scholarly journals Developmental Timing Determines the Protective Effect of Maternal Electroacupuncture on Perinatal Nicotine Exposure-Induced Offspring Lung Phenotype

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Jian Dai ◽  
Bo Ji ◽  
Guozhen Zhao ◽  
Yawen Lu ◽  
Yitian Liu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Hpa Axis ◽  
Lung Development ◽  
Lung Damage ◽  
Developmental Timing ◽  
Nicotine Exposure ◽  
Predisposing Factor ◽  
Once Daily ◽  
Time Periods ◽  
Lung Morphometry

Introduction. Environmental exposure of the developing offspring to cigarette smoke or nicotine is an important predisposing factor for many chronic respiratory conditions, such as asthma, emphysema, pulmonary fibrosis, and so forth, in the exposed offspring. Studies showed that electroacupuncture (EA) applied to maternal “Zusanli” (ST36) acupoints during pregnancy and lactation protects against perinatal nicotine exposure- (PNE-) induced lung damage. However, the most effective time period, that is, prenatal vs. postnatal, to attain this effect has not been determined. Objective. To determine the most effective developmental timing of EA’s protective effect against PNE-induced lung phenotype in the exposed offspring. Methods. Pregnant rats were given (1) saline (“S” group); (2) nicotine (“N” group); (3) nicotine + EA, exclusively prenatally (“Pre-EA” group); (4) nicotine + EA, exclusively postnatally (“Post-EA,” group); and (5) nicotine + EA, administered both prenatally and postnatally (“Pre- and Post-EA” group). Nicotine was injected once daily (1 mg/kg, 100 μl) and EA was administered to bilateral ST36 acupoints once daily during the specified time-periods. At the end of the experimental periods, key hypothalamic pituitary adrenal (HPA) axis markers in pups and dams, and lung function, morphometry, and the central molecular markers of lung development in the offspring were determined. Results. After nicotine exposure, alveolar mean linear intercept (MLI) increased, but mean alveolar number (MAN) decreased and lung PPARγ level decreased, but glucocorticoid receptor (GR) and serum corticosterone (Cort) levels increased, in line with the known PNE-induced lung phenotype. In the nicotine exposed group, maternal hypothalamic corticotropin releasing hormone (CRH) level decreased, but pituitary adrenocorticotropic hormone (ACTH) and serum Cort levels increased. In the “Pre- and Post-EA” groups, PNE-induced alterations in lung morphometry, lung development markers, and HPA axis were blocked. In the “Pre-EA” group, PNE-induced changes in lung morphometry, GR, and maternal HPA axis improved; lung PPARγ and serum Cort levels were slightly but not significantly improved. In contrast, the exclusive “Post-EA” group showed none of these benefits. Conclusions. Maternal EA applied to ST36 acupoints during both pre- and postnatal periods preserves offspring lung structure and function despite perinatal exposure to nicotine. EA applied during the “prenatal period” affords only limited benefits, whereas EA applied during the “postnatal period” is ineffective, suggesting that the EA’s effects in modulating PNE-induced lung phenotype are limited to specific time-periods during lung development.

ONCE-DAILY CICLESONIDE DOES NOT CAUSE HPA-AXIS SUPPRESSION IN PEDIATRIC ASTHMA PATIENTS

2004 ◽  
Vol 5 (5) ◽  
pp. 511
Author(s):  
John W. Georgitis ◽  
Stanley Galant ◽  
Mark Lloyd ◽  
Sudeep Kundu ◽  
James E. Fish ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Pediatric Asthma ◽  
Once Daily ◽  
Asthma Patients

Effect of Intrarectal Prostaglandin E2 Analogue (Enprostil) on Trinitrobenzenesulphonic Acid-Induced Colitis in Rats

2000 ◽  
Vol 28 (1) ◽  
pp. 28-35 ◽  
Author(s):  
Y Onizuka ◽  
K Murase ◽  
H Furusu ◽  
H Isomoto ◽  
Y Mizuta ◽  
...  
Keyword(s):  
Plasma Concentration ◽  
Portal Vein ◽  
Protective Effect ◽  
Colonic Mucosa ◽  
Therapeutic Potential ◽  
Mucosal Damage ◽  
Prostaglandin E ◽  
Once Daily ◽  
Blood Samples ◽  
And Control

