Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Chimpanzees”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1953

Quantitative studies of the virus-host relationship in chimpanzees after inapparent infection with Coxsackie viruses. I. The virus carrier state and the development of neutralizing antibodies.

Following oral administration of Coxsackie viruses (C viruses) to susceptible chimpanzees, these agents can be isolated from the throat for a period of approximately a week, from the blood for a few days, and from the stools for 2 to 3 weeks or even longer. Animals so infected respond with the formation of specific neutralizing antibodies which are maintained for at least 1 to 2 years. Such chimpanzees are immune when challenged orally with homologous strains of virus. They then excrete virus in the stools for 3 or 4 days (passive transfer); no virus can be recovered from the throats and blood of these animals, and neutralizing antibody levels remain unchanged. Animals immune to one antigenic type of C virus can be infected by feeding a different antigenic type. Following such a heterotypic challenge, virus can again be isolated from the throat, blood, and stools; neutralizing antibodies develop to the new strain. Antibodies to the Texas-1 type of C virus were already present in four chimpanzees upon their arrival in the laboratory from Africa. It was possible to set up intestinal carriage of the Texas-1 virus in these animals and to demonstrate a 10- to 100-fold increase in titer of neutralizing, as well as complement-fixing, antibody. Quantitative titrations of the amount of virus present in the stools and throat were performed. Immediately after the first feeding of virus relatively large amounts can be detected in the stools; the titer drops, but may be maintained for as long as 25 days at 10(-2) to 10(-3), furnishing evidence that virus multiplication has taken place. Virus in the throat reached the same order of magnitude at first as in the stools but there was a rapid decline to zero in a few days. The Ohio-1 virus differed from the others in that it persisted in the throat as long as in the stools, and in several instances reached a higher titer in the throat. Following homotypic challenge with all types, virus could be detected in the stools for only a relatively short period of time and at low concentration. Virus-neutralizing substances could not be detected in the stools or throat swabs of convalescent animals, at a time when their serum-neutralizing antibody titers were high. Under the limited conditions of the present experiments, C viruses had no effect on the infection of chimpanzees with three different antigenic types of poliomyelitis virus. Both poliomyelitis and C viruses set up independent infections without apparent interaction between them. No enhancement of the poliomyelitis infection took place, as was plain from the fact that none of the infected chimpanzees became paralyzed. a titration of Texas-1 C virus in four chimpanzees revealed that a suspension of infected tissue diluted to 10(6.0) could cause the development of the carrier state; accidental infection of control animals with other Coxsackie types indicated also that very little virus may be necessary to initiate infection. Seven distinct antigenic types of C virus were inoculated subcutaneously and intramuscularly at the same time into four chimpanzees. The response was the same as that following feeding; virus could be recovered from the throat, blood, and stools, and the animals developed neutralizing antibodies to all seven types of C virus. There was no detectable interference among the viruses. Cortisone did not bring about the reappearance of the virus excretion in chimpanzees previously infected and shown to be intestinal carriers of poliomyelitis and Coxsackie viruses.

Animals↗
PubMed1998

Genital infection of female chimpanzees with human immunodeficiency virus type 1.

To develop an animal model for mucosal HIV-1 infection, adult chimpanzees were inoculated without trauma by depositing the virus inoculum at the entrance to the cervical canal with a rigid catheter to which flexible tubing was attached. By this procedure, persistent infections were established in some chimpanzees with various infectious doses of either cell-associated HIV-1LAI(IIIB) (peripheral blood mononuclear cells from an infected chimpanzee) or with cell-free HIV-1 strains representing subtypes B and E, but not with a subtype A strain. Although some animals did not become infected until after the second or third cervicovaginal exposure, one chimpanzee was clearly infected after one exposure by several criteria, including virus isolation, but this animal did not seroconvert. A second chimpanzee appeared to be resistant to infection despite repeated mucosal exposures at irregular intervals. However, lymphocytes from both of these animals exhibited low-level proliferative responses to HIV-1 but not SIV antigens. Despite these apparently abortive or latent infections, after exposure to HIV-1 by the intravenous route, both animals developed systemic infections and seroconverted. Overall, 8 of 10 chimpanzees were infected systemically after one to three cervicovaginal exposures to HIV-1LAI(IIIB). The results indicate that (1) HIV-1 productive infection of female chimpanzees by the cervicovaginal route generally requires more than one exposure, just as with humans; (2) low level infections without seroconversion can be established after mucosal exposure to HIV; and (3) vaccine efficacy studies involving a single virus challenge of immunized chimpanzees by the cervicovaginal route probably will not be possible.

