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What happens to binocularity in primate strabismus?

Normal humans for whom the positions and movements of the two eyes are constrained to be yoked together are able to extract rich binocular sensory information from the environment. Humans with strabismus are deficient in extracting some of this information. Studies of strabismus in non-human primates can augment what has been learned from humans about relationships between strabismus and sensory binocular function. For example, speculation about the role of binocular vision in primate evolution can help us understand why it is that the advantages of sensory binocular function outweigh the disadvantages of having the positions of the two eyes yoked together. Physiological optics assessments of fixation patterns and accommodative responses in monkeys provide information about how the brain accomplishes and coordinates motor and sensory binocular functions, and sets the stage for determining underlying neural mechanisms responsible for this coordination. Finally, a developmental perspective, concerned with events that occur during an early sensitive period in the life span of an infant primate, can help us understand how nature and nurture interact to set up this complex neural system in normal individuals, and how this process is disrupted in conditions such as strabismus.

Accommodation, Ocular↗

Functional integration of striatal allografts in a primate model of Huntington's disease.

Huntington's disease is an autosomal dominant, inherited disorder that results in progressive degeneration of the basal ganglia (especially the neostriatal caudate nucleus and putamen) and other forebrain structures and is associated with a clinical profile of movement, cognitive and psychiatric impairments for which there is at present no effective therapy. Neuropathological, neurochemical and behavioral features of the disease can all be reproduced in experimental animals by local injection of excitotoxic or metabolic toxins into the neostriatum. All these features of the disease can be alleviated, at least in rats, by transplantation of embryonic striatal tissue into the degenerated striatum, which was the basis for commencing the first clinical trials of striatal transplantation in Huntington's patients. However, although rat striatal xenografts may temporarily reduce apomorphine-induced dyskinesias in monkeys, there has been no demonstration that allograft techniques that work well in rats translate effectively to the much larger differentiated striatum of primates. Here we demonstrate good survival, differentiation and integration of striatal allografts in the primate neostriatum, and recovery in a test of skilled motor performance. Long-term graft survival in primates indicates probable success for clinical transplants in Huntington's disease; in addition, our data suggest that graft placement has a direct influence on the pattern and extent of functional recovery.

Animals↗

Long lasting smooth muscle relaxation by a novel PACAP analogue in guinea-pig and primate airways in vitro.

1. We compared the relaxant effect of pituitary adenylate cyclase activating peptide (PACAP) 1-27 with that of a newly developed PACAP 1-27 analogue, [Arg15,20,21Leu17]-PACAP-Gly-Lys-Arg-NH2, in the guinea-pig trachea and primate bronchi in vitro (n = 4-5). 2. In the guinea-pig trachea precontracted by a submaximally effective carbachol concentration (0.1 microM), cumulative administration of PACAP 1-27 and the beta 2-adrenoceptor agonist salbutamol (3 nM-3 microM) caused significant and concentration-dependent smooth muscle relaxation, with salbutamol being approximately one log-step more potent in this model. However, in primate bronchi precontracted by carbachol (0.1 microM), cumulative administration of PACAP 1-27 and salbutamol caused concentration-dependent smooth muscle relaxation with very similar potencies and maximum relaxant effects. 3. In the guinea-pig trachea, non-cumulative administration of the PACAP 1-27 analogue and the original PACAP 1-27 (0.3-3 microM) caused concentration-dependent relaxation with a very similar maximum relaxant effect and potency. However, the onset and offset of action was markedly slower for the PACAP 1-27 analogue than for the original PACAP 1-27 (< 90% versus < 10% of peak relaxation remaining 6 h after administration). Separate experiments confirmed that the PACAP 1-27 analogue also caused significant relaxation with slower onset and offset of action than did the original PACAP 1-27 in primate bronchi. 4. Peptidase inhibition by captopril (10 microM) and phosphoramidon (1 microM) significantly increased the maximum relaxant effect and duration of action of PACAP 1-27 but not of the PACAP 1-27 analogue, during the 3 h of observation in the guinea-pig trachea. 5. We conclude that [Arg15,20,21Leu17]-PACAP-Gly-Lys-Arg-NH2 produces significant, concentration-dependent and sustained airway smooth muscle relaxation in vitro. The sustained relaxant effect is due, at least in part, to the PACAP 1-27 analogue being less susceptible to cleavage by peptidases than the original peptide PACAP 1-27.

