Akuter thrombembolischer ST-Hebungs-Infarkt bei einem Patienten mit essenzieller Thrombozytose

A 48-year-old man presented with acute chest pain and a greatly increased platelet count. Emergency coronary angiographc revealed thrombotic occlusion of the right coronary artery. Coronary angioplasty and stenting were successfully combined with intracoronary abciximab administration. Due to inadequate postinterventional platelet inhibition an intensified dual antiplatelet therapy with acetylsalicylic acid (ASS) and clopidogrel was applied to prevent stent thrombosis. Due to the thrombo-embolic complication and a platelet count over 1 million/µl a cytoreductive treatment with hydroxyurea was initiated.     

Immunoglobulin Y Levels in Egg Yolk From Three Chicken Genotypes

Laying hens are very efficient producers of antibodies and provide an interesting alternative for large-scale production of specific antibodies. These antibodies also have biochemical advantages over mammalian antibodies (e.g. rabbit antibodies) that can be used to improve immunoassays where antibodies are used. The concentration of IgY in egg yolk is an important production parameter. The purpose of this study was to investigate the genetic variation of IgY levels in egg yolk. We have compared IgY concentrations in egg yolks from two lines, selected for egg production traits at the Swedish University for Agricultural Sciences (Single Comb White Leghorn and Rhode Island Red) and a cross between the two lines (SLU-1392). Single Comb White Leghorns have the highest mean concentration of yolk IgY, 2.21 mg ml^-1 compared to SLU-1392 1.95 mg ml^-1 and Rhode Island Red 1.68 mg ml^-1. The cross thus had an intermediate IgY concentration in relation two the two other lines. There were great differences between individual animals within each line. Our results indicate that it should be possible to increase yolk antibody production by using a high producing chicken line and by genetic selection within the line. We found three individuals with very low yolk IgY concentrations among the Rhode Island Red hens. Newly hatched chickens with limited amounts of IgY from the hen may be more susceptible to infections.     

Rupture of the extensor pollicis longus tendon: a study of aetiological factors.

Although rupture of the extensor pollicis longus (EPL) tendon is a well-known complication of distal radial fractures, a number of patients rupture the EPL because of other conditions. We have retrospectively studied the aetiology of 27 ruptures of the EPL in 26 consecutive patients. Of 19 patients with injured wrists 12 had distal radial fractures, five had blunt trauma, and two had stab wounds that resulted in rupture. In the radial fractures operated on, the EPL rupture was caused by chafing against a dorsal plate (n = 2) or wear against the pins of an external fixator (n = 2). Six patients were taking steroids for systemic diseases and in two cases a local steroid injection was given just before the rupture. We conclude that previous injury is the most common cause of rupture of the EPL. but that rheumatoid arthritis or local or systemic steroids, or both, are also important aetiological factors. Seven patients had an iatrogenic cause for their rupture.     

Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML.

Amplification or duplication of the AML1 gene at chromosome band 21q22 was detected by FISH using a locus-specific probe in three out of 171 unselected patients with therapy-related myelodysplasia (t-MDS) or t-AML (1.7%). In two patients AML1 signals were located tandemly on derivative chromosomes, in one patient on a dic(9;21) and in the the other patient on a derivative chromosome 18 made up of interchanging layers of material from chromosomes 9, 14, 18, and 21. In the third patient three single supernumerary copies of AML1 were located on derivatives of chromosomes 19 and 21. All three patients were older, had previously received therapy with alkylating agents without topoisomerase II inhibitors, had complex karyotypes including abnormalities of chromosomes 5 or 7, and presented acquired point mutations of the TP53 gene. No point mutations of the AML1 gene were observed. The results support a pivotal role of impaired TP53 function in the development of gene amplification or duplication in t-MDS and t-AML.     

Measurements of bone mineral density of the proximal femur by two commercially available dual energy X-ray absorptiometric systems.

Two dual energy X-ray absorptiometric (DXA) instruments have recently become commercially available for local bone densitometry: the QDR-1000 (Hologic Inc.) and the DPX (Lunar Radiation Corp.). We report the precision, influence of femoral rotation, correlation and agreement of bone mineral measurements of the proximal femur by these two instruments. In vitro (femur phantom) short-term precision was 1.1%-3.5%, and the long-term precision was 1.2%-3.8%. In vivo (groups of 10 premenopausal and 10 post-menopausal women) short-term precision of duplicate measurements was 1.6%-4.7%, and long-term precision was 1.9%-5.5%. Overall, the precision for Ward's triangle was over 3% and that for the femoral neck and trochanter, 2%-3%. Rotation of a femur phantom produced a statistically significant change in the bone mineral density (BMD) of the femoral neck. Within a clinically relevant range of femoral rotation (20 degrees inward rotation +/- 5 degrees) the coefficient of variation (CV%) increased by a mean factor of 1.1-1.4. Although the correlation (r less than 0.9) between BMD measurements of the proximal femur by the DPX and QDR-1000 in 30 postmenopausal women was high, there was lack of agreement between the two instruments. We found no statistically significant differences between the right and left femur in 30 postmenopausal women. A bilateral femur scan took a mean total time of about 22 min. We conclude that with the introduction of DXA instruments, the precision of bone mineral measurements of the proximal femur has improved. However, for comparability between commercially available DXA instruments, it might be advantageous if units were standardized.     

