Occurrence and seasonal variation of Perkinsus sp. Infection in wild mollusk populations from coastal waters of Qingdao, northern China.

Perkinsosis has been recognized as one of the major threats to natural and farmed bivalve populations, many of which are of commercial as well as environmental significance. Three Perkinsus species have been identified in China, and the Manila clam (Ruditapes philippinarum) was the most frequently infected species in northern China. Although the occurrence and seasonal variation of Perkinsus spp. have previously been examined, the pathological characteristics of these infections in wild Manila clams and sympatric species in China have seldom been reported. In the present study, the prevalence and intensity of Perkinsus infection in wild populations of Manila clams and 10 sympatric species from three sites were investigated by Ray's fluid thioglycolate medium (RFTM) assay seasonally across a single year. Perkinsus infection was only identified in Manila clams, with a high prevalence (274/284 = 96.48 %) and low intensity (89.8 % with a Mackin value ≤ 2, suggesting generally low-intensity infections) throughout the year. Heavily infected clams were mainly identified in Tianheng in January, which displayed no macroscopic signs of disease. An overview of the whole visceral mass section showed that the trophozoites mostly aggregated in gills and connective tissue of the digestive tract, to a lesser extent in the mantle and foot, and even less frequently in adductor muscle and connective tissues of the gonad. PCR and ITS-5.8S rRNA sequencing of 93 representative RFTM-positive samples revealed a 99.69 to 100 % DNA sequence identity to Perkinsus olseni. Unexpectedly, significantly higher infection intensities were usually identified in January and April when the Condition Index (CI) was relatively high. We propose that factors associated with the anthropogenic harvesting pressure and irregular disturbances should be responsible for the uncommon seasonal infection dynamics of perkinsosis observed in the present study.

Androgen Receptor Transcriptionally Inhibits Programmed Death Ligand-1 Expression and Influences Immune Escape in Bladder Cancer.

In multiple clinical trials, immune checkpoint blockade-based immunotherapy has shown significant therapeutic efficacy in bladder cancer (BCa). Sex is closely related to the incidence rate and prognosis of BCa. As one of the sex hormone receptors, the androgen receptor (AR) is a well-known key regulator that promotes the progression of BCa. However, the regulatory mechanism of AR in the immune response of BCa is still unclear. In this study, the expression of AR and programmed death ligand 1 (PD-L1) was negatively correlated in BCa cells, clinical tissues, and tumor data extracted from The Cancer Genome Atlas Bladder Urothelial Carcinoma cohort. A human BCa cell line was transfected to alter the expression of AR. The results show that AR negatively regulated PD-L1 expression by directly binding to AR response elements on the PD-L1 promoter region. In addition, AR overexpression in BCa cells significantly enhanced the antitumor activity of cocultured CD8+ T cells. Injection of anti-PD-L1 monoclonal antibodies into C3H/HeN mice significantly suppressed tumor growth, and stable expression of AR dramatically enhanced the antitumor activity in vivo. In conclusion, this study describes a novel role of AR in regulating the immune response to BCa by targeting PD-L1, thus providing potential therapeutic strategies for immunotherapy in BCa.

Bioengineered Nanocage from HBc Protein for Combination Cancer Immunotherapy.

Protein nanocages are promising multifunctional platforms for nanomedicine owing to the ability to decorate their surfaces with multiple functionalities through genetic and/or chemical modification to achieve desired properties for therapeutic and diagnostic purposes. Here, we describe a model antigen (OVA peptide) that was conjugated to the surface of a naturally occurring hepatitis B core protein nanocage (HBc NC) by genetic modification. The engineered OVA-HBc nanocages (OVA-HBc NCs), displaying high density repetitive array of epitopes in a limited space by self-assembling into symmetrical structure, not only can induce bone marrow derived dendritic cells (BMDC) maturation effectively but also can be enriched in the draining lymph nodes. Naïve C57BL/6 mice immunized with OVA-HBc NCs are able to generate significant and specific cytotoxic T lymphocyte (CTL) responses. Moreover, OVA-HBc NCs as a robust nanovaccine can trigger preventive antitumor immunity and significantly delay tumor growth. When combined with a low-dose chemotherapy drug (paclitaxel), OVA-HBc NCs could specifically inhibit progression of an established tumor. Our findings support HBc-based nanocages with modularity and scalability as an attractive nanoplatform for combination cancer immunotherapy.

