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Biomedical subjects

G Mick

Publications and source records attributed to G Mick.

18 recordsLinked to original sources

Nutritional regulation of white adipocyte vascular endothelial growth factor (VEGF).

White adipose tissue has distinctive angiogenic properties. White adipocytes are capable of producing vascular endothelial growth factor (VEGF) in response to insulin and catecholamines. Recognizing the dual functions of adipose tissue as an endocrine/metabolic organ and fuel storage depot with an inimitable ability to adjust its organ mass, our aim was to determine whether fasting would affect adipocyte VEGF 165 production. Rats were fed ad libitum, then fasted for 24 hours, and then refed after the 24-hour fast. The isolated white adipocytes from each group and blood endocrine/metabolic profiles were examined at each stage, yielding three sets of results. Using cultured adipocytes, fasting caused a two-fold increase in VEGF 165 formation compared to fed rats that normalized after refeeding. Likewise, freshly prepared adipocytes manifested a three-fold augmentation in adipocyte VEGF 165 mRNA expression and a 60 % increase the transcriptional regulator hypoxia-inducible factor 1 (HIF-1alpha) that normalized after refeeding. Blood studies revealed the expected fasting-related alterations in glucose, beta-hydroxybutyrate and corticosterone. Plasma VEGF concentrations were attenuated by 26 % with fasting, and did not normalize with refeeding. Multiple linear regression analyses uncovered statistically significant inverse correlations between plasma VEGF and blood beta-hydroxybutyrate or serum corticosterone. Blood glucose, in contrast, correlated directly with plasma VEGF. We will discuss the potential role of enhanced adipocyte VEGF formation during starvation in light of the known actions of this factor on vascular endothelial mitogenesis and permeability.

3-Hydroxybutyric Acid↗

[Physiopathology of the migraine attack and mechanisms of action of anti-migraine agents: recent findings in animals].

No current experimental model on migraine is fully satisfactory, and constructing a single model which takes into account all the various clinical and pharmacological aspects does not seem feasible. A critical review of the large number of experimental approaches developed over the past 20 years to investigate migraine attacks and an examination of recent research in the various fields of animal biology seems to be more pertinent in this context. A neurovascular cortical spreading depression could be one of the mechanisms involved in aura formation, but its association with headache is enigmatic, and the implication of hypoxia in its etiopathogenesis remains controversial. Intercritical neuronal hyperexcitability, which has been proposed as a possible biological basis for the onset of migraine, may trigger the development of aura, but also the activation of the trigeminovascular system. An independent but concomitant activation of both phenomena could be driven by a mesencephalic noradrenergic or cortical limbic generator. The trigemino-vascular model of perivascular neurogenic inflammation does not explain certain experimental and pharmacological properties of anti-migraine drugs. The clinical efficacy of the 5-HT1B/D agonists is based on a vasoconstrictive effect and on their inhibition of neurogenic inflammation, while calcitonin gene-related peptide (CGRP) plays a major role in vasodilatation and substance P in neurogenic inflammation. The initiation and initial development of migraine probably involve a prior peripheral sensitization of the trigeminal nociceptors, while the susceptibility to onset of an attack, maintenance of the migrainous state and the clinical variability must certainly rely on central sensitization within the trigeminal caudate nucleus. The numerous experimental approaches to the physiopathology of migraine developed over recent years, each of which provides a basis for the development of new classes of anti-migraine drugs, are not exclusive of one another. Rather, they contribute to providing various specific aspects of a physiopathogenic theory of migraine, which at the present time has to be both wide-ranging and adaptive.

Animals↗

Skull base reconstruction utilizing titanium mesh in chronic CSF leakage repair.

