Functional near-infrared spectroscopy-based neurofeedback training regulates time-on-task effects and enhances sustained cognitive performance.

Time-on-task effect is a common consequence of long-term cognitive demand work, which reflects reduced behavioral performance and increases the risk of accidents. Neurofeedback is a neuromodulation method that can guide individuals to regulate their brain activity and manifest as changes in related symptoms and cognitive behaviors. This study aimed to examine the effects of functional near-infrared spectroscopy-based neurofeedback training on time-on-task effects and sustained cognitive performance. A randomized, single-blind, sham-controlled study was performed: 17 participants received feedback signals of their own dorsolateral prefrontal cortex activity (neurofeedback group), and 16 participants received feedback signals of dorsolateral prefrontal cortex activity from the neurofeedback group (sham-neurofeedback group). All participants received 5 neurofeedback training sessions and completed 2 sustained cognitive tasks, including a 2-back task and a psychomotor vigilance task, to evaluate behavioral performance changes following neurofeedback training. Results showed that neurofeedback relative to the sham-neurofeedback group exhibited increased dorsolateral prefrontal cortex activation, increased accuracy in the 2-back task, and decreased mean response time in the psychomotor vigilance task after neurofeedback training. In addition, the neurofeedback group showed slower decline performance during the sustained 2-back task after neurofeedback training compared with sham-neurofeedback group. These findings demonstrate that neurofeedback training could regulate time-on-task effects on difficult task and enhance performance on sustained cognitive tasks by increasing dorsolateral prefrontal cortex activity.

Associations between body mass index, sleep-disordered breathing, brain structure, and behavior in healthy children.

Pediatric overweight/obesity can lead to sleep-disordered breathing (SDB), abnormal neurological and cognitive development, and psychiatric problems, but the associations and interactions between these factors have not been fully explored. Therefore, we investigated the associations between body mass index (BMI), SDB, psychiatric and cognitive measures, and brain morphometry in 8484 children 9-11 years old using the Adolescent Brain Cognitive Development dataset. BMI was positively associated with SDB, and both were negatively correlated with cortical thickness in lingual gyrus and lateral orbitofrontal cortex, and cortical volumes in postcentral gyrus, precentral gyrus, precuneus, superior parietal lobule, and insula. Mediation analysis showed that SDB partially mediated the effect of overweight/obesity on these brain regions. Dimensional psychopathology (including aggressive behavior and externalizing problem) and cognitive function were correlated with BMI and SDB. SDB and cortical volumes in precentral gyrus and insula mediated the correlations between BMI and externalizing problem and matrix reasoning ability. Comparisons by sex showed that obesity and SDB had a greater impact on brain measures, cognitive function, and mental health in girls than in boys. These findings suggest that preventing childhood obesity will help decrease SDB symptom burden, abnormal neurological and cognitive development, and psychiatric problems.

Evaluation of custom posts and cores fabricated by two digital technologies in core and post space dimensions.

PURPOSE: To evaluate the adaptability between posts and post spaces and the rationality of cores fabricated by two digital custom post-and-core processes. MATERIALS AND METHODS: Titanium post-and-cores were fabricated by digital scanning impression technology or digital scanning wax-pattern technology on tooth defect molds of incisors, premolars, and molars, with traditional lost-wax casts of these teeth as the controls. Micro-CT and a laboratory scanner were used to determine intervals between post wall and root canal wall of the root apex, middle, and cervix of each sample in cross-, sagittal, and coronal sections; intervals between the end of post and tooth; diameters of cervical, middle, and incisal part at cross-, sagittal, and coronal sections of each sample, as well as shoulder widths. RESULTS: The three fabrication processes showed significant differences in intervals between post-and-core prostheses and root canal walls, diameters of all parts of cores, and shoulder widths. Scanning impressions showed significant advantages in the main part of post-and-cores in incisors and premolars, while the scanning wax-pattern process showed obvious inferiorities in premolars and molars. As to core spatial size, values of measured sites in the scanning impression process were closer to the standard than those of the traditional process, while differences between the measured value of the scanning wax-pattern process were much more obvious than in the traditional process. CONCLUSIONS: The use of digital custom post-and-core scanning impressions improved the rationality and precision of post-and-core dimensions compared with two other processes.

'Gold' lost in restoration: Evaluation of core morphology of custom metal posts and cores, and analysis of precious metal debris.

