A Longitudinal Study of the Effects of Bed-Sharing Experience in Infancy on Sleep Outcomes at 2 Years Old.

OBJECTIVE: To assess the effects of bed-sharing experiences in infancy on sleep patterns and sleep problems at 2 years of age. STUDY DESIGN: A total of 1564 children from an ongoing Shanghai Maternal-Child Pairs Cohort were included. Bed-sharing experiences were collected when children were 2, 6, and 24 months old via caregiver-completed questionnaires (whether caregivers shared a bed with children during the night), and children's bed-sharing experiences were classified as follows: no bed-sharing, early-only bed-sharing, late-onset bed-sharing, and persistent bed-sharing. Sleep outcomes at month 24 were assessed using the Brief Infant Sleep Questionnaire. Sleep patterns and problems were compared among the 4 types of bed-sharing experiences. RESULTS: Of the 1564 infants, 10.10% had no bed-sharing, 18.35% had early-only, 27.94% had late-onset, and 43.61% had persistent bed-sharing. Compared with children with no bed-sharing, children with late-onset and persistent bed-sharing had shorter nighttime sleep durations and longer daytime sleep durations (P < .05) and were more likely to snore (aOR 1.87 [95% CI 1.25-2.79]; aOR 1.68 [95% CI 1.14-2.47]) and have sleep onset difficulty (aOR 2.06 [95% CI 1.37-3.09]; aOR 2.07 [95% CI 1.41-3.05]). However, caregivers of infants in the late-onset and persistent bed-sharing groups perceived less problematic sleep (aOR 0.38 [95% CI 0.26-0.56] and aOR 0.40 [95% CI 0.28-0.58]). CONCLUSIONS: Bed-sharing is a common experience among Chinese children. Although bed-sharing may reduce caregivers' perception of children's problematic sleep, late-onset or persistent bed-sharing in infancy is associated with sleep problems at 2 years of age.

Role of viral bioaerosols in nosocomial infections and measures for prevention and control.

The presence of patients with diverse pathologies in hospitals results in an environment that can be rich in various microorganisms including respiratory and enteric viruses, leading to outbreaks in hospitals or spillover infections to the community. All hospital patients are at risk of nosocomial viral infections, but vulnerable groups such as older adults, children and immuno-compromised/-suppressed patients are at particular risk of severe outcomes including prolonged hospitalization or death. These pathogens could transmit through direct or indirect physical contact, droplets or aerosols, with increasing evidence suggesting the importance of aerosol transmission in nosocomial infections of respiratory and enteric viruses. Factors affecting the propensity to transmit and the severity of disease transmitted via the aerosol route include the biological characteristics affecting infectivity of the viruses and susceptibility of the host, the physical properties of aerosol particles, and the environmental stresses that alter these properties such as temperature and humidity. Non-specific systematic and individual-based interventions designed to mitigate the aerosol route are available although empirical evidence of their effectiveness in controlling transmission of respiratory and enteric viruses in healthcare settings are sparse. The relative importance of aerosol transmission in healthcare setting is still an on-going debate, with particular challenge being the recovery of infectious viral bioaerosols from real-life settings and the difficulty in delineating transmission events that may also be a result of other modes of transmission. For the prevention and control of nosocomial infections via the aerosol route, more research is needed on identifying settings, medical procedures or equipment that may be associated with an increased risk of aerosol transmission, including defining which procedures are aerosol-generating; and on the effectiveness of systematic interventions on aerosol transmission of respiratory and enteric viruses in healthcare settings.

Effect of Mono-2-ethyhexyl Phthalate on DNA Methylation in Human Prostate Cancer LNCaP Cells.