OBJECTIVE AND IMPORTANCE: Chronic cerebrospinal fluid leakage is a perplexing management problem in skull base surgery, as well as craniofacial and certain otolaryngologic procedures. When all less invasive techniques have been tried and have failed, craniotomy for direct repair is often done. CLINICAL PRESENTATION: This case represents one such case in which the pathology found required an unusual application of a common surgical adjunct for correction. The patient in question had experienced CSF rhinorrhea intermittently for 10 years prior to presentation. Several intracranial procedures had failed to curtail the rhinorrhea, after failure of lumbar drainage and other less invasive procedures had also failed. The patient was taken to surgery again for an attempt to directly correct the CSF leak, after demonstration of the location of the leak was accomplished with the assistance of contrasted coronal CT images of the anterior fossa. TECHNIQUE: At the time of surgery, comminuted fractures of the floor of the anterior fossa were noted. These fractures were associated with multiple sites of dural impingement. Following meticulous repair of all dural injuries, reconstruction of the floor of the anterior fossa was accomplished with the use of titanium micro mesh. The mesh placement isolated the dura from further contact with the fracture surfaces, preventing recurrent dural injury. CONCLUSION: The use of titanium mesh in skull base surgery has previously been reported in craniofacial and cranial vault procedures. Its use in skull base applications may prove useful in certain situations. This patient remains asymptomatic nearly 2 years after its use, longer than with any previous procedures to correct his chronic CSF leakage.

Cerebrospinal Fluid Rhinorrhea↗

Leptin does not affect adipocyte glucose metabolism: studies in fresh and cultured adipocytes.

Leptin, the 16-kd hormone produced by white fat cells, regulates energy homeostasis, satiety, and multiple sites in the neuroendocrine system. Leptin receptors have been identified in the central nervous system (CNS) and are widespread in peripheral tissues, including fat. Given the association between insulin resistance and obesity, it is important to establish whether leptin has additional effects on peripheral insulin action and glucose metabolism. This study examined whether leptin has a direct autocrine/paracrine action on glucose metabolism in both freshly isolated and 24-hour cultured rat fat cells. Freshly isolated rat adipocytes were incubated for 30 minutes with 200 ng/mL recombinant murine leptin. Thereafter, basal and insulin-stimulated (10(-8) mol/L) glucose transport, glycolysis-Krebs oxidation and lipogenesis ([6-14C]glucose conversion to [14C]O2 and to [14C]triglyceride), and lipolysis were measured. Upon leptin exposure, no statistical differences were detected in glucose transport or metabolism. Increasing the leptin concentration to 1 to 2 microg/mL or prolonging the duration of preincubation with the fat cells to 60 minutes before the metabolic assays did not alter the results. Finally, using two disparate fat cell culture methods with differing substrate additions (pyruvate and high or low glucose concentrations), there was no effect of 24-hour exposure to leptin (200 ng/mL) on basal and insulin-stimulated glucose transport or lipogenesis. We conclude that leptin does not modulate basal or insulin-stimulated glucose metabolism in isolated and cultured fat cells in vitro. However, in vivo, higher pericellular leptin concentrations, as well as other cellular or soluble serum factors, may exist that might lead to a physiologically relevant autocrine action of leptin.

Adipocytes↗

Inhibitory effects of cerulenin on protein palmitoylation and insulin internalization in rat adipocytes.

Protein acylation by long-chain fatty acids has been suggested as a necessary step in membrane trafficking. Because several insulin effects are dependent upon membrane trafficking, the cellular effects of the protein acylation inhibitor cerulenin were examined. Cerulenin blocked palmitoylation of selected rat adipocyte proteins including CD36, the dominant marker for palmitoylation in adipocytes. To measure cerulenin's effects on insulin internalization, rat adipocytes were incubated with 125I-insulin at 37 degrees C in the presence or absence of cerulenin. Surface-bound and intracellular insulin were discriminated by the sensitivity of the former to rapid dissociation by a pH 3 buffer at 4 degrees C. Insulin internalization was inhibited 85% by 0.3 mM cerulenin. Inhibition required preincubation with the agent, was irreversible, was not dependent upon protein synthesis, and was not the result of ATP depletion. Cerulenin was also found to inhibit insulin-stimulated glucose uptake and acetyl-CoA carboxylase activity. Cerulenin had no effect on basal glucose uptake and utilization or on the uptake and retention of fatty acids. In summary, protein acylation may be an important step in insulin-regulated cellular functions dependent upon membrane trafficking, such as insulin internalization.

