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Biomedical subjects

G Steiner

Publications and source records attributed to G Steiner.

341 records · Page 19Linked to original sources
PubMedDate not supplied

Selenium supplementation: plasma glutathione peroxidase an indicator of selenium intake.

Plasma glutathione peroxidase activity is markedly reduced in dietetically treated patients with PKU or MSUD in comparison to health children of the same age. This is due to the low selenium content of their diet. During supplementation with yeast rich in selenium (200 micrograms selenium per day) for 3 months 2 healthy adults did not show any significant change of their plasma GSHPx activity. 5 dietetically treated patients with PKU or MSUD and a reduced selenium state showed a rapid increase of the plasma GSHPx activity after selenium supplementation were started with 120 micrograms Se/m2 x d. The values doubled within the first two days and reached a plateau after 1--3 weeks. The patients showed no clinical anomalities before or during the selenium supplementation besides the inherited defect of amino acid metabolism. Plasma GSHPx activity seems to be a good indicator of short-term changes of selenium intake in patients with reduced selenium state.

Child↗
PubMedDate not supplied

Roles of lipoprotein lipase and hepatic triglyceride lipase in the catabolism in vivo of triglyceride-rich lipoproteins.

To define the roles, in vivo, of hepatic triglyceride lipase and lipoprotein lipase in the catabolism of triglyceride-rich lipoproteins, we investigated the relationship between the activities of the above enzymes in postheparin plasma and the fractional removal rates of very low density lipoproteins (VLDL) and VLDL remnant particles. In 22 patients, the fractional removal rates of VLDL and VLDL-remnant particles were determined from analyses of the disappearance of radioiodinated Sf 60-400 and Sf 12-60 lipoprotein B apoprotein. The maximal activities of hepatic triglyceride lipase and lipoprotein lipase were determined in plasma samples drawn 2-60 minutes after heparin injection (60 U/kg). A positive correlation was observed between the fractional removal rate of VLDL and postheparin plasma lipoprotein lipase activity (r = 0.65). When all 22 patients were considered together, no relationship was demonstrable between remnant fractional removal and postheparin plasma lipoprotein lipase activity. However, humans may be subdivided with respect to the way in which they catabolize remnants. In some, all remnant may be catabolized to form LDL. In others, some of the remnant may also be directly removed from the circulation. Those subjects in whom previous studies indicate that all remnant is converted to LDL demonstrated a positive correlation between remnant fractional removal rate and postheparin plasma lipoprotein lipase activity (n = 8, r - 0.83). No correlations between postheparin plasma hepatic triglyceride lipase activity and any of the fractional removal rates were found. These data are consistent with the following: 1) lipoprotein lipase plays a key regulatory role in the catabolism of triglyceride-rich lipoproteins; 2) this role applies only to those catabolic involving the formation of particles of higher density VLDL remnants and low density lipoprotein; and 3) hepatic triglyceride lipase plays no rate-limiting role in the catabolism of VLDL or VLDL-remnant particles.

Adult↗
PubMedDate not supplied

Relative contribution of triglyceride-rich lipoprotein particle size and number to plasma triglyceride concentration.

These studies were undertaken to determine whether differences in plasma triglyceride concentrations reflected differences in the number or in the size of the triglyceride-rich lipoprotein particles in the circulation. A population of 122 men and women, composed of normotriglyceridemic individuals and individuals with endogenous hypertriglyceridemia (plasma triglyceride concentration from 60 mg/dl to 1400 mg/dl), was studied by one of four independent experimental procedures. Rates of triglyceride production and particle (as reflected by apolipoprotein B) production were simultaneously determined. The data suggest that 71% of any increase in triglyceride production was due to an increase in the production of particles, and only 29% was due to an increase in the amount of triglyceride carried per particle. Direct measurement of the triglyceride-rich lipoprotein particle size by electron microscopy demonstrated that for a fivefold difference in triglyceride borne by the Sf 12-400 lipoproteins (from 100 mg to 500 mg triglyceride/dl plasma), the mean particle size rose by only 29%. Hence, 71% of this difference was due to an increase in particle number. The same results were obtained when triglyceride levels were related to the number of triglyceride-rich lipoproteins in the plasma. The number of particles for these studies was either estimated from apo B concentration or by calculations based on the chemical composition of ultracentrifugal subfractions. These studies have used four different approaches to show that changes of plasma triglyceride concentration primarily reflected a change in the number, not the size, of triglyceride-rich lipoprotein particles. Our studies also demonstrated that 75% to 80% of the triglyceride-rich lipoproteins in both normotriglyceridemic and hypertriglyceridemic subjects were in the Sf 12-60 or intermediate density lipoprotein subfraction.

