12 research outputs found
Pervasive gaps in Amazonian ecological research
Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear un derstanding of how ecological communities respond to environmental change across time and space.3,4
While the increasing availability of global databases on ecological communities has advanced our knowledge
of biodiversity sensitivity to environmental changes,5–7 vast areas of the tropics remain understudied.8–11 In
the American tropics, Amazonia stands out as the world’s most diverse rainforest and the primary source of
Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepre sented in biodiversity databases.13–15 To worsen this situation, human-induced modifications16,17 may elim inate pieces of the Amazon’s biodiversity puzzle before we can use them to understand how ecological com munities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus
crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced
environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple or ganism groups in a machine learning model framework to map the research probability across the Brazilian
Amazonia, while identifying the region’s vulnerability to environmental change. 15%–18% of the most ne glected areas in ecological research are expected to experience severe climate or land use changes by
2050. This means that unless we take immediate action, we will not be able to establish their current status,
much less monitor how it is changing and what is being lostinfo:eu-repo/semantics/publishedVersio
Pervasive gaps in Amazonian ecological research
Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear understanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5,6,7 vast areas of the tropics remain understudied.8,9,10,11 In the American tropics, Amazonia stands out as the world's most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepresented in biodiversity databases.13,14,15 To worsen this situation, human-induced modifications16,17 may eliminate pieces of the Amazon's biodiversity puzzle before we can use them to understand how ecological communities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple organism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region's vulnerability to environmental change. 15%–18% of the most neglected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lost
Participation of cytokines in the necrotic-inflammatory lesions in the heart and skeletal muscles of Calomys callosus  infected with Trypanosoma cruzi Â
Calomys callosus  , a sylvatic reservoir of Trypanosoma cruzi
 , when infected with the Colombian strain (Biodeme Type III, T.
cruzi I ) develops necrotic-inflammatory lesions and intense early
fibrogenesis in the heart and skeletal muscles, that spontaneously
regress. Participation of pro-inflammatory and pro-fibrogenic
cytokines, such as tumor necrosis factor-alpha (TNF-α , gamma
interferon (IFN-γ) , and tumor growth factor-beta (TGF-β), in
the pathogenesis of the lesions is herein studied. Eighty C. callosus
weighing 20 to 30 g were used. Seventy of them were inoculated with the
Colombian strain (105 blood forms) and 10 were maintained as intact
non-infected controls. After infection, C. callosus were sacrificed at
different time-points from 15 to 70 days. The heart and skeletal muscle
were processed for histopathology and cryopreserved for
immunohistochemistry. Early necrotic lesions of parasitized skeletal
muscle and myocardium with intense inflammatory lesions were present.
Search for the in situ presence of TNF-α and IFN-γ, was
performed using rat-IgG anti-mouse antibodies against these cytokines.
For the in situ search of TGF-β, rabbit IgG anti-mouse antibodies
were used. Immunolabeling of the cytokines in tissues of infected C.
callosus was successful. The cytokines TNF-α, IFN-γ, and
TGF-β were detected in the cytoplasm of macrophages and in the
necrotic material from 15 to 45 days post-infection, decreasing their
intensity until complete disappearance by the 65th day, which
correlated with subsiding histopathological lesions. These findings
suggest the participation of these cytokines in the control of parasite
multiplication, in the development of an early fibrogenesis and in the
regression of fibrotic-inflammatory lesions observed in C. callosus
Participation of cytokines in the necrotic-inflammatory lesions in the heart and skeletal muscles of Calomys callosus  infected with Trypanosoma cruzi Â
Calomys callosus  , a sylvatic reservoir of Trypanosoma cruzi
 , when infected with the Colombian strain (Biodeme Type III, T.
cruzi I ) develops necrotic-inflammatory lesions and intense early
fibrogenesis in the heart and skeletal muscles, that spontaneously
regress. Participation of pro-inflammatory and pro-fibrogenic
cytokines, such as tumor necrosis factor-alpha (TNF-α , gamma
interferon (IFN-γ) , and tumor growth factor-beta (TGF-β), in
the pathogenesis of the lesions is herein studied. Eighty C. callosus
weighing 20 to 30 g were used. Seventy of them were inoculated with the
Colombian strain (105 blood forms) and 10 were maintained as intact
non-infected controls. After infection, C. callosus were sacrificed at
different time-points from 15 to 70 days. The heart and skeletal muscle
were processed for histopathology and cryopreserved for
immunohistochemistry. Early necrotic lesions of parasitized skeletal
muscle and myocardium with intense inflammatory lesions were present.