Treatment of Paraquat-Induced Lung Injury With an Anti-C5a Antibody: Potential Clinical Application.

OBJECTIVES: Complement activation product C5a plays a critical role in systemic inflammatory response syndrome induced by viruses, bacteria, and toxic agents including paraquat poisoning. This study is to explore the efficiency of anti-C5a-based intervention on systemic inflammatory responses induced by paraquat poisoning. DESIGN: Study of cynomolgus macaque model and plasma from paraquat-poisoning patients. SETTING: Laboratory investigation. SUBJECTS: Cynomolgus macaque (n = 12) and samples of plasma from patients (n = 16). INTERVENTIONS: The neutralizing antihuman C5a antibody (IFX-1) was administered to investigate the new treatment strategy for paraquat-induced systemic inflammatory responses in cynomolgus macaque model. In addition, C5a activation in plasma of paraquat patients was blocked by IFX-1 to investigate the blockade role of anti-C5a antibody in activation of inflammatory cells. MEASUREMENTS AND MAIN RESULTS: Dysregulated complement activation and the subsequent cytokine storm were found in patients with acute lung injury and in a primate model of paraquat poisoning. Targeted inhibition of C5a by IFX-1 led to marked alleviation of systemic inflammatory responses and multiple organ damage in the primate model. In addition, blockade of C5a activity in plasma from patients completely inhibited activation of CD11b on blood granulocytes from normal donors, suggesting that IFX-1 may alleviate the excessive activation of inflammatory responses and have clinical utility for patients with acute lung injury. CONCLUSIONS: Anti-C5a antibodies such as IFX-1 may be used as effective therapeutics for treatment of those suffering from systemic inflammatory responses induced by chemical poisoning like paraquat.

Treatment with anti-C5a antibody improves the outcome of H7N9 virus infection in African green monkeys.

BACKGROUND: Patients infected with influenza A(H7N9) virus present with acute lung injury (ALI) that is due to severe pneumonia and systemic inflammation. It is often fatal because there are few effective treatment options. Complement activation has been implicated in the pathogenesis of virus-induced lung injury; therefore, we investigated the effect of targeted complement inhibition on ALI induced by H7N9 virus infection. METHODS: A novel neutralizing specific antihuman C5a antibody (IFX-1) was used. This antibody blocked the ability of C5a to induce granulocytes to express CD11b while not affecting the ability of C5b to form the membrane attack complex. African green monkeys were inoculated with H7N9 virus and treated intravenously with IFX-1. RESULTS: The virus infection led to intense ALI and systemic inflammatory response syndrome (SIRS) in association with excessive complement activation. Anti-C5a treatment in H7N9-infected monkeys substantially attenuated ALI: It markedly reduced the lung histopathological injury and decreased the lung infiltration of macrophages and neutrophils. Moreover, the treatment decreased the intensity of SIRS; the body temperature changes were minimal and the plasma levels of inflammatory mediators were markedly reduced. The treatments also significantly decreased the virus titers in the infected lungs. CONCLUSIONS: Antihuman C5a antibody treatment remarkably reduced the ALI and systemic inflammation induced by H7N9 virus infection. Complement inhibition may be a promising adjunctive therapy for severe viral pneumonia.

Fermented Gracilaria lemaneiformis polysaccharides alleviate food allergy by regulating Treg cells and gut microbiota.

