Response of solar-induced chlorophyll fluorescence-based spatial and temporal evolution of vegetation in Xinjiang to multiscale drought.

Climate change and human activities have increased droughts, especially overgrazing and deforestation, which seriously threaten the balance of terrestrial ecosystems. The ecological carrying capacity and vegetation cover in the arid zone of Xinjiang, China, are generally low, necessitating research on vegetation response to drought in such arid regions. In this study, we analyzed the spatial and temporal characteristics of drought in Xinjiang from 2001 to 2020 and revealed the response mechanism of SIF to multi-timescale drought in different vegetation types using standardized precipitation evapotranspiration index (SPEI), solar-induced chlorophyll fluorescence (SIF), normalized difference vegetation index (NDVI), and enhanced vegetation index (EVI) data. We employed trend analysis, standardized anomaly index (SAI), Pearson correlation, and trend prediction techniques. Our investigation focused on the correlations between GOSIF (a new SIF product based on the Global Orbital Carbon Observatory-2), NDVI, and EVI with SPEI12 for different vegetation types over the past two decades. Additionally, we examined the sensitivities of vegetation GOSIF to various scales of SPEI in a typical drought year and predicted future drought trends in Xinjiang. The results revealed that the spatial distribution characteristics of GOSIF, normalized difference vegetation index (NDVI), and enhanced vegetation index (EVI) were consistent, with mean correlations with SPEI at 0.197, 0.156, and 0.128, respectively. GOSIF exhibited the strongest correlation with SPEI, reflecting the impact of drought stress on vegetation photosynthesis. Therefore, GOSIF proves advantageous for drought monitoring purposes. Most vegetation types showed a robust response of GOSIF to SPEI at a 9-month scale during a typical drought year, with grassland GOSIF being particularly sensitive to drought. Our trend predictions indicate a decreasing trend in GOSIF vegetation in Xinjiang, coupled with an increasing trend in drought. This study found that compared with that of the traditional greenness vegetation index, GOSIF has obvious advantages in monitoring drought in the arid zone of Xinjiang. Furthermore, it makes up for the lack of research on the mechanism of vegetation GOSIF response to drought on multiple timescales in the arid zone. These results provide strong theoretical support for investigating the monitoring, assessment, and prediction of vegetation response to drought in Xinjiang, which is vital for comprehending the mechanisms of carbon and water cycles in terrestrial ecosystems.

Importance of GWAS risk loci and clinical data in predicting asthma using machine-learning approaches.

INTRODUCTION: To understand the risk factors of asthma, we combined genome-wide association study (GWAS) risk loci and clinical data in predicting asthma using machine-learning approaches. METHODS: A case-control study with 123 asthmatics and 100 controls was conducted in the Zhuang population in Guangxi. GWAS risk loci were detected using polymerase chain reaction, and clinical data were collected. Machine-learning approaches were used to identify the major factors that contribute to asthma. RESULTS: A total of 14 GWAS risk loci with clinical data were analyzed on the basis of 10 times the 10-fold cross-validation for all machine-learning models. Using GWAS risk loci or clinical data, the best performances exhibited area under the curve (AUC) values of 64.3% and 71.4%, respectively. Combining GWAS risk loci and clinical data, the XGBoost established the best model with an AUC of 79.7%, indicating that the combination of genetics and clinical data can enable improved performance. We then sorted the importance of features and found the top six risk factors for predicting asthma to be rs3117098, rs7775228, family history, rs2305480, rs4833095, and body mass index. CONCLUSION: Asthma-prediction models based on GWAS risk loci and clinical data can accurately predict asthma, and thus provide insights into the disease pathogenesis.

Impact of COVID-19 restrictions on air quality and surface urban heat island effect within the main urban area of Urumqi, China.