1 Objectives: To investigate the deviations between the morphological dimensions of finished cores and desired dimensions made by three available fabricating techniques. To assess the precious metal loss in custom precious metal post and core restorative treatment in the dental clinic. 2 Methods: Titanium posts and cores were fabricated using three different techniques: digital scanning impression technology, digital scanning wax-pattern technology, and the traditional lost-wax casting method. Geomagic Studio was used to fit the scanned model data to the digital design data of the expected preparation and to analyze the 3D deviations between the two. Precious metal debris from the precious metal post and core was collected, processed, weighed and analyzed for precious metal elements by energy-dispersive X-ray spectroscopy layered images. 3 Results: In all 48 pairs of models, there were positive and negative deviations, with the largest mean positive deviation of (0.752 ± 0.037 mm) for models made by the semi-digital scanning wax-pattern technique. A total of 7001.3 mg of metals was recovered from the waste streams collected, which contained precious metals-mainly gold, silver, and platinum. 4 Conclusions: There were discrepancies between the custom core and the expected preparation regardless of the fabrication process used. The digital scanning impression technology showed better dimensional rationality of crown cores. Custom precious metal posts and cores can have an average precious metal loss of 129.7 mg per case in the dental clinic.

A pH/ROS-responsive antioxidative and antimicrobial GelMA hydrogel for on-demand drug delivery and enhanced osteogenic differentiation in vitro.

Long-term inflammation, including those induced by bacterial infections, contributes to the superfluous accumulation of reactive oxygen species (ROS), further aggravating this condition, decreasing the local pH, and adversely affecting bone defect healing. Conventional drug delivery scaffold materials struggle to meet the demands of this complex and dynamic microenvironment. In this work, a smart gelatin methacryloyl (GelMA) hydrogel was synthesized for the dual delivery of proanthocyanidin and amikacin based on the unique pH and ROS responsiveness of boronate complexes. Fourier-transform infrared spectroscopy (FTIR) and X-ray photoelectron spectroscopy (XPS) demonstrated the co-crosslinking of two boronate complexes with GelMA. The addition of the boronate complexes improved the mechanical properties, swelling ratio, degradation kinetics and antioxidative properties of the hydrogel. The hydrogel exhibited pH and ROS responses and a synergistic control over the drug release. Proanthocyanidin was responsively released to protect mouse osteoblast precursor cells from oxidative stress and promote their osteogenic differentiation. The hydrogel responded to pH changes and released sufficient amikacin in a timely manner, thereby exerting an efficient antimicrobial effect. Overall, the hydrogel delivery system exhibited a promising strategy for solving infectious and inflammatory problems in bone defects and promoting early-stage bone healing.

[Inhibition of 1,25-(OH)2D3 on passively sensitized human airway smooth muscle cells].

OBJECTIVE: To investigate the effects of 1,25-(OH)(2)D(3) on the proliferation of passively sensitized human airway smooth muscle cells (HASMCs) and their expressions of MMP-9 and a disintegrin and metalloprotease 33(ADAM33). METHODS: HASMCs were passively sensitized with 10% serum from asthmatic patients. MTT colorimetry assay was used to examine the effect of 1,25-(OH)(2)D(3) on cell proliferation at different concentrations (10(-10) mol/L, 10(-9) mol/L, 10(-8) mol/L, 10(-7) mol/L).By this way, its optimal inhibitory concentration was determined. And then the effects of 1,25-(OH)(2)D(3) at the optimal concentration on cell proliferation was examined by the same MTT assay and cell cycle analysis by flow cytometry. The expressions of MMP-9 and ADAM33 in HASMCs were studied by real-time quantitative RT-PCR and Western blotting analysis. RESULTS: (1) Inhibition of cell proliferation by 1,25-(OH)(2)D(3) was barely detectable at 10(-10) mol/L. But with the increasing concentration ranging from 10(-9) mol/L to 10(-7) mol/L, 1,25-(OH)(2)D(3) markedly inhibited the cell proliferation concentration-dependently and reached the maximum effect at the concentration of 10(-7) mol/L. Accordingly, 10(-7) mol/L was chosen as the optimal concentration of 1,25-(OH)(2)D(3) for the following study. (2) At the concentration of 10(-7) mol/L, 1,25-(OH)(2)D(3) inhibited the cell proliferation of passively sensitized HASMCs in a time-dependent manner and hampered the G(1)/S transition. (3) 1,25-(OH)(2)D(3) pretreatment attenuated the MMP-9 and ADAM33 protein levels in passively sensitized HASMCs by (63.4 ± 3.6)% and (50.9 ± 2.9)%, respectively (P < 0.01). (4) 1,25-(OH)(2)D(3) significantly inhibited the MMP-9 and ADAM33 mRNA levels in passively sensitized HASMCs by (52.2 ± 2.5)% and (67.8 ± 3.2)%, respectively (P < 0.01). CONCLUSION: 1,25-(OH)(2)D(3) has a direct inhibitory effect on passively sensitized HASMCs in vitro, including the inhibition of cell proliferation and the expressions of MMP-9 and ADAM33, which maybe associated with the beneficial role of 1,25-(OH)(2)D(3) in the prevention and therapy of asthmatic airway remodeling.