Food allergy has a significant impact on the health and well-being of individuals, affecting both their physical and mental states. Research on natural bioactive compounds, such as polysaccharides extracted from seaweeds, holds great promise in the treatment of food allergies. In this study, fermented Gracilaria lemaneiformis polysaccharides (F-GLSP) were prepared using probiotic fermentation. Probiotic fermentation of Gracilaria lemaneiformis reduces the particle size of polysaccharides. To compare the anti-allergic activity of F-GLSP with unfermented Gracilaria lemaneiformis polysaccharides (UF-GLSP), an OVA-induced mouse food allergy model was established. F-GLSP exhibited a significant reduction in OVA-specific IgE and mMCP levels in allergic mice. Moreover, it significantly inhibited Th2 differentiation and IL-4 production and significantly promoted Treg differentiation and IL-10 production in allergic mice. In contrast, UF-GLSP only reduced OVA-specific IgE and mMCP in the serum of allergic mice. Furthermore, F-GLSP demonstrated a more pronounced regulation of intestinal flora abundance compared to UF-GLSP, significantly influencing the populations of Firmicutes, Bacteroidetes, Lactobacillus, and Clostridiales in the intestines of mice with food allergy. These findings suggest that F-GLSP may regulate food allergies in mice through multiple pathways. In summary, this study has promoted further development of functional foods with anti-allergic properties based on red algae polysaccharides.

Immunomodulatory Function of Pien Tze Huang in T Cell-Mediated Anti-tumor Activity against B16-F10, MC38 and Hep1-6 Tumor Models.

OBJECTIVE: To investigate the anti-tumor effects of Pien Tze Huang (PZH) in mouse models of B16-F10 melanoma, MC38 colorectal cancer, Hep1-6 hepatocellular carcinoma and chemically induced hepatocellular carcinoma model. METHODS: Various tumor models, including B16-F10, MC38 and Hep1-6 tumor hypodermic inoculation models, B16-F10 and Hep1-6 pulmonary metastasis models, Hep1-6 orthotopic implantation model, and chemically induced hepatocellular carcinoma model, were utilized to evaluate the anti-tumor function of PZH. Tumor growth was assessed by measuring tumor size and weight of solid tumors isolated from C57BL/6 mice. For cell proliferation and death of tumor cells in vitro, as well as T cell activation markers, cytokine production and immune checkpoints analysis, single-cell suspensions were prepared from mouse spleen, lymph nodes, and tumors after PZH treatment. RESULTS: PZH demonstrated significant therapeutic efficacy in inhibiting tumor growth (P<0.01). Treatment with PZH resulted in a reduction in tumor size in subcutaneous MC38 colon adenocarcinoma and B16-F10 melanoma models, and decreased pulmonary metastasis of B16-F10 melanoma and Hep1-6 hepatoma (P<0.01). However, in vitro experiments showed that PZH only had slight impact on the cell proliferation and survival of tumor cells (P>0.05). Nevertheless, PZH exhibited a remarkable ability to enhance T cell activation and the production of interferon gamma, tumor necrosis factor alpha, and interleukin 2 in CD4+ T cells in vitro (P<0.01 or P<0.05). Importantly, PZH substantially inhibited T cell exhaustion and boosted cytokine production by tumor-infiltrating CD8+ T cells (P<0.01 or P<0.05). CONCLUSION: This study has confirmed a novel immunomodulatory function of PZH in T cell-mediated anti-tumor immunity, indicating that PZH holds promise as a potential therapeutic agent for cancer treatment.

Critical roles of the miR-17∼92 family in thymocyte development, leukemogenesis, and autoimmunity.

Thymocyte development requires precise control of PI3K-Akt signaling to promote proliferation and prevent leukemia and autoimmune disorders. Here, we show that ablating individual clusters of the miR-17∼92 family has a negligible effect on thymocyte development, while deleting the entire family severely impairs thymocyte proliferation and reduces thymic cellularity, phenocopying genetic deletion of Dicer. Mechanistically, miR-17∼92 expression is induced by Myc-mediated pre-T cell receptor (TCR) signaling, and miR-17∼92 promotes thymocyte proliferation by suppressing the translation of Pten. Retroviral expression of miR-17∼92 restores the proliferation and differentiation of Myc-deficient thymocytes. Conversely, partial deletion of the miR-17∼92 family significantly delays Myc-driven leukemogenesis. Intriguingly, thymocyte-specific transgenic miR-17∼92 expression does not cause leukemia or lymphoma but instead aggravates skin inflammation, while ablation of the miR-17∼92 family ameliorates skin inflammation. This study reveals intricate roles of the miR-17∼92 family in balancing thymocyte development, leukemogenesis, and autoimmunity and identifies those microRNAs (miRNAs) as potential therapeutic targets for leukemia and autoimmune diseases.