OBJECTIVE: To evaluate whether mono (2-ethylhexyl) phthalate (MEHP) affects genomic DNA methylation and the methylation status of some specific genes such as patched gene (PTCH) and smoothened gene (SMO) in LNCaP cells. METHODS: LNCaP cells were treated with MEHP (0, 1, 5, 10, and 25 µmol/L) for 3 days. An ELISA assay was preformed to detect genomic methylation, including 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC) content. A pyrosequencing assay was applied to assess DNA methylation in PTCH and SMO gene promoters. The correlation between DNA methylation and gene expression was assessed. RESULTS: The proportion of cytosines with 5-mC methylation in LNCaP cells was significantly decreased by MEHP (1, 5, 10, and 25 µmol/L) in a dose-dependent manner (P < 0.01). For genes in the Hedgehog pathway, there was no significant MEHP concentration-dependent difference in the DNA methylation of PTCH and SMO. CONCLUSION: MEHP might affect the progression of prostate cancer through its effect on global DNA methylation.

Maternal Disononyl Phthalate Exposure Activates Allergic Airway Inflammation via Stimulating the Phosphoinositide 3-kinase/Akt Pathway in Rat Pups.

OBJECTIVE: To evaluate the effect of diisononyl phthalate (DINP) exposure during gestation and lacta- tion on allergic response in pups and to explore the role of phosphoinositide 3-kinase/Akt pathway on it. METHODS: Female Wistar rats were treated with DINP at different dosages (0, 5, 50, and 500 mg/kg of body weight per day). The pups were sensitized and challenged by ovalbumin (OVA). The airway response was assessed; the airway histological studies were performed by hematoxylin and eosin (HE) staining; and the relative cytokines in phosphoinositide 3-kinase (PI3K)/Akt pathway were measured by enzyme-linked immunosorbent assay (ELISA) and western blot analysis. RESULTS: There was no significant difference in DINP's effect on airway hyperresponsiveness (AHR) between male pups and female pups. In the 50 mg/(kg·d) DINP-treated group, airway response to OVA significantly increased and pups showed dramatically enhanced pulmonary resistance (RI) compared with those from controls (P<0.05). Enhanced Akt phosphorylation and NF-κB translocation, and Th2 cytokines expression were observed in pups of 50 mg/(kg·d) DINP-treated group. However, in the 5 and 500 mg/(kg·d) DINP-treated pups, no significant effects were observed. CONCLUSION: There was an adjuvant effect of DINP on allergic airway inflammation in pups. Maternal DINP exposure could promote OVA-induced allergic airway response in pups in part by upregulation of PI3K/Akt pathway.

[Changes of the Expression of Brain Derived Neurotrophic Factors in Rats Trachea Induced by Acrolein Exposure].

OBJECTIVE: To investigate expressional changes of brain derived neurotrophic factor (BDNF) in the trachea of rats with acrolein inhalation. METHODS: Twenty two SD rats were divided into 2 groups: the rats in experimental group were subjected to acrolein inhalation for the induce of trachea inflammatory injury, while the rats with saline (NS) inhalation were as control. All the rats were sacrificed in 1,3,6 weeks after acrolein (n = 11 at each time point) or saline inhalation (n = 11 at each time point), the samples of trachea epithelium were harvested. The immunohistochemistry and in situ hybridization was performed to detect the location of BDNF protein and mRNA in trachea. The expression of BDNF mRNA in the trachea tissues were determined by RT-PCR. RESULTS: There are positive cells in epithelium of trachea for BDNF protein and mRNA, with cytoplasm staining. The expression of BDNF mRNA in the trachea was increased at 1 week after acrolein inhalation (P < 0.05, vs. control group), then decreased along with the time and reached to the same level as control group at 3 weeks, then last to 6 weeks (P > 0.05). CONCLUSION: The inflammatory injury in trachea induced by acrolein exposure could be associated with the increased expression of BDNF. BDNF may be one of the crucial inflammatory factors in the process of inflammatory reaction in trachea with acrolein stimulation.

Gender-specific relationship between prenatal exposure to phthalates and intrauterine growth restriction.