Animals↗
PubMed2006

Preparing chimpanzees for laboratory research.

The chimpanzee is the only representative of the Great Apes that is extensively involved in biomedical research in primate laboratories. These apes are used as animal models in a variety of studies, including research on infectious disease, parasitic disease, pharmacokinetic studies, neuroscience, cognition, and behavior. Chimpanzees used in biomedical research in the United States reside largely in six specialized research and holding facilities, and most of the research with them is conducted at these sites. Given the relatively small population of chimpanzees and its importance to biomedical research, it is imperative that we carefully manage the care, production, and use of these animals in biomedical research studies. Selection criteria and preparation techniques are reviewed in this article in an effort to begin a discussion on best practices for choosing and handling chimpanzees participating in biomedical research. The use of routine health assessment information is described for subject selection, as are behavioral issues to be considered. Due to the relatively small number of chimpanzees available, issues related to experimental design and multiple uses of chimpanzees are discussed. Practices related to the transportation and acclimation of chimpanzees are described. Finally, behavioral conditioning procedures are discussed, including habituation, desensitization, and positive reinforcement training that have been applied to reduce animal distress and improve the quality of the science being conducted with chimpanzee subjects.

Acclimatization↗
PubMed1975

Experimental infection of chimpanzees with hepatitis A virus.

The susceptibility of chimpanzees to viral hepatitis type A was examined with immine electron microscopy. Of four seronegative infant chimpanzees, two were inoculated with a hepatitis A acute-phase stool filtrate rich in 27 nm virus-like hepatitis A antigen (HA Ag) particles, and two were inoculated with an HA Ag-negative preinfection stool filtrate. One of each pair of chimpanzees was inoculated intravenously, the other orally. One month later both chimpanzees that had received the HA Ag-positive filtrate developed biochemical, histologic, and clinical evidence of acute viral hepatitis. HA Ag particle (27 nm) were detected in their stools by immune electron microscopy; particle shedding followed a pattern similar to that in human volunteers. Immune electron microscopy also showed that antibody HA Ag had developed in the convalescent-phase sera of the infected chimpanzees. Control animals remained free of illness at this time but did develop hepatitis three to five weeks after exposure to the two infected chimpanzee-. The infectious inoculum was titrated in two additional seronegative chimpanzees. It was concluded that hepatitis a can be successfully transmitted to seronegative chimpanzees. Moreover, these studies provide further evidence that the 27-nm virus-like HA Ag particle is the etiologic agent of viral hepatitis type A.

Animals↗
PubMed1986

Persistent infection of chimpanzees with human T-lymphotropic virus type III/lymphadenopathy-associated virus: a potential model for acquired immunodeficiency syndrome.

