Notes: Optical absorption and positron lifetime measurements have been performed on Fe-doped semi-insulating InP single crystals irradiated with thermal neutrons in a wide dose range from 0.1 to 2.7×1017 n cm−2. Two lifetimes were found: τ1=210 ps is constant in all the irradiation range; and τ2=340 ps reaches an intensity of almost 40% at the higher fluence used. When comparing these results with those obtained on unintentionally doped InP, a large increase of the longest lifetime is observed, from 300 ps in the nondoped InP to 340 ps in the semi-insulating InP. The increase of the second lifetime in InP:Fe means that the positron traps are less attractive to positrons. These positron traps have been associated to a complex defect generated by the main neutron-originated defect, the indium vacancy, and the clusters or interstitial atoms of Fe. The optical absorption spectra show a background absorption related to Fe precipitates in as-grown InP:Fe. This background absorption disappears after neutron irradiation, suggesting the destruction of Fe precipitates by the energetic particles generated in the transmutation process of 115In. © 2001 American Institute of Physics.

Notes: Neutron-irradiated InP single crystals have been investigated by positron-lifetime measurements. The samples were irradiated with thermal neutrons at different fluences yielding concentrations for Sn-transmuted atoms between 2×1015 and 2×1018 cm−3. The lifetime spectra have been analyzed into one exponential decay component. The mean lifetimes show a monotonous increase with the irradiation dose from 246 to 282 ps. The increase in the lifetime has been associated to a defect containing an Indium vacancy. Thermal annealing at 550 °C reduces the lifetime until values closed to those obtained for the as-grown and conventionally doped InP crystals. © 1996 American Institute of Physics.

Notes: A perifusion system of anterior pituitary (AP) tissue was used to investigate the temporal interaction of growth hormone-releasing factor (GRF) and somatostatin (SRIF) in the control of GH secretion in two pig breeds, Göttingen Miniature Pig (GMP), a small obese breed, and German Landrace (GLR), a conventional lean breed. AP tissue pieces derived from sexually mature ovariectomized animals were perifused (6 replicates per treatment) and fractions were collected at 10 min intervals. Basal GH release (ng-mP-1 mg-1 AP) in GLR was twice that of GMP (P 〈 0.001). Exposure to 10 min pulses of 1 nM GRF repeated 3 times at 2 h intervals resulted in rapid stimulatory GH responses (area under the curve) which became attenuated (P 〈 0.05) over time in GMP but not in GLR. Surprisingly, during and following the exposure of AP tissue from GMP to 10-, 20-, or 40-min pulses of 10 nM SRIF alone, GH release was markedly stimulated (P 〈 0.05), while AP tissue from GLR only showed a weak rebound GH release after SRIF pulses. With AP tissue from GLR low concentrations (0.1 nM SRIF) amplified GRF-induced GH release, whereas 1 nM or 10 nM SRIF inhibited GRF-induced GH release. However, concomitant exposure of AP tissue from GMP to 0.1, 1 or 10 nM SRIF during a GRF pulse markedly enhanced the GH response (P 〈 0.05), compared to 1 nM GRF alone, except for 1 nM SRIF which inhibited the GH response to the first GRF pulse. Thus the presence of SRIF, and not only its withdrawal, is an important factor in setting the timing and duration of GH pulses in both breeds. In GLR the concentration of SRIF is more important than the duration and/or type of SRIF pulse. In contrast, in GMP type and/or duration of SRIF pulses seem to be crucial to optimize pulsatile GH release and even determine peak height of GH pulses caused by GRF. These findings indicate clear breed differences in the role of SRIF and in the control of GH release by the interplay of GRF and SRIF. The ‘paradoxical’ effect of SRIF suggests that the role of SRIF is much more complex than that of a mere inhibitor and whose real role could be a modulator either of GH pulse and/or GRF action on GH release.

