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At least 19 recordsLinked to original sources

[The Great Ape Project--human rights for the great anthropoid apes].

The Great Ape Project (GAP) is an appeal of 36 scientist from different disciplines aiming at the legal equalisation of the non-human great apes (chimpanzees, gorillas and orang-utans) with man. The appeal is expressed by a number of essays stating zoological, genetical, ethological, anthropological, ethical and psychological knowledge and, based on these arguments, demanding the abolition of the species barrier between human beings and great apes. The central point of the initiative is the "Declaration on Great Apes", claiming the inclusion of great apes in the "community of equals" and thus securing three basic rights for all great apes: 1. The Right of Life; 2. The Protection of Individual Liberty; 3. The Prohibition of Torture. Not only experiments with great apes and their capture from the wilderness will be banned, but it is also intended to enfranchise as many great apes as possible from research laboratories and zoos. As a legal basis for the achievement of basic rights most of the authors plead for the idea of conferring the moral status of "persons" on great apes. Criticism of the GAP is due to its anthropocentrism. Rejection is especially expressed by advocates of pathocentric ethics who argue that the species barrier will not be abolished but only shifted, running then between the great apes and the remaining living beings. However, the GAP resulted in a greater retention in the use of great apes for experiments in several industrial countries. Additionally, the popular literature published by ethologists in the passed decades has supported a more responsible attitude of the public towards primates. Despite of all efforts the survival of the great apes is greatly endangered within their native countries.

Animal Rights↗

Gibbon ape leukemia virus-Hall's Island: new strain of gibbon ape leukemia virus.

Gibbon ape leukemia virus-Hall's Island (GaLV-H), a type C virus related to previous isolates of GaLV and simian sarcoma virus, was isolated from a gibbon ape with lymphocytic leukemia from a small colony of free-ranging gibbon apes on Hall's Island near Bermuda. We show here by molecular hybridization experiments that GaLV-H is approximately 60% related to three previous isolates of GaLV (GaLV-SF, GaLV-SEATO, and GaLV-Br) and is less closely related to simian sarcoma virus. The oligopyrimidine pattern of a transcript of the terminal 135 +/- 5 nucleotides of the viral RNA of GaLV-H is similar to that of GALV-Br but distinct from that of GaLV-SF and simian sarcoma virus. GaLV-H thus represents a fifth distinct strain of the infectious primate type C viruses, which among the previously described isolates of GaLV is most closely related to GaLV-Br.

Animals↗

Teaching apes to ape language: explaining the imitative and nonimitative signing of a chimpanzee (Pan troglodytes).

Fifteen videotaped conversations of a chimpanzee signing with his trainers were examined in order to determine (a) whether the ape was using imitation to learn about new language forms as some human children do and (b) whether the ape's nonimitative utterances implied knowledge of linguistic structures. The answers to both questions were negative. The evidence suggests that the utterances lacked the semantic and syntactic organization found in the utterances of most children. Instead of learning to use signs as symbols for communicating propositional messages, the ape learned to use gestures as nonsymbolic instrumental responses under the stimulus control of objects in the signing context and verbal and nonverbal cues from the trainers. Other research now underway with chimpanzees may eventually reveal whether this performance is characteristic of chimpanzees in general or is the result of particular training strategies used to teach language to chimpanzees.

Animals↗

Aquatic ape theory, speech origins, and brain differences with apes and monkeys.

Humans and apes show clear differences in brain anatomy. In the human cerebral cortex, for instance, the areas that control the fine movements of the hand, the areas that control the breathing and speech musculature, and the association areas have strongly expanded. It will be argued that these differences are best explained by the aquatic ape theory of human evolution (AAT) and originated in our semi-aquatic past, notably in the adaptations necessary for diving and shellfish collection at sea coasts.

Animals↗

Transplantation of transduced nonhuman primate CD34+ cells using a gibbon ape leukemia virus vector: restricted expression of the gibbon ape leukemia virus receptor to a subset of CD34+ cells.

