Effects of vermicompost fertilization on soil, tomato yield and quality in greenhouse.

The excessive use of chemical fertilizer on vegetables in protected facilities resulted in soil degradation, serious soil-borne diseases, and lower vegetable yield and quality. We examined the effects of vermicompost on soil nutrient, enzyme activities, microbial quantity, tomato growth, yield and quality in greenhouse. The results showed that both broadcast and furrow application of vermicompost improved soil environment, and significantly increased contents of soil organic matter and soil nutrients (nitrogen, phosphorus and potassium). Vermicompost application significantly increased sucrase and catalase activities, abundance of bacteria and actinomycetes, and decreased the abundance of fungi in the soil. Furrow application but not the broadcast application promoted the growth of tomato plants. The vermicompost promoted root activities and leaf photosynthesis, increased chlorophyll, nitrogen and potassium contents in leaves. Broadcast and furrow application of vermicompost significantly increased tomato yield by 22.7% and 32.6%, respectively. Furrow application increased the contents of soluble protein, soluble sugar, vitamin C and titratable acid by 66.1%, 11.0%, 122.6% and 29.9%, respectively, and decreased nitrate content in tomato fruits by 65.7%. However, broadcast application did not affect fruit quality.

Cbl participates in shikonin-induced apoptosis by negatively regulating phosphoinositide 3-kinase/protein kinase B signaling.

Shikonin, a naturally occurring naphthoquinone, exhibits anti-tumorigenic activity. However, its precise mechanisms of action have remained elusive. In the present study, the involvement in the action of shikonin of the ubiquitin ligases Cbl-b and c-Cbl, which are negative regulators of phosphoinositide 3-kinase (PI3K) activation, was investigated. Shikonin was observed to reduce cell viability and induce apoptosis and G2/M phase arrest in lung cancer cells. In addition, shikonin increased the protein levels of B-cell lymphoma 2 (Bcl-2)-associated X and p53 and reduced those of Bcl-2. Additionally, shikonin inhibited PI3k/Akt activity and upregulated Cbl protein expression. In addition, a specific inhibitor of PI3K, LY294002, was observed to have a synergistic effect on the proliferation inhibition and apoptotic induction of A549 cells with shikonin. In conclusion, the results of the present study suggested that Cbl proteins promote shikonin-induced apoptosis by negatively regulating PI3K/Akt signaling in lung cancer cells.

Cbl-b-regulated extracellular signal-regulated kinase signaling is involved in the shikonin-induced apoptosis of lung cancer cells in vitro.

Shikonin (SK), a naturally occurring naphthoquinone, exhibits antitumor activity. However, its precise mechanisms of action are unknown. In the present study, the effects of SK on NCI-H460 human lung cancer cells were investigated. It was found that SK reduced cell viability and induced apoptosis in the NCI-H460 cells. Additionally, SK inhibited extracellular signal-regulated kinase (ERK) activity, which indicates that inhibition of the ERK pathway is probably one of the mechanisms by which SK induced NCI-H460 cell apoptosis. The expression of Cbl-b was significantly increased by treatment with SK for 4 h, and gradually increased to a maximal level at 24 h; the time taken for the upregulation of Cbl-b protein was in accordance to that required for the downregulation of phospho (p)-ERK protein. The Cbl inhibitor Ps341 reversed the SK-induced downregulation of p-ERK and apoptosis of NCI-H460 cells. These results indicate that Cbl-b potentiates the apoptotic action of SK by inhibiting the ERK pathway in lung cancer cells.

Effect of phenylephrine on alveolar fluid clearance in ventilator-induced lung injury.