Prostaglandins exert a protective effect on colonic mucosa in experimentally induced colitis. This study investigated the effect of enprostil, a prostaglandin E2 (PGE2) analogue, on trinitrobenzenesulphonic acid (TNBS)-induced colitis in rats. Each rat received a rectal enema containing TNBS (30 mg), followed 24 h later by intrarectal once-daily enprostil (200 μg). Enprostil-treated and control rats were killed on day 3 (enprostil group, n = 5; control, n = 6) or day 10 (enprostil group, n = 5; control, n = 5) after TNBS treatment. The area of damaged mucosa of the colon was measured relative to the total colonic area. We also determined the macroscopic score of mucosal damage, and measured PGE2, 6-ketoprostaglandin F1α (6-keto-PGF1α) and thromboxane B2 (TXB2) concentration in portal vein blood samples. Enprostil significantly reduced both the area of damaged mucosa (including the ulcer area) and the macroscopic score after 3 days' treatment compared with control. Similarly, enprostil significantly reduced plasma concentration of PGE2, 6-keto-PGF1α and TXB2 during the acute phase at day 3 of treatment compared with control, but not at day 10. These results suggest that PGE2 enema may have therapeutic potential for treating patients with proctitis or left-sided colitis.

scholarly journals Fetal and Neonatal Exposure to Nicotine Disrupts Postnatal Lung Development in Rats: Role of VEGF and Its Receptors

2011 ◽  
Vol 30 (2) ◽  
pp. 244-252 ◽  
Author(s):  
Maria A. Petre ◽  
Jim Petrik ◽  
Russ Ellis ◽  
Mark D. Inman ◽  
Alison C. Holloway ◽  
...  
Keyword(s):  
Lung Development ◽  
Female Rats ◽  
Neonatal Exposure ◽  
Nicotine Exposure ◽  
Smoking During Pregnancy ◽  
Vegf Signaling ◽  
Lung Structure ◽  
And Function ◽  
Postnatal Lung Development ◽  
Endothelial Growth Factor

Many women are unable to quit smoking during pregnancy and therefore are prescribed drugs, including nicotine (nicotine replacement therapy [NRT]), to aid with smoking cessation. However, the consequences to the offspring of pregnant NRT users have not been well studied. The goals of this study were to determine the consequences of fetal and neonatal exposure to nicotine on lung development and function. Female rats were exposed to nicotine for 2 weeks prior to mating until weaning. Lungs were collected from saline and nicotine-treated rats from birth to adulthood to assess postnatal lung structure and function. Although nicotine exposure altered alveolarization at weaning, an effect that resolved by adulthood, it did not affect lung function at any of the ages investigated. However, nicotine exposure significantly decreased lung vascularization. The current study suggests that perinatal exposure to nicotine alters lung development, an effect which may be mediated via decreased vascular endothelial growth factor (VEGF) signaling.

scholarly journals The initial impact of a national BNT162b2 mRNA COVID-19 vaccine rollout

2021 ◽  
Author(s):  
Ahmed Zaqout ◽  
Joanne Daghfal ◽  
Israa Alaqad ◽  
Saleh A.N. Hussein ◽  
Abdullah Aldushain ◽  
...  
Keyword(s):  
Protective Effect ◽  
Incidence Rate ◽  
Confidence Intervals ◽  
Poisson Regression ◽  
Incidence Rates ◽  
Post Vaccination ◽  
Time Periods ◽  
Rate Ratios ◽  
Vaccination Period

AbstractObjectiveWe herein report the initial impact of a national BNT162b2 rollout on SARS-CoV-2 infections in Qatar.MethodsWe included all individuals who by 16 March 2021 had completed ≥14 days of follow up after the receipt of BNT162b2. We calculated incidence rates (IR) and their 95% confidence intervals (CI), during days 1–7, 8–14, 15–21, 22–28, and >28 days post-vaccination. Poisson regression was used to calculate incidence rate ratios (IRR) relative to the first 7-day post-vaccination period.ResultsWe included 199,219 individuals with 6,521,124 person-days of follow up. SARS-CoV-2 infection was confirmed in 1,877 (0.9%), of which 489 (26.1%) were asymptomatic and 123 (6.6%) required oxygen support. The median time from first vaccination to SARS-CoV-2 confirmation was 11.9 days (IQR 7.7–18.2). Compared with the first 7-day post-vaccination period, SARS-CoV-2 infections were lower by 65.8–84.7% during days 15–21, days 22–28, and >28 days (P <0.001 for each). For severe COVID-19, the incidence rates were 75.7– 93.3% lower (P <0.001 for each) during the corresponding time periods.ConclusionOur results are consistent with an early protective effect of BNT162b2 against all degrees of SARS-CoV-2 severity.

