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Biomedical subjects

G Steiner

Publications and source records attributed to G Steiner.

At least 91 records · Page 5Linked to original sources
PubMed1998

The effect of alendronate on cytokine production, adhesion molecule expression, and transendothelial migration of human peripheral blood mononuclear cells.

Since both osteoclasts and macrophages belong to the mononuclear phagocytic system it is conceivable that bisphosphonates not only affect bone metabolism but also inflammatory responses. The migration of mononuclear cells into perivascular tissue is a central event in inflammatory reactions. We studied the effects of the aminobisphosphonate alendronate on the transendothelial migration of human peripheral blood mononuclear cells in an in vitro model. Alendronate (at a concentration of 100 microM) significantly increased the percentage of peripheral blood mononuclear cells that migrated through endothelial cell monolayers. Similar results were obtained with another aminobisphosphonate, viz, pamidronate. An overnight treatment of the endothelial cell monolayers with alendronate did not alter the rate of peripheral blood mononuclear cells that subsequently migrated. The overnight cultivation of the peripheral blood mononuclear cells in the presence of alendronate resulted in an increased surface expression of CD54 (intercellular adhesion molecule-1, ICAM-1) in both CD14(+) and CD3(+) cells; in CD14(+) cells also the expression of CD49d (alpha4 subunit of late activation antigen-4, VLA-4) increased after alendronate treatment. Alendronate treatment of peripheral blood mononuclear cells also resulted in an increased production of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma). We conclude that alendronate has a distinct effect on the transendothelial migration of human peripheral blood mononuclear cells in vitro. Alendronate may either directly or indirectly, e.g., by augmenting the production of proinflammatory cytokines, influence the expression of certain adhesion molecules and thereby facilitate transendothelial migration. These effects could be related to the transient leukopenia reported following intravenous administration of relatively high doses of aminobisphosphonates for the treatment of hypercalcemia of malignancy.

Alendronate↗
PubMed1998

N-acetylneuraminic acids (nana): a potential key in renal calculogenesis.

N-Acetylneuraminic acids (NANA) promote binding of calcium ions to macromolecules and cells, increase the intrinsic viscosity of glycoproteins and facilitate gel formation in water. Since these properties are crucial in urinary calculogenesis, we evaluated NANA levels in urine and serum as well as their expression in kidney tissues. Using a modified thiobarbituric acid assay, the evaluation of free and bound NANA in 24-h urine samples revealed a ratio of 1.87 in 33 non-stone-formers but a reversed ratio of 0.84 in 41 recurrent calcium oxalate stone-formers. Time kinetics revealed a gradual rise in NANA expression until 48 h of culture and a significantly higher release into supernatants of papillary renal epithelial cells (REC) when compared with cortical REC. To examine NANA distribution in kidney tissues, paraffin-embedded biopsies from five normal and six stone-forming kidneys were labeled with the biotinylated NANA-specific lectins Maackia amurensis (MAA) and Sambucus nigra (SNA). Immunohistochemistry revealed intense luminal MAA reactivity of distal tubular REC and collecting ducts in 96.7% and 91.5% of normal and stone-forming kidneys respectively. By contrast, there was a marked difference between normal and stone-forming kidneys for SNA reactivity (17.7% vs 95%) at the same locations. Finally, the glycocalyx of recurrent stone-formers showed altered sialylglycoside linkages [alpha(2,6) instead of alpha(2,3)] that may indicate an altered REC function. Given the calcium-binding potential of NANA, their increased local concentration within the glycocalyx layer in the distal nephron may either initiate stone formation or facilitate attachment of microcrystals to REC.

Adult↗
PubMed1998

Chondrocalcinosis of the hyaline cartilage of the knee: MRI manifestations.

