always be considered when determining which DMARD to use for RA therapy. DMARDs that combine efficacy with negligible renal adverse effects should be used for the treatment of patients susceptible to DMARD-associated renal damage.
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OBJECTIVE: The purposes of the present study were: 1) to investigate how the long-term course of outcome and inflammatory variables could be described in individual patients and suitably summarized in groups of patients; 2) to investigate the associations between outcome and inflammatory variables on the basis of the defined summary measures; and 3) to investigate new prognostic aspects of RA by means of frozen sera and DNA specimens. PATIENTS AND METHODS: During the period 1966-78, 685 Danish Caucasian patients with RA, classified according to the 1958 American Rheumatism Association (ARA) criteria, were admitted to the Department of Rheumatology of Aarhus University Hospital. For scientific purposes all patients went through the same examination programme, including biochemical variables, clinical evaluation of 68 diarthrodial joints, and radiographic evaluation of 46 diarthrodial joints. Since 1987, data from these patients have been organized in a database. The data are arranged according to onset of disease. This thesis is based on about 600,000 data-points from 257 patients. RESULTS: The thesis is based on six studies. The first study shows that early symptomatic improvement of RA during gold treatment was stable over several years, but when evaluated radiographically, the condition continued to deteriorate. In the second study, six main types of radiographic progression were identified: (a) a rare type with no radiographic progression at all (<1%); (b) a type with a slow or moderate onset, but an increasing progression rate (exponential growth type) (9%); (c) a linear type (30%); (d) a type with a moderate to fast onset, and a stable progression rate (the square root type) (11%); (e) a type with a fast onset, but a later decreasing progression rate (the first order kinetics type) (30%) and (f) a type characterized by slow onset, then acceleration and later deceleration (the sigmoid type) (20%). The fact that there was a systematic progression was used to define a system of radiographic events, which could be used as outcome measures in prediction models of the long-term course of RA. The third study shows that low serum levels of the complement-activating serum lectin, mannan (mannose) binding protein (lectin) (MBP = MBL), are associated with a higher erythrocyte sedimentation rate (ESR) (p=0.006), joint swelling score (JS score) (p=0.019), limitation of joint motion score (LM score) (p=0.027), and annual increase in radiographic destruction score (R score) (p=0.053). The fourth study demonstrated a highly significant association between summary measures of inflammatory variables and radiographic outcome, as defined in the second study, indicating that the degree of inflammation is important for the development of destructive joint damage in RA. The fifth study showed that MBL-insufficient patients (two defective structural MBL alleles, or one defective allele combined with a low-expression variant of the normal allele) had a relative risk of a severe radiographic event of 3.1 compared with the MBL competent group (p<0.0001). The sixth study showed that the relative risk (RR) of early interleukin (IL)-1alpha auto-antibodies (aAb) positive patients developing serious radiographic joint destruction was significantly lower than for IL-1alpha aAb-negative patients, RR=0.29 (p=0.04). In rheumatoid factor (RF) positive patients RR was only 0.18 (p=0.02). Patients who seroconverted >2 years after the onset of RA showed the most aggressive development of joint erosion, with RR of serious radiographic joint destruction of 2.56 (p=0.048). Other factors investigated in subgroups of the patients were HLA-DR4, chemokine receptor 5 (CCR 5) genotypes. IL-6 aAb, vascular endothelial growth factor (VEGF) aAb, and interferon (IFN)-gamma aAb. About 80% of the patients were HLA-DR4 positive, indicating the importance of HLA-DR4 as a predisposing factor for RA. There was no association between IL-6 aAb and radiographic outcome, or CCR5 genotypes and radiographic outcome. VEGF aAb and IFN-gamma aAb were quantitatively unimportant. CONCLUSION: In spite of a general improvement in single measures of inflammatory variables, and a general deterioration in radiographic outcome of RA, there is a highly significant association between summary measures of inflammatory variables and radiographic outcome. The progression of radiographic damage in RA follows mathematical patterns. A new method of evaluating the long-term radiographic outcome by means of Kaplan-Meier plots is demonstrated. It is shown that MBL and IL-1alpha aAb are predictors of the prognosis of RA and may play important roles in the pathogenesis of RA.
Brown-Norway (BN) rats are highly susceptible to drug-induced immune dysregulations and when injected with mercuric chloride (HgCl(2)) or sodium aurothiopropanolsulfonate (ATPS), they develop a syndrome characterized by a polyclonal B cell activation depending upon CD4(+) T(h)2 cells that recognize self-MHC class II molecules. Since peripheral tolerance of T(h)2 cells might be crucial in the prevention of immunological manifestations such as allergy, establishing conditions for inducing tolerance to HgCl(2)- or ATPS-mediated immune manifestations appeared to be of large interest. We report here that BN rats neonatally injected with HgCl(2): (i) do not develop the mercury disease, (ii) remain resistant to HgCl(2)-induced autoimmunity at 8 weeks of age and later, provided they are regularly exposed to HgCl(2), (iii) are still susceptible to ATPS-induced immune manifestations, and (iv) exhibit spleen cells that adoptively transfer tolerance to HgCl(2)-induced autoimmunity in naive, slightly irradiated, syngeneic recipients. These findings demonstrate that dominant specific tolerance can be neonatally induced using a chemical otherwise responsible for T(h)2-mediated autoimmunity.