BACKGROUND: No study has examined the association between prenatal phthalate exposure and intrauterine growth retardation (IUGR). This study aimed to investigate whether prenatal exposure to phthalates was associated with increased risk of IUGR. METHODS: A total of 126 mother-newborn pairs, including 42 IUGR cases and 84 control newborns and their mothers, were enrolled in this case-control study. Spot urine samples were collected during the third trimester of pregnancy, and 5 phthalate metabolites (mono-n-butyl phthalate (MBP), monomethyl phthalate (MMP), mono-2-ethylhexyl phthalate (MEHP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP)) were measured. RESULTS: Concentrations of MMP, MEHHP, MEOHP, and SumDEHP (MEHP, MEHHP, and MEOHP) were significantly higher in IUGR cases than in normal controls. In all subjects, urinary concentrations of MEHHP and MEOHP were significantly inversely associated with fetal growth indicators (birth weight and Quetelet's index). When mothers were stratified by infant sex, MEHHP and MEOHP concentrations were still negatively associated with fetal growth indicators, while no significant association was observed in females. In addition, exposure-response relationships were observed between MEHHP/SumDEHP concentrations in maternal urine and IUGR. CONCLUSION: Prenatal exposure to phthalates was associated with increased risk of IUGR, and male newborns were more sensitive to phthalates than females.

Cross-sectional study of the relationship of peripheral blood cell profiles with severity of infection by adenovirus type 55.

BACKGROUND: The immunologic profiles of patients with human adenovirus serotype 55 (HAdV-55) infections were characterized in subjects diagnosed with silent infections (n = 30), minor infections (n = 27), severe infections (n = 34), and healthy controls (n = 30) during a recent outbreak among Chinese military trainees. METHODS: Blood was sampled at the disease peak and four weeks later, and samples were analyzed to measure changes in leukocyte and platelet profiles in patients with different severities of disease. Differential lymphocyte subsets and cytokine profiles were measured by flow cytometry and Luminex xMAP®, and serum antibodies were analyzed by ELISA and immunofluorescence staining. RESULTS: Patients with severe HAdV infections had higher proportions of neutrophils and reduced levels of lymphocytes (p < 0.005 for both). Patients with minor and severe infections had significantly lower platelet counts (p < 0.005 for both) than those with silent infections. The silent and minor infection groups had higher levels of dendritic cells than the severe infection group. Relative to patients with silent infections, patients with severe infections had significantly higher levels of IL-17+CD4+ cells, decreased levels of IL-17+CD8+ cells, and higher levels of IFN-γ, IL-4, IL-10, and IFN-α2 (p < 0.001 for all comparisons). CONCLUSIONS: Patients with different severities of disease due to HAdV-55 infection had significantly different immune responses. These data provide an initial step toward the identification of patients at risk for more severe disease and the development of treatments against HAdV-55 infection.

Enhanced production of 2,3-butanediol by overexpressing acetolactate synthase and acetoin reductase in Klebsiella pneumoniae.

Mutants with overexpression of α-acetolactate synthase (ALS), α-acetolactate decarboxylase, and acetoin reductase (AR), either individually or in combination, were constructed to improve 2,3-butanediol (2,3-BD) production in Klebsiella pneumoniae. The recombinant strains were characterized in terms of the enzyme activity, 2,3-BD yield, and expression levels. The recombinant K. pneumoniae strain (KG-rs) that overexpressed both ALS and AR showed an improved 2,3-BD yield. When cultured in the media with five different carbon sources (glucose, galactose, fructose, sucrose, and lactose), the mutant exhibited higher 2,3-BD productivity and production than the parental strain in all the tested carbon sources except for lactose. The 2,3-BD production of KG-rs in a batch fermentation with glucose as the carbon source was 12% higher than that of the parental strain.

Assessment of Exposure to Polybrominated Dipheny Ethers via Inhalation and Diet in China.