Acetyl-CoA Carboxylase↗

Gating of retinal inputs through the suprachiasmatic nucleus: role of excitatory neurotransmission.

The mammalian circadian clock, located in the hypothalamic suprachiasmatic nucleus (SCN) is important in the regulation of many circadian rhythms, including regulation of pineal gland metabolism and melatonin secretion. Transsection of the optic nerves, disrupting the retinohypothalamic pathway, lesion of the SCN, or lesion of the hypothalamic paraventricular nucleus (PVN) abolish the regulation of pineal serotonin N-acetyltransferase activity by light. Therefore, the pathways linking the retina and the pineal gland must be channelled from the retina through the SCN and the PVN. Many lines of evidence indicate that the major neurotransmitter in the retinal afferents is glutamate. The first aim was therefore to study the retinal target neurons by localising glutamate receptors in the rodent SCN. Using in situ hybridisation, we detected NMDA-R1 and NMDA-R2C mRNA subunits in the SCN. Using immunocytochemistry, immunoreactivity for the AMPA type receptors GluR1, GluR2,3 and GluR4 was also detected in the SCN. Presentation of a short light pulse during the subjective night [i.e. circadian time (CT) 14 or 19], when light induced phase-shifting of activity-rest cycles can be accomplished, also induces expression of the immediate early-genes c-fos and junB in the rodent SCN. The second aim was to use this cellular correlate of behavioural function to determine the location of potential retinal target neurons in the SCN, and to investigate the hypothesis that glutamatergic neurotransmission mediates the effects of light on the circadian system. Thus, the ability of the NMDA receptor antagonist MK-801 to block light-induced c-fos expression in the SCN was studied. In the rat, this antagonist blocked c-fos mRNA expression in a subpopulation of cells in the ventral SCN at doses of 6, but not 2 mg/kg. In contrast, in the hamster both doses blocked light-induced c-fos expression in the ventral SCN. These data provide support for the hypothesis that glutamate mediates effects of light in the SCN, although it appers that the complexes of NMDA receptor subunits, which are involved in light-induced expression of c-fos after light, are relatively insensitive to MK-801. The diversity, heterogeneous distribution, and complexity of glutamate receptor subunits in the SCN suggest that processing of light pulses in the SCN is mediated by several cell types in the SCN. Via an integration process in the clock, the transmission of photic information takes place to other brain structures.

Animals↗

Expression patterns of a glutamate-binding protein in the rat central nervous system: comparison with N-methyl-D-aspartate receptor subunit 1 in rat.

Using radioactive in situ hybridization histochemistry, we examined the topographical patterns of expression of the messenger RNA encoding a glutamate-binding protein (N-methyl-D-aspartate receptor glutamate-binding protein in rat; NMDARgbs) in the central nervous system of the rat. Expression patterns of N-methyl-D-aspartate receptor glutamate-binding protein were compared with those of N-methyl-D-aspartate receptor subunit 1 (NMDAR1) of the N-methyl-D-aspartate receptor on adjacent sections. N-methyl-D-aspartate receptor glutamate-binding protein is not expressed in glial cells. The expression of both N-methyl-D-aspartate receptor glutamate-binding protein and N-methyl-D-aspartate receptor subunit 1 was observed in virtually all neurons throughout the central nervous system. The mean level of N-methyl-D-aspartate receptor subunit 1 expression was higher than that of N-methyl-D-aspartate receptor glutamate-binding protein. Similar topographical patterns of expression of N-methyl-D-aspartate receptor glutamate-binding protein and N-methyl-D-aspartate receptor were observed in most regions, except in discrete thalamic, hypothalamic and brainstem nuclei. Concomitantly for N-methyl-D-aspartate receptor glutamate-binding protein and N-methyl-D-aspartate receptor subunit 1, the highest expression levels were distributed in the mitral layer of main and accessory olfactory bulbs, granule cell layer of the dentate gyrus, polymorphic and pyramidal layers of CA1-3 fields of Ammon's horn. A slightly less prominent expression was observed in the glomerular and granule cell layers of main and accessory olfactory bulbs, anterior olfactory nucleus, layer 2 of piriform cortex, olfactory tubercle and taenia tecta. In the cerebellum, the prominent level of N-methyl-D-aspartate receptor glutamate-binding protein expression was slightly higher in the Purkinje cell layer than in the granule cell layer, an opposite pattern being observed for N-methyl-D-aspartate receptor subunit 1. A moderately high expression level of both messenger RNAs was observed in the medial septal nucleus, nucleus of the diagonal band of Broca, dorsal part of the endopiriform nucleus, and in the anteroventral and anterolateral parts of the bed nucleus of the stria terminalis. In the neocortex, the mean expression level of N-methyl-D-aspartate receptor glutamate-binding protein is moderate, while the mean level of N-methyl-D-aspartate receptor subunit 1 expression is high. With both probes, layer IV is slightly less labeled than the other layers.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