Suppression of allergic airway inflammation in a mouse model by Der p2 recombined BCG.

Allergic asthma is a chronic inflammatory disease mediated by T helper (Th)2 cell immune responses. Currently, immunotherapies based on both immune deviation and immune suppression, including the development of recombinant mycobacteria as immunoregulatory vaccines, are attractive treatment strategies for asthma. In our previous studies, we created a genetically recombinant form of bacille Calmette-Guerin (rBCG) that expressed Der p2 of house dust mites and established that it induced a shift from a Th2 response to a Th1 response in naive mice. However, it is unclear whether rBCG could suppress allergic airway inflammation in a mouse model. In this article we report that rBCG dramatically inhibited airway inflammation, eosinophilia, mucus production and mast cell degranulation in allergic mice. Analysis of interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) levels in bronchoalveolar lavage fluid (BALF) and lung tissue revealed that the suppression was associated with a shift from a Th2 response to a Th1 response. At the same time, rBCG induced a CD4(+) CD25(+) Foxp3(+) T-cell subtype that could suppress the proliferation of Th2 effector cells in vitro in an antigen-specific manner. Moreover, suppression of CD4(+) CD25(+) T cells could be adoptively transferred. Thus, our results demonstrate that rBCG induces both generic and specific immune responses. The generic immune response is associated with a shift from a Th2 to a Th1 cytokine response, whereas the specific immune response against Der p2 appears to be related to the expansion of transforming growth factor-beta (TGF-beta)-producing CD4(+) CD25(+) Foxp3(+) regulatory T cells. rBCG can suppress asthmatic airway inflammation through both immune deviation and immune suppression and may be a feasible, efficient immunotherapy for asthma.

Notch signaling regulates the FOXP3 promoter through RBP-J- and Hes1-dependent mechanisms.

Evidence has shown that Notch signaling modulates CD4(+)CD25(+) regulatory T-cells (Tregs). As transcription factor Foxp3 acts as a master molecule governing the development and function of Tregs, we investigated whether Notch signaling might directly regulate Foxp3 expression. Here, we provide evidence that Notch signaling can modulate the FOXP3 promoter through RBP-J- and Hes1-dependent mechanisms. A conserved RBP-J-binding site and N-box sites were identified within the FOXP3 promoter. We show that the Notch intracellular domain (NIC), the active form of Notch receptors, activates a reporter driven by the FOXP3 promoter. Dissection of the FOXP3 promoter revealed bipartite effects of the RBP-J-binding site and the N-boxes: the RBP-J-binding site positively, while the N-boxes negatively regulated the FOXP3 promoter activity. Moreover, in freshly isolated Tregs, NIC-RBP-J complex is bound to the FOXP3 promoter in Tregs. Our results suggest that Notch signaling might be involved in the development and function of Tregs through regulating Foxp3 expression.

Bioinformatics Analysis of Key Genes and Pathways in Colorectal Cancer.

