PubMed · 11357847
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P D Varosy, T B Newman. 2001-05-10. Acute pharyngitis.. https://pubmed.ncbi.nlm.nih.gov/11357847/
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Hypothalamic-pituitary-adrenal (HPA) responses to stress are initiated by parvicellular neurosecretory neurons in the medial parvicellular (mp) part of the paraventricular hypothalamic nucleus (PVH), which express corticotropin-releasing factor (CRF), among other neuropeptides. We have used an approach guided by patterns of stress-induced Fos expression to explore the manner in which anatomically and phenotypically defined components of the mpPVH respond to acute vs. repeated restraint stress. Hormonal indices of HPA activation in animals exposed to the last of 14 daily repeated restraint sessions were significantly lower than those in rats receiving a single restraint episode. Although this habituation was paralleled by global decrements in activation patterns across all PVH compartments, clear spatial-temporal differences in recruitment profiles were noted between dorsal and ventral aspects of the mpPVH. Thus, acute restraint provoked a biphasic Fos induction, which occurred first within the mpPVH and in an adjoining population of somatostatinergic cells in the periventricular region and only later within other aspects of the PVH. By contrast, Fos responses of habituated animals were monophasic and focused decisively within a discrete ventral aspect of the mpPVH. The ventral population was identified as comprising neurons that express CRF and/or enkephalin and, to a lesser extent, growth hormone-releasing factor. These results indicate a lack of homogeneity among stress-responsive parvicellular neurosecretory neurons and suggest that distinct complements of CRF cells may be preferentially involved in initiating HPA responses to acute stress and sustaining them in the repeated condition.
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Gemtuzumab ozogamicin (Mylotarg) targets leukemia cells expressing the CD33 receptor by means of a monoclonal antibody conjugated to a cytotoxic agent, calicheamicin. Treatment of acute myeloid leukemia (AML) with gemtuzumab ozogamicin may result in liver injury. We reviewed the course of 23 patients who were given gemtuzumab ozogamicin for AML that had relapsed after hematopoietic cell transplantation. Liver toxicity was assessed through physical examination, serum tests, histologic examination, and hepatic venous pressure measurements. Liver injury developed in 11 patients after gemtuzumab ozogamicin administration; it was manifested as weight gain, ascites, and jaundice in 7 patients. Seven patients died with persistent liver dysfunction and either multiorgan failure or sepsis at a median of 40 days after gemtuzumab ozogamicin infusion. Portal pressure measurements were elevated in 2 patients. Results of liver histologic examination in 5 patients showed sinusoidal injury with extensive sinusoidal fibrosis, centrilobular congestion, and hepatocyte necrosis. Six patients experienced AML remission that was sustained for at least 60 days after gemtuzumab ozogamicin infusion. In summary, hepatic sinusoidal liver injury developed after gemtuzumab ozogamicin infusion. Histology showed striking deposition of sinusoidal collagen, suggesting that gemtuzumab ozogamicin targets CD33(+) cells residing in hepatic sinusoids as the mechanism for its hepatic toxicity.