The outbreak of coronavirus in 2019 (COVID-19) posed a serious global threat. However, the reduction in man-made pollutants during COVID-19 restrictions did improve the ecological environment of cities. Using multi-source remote sensing data, this study explored the spatiotemporal variations in air pollutant concentrations during the epidemic prevention and control period in Urumqi and quantitatively analyzed the impact of different air pollutants on the surface urban heat island intensity (SUHII) within the study area. Urumqi, located in the hinterland of the Eurasian continent, northwest of China, in the central and northern part of Xinjiang was selected as the study area. The results showed that during COVID-19 restrictions, concentrations of air pollutants decreased in the main urban area of Urumqi, and air quality improved. The most evident decrease in NO2 concentration, by 77 ± 1.05% and 15 ± 0.98%, occurred in the middle of the first (January 25 to March 20, 2020) and second (July 21 to September 1, 2020) COVID-19 restriction periods, respectively, compared with the corresponding period in 2019. Air pollutant concentrations and the SUHIIs were significantly and positively correlated, and NO2 exhibited the strongest correlation with the SUHIIs. We revealed that variations in the air quality characteristics and thermal environment were observed in the study area during the COVID-19 restrictions, and their quantitative relationship provides a theoretical basis and reference value for improving the air and ecological environment quality within the study area.

Interval training effects on cardiorespiratory capacity of swimmers / Efeito do treinamento intervalado sobre a capacidade cardiorrespiratória de nadadores / Efecto del entrenamiento por intervalos en la capacidad cardiorrespiratoria de nadadores

ABSTRACT Introduction: Cardiopulmonary function is directly related to the body's ability to perform metabolism under aerobic conditions. It is a key characteristic for the training of professional swimmers. It is believed that adding interval training to traditional workouts may contribute to the aerobic endurance of these athletes. Objective: Evaluate the interval training effects on the cardiorespiratory capacity of swimmers. Methods: Twenty volunteer swimmers were randomly divided into two groups for seven weeks. There were 4 hours of class per week, totaling 28 hours of training. In the formal training stage, the experimental group performed intermediate-intensity training, while the control group continued to perform traditional swim team training. The experimental indicators pertinent to the evaluated athletes were collected, tested, and analyzed before and after the experiment. Results: The VO2 of the athletes in the experimental group increased from 3.90±0.67L/min before the experiment to 4.06±0.73L/min after the experiment; VE increased from 156.08±35.76L before the experiment to 180.08±39.42L after the experiment; underwater endurance time increased from 46.80±8.43s before the experiment to 55.49±7.60s after the experiment. Conclusion: Intermittent training improves athletes' physical fitness and sports capacity, being an effective method to improve cardiopulmonary function. Level of evidence II; Therapeutic studies - investigation of treatment outcomes.

RESUMO Introdução: A função cardiopulmonar está diretamente relacionada à capacidade do organismo de executar a metabolização sob condições aeróbicas. É uma característica chave para os treinamentos de nadadores profissionais e acredita-se que a adição do treinamento intervalado nos treinos tradicionais possa contribuir à resistência aeróbica desses atletas. Objetivo: Avaliar o efeito do treinamento intervalado sobre a capacidade cardiorrespiratória dos nadadores. Métodos: Vinte nadadores voluntários foram divididos aleatoriamente em dois grupos durante 7 semanas. Foram 4 horas de aula por semana, totalizando 28 horas de treino. Na etapa de treinamento formal, o grupo experimental realizou essencialmente o treinamento de intensidade intermediária, enquanto o grupo de controle permaneceu executando o treinamento tradicional da equipe de natação. Os indicadores experimentais pertinentes aos atletas avaliados foram coletados, testados e analisados antes e depois do experimento. Resultados: O VO2 dos atletas do grupo experimental aumentou de 3,90±0,67L/min antes do experimento para 4,06±0,73L/min após o experimento; o VE aumentou de 156,08±35,76L antes do experimento para 180,08±39,42L após o experimento; o tempo de resistência subaquática aumentou de 46,80±8,43s antes do experimento para 55,49±7,60s após o experimento. Conclusão: O treinamento intermitente contribui para melhorar a aptidão física e a capacidade esportiva dos atletas, sendo um método eficaz no aprimoramento da função cardiopulmonar. Nível de evidência II; Estudos terapêuticos - investigação dos resultados do tratamento.