The messenger RNAs encoding metabotropic glutamate receptor subtypes are expressed in different neuronal subpopulations of the rat suprachiasmatic nucleus.

Glutamate is the principal transmitter of retinal projections to the rodent suprachiasmatic nucleus, a circadian clock synchronized with the light-dark cycle through the activation of glutamate receptors of the ionotropic type. In vitro, an intracellular mobilization of calcium can be induced by glutamate within cells of the suprachiasmatic nucleus maintained in a calcium-free medium, suggesting a participation of metabotropic glutamate receptors coupled to phospholipase C. Using in situ hybridization histochemistry, we examined the expression of messenger RNAs encoding the mGluR1 and mGluR5 subtypes of metabotropic glutamate receptors in the suprachiasmatic nucleus of the adult rat and during postnatal development. In the adult, mGluR1 was expressed in a small subset of neurons segregated caudally within the ventrolateral subdivision of the nucleus, while mGluR5 was mainly expressed in ventrolateral neurons within the middle third of the nucleus. Both subtypes were expressed in morphologically similar small cells, but mGluR5 was also solely expressed in a small population of larger neurons located at the dorsalmost aspect of the ventrolateral subdivision. In addition, with mGluR1 probe silver grain clusters exhibiting a grain density close but below the significant level were observed throughout the ventrolateral subdivision of the nucleus. At birth, mGluR1 and mGluR5 were similarly expressed throughout the caudal half of the nucleus. The expression of mGluR1 increased during early postnatal development and exhibited an adult pattern at postnatal day 21. The expression of mGluR5 increased from postnatal day 7 and reached the adult pattern at postnatal day 45. These observations suggest that each subtype of metabotropic glutamate receptor coupled to phospholipase C underlies specific roles within the rat suprachiasmatic nucleus during postnatal development and in the adult. In the adult, ionotropic and metabotropic receptors likely co-expressed within neuronal subsets located in the retinal terminal field may have interactive and/or additive effects on intracellular calcium concentration. Metabotropic receptors may thus participate in the mediation of photic information conveyed to a subset of neurons. During postnatal development, metabotropic receptors may play a role in the maturation of glutamatergic synapses associated with the retinal input.

Animals↗

Non-N-methyl-D-aspartate glutamate receptors in glial cells and neurons of the pineal gland in a higher primate.