PURPOSE: To determine the ability of MRI to detect the presence of crystals of calcium pyrophosphate in the articular cartilage of the knee. DESIGN AND PATIENTS: The MR studies of 12 knees (11 cases) were reviewed retrospectively and correlated with radiographs (12 cases) and the findings at arthroscopy (2 cases) and surgery (1 case). A total of 72 articular surfaces were evaluated. Radiographic, surgical or arthroscopic demonstration of chondrocalcinosis was used as the gold standard. Additionally, two fragments of the knee of a patient who underwent total knee replacement and demonstrated extensive chondrocalcinosis were studied with radiography and MRI using spin-echo T1-, T2- and proton-density-weighted images as well as two- and three-dimensional fat saturation (2D and 3D Fat Sat) gradient recalled echo (GRE) and STIR sequences. RESULTS: MRI revealed multiple hypointense foci within the articular cartilage in 34 articular surfaces, better shown on 2D and 3D GRE sequences. Radiographs showed 12 articular surfaces with chondrocalcinosis. In three cases with arthroscopic or surgical correlation, MRI demonstrated more diffuse involvement of the articular cartilage than did the radiographs. The 3D Fat Sat GRE sequences were the best for demonstrating articular calcification in vitro. In no case was meniscal calcification identified with MRI. Hyperintense halos around some of the calcifications were seen on the MR images. CONCLUSION: MRI can depict articular cartilage calcification as hypointense foci using GRE techniques. Differential diagnosis includes loose bodies, post-surgical changes, marginal osteophytes and hemosiderin deposition.

Adult↗
PubMed1998

Important contribution of lipoprotein particle number to plasma triglyceride concentration in type 2 diabetes.

The aim of the present study was to determine the contributions of particle size versus number to differences in plasma triglyceride-rich lipoprotein concentrations in patients with type 2 diabetes. Fasting plasma was obtained from 174 consecutive eligible men and women with type 2 diabetes (with or without insulin treatment, mean age 57.0 + 6.3 years) who were undergoing coronary angiography. The triglyceride-rich (Sf 12-400) lipoproteins (TRL) were subfractionated into the Sf 12-60 and Sf 60-400 subfractions. Particle numbers, estimated by measuring apolipoprotein B by electroimmunoassay, in each of these lipoprotein fractions were related to enzymatically determined triglyceride levels in the triglyceride-rich lipoproteins. Approximately 87% of the triglyceride-rich lipoprotein particles were in the Sf 12-60 fraction and 13% in the Sf 60-400 fraction. Multiple linear regression indicated that 69% (i.e. r2=0.69) of the variance in the triglyceride levels could by explained by differences in TRL particle number and 17% (i. e. r2=0.17) by the differences in particle triglyceride content. These observations are similar in each gender and in those with or without insulin treatment. In conclusion, in type 2 diabetes, the vast majority of triglyceride-rich lipoproteins are smaller particles which are in the Sf 12-60 fraction. Differences in particle number, rather than triglyceride content, account for approximately 70% of the differences in triglyceride levels observed between individuals. Previous demonstrations, in those without diabetes, of an association between small triglyceride-rich lipoproteins with coronary artery disease suggest the importance of these findings to the increased atherosclerosis in diabetes.

Adult↗
PubMed1998

Intermediate-density lipoproteins, diabetes and coronary artery disease.

The results of various studies suggest that hypertriglyceridaemia is associated with an increased risk of coronary artery disease. It is unclear, however, which particular triglyceride (TG)-rich lipoproteins contribute to the risk. Different types of TG-rich lipoprotein differ in function, composition, size and density. TG-rich lipoproteins in the range Svedberg flotation (Sf) 12-60 have been shown to be associated with angiographic severity in both diabetic and non-diabetic individuals. A study in people with type 2 diabetes found that those with moderate coronary artery disease had higher levels of both Sf 12 60 and Sf 60-400. Multivariate analysis showed that this association was independent of both low (LDL)- and high-density lipoprotein (HDL). The association was not seen in patients with severe coronary artery disease, suggesting that these lipoproteins may only be involved in the early stages of atherogenesis. Further research has indicated that the risk correlates positively to the postprandial levels of apolipoprotein B48 in the Sf 20-60 fraction. This suggests that elevated levels of chylomicron remnants are involved in progression of coronary artery disease.

Coronary Disease↗
PubMed1998

Erosive arthritis in systemic lupus erythematosus: analysis of a distinct clinical and serological subset.

Erosive arthritis (EA) in systemic lupus erythematosus (SLE) can be debilitating and deforming with uncertain factors for risk, although antibodies to the A2 hnRNP core protein, known as anti-RA33, have been associated with EA. Two hundred patients under long-term follow-up for SLE were evaluated for EA and associated clinical and serological abnormalities. In addition, sera were tested in a masked fashion for anti-RA33 antibodies in a total of 60 patients: 10 with EA and 50 age-, sex- and ethnically matched controls. Ten of 200 (5%) patients with SLE, mainly non-white women, had EA. There were trends for increased renal involvement (P = 0.06), Sjögren's syndrome (P = 0.07) and Raynaud's phenomenon (P = 0.03) in patients with EA compared to those without EA. Rheumatoid factor (RF) was increased in patients with EA (P < 0.02), as were antibodies to double-stranded DNA (P < 0.05), Sm (P < 0.01) and La/SS-B (P < 0.001). Anti-RA33 antibodies were present in 70% with EA compared to 28% without EA (P < 0.05). RF correlated with anti-RA33 antibodies in patients with EA, but not with the presence of anti-RA33 alone. Thus, anti-RA33 antibodies may identify those patients with SLE who are at risk for EA, and an association with RF suggests a common immune response or pathological mechanism in autoimmune erosive joint disease.