The lymphadenopathy-associated virus (LAV) prototype strain of human T-lymphotropic virus type III/LAV was transmitted to juvenile chimpanzees with no prior immunostimulation by (i) intravenous injection of autologous cells infected in vitro, (ii) intravenous injection of cell-free virus, and (iii) transfusion from a previously infected chimpanzee. All five animals that received more than one 50% tissue culture infective dose were persistently infected with LAV or chimpanzee-passaged LAV for up to 18 months. During this time they developed no illnesses, but they exhibited various degrees of inguinal and axillary lymphadenopathy and significant reductions in rates of weight gain. Detailed blood chemistry and hematologic evaluations revealed no consistent abnormalities, with the exception of immunoglobulin G (IgG) hypergammaglobulinemia, which became apparent in one animal 6 months postinfection and continued at more than 1 year postinfection. Transient depressions followed by increases in the numbers of T4 cells to levels greater than normal were observed in all animals after virus inoculation. However, the number of LAV-infected peripheral blood cells decreased with time after infection. Results of enzyme immunoassays showed that all infected animals seroconverted to IgG anti-LAV within 1 month postinfection and that antibody titers remained high throughout the period of observation. In contrast, only three of the five LAV-infected chimpanzees had detectable IgM antibody responses, and these preceded IgG-specific serum antibodies by 1 to 2 weeks. Virus morphologically and serologically identical to LAV was isolated from peripheral blood mononuclear cells of all infected animals at all times tested and from bone marrow cells taken from one animal 8 months after infection. One chimpanzee that was exposed to LAV only by sharing a cage with an infected chimpanzee developed lymphadenopathy and an IgM response to LAV, both of which were transient; however, no persistent IgG antibody response to LAV developed, and no virus was recovered from peripheral blood cells during a year of follow-up. Thus, LAV readily infected chimpanzees following intravenous inoculation and persisted for extended periods despite the presence of high titers of antiviral antibodies. However, the virus was not easily transmitted from infected to uninfected chimpanzees during daily cage contact.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Challenge of chimpanzees (Pan troglodytes) immunized with human immunodeficiency virus envelope glycoprotein gp120.

The human immunodeficiency virus type 1 (HIV-1), the causative agent of acquired immunodeficiency syndrome, infects humans and chimpanzees. To determine the efficacy of immunization for preventing infection, chimpanzees were immunized with gp120 purified from human T-cell lymphotrophic virus type IIIB (HTLV-IIIB)-infected cell membranes and challenged with the homologous virus, HTLV-IIIB. A challenge stock of HTLV-IIIB was prepared by using unconcentrated HTLV-IIIB produced in H9 cells. The titer of the virus from this stock on human and chimpanzee peripheral blood mononuclear cells and in human lymphoid cell lines was determined; a cell culture infectivity of 10(4) was assigned. All chimpanzees inoculated intravenously with 40 cell culture infectious units or more became infected, as demonstrated by virus isolation and seroconversion. One of two chimpanzees inoculated with 4 cell culture infectious units became infected. Chimpanzees immunized with gp120 formulated in alum developed antibodies which precipitated gp120 and neutralized HTLV-IIIB. Peripheral blood mononuclear cells from gp120-vaccinated and HIV-infected animals showed a significantly greater response in proliferation assays with HIV proteins than did peripheral blood mononuclear cells from nonvaccinated and non-HIV-infected chimpanzees. Two of the gp120-alum-immunized chimpanzees were challenged with virus from the HTLV-IIIB stock. One animal received 400 cell culture infectious units, and one received 40 infectious units. Both animals became infected with HIV, indicating that the immune response elicited by immunization with gp120 formulated in alum was not effective in preventing infection with HIV-1.

Animals↗
PubMed1998

Loss of CD4+ T cells in human immunodeficiency virus type 1-infected chimpanzees is associated with increased lymphocyte apoptosis.

Supportive evidence that apoptosis contributes to loss of CD4+ lymphocytes in human immunodeficiency virus type 1 (HIV-1)-infected humans comes from an apparent lack of abnormal apoptosis in apathogenic lentivirus infections of nonhuman primates, including HIV-1 infection of chimpanzees. Two female chimpanzees were inoculated, one cervically and the other intravenously, with HIV-1 derived from the LAI/LAV-1b strain, which was isolated from a chimpanzee infected with the virus for 8 years. Within 6 weeks of infection, both recipient chimpanzees developed a progressive loss of CD4+ T cells which correlated with persistently high viral burdens and increased levels of CD4+ T-cell apoptosis both in vitro and in vivo. Lymph nodes from both animals also revealed evidence of immune hyperactivation. Intermediate levels of T-cell apoptosis in both peripheral blood and lymph nodes were seen in a third chimpanzee that had been infected with the LAI/LAV-1b strain for 9 years; this animal has maintained depressed CD4/CD8 T-cell ratios for the last 3 years. Similar analyses of cells from 4 uninfected animals and 10 other HIV-1-infected chimpanzees without loss of CD4+ cells revealed no difference in levels of apoptosis in these two control groups. These results demonstrate a correlation between immune hyperactivation, T-cell apoptosis, and chronic loss of CD4+ T cells in HIV-1-infected chimpanzees, providing additional evidence that apoptosis is an important factor in T-cell loss in AIDS. Furthermore, the results show that some HIV-1 strains are pathogenic for chimpanzees and that this species is not inherently resistant to HIV-1-induced disease.