A role for glutamate in signalling mechanisms in the mammalian pineal gland is suggested by the high concentration of the transmitter in pinealocytes and the expression of glutamate receptor subunits in the rat gland. A single type of glutamate binding site has been characterized in the rat and bovine pineal gland, preferentially sensitive to the glutamate agonist alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), a potent inhibitor of melatonin synthesis in vitro. In order to investigate the anatomical basis of a putative role of glutamate in the pineal gland of a higher primate, we performed an immunohistochemical analysis of the cellular localization of AMPA-type glutamate receptor subunits in the pineal gland of the macaque. Staining obtained with an antibody specific to GluR1 receptor subunit showed that this subunit is present in interstitial cells and astrocyte-like cells located in the parenchyma of the distal part of the gland. An antibody specific to GluR4 subunit stained astrocyte-like cells throughout the gland, however mainly in the proximal part, as well as a network of thin and long astrocytic-like processes located exclusively in the distal part of the gland. Staining obtained with an antibody recognizing both GluR2 and GluR3 subunits and the variant GluR4c exhibits a neuropilar-like pattern heterogeneously distributed throughout the gland.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Localization of substance P receptors in central neural structures controlling daily rhythms in nocturnal rodents.

Brain areas involved in the genesis and control of daily rhythms receive a prominent neural input that contains the neurotransmitter substance P (SP), a peptide putatively involved in the synchronization of circadian rhythms by environmental light. We investigated the localization of receptors to SP in the suprachiasmatic nucleus of the hypothalamus (SCN) and in the intergeniculate leaflet of the thalamus (IGL) of the rat and hamster using in situ hybridization histochemistry and immunohistochemistry. Consistently with that previously described in the rat, a neuronal population distributed along the lateral margin and at the dorso-latero-caudal aspect of the hamster SCN expresses moderately the mRNA encoding the SP receptor. In both rat and hamster, immunohistochemical data confirm the previous finding and reveal an almost complete absence of SP receptors in the ventral part of the SCN, which receives a direct projection from the retina. In the IGL of both species, numerous neurons prominently express the mRNA encoding the SP receptor. The immunostaining shows a high density of SP receptors on perikarya and dendrites throughout the nucleus. A dense staining is also observed on individual cells and processes bordering the lumen of blood vessels in the SCN and IGL.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Marginal topography of neurons expressing the substance P receptor in the rat suprachiasmatic nucleus.

Neurons expressing the substance P (SP) receptor (NK1 receptor) in the suprachiasmatic nucleus of the hypothalamus (SCN) have been topographically identified using radioactive in situ hybridization histochemistry. In the anterior hypothalamic area, clustered labeled neurons of small size and exhibiting low levels of gene expression are observed exclusively at the dorsolateral margin of the SCN, straddling cytoarchitectural boundaries of the nucleus. The marginal topography of neurons putative target of a SP-containing retinal input to the ventral SCN indicates that their dendrites bearing the receptor extend towards the retinorecipient part of the nucleus, where they can be modulated by overlapping inputs from the intergeniculate leaflet and the raphe. Eventual interactions between glutamatergic and putative tachykininergic retinal pathways for a coherent photic control of circadian rhythms may therefore occur mainly via intrinsic neuronal connections between their distinct target populations. In addition, since glutamate and SP induce electrophysiological responses in ventrolateral neurons with no interactive effect, neurons integrating both chemical signals, subsequently to their modulation by several influences, may be not located within the ventrolateral SCN. Alternatively but not exclusively, marginal neurons could be a target of SP-containing neurons within the SCN or nearby the nucleus, or from ascending projections from the raphé where serotonin and SP colocalize. The marginal topography of neurons expressing the SP receptor supports the view of the involvement of neurons located in the vicinity of the nucleus in the regulation of circadian rhythms.

Animals↗

Hypothalamic-pituitary dysfunction after radiation for brain tumors.