Colorectal cancer (CRC) is the third most prevalent cancer in the world. Although great progress has been made, the specific molecular mechanism remains unclear. This study aimed to explore the differentially expressed genes (DEGs) and underlying mechanisms of CRC using bioinformatics analysis. In this study, we identified a total of 1353 DEGs in the database of GSE113513, including 715 up- and 638 downregulated genes. Gene ontology analysis results showed that upregulated DEGs were significantly enriched in cell division, cell proliferation, and DNA replication. The downregulated DEGs were enriched in immune response, relation of cell growth and inflammatory response. The Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that upregulated DEGs were enriched in cell cycle and p53 signaling pathway, whereas the downregulated DEGs were enriched in drug metabolism, metabolism of xenobiotics by cytochrome P450, and nitrogen metabolism. A total of 124 up-key genes and 35 down-key genes were identified from the protein-protein interaction networks. Furthermore, we identified five up-modules (up-A, up-B, up-C, up-D, and up-E) and three down-modules (d-A, d-B, and d-C) by module analysis. The module up-A was enriched in sister chromatid cohesion, cell division, and mitotic nuclear division. Pathways associated with cell cycle, progesterone-mediated oocyte maturation, oocyte meiosis, and p53 signaling pathway. Whereas the d-A was mainly enriched in G-protein coupled receptor signaling pathway, cell chemotaxis, and chemokine-mediated signaling pathway. The pathways enriched in chemokine signaling pathway, cytokine-cytokine receptor interaction, and alcoholism. These key genes and pathways might be used as molecular targets and diagnostic biomarkers for the treatment of CRC.

Inhibition of tumor angiogenesis by HMGB1 A box peptide.

High mobility group box 1 protein (HMGB1) is a highly conserved, ubiquitous non-histone nuclear protein, which participates in maintaining nucleosome structure, regulation of gene transcription, and modulating the activity of steroid hormone receptors. Substantial evidence demonstrated that HMGB1 could be secreted into the extracellular milieu, acts as a proinflammatory cytokine and mediates the downstream inflammatory responses in endotoxemia, arthritis and sepsis. Recently, several reports suggested that HMGB1 plays a key role in tumor angiogenesis through multiple mechanisms, including up-regulation of proangiogenic factors, promoting endothelial progenitor cells homing to ischemic tumor tissues and induction of endothelial cell migration and sprouting. And blockade of HMGB1 binding to the receptor for advanced glycation end products (RAGE) with anti-HMGB1 antibody, soluble RAGE or anti-RAGE neutralizing antibody has been proved to inhibit angiogenesis efficiently. Since HMGB1 A box peptide could antagonize the HMGB1 whole length protein by competitively binding to RAGE and has been considered as a HMGB1 specific antagonist, we postulate that the HMGB1 A box peptide could function as an anti-angiogenic agent to inhibit tumor angiogenesis. In our opinion, if the hypothesis proved to be practical, HMGB1 A box peptide could be widely used in clinical settings to treat malignant tumors.

[Effect of dihydroartemisinin on proliferation of human lung adenocarcinoma cell line A549].

BACKGROUND: Recent researches discovered that artemisinin and its derivatives had anti-tumor activity. Dihydroartemisinin is one of the derivatives with higher activity. This study is to explore the effect of dihydroartemisinin on the proliferation of human lung adenocarcinoma cell line A549, so as to provide experimental base for treatment of lung cancer. METHODS: Inhibition of proliferation in vitro was measured by MTT assay. The cell growth curve was drawn according to cell counts. The population doubling time was counted in logarithmic growth phase, DNA contents were measured by flow cytometry. Cell cycles were observed at the same time after the treatment. And the nude mice bearing A549 cancer cells were applied to detect the effect of dihydroartemisinin in vivo. RESULTS: Dihydroartemisinin inhibited A549 cell proliferation in a concentration-dependent manner, after 96h of treatment, the IC50 for dihydroartemisinin inhibition of cell number was 0.23µmol/l. The population doubling time for human lung adenocarcinma in the control group was 21.3h and that in the dihydroartemisinin group was 38.5h . An highly significant difference was observed between the two groups (P < 0.01). Cells in G0 plus G1 were increased after the dihydroartemisinin treatment. The tumor inhibiting rate of dihydroartemisinin was 54.3% in vivo. CONCLUSIONS: Dihydroartemisinin has marked anticancer activity on human lung adenocarcinoma cell line A549 both in vitro and in vivo. The inhibition in vitro is related to blockade of G0 and G1 phases.

[Inhibitive effect on airway mucus overproduction with DNA vaccine based on xenogeneic homologous calcium-activated chloride channel in asthmatic mice].

