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An abnormal level of SO2 is closely related to many diseases. Therefore, developing an effective method for the detection of SO2 in biological environments has important physiological and pathological significance. In this work, a new fluorescent probe (CA-SO2) was designed and synthesized for efficiently and specifically detecting SO2 derivatives through nucleophilic addition reaction. The novel fluorescent probe (CA-SO2) showed high selectivity, fast response time (within 50 s), and low detection limit (LOD = 75 nM). Furthermore, after adding SO2 derivatives to the probe solution, the color of the solution changes from orange to colorless, which allows “naked eye” detection for SO2. Moreover, the probe has a large Stokes shift (129 nm) and excellent biocompatibility. The probe has been successfully applied to the detection of SO2 derivatives in living cells and zebrafish.

Evidence shows that psychosocial stress exacerbates asthma, but there is little intervention to alleviate negative effects of psychosocial stress on asthma. We investigated the role of icariin in anti-inflammation and anti-anxiety potential in a murine model combined psychosocial stress with allergic exposure. The results indicated that icariin administered remarkable increased activity in the center of the open field, reversed airway hyperresponsivenesss, reduced inflammatory cytokine infiltration to the lung and whole body and also in part recovered glucocorticoid responsiveness. Furthermore, our data also showed that icariin significantly inhibited increases of corticosterone and markedly increased glucocorticoid receptor mRNA and protein expression in the lungs of mice exposed to both stress and allergen. Collectively, we speculate that inducing glucocorticoid receptor modulation might be the potential mechanisms of icariin to facilitate corticosteroid responsiveness of cytokine production.

To investigate the features of airway inflammation and hypothalamic-pituitary-adrenal axis (HPAA) activity in patients with asthma accompanied by depression.Adult asthmatics were recruited and enrolled into one of the two groups based on scores on the Hamilton Depression Rating Scale (HAMD): asthmatics with depression (HAMD score ≥8, n = 23), and asthmatics without depression (HAMD score8, n = 41). In addition, 27 healthy individuals and 21 adults with depression only were enrolled as controls. Induced sputum and blood samples were collected for measurement of cytokines and other inflammatory factors. The diurnal rhythm profiles of salivary cortisol and other hormones were obtained for assessment of the HPAA activity.For the group of asthmatics with depression, the mean HAMD score was 19.0, and for the group of asthmatics without depression, the HAMD score averaged 4.9(p.001). Serum and sputum tumor necrosis factor alpha (TNF-α) were significantly higher in asthmatics with depression than those in the other groups (p.05) while serum interferon-gamma (IFN-γ) was lower in asthmatics with depression than that in the other groups (p.05). Twenty-four-hour urinary cortisol, salivary cortisol at 8 a.m. and 4 p.m. were lower in asthmatics with depression compared to other groups (p.05).As compared to healthy individuals and those with asthma or depression alone, individuals with comorbid depression and asthma showed the highest level of pro-inflammatory cytokines and the lowest level of anti-inflammatory cytokines and cortisol. These observations may serve as a valuable reference for diagnosis and clinic therapies of depression in asthmatics.

In order to identify the kinship of Shaolingyuan ancient human excavated from Shaolingyuan archaeological site with high level of certainty, and infer racial origins more clearly and reliably, this paper analyzed the hereditary constitution of this population. We used the “Reverse root canal technique” to extract ancient DNA from 28 teeth in 28 skeletal remains (3057-2784 BP) of Shaolingyuan archaeological site, obtained the sequences of mtDNA Hypervariable region I (HVR-I) by PCR amplifications; then used MEGA 5.5 software to construct phylogenetic trees and compared the sequences among the sequences of interraces, intraraces. The phylogenetic tree showed that there were two major clusters, Cluster 1 with 16 individuals, and Cluster 2 with 5 individuals. Either the genetic gap or the geographic position of the individuals was small. The frequency of SNP site 16223 T > C was 71.4%, significantly higher than other sites. The comparisons of different population demonstrated that there is no significant difference among them. All of them shared the same haplogroup L1’2’3’4’5’6, close to African. Finally, we confirm that there is a very close genetic relationship between some individuals in this cemetery. We regarded Shao-lingyuan Western Zhou cemetery as a family cemetery, and these people belong to East Asia lineage.

