Potential Role of Pectate Lyase and Ca2+in the Increase in Strawberry Fruit Firmness Induced by Short-Term Treatment with High-Pressure CO2

2014 ◽  
Vol 79 (4) ◽  
pp. S685-S692 ◽  
Author(s):  
Mao Hua Wang ◽  
Jin Gook Kim ◽  
Sun Eun Ahn ◽  
Ah Youn Lee ◽  
Tae Min Bae ◽  
...  
Keyword(s):  
High Pressure ◽  
Potential Role ◽  
Pectate Lyase ◽  
Term Treatment ◽  
Fruit Firmness ◽  
Strawberry Fruit ◽  
Short Term ◽  
Short Term Treatment ◽  
High Pressure Co2

scholarly journals Neutrophil DREAM Promotes Neutrophil Recruitment in Vascular Inflammation Via Nuclear Factor Kappa B-Dependent and Independent Mechanisms

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 435-435
Author(s):  
Tripti Kumari ◽  
Jing Li ◽  
Andrew Barazia, ◽  
Vishwanath Jha ◽  
Amber Hansch ◽  
...  
Keyword(s):  
Vascular Inflammation ◽  
Term Treatment ◽  
Neutrophil Recruitment ◽  
Neutrophil Adhesion ◽  
Short Term ◽  
Short Term Treatment ◽  
Tnf Α ◽  
Inflammatory Molecules ◽  
Β2 Integrins

Abstract The interaction between neutrophils and endothelial cells (ECs) is critical for the pathogenesis of vascular inflammation. Neutrophil recruitment to inflamed tissues is initiated by rolling on activated ECs through the interactions between P-/E-selectins and their ligands. Subsequently, activated integrins (mainly αLβ2 and αMβ2) and chemokine receptors bind to their ligands on ECs and mediate slow-rolling, adhesion, crawling, and transmigration of neutrophils. Although many neutrophil adhesion receptors have been identified, the regulation of their ligand-binding function remains not fully understood. Using real-time intravital microscopy with mice lacking downstream regulatory element antagonist modulator (DREAM) and their bone marrow chimeric mice, we demonstrated that hematopoietic cell DREAM contributes to neutrophil recruitment to sites of vascular inflammation induced by TNF-α- but not a G protein-coupled receptor ligand, MIP-2 or fMLP. Our studies using adoptive neutrophil transfers and flow chamber assays revealed that neutrophil DREAM positively regulates the neutrophil recruitment processes under TNF-α-induced inflammatory conditions. Using RNA-seq and biochemical and cell biological studies, we found that neutrophil DREAM upregulates numerous pro-inflammatory molecules and down-regulates anti-inflammatory molecules after TNF-α treatment. In particular, neutrophil DREAM repressed expression of A20, a negative regulator of NF-κB signaling, and enhanced phosphorylation of IκB kinase (IKK) in response to TNF-α, suggesting the role of neutrophil DREAM in NF-κB activity. Furthermore, we observed that DREAM deletion and IKK inhibition significantly diminishes the ligand-binding activity of β2 integrins in neutrophils after short-term treatment with TNF-α and that deletion of neutrophil DREAM does not affect the expression of other neutrophil adhesion receptors, such as PSGL-1, L-selectin, CD44, CXCR2, and CXCR4. As assessed by flow cytometry using conformation-specific reporter antibodies, knockdown of DREAM in neutrophil-like HL-60 cells decreased TNF-α-induced activation of β2 integrins. Neutrophil DREAM promoted degranulation through IKK-mediated SNAP-23 phosphorylation after short-term treatment with TNF-α, implying the role of neutrophil DREAM-IKK signaling in NF-κB-independent signaling. Using intravital microscopy with Berkeley mice (a mouse model of sickle cell disease) deficient in hematopoietic or nonhematopoietic DREAM, we demonstrated that hematopoietic cell DREAM is crucial for inducing intravascular cell-cell aggregation and vaso-occlusive events in microvessels following the TNF-α challenge. Furthermore, infusion of DREAM KO neutrophils, compared with WT neutrophils, significantly reduced neutrophil recruitment and vaso-occlusive events in TNF-α-challenged SCD mice. These results demonstrate that neutrophil DREAM positively regulates β2 integrin function and promotes neutrophil recruitment during sterile inflammation via NF-κB-dependent and independent mechanisms. Our study provides evidence that targeting DREAM might be a novel therapeutic strategy to reduce excessive neutrophil recruitment in inflammatory diseases. Disclosures No relevant conflicts of interest to declare.

