Usefulness of troponin I as a marker of myocardial injury after pediatric cardiac catheterization

Cardiac troponin I (cTnI) is a sensitive and specific marker of myocardial injury. The degree of myocardial injury associated with pediatric cardiac catheterization is unknown. We sought to investigate cTnI after pediatric cardiac catheterization, and to evaluate the degree of elevation observed with specific types of interventions. Seventy-three pediatric catheterizations were evaluated. Diagnostic procedures and interventions not expected to cause myocardial injury were assigned to group I, whereas interventional procedures expected to be associated with cardiac injury were assigned to group II. Group II procedures were further subdivided based on type of intervention. Serum samples were obtained before and after all procedures and analyzed for cTnI. Postprocedure cTnI levels were compared across groups and correlated with age and weight. Procedures in group II were associated with significantly higher cTnI levels than group I (median 2.65 ng/ml; interquartile range 0.9 to 4.9 ng/ml for group II vs 0.3; 0.3 to 1.6 ng/ml for group I, p <0.001). Within group II, cTnI was inversely correlated with age (p <0.05) and weight (p <0.05). Radiofrequency catheter ablation (RFA) caused higher cTnI levels than other types of interventions (median 3.7 ng/ml; 1.9 to 9.5 ng/ml for RFA vs 1.75; 0.7 to 4.9 ng/ml for non-RFA, p <0.05). Most pediatric interventional catheterization procedures are associated with myocardial injury, as evidenced by elevation of cTnI, with RFA causing higher levels than other interventions. Conversely, most diagnostic procedures are associated with no detectable myocardial injury. When compared with adult studies, pediatric patients seem to be at higher risk for myocardial injury from interventional cardiac catheterization.     

Submandibular tumor

Ohne Zusammenfassung V.Tr?ger Klinik für Hals-, Nasen-,Ohrenheilkunde, Unfallkrankenhaus,Warener Stra?e 7, 12683 Berlin, E-Mail: Vanessa.Tr?ger@UKB.de     

Modulation of synaptic transmission by nociceptin/orphanin FQ and nocistatin in the spinal cord dorsal horn of mutant mice lacking the nociceptin/orphanin FQ receptor

Nociceptin/orphanin FQ (N/OFQ) and nocistatin (NST) are two neuropeptides derived from the same precursor protein that exhibit opposing effects on spinal neurotransmission and nociception. Here, we have used whole-cell, patch-clamp recordings from visually identified neurons in spinal cord dorsal horn slices of genetically modified mice to investigate the role of the N/OFQ receptor (N/OFQ-R) in the modulatory action of both peptides on excitatory glutamatergic and inhibitory glycinergic and gamma-aminobutyric acid (GABA)-ergic synaptic transmission. In wild-type mice, N/OFQ selectively suppressed excitatory transmission in a concentration-dependent manner but left inhibitory synaptic transmission unaffected. In contrast, NST reduced only inhibitory but not alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated excitatory synaptic transmission. N/OFQ-mediated inhibition of excitatory transmission was completely absent in N/OFQ-R receptor-deficient (N/OFQ-R(-/-)) mice and significantly reduced in heterozygous (N/OFQ-R(+/-)) mice, whereas the action of NST on inhibitory neurotransmission was completely retained. To test for the relevance of these results for spinal nociception, we investigated the effects of intrathecally injected N/OFQ in the mouse formalin test, an animal model of tonic pain. N/OFQ (3 nmol/mouse) induced significant antinociception in wild-type mice, but had no antinociceptive effects in N/OFQ-R(-/-) mice. These results indicate that the inhibitory action of N/OFQ on excitatory glutamatergic synaptic transmission and its spinal antinociceptive action are mediated via the N/OFQ receptor, whereas the action of NST is independent of this receptor.     

Genetic imbalances in preinvasive tissue of hypopharynx provide evidence for cytogenetic heterogeneity

Multiple chromosomal aberrations have been reported in head and neck squamous cell carcinoma (HNSCC). But less information is available on specific patterns of chromosomal amplifications which distinguish different areas of head and neck tumors. To elucidate genetic mechanisms causing the aggressive growth and high proliferation of hypopharyngeal squamous cell carcinoma (SCC), we performed reverse chromosome painting (RCP) on a total of eight hypopharyngeal SCC including invasive carcinoma and preinvasive tissue. Five hypopharyngeal invasive carcinomas showed amplifications on chromosome 3q. Furthermore, we detected gains on chromosomes 11q and 6p. Compared to the histologically classified preinvasive tissues, we found amplified alterations on chromosome 6p, 11q and 12q, but none of them showed gains on chromosome 3q. This observed heterogeneity in hypopharyngeal SCC might reflect a specific role of chromosome 3q as a late event in the highly invasive capacity of these SCC.     

Experience with midtrimester abortion.

The midtrimester abortion program at a large community hospital was evaluated. During the 3-year study, 1839 patients aborted in the midtrimester by intraamniotic injection of hypertonic saline, prostaglandin F2alpha or a combination of saline and prostaglandin F2alpha. The method, using a combination of saline and prostaglandin F2alpha together with intracervical laminaria, showed significant reduction in the number of failures (4.3 to 1.0%), reduction in the injection-abortion interval from 33.9 to 14.6 hours, shortening of the hospital stay from 2 1/2 to 1 1/3 days, minimum incidence of live abortions (0.9%), infrequent need for oxytocin to effect delivery (7.7%); and low rates of hemorrhage (1.5%) and fever (2.8%). The main disadvantage was an increased rate of incomplete abortions (32.3%), which could be reduced to 27% by patient selection.     

The effect of corticosteroids and other antineoplastic agents on the generation of leukocyte migration inhibition factor

We have shown that hydrocortisone in physiological concentrations can inhibit the production of leukocyte migration inhibition factor (LMIF), but does not diminish the action of this lymphokine. Other agents tested failed to influence LMIF production. Inhibition of LMIF production by corticosteroids was influenced by the nature of the stimulus used for the production as an effect could be seen with PHA or Con A, but not Staphylococcal enterotoxin A (SEA). Production of LMIF was promptly restored after removal of the steroids. Furthermore, addition of a calcium ionophore to PHA restored the production of LMIF even in the presence of corticosteroids. In contrast, addition of exogenous IL-2 did not correct the defect in lymphokine secretion. We believe that inhibition of the production of LMIF by steroid may lead to defective granulocytic function and thus, predispose to infection.