Excessive corticosterone (CORT) is acknowledged to induce neuronal damage in a number of regions of the brain, particularly the hippocampus, the main area implicated in depression. However, little research has been conducted on alterations to hypothalamic neurons in depression and the cellular and molecular basis for these changes. In the present study, we aimed to determine whether CORT causes apoptosis in primary cultured hypothalamic neurons, and to investigate the protective effects of icariin, an active natural ingredient from the Chinese plant, Epimedium sagittatum Maxim. Our study demonstrates that exposure of hypothalamic neurons to CORT causes a significant loss in viability, a significant decrease in mitochondrial membrane potential, an increase in caspase-3 activity, an elevation in intracellular reactive oxygen species elevation and decreased superoxide dismutase activity. However, pretreatment of cells with icariin prior to CORT exposure was identified to noticeably suppress these CORT-induced events. Furthermore, icariin may prevent CORT-induced cell death via activation of the PI3-K/Akt pathway. In conclusion, icariin is able to prevent CORT-induced hypothalamic cell apoptosis via activation of the PI3-K/Akt pathway.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by airway obstruction and progressive lung inflammation, which is insensitive to corticosteroids therapies. In this study, we investigated the mechanism underlying the attenuation of cigarette smoke (CS)-induced respiratory inflammation by baicalin, a flavonoid compound isolated from the root of Scutellaria baicalensis Georgi, in vivo and in vitro. In vivo, mice were exposed to smoke of 15 cigarettes for 1 h/day, 6 days/week for 3 months and dosed with baicalin (25, 50 and 100mg/kg) or dexamethasone (1mg/kg). In vitro, A549 cells were incubated with baicalin (10, 50 and 100 μM) or dexamethasone (10(-12), 10(-10), 10(-8) and 10(-6)M) followed by treatments with cigarette smoke extract (CSE, 2.5 and 5%), or TNF-α (10 ng/ml), or trichostatin A (TSA, 100 ng/ml). We found that baicalin significantly protected pulmonary function and attenuated CS-induced inflammatory response by decreasing inflammatory cells and production of TNF-α, IL-8 and MMP-9. This result was not found in the group treated with dexamethasone. Baicalin also showed efficacy in enhancing histone deacetylase (HDAC)2 activity and protein expression, however, it did not affect HDAC2 mRNA. Further studies revealed that baicalin inhibited HDAC2 phosphorylation, suggesting that it may directly affect the protein structure and effect by modification at post-translational level. Together these results suggest that baicalin has anti-inflammatory effects in cigarette smoke induced inflammatory models in mice and A549 cells, possibly achieved by modulating HDAC2.

This study aimed to investigate the mechanism underlying the attenuation of LPS-induced lung inflammation by icariin in vivo and in vitro. The anti-inflammatory effects of icariin on LPS-induced acute inflammatory and the molecular mechanism were investigated. Pretreatment with icarrin (20mg/kg) could attenuate acute lung inflammation by inhibiting mRNA expressions of tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), metalloproteinase cycloxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in the lung of LPS-treated mice. In addition, icariin suppressed the secretion of TNF-alpha, prostaglandin E2 (PGE(2)) and nitric oxide (NO) as well as NF-kappaB p65 activation. Furthermore, decreased myeloperoxidase (MPO) activity was observed in the lung tissue and LPS-induced cytotoxicity in the RAW 264.7 macrophages cells was also markedly attenuated by icariin. Western blotting analysis and confocal microscopy showed that icariin pretreatment reduced the nucleus transportation and constant level of NF-kappaB p65 in the RAW 264.7 macrophage cells. However, the protective effects of icariin were reversed by a PI3K/Akt inhibitor (wortmannin). Our in vitro and in vivo results suggested that activation of the PI3K/Akt pathway and the inhibition of NF-kappaB were involved in the protective effects of icariin on LPS-induced acute inflammatory responses.

In China, many surveys have shown that most people do not have a correct understanding about cold and administration of anti-cold Chinese patent medicine preparations. The author conducted a systematic summary and analysis on the actual application of anti-cold Chinese patent medicine preparations as well as the warning on safe application of anti-cold Chinese patent medicine preparations in Clinical Medication Information of China Pharmacopoeia, in the expectation of reducing the blind application of anti-cold Chinese patent medicine preparations and providing traditional Chinese medicine pharmacists new ideas in monitoring the safe application of exterior syndrome-relieving Chinese patent medicine preparations.