Animals↗
PubMed2003

The clearance of hepatitis C virus infection in chimpanzees may not necessarily correlate with the appearance of acquired immunity.

Clearance of hepatitis C virus (HCV) infection in humans and chimpanzees is thought to be associated with the induction of strong T-cell responses. We studied four chimpanzees infected with HCV derived from an infectious full-length HCV genotype 1b cDNA. Two of the chimpanzees cleared the infection to undetectable levels for more than 12 months of follow-up; the other two became persistently infected. Detailed analyses of HCV-specific immune responses were performed during the courses of infection in these chimpanzees. Only weak and transient T helper responses were detected during the acute phase in all four chimpanzees. A comparison of the frequency of gamma interferon (IFN-gamma)-producing CD4(+) and CD8(+) T cells in peripheral blood by ELISpot assay did not reveal any correlation between viral clearance and T-cell responses. In addition, analyses of IFN-gamma, IFN-alpha, and interleukin-4 mRNA levels in liver biopsies, presumably indicative of intrahepatic T-cell responses, revealed no distinct pattern in these chimpanzees with respect to infection outcome. The present study suggests that the outcome of HCV infection in chimpanzees is not necessarily attributable to HCV sequence variation and that chimpanzees may recover from HCV infection by mechanisms other than the induction of readily detectable HCV-specific T-cell responses.

Amino Acid Sequence↗
PubMed2005

Functional analysis of human and chimpanzee promoters.

BACKGROUND: It has long been argued that changes in gene expression may provide an additional and crucial perspective on the evolutionary differences between humans and chimpanzees. To investigate how often expression differences seen in tissues are caused by sequence differences in the proximal promoters, we tested the expression activity in cultured cells of human and chimpanzee promoters from genes that differ in mRNA expression between human and chimpanzee tissues. RESULTS: Twelve promoters for which the corresponding gene had been shown to be differentially expressed between humans and chimpanzees in liver or brain were tested. Seven showed a significant difference in activity between the human promoter and the orthologous chimpanzee promoter in at least one of the two cell lines used. However, only three of them showed a difference in the same direction as in the tissues. CONCLUSION: Differences in proximal promoter activity are likely to be common between humans and chimpanzees, but are not linked in a simple fashion to gene-expression levels in tissues. This suggests that several genetic differences between humans and chimpanzees might be responsible for a single expression difference and thus that relevant expression differences between humans and chimpanzees will be difficult to predict from cell culture experiments or DNA sequences.

Animals↗
PubMed1996

A longitudinal study of the kidney function of the chimpanzee (Pan troglodytes) in comparison with humans.

A prospective study of the kidney function of chimpanzees (Pan troglodytes) kept at the Hans Popper Primate Centre has been performed within the last 10 years. The aim of the study was to analyse urine samples for specific gravity, to determine serum creatinine, serum urea, and urinary creatinine, and to calculate creatinine clearance and reference values for healthy chimpanzees. From 1750 urine specimens of adolescent and 568 of infant chimpanzees a mean specific gravity value of 1.013 +/- 0.006 (standard deviation) kg/l and 1.007 +/- 0.003 (standard deviation) kg/l, respectively, was calculated. Serum creatinine was determined in 1864 single samples from 52 chimpanzees; a median value of 101.8 mumol/l (P (5%) 79.6 mumol/l, P (95%) 139.7 mumol/l) was calculated, which is higher than that in humans. Serum urea tests (n = 1831) in the same 52 chimpanzees resulted in a median value of 2.01 mmol/l (P (5%) 0.86 mmol/l, P (95%) 4.78 mmol/l). The calculated median creatinine clearance value of 23.9 ml/min (P (5%) 4.4 ml/min, P (95%) 65.3 ml/min) is lower in chimpanzees than in man. A correction of the creatinine clearance values to the body surface area of 1.73 m2, as routinely performed in humans, gave unusually high results, as there was no proper equation to calculate the surface area of chimpanzees. The use of estimation equations for creatinine clearance values of chimpanzees as developed for humans is therefore not recommended.