scholarly journals Activity of ketoconazole against Mycobacterium tuberculosis in vitro and in the mouse model

2007 ◽  
Vol 56 (8) ◽  
pp. 1047-1051 ◽  
Author(s):  
Sean T. Byrne ◽  
Steven M. Denkin ◽  
Peihua Gu ◽  
Eric Nuermberger ◽  
Ying Zhang
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Term Treatment ◽  
New Drugs ◽  
Bacteriostatic Effect ◽  
Short Term ◽  
Short Term Treatment ◽  
Neutral Conditions

There is an urgent need for the development of new drugs that are active against drug-resistant Mycobacterium tuberculosis strains and can shorten tuberculosis (TB) therapy. It has previously been reported that the azole class of antifungals has anti-TB activity in vitro. This study evaluated ketoconazole (KTC) for activity against M. tuberculosis. The MIC of KTC for different M. tuberculosis strains ranged from 8 to 16 μg ml−1 under both acidic and neutral conditions, with the minimum bactericidal concentration being about twofold higher than the MIC. KTC had enhanced activity against old, non-growing bacilli in vitro when combined with pyrazinamide (PZA) and rifampicin (RIF). A single oral dose of KTC at 75 mg kg−1 led to an inhibitory serum concentration 2 h after administration. The in vivo activity of KTC was evaluated in established pulmonary TB in the murine model, compared alone and in combination with isoniazid (INH), PZA and RIF. KTC alone exhibited little effect after short-term treatment, with a borderline bacteriostatic effect on spleen colony counts but not on lung counts. KTC, when added in combination with INH, PZA and RIF, significantly improved the treatment outcome in the lungs (compared with treatment with INH, PZA and RIF). The lowest numbers of bacilli in lungs were found in mice treated with KTC, PZA and RIF. Further investigation is necessary to determine the role of KTC in the treatment of TB.

Abstract 311: Early Losartan Treatment Prevents the Developmental Programming of Cardiac Dysfunction Caused by Neonatal High Oxygen Exposure in Rats

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Mariane Bertagnolli ◽  
Sarah Béland-Bonenfant ◽  
Anne Dios ◽  
Daniela R Dartora ◽  
Marie-Amélie Lukaszewski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Systolic Function ◽  
Developmental Programming ◽  
Term Treatment ◽  
Short Term ◽  
Short Term Treatment ◽  
High O2 ◽  
Cardiac Alterations

Neonatal oxidative stress is a major postnatal deleterious factor predisposing preterm born infants to classical complications of prematurity (retinopathy, bronchopulmonary dysplasia) which are characterized by impaired vascular development. Our group has previously shown that rats transiently exposed to high O2 as newborns (mimicking human preterms oxidative stress conditions) develop high blood pressure (BP), cardiac remodeling and dysfunction later in life, in part mediated by the renin angiotensin system (RAS). Cardiac RAS activation is characterized by AT1/AT2 receptors imbalance, with increased AT1R at adult age. In order to study the role of RAS at early stages of the developmental programming of cardiac dysfunction caused by high O2 exposure, we assessed whether an early and short-term treatment with AT1R blocker Losartan, prevents cardiac alterations at young male 4 wks-old rats (prior to the elevation of BP in this model). Sprague-Dawley newborns rats were kept with their mother in 80% O2 (O2 group, n=9) or room air (Ctrl, n=9) from days 3-10 of life (P3-P10). Losartan (LOS, n=10, 20 mg/Kg) or water was administered by gavage in O2 rats from P8-P10 (last 2 days of O2 to avoid impact on nephrogenesis). At 4 wks, echocardiography reveals that O2 rats have decreased fraction of shortening compared to Ctrl (FS: 37±2 vs 42±2 %), suggesting impaired systolic function in O2. Cardiac hypertrophy evaluated by heart/body weight and cardiomyocyte surface area (CSA) is also increased in O2 vs Ctrl (141±13 vs 118±4 μm2). LOS treatment prevented the impairment of systolic function in O2 by ameliorating FS (43±2 %) and reducing CSA (121±11 μm2). LOS treatment also modulated RAS genes expression (RT-PCR): LOS restored AT1/AT2 balance in O2 hearts by decreasing AT1b subunit (0.8±0.2 O2 vs 1.3±0.3 O2+LOS vs 0.9±0.2 Ctrl) as well as increasing ACE2 (1.5±0.4 O2 vs 0.8±0.1 O2+LOS vs 1.1±0.4 Ctrl) expressions. In conclusion, a short-term treatment with LOS during neonatal O2 exposure prevents the impairment of cardiac systolic function and hypertrophy at young age. This data reinforces the key role of RAS in the developmental programming of cardiac dysfunction and reveals LOS as an effective strategy to prevent early cardiac alterations caused by neonatal high O2 exposure.