Albuterol↗

Endotoxin sensitization to kinin B(1) receptor agonist in a non-human primate model: haemodynamic and pro-inflammatory effects.

1. Although endotoxaemia induces kinin B(1) receptors in several animal models, this condition is not documented in primates. This study examined the up-regulation of haemodynamic and pro-inflammatory responses to the B(1) agonist des-Arg(10)-kallidin (dKD) in a non-human primate model. 2. Green monkeys (Cercopithecus aethiops St Kitts) received lipopolysaccharide (LPS; 90 microg kg(-1)) or saline intravenously. After 4 h, anaesthetized monkeys were cannulated via the carotid artery to monitor blood pressure changes following intra-arterial injections of dKD or the B(2) agonist bradykinin (BK). Oedema induced by subcutaneous kinin administration was evaluated as the increase in ventral skin folds in anaesthetized monkeys injected with captopril at 4 h to 56 days post-LPS. 3. LPS increased rectal temperature but did not affect blood pressure after 4 h. dKD reduced blood pressure (E(max): 27+/-4 mmHg; EC(50): 130 pmol kg(-1)) and increased heart rate (E(max): 33 b.p.m.) only after LPS. In contrast, the dose-dependent fall in blood pressure with BK was comparable in all groups. The selective B(1) antagonist [Leu(9)]dKD (75 ng kg(-1) min(-1), intravenously) abolished responses to dKD but not BK. 4. dKD injection induced oedema dose-dependently (2.4+/-0.1 mm at 150 nmol) only following LPS (at 4 h to 12 days but not 56 days). In contrast, BK-induced oedema was present and stable in all monkeys. Co-administration of [Leu(9)]dKD (150 nmol) significantly reduced oedema induced by dKD (50 nmol). 5. These results suggest LPS up-regulation of B(1) receptor effects in green monkeys. This non-human primate model may be suitable for testing new, selective B(1) antagonists with therapeutic potential as anti-inflammatory agents.

Animals↗

Distribution and pharmacological characterization of primate NK-1 and NK-3 tachykinin receptors in the central nervous system of the rhesus monkey.

Much attention has focused on tachykinin receptors as therapeutic targets for neuropsychiatric disorders, although their expressional distributions in the primate central nervous system (CNS) remain unclear. We cloned the genes encoding the NK-1 and NK-3 tachykinin receptors (referred to as rmNK-1 and rmNK-3) from the rhesus monkey (Macaca mulatta) brain and examined their pharmacological profiles and regional distributions in the CNS. The deduced rmNK-1 amino-acid sequence differed by only two amino acids from the human NK-1 (hNK-1). The deduced rmNK-3 amino-acid sequence was two amino acids shorter than human NK-3 (hNK-3), with a seven-amino-acid difference in sequence. Ligand binding studies revealed that the affinity of rmNK-1 to substance P (SP) was comparable to that of hNK-1 in cell lines that expressed individual receptors stably. Nonpeptide antagonists had similar effects on the binding of rmNK-1 and hNK-1. Affinity of rmNK-3 for NKB was stronger than for SP and the IC50 value was comparable with that of hNK-3. Ca2+ imaging showed that activations of both rmNK-1 and rmNK-3 by specific ligands, SP and senktide, induced increased intracellular Ca2+ in cell lines that stably expressed individual primate tachykinin receptors. The amounts of rmNK-1 and rmNK-3 mRNAs were quantitatively determined in the monkey CNS. The expression of rmNK-1 was observed in all of the cortical and subcortical regions, including the hippocampus and the amygdala. The putamen contained the most NK-1 mRNA in the brain, with less rmNK-3 mRNA found in the cortex compared to rmNK-1 mRNA. In the monkey hippocampus and amygdala, rmNK-1 mRNA was present at markedly higher concentrations than rmNK-3 mRNA. The present results provide an insight into the distinct physiological nature and significance of the NK-1 and NK-3 tachykinin systems in the primate CNS. These findings are indispensable for establishing model systems in the search for a subtype-specific tachykinin receptor agonist and antagonist for the treatment of neuropsychiatric disorders.

Amino Acid Sequence↗

Vitreous and retinal amino acid concentrations in experimental central retinal artery occlusion in the primate.

