Rapid gas-chromatographic microdetermination of soluphylline in serum

A nitrogen-specific gas-chromatographic method is described for the quantitative analysis of soluphylline without the need for derivatization or evaporation of solvent, and using only 50 microliters of serum. The analysis is performed isothermally on a silicone stationary phase, 2% SP 2250 DA (Supelco). After a single neutral extraction with ethyl acetate containing the internal standard (beta-hydroxypropyl theophylline), an aliquot of the organic solvent is injected directly into the gas chromatograph. The detector sensitivity (least measurable amount) for soluphylline was 1 ng.     

Blue nevus of the prostate: report of two new cases with immunohistochemical and electron-microscopic studies.

Two new cases of prostatic blue nevus are studied with routine histological, immunohistochemical and ultrastructural methods. Both cases showed a chronic lower urinary tract obstruction due to a benign prostatic hyperplasia with spindle-shaped stromal cells loaded with melanin pigment. These cells were positive for S-100 and negative for HMB-45 antibodies, being, to the best of our knowledge, the first time that this antibody has been tested in prostatic pigmented lesions. The electron-microscopy study was performed in the first case, confirming the nature of these pigmented cells as melanocytes derived from the neural crest showing melanosomes in all the stages of differentiation and without complete basal cell membrane. The histogenesis of pigmented lesions of the prostate and the differences between blue nevus and melanosis are discussed, and the literature is reviewed.     

1,3-Dipropyl-8-cyclopentylxanthine attenuates the NMDA response to hypoxia in the rat hippocampus

Excitatory amino acids may cause neuronal damage and death in cerebral hypoxia and ischemia, through the activation of different subtypes of glutamate receptors, in particular of the (NMDA) receptor. In the present work, the effect of hypoxia on the component of the field excitatory postsynaptic potential (fepsp) mediated by the NMDA receptor was studied in the hippocampal CA1 area of the rat. A period of 15 min of hypoxia induced virtual abolition of the NMDA receptor-mediated fepsp and a 94.8 ± 0.7% maximal decrease in the fepsp. A period of 3 min of hypoxia induced a 89.3 ± 12.3% maximal decrease in the NMDA receptor-mediated component of the fepsp and only a 50.8 ± 11.5% maximal decrease in the fepsp. Both periods of hypoxia thus induced a more pronounced depression of the NMDA receptor-mediated component of the fepsp than of the fepsp. We found that 48.5 ± 9.1% decrease (about half of the total decrease) in the NMDA receptor-mediated fepsp, and 51.6 ± 19.6% decrease (approximately all decrease) in the fepsp induced by hypoxia (3 min) were reversed in the presence of the selective adenosine A₁ receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (50 nM), and thus likely to be mediated by endogenous adenosine, through the activation of adenosine A₁ receptors. On the other hand, under the conditions we assumed to be normoxic in our slices, DPCPX (50 nM) induced a much larger increase in the amplitude of the NMDA receptor-mediated fepsp compared to the increase in the fepsp, which suggest that endogenous adenosine is inhibiting predominantly the NMDA receptor-mediated fepsp under these conditions. Hypoxia markedly decreases the NMDA receptor-mediated fepsp in the hippocampal CA₁ area. The contribution of endogenous adenosine to the inhibition of the NMDA receptor-mediated fepsp may be fundamental for its neuroprotective effects.     

Pyrexia of unknown origin: changing spectrum of diseases in two consecutive series.

Comparison was made of the aetiology and methods of diagnosis in two series of patients meeting the classic criteria of pyrexia of unknown origin during 1968-1981 and during 1982-1989 seen in the Department of Internal Medicine at La Paz University Hospital, Madrid, Spain. There was a statistically significant decrease in the percentage of infections and an increase in neoplasms and connective tissue disorders in the second series. The percentage of patients diagnosed by laparatomy was similar in both series but the diagnosis yield at laparotomy was greater in the second period. Pyrexia of unknown origin continues to be a condition which can defy clinical expertise in in spite of advances in diagnostic techniques.     

Supravalvular aortic stenosis and coronary aneurysm]

A 32-year old woman, with endocarditis caused by Streptococcus mitis, and systolic murmur is presented. The Doppler examination was found a systolic gradient of 150 mmHg. Aortography showed a multiple membranous supravalvular aortic stenosis, with aneurysmal dilatation of the left main coronary artery and circumflex artery, associated with bicuspid aortic valve and mild aortic insufficiency. The patient died suddenly by cardiac arrest in stand by to cardiac surgery. Anatomic comprobation was not possible. The coronary artery anomalies associated with the supravalvular aortic stenosis syndrome are reviewed.     