OBJECTIVE: To investigate the effect of phenylephrine (an α-adrenergic agonist) on alveolar fluid clearance (AFC) in ventilator-induced lung injury and the possible mechanism involved. METHODS: A total of 170 male Wistar rats were randomly allocated into 17 groups (n=10) using random number tables. Short-term (40 minutes) mechanical ventilation with high tidal volume (HVT) was performed to induce lung injury, impair active Na+ transport and lung liquid clearance in the rats. Unventilated rats served as controls. To demonstrate the effect of phenylephrine on AFC, phenylephrine at different concentrations (1×10(-5), 1×10(-6), 1×10(-7), 1×10(-8), and 1×10(-9) mol/L) was injected into the alveolar space of the HVT ventilated rats. To identify the influence of adrenergic antagonists, Na(+) channel, and microtubular system on the effect of phenylephrine, phenylephrine at 1×10(-5) mol/L combined with prazosin (an α1-adrenergic antagonist, 1×10(-4) mol/L), yohimbine (an α2-adrenergic antagonist, 1×10(-4) mol/L), atenolol (a ß1- adrenergic antagonist, 1×10(-5) mol/L), ICI-118551 (an ß2-adrenergic antagonist, 1×10(-5) mol/L), amiloride (a Na+ channel blocker, 5×10(-4) mol/L), ouabain (a Na(+)/K(+)-ATPase blocker, 5×10(-4) mol/L), colchicine (a microtubular disrupting agent, 0.25 mg/100 g body weight), or ß-lumicolchicine (an isomer of colchicine, 0.25 mg/100 g body weight) were perfused into the alveolar space of the rats ventilated with HVT for 40 minutes. AFC and total lung water content were measured. RESULTS: Basal AFC in control rats was (17.47±2.56)%/hour, which decreased to (9.64± 1.32)%/hour in HVT ventilated rats (P=0.003). The perfusion of phenylephrine at 1×10(-8), 1×10(-7), 1×10(-6), and 1×10(-5) mol/L significantly increased the AFC in HVT ventilated rats (all P<0.05). This effect of phenylephrine on AFC was suppressed by prazosin, atenolol, and ICI-118551 in HVT ventilated rats by 53%, 31%, and 37%, respectively (all P<0.05). The AFC-stimulating effect of phenylephrine was lowered by 33% and 42% with amiloride and ouabain, respectively (both P<0.05). Colchicine significantly inhibited the effect of phenylephrine (P=0.031). CONCLUSION: Phenylephrine could increase the AFC in HVT-ventilated rats and accelerate the absorption of pulmonary edema.

Plasma metabolic profiling of Alzheimer's disease by liquid chromatography/mass spectrometry.

OBJECTIVES: The identification of Alzheimer's disease (AD) biomarkers may allow for a less invasive and more accurate diagnosis as well as serve as a predictor of future disease progression and treatment response. The aim of this study was to map potential biomarkers in plasma for AD. DESIGN AND METHODS: Plasma metabolic perturbations between AD and healthy old person were investigated using ultra performance liquid chromatography/mass spectrometry (UPLC/MS) and metabonomics approach. The principal component analysis (PCA) of UPLC/MS spectra showed that metabolic changes between two groups. RESULTS: The PCA of UPLC/MS spectra showed that metabolic changes observed between AD and control were clear. Nine potential biomarkers in correlation with the extent of AD were found. CONCLUSIONS: Based on PCA, several potential biomarkers (LPCs, sphingosine and tryptophan) were found and further identified by the following LC/MS/MS analysis. All of them could be the potential early markers of AD.

Effect of beta3-adrenergic agonists on alveolar fluid clearance in hypoxic rat lungs.

BACKGROUND: Recent research suggests that beta(2)-adrenergic agonists increase alveolar fluid clearance (AFC) under physiologic and pathologic conditions. It is unknown whether beta(3)-adrenergic agonists also increase AFC under pathologic conditions. The aim of this study was to investigate the effect of beta(3)-adrenergic agonists on AFC following hypoxic lung injury and the mechanisms involved. METHODS: Hypoxic rats were exposed to 10% oxygen. BRL-37344 (beta(3)-adrenergic agonist) or CGP-12177 (selective beta(3)-adrenergic agonist) alone or combined with beta receptor antagonists, sodium channel blockers, or Na(+)/K(+)-ATPase blockers were perfused into the alveolar space of rats exposed to 10% oxygen for 48 hours. Total lung water content (TLW) and AFC were measured. RESULTS: AFC did not change for the first 24 hours but then decreased after 48-hour exposure to 10% oxygen. The perfusion of BRL-37344 or CGP-12177 significantly increased AFC in normal and hypoxic rats. The AFC-stimulating effect of CGP-12177 was lowered with amiloride (a Na(+) channel blocker) and ouabain (a Na(+)/K(+)-ATPase inhibitor) by 37% and 49%, respectively. Colchicine significantly inhibited the effect of CGP-12177. CONCLUSIONS: These findings suggest that beta(3)-adrenergic agonists can increase AFC during hypoxic lung injury in rats and accelerate the amelioration of pulmonary edema.

[Effects of antisense oligonucleotide to nuclear factor-kappaB on the development of bleomycin-induced pulmonary fibrosis and IL-4 expression therein: experiment with mice].