RESUMEN Introducción: La función cardiopulmonar está directamente relacionada con la capacidad del organismo para realizar el metabolismo en condiciones aeróbicas. Es una característica clave para los entrenamientos de los nadadores profesionales y se cree que la adición del entrenamiento interválico en los entrenamientos tradicionales puede contribuir a la resistencia aeróbica de estos atletas. Objetivo: Evaluar el efecto del entrenamiento por intervalos sobre la capacidad cardiorrespiratoria de los nadadores. Métodos: Veinte nadadores voluntarios fueron divididos aleatoriamente en dos grupos durante 7 semanas. Se impartieron 4 horas de clase a la semana, totalizando 28 horas de entrenamiento. En la etapa de entrenamiento formal, el grupo experimental realizó esencialmente un entrenamiento de intensidad intermedia, mientras que el grupo control permaneció realizando el entrenamiento tradicional del equipo de natación. Los indicadores experimentales pertinentes a los atletas evaluados fueron recogidos, testados y analizados antes y después del experimento. Resultados: El VO2 de los atletas del grupo experimental aumentó de 3,90±0,67L/min antes del experimento a 4,06±0,73L/min después del experimento; el VE aumentó de 156,08±35,76L antes del experimento a 180,08±39,42L después del experimento; el tiempo de resistencia subacuática aumentó de 46,80±8,43s antes del experimento a 55,49±7,60s después del experimento. Conclusión: El entrenamiento por intervalos contribuye a mejorar la forma física y la capacidad deportiva de los atletas, siendo un método eficaz para mejorar la función cardiopulmonar. Nivel de evidencia II; Estudios terapéuticos - investigación de los resultados del tratamiento.

Listeria monocytogenes Inoculation Impedes the Development of Brain Pathology in Experimental Cerebral Malaria by Inhibition of Parasitemia.

Cerebral malaria (CM) is a serious central nervous system dysfunction caused by Plasmodium falciparum infection. In this study, we investigated the effect of Listeria monocytogenes (Lm) inoculation on experimental cerebral malaria (ECM) using Plasmodium berghei ANKA (PbA)-infected C57BL/6 mice. Live Lm inoculation inhibited the parasitemia and alleviated ECM symptoms. The protective effect against ECM symptoms was connected with improved brain pathology manifested as a less-damaged blood-brain barrier, decreased parasite sequestration, and milder local inflammation. Meanwhile, Lm inoculation decreased expression of cell adhesion molecules (ICAM-1 and VCAM-1) and accumulation of pathogenic CD8+ T cells in the brain. In keeping with the suppression of parasitemia, there was an upregulation of IFN-γ, IL-12, MCP-1, and NO expression in the spleen by Lm inoculation upon PbA infection. Early treatment with exogenous IFN-γ exhibited a similar effect to Lm inoculation on PbA infection. Taken together, Lm inoculation impedes the development of brain pathology in ECM, and early systemic IFN-γ production may play a critical role in these protective effects.

Calcitonin Gene-Related Peptide Attenuates Hyperoxia-Induced Oxidative Damage in Alveolar Epithelial Type II Cells Through Regulating Viability and Transdifferentiation.

As a stem cell of alveolar epithelium, the physiological status of alveolar epithelium type II cells (AECII) after hyperoxia exposure is closely related to the occurrence of hyperoxia-induced lung injury and the restoration of normal morphological function of damaged alveolar epithelium. However, the relevant mechanisms involved are not very clear. Therefore, this study aimed to explore the effect of calcitonin gene-related peptide (CGRP) on AECII exposed to hyperoxia and its potential mechanisms. The AECII viability was detected using MTT assay. The malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were detected by spectrophotometry. The transdifferentiation capacity of AECII was evaluated by flow cytometry. The expression levels of Notch1, Hes, HERP, and AECII markers were detected using immunohistochemistry and/or RT-qPCR or immunofluorescence. ELISA was used for the determination of inflammatory markers. The results showed that CGRP significantly promoted cell viability, and markedly suppressed hyperoxia-induced transdifferentiation of AECII; these biological alterations were coincided with decreased MDA level, increased SOD activity, and activated Notch signaling pathway (upregulated expression levels of Notch1, Hes, and HERP). Notably, the in vitro effects of CGRP on Notch signaling pathway were further investigated in animal model, and the HE staining results showed that CGRP reduced in vivo oxidative injury and inflammation in hyperoxia-treated AECII through the promotion of structural and functional regeneration, accompanied by elevated Notch1 expression and activated Notch signaling cascade as shown by immunohistochemistry and QPCR, respectively. Immunohistochemistry of APQ-5 and SPC indicated that CGRP reversed the transdifferentiation of AECIIs in vivo. Our current results were consistent across both in vitro and in vivo settings, and provide a new direction for the prevention and treatment of bronchopulmonary dysplasia (BPD).