The transduction efficiencies of immunoselected rhesus macaque (Macaca mulatta) CD34+ cells and colony-forming progenitor cells based on polymerase chain reaction (PCR) analysis were comparable for an amphotropic Moloney murine leukemia virus (MLV) retroviral vector and a retroviral vector derived from the gibbon ape leukemia virus (GaLV) packaging cell line, PG13. On performing autologous transplantation studies using immunoselected CD34+ cells transduced with the GaLV envelope (env) retroviral vector, less than 1% of peripheral blood (PB) contained provirus. This was true whether bone marrow (BM) or cytokine-mobilized PB immunoselected CD34+ cells were reinfused. This level of marking was evident in two animals whose platelet counts never fell below 50,000/microliter and whose leukocyte counts had recovered by days 8 and 10 after having received 1.7 x 10(7) or greater of cytokine-mobilized CD34+ PB cells/kg. Reverse transcriptase(RT)-PCR analysis of CD34+ subsets for both the GaLV and amphotropic receptor were performed. The expression of the GaLV receptor was determined to be restricted to CD34+ Thy-1+ cells, and both CD34+ CD38+ and CD34+ CD38dim cells, while the amphotropic receptor was present on all CD34+ cell subsets examined. Our findings suggest that, in rhesus macaques, PG13-derived retroviral vectors may only be able to transduce a subset of CD34+ cells as only CD34+ Thy-1+ cells express the GaLV receptor.

ADP-ribosyl Cyclase↗

Ape-like endocast of "ape-man" Taung.

I have identified and illustrated a spherical "dimple" or "depression" on the Taung endocast as indicating the most likely position of the medial end of the lunate sulcus but have not drawn an actual lunate sulcus on Taung because one is not visible. In a recent paper, R. L. Holloway (Am. J. Phys. Anthropol. 77:27-33, 1988) drew a lunate sulcus on his copy of the Taung endocast, incorrectly attributed this sulcus to me, and used it to obtain a ratio of 0.254 to describe "Falk's" position of the lunate sulcus. My published ratio of 0.242 for Taung (Falk: Am. J. Phys. Anthropol. 67:313-315, 1985a) was not considered, although the focus of Holloway's paper was my assessment of the position of the lunate sulcus. Holloway also excluded published ratios for a chimpanzee in my collection from his statistical analysis but, even so, my published ratio for Taung is still only 1.5 standard deviations from his chimpanzee mean. If my chimpanzee brain is included in the sample, the ratio for Taung is 1.2 standard deviations from the mean. Furthermore, one of Holloway's own chimpanzees (B60-7) has a ratio of 0.241, just 0.001 below my ratio for Taung. There is no sulcus where Holloway has drawn one on Taung, his "F(LS)" is not mine, his 2 mm error is not mine, and the correct ratio for my measurement of Taung is the one that I published, not the one that Holloway attributes to me. Assessment of Holloway's chimpanzee data supports my claim that the dimple on the Taung endocast is within the chimpanzee range for the medial end of the lunate sulcus.

Animals↗

Do humans ape? Or do apes human? Imitation and intention in humans (Homo sapiens) and other animals.

A. Whiten, D. M. Custance, J.-C. Gomez, P. Teixidor, and K. A. Bard (1996) tested chimpanzees' (Pan troglodytes) and human children's (Homo sapiens) skills at imitation with a 2-action test on an "artificial fruit." Chimpanzees imitated to a restricted degree; children were more thoroughly imitative. Such results prompted some to assert that the difference in imitation indicates a difference in the subjects' understanding of the intentions of the demonstrator (M. Tomasello, 1996). In this experiment, 37 adult human subjects were tested with the artificial fruit. Far from being perfect imitators, the adults were less imitative than the children. These results cast doubt on the inference from imitative performance to an ability to understand others' intentions. The results also demonstrate how any test of imitation requires a control group and attention to the level of behavioral analysis.

Adolescent↗

Transcriptional activation of apurinic/apyrimidinic endonuclease (Ape, Ref-1) by oxidative stress requires CREB.