Antibodies, Antinuclear↗
PubMed1998

Are autoantibodies active players or epiphenomena?

Autoantibodies have the potential of pathogenicity in several diseases. In rheumatoid arthritis (RA), however, this has not been ultimately proven. RA is characterized by a variety of autoantibodies. Newer insights into characteristics of rheumatoid factors indirectly suggest their pathogenetic involvement. In contrast, antibodies to collagen, despite the availability of an experimental model, do not appear to be pathogenetic in man. Anti-hnRNP antibodies, particularly anti-A2/RA33, are present in RA and experimental models of RA, and therefore, aside from their diagnostic value in established and early RA, could also be involved in the disease process. The nature of Sa, another target antigen in RA, has not yet been elucidated. Filaggrin is the antigen recognized by antikeratin antibodies and antiperinuclear factor; however, citrullin is the target amino acid in filaggrin, and anticitrullin antibodies have a high predictive value. Among a series of cartilage proteins, most have not yet been characterized sufficiently; one, gp39, appears to be of particular interest. Whether or not these antibodies are involved in RA pathogenesis is not yet known. It can be speculated that autoimmunity to some, if not all, of these autoantigens mirrors events important in the development of RA, but further studies on T-cell reactivities and in experimental models are needed to fully understand the involvement.

Animals↗
PubMed1998

Alterations in endothelial F-actin microfilaments in rabbit aorta in hypercholesterolemia.

The current study tests whether hypercholesterolemia influences the distribution of endothelial cell microfilaments during the initiation and growth of fatty streak-type lesions. We classified the lesions occurring over a 20-week period into four types based on the location and extent of macrophage infiltration observed microscopically. The earliest lesion was characterized by leukocytes adherent to the endothelial surface. Minimal lesions were characterized by a few cells in the subendothelium. Intermediate lesions consisted of numerous subendothelial leukocytes in a minimally raised lesion. Advanced fatty streak lesions were elevated, with several layers of leukocytes. The organization of peripheral junctional actin (the dense peripheral band) and of central endothelial cell actin microfilament bundles was studied in each of these lesions by using fluorescent microscopy. We found that in the aorta away from branch sites and in areas away from lesions, the central microfilament distribution was unaffected by hypercholesterolemia. The macrophages entered the wall without any identifiable reorganization in the microfilaments. During the accumulation of subendothelial macrophages in minimal and intermediate lesions, stress fibers were initially increased in comparison to lesion-free areas. In raised advanced lesions, the central microfilaments became thinner and disappeared. However, at flow dividers, where central stress fibers are normally prominent, endothelial cells on the surface of intermediate lesions showed a reduction in central fibers, and peripheral bands became prominent. This finding was associated with changes in cell shape from elongated to cobblestone type. Thus, actin microfilament bundles in endothelial cells underwent substantial changes in distribution during the accumulation of subendothelial macrophages, forming hypercholesterolemia-induced fatty streak-type lesions. These changes may influence endothelial substrate adhesion, permeability, or repair after injury.

Actin Cytoskeleton↗
PubMed1998

Upregulation of cytokine receptors sTNF-R55, sTNF-R75, and sIL-2R in psoriatic arthritis synovial fluid.