Knockdown of Long Noncoding RNAs of Maternally Expressed 3 Alleviates Hyperoxia-Induced Lung Injury via Inhibiting Thioredoxin-Interacting Protein-Mediated Pyroptosis by Binding to miR-18a.

Long-term hyperoxia exposure may cause lung damage with characteristic inflammation. Long noncoding RNA of maternally expressed 3 (MEG3) is up-regulated in lung tissues exposed to hyperoxia; however, the underlying mechanism is unclear. Hyperoxia-induced cells and mouse models were used to study these mechanisms. Molecular assays were used to detect cell viability, cytotoxicity, and expression of miR-18a, MEG3, and inflammatory cytokines. The interaction among MEG3, miR-18a, and thioredoxin-interacting protein (TXNIP) was verified; and pyroptosis-related proteins were analyzed. The in vivo model was established by exposing MEG3 knockdown mice to hyperoxia. Hematoxylin and eosin staining was used to assess pathologic alterations of lung tissues. Hyperoxia suppressed cell viability, induced cell damage, and exacerbated the secretion of IL-1ß and IL-18. Hyperoxia inhibited miR-18a, with increased expression of MEG3, TXNIP, and nonobese diabetic-like receptor family pyrin domain containing 3 (NLRP3). MEG3 aggravated TXNIP expression by binding to miR-18a. Knockdown of MEG3 rescued hyperoxia-induced pyroptosis by up-regulating miR-18a. Furthermore, knockdown of MEG3 inhibited NLRP3 inflammasome activity and caspase-1 signaling by miR-18a. In vivo knockdown of MEG3 and overexpression of miR-18a relieved hyperoxia-induced lung injury via restraining NLRP3 inflammasome-mediated pyroptosis, whereas miR-18a inhibition reversed these effects. In conclusion, knockdown of MEG3 inhibits pyroptosis to alleviate hyperoxia lung injury by suppressing NLRP3 inflammasome and caspase-1 signaling via regulating miR-18a-TXNIP axis.

Somatic gene mutation signatures predict cancer type and prognosis in multiple cancers with pan-cancer 1000 gene panel.

Most cancers are caused by somatic mutations. Some common mutations in the same cancer type can form a "signature" to specifically predict the prognosis or to distinguish it from other cancers. In this study, 710 somatic cell mutations were identified in 142 cases, including digestive, lung and urogenital cancers, and the digestive cancers were further divided into liver, stomach, intestinal, esophageal and cardia cancer. The above mutations were located in 166 genes. In addition, a group of high-frequency mutation genes with specific characteristics were screened to form predictive signatures for each cancer. Verification using TCGA suggested that the signatures could predict the stages, progression-free survival, and overall survival of digestive, intestinal, and liver cancers (P < 0.05). The validation cases further confirmed the predictive role of digestive and liver cancers signatures in diagnosis and prognosis. Overall, this study established predictive signatures for different cancer systems and their subtypes. These findings enable a better understanding in cancer genome, and contribute to the personalized diagnosis and treatment.

Performance of a two-leaf light use efficiency model for mapping gross primary productivity against remotely sensed sun-induced chlorophyll fluorescence data.