OBJECTIVE: To observe the inhibitive effect on airway mucus overproduction with DNA vaccine based on human calcium-activated chloride channel 1 (hCLCA1) in asthmatic mice, who own mCLCA3 being xenogeneic homology of hCLCA1 in airway goblet cell. METHODS: The DNA vaccine was made with hCLCA1 gene inserted into pSecTag2B, and then BALB/c mice were vaccinated by i.m. once every two weeks. When serum antibody showed binding activity to mCLCA3 with ELISA analysis, asthma will be induced with ovalbumin in the vaccinated mice. To detect mucus production, lung sections were PAS stained and their MUC5AC mRNA levels were investigated by reverse transcription polymerase chain reaction (RT-PCR). Mice in control groups were injected with pSecTag2B/mCLCA3, pSecTag2B and saline, respectively. RESULTS: Antiserum of vaccine group after three times vaccination showed good binding activity to three mCLCA3 extracellular domains (ED), and the activity to N-terminal C-terminal ED was stronger than middle-ED. After induced to asthma, the number of goblet cell and MUC5AC mRNA level in vaccine group were lower than these in control group. CONCLUSION: hCLCA1 DNA vaccine can induce mouse to produce serum antibody binding itself mCLCA3, and thus airway mucus overproduction of asthmatic mouse is effectively inhibited.

[The inhibiting effect of niflumic acid on airway hyperresponsiveness in asthmatic mice].

OBJECTIVE: To evaluate the inhibiting effect of niflumic acid (NFA), an inhibitor of calcium-activated chloride channel (ClCa) on airway epithelium, on the airway hyperresponsiveness in asthmatic mice. METHODS: BALB/c mice were randomly divided into an asthma group (A group), a NFA prevention asthmatic group (B group) and a sham-challenged group (C group). The airway pressure time index (APTI) and the content of ET-1 and NO in bronchoalveolar lavage fluid (BALF) in all groups were measured. With the isolated tracheal rings with integral epithelium or epithelium removed from the asthma group (A(1) group and A(2) group) and the sham-challenged group (C(1) group and C(2) group), the contractile responsiveness of various rings to methacholine (mACh) was examined, and its change was observed when the rings were exposed to NFA beforehand. RESULTS: Compared with A group (1.62 +/- 0.14), the APTI in B group (1.21 +/- 0.07) was reduced remarkably (P < 0.01), and the contents of ET-1 [(103 +/- 9) ng/L] and NO [(48.5 +/- 3.2) micromol/L] in BALF of A group were significantly higher than those in B group, [(53 +/- 5) ng/L, (23.7 +/- 2.5) micromol/L (P < 0.01), respectively]. The ratios of maximum contractility in A(1), A(2), C(1) and C(2) groups were (3.79 +/- 0.44), (2.15 +/- 0.21), (1.26 +/- 0.14) and (2.06 +/- 0.18), respectively. The contractility of A(1) group was highest among all groups (all P < 0.01), but could be effectively decreased by NFA. CONCLUSIONS: By inhibiting the special ClCa on the airway epithelium, NFA can inhibit the production of ET-1 and NO by epithelium and thus exert preventive effect on airway hyperresponsiveness in asthma.

[Effects and mechanisms of fibronectin on adhesion and migration of different types of lung cancer cell lines].

BACKGROUND: To observe and explore the effects and mechanisms of fibronectin (FN) on invasion of different types of lung cancers. METHODS: Using tumor invasion models in vitro of plates coated with FN and Boyden chambers with FN filter, differences of adhesion and migration between small cell lung cancer cell line (054A) and adenocarcinoma cell line (A549) were investigated, and proliferative effects of FN on cells were examined. In the meantime the invasive capability changes were observed after cell suspensions were preincubated with anti-α5, anti-α3 and anti-ß1 integrin antibodies, respectively. RESULTS: FN could improve the adhesion, migration and proliferation of A549 more markedly than that of 054A. The number of adhesive cells in A549 cell line changed from 34.7± 5.1 to 189.4±12.3 with time from 2h to 12h compared with that from 19.8±7.9 to 159.2±11.9 in 054A cell line (P < 0.05 or P < 0.01). A549 cell line had 142.7±5.9 migration cells while 054A cell line had 89.4±4.7 (P < 0.01). FN could improved the proliferation in A549 cell line from 0.250±0.019 to 0.754±0.025 (P < 0.01) in concentration-dependent way, but in 054A from 0.205±0.026 to 0.286±0.029. And these effects were mediated mainly by α3ß1 and α5ß1 receptors in A549, but α3ß1 in 054A. CONCLUSIONS: Lung cancers with different origins express so different types and extents of integrin receptors that effects of FN on tumors are various, which is one of important reasons of different invasive capability of lung cancers.