OBJECTIVE: To assess differences in soluble tumor necrosis factor receptor 55 (sTNF-R55), sTNF-R75, and soluble interleukin 2 receptor (sIL-2R) in synovial fluid (SF) of patients with psoriatic arthritis (PsA), a seronegative inflammatory joint disease, in comparison with those of patients with rheumatoid arthiritis (RA) and osteoarthritis (OA). METHODS: sIL-R were measured in SF with commercial sandwich ELISA and the results correlated with serological and clinical disease activity variables. RESULTS: In PsA SF the level of sTNF-R55 was 11.8 +/- 0.8 ng/ml and that of sTNF-R75 13.0 +/- 1.3 ng/ml. sIL-2R concentration in PsA SF was 800 +/- 84 U/ml. Compared to PsA SF, cytokine receptor levels in OA SF were significantly lower: 8.7 +/- 0.8 ng/ml for sTNF-R55 (p < 0.02); 7.1 +/- 0.9 ng/ml for sTNF-R75 (p < 0.0003); and 505 +/- 53 U/ml for sIL-2R (p < 0.009). In contrast RA SF cytokine receptor levels were even higher than those of PsA SF (sTNF-R55: 18.1 +/- 2.0 ng/ml, p < 0.04; sTNF-R75: 29.5 +/- 2.9 ng/ml, p < 0.0002; and for sIL-2R: 1957 +/- 290 U/ml, p < 0.03). CONCLUSION: In PsA SF sTNF-R55, sTNF-R75, and sIL-2R are upregulated compared to OA SF but are lower than in RA SF. Our results for TNF-R agree with recent findings in PsA, since TNF-alpha, an important stimulator for TNF-R, is also significantly lower in PsA than in RA. The upregulation of the cytokine receptors in PsA reconfirms its inflammatory nature, but indicates the more benign course of disease compared with RA.

Arthritis, Psoriatic↗
PubMed1998

Analysis of particle size and lipid composition as determinants of the metabolic clearance of human high density lipoproteins in a rabbit model.

Hypertriglyceridemia is commonly associated with triglyceride (TG) enrichment of high density lipoprotein (HDL) and reduction in HDL cholesterol and apolipoprotein A-I levels. We have recently reported that lipolytic modification of TG-rich HDL, which reduces particle size, enhances its clearance from the circulation. In the present study, we examined the role of particle size and lipid composition in determining the metabolic clearance of human HDL, in the absence of substantial in vivo modification of the particle by hepatic lipase. The rabbit, which has a very low hepatic lipase activity, was used for this purpose. Plasma fractions d < 1.21 g/ml were first isolated by ultracentrifugation from fasting humans with normal (NTG, n=6, mean plasma TG concentration=1.26+/-0.21 (SEM) mmol/l) or elevated plasma TG levels (HTG, n=5, TG=4.49+/-0.65 mmol/l). Small and large HDL particles were separated by gel filtration chromatography and were labeled with either 125I or (131)I. Large HDL were cleared more rapidly than small HDL in 10 out of 11 studies (P=0.006). There was, however, no difference in the fractional catabolic rate (FCR) of large HDL isolated from NTG versus from HTG subjects or in the FCR of small HDL from NTG versus HTG individuals. There was also no correlation between the TG content of HDL and its FCR. In summary, large, lipid-rich human high density lipoproteins (HDL) are cleared more rapidly than small human HDL in rabbits. These results, combined with our previous observation, also support the hypothesis that triglyceride enrichment of HDL, in the absence of substantial lipolytic modification, is not sufficient to enhance its clearance from the circulation.

Adult↗
PubMed1998

[Urinary incontinence in neurogenic defects and urogenital anomalies in childhood].

Dysraphic defects may cause neurogenic incontinence in childhood. Constipation and encopresis are often associated. Depending on the involved segment of the spinal cord hyperreflexia or atonia of the detrusor is observed. Similar findings, without anatomic correlation, can be seen in occult-neurogenic voiding dysfunctions. Therapeutic means aim at preservation of kidney function and the best possible continence. If the symptoms cannot be treated by anticholinergic drugs in a low-capacity, hypertonic bladder, augmentation by bowel segments or continent urinary diversion (e.g. Mainz I pouch) is performed. In the last years modalities of clean intermittent self-catheterization in high-capacity, atonic bladders could be enhanced by the development of new atraumatic catheter systems. Urogenital malformation e.g. proximal epispadias and exstrophic bladder can cause incontinence as well. Recently, new therapeutic concepts were introduced. Ectopic ureter (extraurethral incontinence) in girls or posterior urethral valves in boys as a reason for incontinence must not be forgotten.

Child↗
PubMed1998

Apolipoprotein B-48 and retinyl palmitate are not equivalent markers of postprandial intestinal lipoproteins.

