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At least 19 recordsLinked to original sources
PubMed2006

Clinical response Decision Tree for the Mountain Gorilla (Gorilla beringeii) as a model for great apes.

Disease is one of the main threats to the remaining great ape populations of the world. The decision to intervene in the health of the great apes for population sustainability is controversial. Humans' increasing negative influence on great ape health has mandated the reevaluation of current management policies. The Mountain Gorilla Veterinary Project (MGVP) has been making health intervention decisions since 1986. The decision to intervene has often been made subjectively due to poorly defined criteria that are often influenced by emotion. This paper provides a consistent framework for evidence-based health intervention decision-making. The decision tree is a five-tier process consisting of routine sentinel health observation, intensive follow-up veterinary health observation, outbreak assessment, risk assessment, and risk management. Although this paper focuses on the mountain gorillas, it serves as a basis for evidence-based decision-making in other species.

Animals↗
PubMed2005

Activation of muscarinic K+ channels by arecaidine propargyl ester in isolated guinea-pig atrial myocytes.

Arecaidine propargyl ester (APE) was developed as a potential candidate compound for the treatment of Alzheimer's disease. APE has been shown to have cardiovascular effects. APE produces negative chronotropic and inotropic effects in isolated atria. However, the ionic mechanisms underlying the cardiovascular effects of APE in guinea-pig atria are unclear. The aims of this study were: (1) to examine the shortening effect of APE on action potential duration (APD) and to compare the difference in potency between APE and muscarine in isolated single guinea-pig atrial myocytes by using the current clamp method, (2) to examine by using patch clamp techniques the ionic mechanisms underlying the cardiac effects of APE, and (3) to determine whether the cardiac effects caused by APE affect the usefulness of APE as a potential candidate for the treatment of Alzheimer's disease. The APE significantly reduced the APD in guinea-pig atria and produced no direct effect on ventricular myocytes. APE is approximately 20 times as potent as muscarine in shortening the APD. Attenuation of the APD was consistently accompanied by a hyperpolarization of the resting membrane potential in a concentration-dependent manner. The APE activated muscarinic K+ channels and increased potassium conductance in guinea-pig atrial myocytes. In the cell-attached configuration, the APE contained in the pipette increased the channel-opening probability and decreased the closed-state time interval. The proposal that APE can be used as a potential remedy for the treatment of Alzheimer's disease should be taken into consideration the undesirable cardiovascular side effects that APE causes at lower concentrations.

Animals↗
PubMed2000

Primatology. Human diseases threaten great apes.

Researchers are uncovering disturbing evidence that scientists and tourists are infecting wild primates with human pathogens. In response, ape specialists, including the American Society of Primatologists, are now calling for stricter health standards for researchers and tourists. They are also urging researchers to learn how to diagnose disease in their study animals.

Africa↗
PubMed2004

Tau gene (MAPT) sequence variation among primates.

Filamentous tau deposits are a defining feature of a number of human neurodegenerative diseases. Apes and monkeys have been reported to be differentially susceptible to developing tau pathology. Despite this, only little is known about the organisation and sequence of Tau from nonhuman primates. Here we have sequenced Tau exons 1-13, including flanking intronic regions, and the region in intron 9 that contains Saitohin in chimpanzees, gorillas, and gibbons. Partial sequences were obtained for cynomolgus macaque and green monkey. Chimpanzee brain tau was 100% identical to human tau. Identities were 99.5% for gorilla tau and 99.0% for gibbon tau. Chimpanzee DNA was polymorphic for a repeat in intron 9, which was present in human and gorilla tau, and for the nucleotide at position +29 of the intron that follows exon 10. As was the case of the other nonhuman primates examined, chimpanzee DNA was homozygous for nucleotides used to define the H2 haplotype in human Tau. These differences between human and chimpanzee Tau may contribute to the apparent resistance of chimpanzee brain to developing tau pathology. Sequencing of Saitohin revealed an intact open reading frame in chimpanzee and gorilla, but not in gibbon or macaque.

Alternative Splicing↗
PubMed1987

The aquatic ape theory and some common diseases.

The Aquatic Ape Theory claims that human ancestors once lived in a semi-aquatic habitat. Some human diseases might be explained by our aquatic past. Such problems include hyperventilation, periodic breathing, laryngo- and bronchospasm, vasomotor rhinopathy, seborrhea, dandruff, male pattern alopecia, rhinophyma, osteoarthritis, inguinal hernias, varicose veins, common obesity, myopia, and ear-wax.

