Functional neurogenomic responses to acoustic threats, including a heterospecific referential alarm call and its referent, in the auditory forebrain of red-winged blackbirds.

In animal communication, functionally referential alarm calls elicit the same behavioral responses as their referents, despite their typically distinct bioacoustic traits. Yet the auditory forebrain in at least one songbird species, the black-capped chickadee Poecile atricapillus, responds similarly to threat calls and their referent predatory owl calls, as assessed by immediate early gene responses in the secondary auditory forebrain nuclei. Whether and where in the brain such perceptual and cognitive equivalence is processed remains to be understood in most other avian systems. Here, we studied the functional neurogenomic (non-) equivalence of acoustic threat stimuli perception by the red-winged blackbird Agelaius phoeniceus in response to the actual calls of the obligate brood parasitic brown-headed cowbird Molothrus ater and the referential anti-parasitic alarm calls of the yellow warbler Setophaga petechia, upon which the blackbird is known to eavesdrop. Using RNA-sequencing from neural tissue in the auditory lobule (primary and secondary auditory nuclei combined), in contrast to previous findings, we found significant differences in the gene expression profiles of both an immediate early gene, ZENK (egr-1), and other song-system relevant gene-products in blackbirds responding to cowbird vs. warbler calls. In turn, direct cues of threats (including conspecific intruder calls and nest-predator calls) elicited higher ZENK and other differential gene expression patterns compared to harmless heterospecific calls. These patterns are consistent with a perceptual non-equivalence in the auditory forebrain of adult male red-winged blackbirds in response to referential calls and the calls of their referents.

Liver biopsy in psoriatic arthritis to detect methotrexate hepatotoxicity.

The use of methotrexate in the treatment of psoriatic arthritis is associated with risk of hepatotoxicity. However, monitoring of liver-associated enzymes often lacks sensitivity, and guidelines for serial liver biopsies in psoriatic arthritis are not yet well established. We performed a retrospective review of all patients with psoriatic arthritis receiving methotrexate who were enrolled in the disease-modifying anti-rheumatic drug clinics (DMARD clinics) at the Air Force and Army hospitals in San Antonio, Texas. Information was obtained regarding methotrexate regimen, liver-associated enzyme results, and liver biopsy results. Thirty psoriatic arthritis patients were taking methotrexate in the DMARD clinics. Seventeen patients had a total of 21 biopsies. Biopsies were performed for surveillance dictated by cumulative dose. Liver biopsies were graded on Roenigk scale of I-IV where I is mild steatosis, II is moderate steatosis, IIIa is mild fibrosis, IIIb is severe fibrosis, and IV is cirrhosis. Ten biopsies were grade I, 5 were grade II, 5 were grade IIIa, 1 was grade IIIb, and none were grade IV. In this very small retrospective study, regular monitoring of liver-associated enzymes did not correlate with histologic deterioration in our patients. Until prospective studies are performed, we suggest that routine liver biopsies are necessary to monitor for methotrexate hepatotoxicity in psoriatic arthritis.

Use of desmin immunohistochemistry to distinguish between mesothelial cells and carcinoma in serous fluid cell block preparations.

OBJECTIVE: To evaluate the utility of immunohistochemical stains for desmin in discriminating mesothelial cells from adenocarcinoma in serous fluid cell block preparations. STUDY DESIGN: Cell block preparations from 22 cases (representing 18 patients) that were positive for carcinoma and 5 cases that were negative for malignancy were immunostained with an antibody to desmin. Positive staining was evaluated and scored semiquantitatively in both tumor cells and background mesothelial cells in the malignant cases and mesothelial cells in the negative controls. Staining was evaluated with a score of 0-3 for intensity and 0-5 for distribution. The sum of the two scores was recorded as the total score (TS). RESULTS: Mesothelial cells from all the carcinoma and benign cases stained with desmin (median TS = 5.5, range 4-8), typically strong in intensity and widespread in distribution. Positivity was observed in carcinoma cells in all cases, typically weak and focal (range 2-4). Using a total score of 4 as a cutoff for definitively positive staining, desmin staining was positive in mesothelial cells in 25/25 cases and carcinoma cells in 1/22 cases (P < .0001, Fisher's exact test). Additionally, using the Mann-Whitney ranked sum test on the 20 cases with evaluable mesothelial cells, the medians of the total scores for mesothelial cells (5.5) and carcinoma cells (2.5) were significantly different (P < .0001). CONCLUSION: A total score of > or = 4 was significantly associated with mesothelial cell staining. Use of desmin immunohistochemical staining in cell block preparations may be helpful in distinguishing between mesothelial cells and carcinoma.

Leukocytosis in acute pulmonary embolism.

PURPOSE: The purpose of this investigation is to assess the level of leukocytosis in acute pulmonary embolism (PE). BACKGROUND: Limited data exist regarding leukocytosis in acute PE. One reason that the prevalence of leukocytosis in acute PE is unknown, despite an extensive number of investigations of PE, may relate to the fact that acute PE is usually associated with other conditions that themselves may cause leukocytosis. METHODS: Hospital records of 386 patients with a diagnosis of acute PE were reviewed retrospectively. Patients with no other possible or definite cause of leukocytosis were analyzed separately. A diagnosis of PE was made by a high-probability interpretation of the ventilation/perfusion lung scan or pulmonary angiogram. RESULTS: Among patients with PE in whom other possible or defined causes for leukocytosis were eliminated, 52 of 266 (20%) had a WBC count > 10,000/mm3. None had a WBC count that was > or = 20,000/mm3. Patients with the pulmonary hemorrhage/infarction syndrome had an increased WBC count in 32 of 183 (17%) vs 20 of 83 (24%) in patients who did not have pulmonary hemorrhage/infarction syndrome (not significant). CONCLUSION: A modest leukocytosis may accompany (and possibly be caused by) PE. Its presence should not dissuade the clinician from objectively pursuing the diagnosis of PE.