This study compared retinyl palmitate and apolipoprotein (apo) B-48 as markers of postprandial triglyceride-rich lipoproteins. Nine non-diabetic men received an oral vitamin A-containing fat load. We measured retinyl palmitate, apoB-48, apoB-100, and triglyceride levels in Sf > 400, Sf 60-400 and Sf 20-60 lipoproteins. The peak retinyl palmitate concentration was delayed compared to the peak apoB-48 concentration in each fraction. The discrepancy between retinyl palmitate and apoB-48 was further investigated in another study of 12 men. In that study, a fat load was given and 5 h later, lipolysis was stimulated in vivo with heparin (60 U/kg, i.v.) and the same parameters were followed. Thirty minutes after heparin, triglyceride levels decreased significantly in the three triglyceride-rich lipoprotein fractions (Sf > 400, Sf 60-400 and Sf 20-60). ApoB-48 levels also fell significantly in the three triglyceride-rich lipoprotein fractions. In contrast, retinyl palmitate concentrations did not change significantly in Sf > 400 and Sf 60-400 fractions and increased significantly in the Sf 20-60 fraction. Our results indicate that retinyl palmitate and apolipoprotein B-48 do not mark the same properties of postprandial intestinal lipoproteins. The metabolic pattern of apolipoprotein B-48 parallels that of triglyceride. One possible explanation for these observations is that the apoB-48-containing triglyceride-rich lipoproteins are metabolically heterogeneous and that older particles, those in circulation for a longer period of time, may be cleared more rapidly than newer ones.

Adult↗
PubMed1998

Serum creatinine level is an independent risk factor for the angiographic severity of internal carotid artery stenosis in subjects who have previously had transient ischaemic attacks.

BACKGROUND: Serum creatinine level has been reported to be related to the incidence of strokes. OBJECTIVE: To examine the relationship between serum creatinine level and the severity of extracranial carotid artery atherosclerosis. DESIGN AND METHODS: This is a secondary analysis of data from 88 patients (59 men and 29 women) who had previously had transient ischaemic attacks or minor strokes and had been included in intervention trials of symptomatic carotid disease. Narrowing of internal carotid artery was estimated by angiography. Both internal carotid arteries were measured and the severity was expressed as the sum of percentage stenoses on both sides. The risk profiles of patients with moderate and severe internal carotid artery stenosis were compared. RESULTS: The sex-adjusted mean serum creatinine concentration in those with severe carotid disease was significantly higher than that in those with moderate disease (106.3 +/- 3.3 versus 91.3 +/- 3.7 mumol/l, P = 0.003), but still within the normal range. The risk of having severe disease was compared with risk of having moderate disease for people ranked by their serum creatinine levels. Univariate logistic regression showed that the odds ratio (OR) for having severe involvement of internal carotid artery was greater for patients in mid-tertile of creatinine values than it was for those in the lowest tertile (OR 6.3, 95% confidence interval 2.0-20.4, P = 0.002). The creatinine levels of patients in these two tertiles were within the normal range. The OR was no greater for patients in the highest tertile of creatinine values, which were slightly elevated above the normal range. These OR did not change after adjustment for age, sex, hypertension or systolic blood pressure, diabetes, smoking and lipid levels. CONCLUSION: Results of this study demonstrate for the first time that serum creatinine level, even within the range of upper normal or mildly elevated levels, is related to the angiographic severity of internal carotid artery disease in patients who have previously had transient ischaemic attacks and that this relationship is independent of classic cardiovascular risk factors.

Aged↗
PubMed1997

Anti-A2/RA33 autoantibodies are directed to the RNA binding region of the A2 protein of the heterogeneous nuclear ribonucleoprotein complex. Differential epitope recognition in rheumatoid arthritis, systemic lupus erythematosus, and mixed connective tissue disease.

The recently described anti-A2/RA33 autoantibodies occur in 20-40% of patients with RA, SLE, and mixed connective tissue disease (MCTD). They are directed to the A2 protein of the heterogeneous nuclear ribonucleoprotein complex (hnRNP-A2), an abundant nuclear protein associated with the spliceosome. The NH2-terminal half of the antigen contains two conserved RNA binding domains whereas its COOH-terminal part is extremely glycine-rich. The aim of this study was to characterize the autoepitopes of hnRNP-A2 and to investigate the effects of anti-A2/RA33 autoantibodies on possible functions of the antigen. Using bacterially expressed fragments, two major discontinuous epitopes were identified. One containing the complete second RNA binding domain was recognized by the majority of patients with RA and SLE but not by patients with MCTD. The second epitope contained sequences of both RNA binding domains and was preferentially targeted by patients with MCTD. When the RNA binding properties of the antigen were investigated, oligoribonucleotides containing the sequence motif r(UUAG) were found to bind to a site closely adjacent or overlapping with the epitope targeted by autoantibodies from patients with RA and SLE. Moreover, anti-A2/RA33 autoantibodies from patients with RA or SLE, but not from patients with MCTD, inhibited binding of RNA. Thus, anti-A2/RA33 autoantibodies recognize conformation-dependent epitopes located in a functionally important region of the antigen. Furthermore, the specific recognition of an epitope by MCTD patients may be used as another argument in favor of considering MCTD a distinct connective tissue disease.