Numerous epidemiological and experimental animal studies have indicated that chronic psychological stress may promote tumor development. However, the underlying molecular mechanisms by which chronic stress promotes tumorigenesis remain to be fully elucidated and animal models have not yet been well established. In the present study, an established mouse model of repeated social defeat stress (RSDS), was generated and used to investigate the effect of stress on tumor growth and metastasis. C57BL/6 mice were exposed to RSDS for 10 days, followed by subcutaneousl inoculation with Lewis lung carcinoma cells for seven days. The tumor weight and volume as well as the number of the lung metastatic nodules were then determined. Vascular endothelial growth factor (VEGF) serum levels were measured using ELISAs. In addition, expression levels of VEGF receptor (VEGFR) and L1 cell adhesion molecule (L1CAM) messenger (m)RNA were confirmed using reverse transcription quantitative polymerase chain reaction. Furthermore, protein expression levels of phosphorlyated extracellular signal-regulated kinase (pERK), matrix metalloproteinase (MMP)-2 and MMP-9 were examined using western blot analysis. The results showed that RSDS significantly increased the weight and the volume of the primary tumor as well as the number of the lung metastatic nodules. Serum VEGF levels were significantly higher in the tumor-stress group compared with those of the unstressed tumor mice. In addition, tumors in stressed animals demonstrated markedly enhanced expression of VEGFR-2 and L1CAM mRNA as well as pERK, MMP-2 and MMP-9 protein expression. In conclusion, these results suggested that RSDS contributed to lung cancer progression, angiogenesis and metastasis, which was partially associated with increased VEGF secretion and therefore the activation of the ERK signaling pathway, resulting in the induction of MMP-2 and MMP-9 protein expression.

To extracted DNA from ancient human teeth dated 3000 years ago unearthed in Xi'an and determine the genders for the individuals.Thirty five ancient human teeth were studied. A 'Reverse-root-canal' technique and a Chelex-100 solution were used to extract the DNA. Specific primers for Amelogenin gene were designed for PCR amplification.Genomic DNA was successfully extracted from 30 samples, for which 8 were determined to be males and 22 were females.The 'Reverse-root-canal' technique may be used for extracting DNA from ancient human teeth. Genetics method can supplement physical anthropology for determination of sex for ancient samples.

Airway remodeling is an important characteristic of asthma, linking inflammation with airway hyperresponsiveness. Baicalin, a major active component, was isolated from Radix Scutellariae. Many studies show that baicalin has anti-inflammatory, anti-bacterial, and anti-allergic effects. Here we investigate the influence of baicalin on asthmatic airway remodeling and the mechanism underlining the anti-remodeling effect in vivo. Asthmatic airway remodeling mice model was established by ovalbumin exposure. Seventy female BALB/c mice were randomly assigned to seven experimental groups: blank, ovalbumin, hexadecadrol, control, and baicalin (25 mg/kg, 50 mg/kg, 100 mg/kg) groups. Pulmonary function was measured using a whole-body plethysmograph in conscious and unrestrained mice. The lung pathology was observed and measured. The production of cytokines in bronchoalveolar lavage fluid and serum was measured using enzyme-labeled immunosorbent assay kits, and the expression levels of transforming growth factor-β 1 and vascular endothelial growth factor were detected by immunohistochemistry. The protein expression levels of transforming growth factor-β 1, vascular endothelial growth factor, extracellular signal–regulated kinase, and p21ras were measured using Western blot. The results show that ovalbumin exposure significantly increased the expression of interleukin-13 in BALF and serum, and transforming growth factor-β 1, vascular endothelial growth factor, extracellular signal–regulated kinase and p21ras expressions in the lungs. Baicalin attenuated the effects of ovalbumin significantly. It can be concluded that baicalin has significant anti-remodeling effect on ovalbumin-induced asthmatic airway remodeling mice model by decreasing expression of transforming growth factor-β 1, interleukin-13, and vascular endothelial growth factor and inhibiting the activation of the extracellular signal–regulated kinase pathway.

