Conservation effectiveness of protected areas for Hong Kong butterflies declines under climate change

Protected areas are important in conserving the rapid decline of biodiversity in the Anthropocene. Yet uncertainty persists whether protected areas will continue to meet conservation goals if climate change causes community or ecosystem shifts. Previous research has proven equivocal with some studies finding protected areas fail conservation objectives and others finding objectives are largely met. The effectiveness of protected area systems within tropical Asia and for insects are particularly under-studied. Using species distribution modeling of 68 butterfly species (15,346 locality records), we carried out an evaluation of the effectiveness of protected areas in Hong Kong, one of the most well-covered (40% land area) protected area systems in the Asian tropics, and projected how the ability to protect biodiversity would change under different climate change scenarios and different conservation target schemes. Under climate change, 15–37% of the modeled species in 2000 were projected to become extirpated by 2050. Under all conservation target schemes, the proportion of species unprotected increased or leveled, by up to as much as 7%. If buffer grids were considered as unprotected, the increase in these gap species was much greater, by up to as much as 22%. These results together indicate that under climate change, the effectiveness of protected areas for butterflies in Hong Kong is likely to decrease despite the territory’s relatively high proportion of protected area coverage. We also highlight here the importance of the fortification of partly protected areas in mediating biodiversity loss under the impacts of global change.     

Structures and biological functions of IL-31 and IL-31 receptors

Interleukin-31, produced mainly by activated CD4⁺ T cells, is a newly discovered member of the gp130/IL-6 cytokine family. Unlike all the other family members, IL-31 does not engage gp130. Its receptor heterodimer consists of a unique gp130-like receptor chain IL-31RA, and the receptor subunit OSMRβ that is shared with another family member oncostatin M (OSM). Binding of IL-31 to its receptor activates Jak/STAT, PI3K/AKT and MAPK pathways. IL-31 acts on a broad range of immune- and non-immune cells and therefore possesses potential pleiotropic physiological functions, including regulating hematopoiesis and immune response, causing inflammatory bowel disease, airway hypersensitivity and dermatitis. This review summarizes the recent findings on the biological characterization and physiological roles of IL-31 and its receptors.     

Analysis of renal lesions in Chinese tuberous sclerosis complex patients with different types of TSC gene mutations

We sought to explore the relationship between renal lesion features and genetic mutations in tuberous sclerosis complex (TSC) patients. TSC patients with renal lesions were subjected to TSC1/2 gene next-generation sequencing (NGS). TSC1/2 mutation types and imaging examinations were screened for combined analysis of genetic and clinical features. Seventy-three probands among TSC patients with renal lesions were included. Twenty affected relatives were also included. In total, 93 patients were included. Eighty patients (86.0%) had bilateral renal angiomyolipomas (AMLs), and one had epithelioid AML. Two patients had polycystic kidney disease, one had renal cell carcinoma, and one had Wilms tumor. Among the 73 probands, four had TSC1 mutations, 53 had TSC2 mutations, and 16 had no mutations identified (NMI). There was no statistically significant difference between TSC1 mutation, TSC2 mutation and NMI group (P= 0.309), or between familial and sporadic groups (P= 0.775) when considering AML size. There was no statistically significant difference between pathogenic/likely pathogenic and benign/likely benign/NMI groups (P= 0.363) or among patients with different mutation types of TSC2 (P= 0.906). The relationship between the conditions of TSC gene mutations and the severity of renal lesions still needs more analysis. Patients with NMI, particularly those with familial disease, need more attention because the pathogenesis remains unknown.     

Myelin-specific regulatory T cells accumulate in the CNS but fail to control autoimmune inflammation

Treatment with ex vivo-generated regulatory T cells (T-reg) has been regarded as a potentially attractive therapeutic approach for autoimmune diseases. However, the dynamics and function of T-reg in autoimmunity are not well understood. Thus, we developed Foxp3gfp knock-in (Foxp3gfp.KI) mice and myelin oligodendrocyte glycoprotein (MOG)(35-55)/IA(b) (MHC class II) tetramers to track autoantigen-specific effector T cells (T-eff) and T-reg in vivo during experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. MOG tetramer-reactive, Foxp3(+) T-reg expanded in the peripheral lymphoid compartment and readily accumulated in the central nervous system (CNS), but did not prevent the onset of disease. Foxp3(+) T cells isolated from the CNS were effective in suppressing naive MOG-specific T cells, but failed to control CNS-derived encephalitogenic T-eff that secreted interleukin (IL)-6 and tumor necrosis factor (TNF). Our data suggest that in order for CD4(+)Foxp3(+) T-reg to effectively control autoimmune reactions in the target organ, it may also be necessary to control tissue inflammation.     