Estimating terrestrial gross primary production is an important task when studying the carbon cycle. In this study, the ability of a two-leaf light use efficiency model to simulate regional gross primary production in China was validated using satellite Global Ozone Monitoring Instrument - 2 sun-induced chlorophyll fluorescence data. The two-leaf light use efficiency model was used to estimate daily gross primary production in China's terrestrial ecosystems with 500-m resolution for the period from 2007 to 2014. Gross primary production simulated with the two-leaf light use efficiency model was resampled to a spatial resolution of 0.5° and then compared with sun-induced chlorophyll fluorescence. During the study period, sun-induced chlorophyll fluorescence and gross primary production simulated by the two-leaf light use efficiency model exhibited similar spatial and temporal patterns in China. The correlation coefficient between sun-induced chlorophyll fluorescence and monthly gross primary production simulated by the two-leaf light use efficiency model was significant (p<0.05, n=96) in 88.9% of vegetated areas in China (average value 0.78) and varied among vegetation types. The interannual variations in monthly sun-induced chlorophyll fluorescence and gross primary production simulated by the two-leaf light use efficiency model were similar in spring and autumn in most vegetated regions, but dissimilar in winter and summer. The spatial variability of sun-induced chlorophyll fluorescence and gross primary production simulated by the two-leaf light use efficiency model was similar in spring, summer, and autumn. The proportion of spatial variations of sun-induced chlorophyll fluorescence and annual gross primary production simulated by the two-leaf light use efficiency model explained by ranged from 0.76 (2011) to 0.80 (2013) during the study period. Overall, the two-leaf light use efficiency model was capable of capturing spatial and temporal variations in gross primary production in China. However, the model needs further improvement to better simulate gross primary production in summer.

[Transfection Efficiency of Ad5F11p-GFP on CIK and NK-92 Cells and Its Influence on Biological Characteristics].

OBJECTIVE: To study transfection efficiency of Ad5F11p-GFP and its influence on biological characteristics of CIK and NK-92 cells in order to predict the application of Ad5F11p vector in immunotherapy. METHODS: Two kinds of immune cells, cytokine-induced killer (CIK) cells and natural-killer (NK) cell line NK-92 cells, were transfected by Ad5F11p-GFP at different multiplicity of transfection (MOI), and untransfected immune cells were used as negative control. GFP expression was determined by flow cytometry, the cell morphology was observed with microscope, the cell proliferation was analyzed by trypan blue staining, specific cytotoxicity of NK-92 cells was determined by LDH assay. RESULTS: About 90% of transfection efficiency for NK-92 cells could be achieved at a MOI of 25, while the transfection efficiency for CIK was less than 40% at a MOI of 200. In addition, the transfection efficiency basically unchanged at the same MOI for 48 h and 96 h, and the immune cells transfected with the virus trended to form agglomeration, displaying slower proliferation, increase of IFN-γ release and enhancement of tumor killing activity. CONCLUSION: Ad5F11p- modified NK-92 shows a good prospect for adoptive immunotherapy.

Parasite densities modulate susceptibility of mice to cerebral malaria during co-infection with Schistosoma japonicum and Plasmodium berghei.

BACKGROUND: Malaria and schistosomiasis are endemic and co-exist in the same geographic areas, even co-infecting the same host. Previous studies have reported that concomitant infection with Schistosoma japonicum could offer protection against experimental cerebral malaria (ECM) in mice. This study was performed to evaluate whether alterations in parasite density could alter this protective effect. METHODS: Mice were inoculated with 100 or 200 S. japonicum cercariae followed by infection with high or low density of Plasmodium berghei ANKA strain eight weeks after the first infection. Then, parasitaemia, survival rate and blood-brain-barrier (BBB) damage were assessed. Interferon-gamma (IFN-γ), interleukin (IL)-4, IL-5, IL-13, IL-10, and TGF-ß levels were determined in splenocyte supernatants using enzyme-linked immunosorbent assay (ELISA). Cell surface/intracellular staining and flow cytometry were used to analyse the level of CD4(+)/CD8(+) T cells, CD4(+)CD25(+)Foxp3(+) Tregs, IL-10-secreting Tregs, and IL-10(+)Foxp3-CD4(+) T cells in the spleen, and CD4(+)/CD8(+) T cells infiltrating the brain. RESULTS: Co-infection with low density P. berghei and increased S. japonicum cercariae significantly increased the levels of IL-4, IL-5, IL-13, TGF-ß and Tregs, but significantly decreased the levels of IFN-γ and the percentage of CD4(+) T cells and CD8(+) T cells in the spleen and CD8(+) T cell infiltration in the brain. Increased worm loads also significantly decreased mortality and BBB impairment during ECM. When challenged with higher numbers of P. berghei and increased cercariae, the observed cytokine changes were not statistically significant. The corresponding ECM mortality and BBB impairment also remained unchanged. CONCLUSIONS: This study demonstrates that protection for ECM depends on the numbers of the parasites, S. japonicum and P. berghei, during co-infection. Alterations in the regulatory response appear to play a key role in this adaptation.