OBJECTIVE: This paper is to assess the current status of polybrominated diphenyl ethers (PBDEs) contamination in the environment in China and estimate the exposure to PBDEs in non-occupational populations. METHODS: A total of 80 research papers published from January 2001 to October 2013 were selected. Geographic information system (GIS) was used in mapping PBDE concentrations and distributions in environmental media. Ni's model was applied to calculate ∑PBDE-intake via the intakes of contaminated food, water and air in the Pearl River Delta and Yangtze River Delta. RESULTS: BDE-209 was found to be the major PBDE congener in the environmental media and food in China. PBDE concentrations varied among different areas, among which the contamination in Guangdong Province was most serious. Daily intake of ∑PBDEs was 225.1-446.0 ng/d for adults in the Pearl River Delta, which was higher than the intake for those living in the Yangtze River Delta (148.9-369.8 ng/d). CONCLUSION: Atorvastatin can attenuate LPS-induced TNF-α expression and production by activating HO-1 via the ERK and p38 MAPK pathways, suggesting that atorvastatin can be used in treatment of inflammatory diseases such as sepsis, especially in those with atherosclerotic diseases.

Development of a reference dose for BDE-47, 99, and 209 using benchmark dose methods.

Eleven recently completed toxicological studies were critically reviewed to identify toxicologically significant endpoints and dose-response information. Dose-response data were compiled and entered into the USEPA's benchmark dose software (BMDS) for calculation of a benchmark dose (BMD) and a benchmark dose low (BMDL). After assessing 91 endpoints across the nine studies, a total of 23 of these endpoints were identified for BMD modeling, and BMDL estimates corresponding to various dose-response models were compiled for these separate endpoints. Thyroid, neurobehavior and reproductive endpoints for BDE-47, -99, -209 were quantitatively evaluated. According to methods and feature of each study, different uncertainty factor (UF) value was decided and subsequently reference doses (RfDs) were proposed. Consistent with USEPA, the lowest BMDLs of 2.10, 81.77, and 1698 µg/kg were used to develop RfDs for BDE-47, -99, and -209, respectively. RfDs for BDE-99 and BDE-209 were comparable to EPA results, and however, RfD of BDE-47 was much lower than that of EPA, which may result from that reproductive/developmental proves to be more sensitive than neurobehavior for BDE-47 and the principal study uses very-low-dose exposure.

Dual-role regulator of a novel miR-3040 in photoperiod-mediated wing dimorphism and wing development in green peach aphid.

Wing dimorphism is regarded as an important phenotypic plasticity involved in the migration and reproduction of aphids. However, the signal transduction and regulatory mechanism of wing dimorphism in aphids are still unclear. Herein, the optimal environmental conditions were first explored for inducing winged offspring of green peach aphid, and the short photoperiod was the most important environmental cue to regulate wing dimorphism. Compared to 16 L:8 D photoperiod, the proportion of winged offspring increased to 90% under 8 L:16 D photoperiod. Subsequently, 5 differentially expressed microRNAs (miRNAs) in aphids treated with long and short photoperiods were identified using small RNA sequencing, and a novel miR-3040 was identified as a vital miRNA involved in photoperiod-mediated wing dimorphism. More specifically, the inhibition of miR-3040 expression could reduce the proportion of winged offspring induced by short photoperiod, whereas its activation increased the proportion of winged offspring under long photoperiod. Meanwhile, the expression level of miR-3040 in winged aphids was about 2.5 times that of wingless aphids, and the activation or inhibition of miR-3040 expression could cause wing deformity, revealing the dual-role regulator of miR-3040 in wing dimorphism and wing development. In summary, the current study identified the key environmental cue for wing dimorphism in green peach aphid, and the first to demonstrate the dual-role regulator of miR-3040 in photoperiod-mediated wing dimorphism and wing development.

[Health Risk Assessment for an Arsenic-contaminated Site Based on Monte Carlo Simulation and Parameters Optimization].