PURPOSE: Vitreous and retinal amino-acid concentrations were evaluated in a primate model of central retinal artery occlusion (CRAO) to study the role of glutamate excitotoxicity in acute retinal ischaemia. METHODS: Unilateral, acute CRAO was produced by temporary clamping of the central retinal artery for 190 min in four elderly rhesus monkeys. Fundus photography, fluorescein angiography, and electroretinogram were performed before and during CRAO, and after unclamping the artery. Vitreous samples were obtained before and after CRAO in both eyes, and analysed for 13 amino-acid concentrations using high-pressure liquid chromatography. The animals were killed 350 min after retinal reperfusion, and the retinal tissue was submitted for amino-acid analysis. RESULTS: In all four eyes, the macula showed the 'cherry red spot'. The CRAO was confirmed by fluorescein angiography and decreased b-wave on electroretinogram. Retinal histology confirmed ischaemic changes in the inner retina. Changes in all 13 vitreous amino-acid concentrations after CRAO (including glutamate) were not significantly different between study and control eyes (P = 0.09 to 0.82). All retinal amino-acid concentrations (including glutamate) were not significantly different between two eyes (P = 0.07-0.93). CONCLUSIONS: In the primate model of acute inner retinal ischaemia induced by transient CRAO, we were unable to detect significantly elevated concentrations of vitreous and retinal glutamate. Our primate model has the advantage of closely modelling the CRAO in humans. Further basic and clinical studies are needed to elucidate the role of glutamate excitotoxicity in retinal ischaemia.

Acute Disease↗

Differences among nonhuman primates in susceptibility to bone marrow progenitor transduction with retrovirus vectors.

Nonhuman primates are increasingly being used as models for pre-clinical assessment of retrovirus vector expression and function following stem and progenitor cell transduction. We compared the relative susceptibility of CD34+ marrow progenitors from four nonhuman primate species and humans to transduction with amphotropic pseudotyped retrovirus vectors containing the Neo gene. The rate of functional gene transfer was measured by colony formation under G418 selection. Marrow progenitors from pigtail macaques (Macaca nemestrina) were transduced at about twice the rate (19.1 +/- 4.3%) as those from rhesus (11.2 +/- 3.7%) and cynomolgus (7.6 +/- 1.9%) macaques, baboons (7.8 +/- 1.8%), and humans (9.6 +/- 1.7%). Semiquantitative RT/PCR analysis suggests this difference may be due to elevated expression of the amphotropic receptor Pit2 in pigtailed macaque CD34+ cells. Further, transduction rates increased an average 1.6 +/- 0.4-fold when the culture temperature was lowered to 33 degrees C, and 2.1 +/- 0.3-fold when the culture dishes were coated with the fibronectin fragment CH-296. The data presented here point to important differences among nonhuman primate models as well as transduction culture conditions, and suggest that pigtailed macaques may be particularly useful for assessing expression and function of therapeutic retrovirus vectors. Gene Therapy (2000) 7, 359-367.

Animals↗

Efficient and stable Sendai virus-mediated gene transfer into primate embryonic stem cells with pluripotency preserved.

Efficient gene transfer and regulated transgene expression in primate embryonic stem (ES) cells are highly desirable for future applications of the cells. In the present study, we have examined using the nonintegrating Sendai virus (SeV) vector to introduce the green fluorescent protein (GFP) gene into non-human primate cynomolgus ES cells. The GFP gene was vigorously and stably expressed in the cynomolgus ES cells for a year. The cells were able to form fluorescent teratomas when transplanted into immunodeficient mice. They were also able to differentiate into fluorescent embryoid bodies, neurons, and mature blood cells. In addition, the GFP expression levels were reduced dose-dependently by the addition of an anti-RNA virus drug, ribavirin, to the culture. Thus, SeV vector will be a useful tool for efficient gene transfer into primate ES cells and the method of using antiviral drugs should allow further investigation for regulated SeV-mediated gene expression.

Animals↗

Prefrontal cortical projections to the midbrain in primates: evidence for a sparse connection.