It has already been recognized that psychosocial stress evokes asthma exacerbation; however, the mechanism of how stress gets inside the body is not clear. This study aimed to observe the impact of psychosocial stress on airway inflammation and its mechanism in the ovalbumin-induced asthmatic mice combined with social disruption stress.Thirty-six male BALB/c mice were randomly divided into: control group, asthma group (ovalbumin-induced), asthma plus social disruption stress group (SDR), and SDR group. The open field video tracking system was used to assess animal behaviors. The invasive pulmonary resistance (RL) and dynamic lung compliance (cdyn) test system from Buxco was applied to detect pulmonary function. The enzyme-linked immunosorbent assay (ELISA) was utilized to determine OVA-IgE, T-helper type 2 (Th2) cytokines (IL-4, IL-5, IL-13) and corticosterone in mouse serum, the Th2 cytokines (IL-4, IL-5, IL-13, IL-6, TNF-α) in bronchoalveolar lavage fluid (BALF), and IL-6 and TNF-α levels in the supernatant of splenocytes cultured in vitro. Hematoxylin-eosin (HE) staining was used to assess airway inflammation in lung histology. The cell count kit-8 assay (CCK-8) was applied to evaluate the inhibitory effect of corticosterone on splenocyte proliferation induced by lipopolysaccharide (LPS). Real time-PCR and Western blotting were utilized to determine glucocorticoid receptor (GR) mRNA and GR protein expression in lungs.The open field test showed that combined allergen exposure and repeated stress significantly shortened the time the mice spent in the center of the open field (P0.01), increased ambulatory activity (P0.01) and the count of fecal boli (P0.01), but deceased vertical activity (P0.01). Results from pulmonary function demonstrated that airway hyperresponsiveness (AHR) was enhanced by psychosocial stress compared with allergy exposure alone. The ELISA results showed that cytokines in serum and BALF were significantly increased (P0.05). Moreover, the lung histology showed that infiltrated inflammatory cells were significantly increased in the asthma-SDR group compared with the asthma group (P0.05). Interestingly, serum corticosterone was remarkably raised by psychosocial stress (P0.05). In addition, the inhibitory effect of corticosterone on IL-6 and TNF-α in LPS-stimulated splenocyte cultures in vitro was diminished in the asthma-SDR group compared to the asthma group. The CCK-8 test revealed that the inhibition effect of corticosterone on splenocyte proliferation induced by LPS was significantly impaired in the SDR and asthma-SDR groups, while no significant effect was observed in the control and asthma groups. Furthermore, expression of GR mRNA and GR protein were significantly reduced in the lung tissues of the asthma-SDR group (P0.05).Social disruption stress can promote anxiety behavior, activate the hypothalamic-pituitary-adrenal (HPA) axis, increase AHR and inflammation, and also impair glucocorticoid sensitivity and its function in a murine model of asthma. The down-regulation of GR expression induced by social disruption stress is in part associated with glucocorticoid insensitivity, which leads to asthma exacerbation.

Objective: To investigate serum and sputum cytokine profiles in asthma and chronic obstructive pulmonary disorder (COPD). Methods: Clinical characteristics, blood and sputum samples were collected from asthma (n = 37) and COPD (n = 36) patients, and healthy subjects (n = 39). Cytokines were measured by enzyme-linked immunosorbent assay (ELISA) and inflammation antibody array; levels were analysed according to smoking status and presence of eosinophilia in the airways of COPD/asthma patients, and compared with those in healthy subjects. Results: ELISA revealed a significant difference in the expression of only a few cytokines in the COPD versus asthma groups, and in both patient groups compared with healthy subjects. The antibody array showed greater differentiation in inflammatory mediators. In the subphenotype analysis, the differential expression of cytokines was more significant between eosinophilic and noneosinophilic airway inflammation than between asthma and COPD, according to both the ELISA and antibody array. There was little difference in cytokine expression between smoking and nonsmoking subgroups. Conclusions: Differential expression of inflammatory mediators is present between patients with COPD or asthma, and eosinophilic or noneosinophilic airway inflammation, and contributes to understanding the cytokine network of airway inflammation.