Animals↗
PubMed2003

Analysis of the TCR beta variable gene repertoire in chimpanzees: identification of functional homologs to human pseudogenes.

Chimpanzees are used for a variety of disease models such as hepatitis C virus (HCV) infection, where Ag-specific T cells are thought to be critical for resolution of infection. The variable segments of the TCR alphabeta genes are polymorphic and contain putative binding sites for MHC class I and II molecules. In this study, we performed a comprehensive analysis of genes that comprise the TCR beta variable gene (TCRBV) repertoire of the common chimpanzee Pan troglodytes. We identified 42 P. troglodytes TCRBV sequences representative of 25 known human TCRBV families. BV5, BV6, and BV7 are multigene TCRBV families in humans and homologs of most family members were found in the chimpanzee TCRBV repertoire. Some of the chimpanzee TCRBV sequences were identical with their human counterparts at the amino acid level. Notably four successfully rearranged TCRBV sequences in the chimpanzees corresponded to human pseudogenes. One of these TCR sequences was used by a cell line directed against a viral CTL epitope in an HCV-infected animal indicating the functionality of this V region in the context of immune defense against pathogens. These data indicate that some TCRBV genes maintained in the chimpanzee have been lost in humans within a brief evolutionary time frame despite remarkable conservation of the chimpanzee and human TCRBV repertoires. Our results predict that the diversity of TCR clonotypes responding to pathogens like HCV will be very similar in both species and will facilitate a molecular dissection of the immune response in chimpanzee models of human diseases.

Amino Acid Sequence↗
PubMed1975

Contrasting effects of morphine on schedule-controlled behavior in the chimpanzee and baboon.

Schedule-controlled key pressing was maintained in two chimpanzees and three baboons under a multiple 10-minute fixed-interval (FI 10-min) 30-response fixed-ratio (FR 30) schedule of food delivery. Characteristic rates and patterns of responding were maintained under the FI and FR schedules, and the performance of the two species differed in no systematic way. The acute i.m. administration of morphine (0.1-3.0 mg/kg) prior to selected 2-hour sessions increased mean rates of responding under the FI schedule in the chimpanzee, but decreased responding in the baboon. At a dose of 3.0 mg/kg of morphine, responding under the FI schedule in the chimpanzee increased 4-fold and responding in the baboon decreased to less than 25% of control levels. Mean response rates under the FR schedule were also increased by morphine in the chimpanzee, but responding under the FR schedule was little affected in the baboon except at the higher doses which decreased response rates below control levels. Respiratory rate in the chimpanzee was markedly depressed at 5.6 mg/kg of morphine and one chimpanzee died. A similar depression of respiration was not observed in the increase responding in a nonhuman primate, the chimpanzee, and that the behavioral effects of morphine in the chimpanzee are qualitatively different from the effects in monkeys.

Animals↗
PubMed1988

Antifilarial activity of CGP 20,376 in chimpanzees (Pan t. troglodytes) naturally infected with Dipetalonema vanhoofi.