[The protective effect of chlorophyllin against oxidative damage and its mechanism].

OBJECTIVE: To investigate whether chlorophyllin could protect human umbilical vein endothelial cell (HUVEC) against oxidative damage by inducing the expression of heme oxygenase-1 (HO-1) and to explore the underlying mechanism. METHODS: The cellular protection of chlorophyllin against oxidative damage was detected by cell-survival assay with flow cytometry. The level of free radicals was detected directly by electron spin resonance spectra. The induced expression of HO-1 was shown by RT-PCR, Western blot, immunofluorescence confocal laser microscopy and enzymatic activity test. Whether the activation of PI3K/Akt pathway was involved was detected by Western blot. RESULTS: Chlorophyllin could protect HUVEC against oxidative damage caused by H2O2 via scavenging the excessive free radicals. Chlorophyllin treatment could induce expression of HO-1 in a dose- and time-dependent manner. The activation of PI3K/Akt pathway was required in the induction of HO-1. LY294002, the specific inhibitor of PI3K, could suppress the activation of PI3K/Akt and the induced expression of HO-1 in a dose-dependent manner. CONCLUSIONS: Chlorophyllin shows cellular protection against oxidative damage by counteracting the excessive free radicals. Up-regulation of HO-1 expression plays a pivotal role in the protection of chlorophyllin, while the activation of PI3K/Akt signaling pathway is required in the induction of HO-1.

[Analysis of developing feature of pneumoconiosis].

OBJECTIVE: To get the message about the developing feature of pneumoconiosis by analyzing the data from 353 cases of pneumoconiosis diagnosed in our hospital recent 6 years. METHODS: To analyze the onset age, onset service years and incubation period of 353 cases of pneumoconiosis, especially in silicosis, coal worker's pneumoconiosis and potter's pneumoconiosis. RESULTS: 353 patients referred to 10 species of pneumoconiosis, the silicosis, coal worker's pneumoconiosis and potter's pneumoconiosis were accounted for 28.90%, 43.34% and 15.01% of total pneumoconiosis respectively. Diagnosed patients who began to exposed to dust during 1950's to 1980's accounted for 84.99% of all the diagnosed patients. The onset age, onset service years and incubation period of silicosis, coal worker's pneumoconiosis and potters pneumoconiosis all showed a shorten trend compared each other every decade, especially after 1980's, but excluded potter's pneumoconiosis because of that the ceramics industry switched to other products in Beijing. There was a positive correlation relationship between average onset age and incubation period in three main species of pneumoconiosis mentioned above, but no significant difference could be seen in average promotion years. Additionally, comparing with other type of work, jade machining workers showed such a characteristic as younger onset and short incubation period. CONCLUSION: The development situation of silicosis, coal worker's pneumoconiosis is still no so optimistic, and the strict surveillance and administration especially to the township enterprises with poor production conditions should get further strengthen.

[Effects of baicalin on pulmonary functions of acute respiratory distress syndrome induced by oleic acid in rats].

OBJECTIVE: To investigate the effect of baicalin on pulmonary functions and its mechanism during the development of acute respiratory distress syndrome (ARDS) induced by oleic acid (OA) in rats. METHODS: Rats were randomized into 5 groups: control, ARDS (OA induction, 0.12 mg/kg), baicalin-treated group (150 mg/kg), baicalin-treated group (300 mg/kg) and baicalin-treated group (450 mg/kg). The blood samples and lung tissue were collected at 10 min, 1, 2 and 6 h after OA injection. The lung concentration of myeloperoxidase (MPO) was detected by an ELISA (enzyme-linked immunosorbent assay) kit. Meanwhile, blood gas analysis and pulmonary pathological examination were also performed. RESULTS: The level of arterial oxygen partial pressure and oxygenation index decreased (P < 0.01 vs. control) and oxygenation index (190 mm Hg, 1 mm Hg = 0.133 kPa) reached the diagnostic standard of ARDS at 2 h in ARDS group. In baicalin-treated group (150 mg/kg and 300 mg/kg), the level of arterial oxygen partial pressure and oxygenation index increased versus the ARDS group. In baicalin-treated group (450 mg/kg), the level of arterial oxygen partial pressure was undifferentiated at 1, 2 and 6 h (P > 0.05) and decreased at 10 min (46.8 mm Hg, P < 0.05) versus the ARDS group. The level of MPO increased in baicalin-treated (300 mg/kg) and ARDS groups. Compared with the ARDS group, the level of MPO decreased significantly in baicalin-treated group (300 mg/kg) at 10 min, 1 and 2 h. Meanwhile, the pulmonary pathological damage improved in baicalin-treated group (300 mg/kg). CONCLUSION: An appropriate dose of baicalin may improve hypoxemia of ARDS induced by OA in rats. It may be due to the inhibition of MPO activity.