OBJECTIVE: To investigate the expression of nuclear factor-kappaB (NF-kappaB) in the cells in the bronchoalveolar lavage fluid (BALF) of idiopathic pulmonary fibrosis (IPF) and its effects on IL-4 expression therein, and to investigate the therapeutic role of antisense oligonucleotide (ASON) to NF-kappaB on IPF. METHODS: C57BL/6 mice were randomly divided into 4 groups: bleomycin (BLM) group (n = 35, injected with BLM through caudal vein), control group [n = 20, injected with normal saline (NS) via caudal vein], ASON group (n = 35, injected with ASON to p65, a subunit of NF-kappaB, at the dose of 900 microg), and SON group (n = 35, injected with sense oligonucleotide to p65 subunit). Six hours after intravenous injection, the BLM, ASON, and SON groups were treated with BLM-A5 (5 mg/kg dissolved in 20 microl NS) by intratracheal installation, and the control group was treated with NS (20 microl). 0.5, 1, 3, 7, 14, and 28 days following intratracheal instillation of BLM or 0.5, 1, 14 days following intratracheal instillation of NS, 5 mice of every group were sacrificed and bronchoalveolar lavage was performed. The BALF was collected and assayed with ELISA for IL-4. Immunohistochemistry (IHC) and microscope image analysis were completed to detect the expression of p65 and IL-4 in the bronchoalveolar lavage cells. Another 5 mice from each group were sacrificed 28 days after intratracheal instillation with their total right lungs taken out to undergo pathohistological examination. The content of hydroxyproline in the left lung was detected by high performance liquid chromatography and ELISA. RESULTS: (1) Twenty-eight days after intratracheal instillation, the BLM and the SON groups showed consolidation of the lung parenchyma with loss of the alveolar architecture and increased cellularity, while the ASON and control groups showed no significant pulmonary consolidation or fibrosis. (2) Twenty-eight days after intratracheal instillation, the hydroxyproline content of the BLM group was 876.8 +/- 91.1 nmol/lung, significantly higher than that of the control group (347.6 +/- 53.9 nmol/lung, t = -9.833, P < 0.001); the hydroxyproline content of the ASON group was 505.6 +/- 34.8 nmol/lung, significantly lower than that of the BLM group (t = -9.862, P < 0.001); however, the hydroxyproline content of the SON group was 775.2 +/- 68.9 nmol/lung, not significantly different from that of the BLM group (t = 2.118, P = 0.102). (3) One day after the intratracheal instillation of BLM, the value of average integral optical density of p65 in the bronchoalveolar lavage cells of the BLM, SON, and ASON groups were 275 +/- 13, 233 +/- 60, 233 +/- 60, and 126 +/- 34 respectively, all significantly higher that of the control group (38 +/- 18, t = 27.350, 8.039, and 6.107, P < 0.001, = 0.001, and = 0.004), that of the ASON group being significantly lower than those of the BLM and SON groups (t = 7.664 and -3.407, P = 0.002 and 0.027). (4) IHC showed that 1 day after the intratracheal instillation, the value of average integral optical density of IL-4 of the BLM, SON, and ASON groups were 134 +/- 16, 128 +/- 2, and 80 +/- 9 respectively, all significantly higher than that of the control group (33 +/- 12, t = 10.346, -5.927, and 5.313, P < 0.001, = 0.004, = 0.006), that of the ASON group being significantly lower than those of the BLM and SON groups (t = 6.967 and -3.591, P = 0.002 and 0.023). (5) ELISA showed that 1 day after the intratracheal instillation the IL-4 level BLM, SON, and ASON groups were (20.8 +/- 7.2) ng/L, (21.4 +/- 8.0) ng/L, and (9.7 +/- 1.4) ng/L respectively, all significantly higher than that of the control group [(1.6 +/- 3.6) ng/L, t = 6.494, 4.143, and 4.331, P = 0.003, 0.014, and 0.012], that of the ASON group being significantly lower than those of the BLM and SON groups (t = -3.553 and -3.577, P = 0.024 and 0.023) (6) Correlation analysis showed that 1 day after intratracheal instillation the expression of p65 was positively correlated with IL-4 expression in the bronchoalveolar lavage cells in the treatment group (r = 0.890, P < 0.05) and the ASON group (r = 0.909, P < 0.05). CONCLUSION: The expression of NF-kappaB is significantly increased and augments the expression of IL-4 indirectly in the BALF cells during the process of BLM-induced lung fibrosis. ASON significantly inhibits the NF-kappaB activation and the IL-4 expression, and may be useful in gene therapy for pulmonary fibrosis.

