Biomedical subjects

John D Herrington

Publications and source records attributed to John D Herrington.

3 recordsLinked to original sources

PubMed2005

Neural mechanisms of affective interference in schizotypy.

Negatively valenced stimuli foster cognitive impairment in schizotypy and schizophrenia. To identify relevant brain mechanisms, the authors had 16 positive-schizotypy and 16 control participants perform an emotional Stroop task, judging the ink color of negative and neutral words during functional magnetic resonance imaging (fMRI) of regional brain activity. Schizotypy individuals showed increased right and decreased left activity in dorsolateral prefrontal cortex, indicating a deficit in maintenance of attentional set in the presence of negative emotional distractors. They also showed abnormal activity in ventral limbic areas, including decreased activity in nucleus accumbens and increased activity in hippocampus and amygdala, a circuit involved in the integration of cognitive and affective processes. These results indicate that aspects of emotion-cognition processes and the brain mechanisms that implement them are similar in schizotypy and schizophrenia.

Adult↗

PubMed2005

Emotion-modulated performance and activity in left dorsolateral prefrontal cortex.

Functional MRI (fMRI) was used to examine the relationship between processing of pleasant and unpleasant stimuli and activity in prefrontal cortex. Twenty volunteers identified the colors in which pleasant, neutral, and unpleasant words were printed. Pleasant words prompted more activity bilaterally in dorsolateral prefrontal cortex (DLPFC) than did unpleasant words. In addition, pleasant words prompted more activity in left than in right DLPFC. Response speed to pleasant words was correlated with DLPFC activity. These data directly link positive affect, enhanced performance, and prefrontal activity, providing some of the first fMRI evidence supporting models of emotional valence and frontal brain asymmetry based on electroencephalography (EEG).

Adult↗

PubMed2005

Tumor lysis syndrome after bortezomib therapy for plasma cell leukemia.

Tumor lysis syndrome (TLS) is a manifestation of metabolic disturbances that can lead to severe treatment complications and ultimately life-threatening events. This syndrome has been reported in solid tumors but is more common in bulky, hyperproliferative malignancies. Tumor lysis syndrome in plasma cell malignancies is less common due to the low turnover rate of the malignant B cells. Bortezomib is the first proteasome inhibitor approved by the United States Food and Drug Administration as second- and third-line therapy for patients with relapsed multiple myeloma. We describe the case of a patient with plasma cell leukemia treated with bortezomib who developed TLS. Bortezomib was begun as single-agent therapy that resulted in the development of TLS after the third dose of the first cycle. Evaluation with the Naranjo Adverse Drug Reaction Probability Scale indicated a probable relationship between TLS and bortezomib in this patient. Patients receiving bortezomib may be at risk for TLS, especially if they have high tumor burden, rapidly proliferative disease, and unfavorable cytogenetics.

Antineoplastic Agents↗