CGP 20,376, a benzthiazole and new antifilarial agent, was investigated at CIRMF in eight wild born chimpanzees naturally infected with Dipetalonema vanhoofi. Single oral doses (3.75, 7.5, 11 and 15 mg/kg) were administered. Drug levels during the first hour after administration were assessed in seven chimpanzees at 10 minute intervals in the blood. Levels of unchanged drug (CGP 20,376) were higher than those of its metabolite (CGP 20,308). However, there was considerable variation between individuals, although the results for each animal were consistent. Because of investigational limitations a complete drug profile could not be established. Unsheathed microfilariae of D. vanhoofi were monitored during the first hour following drug administration in seven chimpanzees. In five the microfilaraemia dropped to low counts within 10 minutes and remained below the initial values for the next 50 minutes while in two other chimpanzees it showed a more irregular reduction. Periodic microfilarial counts over the next 20 months, at roughly 30 day intervals, showed that three chimpanzees, treated with 7.5, 11 and 15 mg/kg respectively, remained free of circulating microfilariae from Day 1 to Day 600, the chimpanzee treated with 3.75 mg/kg remained microfilaremic and, in three chimpanzees low numbers of microfilariae reappeared within one year, whereas in the remaining ape they reappeared after one year. No major clinical adverse effects were observed, but liver function tests showed mild reversible changes at the 11 and 15 mg/kg doses. CGP 20,376 was therefore microfilaricidal, except for the lowest dose, and it was possibly macrofilaricidal in those chimpanzees which remained free of microfilariae for 600 days. Clinically CGP 20,376 was well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Lack of chronic immune activation in HIV-infected chimpanzees correlates with the resistance of T cells to Fas/Apo-1 (CD95)-induced apoptosis and preservation of a T helper 1 phenotype.

Chimpanzees are one of the few species, along with humans, susceptible to persistent HIV-1 infection. However, HIV-infected chimpanzees do not exhibit the marked immune system alterations seen in humans and remain relatively resistant to AIDS. In humans, HIV infection leads to unresponsiveness of T cells in response to TCR stimulation, associated with increased T cell death by apoptosis. In an effort to understand some of the mechanisms used to limit lentivirus infection in African nonhuman primates, we compared apoptosis in infected humans vs chimpanzees in CD4 and CD8 T cells in relation with the expression of Bcl-2 and Fas molecules. The intensity of apoptosis in CD4 and CD8 T cells from infected chimpanzees was very low, was not inducible by several TCR-dependent activators, and was comparable to that detected in noninfected chimpanzees. Moreover, CD45RO+ and HLA-DR+ subsets, which were shown to exhibit ex vivo a high propensity to undergo apoptosis in infected humans, were not modified in infected chimpanzees. Interestingly, in contrast to the situation found in infected humans, Fas ligation by agonistic Abs or recombinant human Fas ligand on CD4 and CD8 T cells from infected chimpanzees did not induce apoptosis in these subsets even when Bcl-2 was down-regulated. Finally, this resistance to apoptosis was associated with the predominance of CD3 T cells with a Th1 phenotype. Together these observations argue for a strong relationship among the absence of chronic immune stimulation in HIV-1-infected chimpanzees, the normal control of lymphocyte survival, and the resistance to disease progression.

Animals↗
PubMed2002

Survey of savanna chimpanzees (Pan troglodytes verus) in Southeastern Sénégal.

A survey of the western subspecies of chimpanzee (Pan troglodytes verus) was conducted from 1 February to 9 April 2000 in Sénégal, West Africa, by the Miami Assirik Pan Project (MAPP). In addition to the Assirik area of the Parc National du Niokolo Koba (PNNK), areas south and east of the park were surveyed. Nests made by chimpanzees were used to estimate chimpanzee distribution and densities. Within the PNNK, chimpanzees were estimated to occur at an average of 0.13 individuals/km(2). Chimpanzee nests were recorded in nine of 10 locales surveyed outside of the PNNK, as well as within the park. Data on 994 nests made by chimpanzees were recorded outside the PNNK, while 736 nests were recorded inside the park. Nest density in areas surveyed outside the PNNK, such as Bandafassi, Tomboronkoto, and Segou, was comparable to that of Assirik in habitats where nests were concentrated (i.e., evergreen gallery forest). The purpose of MAPP was to initiate long-term research of chimpanzees in southeastern Sénégal, as a follow-up to the Stirling African Primate Project (SAPP) of the 1970s. We sought to replicate the standards set by the SAPP project, except when technological innovations allowed improvement in data collection procedures (e.g., the global positioning system (GPS)).