BACKGROUND: Patients with brain tumors who are treated with radiation frequently have growth hormone deficiency, but other neuroendocrine abnormalities are presumed to be uncommon. METHODS: We studied endocrine function in 32 patients (age, 6 to 65 years) 2 to 13 years after they had received cranial radiotherapy for brain tumors. The doses of radiation to the hypothalamic-pituitary region ranged from 3960 to 7020 rad (39.6 to 70.2 Gy). Nine patients also received 1800 to 3960 rad (18.0 to 39.6 Gy) to the craniospinal axis. Serum concentrations of thyroid, gonadal, and pituitary hormones were measured at base line and after stimulation. RESULTS: Nine patients (28 percent) had symptoms of thyroid deficiency, and 20 patients (62 percent) had low serum total or free thyroxine or total triiodothyronine concentrations. Of the 23 patients treated only with cranial radiation, 15 (65 percent) had hypothalamic or pituitary hypothyroidism. Of the nine patients who also received spinal (and thus direct thyroid) radiation, three (33 percent) had evidence of primary thyroid injury. Seven of the 10 postpubertal, premenopausal women (70 percent) had oligomenorrhea, and 5 (50 percent) had low serum estradiol concentrations. Three of the 10 men (30 percent) had low serum testosterone concentrations. Overall, 14 of the 23 postpubertal patients (61 percent) had evidence of hypogonadism. Mild hyperprolactinemia was present in 50 percent of the patients. Responses to stimulation with corticotropin-releasing hormone and corticotropin were normal in all patients except one, who had panhypothalamic dysfunction. However, serum 11-deoxycortisol responses to the administration of metyrapone were low in 11 of the 31 patients (35 percent) tested. Three of the 32 patients, (9 percent) had no endocrine abnormalities, 9 (28 percent) had an abnormal result on tests of thyroid, gonadal, prolactin, or adrenal function, 8 (25 percent) had abnormalities in two axes, 8 (25 percent) in three axes, and 4 (12 percent) in all four axes. CONCLUSIONS: Cranial radiotherapy in children and adults with brain tumors frequently causes abnormal hypothalamic-pituitary function. The most frequent changes are hypothyroidism and gonadal dysfunction, although subtle abnormalities in adrenal function may also be present.

Adolescent↗

Retinal projection to the olfactory tubercle and basal telencephalon in primates.

The retinal projection to the basal telencephalon was studied in eight species of primates from the suborders Strepsirhini and Haplorhini, including one anthropoid primate, the gibbon. Animals received an intraocular injection of tritiated amino acids and the distribution of retinal fibers and terminals was demonstrated by autoradiographic techniques in horizontal and coronal sections. In all species a discrete group of labeled retinal fibers is observed to branch off from the dorsolateral aspect of the optic tract at the level of the suprachiasmatic nucleus. These fibers, destined to the basal telencephalon, are topographically distinct from the retinal fibers which innervate the suprachiasmatic nucleus and medial hypothalamic regions. The fibers of the retinotelencephalic tract course dorsally above the supraoptic nucleus through the lateral hypothalamic area and then proceed further rostrally and laterally below the diagonal band of Broca towards the olfactory tubercle. Within the olfactory tubercle, terminal distribution of label is observed in the mediocaudal region along the granular cell layer II. In the macaque this cellular layer shows a characteristic thickening in the region of retinal terminals which is evident in both coronal and horizontal section. In some species this labeled region is seen within the superficial bulge of the tubercle on the ventral aspect of basal telencephalon. In all primates the retinal projection to olfactory tubercle is bilateral. In prosimians label is predominantly contralateral to the injected eye, in New World monkeys label is equally distributed on both sides of the brain and in Old World monkeys label is mainly found ipsilaterally. Retinal fibers were also seen in the periamygdaloid region but never extended as far as piriform cortex. These results, in addition to previous studies in other mammalian orders, confirm that the basal telencephalon, and in particular the olfactory tubercle, constitutes a region of visual and olfactory convergence. This sensory integration may be related to photic and chemosensory modulation of reproductive physiology and behavior.

Animals↗

Evidence for a substance P containing subpopulation in the primate suprachiasmatic nucleus.

