Survival impact of postoperative radiotherapy in patients with olfactory neuroblastoma: 513 cases from the SEER database.

PUPOSE: To evaluate the impact of postoperative radiotherapy (PORT) on survival in olfactory neuroblastoma (ONB) patients with different tumor staging. MATERIAL AND METHODS: Patients with ONB were selected in the Surveillance, Epidemiology and End Results (SEER) database from 2004-2016. Survival analyses were performed using Kaplan-Meier (K-M) method, Cox regression analysis, and competing risk model. RESULTS: A total of 513 patients were included in the study. Univariate and multivariate analysis results demonstrated that PORT was not an independent prognostic factor for overall survival (OS) of modified Kadish stage A and B patients (P=0.699 and P=0.248, respectively). Kadish stage C and D patients who underwent PORT had significantly better OS than those who did not undergo PORT (P=0.03 and P<0.0001). K-M curves revealed that the 5- and 10-year OS rates of patients who underwent PORT vs. non-PORT were 85.3% vs. 70.4% and 68.2% vs. 56.8% in stage C patients, respectively. For stage D patients, the 5-year OS rates were 70.7% and 42.6%, and 10-year OS rates were 53.4% and 29.5% in the PORT and non-PORT groups, respectively. The competitive risk model revealed that the 5-year cancer-specific cumulative mortality incidence decreased by 26.6% while the 10-year mortality incidence decreased by 41.4% in Kadish stage C patients who were treated using PORT; meanwhile, for Kadish stage D patients who were treated with PORT, the 5- and 10-year mortality incidences were reduced by 35.3% and 42.6%, respectively. Furthermore, we found that chemotherapy was not related to the prognosis of ONB patients (all P>0.05). CONCLUSION: Our results indicate that PORT improved survival outcomes of modified Kadish stage C and D ONB patients. However, PORT may not affect survival for modified Kadish stage A and B individuals. Chemotherapy was not recommended for ONB; therefore, further studies are warranted to determine its therapeutic significance.

Repolarization interactions between cardiac segments of varying action potential duration.

We studied interactions between action potential duration (APD) disperse zones using a double compartment bath in which an APD lengthening solution (Ni++ 2 mmol/L, in Tyrode's solution) was added to one compartment (which contained a portion of the fiber labeled "segment A") followed by addition of an APD shortening solution (6 to 10 mmol/K+) to the other compartment ("segment B"). Standard microelectrode techniques were used in canine Purkinje fibers. With Ni++ in segment A, there was a dispersion in APD measured at both 50% (APD50) and 95% (APD95) of repolarization. After selective addition of K+ to segment B, APD50 dispersion remained constant while APD95 dispersion increased, which indicated a change in the slope of repolarization, a factor with possible arrhythmogenic potential. In addition, a characteristic transitional action potential was seen adjacent to the partition. This had a timely and normally sloping early repolarization followed by a much more gradually sloping shelf. Premature action potentials arising during this shelf had diminished upstrokes. Results of these experiments may be useful in evaluating APD dispersion in relation to arrhythmias.

In vitro characteristics of repolarization abnormality--a possible cause of arrhythmias.

When membrane potential (Vm) remains at depolarized levels for prolonged intervals, quiescence and/or repetitive activations occur. In situ such events would be associated with arrhythmias. One way for such a state to occur is abnormal delay of repolarization leading to marked prolongation of action potential (AP) duration (APD). We studied canine Purkinje fibers in which abnormal AP prolongation had been induced by hypoxic, acidic Tyrode's with or without epinephrine, or by Ni++. AP's exhibited a prolonged secondary plateau with or without early afterdepolarizations (EAD's); they were up to ten minutes in duration. With programmed stimulation, APD's displayed a markedly exaggerated interval dependence with slight increases in diastolic interval causing transitions from normal to abnormal and very long AP's. Normalization of AP's occurred during prolonged rapid pacing trains and only gradually returned to abnormality after cessation of pacing. We also induced EAD's via programmed stimulation at plateau Vm levels. Repolarization could be brought on abruptly via these stimulus-induced EAD's; in certain instances trains of EAD's were required. The above characteristics of the state for which the term "repolarization failure" seems appropriate may have implications for in situ arrhythmias, e.g. in "Torsade de Pointes" ventricular tachycardia.