Effects of the selective noradrenergic neurotoxin DSP4 on cerebellar Purkinje neuron electrophysiology

The effect of the adrenergic neurotoxin DSP4 on cerebellar electrophysiology was studied in the rat. DSP4, administered parenterally, depleted cerebellar norepinephrine by 76%. The depressant response of cerebellar Purkinje neurons to phencyclidine, a drug which acts on adrenergic presynaptic terminals to release NE, was markedly reduced after DSP4 pretreatment. In contrast with 60HDA, which increased firing rates of the Purkinje cells, DSP4 did not change the rate or pattern of Purkinje cell discharge. Taken together these results suggest that DSP4 may be a valuable tool for studying central adrenergic pathways, but that this drug has properties which differ from 60HDA.     

Automated thermal imaging monitors the local response to cervical cancer brachytherapy

Malignant tumors have high metabolic and perfusion rates, which result in a unique temperature distribution as compared to healthy tissues. Here, we sought to characterize the thermal response of the cervix following brachytherapy in women with advanced cervical carcinoma. Six patients underwent imaging with a thermal camera before a brachytherapy treatment session and after a 7-day follow-up period. A designated algorithm was used to calculate and store the texture parameters of the examined tissues across all time points. We used supervised machine learning classification methods (K Nearest Neighbors and Support Vector Machine) and unsupervised machine learning classification (K-means). Our algorithms demonstrated a 100% detection rate for physiological changes in cervical tumors before and after brachytherapy. Thus, we showed that thermal imaging combined with advanced feature extraction could potentially be used to detect tissue-specific changes in the cervix in response to local brachytherapy for cervical cancer.     

Nucleotide sequence comparison of five human pepsinogen A (PGA) genes: evolution of the PGA multigene family

To unravel the genetic basis for the pepsinogen A (PGA) protein polymorphism, we have isolated and characterized a number of PGA genes, distinguishable by polymorphic EcoRI fragments of 12.0, 15.0, and 16.6 kb. Using a HindIII or AvaII polymorphism, we can discriminate between different 15.0 (15.0 and 15.0*) and 12.0 (12.0s and 12.0l) genes, respectively. The coding sequences of a 15.0 and a 16.6 gene were determined, together with considerable stretches of the 5'- and 3'-flanking regions and introns. The genes were demonstrated to encode Pg5 and Pg4, respectively. Because substitutions in codons 43 and 207 appeared to be critical in the determination of the encoded proteins, we sequenced only these regions in the two 12.0 genes and the 15.0* gene. On the basis of these partial sequences, we assume that these genes encode Pg3. In the evolutionary model of the PGA gene cluster presented here, the 12.0 genes arose by an unequal, but homologous crossover. The results of sequence analysis of the second intron of the 12.0s, 12.0l, 15.0, and 16.6 genes suggest that the two 12.0 genes have arisen from two different crossover events.