[Therapeutic efficacy of chemotherapy with VIP for small cell lung cancer].

BACKGROUND: To evaluate the effect of combination chemotherapy with etoposide plus ifosfamide and cisplatin (VIP) for small cell lung cancer (SCLC). METHODS: One-hundred and twenty patients with localized SCLC who never received chemotherapy were randomly divided into VIP regimen group and EP regimen group. The response and toxicity were evaluated after 3 cycle chemotherapy with VIP or EP respectively. In addition, salvage chemotherapy by VIP was given to 25 patients, who had progression or recurrence of the cancer after treatment with EP regimen, and the response was assessed after 3 cycles of the treatment. RESULTS: In 118 evaluable patients, response rate was 89.6% for VIP regimen group and 78.3% for EP regimen group. There was no remarkable difference of response rates between the two groups. Toxicity of the two regimens was similar. However, complete response rate for VIP regimen group (43.1%) was significantly higher than that for EP regimen group (25.0%) (P < 0.05). In 23 patients who were progressive or relapsed after treatment with EP regimen, the complete response, partial response, progression and total response were 13.0%, 39.1%, 47.8% and 52.2% respectively. CONCLUSIONS: VIP regimen may be used as the first-line chemotherapy for localized SCLC, its efficacy is superior to that of EP regimen. VIP can also be used as salvage chemotherapy regimen for patients with SCLC who failed to EP regimen chemotherapy.

[Research of anti-proliferation of curcumin on A549 human lung cancer cells and its mechanism].

OBJECTIVE: To investigate the mechanism of anti-tumor effects of curcumin on human lung cancer cell (A549). METHOD: MTT colorimetry method, fluoroscope, FCM combine PI and Annexin V-FITC double pigmentation method and Western blot method were used. RESULT: Under the effect of the curcumin, cell grew against the wall and suspended in the culture liquid, the A549 cell nucleolus were found fragmentated into different size of apoptosis body under fluoroscopy. The cell proliferation were obvious suppressed after treated with different concentration curcumin for 72 hours. The IC50 were 18 micromol/L by using linear regression. The apoptosis induced by curcumin of A549 cell is concentration dependent. With curcumin increased from 5 micromol/L to 30 micromol/L, Annexin-FITC single positive cell (early apoptosis cell) increased from 3.4% to 59.1%. When curcumin concentration reached 40 micromol/L, PI and Annexin V-FITC double positive cell (secondary apoptosis necrosis cell) became major part of cells, and the cell showed G2 phase block. Observed with western blot method, with the increase of curcumin concentration to 10 micromol/L, the expression of PARP increased simultaneously. CONCLUSION: Curcumin can interfere cell growth cycle of A549 cell and suppress cell growth. The suppression effect is concentration dependent. The effect depends not only from the nonspecific cytotoxic but also from induced cell apoptosis.

Resveratrol down-regulates survivin and induces apoptosis in human multidrug-resistant SPC-A-1/CDDP cells.

We studied the effect of resveratrol treatment on multidrug-resistant human non-small cell lung cancer cells. Human multidrug-resistant SPC-A-1/CDDP cells were treated with resveratrol at a concentration of 25, 50, or 100 microM in in vitro studies and nude mice were implanted with multidrug-resistant SPC-A-1/and fed a special diet that included resveratrol at a dose of either 1 g/kg/day or 3 g/kg/day in in vivo studies. No adverse toxicological effects of resveratrol treatment were observed. The rate of cell proliferation, apoptosis ratio, cell cycle phase distribution, IC50 values of cisplatin, gefitinib, and paclitaxel, implanted tumour volume, and expression of survivin in resveratrol-treated and control mice were then determined. Resveratrol significantly inhibited the proliferation of SPC-A-1/CDDP cells, induced apoptosis, arrested the cell cycle phase between G0-G1 and S phase or at the G2/M phase, decreased the IC50 values of multiple chemotherapeutic drugs, and showed anti-tumour effects in nude mice that had been implanted with SPC-A-1/CDDP cells. In additional, resveratrol affected the proliferation of SPC-A-1/CDDP cells in a dose- and time-dependent manner. Expression of survivin in SPC-A-1/CDDP cells decreased after they were treated with all concentrations of resveratrol and resveratrol was also found to have a dose-dependent effect on survivin expression. Resveratrol can induce apoptosis in multidrug-resistant human NSCLC SPC-A-1/CDDP cells by down-regulating the expression of survivin.