To study the correlation between the inflammatory factors in the serum and the induced sputum and the hypothalamic-pituitary-adrenal (HPA) axis function in advanced lung adenocarcinoma patients of different syndromes.Totally 71 patients with advanced lung adenocarcinoma were assigned to three groups according to syndrome differentiation, i.e., Shen-yang deficiency (SYD) group (28 cases), Fei-qi deficiency (FQD) group (23 cases), and yin deficiency fire excess (YDFE) group (20 cases). Another 41 healthy subjects were enrolled as the normal control group. Sputum was induced and blood samples were collected for measurement of cytokines including tumor necrosis factor alpha (TNF-alpha), transforming growth factor beta (TGF-beta), interleukin-6 (IL-6), and interferon gamma (INF-gamma). The cytokine assay was performed using Bio-Plex Pro multi assay technology. 24-h collection of urine was performed and salivary samples of the diurnal rhythm profiles [including urinary free cortisol (UFC), urinary 17-hydroxycorticosteroids (17-OH), urinary 17-ketosteroid (17-KS), and cortisol in the serum and saliva] were obtained for assessment of the HPA axis activity.A higher level of serum IL-6 and a lower level of 24-h UFC and 17-OH were found in the SYD group (P0.05). The urinary 17-KS was obviously lower in the SYD group than in the normal control group and the YDEE group (P0.05). Compared with the FQD group and the normal control group, a higher serum level of TNF-alpha and a lower level of IFN-gamma were found in the SYD group and the YDFE group (P0.05). The TNF-alpha and TGF-beta levels in the induced sputum obviously increased in the SYD group (P0.05). The IFN-gamma level in the induced sputum obviously decreased in the YDFE group (P0.05). The serum and salivary cortisol obviously decreased from 8: 00 am to 8:00 am the next morning in the SYD group (P0.05). The serum cortisol level was negatively correlated with serum TNF-alpha (r = -0.26, P = 0.03) and serum IL-6 (r = -0.25, P = 0.03). The salivary cortisol level was negatively correlated with IL-6 in the induced sputum (r = -0.29, P = 0.02). The serum IFN-gamma was positively correlated with urinary 17-OH (r = 0.21, P = 0.03).The inflammatory factors of advanced lung adenocarcinoma patients of SYD syndrome were up-regulated, with the most obvious decreased or disarranged HPA axis functions. The levels of IL-6, TNF-alpha, and IFN-gamma were closely correlated with the HPA axis functions. The transformation from qi deficiency, yin deficiency to Shen-yang deficiency existed in lung adenocarcinoma patients. The levels of IL-6, TNF-alpha, and IFN-gamma in the serum and the induced sputum, as well as the HPA axis functions are important indices for microscopic syndrome typing of lung adenocarcinoma.

Effects of icariin on airway inflammation in asthmatic rats and the intervention of LPS induced inflammation are interfered with the machanism of icariin. Our study aimed to observe the effect of icariin on ovalbumin-induced imbalance of Th1/Th2 cytokine expression and its mechanism.Sixty male SD rats were randomly divided into control group (PBS), asthma group (ovalbumin (OVA)-induced), dexamethasone group, and OVA+icariin low, medium and high dose groups (5, 10, 20 mg/kg, respectively). Each group had ten rats. The model of OVA sensitization was a rat asthma model. Enzyme-linked immunosorbent assay (ELISA) method was used to observe the effects of icariin on interleukin-4 (IL-4) and inerferon γ (IFN-γ) in rats' lung tissue. Immunohistochemical staining was applied to detect the intervention effects of icariin on T cells (T-bet) and gatabinding protein 3 (GATA-3) in rat pulmonary tissue. Realtime RT-PCR was used to observe the intervention effects of icariin on T-bet and GATA-3 mRNA expression in rat pulmonary tissue and spleen lymphocytes. Western blotting was used to observe the icariin intervention effects on T-bet, GATA-3 and nuclear factor-Kappa B (NF-κB) p65 protein expressions in rat pulmonary tissue.The ELISA results from pulmonary tissue showed that IL-4 expression was significantly reduced (P0.05), while the IFN-γ expression increased but not significantly when we compared OVA+icariin medium and high dose groups with the asthma group. Immunohistochemical staining of pulmonary tissue showed that the GATA-3 decreased significantly while the T-bet staining did not change in the OVA+icariin high dose group. In pulmonary tissue and spleen lymphocytes T-bet and GATA-3 mRNA expressions were significantly reduced (P0.05) in icariin treatment groups compared with the asthma model group. GATA-3 and T-bet mRNA in rat spleen lymphocytes in the asthma group were higher than in the control group. GATA-3 mRNA expression in pulmonary tissue significantly decreased (P0.05) while T-bet mRNA expression decreased but not significantly in the icariin treatment group compared with the asthma group. T-bet and GATA-3 protein expressions in pulmonary tissue increased significantly compared with the asthma group, which meant that icariin could inhibit the increase of GATA-3 protein, but not of T-bet. The bronchus, blood vessels and periphery pulmonary tissue had infiltration of inflammatory cells in the OVA+icariin high dose group while NF-κB p65 cells were reduced, and expression of NF-κB p65 in this group was less than in the asthma group. The expression of total p65 protein decreased with icariin treatment while the expression of cytoplasmic p65 protein increased.Icariin could regulate the imbalance of Th1/Th2 cytokines in asthmatic rat pulmonary tissue. Icariin could regulate the imbalance of Th1/Th2 associated transcription factors T-bet and GATA-3 in asthmatic rat pulmonary tissue and spleen lymphocytes. Icariin could inhibit the activation of NF-κB p65 protein in asthmatic rat pulmonary tissue.