Inhibition of complement activation alleviates acute lung injury induced by highly pathogenic avian influenza H5N1 virus infection.

The acute lung injury (ALI) that occurs after the highly pathogenic avian influenza H5N1 virus infection is associated with an abnormal host innate immune response. Because the complement system plays a central role in innate immunity and because aberrant complement activation is associated with a variety of autoimmune and inflammatory diseases, we investigated the complement involvement in the pathogenesis of ALI induced by H5N1 virus infection. We showed that ALI in H5N1-infected mice was caused by excessive complement activation, as demonstrated by deposition of C3, C5b-9, and mannose-binding lectin (MBL)-C in lung tissue, and by up-regulation of MBL-associated serine protease-2 and the complement receptors C3aR and C5aR. Treatment of H5N1-infected mice with a C3aR antagonist led to significantly reduced inflammation in lungs, alleviating ALI. Furthermore, complement inhibition with an anti-C5a antibody or complement depletion with cobra venom factor after H5N1 challenge resulted in a similar level of protection to that seen in C3aR antagonist-treated mice. These results indicate that excessive complement activation plays an important role in mediating H5N1-induced ALI and that inhibition of complement may be an effective clinical intervention and adjunctive treatment for H5N1-induced ALI.

Glycogen synthase kinase 3 controls T-cell exhaustion by regulating NFAT activation.

Cellular immunity mediated by CD8+ T cells plays an indispensable role in bacterial and viral clearance and cancers. However, persistent antigen stimulation of CD8+ T cells leads to an exhausted or dysfunctional cellular state characterized by the loss of effector function and high expression of inhibitory receptors during chronic viral infection and in tumors. Numerous studies have shown that glycogen synthase kinase 3 (GSK3) controls the function and development of immune cells, but whether GSK3 affects CD8+ T cells is not clearly elucidated. Here, we demonstrate that mice with deletion of Gsk3α and Gsk3ß in activated CD8+ T cells (DKO) exhibited decreased CTL differentiation and effector function during acute and chronic viral infection. In addition, DKO mice failed to control tumor growth due to the upregulated expression of inhibitory receptors and augmented T-cell exhaustion in tumor-infiltrating CD8+ T cells. Strikingly, anti-PD-1 immunotherapy substantially restored tumor rejection in DKO mice. Mechanistically, GSK3 regulates T-cell exhaustion by suppressing TCR-induced nuclear import of NFAT, thereby in turn dampening NFAT-mediated exhaustion-related gene expression, including TOX/TOX2 and PD-1. Thus, we uncovered the molecular mechanisms underlying GSK3 regulation of CTL differentiation and T-cell exhaustion in anti-tumor immune responses.

The Probiotic Bacillus hwajinpoensis Colonizes the Digestive System of Crassostrea gigas Larvae and Protects Them from Vibrio alginolyticus Infection.

The Pacific oyster Crassostrea gigas is one of the most important cultured marine species around the world. Production of Pacific oysters in China has depended primarily on hatchery produced seeds since 2016, with the successful introduction and development of triploid oysters. However, the seed supply of Pacific oysters is threatened by recurring mass mortality events in recent years. Vibriosis is the most commonly encountered disease associated with intensive oyster culture in hatcheries and nurseries. Vibrio alginolyticus and Bacillus hwajinpoensis were the two strains with pathogenic and probiotic effects, respectively, identified during the Pacific oyster larvae production. To monitor their colonization process in Pacific oyster larvae, green fluorescent protein (GFP) and red fluorescent protein (RFP) were labeled to the pathogenic V. alginolyticus and the probiotic B. hwajinpoensis stain, respectively. The pathogenic and probiotic effects of the two strains during the colonization process were then assessed. Stabile expression of GFP and RFP were observed in corresponding stains, and the capabilities of growth, biofilm formation and in vitro adhesion of GFP- and RFP- tagged stains were not significantly different from those of the wild-type strains. Usage of probiotics of 105 CFU/mL significantly inhibited the growth of pathogenic V. alginolyticus and reduced the mortality of D-sharped larvae. Both the pathogenic and probiotic strains employed a similar route to enter and colonize the oyster larvae, which indicates that competing with pathogens for binding and spreading sites were one of the mechanisms of B. hwajinpoensis to provide the probiotic effects to oyster larvae. In summary, employment of fluorescence-tagged pathogenic and probiotic strains simultaneously provides us with an excellent bioassay model to investigate the potential mechanisms of probiotics.