Apurinic/apyrimidinic endonuclease (APE alias Ref-1) is a multifunctional enzyme involved in DNA repair and redox regulation of transcription factors (e.g., AP-1). It also acts as a repressor of its own and other genes. Recently, it was shown that the level of APE mRNA and protein is enhanced upon treatment of cells with oxidative agents, such as hydrogen peroxide (H(2)O(2)), which gives rise to an adaptive response of cells to oxidative stress. Induction of APE is due to APE promoter activation. To elucidate the mechanism of transcriptional activation of APE by oxidative agents, we introduced mutations into the cloned human APE promoter and checked its activity in transient transfection assays. Here we demonstrate that mutational inactivation of a CREB binding site (CRE) present within the promoter completely abolished APE promoter activation by H(2)O(2), indicating that CREB is required for APE induction. The CRE element in the context of the APE promoter sequence binds c-Jun and ATF-2, which was shown in gel retardation experiments. Under conditions of induction of APE by H(2)O(2), the expression of c-Jun was significantly enhanced, which supports the view that induction of c-Jun is involved in signaling leading to APE promoter activation by oxidative stress.

Activating Transcription Factor 2↗

Incision activity of human apurinic endonuclease (Ape) at abasic site analogs in DNA.

The major apurinic/apyrimidinic (AP) endonuclease of human cells, the Ape protein, incises DNA adjacent to abasic sites to initiate DNA repair and counteract the cytotoxic and mutagenic effects of AP sites. Here we address the determinants of Ape AP endonuclease activity using duplex DNA substrates that contain synthetic analogs of AP sites: tetrahydrofuranyl (F), propanediol (P), ethanediol (E), or 2-(aminobutyl)-1,3-propanediol (Q). The last of these, a branched abasic structure, was a poor substrate for which Ape had kcat > 1000-fold lower than for F. In contrast, the specificity constant (kcat/Km) for E or P of Ape purified from HeLa cells was only 5-8-fold lower than for F. Positioning a phosphorothioate ester immediately 5' to F inhibited Ape incision activity 20-fold (Rp isomer) or > 10,000-fold (Sp isomer). Although Ape did not have detectable endonuclease activity toward single-stranded substrates or unmodified double-stranded DNA, the enzyme displayed a low level of 3'-exonuclease activity for duplex DNA (< 0.03% of its AP endonuclease activity), which was influenced by the reaction conditions. The base positioned opposite F did not dramatically affect the cleavage efficiency of Ape, but an F:F arrangement was cleaved at approximately one-third of the efficiency of F:C. A 3'-mismatch diminished P and E cleavage only slightly and F not at all. A 5'-mismatch reduced the Ape cleavage rate 4-10-fold for F and approximately 100-fold for P and E. A series of substrates with F at different positions along the oligonucleotide showed that Ape requires > or = 4 base pairs 5' to the abasic site and > or = 3 base pairs on the 3'-side. The implications of these results for substrate recognition by Ape are discussed.

Base Sequence↗

Enamel hypoplasia in deciduous teeth of great apes: do differences in defect prevalence imply differential levels of physiological stress?