The Role of Colloidal Bismuth Subcitrate in the Short-Term Treatment of Duodenal Ulcer

1986 ◽  
Vol 21 (sup122) ◽  
pp. 30-34 ◽  
Author(s):  
L. Barbara ◽  
R. Corinaldesi ◽  
E. Rea ◽  
A. Paternicò ◽  
V. Stanghellini
Keyword(s):  
Duodenal Ulcer ◽  
Term Treatment ◽  
Short Term ◽  
Short Term Treatment ◽  
Colloidal Bismuth Subcitrate ◽  
Bismuth Subcitrate ◽  
Colloidal Bismuth

scholarly journals Effect of cyclosporine on endothelial albumin leakage in rats.

1992 ◽  
Vol 3 (1) ◽  
pp. 51-57
Author(s):  
L C Moore ◽  
J Mason ◽  
L Feld ◽  
J B Van Liew ◽  
F J Kaskel
Keyword(s):  
Volume Expansion ◽  
Marked Reduction ◽  
Term Treatment ◽  
Albumin Concentration ◽  
Plasma Extravasation ◽  
Short Term ◽  
Short Term Treatment ◽  
Albumin Leakage ◽  
Blood Volumes

Short-term treatment of rats with cyclosporine (cyclosporine A [CsA]; Sandimmune) results in a marked reduction in intravascular plasma volume, a factor that might contribute to the renal dysfunction associated with this potent immunosuppressant. To examine the role of plasma extravasation in CsA-induced hypovolemia, intravascular plasma volumes (PV), blood volumes, [125I]albumin disappearance, and changes in hematocrit (Hct) were measured in Inactin-anesthetized rats subjected to minimal surgery. The rats were treated for 3 wk with either 25 mg/kg/day of CsA s.c. or vehicle. Plasma creatinine and urea were significantly elevated, and magnesium was reduced in the CsA group (N = 6) as compared with controls (CON) (N = 6). CsA treatment had no effect on urinary protein and albumin excretion. Blood volume was significantly lower in CsA than in CON (8.4 +/- 0.5 versus 10.6 +/- 0.3 mL/100 g body wt) as was PV (4.3 +/- 0.2 versus 5.5 +/- 0.2 mL/100 g body wt). Two hours after injection, plasma [125I]albumin concentration had fallen by 41 +/- 4% in CsA versus 23 +/- 5% in CON. Because Hct, and, hence PV, was unchanged in both groups during these 2 h, these data indicate enhanced endothelial albumin leakage in the CsA group. In two additional groups of six rats each, acute volume expansion with fresh whole blood (2 mL/100 g body wt) resulted in extravasation of plasma. Hct rose by 8.0 +/- 0.2% in CsA versus 3.8 +/- 0.2% in CON after 150 min, corresponding to 27 +/- 3 and 15 +/- 2% decreases in total PV, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

42. The mood stabilizer valproic acid down regulates neuronal cyclooxygenase-2 expression: Central role of nuclear factor-kappa B after long-term, but not short-term treatment

2009 ◽  
Vol 23 ◽  
pp. S21
Author(s):  
Vikramjeet Singh ◽  
Francisco J. Caballero ◽  
Marco A. Calzado ◽  
Eduardo Candelario-Jalil ◽  
Friederike von Müller ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Nuclear Factor Kappa B ◽  
Mood Stabilizer ◽  
Term Treatment ◽  
Cyclooxygenase 2 ◽  
Nuclear Factor ◽  
Short Term ◽  
Short Term Treatment

scholarly journals Effects of short-term treatment of high pressure CO2on the changes in fruit quality during the storage of 'Maehyang' strawberries

2014 ◽  
Vol 41 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Sun-Eun Ahn ◽  
Mao-Hua Wang ◽  
Ah-Youn Lee ◽  
Yong-Soo Hwang
Keyword(s):  
High Pressure ◽  
Fruit Quality ◽  
Term Treatment ◽  
Short Term ◽  
Short Term Treatment

Role of fibrinogen in atherosclerosis: therapeutic effects of bezafibrate in short-term treatment

1987 ◽  
pp. 431-437
Author(s):  
G. Pagano ◽  
G. Niort ◽  
P. Nuccio ◽  
A. Bulgarelli
Keyword(s):  
Term Treatment ◽  
Therapeutic Effects ◽  
Short Term ◽  
Short Term Treatment
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