To observe the effect of Bushen Huoxue Recipe (BSHXR, a Chinese medicine recipe for Shen reinforcing and blood circulation activating) on the levels of urinary albumin, interleukin-6 (IL-6), transforming growth factor-beta1 (TGF-beta1), and monocyte chemotactic protein-1 (MCP-1) in chronic nephritis patients of Shen-deficiency blood-stasis syndrome.Forty-five patients were blocking assigned randomly to two groups, fifteen patients in the control group and thirty in the treatment group. All orally took Monopril 10 mg, once daily. But BSHXR was given additionally to patients in the treatment group after decocting,one dose per day (taken in two times). The treatment course for both groups was eight weeks. Besides, a normal control group consisting of six healthy subjects from health examination of Shuguang Hospital was set up. The 24-h urinary albumin and contents of TGF-beta1, IL-6 and MCP-1 in urine of all subjects were observed.Compared with before treatment the 24-h urinary albumin was obviously reduced in the treatment group, showing significant difference (P0.01). The urinary 24-h albumin decreased in the control group, with statistical significance (P0.05). Statistical difference existed between the treatment group and the control group after treatment (P0.01). Compared with before treatment, urinary levels of IL-6, TGF-beta1, and MCP-1 were all down-regulated in the treatment group and the control group after treatment (P0.01), and the decreasing of IL-6 and TGF-beta1, levels was more significant in the treatment group statistically (P0.05).BSHXR could attenuate the albuminuria in patients of chronic nephritis. Its mechanism might be possibly correlated with its down-regulation of IL-6, TGF-beta1, and MCP-1 levels.

To investigate the effect and acting mechanism of Bushen Huoxue Recipe (BHR) on the state of extracellular matrix in glomerulosclerosis (GS) rats model.GS rat model was established by unilateral nephrectomy and adriamycin injection. Model rats were randomly divided into 4 groups: the normal control group, the model group, the test group treated by BHR, and the positive control group treated with fosinopril sodium, with 11 rats in each group. The 24 h urinary protein and renal function of rats were observed, the contents of matrix metalloproteinase 1 (MMP-1), tissue inhibitor of metalloproteinase 1 (TIMP-1) in renal tissue and transforming growth factor-beta1 (TGF-beta1) in blood plasma, and renal tissue were detected.Compared with those in the normal control group, 24 h urinary protein was increased and renal function was deprived in the model group; TIMP-1 expression increased, MMP1 expression decreased in renal tissue of rats in the model group, showing statistical difference between groups (P0.05). As compared with the model group, the abnormal changes of TIMP-1 and MMP1 expressions were ameliorated in the two groups treated either by BHR or fosinopril (P0.05). The content of TGF-beta1 in the model group, either in blood or in renal tissue, was significantly higher than those in the normal control group respectively (P0.01), showing no significant change after BHR treatment.The protective effect of BHR on renal function in rats with GS is possibly by way of influencing expressions of TGF-beta1, TIMP-1 and MMP1 to regulate the state of extracellular matrix and lessen the matrix aggregation.

Neurons are damaged following prolonged exposure to high concentrations of corticosterone, particularly during chronic inflammatory and immune diseases. One of the main mechanisms underlying neuronal injury is apoptosis. In the present study the neuroprotective effects of icariin, an active natural ingredient from the Chinese plant Epimedium sagittatum maxim against corticosterone-induced apoptosis were examined in primary cultured rat hippocampal neuronal cells. Pre-treatment of neuronal cells with icariin suppressed corticosterone-induced cytotoxicity in a dose-dependent manner. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP) nick-end-labeling assay (TUNEL) labeling demonstrated that icariin significantly reduced TUNEL-positive cell numbers induced by exposure of cultured neurons to corticosterone. Moreover, icariin markedly inhibited corticosterone-induced mitochondrial dysfunction, including improved mitochondrial membrane potential and inhibition of caspase-3 activation. Using western blot analysis, corticosterone activated p38MAPK, extracellular regulated kinase 1/2(ERK1/2) ,and c-jun N-terminal protein kinase 1(JNK1) ,while icariin blocked p38 MAPK, but not JNK1 or ERK1/2. Pharmacological approaches showed that the activation of p38MAPK plays a critical role in corticosterone-induced mitochondrial dysfunction and apoptosis. Taken together, the present results suggest that the protective effects of icariin on apoptosis in hippocampal neuronal cells are potentially mediated through blockade of p38 MAPK phosphorylation.