MHC class II regulation of CD8+ T cell tolerance and implications in autoimmunity and cancer immunotherapy.

Major histocompatibility complex (MHC) class II-reactive CD8+ T cells are found in humans and animals, but little is known about their identity, development, and function. In this study, we discover a group of CD8+ T cells reactive to both MHC class I and II molecules in MHC class II-deficient mice. We clone their T cell receptors (TCRs) and analyze their development and function. In wild-type animals, thymocytes bearing those TCRs are purged by negative selection. In the absence of MHC class II, they develop into mature CD8+ T cells. When encountering MHC class II in the periphery, they undergo robust activation and proliferation, attack self-tissues, and cause lethal autoimmune diseases. In adoptive T cell therapy, those CD8+ T cells are able to efficiently control MHC class II-expressing tumors. This study opens the door to investigation of dual-reactive CD8+ T cells, their development and selection in the thymus, and the perils and promises when their normal development and selection are compromised.

Thermal Remediation of Soil Contaminated with Polycyclic Aromatic Hydrocarbons: Pollutant Removal Process and Influence on Soil Functionality.

Thermal remediation has been widely used for the removal of polycyclic aromatic hydrocarbon (PAH) from contaminated soil. The method has a high removal rate for semi-volatile organic pollutants; however, soil functionality is affected by the method because of the alteration of the soil properties. In this study, experimental soil was impregnated with phenanthrene (Phe), pyrene (Pyr), and benzo(a)pyrene (BaP); after natural air-dry aging, the thermal remediation experiment was carried out, using a tube-furnace and thermal gravimetry-Fourier transform infrared (TG-FTIR) equipment. More than 84% of the Phe and Pyr were lost in the aging stage, whereas the BaP was stable with 41% retention in the soil. After the thermal treatment, the desorption and decomposition of the pollutants and organic matter led to the removal of the PAHs; about 1% of the PAHs remained in the soil treated at 400 °C. The presence of the PAHs can promote the thermal reaction by slightly reducing the reaction activation energy by ~7-16%. The thermal remediation had a significant influence on the physical properties of the soil and destroyed the bioavailability by reducing the organic matter content. Therefore, a comprehensive consideration of effective PAH removal while preserving soil functionality may require a low temperature (100 °C) method for thermal remediation.

Sulfate oligosaccharide of Gracilaria lemaneiformis modulates type 1 immunity by restraining T cell activation.

Seaweeds are important "blue food" and some seaweeds have been demonstrated that have the immunoregulation activities and benefit for human health. However, which immune cell subsets are targeted and how immune processes are regulated by those seaweeds remain poorly understood. Here we identified sulfated oligosaccharide of Gracilaria lemaneiformis (GLSO) inhibits IFNγ production by T cells in ovalbumin (OVA) immunized mice and in vitro activation system of OVA-specific CD4+ T cells. Furthermore, GLSO predominantly targets T cells but not dendritic cells, and regulates the late stage of expression of T cell activation and differentiation markers. Mechanistically, results of transcriptomic and proteome analysis indicate that GLSO inhibits mTOR activity, glycolysis, cell cycle and DNA replication. Thus, GLSO has an immunomodulatory function in Th1 immune responses by restraining T cell activation. Our study unravels the anti-inflammatory mechanism of GLSO and provides a new insight for industrial development of seaweeds as health food.