This paper presents new data on enamel hypoplasia in the deciduous canine teeth of great apes. The enamel defect under consideration is known as localized hypoplasia of primary canines (LHPC), and is characterized by an area of thin or missing enamel on the labial surface of deciduous canine teeth (Skinner [1986a] Am. J. Phys. Anthropol. 69:59-69). Goals of this study are: 1) to determine if significant differences in the frequency of LHPC occur among three genera of great apes, and 2) to evaluate variation in LHPC prevalence among great apes as evidence of differential physiological stress. Infant and juvenile apes with deciduous teeth were examined at the Cleveland Museum of Natural History (n = 100) and at the Smithsonian Institution, National Museum of Natural History (n = 36). Deciduous teeth were observed under oblique incandescent light, with the naked eye and with a 10x hand lens. Enamel hypoplasia was scored using Federation Dentaire International (FDI)-Defects of Dental Enamel (DDE) standards. Hypoplasias were recorded by drawing defect location and size on a dental chart, and by measuring defect size and location with Helios needlepoint dial calipers. The prevalence of LHPC is reported by genus and sex, using two approaches: 1) the frequency of affected individuals-those having one or more deciduous canine teeth scored positive for LHPC; and 2) the number of canine teeth scored positive for LHPC as a percentage of all canine teeth observed. Variation in defect size and location will be described elsewhere. Localized hypoplasia of primary canine teeth was found in 62.5% of 128 individual apes, and in 45.5% of 398 great ape deciduous canines. As in humans, LHPC is the most common form of enamel hypoplasia in deciduous teeth of great apes, while LEH is rare or absent. The distribution and pattern of expression of LHPC in great apes is similar to that described in humans: side differences are not significant, but mandibular canines exhibit the defect two to five times more often than maxillary canine teeth. Differences in LHPC prevalence by sex are small and not significant. Intergeneric differences are large and non-random: chimpanzees (Pan) exhibit a significantly lower frequency of LHPC (22%, n = 50) by individual count, than either the orangutan (Pongo, 88.0%, n = 25) or the gorilla (Gorilla, 88.7%, n = 53). Tooth count prevalences exhibit a similar pattern of variation and are also statistically significant. These findings suggest that large bodied great apes (gorilla and orangutan) may be under greater physiological stress during perinatal and early postnatal development than the chimpanzee. The size, position, and timing of LHPC lesions are currently under analysis and may yield more insight into the etiological origin of this enamel defect.

Animals↗

Enamel hypoplasia in the deciduous teeth of great apes: variation in prevalence and timing of defects.

The prevalence of enamel hypoplasia in the deciduous teeth of great apes has the potential to reveal episodes of physiological stress in early stages of ontogenetic development. However, little is known about enamel defects of deciduous teeth in great apes. Unresolved questions addressed in this study are: Do hypoplastic enamel defects occur with equal frequency in different groups of great apes? Are enamel hypoplasias more prevalent in the deciduous teeth of male or female apes? During what phase of dental development do enamel defects tend to form? And, what part of the dental crown is most commonly affected? To answer these questions, infant and juvenile skulls of two sympatric genera of great apes (Gorilla and Pan) were examined for dental enamel hypoplasias. Specimens from the Powell-Cotton Museum (Quex Park, UK; n = 107) are reported here, and compared with prior findings based on my examination of juvenile apes at the Cleveland Museum of Natural History (Hamman-Todd Collection; n = 100) and Smithsonian Institution (National Museum of Natural History; n = 36). All deciduous teeth were examined by the author with a x10 hand lens, in oblique incandescent light. Defects were classified using Fédération Dentaire International (FDI)/Defects of Dental Enamel (DDE) standards; defect size and location on the tooth crown were measured and marked on dental outline charts. Enamel defects of ape deciduous teeth are most common on the labial surface of canine teeth. While deciduous incisor and molar teeth consistently exhibit similar defects with prevalences of approximately 10%, canines average between 70-75%. Position of enamel defects on the canine crown was analyzed by dividing it into three zones (apical, middle, and cervical) and calculating defect prevalence by zone. Among gorillas, enamel hypoplasia prevalence increases progressively from the apical zone (low) to the middle zone to the cervical zone (highest), in both maxillary and mandibular canine teeth. Results from all three study collections reveal that among the great apes, gorillas (87-92%) and orangutans (91%) have a significantly higher prevalence of canine enamel defects than chimpanzees (22-48%). Sex differences in canine enamel hypoplasia are small and not statistically significant in any great ape. Factors influencing intergroup variation in prevalence of enamel defects and their distribution on the canine crown, including physiological stress and interspecific dento-gnathic morphological variation, are evaluated.

Age Factors↗

Expression of a multifunctional DNA repair enzyme gene, apurinic/apyrimidinic endonuclease (APE; Ref-1) in the suprachiasmatic, supraoptic and paraventricular nuclei.