Frontal cortical efferent fibers are thought to have important regulatory influence on cortico-basal ganglia (BG) circuits. The cortico-midbrain (substantia nigra/ventral tegmental area, SN/VTA) pathway has received particular attention in psychiatric diseases, most notably schizophrenia. Work in rodents demonstrates that the prefrontal cortico (PFC)-midbrain pathway plays a central role in regulating the firing pattern of dopamine (DA) neurons. These findings have led to some important hypotheses concerning PFC/BG interaction in schizophrenia. Descending PFC projections to the SN/VTA have been primarily documented in the rodent. The aim of this study was to determine the degree and organization of PFC afferents to these areas in the Macaque monkey. Anterograde tracer injections were made into discrete orbital, cingulate, and dorsolateral prefrontal areas. Projections were charted to the SN and VTA. Overall, there were very few fibers in the ventral midbrain following injections confined to specific areas of the PFC. To determine the relationship of the descending fibers to the midbrain DA neurons, sections were double stained for the tracer molecules and for tyrosine hydroxylase. In all cases, the prefrontal projections and the TH-positive cells did not appear to be in close juxtaposition. The results show a very limited projection from the PFC to the midbrain DA neurons in primates, terminating both within the SN proper as well as in the VTA. They arise from a broad region of the PFC, including the DLPF, cingulate, and orbital cortices. However, despite the relative lack of cortical input to the midbrain cells, these neurons are rich in glutamate receptors in primates. Thus, while, based on these anatomical studies, direct cortical control of DA neurons remains debatable in primates; the cortex may directly impact other sources of glutamatergic control.

Animals↗

MIC genes in non-human primates.

MIC molecules belong to the immunoglobulin superfamily, are encoded within the MHC region and are recognized by gamma/delta T-cell receptors. In humans, at least two functional genes (MIC-A* and MIC-B*) and two pseudogenes (MIC-C* and MIC-D*) exist. Functional MIC gene copies are characterized by a high degree of polymorphism, while pseudogenes bear several debilitating mutations either in the putative extracellular region or in the transmembrane region of the molecule. In this study we sequenced these segments of MIC genes in seven non-human primates in order to determine whether debilitating mutations were present. All the MIC primate genes studied were highly homologous to their human counterparts, and cystein residues involved in the maintenance of the immunoglobulin-like structure were highly conserved. Furthermore, none of the MIC genes studied contained stop codons in the extracellular or transmembrane segments of the molecule, which suggests that at least one functional gene copy exists in non-human primates. A distinct family of MHC immunoglobulin-like genes was recently identified within the MHC class I region in humans (Bahram et al., 1994; Leelayuwat et al., 1994). Members of this MIC (MHC class I chain related) gene family belong to the immunoglobulin superfamily. Similar to classical class I MHC genes, they are characterized by three distinct extracellular domains (alpha 1-3), a transmembrane (TM) segment and a cytoplasmic segment, each encoded by a separate exon (Bahram et al., 1994; Bahram et al., 1996). Other similarities between MIC genes and classical MHC genes include a high degree of polymorphism (Fodil et al., 1996; Pellet et al., 1997) and recognition by T-cell receptors (Groh et al., 1998). These findings suggest that the putative MIC-A* chain has evolved for a function that is related to, but quite distinct from, that of typical MHC class I chains.

Amino Acid Sequence↗

Zolpidem displays heterogeneity in its binding to the nonhuman primate benzodiazepine receptor in vivo.

The distinctive pharmacological activity of zolpidem in rats compared with classical benzodiazepines has been related to its differential affinity for benzodiazepine receptor (BZR) subtypes. By contrast, in nonhuman primates the pharmacological activity of zolpidem was found to be quite similar to that of classical BZR agonists. In an attempt to explain this discrepancy, we examined the ability of zolpidem to differentiate BZR subtypes in vivo in primate brain using positron emission tomography. The BZRs were specifically labeled with [11C]flumazenil. Radiotracer displacement by zolpidem was monophasic in cerebellum and neocortex, with in vivo Hill coefficients close to 1. Conversely, displacement of [11C]flumazenil was biphasic in hippocampus, amygdala, septum, insula, striatum, and pons, with Hill coefficients significantly smaller than 1, suggesting two different binding sites for zolpidem. In these cerebral regions, the half-maximal inhibitory doses for the high-affinity binding site were similar to those found in cerebellum and neocortex and approximately 100-fold higher for the low-affinity binding site. The low-affinity binding site accounted for < 32% of the specific [11C]-flumazenil binding. Such zolpidem binding characteristics contrast with those reported for rodents, where three different binding sites were found. Species differences in binding characteristics may explain why zolpidem has a distinctive pharmacological activity in rodents, whereas its pharmacological activity in primates is quite similar to that of classical BZR agonists, except for the absence of severe effects on memory functions, which may be due to the lack of substantial zolpidem affinity for a distinct BZR subtype in cerebral structures belonging to the limbic system.