Immunohistochemical detection of substance P (SP) in the suprachiasmatic nucleus (SCN) of the Old World monkey, Macaca fascicularis, was performed using two different rabbit polyclonal antisera. Immunostaining revealed a large population of neurons located in the dorsal subdivision of the nucleus identified by Nissl stain. This neuronal group represents the only cluster of SP-like immunoreactive (SP-IR) perikarya observed within the hypothalamus. In contrast with our present finding in the macaque, earlier studies only reported a few scattered SP-IR neurons in the SCN of other mammalian species. In agreement with previous descriptions of neuropeptides in the SCN, the topographical distribution of SP-IR neurons in the monkey confirms that cellular segregation is a significant feature of the mammalian SCN. This particular peptidergic subpopulation may represent a characteristic of the monkey circadian pacemaker. Together with other anatomical data previously reported in monkey and man, this finding also relates to the anatomical evolution of the circadian system from non-primates to humans. Although convincing data support the implication of SP in cyclic neuroendocrine regulations, the role of this tachykinin in circadian rhythmicity remains to be elucidated.

Animals↗

Retinohypothalamic pathway: a breach in the law of Newton-Müller-Gudden?

Theories of binocular vision originally imagined by Newton provided the foundation for subsequent investigations of the visual system by early anatomists and physiologists. These studies led to the widely accepted concept that degree of optic fiber decussation in the chiasm is inversely related to frontal orientation of the optical axes of the eyes (law of Newton-Müller-Gudden). A survey of 23 species from 11 mammalian orders demonstrates that, in contrast to other visual pathways, the retinohypothalamic projection does not obey this general principle. In further contradiction, an unexpected finding in primates is the predominance of ipsilateral, rather than contralateral, retinal input to the suprachiasmatic nucleus. This unusual organization underlines the functional and evolutionary specificities of this 'non-image forming' visual pathway.

Animals↗

Retinal projection to mammalian telencephalon.

Retinal projections were studied in species from 8 orders of mammals using anterograde tracing techniques. The olfactory tubercle of basal telencephalon receives a projection from the retina in all animals. In all species the course of labelled fibers is similar and the terminal distribution of label along the internal border of the granular cell layer is restricted to the mediocaudal region of the tubercle. These shared characteristics suggest that this pathway is a typical mammalian feature, possibly providing for convergence of visual and chemosensory information in telencephalon.

Animals↗

Cord blood and postnatal serum leptin and its relationship to steroid use and growth in sick preterm infants.

OBJECTIVE: To study the effect of prenatal and postnatal glucocorticoids use on serum leptin and weight gain in sick preterm infants and its correlation with caloric intake. METHODS: Serum leptin was measured in 24 neonates at day 1 (cord), 14 and 28 by radioimmunoassay. Total caloric intake (enteral and parenteral) and weight were measured on days 14 and 28 of life. RESULTS: Mean birth weight and gestational age of study infants were 864 +/- 273 g (mean +/- SD) (range 520-1755 g), and 26.6 +/- 2.4 weeks (23-32 weeks) respectively. Cord blood leptin was greater in infants whose mothers received antenatal steroids (1.98 +/- 1.05 ng/ml vs 0.94 +/- 0.39 ng/ml, p=0.004). Serum leptin increased postnatally from 1.52 +/- 1.0 ng/ml at birth to 2.2 +/- 1.3 ng/ml on day 28 of life (p=0.03). Mean serum leptin had an inverse exponential relationship with postnatal weight gain by day 28 of life (R2=0.56). Total caloric intake on days 14 and 28 of life did not correlate with postnatal weight gain. CONCLUSIONS: Increased serum concentration of leptin following glucocorticoids may be associated with poor weight gain in sick preterm infants.

Betamethasone↗

Hyponatremia secondary to reset osmostat in a child with a central nervous system midline defect and a chromosomal abnormality.

A newborn with a CNS midline defect and persistent hyponatremia was diagnosed with a "reset" osmostat using a 3% hypertonic saline test. The diagnosis was established by measuring urinary arginine vasopressin (UAVP) and plasma osmolality (P(Osmoil)). In this infant a chromosome abnormality with the karyotype 46, X, -X, +der(X) t(X;13) (p22.1;q22) was associated with the midline defect and a reset osmostat.

Arginine Vasopressin↗