A Novel Salt-Bridge Electroflocculation Technology for Harvesting Microalgae.

Microalgae biomass, as a promising alternative feedstock, can be refined into biodiesel, pharmaceutical, and food productions. However, the harvesting process for quality biomass still remains a main bottleneck due to its high energy demand. In this study, a novel technique integrating alkali-induced flocculation and electrolysis, named salt-bridge electroflocculation (SBEF) with non-sacrificial carbon electrodes is developed to promote recovery efficiency and cost savings. The results show that the energy consumption decreased to 1.50 Wh/g biomass with a high harvesting efficiency of 90.4% under 300 mA in 45 min. The mean particle size of algae flocs increased 3.85-fold from 2.75 to 10.59 µm, which was convenient to the follow-up processing. Another major advantage of this method is that the salt-bridge firmly prevented cells being destroyed by the anode's oxidation and did not bring any external contaminants to algal biomass and flocculated medium, which conquered the technical defects in electro-flocculation. The proposed SBEF technology could be used as a low cost process for efficient microalgae harvest with high quality biomass.

A prophylactic effect of aluminium-based adjuvants against respiratory viruses via priming local innate immunity.

Infection caused by respiratory viruses can lead to a severe respiratory disease and even death. Vaccination is the most effective way to prevent the disease, but it cannot be quickly applied when facing an emerging infectious disease. Here, we demonstrated that immunization with an aluminium-zinc hybrid particulate adjuvant (FH-001) alone, bearing great resemblance in morphology with commonly used aluminium-based adjuvants in vaccines, could quickly induce mice to generate a broadly protective immune response to resist the lethal challenge of influenza B viruses. Furthermore, a multi-omics-based analysis revealed that the alveolar macrophage and type I interferon pathway, rather than adaptive immunity and type II interferon pathway, were essential for the observed prophylactic effect of FH-001. More importantly, a similar protective effect was observed against influenza A virus strain A/Shanghai/02/2013(H7N9), A/California/04/2009(H1N1) and respiratory syncytial virus. Therefore, we introduced here a new and promising strategy that can be quickly applied during the outbreak of emerging respiratory viruses.

Glycogen synthase kinase 3 drives thymocyte egress by suppressing ß-catenin activation of Akt.

Molecular pathways controlling emigration of mature thymocytes from thymus to the periphery remain incompletely understood. Here, we show that T cell­specific ablation of glycogen synthase kinase 3 (GSK3) led to severely impaired thymic egress. In the absence of GSK3, ß-catenin accumulated in the cytoplasm, where it associated with and activated Akt, leading to phosphorylation and degradation of Foxo1 and downregulation of Klf2 and S1P1 expression, thereby preventing emigration of thymocytes. A cytoplasmic membrane-localized ß-catenin excluded from the nucleus promoted Akt activation, suggesting a new function of ß-catenin independent of its role as a transcriptional activator. Furthermore, genetic ablation of ß-catenin, retroviral expression of a dominant negative Akt mutant, and transgenic expression of a constitutively active Foxo1 restored emigration of GSK3-deficient thymocytes. Our findings establish an essential role for GSK3 in thymocyte egress and reveal a previously unidentified signaling function of ß-catenin in the cytoplasm.

Discovery of new genetic loci for male sexual orientation in Han population.