Effect of pretreatment with high-dose ulinastatin in preventing radiation-induced pulmonary injury in rats.

In order to develop a better management strategy for radiation-induced pulmonary injury, we compared the protective effect of pretreatment and aftertreatment with different doses of ulinastatin. Two hundred and forty female Sprague-Dawley rats were randomized into five groups. Group R received radiation only, groups P1 and P2 were pretreated with different doses of i.v. ulinastatin for 3 days pre- and 4 days post-irradiation, and groups A1 and A2 were treated for 7 days post-irradiation only. Rats were sacrificed at 2 h, and at 4, 8, 16, and 24 weeks post-irradiation. The expressions of TGF-beta1, TNF-alpha, IL-6, hydroxyproline and laminin were determined. No adverse toxicological effects of ulinastatin pretreatment were observed. Mortality and ratio of fibrotic area was lowest in group P1(5/45; 30.6+/-3.11%, P<0.05 vs. A2). Expressions of TGF-beta1 and IL-6 in group P1 were significantly lowest at 4 weeks (3.01+/-0.35, 549+/-58, 32.3+/-3.27, P<0.01), and expressions of hydroxyproline and laminin were also lowest at 24 weeks (741+/-68 and 82.6+/-6.91, P<0.01) in comparison with other groups. Significant differences were observed in expression of TGF-beta1 and TNF-alpha in lung between group P1 and group A1 at 4 weeks (263+/-11% vs. and 187+/-9%, 189+/-8% vs. 154+/-9%, P<0.01, P<0.05 respectively). Pretreatment with high dose ulinastatin resulted in a milder inflammatory response and suppressed pulmonary fibrosis, which may serve as a favorable management strategy.

[To explore the mechanisms of neurogenic inflammation and airway hyperresponsiveness of rat by inhaled sulfur].

AIM: To explore the physiopathological mechanisms of airway injury and the effect on the airway responsiveness of rat by inhaled sulfur dioxide(SO2). METHODS: Sixteen SD male rats were divided randomly into 2 groups (n = 8): the control group and SO2 group. The control group was exposed o pure air. SO2 group was exposed to SO2 of the content 1.0 mg/(m(3) x h) 6h daily for consecutive 3 d. At 4th day, we determined the airway responsiveness, collected the bronchoalveolar lavage fluid (BALF), plasma and lung tissue. Then we counted the total cellular score in BALF, measured the plasma SP content and made the immunohistochemistry staining on the lung tissue (HE and SP methods). RESULTS: Compared with the control group, the total cellular score in BALF and plasma SP content in SO2 group's increased significantly ( P < 0.01). HE staining showed there were a great deal of inflammatory cells infiltration under the tunica mucosa bronchiorum; and SP immunohistochemistry staining indicated there were significant changes in numbers of SP-IR positive fibers of SO2group. CONCLUSION: Exposure to low concentration of SO2 would injure healthy rat's airway, and induce airway hyperresponsiveness, neurogenic inflammation is one of its critical pathophysiological mechanisms.

[Respiratory syncytial virus infection enhances airway hyperresponsiveness in guinea pigs and the underlined mechanism].

AIM: To study the relation between Respiratory Syncytial Virus infection and asthma development by measuring airway responsiveness (AR) and M2R function. METHODS: Guinea pigs (n = 34) were randomly divided into 4 groups: Hep-2/NS group (group A, n = 9), RSV/NS group (group B, n =9), Hep-2/OVA group (group C, n = 8) and RSV/OVA group(group D, n = 8). On day 21 after infection we tested AR and M2R. Then counted eosinophils in BALF and observed pathological change. RESULTS: Intraairway pressure(IP mmH20) of group B had no significant difference with group A(P > 0.01), and the extent of IP decrease also had no difference between groups A and B (P > 0. 05), but IP of C group were much higher than group A (P<0.05), with extent of IP decrease lower than group A (P < 0.05). And IP of group D were higher than group C (P < 0.01), with the extent of IP decrease much lower than group C (P < 0.05). CONCLUSION: RSV infection could enhance OVA-induced M2R dysfunction, then develop AHR.