Based on previous findings that the inhibitory hypophysiotropic factor somatostatin (somatotropin-release-inhibiting hormone, SRIH) is markedly reduced in growth hormone (GH)-deficient transgenic or spontaneous Snell dwarf mice, the present study was undertaken to determine whether hypophysiotropic SRIH expression was reduced in a type of dwarf mouse (Ames, df/df) in which SRIH had not been assessed, and whether the supposed reduction was present throughout life or was the result of regression after initial normal differentiation. Brain sections from normal (DF/?) and df/df mice were immunostained for SRIH using both standard and ‘Elite’ avidin-biotin complex reagents (Vectastain kits, Vector Laboratories, Inc., Burlingame, Calif., USA). Selected adult mice were treated with intracerebroventricular colchicine to maximize SRIH retention in perikarya. The developmental pattern of hypophysiotropic SRIH was assessed in brains of DF/? and df/df mice at 1, 3, 7, 14, 21, 60, and 90 days (d) postnatally. SRIH-immunoreactive neurons in the anterior periventricular nucleus (PeN) were quantified at each age. Although the use of Elite reagents or Elite and colchicine pretreatment increased (p < 0.001) the number of immunoreactive cells that were detectable in adult (60- to 90-day-old) df/df mice, the number of PeN SRIH neurons was reduced to 28% (p < 0.01) in untreated, and to 47% (p < 0.01) in colchicine-treated, df/df compared with DF/?, mice. In other CNS areas, SRIH immunostaining was comparable for df/df and DF/? mice, including neuron numbers in the medial basal hypothalamus of untreated mice. In postnatal development, SRIH was detectable in median eminence (ME) terminals at birth in some mice of both phenotypes, and at 3 d in all DF/? mice; ME SRIH was detectable in all mice by 7 d. In PeN, SRIH cells were first detectable consistently in normals at 3 d, and in dwarfs at 7 d. In DF/? mice, numbers of immunoreactive SRIH perikarya increased from 3 to 21 d, then plateaued. In dwarfs, SRIH cell numbers increased through 14 d. Numbers of SRIH perikarya were lower in df/df than in DF/? at 7, 14, 21, 60, and 90 d (all p < 0.05 or less). Thus, in Ames dwarf mice, as in other GH-deficient models, SRIH is markedly reduced in hypophysiotropic, ME-projecting neurons. The developmental pattern of hypophysiotropic SRIH in Ames dwarf mice is different from that of hypophysiotropic dopaminergic (DA) neurons in these animals, which are also prolactin (PRL)-deficient. Although DA levels and cell numbers are reduced markedly in adult df/df mice, both parameters have been found to be comparable to those of DF/? mice for the first 2-3 weeks postnatally. The consistent PeN SRIH deficit in dwarfs may reflect the importance of GH feedback earlier in development, because GH production in normal mice begins before birth, whereas PRL is not detectable until 7 d postnatally. The findings indicate that absent GH production has a marked negative effect on differentiation and levels of peptide expression in hypophysiotropic SRIH neurons.
Pediatric patients undergoing surgical correction of congenital heart diseases using cardiopulmonary bypass (CPB) are subjected to hypothermia. Core temperature is cooled down to 26–28°C during CPB. Postoperative hypothermia in these patients remains a source of long-intensive care unit (ICU) stay. Therefore, this study was performed to build a rewarming strategy aiming to improve the cardiac performance, minimize the early after-drop in both core and foot temperatures, and to achieve early achievement of homeostasis. Thirty pediatric patients of acyanotic congenital heart diseases were randomly allocated into one of three equal groups of 10. Group I was kept at 3°C between nasopharyngeal and heater-cooler unit water temperatures during rewarming whereas group II and group III were kept at 5°C and 7°C, respectively. The following parameters were measured: 1) cardiac performance (cardiac index and peak velocity); 2) cumulative amrinone consumption, blood lactate levels, and total body oxygen consumption; 3) intraoperative and postoperative peak and trough core and foot temperatures; and 4) time to extubation and ICU stay. Group I patients showed statistically significant increase in cardiac index and peak velocity compared with groups II and III, at p < 0.05 and p < 0.025, respectively. Statistically, the consumption of amrinone was significantly decreased in group I compared with groups II and III, with p < 0.005 and p < 0.0005, respectively, at 6 hours postoperatively. Group I showed an insignificant increase in blood lactate level, where groups II and III showed significant increases compared with controls (p < 0.001 at 6 hours postoperatively). Intraoperatively, both trough core and peak foot temperatures of group I patients statistically were significantly higher than in group III patients at p < 0.0005 and p < 0.05, respectively. The same applies in the ICU as regards to the time to core temperature (p < 0.005) and the rate of foot warming (p < 0.01). It was found that a difference of 3°C (group I) between nasopharyngeal and heater-cooler unit water temperatures during rewarming demonstrated the best outcome compared with 5°C and 7°C differences (groups II and III, respectively). This outcome was obvious in the following parameters: 1) the best cardiac performance (cardiac index and peak velocity); 2) the lowest values of cumulative amrinone consumption and blood lactate level; 3) the least after-drop in both core and foot temperatures; and 4) achievement of early homeostasis, shortest ICU stays, and conservation of the ICU resources.