Prostaglandins and CGRP release from cardiac sensory nerves

Summary (1) The possible influence of Prostaglandins (PG) E₁ and I₂ as well as ischaemia, ouabain and bradykinin on the outflow of calcitonin gene-related peptide (CGRP)- and neuropeptide Y (NPY)-like immunoreactivity (LI) from the guinea-pig heart was studied in vitro. (2) Exposure to PGE₁ (10^–5 M), but not PGI₂ (10^–5 M), induced an increased outflow, suggesting release of CGRP-LI. PGE₁ simultaneously increased the contractile force and heart rate while no effects were observed on perfusate volume or outflow of NPY-LI. PGI₂ had no effect on contractile parameters or coronary flow. In separate experiments on capsaicin-pretreated animals, the stimulatory effects of PGE₁ on heart rate and contractile force remained unchanged while no increased CGRP-LI outflow was detectable. (3) Ouabain, bradykinin and reperfusion after total stop-flow ischaemia was associated with an indomethacin-resistant increase in perfusate levels of CGRP-LI but not of NPY-LI. While ouabain markedly increased the contractile force, exposure to bradykinin or ischaemia did not induce any clear-cut changes in contractile force or heart rate. (4) Capsaicin-exposure evoked a markedly increased outflow of CGRP-LI but not of NPY-LI in combination with an increase in heart rate and a decrease in contractile force. Repeated administration of capsaicin induced tachyphylaxis. The stimulatory effects of capsaicin on CGRP-LI outflow and heart rate, but not the negative inotropic effect, did not occur in capsaicin-pretreated animals. (5) It is concluded that PGE₁, but not PGI₂, can activate cardiac capsaicin-sensitive fibres as revealed by increased outflow of CGRP-LI. The cardiostimulatory effects induced by PGE₁ are not related to CGRP release, however. A possible prostaglandin link in the CGRP-LI released by ouabain, bradykinin or ischaemia seems unlikely. Send offprint requests to: A. Franco-Cereceda at the above address     

Alpha-ketoacids stimulate rat renal cysteine conjugate beta-lyase activity and potentiate the cytotoxicity of S-(1,2-dichlorovinyl)-L-cysteine

Renal cysteine conjugate beta-lyase (beta-lyase) catalyzes the bioactivation of nephrotoxic cysteine S-conjugates. beta-Lyase activity is present in both renal cytosolic and mitochondrial fractions, and, although the cytosolic beta-lyase is identical to glutamine transaminase K, the mitochondrial beta-lyase has not been characterized. Because beta-lyase is a pyridoxal phosphate (PLP)-dependent enzyme, pyridoxamine phosphate (PMP) formation may occur during the metabolism of cysteine S-conjugates. In this study, the effects of alpha-ketoacids, which may convert the PMP form of the enzyme to the pyridoxal phosphate form, on the metabolism and cytotoxicity of cysteine S-conjugates were examined; the PMP enzyme is catalytically inactive in beta-elimination reactions, but is catalytically active in transamination reactions. Both alpha-keto-gamma-methiolbutyrate (KMB) and alpha-ketobutyrate enhanced the metabolism of S-(2-benzothiazolyl)-L-cysteine (BTC) to 2-mercaptobenzothiazole by rat renal cytosol or mitochondria. KMB and phenylpyruvate potentiated both the cytotoxicity of S-(1,2-dichlorovinyl)-L-cysteine (DCVC) in isolated rat renal proximal tubular cells and the inhibition of mitochondrial respiration produced by DCVC. These results are consistent with the formation of PMP during the renal cytosolic or mitochondrial metabolism of cysteine S-conjugates. Mitochondrial beta-lyase was previously localized in the outer membrane. To examine whether beta-lyase activity is present in mitoplasts, but in the PMP form, the effects of KMB on the metabolism of BTC to 2-mercaptobenzothiazole and on the DCVC-induced inhibition of state 3 respiration in mitoplasts were studied. The majority of the mitochondrial beta-lyase activity was present in the outer membrane, and the specific activity of the outer membrane beta-lyase was greater than that of the mitoplast beta-lyase. KMB produced equivalent stimulation of beta-lyase activity in intact mitochondria, in mitochondrial outer membranes, and in mitoplasts and potentiated DCVC-induced inhibition of respiration in intact mitochondria, but not in mitoplasts. These results provide additional evidence for the central role of beta-lyase in the bioactivation of nephrotoxic cysteine S-conjugates.