Adult↗
PubMedDate not supplied

Myxoid chondrosarcoma of the os calcis: a case report.

This case report of a myxoid chondrosarcoma of the os calcis is presented because of its rarity. The clinical, roentgenographic, and pathological features are discussed, and the difficulty in diagnosis is elaborated.

Aged↗
PubMedDate not supplied

Cost of medications for patients with ischemic heart disease in a rural family practice center.

BACKGROUND: Cardiovascular disease is the leading cause of death, and multiple medications are often needed to control symptoms and risk factors. Little research has explored the cost of medications for a typical patient with chronic ischemic heart disease. We undertook a study to determine the cost of medications and how they are paid for by patients in one rural clinic. METHODS: One hundred four patients met criteria for chronic ischemic heart disease. We obtained patient information, risk factors, and current medications using retrospective chart reviews. We then calculated usual and customary costs per month for each of the 355 cardiac and 214 noncardiac prescriptions. After we determined which patients qualified for third party reimbursement or the community health center medication discount program, we calculated the actual out-of-pocket cost to the patient for each prescription. RESULTS: Average monthly medication costs were $104.77 for cardiac medications and $115.54 for noncardiac medications, for a total of $220.31. Patients were reimbursed for approximately 64 percent of the total medications costs, making average out-of-pocket medication costs $41.52 for cardiac medications and $36.86 for noncardiac medications, for a total of $78.38. Seventy-one percent of patients were reimbursed by their insurance company, 19 percent qualified for the medication discount program, and 10 percent had no assistance. Patient risk factors included positive family history of chronic ischemic heart disease (71 percent), hypertension (64 percent), history of smoking (61 percent), currently smoking (26 percent), diabetes (25 percent), and recently elevated cholesterol levels (67 percent of 76 patients). CONCLUSIONS: Medication costs for patients with chronic ischemic heart disease are expensive and burdensome. Third party payers and the medication discount program relieved a considerable (64 percent) but inadequate amount of prescription costs. Multiple risk factors coexist with these medication costs. Patient behavior modification and an aggressive approach to risk reduction might reduce these costs.

Adult↗
PubMedDate not supplied

Multicenter validation of recombinant, natural and synthetic antigens used in a single multiparameter assay for the detection of specific anti-nuclear autoantibodies in connective tissue disorders.

OBJECTIVES: We investigated the feasibility of using a single multi-parameter test based mainly on recombinant autoantigens for the detection of anti-nuclear autoantibodies, and analyzed the agreement between this test format and conventional techniques. METHODS: The presence of autoantibodies was determined by a line immunoassay (LIA) in 755 sera derived from patients with different autoimmune connective tissue disorders. All sera were previously tested by standard assays that are routinely used at the 8 participating European centers. RESULTS: The overall sensitivity and specificity of autoantibody detection by LIA was similar or higher as compared to combined conventional techniques (CCT). In particular, the detection of anti-Ro52 in systemic lupus erythematosus (SLE) sera (P = 0.004) and anti-LA in both SLE (P < 0.0009) and in Sjögren's syndrome (P < 0.0009) sera was significantly more sensitive when using LIA compared to CCT. By contrast, CCT was never more sensitive than LIA for any of the markers. CONCLUSION: The LIA is a reliable alternative to a combination of conventional techniques for the detection of specific anti-nuclear autoantibodies. The multi-parameter test also reveals autoantibody reactivities that may not be detected when only a limited number of conventional techniques are applied.

Antibodies, Antinuclear↗
PubMedDate not supplied

Induction of anti-RA33 hnRNP autoantibodies and transient spread to U1-A snRNP complex of spliceosome by idiotypic manipulation with anti-RA33 antibody preparation in mice.