Risk assessment is a critical part of risk management for contaminated sites. However， in the specific management practice of As-contaminated sites， it is difficult to obtain realistic health risks for contaminated sites based on the total amount of pollutants and determined values of the model， thus preventing the control requirements of later remediation to be met. An increasing number of studies have recently been conducting risk assessments by considering bioavailability， modification parameters， and combined probabilistic models. To improve the accuracy of risk assessment results， taking a large As-contaminated site as a case， 432 sampling sites were set up and collected at different depths to analyze the level and distribution characteristics of As pollution， and probabilistic risk assessment was conducted with the modification of model parameters through literature research and Monte Carlo simulation. Then， the impact of traditional methods and probabilistic methods on health risk assessment was explored in comparison. The results indicated that ω（As） in the top soil of the study area ranged from 2.70-97.0 mg·kg-1， with a spatial variation coefficient of 0.61 and weaker spatial continuity. The carcinogenic risk and hazard index obtained by the traditional risk assessment method were 2.12E-4 and 8.36， respectively， which obviously overestimated the actual risk level and were not conductive to the refined management of As-contaminated sites. Combined with modification of model parameters and probabilistic risk assessment， the non-carcinogenic risk for adults and children was found to be at an acceptable level， and the carcinogenic risk was reduced by nearly an order of magnitude compared to that in the conventional method. Considering the relative biological effectiveness （RBA） of As， the 95% quantile of the total carcinogenic risk was 1.24E-5， a reduction of up to 36.41% compared to the uncorrected corresponding risk value of 1.95E-5. The carcinogenic risk of soil As for adults and children in the study area exceeded acceptable risk levels 1E-6， with oral ingestion of soil being the primary route of exposure. In addition， the results of the sensitivity analysis of the parameters showed that As concentration， daily oral ingestion rate of soils， and exposure duration of children had relatively larger effects for health risks. This work will provide a methodological and theoretical basis for achieving accurate risk assessment of As-contaminated sites and provide concepts for refined risk management.

[Spatial and Temporal Distribution Characteristics of Ozone Concentration and Population Health Benefit Assessment in the Yangtze River Delta Region from 2017 to 2020].

In recent years, the ozone (O3) concentration has showed a rising trend in China, becoming second only to PM2.5 as an important factor affecting air quality. To grasp the spatial-temporal variations characteristics of O3 and the associated health impacts during the implementation of the three-year plan on defending the blue sky in the Yangtze River Delta (YRD) region, data collected from 210 monitoring stations in the YRD from 2017 to 2020 were analyzed using the global Moran's index and Getis-Ord Gi* index methods, and the associated health benefits of reduced O3 exposure were evaluated using the health risk and environmental value assessment methods. The results showed that during the study period, the interquartile range (IQR) of the annual average O3 concentration and that of the warm season both presented a declining trend. The average O3 concentrations in both warm and cold seasons showed a similar spatial distribution pattern, with the northern part exhibiting the higher concentrations and the southern part showing the lower concentrations. Furthermore, the O3 concentrations in the warm season were characterized by high O3 concentrations clustering in the northern and central part of the region. The proportion of the population exposure to annual average O3 concentration over 160 µg·m-3 decreased from 72.3% in 2017 to 34.8% in 2020 in the YRD. Although the population-weighted annual mean O3 concentration in the whole YRD region showed a downward trend, some cities in western Anhui province, northern Jiangsu province, and central Jiangsu province showed fluctuations and even an increasing trend. In terms of health benefits, there were 3782 cases (95% CI:2050-5511 cases) of avoided premature deaths associated with reduced O3 concentrations in the warm season in 2020 compared to 2017. The total health benefit was 26198 million yuan (95% CI:14201-38175 million yuan). Compared to the cost of the main O3 precursor emission reduction, the cost-benefits ratio was 1:1.67 to 3.23.