Bronchial asthma (BA) and chronic obstructive pulmonary disease (COPD) are both inflammatory airway diseases with different characteristics. However, there are many patients who suffer from both BA and COPD. This study was to evaluate changes of inflammatory airway features and hypothalamic-pituitary-adrenal (HPA) axis function in asthmatic rats combined with COPD.Brown Norway (BN) rats were used to model the inflammatory airway diseases of BA, COPD and COPD + BA. These three models were compared and evaluated with respect to clinical symptoms, pulmonary histopathology, airway hyperresponsiveness (AHR), inflammatory cytokines and HPA axis function.The inflammatory airway features and HPA axis function in rats in the COPD + BA model group were greatly influenced. Rats in this model group showed features of the inflammatory diseases BA and COPD. The expression of inflammatory cytokines in this model group might be up or downregulated when both disease processes are present. The levels of corticotrophin releasing hormone mRNA and corticosterone in this model group were both significantly decreased than those in the control group (P0.05).BN rat can be used as an animal model of COPD + BA. By evaluating this animal model we found that the features of inflammation in rats in this model group seem to be exaggerated. The HPA axis functions in rats in this model group have been disturbed or impaired, which is prominent at the hypothalamic level.

The most common cause of death from paraquat (PQ) poisoning is respiratory failure from pulmonary fibrosis, which develops through pathological overproduction of extracellular matrix proteins such as collagens. In this study, a MicroCT system was used to observe dynamic changes of pulmonary fibrosis in rats with PQ poisoning, and find the characteristics of interstitial lung diseases via density-based and texture-based analysis of CT images of the lung structure.A total of 15 male SD rats were randomly divided into a control group (n=5) and a PQ poisoning group (n=10). The rats in the poisoning group were intraperitoneally administered with 4 mg/ mL PQ at 14 mg/kg, and the rats in the control group were administered with the same volume of saline. The signs of pulmonary fibrosis observed by the MicroCT included ground-glass opacity, nodular pattern, subpleural interstitial thickening, consolidation honeycomb-like shadow of the lung.Compared with the control group, the rats with acute PQ poisoning had different signs of pulmonary fibrosis. Ground-glass opacity and consolidation of the lung appeared at the early phase of pulmonary fibrosis, and subpleural interstitial thickening and honeycomb-like shadow developed at the middle or later stage. MicroCT images showed that fibrotic lung tissues were denser than normal lungs, and their density was up-regulated with pulmonary fibrosis. There was no difference in the progress of pulmonary fibrosis between the right lung and the left lung (P0.05), but there were differences in fibrosis degree at different sites in the lung (P0.05 or P0.01). Pulmonary fibrosis was mainly seen in the exterior area of the middle-lower part of the lung.Imaging can show the development of pulmonary fibrosis in PQ poisoning rats, and this method may help to administer drugs more reasonably in treating pulmonary fibrosis.

This retrospective study evaluated the diagnostic accuracy of 2-(F18)-fluoro-2-deoxy-D-glucose-positron emission tomography ((18)F-FDG-PET)/computed tomography (PET/CT) in the preoperative diagnosis of metastatic mediastinal and hilar lymph node in patients with non-small-cell lung cancer (NSCLC).A total of 39 patients received preoperative (18)F-FDG PET/CT and the postoperative biopsy. We compared preoperative PET/CT scan results with corresponding intraoperative histopathalogic findings in 39 NSCLC patients. The sensitivity, specificity, accuracy, positive and negative predictive value of (18)F-FDG PET/CT were assessed.Histopathologic examination confirmed metastasis in 57 out of the 208 excised lymph nodes; 23 of the 57 nodes were mediastinal and hilar lymph nodes. The sensitivity, specificity, accuracy, positive predictive value and negative predictive value of PET/CT in the preoperative diagnosis of mediastinal lymph node metastasis in NSCLC patients were 65%, 96.8%, 92%, 78.5% and 90%, respectively.PET/CT scan showed good accuracy in the preoperative diagnosis of mediastinal and hilar lymph node metastasis in the patients with NSCLC. We recommend that PET/CT scanning be used as a first-line evaluation tool for tumor diagnosis, therapy evaluation and follow-up.