Animals↗
PubMed2000

Degenerative joint disease in African great apes: an evolutionary perspective.

Degenerative joint disease is investigated in the spine and major peripheral joints (shoulder, elbow, hip and knee) in samples of chimpanzees (Pan troglodytes schweinfurthii; P. troglodytes troglodytes), lowland gorillas (Gorilla gorilla gorilla), and bonobos (P. paniscus). The P. troglodytes schweinfurthii sample comes from Gombe National Park, Tanzania, while the other samples are derived from museum materials originally collected in west/central Africa. Total data for African ape samples include 5807 surfaces for ascertainment of vertebral osteophytosis, 12,479 surfaces for determination of spinal osteoarthritis, and 1211 joints for evaluation of peripheral joint osteoarthritis. All apes display significantly less spinal disease than in a comparable human sample, and these differences are most likely a consequence of human biomechanical adaptations for bipedal locomotion. Apes are also generally less involved in the major peripheral joints than are humans, but human groups are themselves highly variable in prevalence of peripheral osteoarthritis. These data agree with other findings of low prevalence of degenerative joint prevalence in free-ranging apes, but contrast markedly with evidence derived from colony-reared Old World monkeys.

Africa↗
PubMed1975

Ulcerative colitis in apes: A comparison with the human disease.

The pathological changes in the colons of two young gorillas and an adult orang-utan which developed diarrhoea and died, are described. Since no causative agents could be identified and the changes were indistinguishable from the active phase of ulcerative colitis in humans, these cases were considered examples of this disease in apes. Evidence of early healing was found in one case and the suitability of apes and monkeys as possible animal models of the human disease is discussed.

Animals↗
PubMed2001

Host range studies of GB virus-B hepatitis agent, the closest relative of hepatitis C virus, in New World monkeys and chimpanzees.

GB virus-B (GBV-B) is a member of the Flaviviridae family of viruses. This RNA virus causes acute resolving hepatitis in experimentally infected tamarins, but its natural host remains unknown. GBV-B and a related virus, GBV-A, were recovered from serum containing the "GB agent," which was believed to have originated from a surgeon (initials: GB) with acute hepatitis. GBV-B has special interest because it is the virus related most closely to hepatitis C virus, which is an important cause of acute and chronic liver disease in humans. In the present study, we found that the host range of GBV-B includes owl monkeys. Tamarins and owl monkeys belong to two different families of New World monkeys. The natural history of GBV-B in the two owl monkeys studied was similar to that previously found for tamarins and was characterized by early appearance of viremia and viral clearance. However, the peak viral titers of GBV-B observed in owl monkeys (10(5) genome equivalents [GE] /ml) were lower than those observed in experimentally infected tamarins (10(7)-10(8) GE/ml) and acute hepatitis was observed in only one animal. If GBV-B were indeed a virus of humans, it would be expected to infect chimpanzees, a surrogate of humans, because all recognized human hepatitis viruses are transmissible to chimpanzees and cause hepatitis. However, in the present study, we failed to transmit GBV-B to a naive chimpanzee. In addition, a second naive chimpanzee transfected intrahepatically with RNA transcripts from an infectious clone of GBV-B did not become infected. Thus, chimpanzees are apparently not susceptible to GBV-B. Finally, we failed to detect GBV-B in acute-phase serum from surgeon GB. Our data suggest that GBV-B is not a human virus and that GBV-B, like GBV-A, is a virus of New World monkeys.

Acute Disease↗
PubMed1980

Infectious diseases of the great apes of Africa.

The chimpanzee is the most extensively used ape in biomedical research. Its phylogenetic relationship to man has made it one of the most desirable of research animals. However, because of this closeness to man, the chimpanzee is highly susceptible to human (and other primate) infectious agents, particularly viruses. This susceptibility makes the chimpanzee the only known available test system for aetiological studies on such diseases as hepatitis, neurological diseases of suspected viral origin, etc. Very few infectious disease data are available on the gorilla. What is known suggests a parallelism with the chimpanzee and man. Serological data, however, strongly suggest that subclinical infection without overt disease occurs following contact with human and other animal infectious agents. The need for studies of infectious diseases in the wild is stressed. The susceptibility of these species to human disease incitants emphasizes the need for rigid precautions to avoid exposure and to maintain healthy animals.