Epidemiological studies have demonstrated that the genetic factors partly influence the development of same-sex sexual behavior, but most genetic studies have focused on people of primarily European ancestry, potentially missing important biological insights. Here, we performed a two-stage genome-wide association study (GWAS) with a total sample of 1478 homosexual males and 3313 heterosexual males in Han Chinese populations and identified two genetic loci (rs17320865, Xq27.3, FMR1NB, Pmeta = 8.36 × 10-8, OR = 1.29; rs7259428, 19q12, ZNF536, Pmeta = 7.58 × 10-8, OR = 0.75) showing consistent association with male sexual orientation. A fixed-effect meta-analysis including individuals of Han Chinese (n = 4791) and European ancestries (n = 408,995) revealed 3 genome-wide significant loci of same-sex sexual behavior (rs9677294, 2p22.1, SLC8A1, Pmeta = 1.95 × 10-8; rs2414487, 15q21.3, LOC145783, Pmeta = 4.53 × 10-9; rs2106525, 7q31.1, MDFIC, Pmeta = 6.24 × 10-9). These findings may provide new insights into the genetic basis of male sexual orientation from a wider population scope. Furthermore, we defined the average ZNF536-immunoreactivity (ZNF536-ir) concentration in the suprachiasmatic nucleus (SCN) as lower in homosexual individuals than in heterosexual individuals (0.011 ± 0.001 vs 0.021 ± 0.004, P = 0.013) in a postmortem study. In addition, compared with heterosexuals, the percentage of ZNF536 stained area in the SCN was also smaller in the homosexuals (0.075 ± 0.040 vs 0.137 ± 0.103, P = 0.043). More homosexual preference was observed in FMR1NB-knockout mice and we also found significant differences in the expression of serotonin, dopamine, and inflammation pathways that were reported to be related to sexual orientation when comparing CRISPR-mediated FMR1NB knockout mice to matched wild-type target C57 male mice.

Poplar plantation has the potential to alter the water balance in semiarid Inner Mongolia.

Poplar plantation is the most dominant broadleaf forest type in northern China. Since the mid-1990s plantation was intensified to combat desertification along China's northwestern border, i.e., within Inner Mongolia (IM). This evoked much concern regarding the ecological and environmental effects on areas that naturally grow grass or shrub vegetation. To highlight potential consequences of large-scale poplar plantations on the water budget within semiarid IM, we compared the growing season water balance (evapotranspiration (ET) and precipitation (PPT)) of a 3-yr old poplar plantation (Kp(3)) and a natural shrubland (Ks) in the Kubuqi Desert in western IM, and a 6-yr old poplar plantation (Bp(6)) growing under sub-humid climate near Beijing. The results showed that, despite 33% lower PPT at Kp(3), ET was 2% higher at Kp(3) (228 mm) as compared with Ks (223 mm) in May-September 2006. The difference derived mainly from higher ET at the plantation during drier periods of the growing season, which also indicated that the poplars must have partly transpired groundwater. Estimated growing season ET at Bp(6) was about 550 mm and more than 100% higher than at Kp(3). It is estimated that increases in leaf area index and net radiation at Kp(3) provide future potential for the poplars in Kubuqi to exceed the present ET and ET of the natural shrubland by 100-200%. These increases in ET are only possible through the permanent use of groundwater either directly by the trees or through increased irrigation. This may significantly change the water balance in the area (e.g., high ET at the cost of a reduction in the water table), which renders large-scale plantations a questionable tool in sustainable arid-land management.

Study on physical training in the lipid metabolism regulation of obese adolescents / Estudo sobre treinamento físico na regulação do metabolismo lipídico em adolescentes obesos / Estudio sobre el entrenamiento físico en la regulación del metabolismo lipídico en adolescentes obesos

ABSTRACT Introduction In proportion to the development of the economy, the problem of obesity among adolescents is also increasing. This abnormal lipid metabolism index can influence other physical diseases besides harming the social development of youth. Objective Investigate physical training and the regulation of lipid metabolism in adolescents, improving the metabolic index of obese youth. Methods 80 obese adolescents with equal numbers of both genders were randomly assigned into experimental and control groups. The experimental group received daily 80-min sports training (aerobics, walking, badminton, swimming, and other sports with low intensity and long duration) six times a week for one month, without distinction of exercise intensity or frequency for gender. A comparison method was performed between the groups before and after the intervention with indicators including body weight, BMI, fluid ratio, water measurement, waist, hip, skinfold thickness, FBG, CT, Tg, HDL - C, and LDL - C, among others. Results Physical training can effectively improve adolescents' body shape. Blood indices and other indicators except for HDL-C positively correlate with this body shape. Physical training substantially improved lipid metabolism in obese adolescents. Conclusion The exercise regimen of this experiment proved to be simple and manageable, offering adolescents a healthier physical and more confidence in their daily study, life, and social interaction, but also reducing several diseases caused by obesity. Due to the ease of replication, the sample size can be expanded to universal conclusions, making it feasible to popularize. Level of evidence II; Therapeutic studies - investigation of treatment outcomes.