Animals↗
PubMed2003

Histologic examination of bone development in juvenile chimpanzees.

The purpose of this study is to determine whether histologic skeletal development in chimpanzees (Pan troglodytes) differs from that in humans. Currently, minimal quantitative data are available on the bone histology of great apes. In addition to providing baseline data on juvenile chimpanzee bone histology, the data generated by this study have potential applications for studying the comparative development between chimpanzees and humans and other primates, as well as investigating the evolution of human bone development, differences in development among limb elements, and differences in histology related to locomotor function. The study sample includes thin sections from the femoral, tibial, and fibular midshafts of 13 chimpanzees originally prepared by Kerley ([1966] Tulane Stud. Zool. 13:71-82) as part of a study on skeletal age changes in the chimpanzee. Twelve juveniles, ranging in known age from 2-15.3 years, and one adult, with a known age of 35 years, are represented. For each specimen, numbers of osteons, osteon fragments, and non-Haversian canals were counted, and percent lamellar bone was estimated. Results were compared with data extracted from Kerley ([1965] Am. J. Phys. Anthropol. 23:149-164) on a juvenile human sample. Results indicate that juvenile chimpanzees and humans exhibit similar age-related changes in histologic variables. However, age is not as strong a predictor of variation in microstructural variables in chimpanzees as it is in humans.

Animals↗
PubMed1975

Epidermal patterns of the hands and feet of the pygmy Chimpanzee (Pan paniscus).

The characteristics of the epidermal ridge system were studied in a series of eighteen lesser or pygmy chimpanzees (Pan paniscus). The general ridge alignments are very similar to those of the chimpanzee (Pan troglodytes); Biegert ('61). On the average the pattern intensity (P. I.) of the palm configurations is considerably higher in the pygmy chimpanzee than in the chimpanzee, thus representating the highest total palm pattern intensity of all species of the hominoidea. The sole configurations show parallel main results to those of the palm; however, the decreased sole pattern frequency of the pygmy chimpanzee is of a smaller predominance only as compared to the values of the other species of this superfamily. The preliminary data on the finger tip patterns, translated into P. I. values, are much higher than in chimpanzees and within the range of the mean values of gorillas (Brehme, '73), while those of the toes of pygmy chimpanzees seem to possess the lowest P. I. values of the African apes.

Animals↗
PubMed1994

Patterns of predation by chimpanzees on red colobus monkeys in Gombe National Park, 1982-1991.

Predatory patterns in wild chimpanzees are important evidence in the continuing debate about the role of hunting in the behavior of early hominids. Data are presented on the predator-prey ecology of red colobus monkeys Colobus badius tephrosceles) and chimpanzees (Pan troglodytes schweinfurthii) in Gombe National Park, Tanzania, from 1982 through 1991. During this period chimpanzees were observed to kill 429 mammalian prey items, 350 of which were red colobus. Hunts were undertaken by chimpanzees in 71.5% of encounters with red colobus, and in 52.2% of all hunts at least one colobus was caught. Hunting occurred in all months, but its frequency peaked in the late dry season months of August and September, and was lowest in the rainy months of April and May. There was greater seasonality of hunting from 1982 to 1991 than previously reported for Gombe. Hunting success varied between 40% in the rainy season and 65% in the dry season. Sixty multiple kills of colobus were reported in which from two to seven colobus were killed. Approximately 75% of all colobus caught were immatures; juveniles were the most preyed upon age class. Adult and adolescent male chimpanzees made 89.3% of all kills; the 10.7% of kills made by adult females was an increase over the 4% figure for female kills reported in the preceding decade. Hunting showed a strong "binge" tendency, with the explanation for binges likely related to social rather than ecological factors. These results are discussed in light of earlier hunting data for Gombe chimpanzees, and compared with data from other chimpanzee field studies.

Age Factors↗