Search for the in situ presence of TNF-α and IFN-γ, was
performed using rat-IgG anti-mouse antibodies against these cytokines.
For the in situ search of TGF-β, rabbit IgG anti-mouse antibodies
were used. Immunolabeling of the cytokines in tissues of infected C.
callosus was successful. The cytokines TNF-α, IFN-γ, and
TGF-β were detected in the cytoplasm of macrophages and in the
necrotic material from 15 to 45 days post-infection, decreasing their
intensity until complete disappearance by the 65th day, which
correlated with subsiding histopathological lesions. These findings
suggest the participation of these cytokines in the control of parasite
multiplication, in the development of an early fibrogenesis and in the
regression of fibrotic-inflammatory lesions observed in C. callosus
Fibrogenesis and collagen resorption in the heart and skeletal muscle of Calomys callosus  experimentally infected with Trypanosoma cruzi: immunohistochemical identification of extracellular matrix components
Intense inflammatory lesions and early development of interstitial
fibrosis of the myocardium and skeletal muscle with spontaneous
regression, have been described in Calomys callosus  infected
with Trypanosoma cruzi  . The genetic types of collagen present
in this model were investigated through immunohistochemistry using
specific antibodies, combined with histopathology and Picro-Sirius
staining of collagen. Thirty-five calomys were infected with the
Colombian strain of T. cruzi and sacrificed at 24, 30, 40, 60 and 90
days post-infection. Inflammatory lesions and fibrogenesis were
prominent at the early phase of infection and significantly decreased
during late infection. Immunoisotyping of the matrix components was
performed by indirect immunofluorescence on 5 µm thick cryostat
sections using specific antibodies against laminin, fibronectin and
isotypes I, III and IV of collagen. In the early phase, positive
deposits of all the matrix components were present, with predominance
of fibronectin, laminin and collagens types I and III in the myocardium
and of types III and IV in the skeletal muscles. From the 40th day,
type IV collagen predominates in the heart. At the late phase of
infection (60th to 90th day), a clear fragmentation and decrease of all
the matrix components were detected. Findings of the present study
indicate that a modulation of the inflammatory process occurs in the
model of C. callosus , leading to spontaneous regression of fibrosis
independent of the genetic types of collagen involved in this process
Treatment with benznidazole in association with immunosuppressive drugs in mice chronically infected with Trypanosoma cruzi: investigation into the possible development of neoplasias
Benznidazole is recommended in Brazil for the treatment of Trypanosoma cruzi infection in acute and early chronic phases of Chagas' disease. Observations by others have indicated a higher incidence of neoplasias in immunosuppressed patients, presenting Chagas' disease reactivation, submitted to treatment with benznidazole. In the present study, we investigated whether there is a potentiation in the generation of lymphomas in chronically infected mice, treated with immunosuppressive drugs and benznidazole. For this, 142 Swiss mice chronically infected with the 21 SF strain of T. cruzi and 72 normal Swiss mice were used. Both infected and normal mice were divided into experimental groups and submitted to one of the following treatment regimens: benznidazole alone; immunosuppressive drugs (azathioprine, betamethasone and cyclosporin); a combination of immunosuppressive drugs and benznidazole; and untreated controls. In the infected group treated with benznidazole, one mouse developed a non-Hodgkin's lymphoma. This finding has been interpreted as a spontaneous tumor of mice. The study of the chronically infected mice treated with the combination of immunosuppressive drugs and benznidazole demonstrated an absence of lymphomas or other neoplasias. These findings support the indication of benznidazole, as the drug of choice, for immunosuppressed patients that develop a reactivation of Chagas' disease