RESUMO Introdução Proporcionalmente ao desenvolvimento da economia, aumenta também o problema da obesidade entre os adolescentes. Esse índice anormal no metabolismo lipídico pode influenciar outras doenças físicas além de prejudicar o desenvolvimento social na juventude. Objetivo Investigar o treinamento físico e a regulação do metabolismo lipídico em adolescentes, melhorando o índice metabólico dos jovens obesos. Métodos 80 adolescentes obesos com número igual de ambos os sexos foram distribuídos aleatoriamente em grupos controlados de experimento e controle. O grupo experimental recebeu treinamentos esportivos diários de 80 minutos (aeróbica, caminhada, badminton, natação e outros esportes com baixa intensidade e longa duração), seis vezes por semana durante um mês, sem distinção de intensidade ou frequência dos exercícios para os sexos. Foi realizado o método de comparação entre os grupos, antes e após a intervenção, com indicadores incluindo peso corporal, IMC, taxa de líquidos, medição de água, cintura, quadril, espessura de dobras cutâneas, FBG, CT, Tg, HDL - C, LDL - C entre outros. Resultados O treinamento físico pode melhorar efetivamente a forma corporal dos adolescentes. Índices sanguíneos e outros indicadores com exceção do HDL-C estão positivamente correlacionados com essa forma corporal. O treinamento físico melhorou substancialmente o metabolismo lipídico de adolescentes obesos. Conclusão O esquema de exercícios deste experimento demonstrou-se simples e viável, oferecendo aos adolescentes um físico mais saudável e mais confiança no processo de estudo diário, vida e interação social, mas também reduzir diversas doenças causadas pela obesidade. Devido a facilidade de replicação, o número de amostrar pode ser expandido para conclusões universais, viabilizando a sua popularização. Nível de evidência II; Estudos terapêuticos - investigação dos desfechos do tratamento.

RESUMEN Introducción Proporcionalmente al desarrollo de la economía, el problema de la obesidad entre los adolescentes también aumenta. Este índice anormal en el metabolismo lipídico puede influir en otras enfermedades físicas además de perjudicar el desarrollo social en la juventud. Objetivo Investigar el entrenamiento físico y la regulación del metabolismo lipídico en adolescentes, mejorando el índice metabólico de los jóvenes obesos. Métodos 80 adolescentes obesos con igual número de ambos sexos fueron distribuidos aleatoriamente en los grupos de experimento y de control. El grupo experimental recibió 80 minutos diarios de entrenamiento deportivo (aeróbic, marcha, bádminton, natación y otros deportes de baja intensidad y larga duración), seis veces a la semana durante un mes, sin distinción de intensidad o frecuencia de los ejercicios para los sexos. Se realizó un método de comparación entre los grupos, antes y después de la intervención, con indicadores que incluían el peso corporal, el IMC, la tasa de líquidos, la medición del agua, la cintura, la cadera, el grosor de los pliegues cutáneos, FBG, CT, Tg, HDL - C, LDL - C, entre otros. Resultados El entrenamiento físico puede mejorar eficazmente la forma corporal de los adolescentes. Los índices sanguíneos y otros indicadores, excepto el HDL-C, están positivamente correlacionados con esta forma corporal. El entrenamiento físico mejoró sustancialmente el metabolismo de los lípidos en los adolescentes obesos. Conclusión El esquema de ejercicios de este experimento demostró ser simple y factible, ofreciendo a los adolescentes un físico más saludable y más confianza en el proceso de estudio diario, la vida y la interacción social, pero también reduciendo varias enfermedades causadas por la obesidad. Debido a la facilidad de replicación, el tamaño de la muestra puede ampliarse para obtener conclusiones universales, lo que permite su popularización. Nivel de evidencia II; Estudios terapêuticos - investigación de los resultados del tratamiento.