[A multicentre study on the pathogenic agents in 665 adult patients with community-acquired pneumonia in cities of China].

OBJECTIVE: To investigate the pathogenic causes of community-acquired pneumonia (CAP) in adult patients in China, the relation of previous antibiotic use and the Pneumonia Patient Outcome Research Team (PORT) classification to microbial etiology, and the prevalence of drug resistance of common CAP bacteria. METHODS: A prospective study was performed on 665 consecutive adult patients with CAP at 12 centers in 7 Chinese cities during one year. The etiology of pneumonia was considered if one of the following criteria was met: (1) valid sputum sample yielding one or more predominant strains; (2) blood cultures yielding a bacterial pathogen; (3) seroconversion, a > or = 4-fold increase or decrease titers of antibodies to Mycoplasma pneumoniae, Chlamydia pneumoniae and Legionella pneumophila. Minimum inhibitory concentration (MIC) of respiratory tract isolates was determined using the agar dilution method. RESULTS: Pathogens were identified in 324/610 patients (53.1%) with valid serum samples and sputum cultures as follows: Mycoplasma pneumoniae (126, 20.7%), Streptococcus pneumoniae (63, 10.3%), Haemophilus influenzae (56, 9.2%), Chlamydia pneumoniae (40, 6.6%), Klebsiella pneumoniae (37, 6.1%), Legionella pneumophila (31, 5.1%), Staphylococcus aureus (23, 3.8%), Escherichia coli (10, 1.6%), Moraxella catarrhalis (8, 1.3%), Pseudomonas aeruginosa (6, 1.0%). Of 195 patients with a bacterial pathogen, an atypical pathogen was identified in 62 (10.2%) cases. The non-susceptibility rate of Streptococcus pneumoniae to penicillin, azithromycin, and moxifloxacin was 20.3%, 75.4% and 4.3% respectively. CONCLUSIONS: Atypical pathogens have important role in CAP, with Mycoplasma pneumoniae being the most common pathogen, and mixed infection of atypical pathogens with bacteria was found in 10.2% of the cases. Streptococcus pneumoniae and Haemophilus influenzae remain the most important bacteria for CAP. More than 75.0% of Streptococcus pneumoniae was resistant to macrolides and 20.3% was resistant to penicillin.

[Effects of beta-adrenergic agonists on alveolar fluid clearance in rat lungs].

OBJECTIVE: To study the effects of three selective beta-adrenergic agonists on alveolar fluid clearance (AFC) in the isolated rat lungs. METHODS: Isotonic 5% albumin solutions with different pharmacological agents were instilled into the distal airways in the isolated rat lungs. The lungs were inflated with 100% oxygen at 7 cm H2O (1 cm H2O = 0.098 kPa) and placed in a humid incubator at 37 degrees C. AFC was estimated by the progressive increase in the albumin concentration over 1 h. RESULTS: The baseline AFC was 6.9% +/- 2.2%. Beta(1)-adrenergic agonist denopamine, beta(2)-adrenergic agonist terbutaline and beta(3)-adrenergic agonist BRL-37344 increased AFC significantly (17.1% +/- 2.4%, 19.5% +/- 1.2% and 19.9% +/- 2.5%, respectively). Beta(1)-adrenergic antagonist atenolol abolished the effects of denopamine (AFC was 6.1% +/- 0.9%), but did not inhibit the effects of terbutaline and BRL-37344. Beta(2)-adrenergic antagonist ICI-118551 abolished the effects of terbutaline and BRL-37344 (AFC were 5.7% +/- 0.6% and 7.8% +/- 2.6%), and also partially inhibited the effects of denopamine (AFC was 12.7% +/- 1.8%). Beta(3)-adrenergic antagonist SR-59230A partially inhibited the effects of BRL-37344 and terbutaline (AFC were 13.8% +/- 3.1% and 14.5% +/- 3.5%), but did not change the effects of denopamine. CONCLUSIONS: Denopamine, terbutaline and BRL-37344 are potent stimulators of AFC in the rat lungs. The effects of denopamine and terbutaline are mediated via beta(1)- and beta(2)-adrenoceptors, respectively. The effects of BRL-37344 may be mediated via beta(2)-adrenoceptors. ICI-118551 and SR-59230A may have some beta(1)- and beta(2)-inhibitory effects, respectively.