USP7 promotes the osteoclast differentiation of CD14+ human peripheral blood monocytes in osteoporosis via HMGB1 deubiquitination.

Background: Abnormal osteoclast and osteoblast differentiation is an essential pathological process in osteoporosis. As an important deubiquitinase enzyme, ubiquitin-specific peptidase 7 (USP7) participates in various disease processes through posttranslational modification. However, the mechanism by which USP7 regulates osteoporosis remains unknown. Herein, we aimed to investigate whether USP7 regulates abnormal osteoclast differentiation in osteoporosis. Methods: The gene expression profiles of blood monocytes were preprocessed to analyze the differential expression of USP genes. CD14+ peripheral blood mononuclear cells (PBMCs) were isolated from whole blood collected from osteoporosis patients (OPs) and healthy donors (HDs), and the expression pattern of USP7 during the differentiation of CD14+ PBMCs into osteoclasts was detected by western blotting. The role of USP7 in the osteoclast differentiation of PBMCs treated with USP7 siRNA or exogenous rUSP7 was further investigated by the F-actin assay, TRAP staining and western blotting. Moreover, the interaction between high-mobility group protein 1 (HMGB1) and USP7 was investigated by coimmunoprecipitation, and the regulation of the USP7-HMGB1 axis in osteoclast differentiation was further verified. Osteoporosis in ovariectomized (OVX) mice was then studied using the USP7-specific inhibitor P5091 to identify the role of USP7 in osteoporosis. Results: The bioinformatic analyses and CD14+ PBMCs from osteoporosis patients confirmed that the upregulation of USP7 was associated with osteoporosis. USP7 positively regulates the osteoclast differentiation of CD14+ PBMCs in vitro. Mechanistically, USP7 promoted osteoclast formation by binding to and deubiquitination of HMGB1. In vivo, P5091 effectively attenuates bone loss in OVX mice. Conclusion: We demonstrate that USP7 promotes the differentiation of CD14+ PBMCs into osteoclasts via HMGB1 deubiquitination and that inhibition of USP7 effectively attenuates bone loss in osteoporosis in vivo.The translational potential of this article:The study reveals novel insights into the role of USP7 in the progression of osteoporosis and provides a new therapeutic target for the treatment of osteoporosis.

[The role of BDNF in brain ischemia pulmonary edema].

Brain ischemia pulmonary edema(BIPE)is a critical type of the neurogenic pulmonary edema (NPE), with acute development and progression and high mortality. The study on mechanism of BIPE has important scientific significance and substantial practice values. NPE, as a complicated physiopathology condition, is not resulted from single factor but systemic events including the changes in nervous system, body fluid regulation and endocrine involved in central nervous system after the injury. The studies on this topic in this current issue suggested that brain-derived neurotrophic factor (BDNF) could involve in the pathogenesis procedure of NPE following brain ischemia, which indicated that the crucial role of BDNF in the NPE after BIPE. The findings of these studies pave a way for the treatment of BIPE by using BDNF administration in future clinic trail.

[Expression of trkB gene in the pulmonary tissue of rats with lung injury induced by cerebral ischemia].

OBJECTIVE: To investigate the expression of tyrosine kinase B (trkB) in lung tissue of rats with lung injury induced by brain ischemia. METHODS: Twenty six adult SD rats were divided into sham group and brain ischemia lung injury (BILI) group. All rats were sacrificed at 3 days after the operation of modeling, lung tissues were then harvested to measure the protein and mRNA level of trkB by the methods of western blot and RT-PCR, the location of trkB positive cells was observed by immunochemistry study. RESULTS: trkB mRNA level in the lung tissue of rats with brain ischemia presented a significant increase, in corresponding to the upregulation of BDNF protein levels, when compared with sham one (P<0.05). trkB was localized in endothelia cells and smooth muscle. CONCLUSION: The upregulated expression of trkB expression may be associated with lung injury after brain ischemia.

[Expression changes of BDNF in lung of rats subjected to brain ischemia].