Implications for matrix metalloproteinases as modulators of pediatric lung disease

2003 ◽  
Vol 284 (4) ◽  
pp. L557-L565 ◽  
Author(s):  
Margaret K. Winkler ◽  
Jane K. Foldes ◽  
Robert C. Bunn ◽  
John L. Fowlkes
Keyword(s):  
Respiratory Failure ◽  
Matrix Metalloproteinases ◽  
Lung Disease ◽  
Lung Development ◽  
Large Family ◽  
Lung Damage ◽  
Gelatinase Activity ◽  
Normal Human ◽  
Pediatric Lung Disease ◽  
Diseased Lung

Matrix metalloproteinases (MMPs) are a large family (>20) of cation-dependent proteinases believed to be important modulators of normal human lung development and potentially harmful mediators of lung damage. Little is known about MMP production and secretion by the lung during childhood or how alterations in MMP levels may be involved in lung damage. We examined endotracheal aspirates from children (<19 years) without lung disease for the presence of MMP activity. Only gelatinase activity was detectable, and inhibitor profiles suggest they represented one or more MMPs. Comparison of gelatinase activity, MMP expression, and MMP activity in children without pulmonary disease with children who required mechanical ventilation for respiratory failure show: 1) gelatinase activity was approximately five- to sixfold higher in respiratory failure; 2) MMP-7, MMP-8, and MMP-9 concentrations and MMP-8 and MMP-9 activities were markedly elevated in respiratory failure; and 3) MMP-7, MMP-8, and MMP-9 levels were significantly correlated in children with lung disease. These studies provide compelling evidence that specific MMPs are present in the diseased lung and may participate in the pathogenesis of pediatric respiratory failure.

Cilostazol Effect on Amikacin-Induced Ototoxicity: An Experimental Study

2016 ◽  
Vol 21 (4) ◽  
pp. 250-253 ◽  
Author(s):  
Mohammad Waheed El-Anwar ◽  
Said Abdelmonem ◽  
Ebtessam Nada ◽  
Dalia Galhoom ◽  
Ahmed A. Abdelsameea
Keyword(s):  
Experimental Study ◽  
Protective Effect ◽  
Adult Male ◽  
Otoacoustic Emissions ◽  
Male Rats ◽  
Control Group ◽  
Once Daily ◽  
Frequency Bands ◽  
Transient Evoked Otoacoustic Emissions

Objectives: To find out the possible protective effect of cilostazol against amikacin-induced ototoxicity. Methods: This study was carried out on 24 adult male rats classified into 4 equal groups of 6 animals each. (1) The control group was administered saline (1 ml/day, p.o.) for 14 days. (2) The amikacin group was administered amikacin (200 mg/kg, i.m.) once daily for 14 days. (3) The cilostazol-amikacin (14 days) group was administered cilostazol (30 mg/kg, p.o.) once daily and amikacin (200 mg/kg, i.m.) once daily for 14 days. (4) The cilostazol (28 days)-amikacin (14 days) group was administered cilostazol (30 mg/kg, p.o.) once daily for 28 days and amikacin (200 mg/kg, i.m.) once daily for 14 days. Changes in the transient evoked otoacoustic emissions (TEOAEs) in the 4 groups were interpreted statistically. Results: No reported significant differences in TEOAE levels were detected between the groups at the start of the study. In all frequency bands, TEOAEs disappeared after amikacin treatment in the amikacin-alone group and remained absent in the amikacin-cilostazol (14 days) group, while TEOAEs reappeared in the amikacin-cilostazol (28 days) group. Conclusion: Cilostazol treatment for 28 days had a protective effect against amikacin-induced ototoxicity in rats.

scholarly journals Impact of Tobacco Smoke and Nicotine Exposure on Lung Development

CHEST Journal ◽  
2016 ◽  
Vol 149 (2) ◽  
pp. 552-561 ◽  
Author(s):  
Kevin Gibbs ◽  
Joseph M. Collaco ◽  
Sharon A. McGrath-Morrow
Keyword(s):  
Tobacco Smoke ◽  
Lung Development ◽  
Nicotine Exposure
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