Animals↗

Central integrative role of oestrogen in modulating the communication between the placenta and fetus that results in primate fecal-placental development.

This review summarizes the experimental evidence supporting the concept that oestrogen has a central integrative role in modulating the communication that occurs between the placenta and the fetus which results in primate fetal-placental development. Thus oestrogen, acting within placental trophoblasts, regulates the functional differentiation of syncytiotrophoblasts, manifested as an upregulation of key components of the progesterone biosynthetic pathway and the 11beta-hydroxysteroid dehydrogenase (11beta-HSD)-1 and -2 enzymes controlling cortisol-cortisone interconversion. The increase in 11beta-HSD expression results in the switch in the qualitative and quantitative patterns of transplacental corticosteroid metabolism that induces maturation of the primate fetal hypothalamic pituitary adrenocortical axis. The studies outlined in this review, therefore, provide new insight into the role that oestrogen plays during the course of primate pregnancy and demonstrate that an oestrogen-dependent signalling system exists in utero that coordinates the placental and fetal dialogue critical to development of the placenta and endocrine systems underlying neonatal self-sufficiency.

11-beta-Hydroxysteroid Dehydrogenases↗

Neurobiology of early life stress: nonhuman primate models.

Numerous studies have shown that early life stress in nonhuman primates produces profound and long-lasting changes in behavior and biological function. We review several aspects of the neurobiology of early life stress, focusing on nonhuman primate experimental paradigms. There is experimental evidence that even prenatal stress can produce profound alterations in biological factors such as regulation of the hypothalamic-pituitary-adrenal (HPA) axis, biogenic amines, and immune function, as well as in behavioral measures of attention and sociability. An ongoing struggle in research studies is defining the relative contributions of nature and nurture in mediating the long-term effects of stress. Studies of social support contend that this has the capacity to buffer the deleterious effects of stressful early rearing environments, whereas social deprivations appear to have negative behavioral and medical outcomes, most notably deficits in immune function. From studies involving variable foraging demand (VFD)-reared nonhuman primates and other models, we suggest that many of the behavioral and biochemical changes produced resemble those seen in humans who suffer from depressive and anxiety conditions. Finally, there appears to be remarkable consistency of key neurobiological findings across species.

Animals↗

Sleep-related behavioural adaptations in free-ranging anthropoid primates.

Several aspects of behaviour relating to sleep in monkeys and apes are reviewed, including sleeping site selection, approach to and departure from sleeping sites, social behaviour at the sites, and nocturnal activities. Illustrative examples are given for each topic. Good sleeping sites for primates give protection from predators and/or some physical comfort from the elements and other sources of disturbance. Availability of sleeping sites may determine ranging patterns and whether an area is exploited or not. Times of retiring and resumption of daytime activities are influenced by foraging and ranging requirements. Social relationships and their influencing factors continue during the night, including dominance, kinship, affiliation and sex. Social partners may be used for thermoregulation and for increasing postural stability. Primates show a range of solutions to the problems surrounding sleep, and similarities and differences between monkeys and the large-bodied, nest-building great apes are described. Knowledge of natural sleep-related phenomena in non-human primates can provide valuable insights for human sleep research, and vice-versa.

Journal Article↗

Bone regeneration using recombinant human bone morphogenetic protein-2 (rhBMP-2) in alveolar defects of primate mandibles.

The efficacy of bone morphogenetic protein (BMP) for bone reconstruction has been widely studied in numerous animal experiments, but insufficient information exists about its ability to regenerate bone in primates. The purpose of this study was to evaluate the effects of recombinant human BMP-2 (rhBMP-2) on bone formation in alveolar bone defects in the mandibles of young primates. Marginal bone defects were created in the mandibles of nine 5-year-old rhesus monkeys and rhBMP-2 permeated in a polylactic-co-glycolic acid-coated gelatin sponge (PGS) was implanted into the bone defects. The resected bone treated with rhBMP-2 regenerated completely at 12 weeks postoperatively, and remodelling and consolidation of new bone were seen histologically. This study provides evidence of considerable bone regeneration in alveolar defects after surgical implantation of rhBMP-2 in non-human primates. This technique may be an effective alternative to autogenous bone grafts for reconstructive surgery in clinical practice.