Isolation and characterization of PSI–LHCI super-complex and their sub-complexes from a red alga <Emphasis Type="Italic">Cyanidioschyzon merolae</Emphasis>

Photosystem I (PSI)–light-harvesting complex I (LHCI) super-complex and its sub-complexes PSI core and LHCI, were purified from a unicellular red alga Cyanidioschyzon merolae and characterized. PSI–LHCI of C. merolae existed as a monomer with a molecular mass of 580 kDa. Mass spectrometry analysis identified 11 subunits (PsaA, B, C, D, E, F, I, J, K, L, O) in the core complex and three LHCI subunits, CMQ142C, CMN234C, and CMN235C in LHCI, indicating that at least three Lhcr subunits associate with the red algal PSI core. PsaG was not found in the red algae PSI–LHCI, and we suggest that the position corresponding to Lhca1 in higher plant PSI–LHCI is empty in the red algal PSI–LHCI. The PSI–LHCI complex was separated into two bands on native PAGE, suggesting that two different complexes may be present with slightly different protein compositions probably with respective to the numbers of Lhcr subunits. Based on the results obtained, a structural model was proposed for the red algal PSI–LHCI. Furthermore, pigment analysis revealed that the C. merolae PSI–LHCI contained a large amount of zeaxanthin, which is mainly associated with the LHCI complex whereas little zeaxanthin was found in the PSI core. This indicates a unique feature of the carotenoid composition of the Lhcr proteins and may suggest an important role of Zea in the light-harvesting and photoprotection of the red algal PSI–LHCI complex.     

Impaired ABCA1-dependent lipid efflux and hypoalphalipoproteinemia in human Niemann-Pick type C disease

The cholesterol trafficking defect in Niemann-Pick type C (NPC) disease leads to impaired regulation of cholesterol esterification, cholesterol synthesis, and low density lipoprotein receptor activity. The ATP-binding cassette transporter A1 (ABCA1), which mediates the rate-limiting step in high density lipoprotein (HDL) particle formation, is also regulated by cell cholesterol content. To determine whether the Niemann-Pick C1 protein alters the expression and activity of ABCA1, we determined the ability of apolipoprotein A-I (apoA-I) to deplete pools of cellular cholesterol and phospholipids in human fibroblasts derived from NPC1+/+, NPC1+/-, and NPC1-/- subjects. Efflux of low density lipoprotein-derived, non-lipoprotein, plasma membrane, and newly synthesized pools of cell cholesterol by apoA-I was diminished in NPC1-/- cells, as was efflux of phosphatidylcholine and sphingomyelin. NPC1+/- cells showed intermediate levels of lipid efflux compared with NPC1+/+ and NPC1-/- cells. Binding of apoA-I to cholesterol-loaded and non-cholesterol-loaded cells was highest for NPC1+/- cells, with NPC1+/+ and NPC1-/- cells showing similar levels of binding. ABCA1 mRNA and protein levels increased in response to cholesterol loading in NPC1+/+ and NPC1+/- cells but showed low levels at base line and in response to cholesterol loading in NPC1-/- cells. Consistent with impaired ABCA1-dependent lipid mobilization to apoA-I for HDL particle formation, we demonstrate for the first time decreased plasma HDL-cholesterol levels in 17 of 21 (81%) NPC1-/- subjects studied. These results indicate that the cholesterol trafficking defect in NPC disease results in reduced activity of ABCA1, which we suggest is responsible for the low HDL-cholesterol in the majority of NPC subjects and partially responsible for the overaccumulation of cellular lipids in this disorder.     

Transplantation of Induced Pluripotent Stem Cells Improves Functional Recovery in Huntington's Disease Rat Model

The purpose of this study was to determine the functional recovery of the transplanted induced pluripotent stem cells in a rat model of Huntington''s disease with use of ¹⁸F-FDG microPET/CT imaging.

Methods

In a quinolinic acid-induced rat model of striatal degeneration, induced pluripotent stem cells were transplanted into the ipsilateral lateral ventricle ten days after the quinolinic acid injection. The response to the treatment was evaluated by serial ¹⁸F-FDG PET/CT scans and Morris water maze test. Histological analyses and Western blotting were performed six weeks after stem cell transplantation.

Results

After induced pluripotent stem cells transplantation, higher ¹⁸F-FDG accumulation in the injured striatum was observed during the 4 to 6-weeks period compared with the quinolinic acid-injected group, suggesting the metabolic recovery of injured striatum. The induced pluripotent stem cells transplantation improved learning and memory function (and striatal atrophy) of the rat in six week in the comparison with the quinolinic acid-treated controls. In addition, immunohistochemical analysis demonstrated that transplanted stem cells survived and migrated into the lesioned area in striatum, and most of the stem cells expressed protein markers of neurons and glial cells.

Conclusion

Our findings show that induced pluripotent stem cells can survive, differentiate to functional neurons and improve partial striatal function and metabolism after implantation in a rat Huntington''s disease model.     