Notes: The application of a Percoll density gradient cell separation procedure to the pituitary gland of neonatal, prepubertal and mature pigs is described. After enzymatic dispersion, cell viability was 90% to 98% as determined by uptake of Trypan Blue. Recovery of dissociated cells after application of the gradient ranged from 80% to 95%. The dissociated cells were separated in several fractions that were characterized immunocytochemically using different antisera. We obtained highly enriched fractions of gonadotrope (gonadotropins), somatotrope (growth hormone) and lactotrope (prolactin) cells for each age. Concentration of the cell types (purity) was higher than 60% in the following fractions: 1) gonadotropin cells, fraction 15 (1.033 g/cc of density) from mature animals; 2) growth hormone cells, fraction 3 (1.121 g/cc of density) from neonatal animals and fraction 9 (1.087 g/cc) from prepubertal animals; and 3) prolactin cells, fraction 7 (1.094 g/cc) and 10 (1.082 g/cc) from neonatal animals and fraction 14 (1.051 g/cc) from mature pigs. In thyrotrope (thyroid-stimulating hormone) and corticotrope (adrenocorticotropin) cells, enriched fractions were also obtained, although the values of purity were lower (20% to 58%). In conclusion, the proposed cell separation and enrichment technique is suitable for the isolation, purification and examination of porcine pituitary cell types and subpopulations, and offers major advantages such as simplicity, rapidity, efficiency and reproducible results.

Notes: There is increasing evidence that nitric oxide (NO) produced by NO synthase (NOS), and their signalling partners, guanylyl cyclase and cGMP, play a relevant role in growth hormone (GH) secretion from somatotrophs. We previously demonstrated that both GH-releasing hormone (GHRH; 10−8 M) and low concentrations of somatostatin (10−15 M) stimulate pig GH release in vitro, whereas a high somatostatin concentration (10−7 M) inhibits GHRH-induced GH secretion. To ascertain the possible contribution of the NOS-NO and guanylyl cyclase-cGMP routes to these responses, cultures of pituitary cells from prepubertal female pigs were treated (30 min) with GHRH (10−8 M) or somatostatin (10−7 or 10−15 M) in the absence or presence of activators or blockers of key steps of these signalling cascades, and GH release was measured. Two distinct activators of NO route, SNAP (5 × 10−4 M) or L-AME (10−3 M), similarly stimulated GH release when applied alone (with this effect being blocked by 10−7 M somatostatin), but did not alter the stimulatory effect of GHRH or 10−15 M somatostatin. Conversely, two NO pathway inhibitors, NAME (10−5 M) or haemoglobin (20 µg/ml) similarly blocked GHRH- or 10−15 M somatostatin-stimulated GH release. 8-Br-cGMP (10−8 to 10−4 M) strongly stimulated GH release, suggesting that cGMP may function as a subsequent step in the NO pathway in this system. Interestingly, 10−7 M somatostatin did not inhibit the stimulatory effect of 8-Br-cGMP. Moreover, although 8-Br-cGMP did not modify the effect of GHRH, it enhanced GH release stimulated by 10−15 M somatostatin. Accordingly, a specific guanylyl cyclase inhibitor, LY-83, 583 (10−5 M) did not alter 10−15 M somatostatin-induced GH release, whereas it blocked GHRH-induced GH secretion. These results demonstrate for the first time that the NOS/NO signalling pathway contributes critically to the stimulatory effects of both GHRH and low-concentration somatostatin on GH release, and that, conversely, the subsequent guanylyl cyclase/cGMP step only mediates GHRH- and not low-concentration somatostatin-induced GH secretion from somatotrophs.

Notes: Visceral leishmaniasis (VL), an endemic parasitosis in Spain, is increasing as an important opportunistic infection in AIDS patients. We describe four cases of severe haemophilic patients with end-stage HIV disease who present with visceral leishmaniasis. We report the clinical course, methods of diagnosis and response to therapy. From the assessed clinical data it does not appear to be any difference with regard to VL either in other HIV risk groups or in immunocompetent groups. In contrast with previous reports, we have found that despite their immunodepressed state, positive serology for Leishmania was found in three of the four cases. A similar observation has been made in patients with VL who are immunodepressed because of other reasons. We also confirm previous reports of poor response and intolerance of antimony treatment, the deteriorating course of the disease in AIDS patients and that there is only a slight relationship between the disease and the cause of patient death. We agree with the proposition that this pathology ought to be included in the definition critera for AIDS.