OBJECTIVE: Anti-RA33 antibodies occur in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and mixed connective tissue disease (MCTD) and target the A2/B1 protein of the heterogeneous nuclear ribonucleoprotein (hnRNP) complex 4 which forms part of the spliceosome. The aim of the present study was to evaluate the immune response and pathological features induced in mice immunized with anti-RA33 antibodies or patient-derived recombinant single-chain variable fragments (scFv) of anti-RA33 antibodies. METHODS: In the first set of the experiment, two strains of mice (C57BL/6J and BALB/c) were immunized with IgG preparations obtained from two patients with RA and one normal donor. One of the patients had high titer anti-RA33 antibodies; the other one showed weak borderline reactivity. In the second set of the experiment three groups of C57BL/6J mice were immunized, respectively, with affinity-purified (AP) anti-RA33 antibodies, scFv of anti-RA33 antibodies and normal human IgG. The immunological response induced in immunized mice was studied by immunoblotting and line immunoassay (LIA). The presence of arthritis, serositis or myositis was assessed six-months following initial immunization. RESULTS: While anti-RA33 antibodies developed in only two of the mice immunized with different human IgG fractions, anti-RA33 antibodies were clearly detected in 7 sera of 13 mice immunized with AP anti-RA33 antibodies three months after the boost immunization and, moreover, also in 2 sera of 13 mice immunized with scFv of anti-RA33 antibodies. In contrast, mice immunized with normal human IgG did not develop anti-RA33 antibodies. Interestingly, transient autoantibody production against another nuclear autoantigen, U1 snRNP, was observed in 3 C57BL/6J mice immunized with scFv and in 1 mouse immunized with AP autoantibodies. However, these immunological responses were not associated with pathological findings. CONCLUSIONS: Active immunization of naive mice with AP anti-RA33 antibodies and scFv of anti-RA33 antibodies resulted on the one hand in the production of murine anti-RA33 antibodies and led, on the other hand, to transient "autoantibody spread" to snRNP component of the spliceosome and other nuclear autoantigens. This "autoantibody spread" probably reflected disregulation of the idiotypic anti-idiotypic cascade.

Animals↗
PubMedDate not supplied

Preliminary report on cytokine determination in human synovial fluids: a consensus study of the European Workshop for Rheumatology Research. The Cytokine Consensus Study Group of the European Workshop for Rheumatology Research.

A consensus study involving several European research groups was conducted in order to assess the reliability and reproducibility of cytokine measurements in biological fluids. Six synovial fluids and one serum--some of them spiked with recombinant human cytokines--were aliquoted and distributed blindly to different laboratories. The samples were tested for tumor necrosis factor alpha (TNF-alpha), interleukin-1 alpha (IL-1 alpha) and 1 beta, IL-6, IL-2, interferon gamma (IFN-gamma), and the soluble receptors of IL-2 (IL-2R) and TNF (TNF-sR55 and -sR75), using various immunoassays and, occasionally, bioassays. The same ELISA used in different laboratories yielded comparable results, whereas different ELISAs usually detected the highest levels in the same samples, but yielded different absolute values. This finding highlights the necessity of establishing international standards for all immunoassays. Many other questions arose during this preliminary study, and further investigations are planned to clarify them.

Cytokines↗
PubMedDate not supplied

The Austrian Early Arthritis Registry.

The Austrian Early Arthritis Registry (Austrian Early Arthritis Action, EAA) enrols and follows patients with inflammatory arthritis of very short (< 12 weeks) duration. Currently, data on 375 patients (almost 2000 individual follow-up examinations) have been entered into the EA database. Evaluations of data from 182 patients with a follow-up of at least one year are available. 65% of these patients have RA, as diagnosed using the ACR classification criteria in a cumulative fashion. Approximately 15% of these patients still have no established diagnosis and are being carried forward and observed as cases of "undifferentiated arthritis". In RA patients, the mean DAS 28 decreased significantly from an initial mean score of 5.5 (high disease activity) into the range of low disease activity. At the end of one year a DAS 28 of < 3.2 was observed in 52% of the RA patients. Radiological progression in these RA patients, who also received treatment very early, appears to be less severe than in other cohorts, although direct comparisons are impossible due to different methods of patient selection. In addition, the serological data from our cohort in cooperation with other study groups will allow development and validation of possible prediction algorithms for early arthritis patients which could improve the diagnostic and therapeutic approach to this patient group.

