Global biodiversity is in decline. This is of concern for aesthetic and ethical reasons, but possibly also for practical reasons, as suggested by experimental studies, mostly with plants, showing that biodiversity reductions in small study plots can lead to compromised ecosystem function. However, inferring that ecosystem functions will decline due to biodiversity loss in the real world rests on the untested assumption that such loss is actually occurring at these small scales in nature. Using a global database of 168 published studies and >16,000 nonexperimental, local-scale vegetation plots, we show that mean temporal change in species diversity over periods of 5–261 y is not different from zero, with increases at least as likely as declines over time. Sites influenced primarily by plant species’ invasions showed a tendency for declines in species richness, whereas sites undergoing postdisturbance succession showed increases in richness over time. Other distinctions among studies had little influence on temporal richness trends. Although maximizing diversity is likely important for maintaining ecosystem function in intensely managed systems such as restored grasslands or tree plantations, the clear lack of any general tendency for plant biodiversity to decline at small scales in nature directly contradicts the key assumption linking experimental results to ecosystem function as a motivation for biodiversity conservation in nature. How often real world changes in the diversity and composition of plant communities at the local scale cause ecosystem function to deteriorate, or actually to improve, remains unknown and is in critical need of further study.

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Global meta-analysis reveals no net change in local-scale plant biodiversity over time

The cytokine profile produced by peripheral blood mononuclear cells (PBMC) in response to leishmania antigens and the ability of interleukin-10 (IL-10) and transforming growth factor β (TGF-β) to modulate the immune response were evaluated in 21 mucosal leishmaniasis patients. Patients with mucosal disease exhibited increased gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) secretion and decreased IL-10 secretion compared to patients with classical cutaneous leishmaniasis. CD4+ Th1 cells were the main source of IFN-γ and TNF-α production in mucosal leishmaniasis patients. Evaluation of cytokine gene expression in PBMC of these patients showed that there was strong up-regulation of IFN-γ transcripts upon stimulation with leishmania antigen, in contrast to the baseline levels of IL-10 mRNA. IL-10 suppressed IFN-γ production by 48% in cell cultures from cutaneous leishmaniasis patients and by 86% in cell cultures from healthy subjects stimulated with purified protein derivative, whereas in similar conditions IL-10 suppressed IFN-γ production by 19% in cell cultures from mucosal leishmaniasis patients stimulated with leishmania antigen. TGF-β suppressed IFN-γ levels to a greater extent in healthy subjects than in mucosal leishmaniasis and cutaneous leishmaniasis patients. These data indicate that a poorly modulated T-cell response in mucosal leishmaniasis patients leads to production of high levels of proinflammatory cytokines, such as IFN-γ and TNF-α, as well as a decreased ability of IL-10 and TGF-β to modulate this response. These abnormalities may be the basis for the pathological findings observed in this disease.

Up-Regulation of Th1-Type Responses in Mucosal Leishmaniasis Patients

Publisher Summary Among the protozoa of the Trypanosomatidae family, a large number of species represent agents of diseases, such as Chagas' disease. This chapter reviews some aspects of the cell biology of Trypanosoma cruzi, giving emphasis to those aspects related to the ultrastructure of pathogenic protozoa. Protozoa of the Trypanosomatidae family show, during their, life cycle, several forms which can be easily identified by light microscopy in Giemsa-stained preparations. The chapter also explains the life cycle of T. cruzi. In the life cycle of T. cruzi, there are forms which are able to divide. There is one form, considered to be highly differentiated and responsible for the infectivity of these protozoa, which does not divide. It is highlighted that the trypomastigote form can transform into a rounded form which possesses a free flagellum. This form, which appears in the stomach, is able to transform into either short epimastigotes that start a process of multiplication in the intestinum or into long epimastigotes which move to the more posterior region of the digestive tract of the bug. Cell surface is also emphasized in the chapter.

Cell Biology of Trypanosoma cruzi

Tropical savannas have been increasingly viewed as an opportunity for carbon sequestration through fire suppression and afforestation, but insufficient attention has been given to the consequences for biodiversity. To evaluate the biodiversity costs of increasing carbon sequestration, we quantified changes in ecosystem carbon stocks and the associated changes in communities of plants and ants resulting from fire suppression in savannas of the Brazilian Cerrado, a global biodiversity hotspot. Fire suppression resulted in increased carbon stocks of 1.2 Mg ha −1 year −1 since 1986 but was associated with acute species loss. In sites fully encroached by forest, plant species richness declined by 27%, and ant richness declined by 35%. Richness of savanna specialists, the species most at risk of local extinction due to forest encroachment, declined by 67% for plants and 86% for ants. This loss highlights the important role of fire in maintaining biodiversity in tropical savannas, a role that is not reflected in current policies of fire suppression throughout the Brazilian Cerrado. In tropical grasslands and savannas throughout the tropics, carbon mitigation programs that promote forest cover cannot be assumed to provide net benefits for conservation.

The biodiversity cost of carbon sequestration in tropical savanna

Purine and pyrimidine metabolism in the trypanosomatidae

SYNOPSIS. A defined medium for an insect trypanosomatid, “Leptomonas pessoai” (probably a member of the genus Herpetomonas) isolated from the reduviid Zelus leucogrammus, allows growth up to 37 C. No marked differences were evident for growth at 37 C. The requirements for amino acids, vitamins, purine, and hemin, and pH range were like those established for Crithidia fasciculata. Again like C. fasciculata, it remains alive at 4 C for at least 3 months in a clycerolated defined medium.

Growth of an Insect Trypanosomatid at 37 C in a Defined Medium

Morphological, cultural, and biochemical criteria that have been used in describing lower trypanosomatids, genera Blastocrithidia, Crithidia, Leptomonas, Herpetomonas, Rhynchoidomonas, and Phytomonas are reviewed. Kinetoplast structure, carbohydrate utilization, electrophoretic mobilities of isoenzymes, and kDNA fingerprinting are among the recommended criteria for species differentiation. Temperature, pH, and osmolarity tolerance are useful growth parameters. Generic placement may be assisted by the determination of nitrogenous excretion products and ornithine-arginine cycle enzymes.

Guidelines for the Description of New Species of Lower Trypanosomatids1

Tratado de microbiologia

https://www.cell.com/trends/parasitology/pdf/0169-4758(90)90388-K.pdf

Trypanosomatid parasites of plants (phytomonas)

SYNOPSIS

Crithidia deanei from the reduviid hemipteron, Zelus leucogrammus, unlike most lower trypanosomatids cultivated in defined medium, required only 2 amino acids, methionine and tyrosine; only 4 vitamins, folic acid, thiamine, biotin, and nicotinamide; and neither hemin nor a purine source. Electron microscopy reveals an endosymbiont, probably bacterial, which presumably provides the other basic trypanosomatid essential nutrients.

Isaac Roitman

Papers

Growth of an Insect Trypanosomatid at 37 C in a Defined Medium

Guidelines for the Description of New Species of Lower Trypanosomatids1

Tratado de microbiologia

Trypanosomatid parasites of plants (phytomonas)

Simple Nutrition of Crithidia deanei, a Reduviid Trypanosomatid with an Endosymbiont*