Apurinic/apyrimidinic endonuclease (APE; also referred to as Ref-1) repairs oxidative damage to DNA and regulates the redox state of DNA binding proteins. This later property influences the ability of DNA binding proteins, which include Fos and Jun, to bind to AP-1 complexes. Since DNA binding proteins may play important roles in regulating neuronal activity in the hypothalamus, we examined the expression of APE in the hypothalami of rats. In situ hybridization studies revealed high levels of APE mRNA expression in the suprachiasmatic nuclei (SCN), supraoptic nuclei (SON) and paraventricular nuclei (PVN). Since the SCN are the site of a biological clock, we examined whether APE gene expression was regulated by the circadian cycle or by light. Quantitative in situ hybridization studies showed that APE mRNA levels remained constant over the circadian cycle and were not increased by light exposure at night. We also tested if APE expression was under osmotic control in the SON and PVN. Hypertonic stimulus, however, did not induce further expression of APE mRNA in either the SON or the PVN. These findings identify the SCN, SON and PVN as sites of high level APE gene expression. These data suggest that APE may play an important role in these structures either to facilitate DNA repair or DNA binding protein action.

Animals↗

Regulated expression of APE apurinic endonuclease mRNA during wound healing in porcine epidermis.

Abasic (AP) sites in DNA are cytotoxic and mutagenic and their repair is initiated by AP endonucleases. The major AP endonuclease of mammalian cells is encoded by the APE gene. Ape protein has also been proposed to modulate the activity of some transcription factors independently of its AP endonuclease activity. We investigated whether APE expression is coordinated with cell division, which could diminish mutagenesis. The level of APE mRNA was followed during wound healing in porcine epidermis, in which surgical wounding prompts rapid cell proliferation followed by a differentiation program to regenerate normal skin. In situ hybridization with a probe from human APE cDNA revealed strongly decreased expression in rapidly proliferating migrating cells during the first 1-3 days following wounding, succeeded by sharply increased APE expression that exceeded the pre-wounding levels by days 9-17. These changes were not observed in the surrounding undamaged tissue. In contrast to the foregoing in vivo results, APE expression in cultured primary human fibroblasts (IMR90) or myeloid leukemia cells (K562) was not coordinated with cell division. This biphasic APE expression during wound healing could relate to transcription factor regulation or it could allow unhindered DNA synthesis or prepare the developing epidermis to handle DNA damage. However, if transient under-expression of APE-encoded repair enzyme does occur, it might render regenerating skin especially vulnerable to mutagenesis during the cell proliferation phase.

Animals↗

Meningeal arterial patterns in great apes: implications for hominid vascular evolution.

Arterial meningeal patterns were observed for 100 hemispheres from great ape endocasts (Pan paniscus, Pan troglodytes, Gorilla gorilla, and Pongo pygmaeus). Eight patterns emerged based on the relative contributions to the walls and dura mater of the middle part of the braincase of meningeal arteries that stem from two sources. These arteries enter the braincase through either the orbit (delivering blood from the internal carotid artery) or through the base of the middle cranial fossa (via the middle meningeal artery whose blood comes from the external carotid artery). The three genera of apes manifest different frequencies of the eight patterns, with orangutans highly dependent on orbital meningeal arteries at one extreme, and chimpanzees showing the greatest reliance on the middle meningeal artery at the other. As was the case in an earlier study of rhesus monkeys, there is a trend across the two genera of African apes for increased mean cranial capacity to be associated with increased reliance on the internal carotid artery for supplying the middle portion of the braincase. However, unlike the case for macaques, this trend does not reach statistical significance in African apes. Because it is rare for humans to manifest significant arterial contributions from the orbit to the middle cranial fossa, the comparative data on monkeys, apes, and humans suggest that, during the course of vascular evolution in Homo, the middle meningeal artery eventually took over supply of the entire middle cranial fossa. This hypothesis should be tested in the hominid fossil record. Earlier work on meningeal arterial patterns in apes has traditionally relied on Adachi's system that was determined from humans and focuses on the origin of the middle branch of the middle meningeal artery. As a result, the extensive orbital contributions to the middle portion of the braincase that characterize apes were not recognized and the eight patterns described in this paper were often erroneously assigned to the three patterns that adequately describe only humans. Adachi's system should therefore be abandoned for nonhuman primates and early hominids. A correct understanding of meningeal arterial evolution cannot be achieved until the orbital contributions to the meningeal arteries are recognized and incorporated into an evolutionary study that spans from apes to fossil hominids to living people.

Animals↗