To determine the expression and possible function of CIC-5 during the rat tooth germ development.Isolated total mRNA and protein from the rat tooth germs which were at different stages of development. RT-PCR and Western blot were used to investigate the mRNA and protein expression of the CIC-5 in the rat tooth germ.The mRNA and protein of CIC-5 expressed in the late bell stage, but undetected inThe mRNA and protein of CIC-5 expressed in the late bell stage, but undetected in the early or middle bell stage.These results showed the spatial temporal distribution of expression of CIC-5 during the different stages of the rat tooth germ development and suggested that it might contribute to the rat tooth germ development.

To determine the transfection efficiency and transient expression of pIDO-EGFP gene in primarily cultured C57 articular cartilage of mice, and to establish a transfection method of the primarily cultured articular cartilage in mice.Plasmid IDO-EGFP was amplified in Escherichia coli. The primarily cultured mouse chondrocytes which were initially obtained from articular cartilage were cultured in vitro and transfected with pIDO-EGFP by lipofectamine2000 reagent under optimized condition. Transfection process and transient expression were evaluated by fluorescent microscopy and laser scanning confocal microscopy (LSCM), and transfection efficiency was determined by flow cytometry.There was obvious expression of EGFP at 24 h after transfection. The transfection efficiency of pIDO-EGFP into primarily cultured mouse chondrocytes reached 36.43% at 48 hours and the transfection did not affect the process of cell adherence.IDO gene has been successfully transfected into primarily cultured chondrocytes by means of lipofectamine2000 reagent and the chondrocytes can survive in vitro. Satisfactory efficiency of transient transfection can be reached under optimized condition, which will provide a basis for gene introduction and modification of tissue engineered cartilage.

To investigate the association of CYP2C9*3 and *6 with hyperlipidaemia in Chinese.Four hundred and seventy-six Chinese participated in the study, including 211 uncomplicated hyperlipidaemic patients and 265 healthy controls. PCR-RFLP was used to identify CYP2C9*3 and *6.CYP2C9*6 was not detected in this study. The allelic frequency of CYP2C9*3 was 0.039 (95% CI 0.022, 0.056). A nonsignificant difference existed in CYP2C9*3 frequencies between males and females (P = 0.605, OR = 1.194, 95% CI 0.610, 2.336), patients and controls (P = 0.063, OR = 0.506, 95% CI 0.244, 1.049) in the total population. However, in the female group, CYP2C9*3 frequency in patients with hyperlipidaemia was significantly lower than that in controls (P0.0001, OR = 0.062, 95% CI 0.008, 0.476).The association of CYP2C9*3 with hyperlipidaemia was specific for females in this Chinese population.

To investigate expression of PTEN protein in oromaxillofacial tumor cell lines and to compare the difference of PTEN protein expression between highly metastatic cancer cell lines and their parent cell lines.ABC immunohistochemical staining was applied for detecting expression of PTEN protein in 8 kinds of cancer cell lines, including tongue cancer cell lines Tca8113 and HSC-3,oral bottom cancer cell line HSC-2, buccal cancer cell line BcaCD885, mucoepidermoid carcinoma cell line MEC-1, adenoid cystic carcinoma cell line SACC83, highly metastatic tongue cancer cell line Tb-TLP and highly metastatic mucoepidermoid carcinoma cell line M3SP2.Of the 8 kinds of cancer cell lines, 5 kinds of cancer cell lines were positive for PTEN protein expression. PTEN protein was located in cytoplasm around nucleus. 3 kinds of cancer cell lines, BcaCD885, Tb-TLP and M3SP2, lacked expression of PTEN protein.Deficiency of PTEN protein expression may play a certain role in cancer cell metastasis.

Objective: To determine the attitude of some Chinese orthodontists towards the relationship between orthodontic treatment and temporomandibular disorders (TMDs). Subjects and methods: 25 orthodontists, in six public hospitals (Xi'an, the capital of Shaanxi Province, China), were asked to complete a 10-item questionnaire concerning orthodontics/TMD. Results: 84% of orthodontists often asked their patients about the signs and symptoms of TMD before orthodontic treatment and 92% reported examining the TMJ region. 76% of orthodontists thought orthodontic treatment may possibly lead to a greater incidence of TMD, while 84 per cent claimed that orthodontic treatment might prevent TMD. Methods of orthodontic treatment, patient's age, and occlusal interference were regarded as risk factors leading to increased incidence of TMD. Conclusions: Some Chinese orthodontists realise the importance of the relationship between orthodontic treatment and TMD. Most thought that unsuitable orthodontic treatment might increase the development of TMD and that orthodontic treatment could prevent TMD.