Activities of Daily Living↗
PubMedDate not supplied

Anti-RA33 autoantibodies may recognize epitopes in the N-terminal region of hnRNP-A2 (RA33).

The nuclear autoantigen RA33, which is identical to the A2 protein of the heterogeneous nuclear ribonucleoprotein (hnRNP-A2), is a nucleic acid binding protein of 341 amino acids. The N-terminal part contains two RNA binding domains whereas the C-terminal part consists of a long glycine-rich region starting around amino acid 192. Autoantibodies to hnRNP-A2/RA33 can be detected in 20-40% of sera from RA, SLE and MCTD patients. So far, it has not been known which regions of A2/RA33 are recognized by these autoantibodies. To address this issue, tryptic fragments of natural A2/RA33 were investigated by immunoblotting using 14 sera from anti-RA33 positive patients with RA (n = 5), SLE (n = 5) and MCTD (n = 4). Most sera reacted with a 22 kD fragment comprising the N-terminal part of the protein. However, a smaller 18 kD fragment was recognized only by 3 RA and 3 MCTD sera whereas two of five SLE sera were reactive with two larger fragments of 26 and 29 kD. In order to further characterize the epitope(s) C-terminal deletion mutants of recombinant A2/RA33 were investigated by immunoblotting employing 27 sera from anti-RA33 positive patients with RA (n = 10), SLE (n = 8), and MCTD (n = 9). All sera recognized a fragment terminating at amino acid 212 which contained the complete N-terminal region as well as 20 amino acids of the glycine-rich section. Thus, these data indicate that the N-terminal part of A2/RA33 contains epitopes for antiA2/RA33 autoantibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, Nuclear↗
PubMedDate not supplied

A two-year clinical study of the effects of two triphasic oral contraceptives on plasma lipids.

OBJECTIVE: Oral contraceptive formulations can alter plasma lipid and lipoprotein levels; however, lower-dose triphasic tablets show only minimal metabolic effects during 6 or 12 cycles of use. Involvement of lipids in chronic cardiovascular conditions, plus long-term use of oral contraceptive tablets, prompted this first 24-cycle study of the effect of triphasic formulations on young women. METHODS: 69 women assigned randomly to an ethinyl estradiol/levonorgestrel formulation (Triphasil) or an ethinyl estradiol/norethindrone formulation (Ortho 7/7/7) and 25 control women (no hormonal contraception) had blood sampled for lipids and lipoproteins pre-trial, and at 3- or 6-cycle intervals for 24 cycles. RESULTS: At cycle 24, control women experienced no significant change from baseline in any variable except apolipoprotein B (apo B). Plasma apo B increased 42% (P < .01), reflecting the LDL apo B increase (42%, P < .01). Both combination formulations significantly increased apo B (plasma, VLDL, IDL and LDL); the increases ranged between 47% and 84%. Plasma apo A1 rose (15%, P < .001) in the Ortho 7/7/7 group only. Plasma and LDL triglycerides were increased significantly (P < .001) by the norethindrone product, 43% and 81%, respectively, and plasma and LDL cholesterol, 14% and 28%, respectively. Cholesterol decreased in all other subfractions, including HDL (11%, P < .01). HDL cholesterol decreased significantly in the Triphasil group (8%, P < .05); no other cholesterol subfractions changed significantly. All cycle-24 lipid and lipoprotein values remained well within respective normal ranges. CONCLUSION: Although 2-year exposure to the triphasic oral contraceptive formulations changed the lipid risk factors for cardiovascular disease only within normal ranges, there remains potential for long-term health effects when compounded with other risk factors.

Adolescent↗
PubMedDate not supplied

Anti-RA 33 as a marker antibody of rheumatoid arthritis in a Finnish population.

To obtain information on anti-RA 33 as a marker antibody of rheumatoid arthritis (RA), a panel of Finnish sera were tested by immunoblotting with partially purified RA 33 antigen. Six of 100 specimens from patients with RA, one of 39 specimens from subjects who later developed seropositive RA, and one of 50 specimens from subjects with "false-positive" rheumatoid factor reactions were positive. The findings are compatible with the concept that anti-RA 33 is associated with RA from its onset and can even precede the disease. However, the prevalence of this antibody in Finnish RA patients is remarkably low compared to patients from continental Europe.

Adult↗