Simian 2.2 PRO
Oludare Padilla
The simians are sister group to the tarsiers (Tarsiiformes), together forming the haplorhines. The radiation occurred about 60 million years ago (during the Cenozoic era); 40 million years ago, simians colonized South America, giving rise to the New World monkeys. The remaining simians (catarrhines) split about 25 million years ago into Cercopithecidae and apes (including humans).
Extant simians are split into two distinct groups. The New World monkeys in parvorder Platyrrhini split from the rest of the simian line about 40 million years ago (Mya), leaving the parvorder Catarrhini occupying the Old World. This latter group split about 25 Mya between the Cercopithecidae and the apes. This shows that the Cercopithecidae are closer related to the apes than to the Platyrrhini.
Some lines of extinct simian also are either placed into the Eosimiidae (to reflect their Eocene origin) and sometimes in Amphipithecidae, thought to originate in the Early Oligocene. Additionally, Phileosimias is sometimes placed in the Eosimiidae and sometimes categorised separately.[11]
Below is a cladogram with some of the extinct simian species with the more modern species emerging within the Eosimiidae. The simians originated in Asia, while the crown simians were in Afro-Arabia.[12][13][5][14][7][15] It is indicated approximately how many Mya the clades diverged into newer clades.
Usually the Ekgmowechashalidae are considered to be Strepsirrhini, not Haplorhini.[16] A 2018 study places Eosimiidae as a sister to the crown haplorhini.[17] In 2020 papers, the Proteopithecidae are part of the Parapithecoidea,[15][18] and Nosmips aenigmaticus (previously in Eosimidae[13]) is a basal simian.[18] In a 2021 paper, the following basal simians were found:[19]
Dolichocebus annectens and Parvimico materdei would normally, given their South American location and their age and other factors, be considered Platyrrhini. The original Eosmiidae appear polyphyletic with Nosmips, Bahinia, and Phileosimias at different locations from other eosimians.
In a section of their 2010 assessment of the evolution of anthropoids (simians) entitled "What is an Anthropoid", Williams, Kay, and Kirk set out a list of biological features common to all or most anthropoids, including genetic similarities, similarities in eye location and the muscles close to the eyes, internal similarities between ears, dental similarities, and similarities on foot bone structure.[6] The earliest anthropoids were small primates with varied diets, forward-facing eyes, acute color vision for daytime lifestyles, and brains devoted more to vision and less to smell.[6] Living simians in both the New World and the Old World have larger brains than other primates, but they evolved these larger brains independently.[6]
The Latin word for "ape" is simia, which itself comes from simus, "snub-nosed". Simian is usually a scientific word; thus, for instance, biologists study simian viruses in the search for cures to AIDS and other diseases. But simian can be used by the rest of us to describe human behavior. Human babies often cling to their mothers in a simian way, and kids playing on a jungle gym may look like simians. But if you notice that a friend has a simian style of walking or eating bananas, it might be best not to tell him.
Clinical evidence suggests that cellular immunity is involved in controlling human immunodeficiency virus-1 (HIV-1) replication. An animal model of acquired immune deficiency syndrome (AIDS), the simian immunodeficiency virus (SIV)-infected rhesus monkey, was used to show that virus replication is not controlled in monkeys depleted of CD8+ lymphocytes during primary SIV infection. Eliminating CD8+ lymphocytes from monkeys during chronic SIV infection resulted in a rapid and marked increase in viremia that was again suppressed coincident with the reappearance of SIV-specific CD8+ T cells. These results confirm the importance of cell-mediated immunity in controlling HIV-1 infection and support the exploration of vaccination approaches for preventing infection that will elicit these immune responses.
Simian malaria from wild non-human primate populations is increasingly recognised as a public health threat and is now the main cause of human malaria in Malaysia and some regions of Brazil. In 2022, Malaysia became the first country not to achieve malaria elimination due to zoonotic simian malaria. We review the global distribution and drivers of simian malaria and identify priorities for diagnosis, treatment, surveillance, and control. Environmental change is driving closer interactions between humans and wildlife, with malaria parasites from non-human primates spilling over into human populations and human malaria parasites spilling back into wild non-human primate populations. These complex transmission cycles require new molecular and epidemiological approaches to track parasite spread. Current methods of malaria control are ineffective, with wildlife reservoirs and primarily outdoor-biting mosquito vectors urgently requiring the development of novel control strategies. Without these, simian malaria has the potential to undermine malaria elimination globally.
Fibroblast cell lines were established from mouse embryos homozygous for a targeted disruption of the Igf1r gene, encoding the type 1 receptor for insulin-like growth factor I (IGF-I) and from their wild-type littermates. The cells from the wild-type embryos (W cells) grow in serum-free medium supplemented with platelet-derived growth factor, epidermal growth factor, and IGF-I, whereas the cells from Igf1r(-/-) embryos (R- cells) do not, although they grow at a reduced rate in 10% fetal calf serum. The simian virus 40 (SV40) large T antigen, expressed from a transfected plasmid, can transform W cells, which form foci in monolayer cultures and colonies in soft agar (anchorage-independent growth). In contrast, the SV40 large tumor antigen, although normally expressed from the transfected template, is unable to transform R- cells, which remain contact-inhibited and fail to grow in soft agar. The transformed phenotype is restored if the R- cells carrying the SV40 large tumor antigen are stably transfected with a plasmid expressing the human IGF-I receptor. These results demonstrate that signaling via the IGF-I receptor is an indispensable component of the SV40 transformation pathway. This conclusion is further supported from the results of antisense RNA experiments with tumor cell lines showing that interference with the function of the IGF-I receptor has a profound effect on anchorage-independent growth, even under conditions that only modestly affect growth in monolayers.
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