Characterization of immune responses to single or mixed infections with P. yoelii 17XL and P. chabaudi AS in different strains of mice.

The outcome of Plasmodium yoelii 17XL (P.y17XL)-infected BALB/c and DBA/2 mice, ranging from death to spontaneous cure, depends largely on the establishment of effective Th1 and Th2 responses and a successful switch between Th1 and Th2 responses, as well as appropriate functioning of CD4(+)CD25(+)Foxp3(+)regulatory T cells (Tregs). The infection with another malaria-causing parasite, Plasmodium chabaudi AS (P.cAS), leads to a different outcome in BALB/c and DBA/2 mice compared to mice infected with P.y17XL alone. To understand the consequence of co-infection with P.y17XL and P.cAS, we determined the proliferation curve of parasites, pro-inflammatory/anti-inflammatory cytokine profiles, and the dynamic changes of the number of Tregs in DBA/2 and BALB/c mice with single or mixed-species infections. The infective mode in mixed-species infections was the same as single P.y17XL infections. The multiplication of P.y17XL parasites prevailed in BALB/c and DBA/2 mice with early mixed infections, as detected by RTQ-PCR. Subsequently, the multiplication of P.cAS parasites dominated in DBA/2 mice with mixed infections, while BALB/c mice succumbed to infection. In addition, the dynamic changes in IFN-gamma and IL-4 production in mice with mixed infections, used as a measure of Th1 and Th2 responsiveness, were consistent with P.y17XL-infected mice. Treg activation and the IL-10 level were also closely related to susceptibility to infection. Our findings demonstrate that the characteristics of the immune response during infections with mixed species are dependent on the mode of proliferation of different species of Plasmodium. Indeed, different species of Plasmodium can influence each other in the same host.

Polymorphism of the mouse gene for the interleukin 10 receptor alpha chain (Il10ra) and its association with the autoimmune phenotype.

Several studies suggest that interleukin (IL)-10 pathway is involved in murine lupus, while no linkage of IL-10 gene polymorphism to disease susceptibility has been reported in studies with lupus-prone mice. Since IL-10 functions through the specific IL-10 receptor alpha (IL-10RA) chain and the IL-10RA gene (Il10ra) is linked to the susceptibility loci of atopic dermatitis and Crohn's disease identified using mouse models, we supposed that IL-10RA might be involved in murine lupus. By flow cytometry analysis, we found that NZW mice, one of the parental strains of lupus-prone (NZBxNZW) F1 mice, express extremely low levels of IL-10RA compared with NZB mice, the other parental strain, and the healthy BALB/c and C57BL/6 mice. Sequence analyses of Il10ra cDNA of NZW mice showed multiple nucleotide mutations compared with that of NZB and C57BL/6 strains, some of which would result in amino acid substitutions in the IL-10RA protein. Lupus-prone MRL mice shared the same polymorphism with NZW. Analyses using (NZBxNZW) F1xNZB backcross mice showed that high serum levels of IgG antichromatin antibodies were regulated by a combinatorial effect of the NZW Il10ra allele and a heterozygous genotype for Tnfa microsatellite locus. Our data suggest that the polymorphic NZW-type Il10ra may be involved in the pathologic production of antichromatin antibodies and, if so, may contribute in part to the development of systemic lupus erythematosus as one susceptibility allele.