OBJECTIVE: To investigate the expression of brain-derived neurotrophic factor (BDNF) in lung injury induced by brain ischemia in rats. METHODS: 46 adult SD rats were assigned randomly to sham operation group and brain ischemia lung injury group (BILI, n = 23 in each group). Rats were subjected brain ischemia and allowed to survived 3 d. After performed neurological functional severe deficit evaluation, lung edema was observed (n=5). The BDNF expression for its mRNA and protein in lung tissues was determined by using ELISA (n=5) and RT-PCR technique (n=8). The localization of BDNF was also determined by immunohistochemistry (n=5). RESULTS: After brain ischemia for 3 days, the severe neurological functional deficit and edema in lung were seen. BDNF was located in cytoplasma of smooth muscle and epithial cells in the lung. The level of BDNF mRNA (indicated by RT-PCR) and the protein level (indicated by ELISA) were all upregulated at 3 days after brain ischemia (P<0.05). CONCLUSION: Lung edema occurred after brain ischemia in rats is concomitant with BDNF expression, which consists of the mechanism involved lung injury induced by brain ischemia.

[Expression changes of MEK in lung of rats subjected to brain ischemia].

OBJECTIVE: To explore the expression changes of mitogen extracellular kinase (MEK) in injured lung after brain ischemia in rats. METHODS: Adult SD rats were assigned randomly to sham operation group and brain ischemia lung injury (BILI) group. Rats in BILI group were subjected brain ischemia and allowed to survived 3 d. Pathalogical changes in lung were indicated by HE staining. The MEK expression was determined by RT-PCR and Western blot technique. RESULTS: After brain ischemia, the bulk of inflammatory cells invaded into lung were observed. Upregulated level of MEK mRNA and protein were found at 3 days after ischemia (P<0.05). CONCLUSION: The upregulated expression of MEK implied that the MEK may play some roles in lung injury after brain ischemia.

[Expression of TNF-alpha in lung tissue of rats with lung injury induced by brain ischemia].

OBJECTIVE: To investigate the expression of tumor necrosis factor-alpha (TNF-alpha) in the lung tissue of rats with lung injury induced by brain ischemia. METHODS: The rat model of lung injury induced by brain ischemia was established. At 24 h, 48 h, 72 h after brain ischemia, lung tissues were harvested from each rats, the expressions of TNF-alpha mRNA and protein and its distributions in the lung tissue were measured by the methods of RT-PCR (n=8), Western blot (n=8), and immunohistochemistry (n=5), respectively. RESULTS: The increase of TNF-alpha mRNA and protein levels were found in the lung tissues after brain ischemia, when compared with sham group (P<0.05). The morphological study with immunohistochemical staining observed TNF-alpha positive reaction in epithelial cells and some macrophages in the lung tissues after brain ischemia. CONCLUSION: The expression of TNF-alpha in the lung tissue could be upregulated in the rats with brain ischemia.

[Expression changes of IL-1beta in lung of rats subjected to brain ischemia].

OBJECTIVE: To study the expression changes of interleukin-1beta (IL-1beta) in the lung of rats with brain ischemia. METHODS: Adult SD rats were divided into sham operation group and brain ischemia lung injury (BILI) group randomly. Focal cerebral ischemia inflammatory lung injury model was developed with intraluminal thread technique. Lungs were harvested from rats at different time point respectively. RT-PCR (24 h), Western blot (48 h) and immunohistochemistry (72 h) were employed to detect the expressional changes and the distributions of IL-1beta in the lung tissues. RESULTS: IL-1beta immunohistochemical positive reaction was observed in epithelia cell and neutrophil as well as macrophage. Increased protein level and mRNA expression for IL-1beta were found in lung after brain ischemia compared with those of sham group. CONCLUSION: IL-1beta, as a crucial inflammatory factor, could be associated with airway inflammation in lung following brain ischemia in rats.