Animals↗
PubMed1964

HOMOTRANSPLANTATION.

Explore the source record for details and available documents.

Antigen-Antibody Reactions↗
PubMed2001

Review of findings of the Andhra Pradesh Eye Disease Study: policy implications for eye-care services.

The Andhra Pradesh Eye Disease Study (APEDS) was conducted in order to design long-term strategies to reduce blindness in the background of non-availability of recent population-based data on various aspects of blindness. The objectives of APEDS were to determine the prevalence and causes of blindness and visual impairment, prevalence of and risk factors for major eye diseases, barriers to eye-care services, and quality of life among the visually impaired. Multistage sampling was used to select 11,786 subjects of all ages from 24 urban clusters and 70 rural clusters in one urban and three rural areas belonging to different parts of Andhra Pradesh, with the aim of obtaining a study sample representative of the urban-rural and socioeconomic distribution of the population of this state. A total of 10,293 subjects underwent a detailed interview and dilated eye examination by trained professionals. The adjusted prevalence of blindness (presenting visual acuity <6/60 or central visual field <20 degrees in the better eye) was 1.84%, and moderate visual impairment (presenting visual acuity <6/18-6/60 or equivalent visual field loss in the better eye) was 8.1%. Cataract and refractive error were responsible for 60.3% of blindness and 85.7% of moderate visual impairment. Increasing age, decreasing socioeconomic status, female gender, and rural area of residence were associated with higher risk of blindness. Projections from APEDS suggest that there were 18.7 million blind people in 2000 in India, and that this number is likely to increase to 24.1 million and 31.6 million in 2010 and 2020 respectively, if the current trend continues. This review summarizes the findings of APEDS and discusses the implications of these data on the policy and planning of eye-care services.

Blindness↗
PubMedDate not supplied

Primate hepatitis B viruses - genetic diversity, geography and evolution.

There are six well characterised genotypes (A-F) of human hepatitis B virus that have distinct geographic ranges which generally relate to chronic HBV infection. A seventh human genotype (G) has recently been described, but there is limited information on ethnic and geographic distribution. Despite the fact that early studies indicated that HBV antigens were present in other primates, the prevailing dogma that HBV was a human disease precluded alternative explanations. Within the past 5 years, hepatitis B viruses have been characterised from all the Old World great apes (orangutan, gibbons, gorillas and chimpanzees) and from a New World woolly monkey. Each group of non-human primates appears to have a distinct strain of hepatitis B virus that can be distinguished from human sequences based upon the nucleotide sequence and selected amino acid changes in the viral proteins. The woolly monkey HBV is most divergent from other primate and human sequences, while the great ape HBV sequences cluster together with separate branches for each group.

Animals↗
PubMed2003

Chronic hepatitis C virus infection established and maintained in chimpanzees independent of dendritic cell impairment.

Chronic hepatitis C virus (HCV) infection in humans is associated with an impairment of dendritic cells (DC). It has been hypothesized that impairment of DC function may be a central mechanism facilitating the establishment of a chronic carrier state. However, the majority of patients studied with DC impairment to date have been identified and, thus, inadvertently selected because of clinical manifestations leading to their diagnosis, which may have been many years following actual infection. We set out to determine whether impaired DC function occurred in the earlier asymptomatic phase of infection and turned to a well-defined cohort of HCV-infected chimpanzees in which the specific date of infection and the nature of the inoculum were well characterized. Results revealed that, in contrast to the observations in human subjects with advanced clinical hepatitis, there was neither impairment of the allostimulatory capacity of monocyte-derived DC from HCV chronic carriers nor impairment of the maturation process. Decreased allostimulatory capacity was only detected in 2 animals and, interestingly, in those that possessed the highest viral loads. Nevertheless, HCV sequences were undetectable in any of the DC derived from HCV-infected chimpanzees. In conclusion, these findings suggest that the mechanisms of establishing persistent HCV infection are separate and independent from those responsible for impaired DC function. Indeed, the maturation and allostimulatory impairment, as described in patient studies, are not necessary prerequisites but rather possible consequences of persistent and active HCV infection associated with disease progression.

Animals↗