BACKGROUND: Rheumatoid arthritis patients treated with gold salts occasionally develop a glomerulonephritis and an increase in serum IgE concentration. Brown-Norway (BN) rats injected with aurothiopropanolsulphonate (ATPS) exhibit an increase in serum IgE concentration, produce antilaminin antibodies (Abs) and develop glomerular linear immunoglobulin (Ig) deposits, occasionally a membranous glomerulopathy and vascular granular Ig deposits. Lewis (LEW) rats are resistant. METHODS: The genetic requirements governing the appearance of these manifestations were studied in congenic rats, and in F1 hybrids injected with ATPS. RESULTS: Non-MHC-linked genes from the BN strain were absolutely required for all the traits to be observed. The RT1n (BN) or RT1(1) (LEW) haplotypes at the MHC were permissive for all the manifestations to appear and two RT1(1) alleles were associated with the highest response. However, granular Ig deposits were only observed in RT1n rats. The high serum IgE concentration and the antilaminin Ab level were associated with the presence of glomerular Ig deposits but were not associated with the presence of vascular Ig deposits. CONCLUSIONS: This study shows that susceptibility to ATPS was mainly dependent upon non-MHC-linked BN genes and that the involvement of MHC-linked genes differed depending upon the character considered. There is an epistatic effect between the various genes.
The pathogenesis of gold-induced autoimmunity and membranous glomerulopathy is not well understood. HgCl2 and D-penicillamine, other chemicals known to trigger membranous glomerulopathy in humans, induce autoimmune manifestations in Brown-Norway (BN) rats but not in Lewis (LEW) rats. These chemicals trigger T-cell clones which are specific for self class II molecules from the major histocompatibility complex and are probably responsible for the polyclonal B-cell activation observed. The aim of this work was to test the effects of aurothiopropanolsulphonate (ATPS) in BN and LEW rats. In BN rats, ATPS induced a polyclonal B-cell activation marked by lymphoproliferation, hyperimmunoglobulinaemia affecting mainly IgE, and by the production of numerous autoantibodies. A glomerulonephritis occurred, initially due to anti-glomerular basement membrane antibody deposition, and later to the formation of granular deposits, occasionally resulting in a typical membranous glomerulopathy. Self class-II-specific T-cells were found that might be responsible for the polyclonal B-cell activation. Lewis rats were free of glomerulopathy but, like BN rats, exhibited an interstitial nephritis and some degree of polyclonal B-cell activation. These findings demonstrate that, depending on the strain, ATPS triggers different B-cell clones inducing different degrees of autoimmunity.
This article describes the current drug therapies used to manage rheumatoid arthritis (RA). A brief description of the pathology, pathogenesis, and clinical features of RA is presented. The purpose of the article is to increase an awareness among physical therapists regarding the medications their patients might be taking and how these agents might influence the outcome of physical therapy intervention. The general approach to prescribing medication is presented according to the status of the disease. The attributes of nonsteroidal antiinflammatory drugs, corticosteroids, slow-acting antirheumatic drugs, and cytotoxic and experimental drugs used in RA are described. Given the potential benefits, side effects, and adverse reactions of these potentially powerful medications, it is important for the physical therapist to monitor closely what is happening to the patient with respect to the use or nonuse of the medication.
Cutaneous toxicity from drugs used to treat RA is a major perceived problem. Over a 2-yr period we have prospectively reviewed 114 patients with a suspected adverse cutaneous reaction to anti-rheumatic drugs. In 71 (62%), the rash was thought to be unrelated to drug therapy. This group included 10 in whom the rash had resolved before review (usually < 1 week), 38 with a rash related to their rheumatoid disease and 23 with eruptions unrelated to either drugs or arthritis. Forty-three (38%) patients had rashes thought to be related to their drug therapy. Gold therapy (both oral and intramuscular) was implicated most frequently (31 patients). However, the majority of these (23) had a pityriasiform/discoid eczematous eruption that responded to potent topical steroids occasionally with a reduction in gold dosage. In this sample it was possible to continue drug therapy in 82% of patients with what were initially thought to be cutaneous adverse drug reactions. Careful evaluation should allow a majority of patients to continue drug therapy from which they are often gaining benefit.