Absorbable Implants↗

Fresh porcine cardiac valves are not rejected in primates.

OBJECTIVE: Transplanted porcine hearts are hyperacutely rejected by human immunoglobulin M antibodies against a porcine vascular endothelial molecule, galactose alpha-1,3-galactose, with ensuing human complement activation and membrane attack complex deposition. It is unclear, however, whether porcine valve endothelium triggers a similar immune response. We sought to investigate whether fresh porcine valves implanted into primates are rejected. METHODS: Wild-type porcine hearts before (n = 6) and after (n = 3) heterotopic transplantation into baboons underwent sectioning and were examined by hematoxylin and eosin staining and immunohistochemistry for galactose alpha-1,3-galactose, primate immunoglobulin M, and membrane attack complex. RESULTS: Examination of untransplanted porcine hearts showed that although cardiac microvascular endothelium strongly expressed the galactose alpha-1, 3-galactose antigen, galactose alpha-1,3-galactose was not detected on the endothelium of porcine aortic and pulmonary valves. Porcine hearts transplanted into baboon recipients were hyperacutely rejected 60 to 80 minutes after implantation. Despite dramatic tissue damage associated with extensive immunoglobulin M and membrane attack complex binding on the microvascular endothelium, the aortic and pulmonary valves were entirely spared. Valves remained morphologically intact at explant and showed no signs of immunoglobulin M- and membrane attack complex-mediated damage. CONCLUSIONS: The absence of galactose alpha-1,3-galactose expression may protect unfixed porcine valves from xenograft rejection in primates. Further investigation of viable porcine valves appears warranted.

Animals↗

The evolution of neuroendocrine mechanisms regulating sexual behaviour in female primates.

The common marmoset is a small New World primate that lives in extended family groups. Female marmosets show rhythmic changes in proceptivity during their 28-Day ovarian cycle, but fluctuations in sexual receptivity are relatively subtle. Receptivity persists even after ovariectomy and adrenalectomy in the female marmoset. In the intact female, increases in proceptivity at mid cycle are due to the activational effects of oestradiol. Treatment of the ovariectomized female with oestradiol-17beta stimulates proceptivity and this effect is blocked by thermal or excitotoxic (neuronal cell body specific) lesions in the anterior or medial hypothalamus. Implantation of oestradiol into the anterior hypothalamus (via guide cannulae) also activates proceptivity. Luteinizing hormone releasing hormone (LHRH) may also form part of the neuroendocrine mechanism controlling proceptivity in the intact female, given that exogenous LHRH stimulates proceptivity in ovariectomized, oestrogen-primed marmosets. These effects of oestradiol (and LHRH) on proceptive displays are much more pronounced than any effects involving sexual receptivity. Conversely, treatment of the ovariectomized female with progesterone, at doses sufficient to produce luteal phase concentrations of circulating hormone, causes a marked suppression of proceptivity, but only small decreases in sexual receptivity. These experiments on marmosets remain some of the very few studies to define how hormones influence the brain and sexual behaviour in female primates. They support the conclusion that sexual receptivity is not under rigid neuroendocrine control in female anthropoids, and that there is no peri-ovulatory period of oestrus, such as occurs in most non-primate mammals.

Adrenalectomy↗

The Primate Embryo Gene Expression Resource in embryology and stem cell biology.

The analysis of temporal patterns of gene expression in embryos is an essential component of any research program seeking to understand molecular mechanisms that control development. Little is known of early regulatory mechanisms that operate in primate oocytes and preimplantation-stage embryos. Such studies have been hindered by the cost of obtaining, and limited availability of, non-human primate oocytes and embryos, and by ethical and legal constraints on studies of human embryos. Over the past 4 years we have established the Primate Embryo Gene Expression Resource (PREGER) to circumvent these limitations. A set of over 200 samples of rhesus monkey oocytes and embryos has been converted to cDNA libraries, which are, in turn, used for a variety of molecular analyses. Both the libraries and cDNA dot blots can be distributed free of charge to anyone wishing to study gene expression at these stages. This includes providing an inexpensive and rapid method for confirming and extending results of gene discovery approaches such as microarray analysis. PREGER includes an on-line resource with a database and other useful tools for embryologists. The resource is being expanded to incorporate samples from other species and from embryonic stem cells.

Animals↗