Background: Iron is the most abundant element on earth and an essential metal for life. It is used extensively by proteins involved in the electron transport chain, the active centers of many enzymes and oxygen transport. It is essential for the adequate development and functioning of the brain. The regulation of the iron metabolism is crucial since both the iron deficiency and the iron overload can cause a disease. Aim of the Work: To detect the effects of iron exposure during the postnatal period on the putamen, the subthalamic nucleus and the substantia nigra in adult albino rats. Material and Methods: A total number of twenty albino rats were used in the study. They were equally divided into a control group and an experimental group. The control group received tap water orally. The experimental group received 15 mg/ kg of ferrous gluconate orally. The regimen started at postnatal day 12 and continued until three months old. The rats were anaesthetized and the brains were extracted. The specimens from the fixed brains were dissected and processed for the light and the electron microscopic examination. Morphometric measurements were also done. Results: The light microscopic study of the treated group revealed neurons of putamen had dense darkly stained nuclei and vacuolations appeared within the neuropil. Wide spaces between darkly stained neurons of the subthalamic nucleus were detected. The neuropil of the substantia nigra pars compacta (SNc) had many vacuoles and most of the neurons had darkly stained nuclei. Immunohistochemistry of the putamen using anti-TH demonstrated a reduction of TH expression in a patchy manner. Immunohistochemistry of SNc showed a weak TH immunoreactivity in the neuropil of the treated group and a reduction in the number of TH immunopositive neurons in comparison with the control group. The electron microscopic study of the SNc and putamen of the treated group showed degeneration of the mitochondria, vacuolization of the cytoplasm, heterochromatic nuclei with irregular outline and marked loss of cell organelles in the cytoplasm. Morphometric studies revealed significant reduction in the cell count and surface area of the neurons in SNc and putamen of the treated group in comparison with the control group. Conclusion: Iron overdose during postnatal period produces degeneration of the putamen, subthalamic nucleus and substantia nigra in the adult albino rat.
Background: Central nervous system (CNS), in particular, depends on thyroid hormones (TH) for the growth and upkeep of normal physiological processes. The preferred medication for thyroid replacement therapy continues to be levothyroxine, a synthetic thyroid hormone. Objectives:The goal of the current study was to determine whether maternally induced hypothyroidism could have an impact on the postnatal development of albino rat visual cortex and whether levothyroxine might have any protective effects or not. Material and Methods: Twenty one (21) pregnant rats were randomly divided equally into three groups; control group (received distilled water orally daily from first day of gestation until day 20 after delivery), hypothyroid group (received Carbimazole orally in a dose of 5 mg/rat/ day from first day of gestation until day 20 after delivery) and hypothyroid group treated with levothyroixine (received Carbimazole orally in a dose of 5mg/ rat/ day for the same period concomitantly with Levothyroxine subcutaneously at a dose of 5µg/day/rat from day 10 of gestation until 20 day after delivery). Pups (newborn, 10 and 20 days) were anesthetized, sacrificed; their brains were processed for histological evaluation. Morphometric and statistical studies were done. Results: Hypothyroidism induced visual cortex histological insults in the form of decreased cortical thickness and nuclear size and increase in packing of cells. Darkly stained cells were noticed. Clustering of pyramidal cells in ganglionic layer was not evident. Borders between layers couldn't be easily distinguished. These insults were ameliorated in hypothyroid rats treated with Levothyroxine. Conclusion: Levothyroxine might protect against maternal hypothyroidism induced visual cortical neurotoxicity.
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