Oral leiomyosarcomas: report of two cases with immunohistochemical profile.

Leiomyosarcoma of the oral cavity is a very rare tumor associated with aggressive clinical behavior and low survival. In this paper, we report 2 cases of leiomyosarcoma, affecting the gingival mucosa of a 54-year-old female and the maxillary bone of a 63-year-old male. Histologically, the tumors were composed of variably oriented fascicles of spindle-shaped cells with cigar-shaped nuclei and eosinophilic cytoplasm. The lesions were treated by surgical resection. Immunoreactivity to anti-vimentin, anti-smooth muscle actin, anti-desmin, anti-laminin, and anti-muscle-specific actin antibodies were found; conversely, the tumor cells were negative for anti-S100 and AE1/AE3 proteins. This report emphasizes the role of immunohistochemical study for correct diagnosis of leiomyosarcoma.     

Cytokine production, activation marker, and skin homing receptor in children with atopic dermatitis and bronchial asthma

T cells are known to develop a critical role in the pathogenesis of atopic dermatitis (AD) and bronchial asthma. T cells involved in AD express the skin homing receptor CLA, but no lung homing receptor has been identified in bronchial asthma. We compared different cell markers and the cytokine production in T cells from children with AD or bronchial asthma. We studied the involvement of CLA+ and CLA- T-cell subpopulations in these diseases. We studied 20 children with acute AD lesions, 15 with mild persistent asthma, and 15 non-atopic controls. All patients were sensitized to house dust mite (DP) and evaluated during the acute phase. Total and specific IgE were measured by immunoassay and the expression of different cell markers and the cytokine production was analyzed by flow cytometry in peripheral blood mononuclear cells. Total IgE was significantly higher in AD children and IgE to DP in the asthmatic children. There was a significant increase in CD25+ CD4+ cells in asthmatic children and in HLA-DR+ CD4+ and HLA-DR+ CD8+ cells in AD. In the CD4+ subsets, there was an increase in IL-13, IL-5 and TNF-alpha in AD compared to controls, a decrease in IFN-gamma in asthmatic children compared to controls, and an increase in IL-13, IL5, IL2, TNF-alpha, and IFN-gamma in the AD compared to asthmatic children. Changes in cytokine production were mainly detected in CLA+ cells in AD and in CLA- cells in asthma. Differences exist in total and specific IgE, activation markers, and cytokine patterns between AD children and children with asthma, with the former expressing a Th2 pattern whereas in asthmatic children we only detected a decrease in IFN-gamma. Moreover, the subpopulations (CLA+ vs. CLA-) expressing these changes were different, indicating that the underlying mechanisms in the two diseases are not exactly the same.     

B(2)-receptor modulation of the reactivity to phenylephrine and angiotensin II in the carotid artery of normotensive rats after trandolapril treatment.

This study was designed to study the effects of angiotensin converting enzyme inhibitors (ACEI) following treatment with trandolapril (0.3 mg kg(-1) day(-1)) on carotid arterial responsiveness in normotensive Wistar rats. Carotid arteries were obtained from control or trandolapril-treated animals and mounted in an isolated organ bath. Reactivity to angiotensin II (Ang II), phenylephrine (Phe) and KCl was studied. Agonist concentration-response curves were constructed in either the absence or presence of the endothelium or after incubation with L-NAME (10(-6) M), HOE140 (10(-7) M) or indomethacin (10(-5) M). Trandolapril treatment decreased the Ang II and Phe potencies in carotid arteries, but did not affect the maximal response. The KCl responses (potency and Emax) were similar in both control and trandolapril-treated arteries. The absence of endothelium increased the response to both agonists in control and trandolapril-treated arteries; however, the inhibitory component from the endothelial layer of the Phe response was greater in trandolapril-treated animals than in control animals. The presence of L-NAME or HOE140 abolished the changes in the potency values of trandolapril-treated animals. The presence of indomethacin did not change the effect of trandolapril on the potency values of both agonists. We conclude that trandolapril treatment decreased the carotid arterial reactivity in normotensive rats and that this effect is endothelium-dependent. Furthermore, the involvement of B(2)-receptors and NO production, but not of prostaglandins, is suggested in this mechanism.