Arthritis, Rheumatoid↗
PubMed1997

Chylomicronemia due to apolipoprotein CIII overexpression in apolipoprotein E-null mice. Apolipoprotein CIII-induced hypertriglyceridemia is not mediated by effects on apolipoprotein E.

The mechanism of apolipoprotein (apo) CIII-induced hypertriglyceridemia remains uncertain. We crossed apoCIII transgenic and apoE gene knockout (apoE0) mice, and observed severe hypertriglyceridemia with plasma triglyceride levels of 4,521+/-6, 394 mg/dl vs. 423+/-106 mg/dl in apoE0 mice, P < 0.00001 for log(triglycerides [TG]). Cholesterols were 1,181+/-487 mg/dl vs. 658+/-151 mg/dl, P < 0.0001. Lipoprotein fractionation showed a marked increase in triglyceride-enriched chylomicrons+VLDL. This increase was limited to the lowest density (chylomicrons and Sf 100-400) subfractions. Intermediate density lipoproteins (IDL)+LDL increased moderately, and HDL decreased. There was no significant increase in triglyceride production in apoCIII transgenic/apoE0 mice. The clearance of VLDL triglycerides, however, was significantly decreased. Lipoprotein lipase in postheparin plasma was elevated, but activation studies suggested LPL inhibition by both apoCIII transgenic and apoCIII transgenic/apoE0 plasma. ApoCIII overexpression also produced a marked decrease in VLDL glycosaminoglycan binding which was independent of apoE. The predominant mechanism of apoCIII-induced hypertriglyceridemia appears to be decreased lipolysis at the cell surface. The altered lipoprotein profile that was produced also allowed us to address the question of the direct atherogenicity of chylomicrons and large VLDL. Quantitative arteriosclerosis studies showed identical results in both apoCIII transgenic/apoE0 and apoE0 mice, supporting the view that very large triglyceride-enriched particles are not directly atherogenic.

Animals↗
PubMed1997

Interaction of tetracycline with RNA: photoincorporation into ribosomal RNA of Escherichia coli.

Photolysis of [3H]tetracycline in the presence of Escherichia coli ribosomes results in an approximately 1:1 ratio of labelling ribosomal proteins and RNAs. In this work we characterize crosslinks to both 16S and 23S RNAs. Previously, the main target of photoincorporation of [3H]tetracycline into ribosomal proteins was shown to be S7, which is also part of the one strong binding site of tetracycline on the 30S subunit. The crosslinks on 23S RNA map exclusively to the central loop of domain V (G2505, G2576 and G2608) which is part of the peptidyl transferase region. However, experiments performed with chimeric ribosomal subunits demonstrate that peptidyltransferase activity is not affected by tetracycline crosslinked solely to the 50S subunits. Three different positions are labelled on the 16S RNA, G693, G1300 and G1338. The positions of these crosslinked nucleotides correlate well with footprints on the 16S RNA produced either by tRNA or the protein S7. This suggests that the nucleotides are labelled by tetracycline bound to the strong binding site on the 30S subunit. In addition, our results demonstrate that the well known inhibition of tRNA binding to the A-site is solely due to tetracycline crosslinked to 30S subunits and furthermore suggest that interactions of the antibiotic with 16S RNA might be involved in its mode of action.

Base Sequence↗
PubMed1997

Diabetes and atherosclerosis--a lipoprotein perspective.

Atherosclerosis is the most frequent complication of diabetes. It affects all major vascular beds. The metabolic derangements that occur in diabetes may underlie many of the reasons for this. These abnormalities include alterations in the metabolism of lipoproteins, particularly the triglyceride-rich lipoproteins. Studies are currently being conducted to determine whether correcting the dyslipoproteinaemias associated with diabetes will reduce the risk of atherosclerosis in the diabetic population.

Arteriosclerosis↗