Photosynthetic performance and growth traits in Pennisetum centrasiaticum exposed to drought and rewatering under different soil nutrient regimes

Responses of plants exposed to drought and rewatering have been well documented; however, little is known concerning strategies of psammophyte to drought and rewatering under different soil nutrient regimes. For this study, Pennisetum centrasiaticum under two soil nutrient regimes was subjected to progressive drought and subsequent rewatering. Soil water status, gas exchange characteristics, chlorophyll a fluorescence characteristics as well as biomass traits were measured to investigate ecophysiological responses. Net photosynthesis rate (P _n), stomatal conductance (g _s), water use efficiency, maximum quantum efficiency of photosynthesis system II (PSII, F _V/F _M), electron transport flux per cross section (ET₀/CS₀), and performance index on cross section basis (PI_CS) were suppressed during drought periods for both nutrient regimes. Meanwhile, leaf intercellular CO₂ concentration (C _i ), minimal fluorescence intensity (F ₀), and dissipated energy flux per cross section (DI₀/CS₀) increased. Reversible downregulation of PSII photochemistry and enhanced thermal dissipation of excess excitation energy (DI₀/CS₀) contributed to enhanced photo-protection in drought-stressed plants. Thus, the results indicate that P. centrasiaticum is capable of withstanding and surviving extreme drought events, and the recovery pattern of stressed P. centrasiaticum under both nutrient regimes was similar. However, fertilization increased the biomass and the variation in gas exchange and chlorophyll a fluorescence characteristics during drought periods. Additionally, fertilization accelerated the process of drought and aggravated stress under extreme drought events. Thus, the fertilization strategy used in P. centrasiaticum restoration should be carefully selected—fertilization may not always be beneficial.     

Activated mouse CD4+Foxp3? T cells facilitate melanoma metastasis via Qa-1-dependent suppression of NK-cell cytotoxicity

The regulatory activities of mouse CD4⁺Foxp3⁺ T cells on various immune cells, including NK cells, have been well documented. Under some conditions, conventional CD4⁺Foxp3⁻ T cells in the periphery are able to acquire inhibitory function on other T cells, but their roles in controlling innate immune cells are poorly defined. As a potential cellular therapy for cancer, ex vivo activated CD4⁺Foxp3⁻ effector T cells are often infused back in vivo to suppress tumor growth and metastasis. Whether such activated T cells could affect NK-cell control of tumorigenesis is unclear. In the present study, we found that mitogen-activated CD4⁺Foxp3⁻ T cells exhibited potent suppressor function on NK-cell proliferation and cytotoxicity in vitro, and notably facilitated B16 melanoma metastasis in vivo. Suppression of NK cells by activated CD4⁺Foxp3⁻ T cells is cell-cell contact dependent and is mediated by Qa-1:NKG2A interaction, as administration of antibodies blocking either Qa-1 or NKG2A could completely reverse this suppression, and significantly inhibited otherwise facilitated melanoma metastasis. Moreover, activated CD4⁺Foxp3⁻ cells from Qa-1 knockout mice completely lost the suppressor activity on NK cells, and failed to facilitate melanoma metastasis when transferred in vivo. Taken together, our findings indicate that innate anti-tumor response is counter regulated by the activation of adaptive immunity, a phenomenon we term as “activation-induced inhibition”. Thus, the regulatory role of activated CD4⁺Foxp3⁻ T cells in NK-cell activity must be taken into consideration in the future design of cancer therapies.     

Candidate gene expression affects intramuscular fat content and fatty acid composition in pigs

The objective of this study was to correlate the expression pattern of candidate genes with the intramuscular fat (IMF) content and fatty acid composition of the Longissimus dorsi muscle of Duroc × Shanzhu commercial crossbred pigs. Animals of both sexes were slaughtered at a body weight of about 90 kg. The IMF content and fatty acid composition of the Longissimus dorsi muscle were measured and correlated with candidate genes mRNA expression (AdPLA, ADRB3, LEPR, MC4R, PPARγ, PPARα, LPL, PEPCK, and SCD). Females presented higher IMF content (p < 0.05) than males. The total saturated fatty acid (SFA) in males was greater (p < 0.01), whereas the total monounsaturated fatty acid (MUFA) (p < 0.01) and polyunsaturated fatty acid (PUFA) (p < 0.05) were lower than in females. The expressions of AdPLA, MC4R, PEPCK, and SCD correlated with the IMF content (p < 0.05). AdPLA showed a positive association with MUFA and a negative association with SFA (p < 0.05). LEPR and MC4R were both positively and significantly associated with C18:3 and C20:0 (p < 0.05). PPARα and PPARγ were negatively correlated with SFA, and PPARγ was positively associated with MUFA (p < 0.05). LPL was positively associated with MUFA and negatively associated with SFA (p < 0.05). PEPCK was negatively correlated with PUFA (p < 0.05). SCD was positively associated with MUFA (p < 0.05). The revealed correlations may confirm that these candidate genes are important for fat deposition and fatty acid composition in pigs, and the evaluation and use of these genes may be useful for improving porcine meat quality.